unique_id,web-scraper-start-url,sub_chapters_x,sub_chapters-href,paragraph,is_paragraph,sub_section_headings,fig_num,sub_chapters_y,images-src,image_caption
97ebdeb2-7d1f-4119-99ac-a7f7f9ebbb77,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"To get warmed up, let us start with the simplest one, pleurisy.",True,,,,,
7009c4e3-0b80-4c44-887c-8b2524aa62db,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Pleurisy is synonymous with pleuritis and refers to inflammation of the pleural membranes that may be accompanied by pleural exudate or may remain “dry.” Inflammation of the membranes may be mild and transient due to common conditions such as bacterial or viral infection, or it may be severe and chronic and indicative of more serious conditions, such as lupus and rheumatoid arthritis.",True,,,,,
407a2c51-13bf-4dda-a164-eb5fbdd989df,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The inflammation causes thickening of the membranes that may cause them to impinge on the pleural space. Prolonged inflammation leads to an accumulation of pleural macrophages, and these in turn initiate a proliferation of fibrocytes. The inflammatory process may prevent the membranes from moving freely, and in some patients the two inflamed membranes sliding against each other can produce an audible pleural friction rub, which sounds like leather rubbing against leather or walking on fresh snow. The hallmark symptom of a pleural rub is sudden onset chest pain associated with inhalation and cough.",True,,,,,
7c6236df-56f7-4a85-b6fc-d15fcacccc79,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"In prolonged pathological conditions, the membranes may adhere, and calcium deposits can appear in old pleural fibrosis and are often associated with chronic conditions such as asbestosis. When significant, this level of fibrosis may restrict respiratory movement.",True,,,,,
7fe0cd64-f257-4e5f-87ad-64d866728ae2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,Pleural Effusion,False,Pleural Effusion,,,,
0def0019-efda-4bf8-be84-5b336770125a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"In our description of pleurisy we eluded to our next pleural disorder, pleural effusion. The normally small amount of pleural fluid is sufficient to lubricate the movement of the lungs and is not detectable on x-ray without specialized radiography. Pleural effusion is the abnormal accumulation of fluid in the pleural space and is easily detectable. As with the formation of fluid accumulation in any part of the body, a normal fluid level in the pleural space is dependent on a balanced rate of formation and reabsorption. In pleural effusion, this balance is lost.",True,Pleural Effusion,,,,
902fd1dd-cadc-4a50-8f63-14d5cccf816f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Initially it was thought that pleural fluid was formed by hydrostatic pressure in capillaries in the parietal membrane pushing fluid into the pleural space, and the fluid was then absorbed by capillaries in the visceral membrane. However, there is mounting evidence to show that reabsorption is actually performed by the lymph vessels in the parietal membrane. The low hydrostatic pressure and large capacity of these vessels helps maintain the normal, small volume of pleural fluid. Pleural effusion can be caused by:",True,Pleural Effusion,,,,
efd6567f-5f5c-4501-bbea-0cacb9da552d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"For example, pleural effusion in cardiac pulmonary edema occurs as fluid leaks across the visceral pleura from the lung.",True,Pleural Effusion,,,,
d24c3129-0e09-4597-aba0-f501519a0c12,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Two broad classifications exist, transudate and exudate, so let us compare them now (summary in table 9.1).",True,Pleural Effusion,,,,
15308720-28b8-4057-8aba-0d06e11d901b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Transudative effusion occurs when there is a disturbance in the Starling’s forces influencing fluid movement across the capillary. As such transudate can be caused by an increase in hydrostatic force pushing fluid out of the capillary, such as in congestive heart failure, or a decrease in the plasma oncotic pressure retaining fluid in the capillary, such as in kidney or liver disease. This results in a transudate with low specific gravity, protein concentration, and cell count.",True,Pleural Effusion,,,,
7cff022c-a76f-4a82-b17e-f78a5fdd876d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
7cff022c-a76f-4a82-b17e-f78a5fdd876d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
7cff022c-a76f-4a82-b17e-f78a5fdd876d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
7cff022c-a76f-4a82-b17e-f78a5fdd876d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
1e0b031d-9c50-4863-b745-92487d68f087,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,Table 9.1: Comparison of transudative and exudative pleural effusions.,True,Pleural Effusion,,,,
d28a84a9-71ac-4502-8ece-95fa5e2224ec,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The manifestation of pleural effusion varies with the quantity of fluid accumulation and the time line. Symptoms may in fact be absent when the effusion is small. In the case of exudative pleurisy, an initial rub pain may disappear as exudate accumulates and separates the rubbing pleural surfaces.",True,Pleural Effusion,,,,
d575ecdb-955c-4b19-916f-a59a4460db7f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,As the effusion volume increases the patient is likely to experience dyspnea and physical exam will more likely include dullness to percussion and absence of breath sounds as the effusion forms a fluid pillow around the lung.,True,Pleural Effusion,,,,
2b911b0a-c25c-424a-9007-658fd882bfdd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
2b911b0a-c25c-424a-9007-658fd882bfdd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
2b911b0a-c25c-424a-9007-658fd882bfdd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
2b911b0a-c25c-424a-9007-658fd882bfdd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
6a213ac2-3232-4642-b5ea-84dc3b2e1882,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"As we have already mentioned, the pleural fluid’s composition can provide a great deal of information about the underlying mechanism. We have already mentioned the ability to distinguish between an exudate and a transudate by analysis of the fluid. But gross inspection of the fluid can be revealing before lab tests are ready.",True,Pleural Effusion,,,,
39e4babc-3e32-4837-a9aa-93149918524f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
39e4babc-3e32-4837-a9aa-93149918524f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
39e4babc-3e32-4837-a9aa-93149918524f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
39e4babc-3e32-4837-a9aa-93149918524f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
c7344b21-2aa5-4a33-9e99-55431504c570,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
c7344b21-2aa5-4a33-9e99-55431504c570,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
c7344b21-2aa5-4a33-9e99-55431504c570,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
c7344b21-2aa5-4a33-9e99-55431504c570,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
fc06e3ad-477c-4c24-8714-7e8253b62da5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
fc06e3ad-477c-4c24-8714-7e8253b62da5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
fc06e3ad-477c-4c24-8714-7e8253b62da5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
fc06e3ad-477c-4c24-8714-7e8253b62da5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
55dda68d-a0fb-4804-8f51-27432e0a7d33,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
55dda68d-a0fb-4804-8f51-27432e0a7d33,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
55dda68d-a0fb-4804-8f51-27432e0a7d33,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
55dda68d-a0fb-4804-8f51-27432e0a7d33,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
3611c3f5-376f-4308-b83c-4012058f7bab,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,Pneumothorax,False,Pneumothorax,,,,
c7166aaa-f88c-45d5-8fb8-aea658aa589c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Normally the negative pressure inside the pleural space opposes the lung’s recoil and holds the lung surface to the interior of the thorax. If the pleural membranes are disrupted this subatmospheric or negative pressure is lost and the lung can recoil, or collapse. This is a pneumothorax.",True,Pneumothorax,,,,
c2586289-886f-4131-85d6-2457ba18e76c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The causal events of losing the negative pleural pressure divide pneumothoraces into one of two categories: spontaneous or traumatic. (A third category exists, artificial pneumothorax, which was intentionally induced as part of procedures that are very rarely used today.)",True,Pneumothorax,,,,
38f879f0-5ff6-43f0-95ec-fc890ff997cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
38f879f0-5ff6-43f0-95ec-fc890ff997cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
38f879f0-5ff6-43f0-95ec-fc890ff997cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
38f879f0-5ff6-43f0-95ec-fc890ff997cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
df047406-e161-4f2b-b683-a315a1315378,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
df047406-e161-4f2b-b683-a315a1315378,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
df047406-e161-4f2b-b683-a315a1315378,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
df047406-e161-4f2b-b683-a315a1315378,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
0fe5da22-93a8-4711-8d35-5624a9f89b5f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The most common cause of spontaneous pneumothorax in pulmonary patients is a ruptured bleb or bulla. These thin-walled, air-filled cavities are found near the pleural surface, particularly in cases of emphysema. In the past, TB was thought to be the most common cause of pneumothorax as its destructive path encroached on the pleural space.",True,Pneumothorax,,,,
e8f8516a-c8ad-4295-b55f-73cb46039a26,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Traumatic pneumothorax is often a consequence of chest injury that involves laceration of the pleura. This might be due to a broken rib or penetrative wound to the chest that allows air to enter the pleural space and equilibrate with the atmosphere. The injury might not be malicious though as some procedures might inadvertently or unavoidably perforate the pleura, such as thoracentesis, pleural biopsy, lung biopsy, or subclavian vein puncture. Trauma from within the lung may also occur. Similar to the mechanism of a rupturing bleb, if excessive airway pressures are used during mechanical ventilation there is the risk that airspaces are disrupted and barotrauma involves the visceral pleura.",True,Pneumothorax,,,,
fab6752f-0cd2-4f94-b1d6-360dba928893,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"is often a consequence of chest injury that involves laceration of the pleura. This might be due to a broken rib or penetrative wound to the chest that allows air to enter the pleural space and equilibrate with the atmosphere. The injury might not be malicious though as some procedures might inadvertently or unavoidably perforate the pleura, such as",True,Pneumothorax,,,,
e45fe667-2ec7-4033-8c5e-04c092a2b507,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,", pleural biopsy, lung biopsy, or subclavian vein puncture. Trauma from within the lung may also occur. Similar to the mechanism of a rupturing bleb, if excessive airway pressures are used during mechanical ventilation there is the risk that airspaces are disrupted and barotrauma involves the visceral pleura.",True,Pneumothorax,,,,
a204c5c6-7a42-4146-a852-8691884ffd56,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
a204c5c6-7a42-4146-a852-8691884ffd56,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
a204c5c6-7a42-4146-a852-8691884ffd56,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
a204c5c6-7a42-4146-a852-8691884ffd56,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
40ccba21-8fb6-4af3-aba0-bff1653d3e37,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Tension pneumothorax may arise if the disruption to the pleural is such that the injury acts like a valve. During inspiration when thoracic pressure falls air enters the airways and also the thoracic cavity via the injury. During expiration when the thoracic pressure increases, the wound closes, stopping the air that entered the thoracic cavity from leaving. So with each inspiration more air enters while little or none leaves during the subsequent expiration. The accumulating volume can begin to push the heart and mediastinum to the contralateral side. This may severely affect cardiac output and rapidly become life threatening.",True,Pneumothorax,,,,
c8ef4a3e-bc72-41a2-832a-f0993ef52345,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
c8ef4a3e-bc72-41a2-832a-f0993ef52345,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
c8ef4a3e-bc72-41a2-832a-f0993ef52345,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
c8ef4a3e-bc72-41a2-832a-f0993ef52345,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
34b024cb-5165-4749-a052-0d8070d763e3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Pneumothorax,,,,
a8850dcf-5c61-474b-b4f7-bdb65edf15a6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumothorax,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-3,"West, John B. “Chapter 5: Restrictive Diseases.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Pneumothorax,,,,
c7a02ca7-64e6-4d0c-a8a9-168b2225c20a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"To get warmed up, let us start with the simplest one, pleurisy.",True,Pneumothorax,,,,
6d5700d0-7bdc-4b79-a81d-0225014381b0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Pleurisy is synonymous with pleuritis and refers to inflammation of the pleural membranes that may be accompanied by pleural exudate or may remain “dry.” Inflammation of the membranes may be mild and transient due to common conditions such as bacterial or viral infection, or it may be severe and chronic and indicative of more serious conditions, such as lupus and rheumatoid arthritis.",True,Pneumothorax,,,,
28056da2-5b3a-4286-82fd-311c9a2cb181,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The inflammation causes thickening of the membranes that may cause them to impinge on the pleural space. Prolonged inflammation leads to an accumulation of pleural macrophages, and these in turn initiate a proliferation of fibrocytes. The inflammatory process may prevent the membranes from moving freely, and in some patients the two inflamed membranes sliding against each other can produce an audible pleural friction rub, which sounds like leather rubbing against leather or walking on fresh snow. The hallmark symptom of a pleural rub is sudden onset chest pain associated with inhalation and cough.",True,Pneumothorax,,,,
b928ae44-7d37-4f70-a8ec-7ae8e78fa01e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"In prolonged pathological conditions, the membranes may adhere, and calcium deposits can appear in old pleural fibrosis and are often associated with chronic conditions such as asbestosis. When significant, this level of fibrosis may restrict respiratory movement.",True,Pneumothorax,,,,
da0f74eb-b8ce-46fd-b882-f6236730dfe0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,Pleural Effusion,False,Pleural Effusion,,,,
91cb008f-74c2-4632-882a-8c071e0ed2a8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"In our description of pleurisy we eluded to our next pleural disorder, pleural effusion. The normally small amount of pleural fluid is sufficient to lubricate the movement of the lungs and is not detectable on x-ray without specialized radiography. Pleural effusion is the abnormal accumulation of fluid in the pleural space and is easily detectable. As with the formation of fluid accumulation in any part of the body, a normal fluid level in the pleural space is dependent on a balanced rate of formation and reabsorption. In pleural effusion, this balance is lost.",True,Pleural Effusion,,,,
c3bf9bbc-fe7c-4331-aaf9-3ca96002fc3f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Initially it was thought that pleural fluid was formed by hydrostatic pressure in capillaries in the parietal membrane pushing fluid into the pleural space, and the fluid was then absorbed by capillaries in the visceral membrane. However, there is mounting evidence to show that reabsorption is actually performed by the lymph vessels in the parietal membrane. The low hydrostatic pressure and large capacity of these vessels helps maintain the normal, small volume of pleural fluid. Pleural effusion can be caused by:",True,Pleural Effusion,,,,
6d971ee1-51c5-46a0-a945-e79b37cc6004,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"For example, pleural effusion in cardiac pulmonary edema occurs as fluid leaks across the visceral pleura from the lung.",True,Pleural Effusion,,,,
689fc251-8bfb-4c4c-b328-deed63e8d847,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Two broad classifications exist, transudate and exudate, so let us compare them now (summary in table 9.1).",True,Pleural Effusion,,,,
b713a187-4300-4cb5-80e9-d5608997f4fc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Transudative effusion occurs when there is a disturbance in the Starling’s forces influencing fluid movement across the capillary. As such transudate can be caused by an increase in hydrostatic force pushing fluid out of the capillary, such as in congestive heart failure, or a decrease in the plasma oncotic pressure retaining fluid in the capillary, such as in kidney or liver disease. This results in a transudate with low specific gravity, protein concentration, and cell count.",True,Pleural Effusion,,,,
3623bd51-c46f-442e-91b3-d8d121b5c14e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
3623bd51-c46f-442e-91b3-d8d121b5c14e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
3623bd51-c46f-442e-91b3-d8d121b5c14e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
3623bd51-c46f-442e-91b3-d8d121b5c14e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
b2023634-12b9-4900-8966-17f56c25fddc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,Table 9.1: Comparison of transudative and exudative pleural effusions.,True,Pleural Effusion,,,,
ff527ed9-70ec-4487-9b8e-91aedf71f012,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The manifestation of pleural effusion varies with the quantity of fluid accumulation and the time line. Symptoms may in fact be absent when the effusion is small. In the case of exudative pleurisy, an initial rub pain may disappear as exudate accumulates and separates the rubbing pleural surfaces.",True,Pleural Effusion,,,,
c382be13-3d22-4dcd-878b-52aabdd88f4b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,As the effusion volume increases the patient is likely to experience dyspnea and physical exam will more likely include dullness to percussion and absence of breath sounds as the effusion forms a fluid pillow around the lung.,True,Pleural Effusion,,,,
58ecefba-8672-4340-b7b7-a7ac1875c82e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
58ecefba-8672-4340-b7b7-a7ac1875c82e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
58ecefba-8672-4340-b7b7-a7ac1875c82e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
58ecefba-8672-4340-b7b7-a7ac1875c82e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
8aa14dae-745d-4370-990c-dd0c80007238,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"As we have already mentioned, the pleural fluid’s composition can provide a great deal of information about the underlying mechanism. We have already mentioned the ability to distinguish between an exudate and a transudate by analysis of the fluid. But gross inspection of the fluid can be revealing before lab tests are ready.",True,Pleural Effusion,,,,
6c59470c-fac5-4568-90b0-17683899422b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
6c59470c-fac5-4568-90b0-17683899422b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
6c59470c-fac5-4568-90b0-17683899422b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
6c59470c-fac5-4568-90b0-17683899422b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
9907c7c8-6645-472b-931d-9903ad85cb67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
9907c7c8-6645-472b-931d-9903ad85cb67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
9907c7c8-6645-472b-931d-9903ad85cb67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
9907c7c8-6645-472b-931d-9903ad85cb67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
5fb1edd2-1b0e-40fb-8b86-a268a72e374f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
5fb1edd2-1b0e-40fb-8b86-a268a72e374f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
5fb1edd2-1b0e-40fb-8b86-a268a72e374f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
5fb1edd2-1b0e-40fb-8b86-a268a72e374f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
a0d647a5-28d2-47ed-988e-cc7b8d5f0196,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
a0d647a5-28d2-47ed-988e-cc7b8d5f0196,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
a0d647a5-28d2-47ed-988e-cc7b8d5f0196,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
a0d647a5-28d2-47ed-988e-cc7b8d5f0196,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
95ef044d-27bd-438b-a098-3baf7f855f5c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,Pneumothorax,False,Pneumothorax,,,,
dc21b918-0174-4104-ba57-3f5969013091,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Normally the negative pressure inside the pleural space opposes the lung’s recoil and holds the lung surface to the interior of the thorax. If the pleural membranes are disrupted this subatmospheric or negative pressure is lost and the lung can recoil, or collapse. This is a pneumothorax.",True,Pneumothorax,,,,
3e073d57-6b5e-4082-ba6d-4dd38bd59687,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The causal events of losing the negative pleural pressure divide pneumothoraces into one of two categories: spontaneous or traumatic. (A third category exists, artificial pneumothorax, which was intentionally induced as part of procedures that are very rarely used today.)",True,Pneumothorax,,,,
1724eaf0-35df-4082-8905-7c646a6be544,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
1724eaf0-35df-4082-8905-7c646a6be544,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
1724eaf0-35df-4082-8905-7c646a6be544,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
1724eaf0-35df-4082-8905-7c646a6be544,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
4ebcf7a2-12c9-4797-a6c8-92086deac997,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
4ebcf7a2-12c9-4797-a6c8-92086deac997,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
4ebcf7a2-12c9-4797-a6c8-92086deac997,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
4ebcf7a2-12c9-4797-a6c8-92086deac997,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
ba66106f-e38a-4018-96a4-f2fd0f510abd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The most common cause of spontaneous pneumothorax in pulmonary patients is a ruptured bleb or bulla. These thin-walled, air-filled cavities are found near the pleural surface, particularly in cases of emphysema. In the past, TB was thought to be the most common cause of pneumothorax as its destructive path encroached on the pleural space.",True,Pneumothorax,,,,
382ff195-5400-4a0b-9e1b-b51e573ab960,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Traumatic pneumothorax is often a consequence of chest injury that involves laceration of the pleura. This might be due to a broken rib or penetrative wound to the chest that allows air to enter the pleural space and equilibrate with the atmosphere. The injury might not be malicious though as some procedures might inadvertently or unavoidably perforate the pleura, such as thoracentesis, pleural biopsy, lung biopsy, or subclavian vein puncture. Trauma from within the lung may also occur. Similar to the mechanism of a rupturing bleb, if excessive airway pressures are used during mechanical ventilation there is the risk that airspaces are disrupted and barotrauma involves the visceral pleura.",True,Pneumothorax,,,,
96dc3d60-e417-4f75-84ac-f7aa1cfd3d85,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"is often a consequence of chest injury that involves laceration of the pleura. This might be due to a broken rib or penetrative wound to the chest that allows air to enter the pleural space and equilibrate with the atmosphere. The injury might not be malicious though as some procedures might inadvertently or unavoidably perforate the pleura, such as",True,Pneumothorax,,,,
103e73a7-9bdb-4132-aeb3-fcfea392b09c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,", pleural biopsy, lung biopsy, or subclavian vein puncture. Trauma from within the lung may also occur. Similar to the mechanism of a rupturing bleb, if excessive airway pressures are used during mechanical ventilation there is the risk that airspaces are disrupted and barotrauma involves the visceral pleura.",True,Pneumothorax,,,,
46ec9129-1ea4-44d7-bbe4-2b930c6ac776,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
46ec9129-1ea4-44d7-bbe4-2b930c6ac776,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
46ec9129-1ea4-44d7-bbe4-2b930c6ac776,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
46ec9129-1ea4-44d7-bbe4-2b930c6ac776,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
be9a34e7-3e93-4d77-9d36-e04d450b58fd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Tension pneumothorax may arise if the disruption to the pleural is such that the injury acts like a valve. During inspiration when thoracic pressure falls air enters the airways and also the thoracic cavity via the injury. During expiration when the thoracic pressure increases, the wound closes, stopping the air that entered the thoracic cavity from leaving. So with each inspiration more air enters while little or none leaves during the subsequent expiration. The accumulating volume can begin to push the heart and mediastinum to the contralateral side. This may severely affect cardiac output and rapidly become life threatening.",True,Pneumothorax,,,,
df8efd10-f1a0-41a8-a508-bc0f96d1a2e7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
df8efd10-f1a0-41a8-a508-bc0f96d1a2e7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
df8efd10-f1a0-41a8-a508-bc0f96d1a2e7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
df8efd10-f1a0-41a8-a508-bc0f96d1a2e7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
741874fd-7cdf-457b-a22a-b7d65e568c5d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Pneumothorax,,,,
46f61cf8-840d-435b-ab18-6c89d80fb47a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleural Effusion,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-2,"West, John B. “Chapter 5: Restrictive Diseases.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Pneumothorax,,,,
193ae403-ae52-4004-bd83-6bd57f64deb5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"To get warmed up, let us start with the simplest one, pleurisy.",True,Pneumothorax,,,,
3fc38b80-2d8b-431d-9a2c-1263a2d7157b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Pleurisy is synonymous with pleuritis and refers to inflammation of the pleural membranes that may be accompanied by pleural exudate or may remain “dry.” Inflammation of the membranes may be mild and transient due to common conditions such as bacterial or viral infection, or it may be severe and chronic and indicative of more serious conditions, such as lupus and rheumatoid arthritis.",True,Pneumothorax,,,,
9644b9a7-b69f-485b-b4f2-a51ea592440e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The inflammation causes thickening of the membranes that may cause them to impinge on the pleural space. Prolonged inflammation leads to an accumulation of pleural macrophages, and these in turn initiate a proliferation of fibrocytes. The inflammatory process may prevent the membranes from moving freely, and in some patients the two inflamed membranes sliding against each other can produce an audible pleural friction rub, which sounds like leather rubbing against leather or walking on fresh snow. The hallmark symptom of a pleural rub is sudden onset chest pain associated with inhalation and cough.",True,Pneumothorax,,,,
4811dbba-8f0a-43b3-a59e-d72256dc2c82,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"In prolonged pathological conditions, the membranes may adhere, and calcium deposits can appear in old pleural fibrosis and are often associated with chronic conditions such as asbestosis. When significant, this level of fibrosis may restrict respiratory movement.",True,Pneumothorax,,,,
fd70499f-0739-4c46-ba3f-fbfbadd873ca,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,Pleural Effusion,False,Pleural Effusion,,,,
02cba639-69cc-47d3-8a39-fd50c3dc0893,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"In our description of pleurisy we eluded to our next pleural disorder, pleural effusion. The normally small amount of pleural fluid is sufficient to lubricate the movement of the lungs and is not detectable on x-ray without specialized radiography. Pleural effusion is the abnormal accumulation of fluid in the pleural space and is easily detectable. As with the formation of fluid accumulation in any part of the body, a normal fluid level in the pleural space is dependent on a balanced rate of formation and reabsorption. In pleural effusion, this balance is lost.",True,Pleural Effusion,,,,
fa945595-3a44-405c-bc74-08862f80cc20,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Initially it was thought that pleural fluid was formed by hydrostatic pressure in capillaries in the parietal membrane pushing fluid into the pleural space, and the fluid was then absorbed by capillaries in the visceral membrane. However, there is mounting evidence to show that reabsorption is actually performed by the lymph vessels in the parietal membrane. The low hydrostatic pressure and large capacity of these vessels helps maintain the normal, small volume of pleural fluid. Pleural effusion can be caused by:",True,Pleural Effusion,,,,
140c2f00-7142-4532-be32-8a6cb9e1d105,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"For example, pleural effusion in cardiac pulmonary edema occurs as fluid leaks across the visceral pleura from the lung.",True,Pleural Effusion,,,,
2ae212ec-31e5-47f9-871f-dcc4c168b76b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Two broad classifications exist, transudate and exudate, so let us compare them now (summary in table 9.1).",True,Pleural Effusion,,,,
21ec79a4-03d8-4153-af3f-783b05740afa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Transudative effusion occurs when there is a disturbance in the Starling’s forces influencing fluid movement across the capillary. As such transudate can be caused by an increase in hydrostatic force pushing fluid out of the capillary, such as in congestive heart failure, or a decrease in the plasma oncotic pressure retaining fluid in the capillary, such as in kidney or liver disease. This results in a transudate with low specific gravity, protein concentration, and cell count.",True,Pleural Effusion,,,,
c8d8f304-c236-4a07-ac6f-29348ab1e8d9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
c8d8f304-c236-4a07-ac6f-29348ab1e8d9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
c8d8f304-c236-4a07-ac6f-29348ab1e8d9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
c8d8f304-c236-4a07-ac6f-29348ab1e8d9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
cc5bcd51-1181-475a-b78f-bb89eb60c6bc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,Table 9.1: Comparison of transudative and exudative pleural effusions.,True,Pleural Effusion,,,,
dc772fba-0f5a-4805-bf54-5cea04c7e7f4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The manifestation of pleural effusion varies with the quantity of fluid accumulation and the time line. Symptoms may in fact be absent when the effusion is small. In the case of exudative pleurisy, an initial rub pain may disappear as exudate accumulates and separates the rubbing pleural surfaces.",True,Pleural Effusion,,,,
039ecf79-0b5c-4725-948b-2cdbe6425412,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,As the effusion volume increases the patient is likely to experience dyspnea and physical exam will more likely include dullness to percussion and absence of breath sounds as the effusion forms a fluid pillow around the lung.,True,Pleural Effusion,,,,
14a3266c-122f-4976-9ff7-8d37b6bd7bc7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
14a3266c-122f-4976-9ff7-8d37b6bd7bc7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
14a3266c-122f-4976-9ff7-8d37b6bd7bc7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
14a3266c-122f-4976-9ff7-8d37b6bd7bc7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
588b8ad5-b3f4-4367-80e6-987482a656c5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"As we have already mentioned, the pleural fluid’s composition can provide a great deal of information about the underlying mechanism. We have already mentioned the ability to distinguish between an exudate and a transudate by analysis of the fluid. But gross inspection of the fluid can be revealing before lab tests are ready.",True,Pleural Effusion,,,,
29eb258f-0c47-49ba-a17f-4be145804d8e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
29eb258f-0c47-49ba-a17f-4be145804d8e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
29eb258f-0c47-49ba-a17f-4be145804d8e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
29eb258f-0c47-49ba-a17f-4be145804d8e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
f3f4c061-7703-4d06-b20c-3b11082d2d26,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
f3f4c061-7703-4d06-b20c-3b11082d2d26,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
f3f4c061-7703-4d06-b20c-3b11082d2d26,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
f3f4c061-7703-4d06-b20c-3b11082d2d26,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
b5227ea8-bc09-4eef-ad2b-f51c8a3c08ca,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
b5227ea8-bc09-4eef-ad2b-f51c8a3c08ca,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
b5227ea8-bc09-4eef-ad2b-f51c8a3c08ca,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
b5227ea8-bc09-4eef-ad2b-f51c8a3c08ca,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
1fbde6e2-d611-4b20-9e17-055a8ccc4452,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
1fbde6e2-d611-4b20-9e17-055a8ccc4452,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
1fbde6e2-d611-4b20-9e17-055a8ccc4452,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
1fbde6e2-d611-4b20-9e17-055a8ccc4452,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
7e403a0a-d561-4e39-bc90-1979596aebf0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,Pneumothorax,False,Pneumothorax,,,,
393987e2-40d5-4f85-a164-eb8bf6135903,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Normally the negative pressure inside the pleural space opposes the lung’s recoil and holds the lung surface to the interior of the thorax. If the pleural membranes are disrupted this subatmospheric or negative pressure is lost and the lung can recoil, or collapse. This is a pneumothorax.",True,Pneumothorax,,,,
06b2e346-2582-4ffa-8a41-a1748fe99c1d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The causal events of losing the negative pleural pressure divide pneumothoraces into one of two categories: spontaneous or traumatic. (A third category exists, artificial pneumothorax, which was intentionally induced as part of procedures that are very rarely used today.)",True,Pneumothorax,,,,
547ecc44-7c9a-426b-b23c-6f2a37f736cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
547ecc44-7c9a-426b-b23c-6f2a37f736cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
547ecc44-7c9a-426b-b23c-6f2a37f736cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
547ecc44-7c9a-426b-b23c-6f2a37f736cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
7208bba5-9a3d-44c4-8d49-9051b3262577,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
7208bba5-9a3d-44c4-8d49-9051b3262577,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
7208bba5-9a3d-44c4-8d49-9051b3262577,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
7208bba5-9a3d-44c4-8d49-9051b3262577,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
1644f18e-1fd8-41f6-879a-1c0a356147ff,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The most common cause of spontaneous pneumothorax in pulmonary patients is a ruptured bleb or bulla. These thin-walled, air-filled cavities are found near the pleural surface, particularly in cases of emphysema. In the past, TB was thought to be the most common cause of pneumothorax as its destructive path encroached on the pleural space.",True,Pneumothorax,,,,
e1aa80a1-e083-4afb-8e53-99b41cc7c42a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Traumatic pneumothorax is often a consequence of chest injury that involves laceration of the pleura. This might be due to a broken rib or penetrative wound to the chest that allows air to enter the pleural space and equilibrate with the atmosphere. The injury might not be malicious though as some procedures might inadvertently or unavoidably perforate the pleura, such as thoracentesis, pleural biopsy, lung biopsy, or subclavian vein puncture. Trauma from within the lung may also occur. Similar to the mechanism of a rupturing bleb, if excessive airway pressures are used during mechanical ventilation there is the risk that airspaces are disrupted and barotrauma involves the visceral pleura.",True,Pneumothorax,,,,
4fc63b19-bfbc-4150-975b-2b9035dba488,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"is often a consequence of chest injury that involves laceration of the pleura. This might be due to a broken rib or penetrative wound to the chest that allows air to enter the pleural space and equilibrate with the atmosphere. The injury might not be malicious though as some procedures might inadvertently or unavoidably perforate the pleura, such as",True,Pneumothorax,,,,
24362905-d1ce-4c8f-86c6-057d72bbfc66,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,", pleural biopsy, lung biopsy, or subclavian vein puncture. Trauma from within the lung may also occur. Similar to the mechanism of a rupturing bleb, if excessive airway pressures are used during mechanical ventilation there is the risk that airspaces are disrupted and barotrauma involves the visceral pleura.",True,Pneumothorax,,,,
2e0c13ea-d92f-43a7-8de9-7836661ead80,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
2e0c13ea-d92f-43a7-8de9-7836661ead80,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
2e0c13ea-d92f-43a7-8de9-7836661ead80,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
2e0c13ea-d92f-43a7-8de9-7836661ead80,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
be557eb7-977d-4e40-8eda-f9d1b13de2dc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Tension pneumothorax may arise if the disruption to the pleural is such that the injury acts like a valve. During inspiration when thoracic pressure falls air enters the airways and also the thoracic cavity via the injury. During expiration when the thoracic pressure increases, the wound closes, stopping the air that entered the thoracic cavity from leaving. So with each inspiration more air enters while little or none leaves during the subsequent expiration. The accumulating volume can begin to push the heart and mediastinum to the contralateral side. This may severely affect cardiac output and rapidly become life threatening.",True,Pneumothorax,,,,
d9878459-6911-48eb-8acc-7ddc85059ad1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
d9878459-6911-48eb-8acc-7ddc85059ad1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
d9878459-6911-48eb-8acc-7ddc85059ad1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
d9878459-6911-48eb-8acc-7ddc85059ad1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
f1b103ff-e100-43bd-8843-88b1721cd165,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Pneumothorax,,,,
b8a884f0-95ee-4111-8d03-60c2a7a5ca6c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pleurisy,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/#chapter-41-section-1,"West, John B. “Chapter 5: Restrictive Diseases.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Pneumothorax,,,,
ac0f705c-a915-43f6-9d06-5a856b0ed98e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"To get warmed up, let us start with the simplest one, pleurisy.",True,Pneumothorax,,,,
7e880967-3b78-44ec-8bae-2ca8f6de29a7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Pleurisy is synonymous with pleuritis and refers to inflammation of the pleural membranes that may be accompanied by pleural exudate or may remain “dry.” Inflammation of the membranes may be mild and transient due to common conditions such as bacterial or viral infection, or it may be severe and chronic and indicative of more serious conditions, such as lupus and rheumatoid arthritis.",True,Pneumothorax,,,,
fb000bbf-823e-4672-b00b-20a9979caa36,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The inflammation causes thickening of the membranes that may cause them to impinge on the pleural space. Prolonged inflammation leads to an accumulation of pleural macrophages, and these in turn initiate a proliferation of fibrocytes. The inflammatory process may prevent the membranes from moving freely, and in some patients the two inflamed membranes sliding against each other can produce an audible pleural friction rub, which sounds like leather rubbing against leather or walking on fresh snow. The hallmark symptom of a pleural rub is sudden onset chest pain associated with inhalation and cough.",True,Pneumothorax,,,,
2d6cdf2a-1da5-46ad-bf0d-3a6131126213,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"In prolonged pathological conditions, the membranes may adhere, and calcium deposits can appear in old pleural fibrosis and are often associated with chronic conditions such as asbestosis. When significant, this level of fibrosis may restrict respiratory movement.",True,Pneumothorax,,,,
df112591-93a2-43b6-9955-4eb4d3d6cc5f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,Pleural Effusion,False,Pleural Effusion,,,,
621f7764-2564-4502-9c54-a26a4f035151,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"In our description of pleurisy we eluded to our next pleural disorder, pleural effusion. The normally small amount of pleural fluid is sufficient to lubricate the movement of the lungs and is not detectable on x-ray without specialized radiography. Pleural effusion is the abnormal accumulation of fluid in the pleural space and is easily detectable. As with the formation of fluid accumulation in any part of the body, a normal fluid level in the pleural space is dependent on a balanced rate of formation and reabsorption. In pleural effusion, this balance is lost.",True,Pleural Effusion,,,,
14104d19-2957-47a7-b7e4-6923838fa20e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Initially it was thought that pleural fluid was formed by hydrostatic pressure in capillaries in the parietal membrane pushing fluid into the pleural space, and the fluid was then absorbed by capillaries in the visceral membrane. However, there is mounting evidence to show that reabsorption is actually performed by the lymph vessels in the parietal membrane. The low hydrostatic pressure and large capacity of these vessels helps maintain the normal, small volume of pleural fluid. Pleural effusion can be caused by:",True,Pleural Effusion,,,,
759d6022-bda7-4a95-bb8a-48d08b1c8685,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"For example, pleural effusion in cardiac pulmonary edema occurs as fluid leaks across the visceral pleura from the lung.",True,Pleural Effusion,,,,
332fb5e9-7327-47ae-b15b-98ec5b83880f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Two broad classifications exist, transudate and exudate, so let us compare them now (summary in table 9.1).",True,Pleural Effusion,,,,
e7c00bdd-9998-4950-a002-e4eeddbbbdff,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Transudative effusion occurs when there is a disturbance in the Starling’s forces influencing fluid movement across the capillary. As such transudate can be caused by an increase in hydrostatic force pushing fluid out of the capillary, such as in congestive heart failure, or a decrease in the plasma oncotic pressure retaining fluid in the capillary, such as in kidney or liver disease. This results in a transudate with low specific gravity, protein concentration, and cell count.",True,Pleural Effusion,,,,
67dd7178-f69d-456c-88bb-3aaaf13e4a69,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
67dd7178-f69d-456c-88bb-3aaaf13e4a69,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
67dd7178-f69d-456c-88bb-3aaaf13e4a69,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
67dd7178-f69d-456c-88bb-3aaaf13e4a69,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Exudative effusion is caused by increased capillary permeability, such as that caused by the inflammatory process. Relate this back to your understanding of exudative pleurisy (figure 9.1). As larger molecules can exit the leaky capillaries, exudative effusion has a higher specific gravity, higher protein concentration, and likely a higher cell count.",True,Pleural Effusion,Figure 9.1,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
25c8c5d4-fe56-44ef-9714-7ec69a160611,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,Table 9.1: Comparison of transudative and exudative pleural effusions.,True,Pleural Effusion,,,,
9e75aae9-3897-4841-818c-bb0add5d6c1f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The manifestation of pleural effusion varies with the quantity of fluid accumulation and the time line. Symptoms may in fact be absent when the effusion is small. In the case of exudative pleurisy, an initial rub pain may disappear as exudate accumulates and separates the rubbing pleural surfaces.",True,Pleural Effusion,,,,
dfa9bd9c-6318-42ad-8b12-1daa877056fc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,As the effusion volume increases the patient is likely to experience dyspnea and physical exam will more likely include dullness to percussion and absence of breath sounds as the effusion forms a fluid pillow around the lung.,True,Pleural Effusion,,,,
4c8719b9-88e2-44c3-b12a-9200860f2086,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
4c8719b9-88e2-44c3-b12a-9200860f2086,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
4c8719b9-88e2-44c3-b12a-9200860f2086,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
4c8719b9-88e2-44c3-b12a-9200860f2086,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"As the severity of the effusion increases the patient will be severely short of breath, and the risk of the effusion pushing mediastinal structures to the contralateral side becomes significant and urgent (figure 9.1) as even mild displacement of the mediastinum can reduce cardiac output and produce hypotension. More significant displacement can become life threatening.",True,Pleural Effusion,Figure 9.1,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.1.jpeg,Figure 9.1: Severe pleural effusion leading to displacement of the mediastinum and heart to the right. This patient’s condition is critical because of the threat to cardiac output.
021fcf05-6f39-4f46-bbac-1be7ceb852fa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"As we have already mentioned, the pleural fluid’s composition can provide a great deal of information about the underlying mechanism. We have already mentioned the ability to distinguish between an exudate and a transudate by analysis of the fluid. But gross inspection of the fluid can be revealing before lab tests are ready.",True,Pleural Effusion,,,,
ffedb4a3-0780-4d75-a3e7-a36aebbf6c7b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
ffedb4a3-0780-4d75-a3e7-a36aebbf6c7b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
ffedb4a3-0780-4d75-a3e7-a36aebbf6c7b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
ffedb4a3-0780-4d75-a3e7-a36aebbf6c7b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Fluid drawn through thoracentesis that appears clear and straw colored (figure 9.2) is likely to be transudate. The clarity of the fluid relates to a low protein content reflecting intact capillaries, and you should be looking for disturbances in Starling’s forces. Lab results can confirm the integrity of the capillary beds. Clinically the pleural fluid’s protein content and lactate dehydrogenase concentration are used and are expressed as a ratio with the patient’s plasma concentrations. Light’s criteria set diagnostic thresholds for these ratios to determine transudative or exudative effusions.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
5c2e17f7-73c7-4491-b299-ccf02ed1d8e9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
5c2e17f7-73c7-4491-b299-ccf02ed1d8e9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
5c2e17f7-73c7-4491-b299-ccf02ed1d8e9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
5c2e17f7-73c7-4491-b299-ccf02ed1d8e9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The higher protein of exudative effusion gives the fluid a more turbid or cloudy appearance, and high protein content may even give the fluid a foamy head (figure 9.2). Further lab analysis of the composition and cell content of the exudate can help determine the underlying cause of the leak. For example, presence of polymorphonuclear leukocytes is highly suggestive of pyrogenic infection, whereas predominance of lymphocytes is indicative of TB or malignancy.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
1b58fe9f-0787-43f9-88a5-c42739e9791f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
1b58fe9f-0787-43f9-88a5-c42739e9791f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
1b58fe9f-0787-43f9-88a5-c42739e9791f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
1b58fe9f-0787-43f9-88a5-c42739e9791f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Presence of lysed red blood cells will give the fluid a red turbid appearance (figure 9.2) and is indicative of trauma or malignancy, and again will require further investigation. If a malignancy has penetrated the lymphatics, such as the thoracic duct, the resultant chylous exudate will have a milky appearance.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
01407897-18a5-4f98-8e0b-182419b1bb03,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
01407897-18a5-4f98-8e0b-182419b1bb03,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
01407897-18a5-4f98-8e0b-182419b1bb03,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
01407897-18a5-4f98-8e0b-182419b1bb03,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"A purulent fluid (figure 9.2) is indicative of infection within the pleural space and culturing the fluid will allow the pathogen to be determined. When pleural fluid is grossly purulent or contains pyogenic organisms we refer to this as pleural empyema. The most common route of entry for organisms is from underlying pneumonia or lung abscess, or through penetrative surgery or chest wound. The patient usually presents with fever and other manifestations of bacterial infection.",True,Pleural Effusion,Figure 9.2,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.2.png,Figure 9.2: Appearance of pleural fluid and diagnosis.
019c1da4-fc14-469a-9eb1-b71c22ef651c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,Pneumothorax,False,Pneumothorax,,,,
888d2fb0-6d87-4cb9-8ebd-666513d8bb02,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Normally the negative pressure inside the pleural space opposes the lung’s recoil and holds the lung surface to the interior of the thorax. If the pleural membranes are disrupted this subatmospheric or negative pressure is lost and the lung can recoil, or collapse. This is a pneumothorax.",True,Pneumothorax,,,,
71bb8ff2-425b-482f-8432-e525b238c55b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The causal events of losing the negative pleural pressure divide pneumothoraces into one of two categories: spontaneous or traumatic. (A third category exists, artificial pneumothorax, which was intentionally induced as part of procedures that are very rarely used today.)",True,Pneumothorax,,,,
df6a84c9-aeef-4ca4-85fb-3ca168b20fde,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
df6a84c9-aeef-4ca4-85fb-3ca168b20fde,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
df6a84c9-aeef-4ca4-85fb-3ca168b20fde,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
df6a84c9-aeef-4ca4-85fb-3ca168b20fde,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Spontaneous pneumothorax occurs in the absence of accidental or intentional trauma. When it occurs in otherwise healthy individuals it is usually the fault of anatomy and occurs mostly in tall, thin individuals with a long and narrow chest. If you compare the two body morphs in figure 9.3, the tall, thin torso has a lot of lung mass hanging below a relatively small apical section of pleural membrane compared to the other torso.",True,Pneumothorax,Figure 9.3,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.3.png,"Figure 9.3: A tall, thin body morph (right) is more prone to a spontaneous pneumothorax."
0ddb6643-b66b-4b35-8cbf-1bc99f0ccb99,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
0ddb6643-b66b-4b35-8cbf-1bc99f0ccb99,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
0ddb6643-b66b-4b35-8cbf-1bc99f0ccb99,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
0ddb6643-b66b-4b35-8cbf-1bc99f0ccb99,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The proportionately greater weight of lung per unit surface area at the apex increases the risk that bulla form (figure 9.4), then rupture causing loss of pleural membrane adhesion.",True,Pneumothorax,Figure 9.4,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.4.png,Figure 9.4: Rupturing bulla and blebs can lead to spontaneous pneumothorax.
7d9c17cd-020e-40d6-9fe5-5416f3e2a504,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The most common cause of spontaneous pneumothorax in pulmonary patients is a ruptured bleb or bulla. These thin-walled, air-filled cavities are found near the pleural surface, particularly in cases of emphysema. In the past, TB was thought to be the most common cause of pneumothorax as its destructive path encroached on the pleural space.",True,Pneumothorax,,,,
d9151036-a05b-41b1-bcaf-8ad50445d016,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Traumatic pneumothorax is often a consequence of chest injury that involves laceration of the pleura. This might be due to a broken rib or penetrative wound to the chest that allows air to enter the pleural space and equilibrate with the atmosphere. The injury might not be malicious though as some procedures might inadvertently or unavoidably perforate the pleura, such as thoracentesis, pleural biopsy, lung biopsy, or subclavian vein puncture. Trauma from within the lung may also occur. Similar to the mechanism of a rupturing bleb, if excessive airway pressures are used during mechanical ventilation there is the risk that airspaces are disrupted and barotrauma involves the visceral pleura.",True,Pneumothorax,,,,
88f699c9-a0b3-413b-959b-d7f94f7139ee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"is often a consequence of chest injury that involves laceration of the pleura. This might be due to a broken rib or penetrative wound to the chest that allows air to enter the pleural space and equilibrate with the atmosphere. The injury might not be malicious though as some procedures might inadvertently or unavoidably perforate the pleura, such as",True,Pneumothorax,,,,
bb9811ec-ed49-4a6c-ac95-2b67ca85ca88,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,", pleural biopsy, lung biopsy, or subclavian vein puncture. Trauma from within the lung may also occur. Similar to the mechanism of a rupturing bleb, if excessive airway pressures are used during mechanical ventilation there is the risk that airspaces are disrupted and barotrauma involves the visceral pleura.",True,Pneumothorax,,,,
e7eb4265-1055-4810-a429-183836d3a3ee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
e7eb4265-1055-4810-a429-183836d3a3ee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
e7eb4265-1055-4810-a429-183836d3a3ee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
e7eb4265-1055-4810-a429-183836d3a3ee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"The pneumothorax is readily identified with translucency on the affected side. The pathophysiology of a pneumothorax (figure 9.5) leads to hypoxia and hypercapnia in the affected lung through changes in perfusion and ventilation. Perfusion to the affected side is markedly reduced as the vasoconstrictive response to local hypoxia and the loss of radial traction to vessels profoundly increases vascular resistance. Consequently, perfusion shifts to the contralateral and unaffected lung. Similarly ventilation to the collapsed lung is minimal as airspaces are collapsed and airway resistance is very high, but the chemoreceptive reflexes increase ventilation to the unaffected lung where resistance is normal. Because perfusion and ventilation are shifted to the normal lung, V/Q mismatching may be compensated to some degree and severe hypoxemia may be avoided. When pneumothorax occurs patients usually describe a rapid onset of dyspnea and initial sudden sharp pain. The pain often then transitions into a dull ache.",True,Pneumothorax,Figure 9.5,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.5.png,Figure 9.5: Pathophysiology of a pneumothorax
5e8a82c2-4ccd-4a26-8de0-a1f5aac8d6bd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Tension pneumothorax may arise if the disruption to the pleural is such that the injury acts like a valve. During inspiration when thoracic pressure falls air enters the airways and also the thoracic cavity via the injury. During expiration when the thoracic pressure increases, the wound closes, stopping the air that entered the thoracic cavity from leaving. So with each inspiration more air enters while little or none leaves during the subsequent expiration. The accumulating volume can begin to push the heart and mediastinum to the contralateral side. This may severely affect cardiac output and rapidly become life threatening.",True,Pneumothorax,,,,
efc8a0e5-e03b-4006-9d9b-47067259b5a5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,Pneumothorax,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
efc8a0e5-e03b-4006-9d9b-47067259b5a5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,Pleural Effusion,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
efc8a0e5-e03b-4006-9d9b-47067259b5a5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,Pleurisy,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
efc8a0e5-e03b-4006-9d9b-47067259b5a5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,These CT scans in figure 9.6 shows a spontaneous pneumothorax (left panel) and a tension pneumothorax (right panel) with significant shift of the mediastinum over the contralateral hemithorax. So now you should be able to distinguish between the causes and mechanisms of these pleural disorders and determine their effects on pulmonary and cardiac function.,True,Pneumothorax,Figure 9.6,9. Pleural Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/9.6.png,Figure 9.6: CT comparison of an uncomplicated pneumothorax and a tension pneumothorax.
cbd75241-fcb4-434c-b0a1-eca704ab7b1d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Pneumothorax,,,,
681401a7-1e3e-4bb7-bc90-1a5f14a1120a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,9. Pleural Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pleural-diseases/,"West, John B. “Chapter 5: Restrictive Diseases.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Pneumothorax,,,,
69f961c0-969d-40e6-8ade-b643ff59d2c7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"The lung is no different from any other organ in that it is susceptible to disorders of the immune system. One might argue that it is surprising that the lung does not encounter more problems, given the lung’s exposure to the environment and the myriad antigens it encounters. Before we start looking at a few specific disorders, let us quickly review the four mechanisms through which the immune system might disrupt lung tissue.",True,Pneumothorax,,,,
1a94ccb8-a877-481c-afba-6bd5bbb2d630,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"A type 1 reaction, or immediate hypersensitivity (table 8.1), is a result of overexpression of IgE (table 8.1). When an antigen binds to the overexpressed IgE on the surface of mast cells, the cell releases histamine and leukotrienes that in turn induce an inappropriate or exaggerated inflammatory response. Allergic asthma is an example of a type 1 reaction.",True,Pneumothorax,,,,
701e3fef-85c0-405b-8b02-3a1a6713794d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,overexpression,False,overexpression,,,,
49e8b3ef-78fa-49c0-a782-676e724ef6a7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"A type 2 reaction, or antibody-dependent cytotoxic reaction (table 8.1), is the result of a circulating antibody reacting with a component of a cell or tissue. The formation of this inappropriate immune complex results in the cell or tissue being flagged for attack by the immune system. Goodpasture’s syndrome is an example of a type 2 reaction.",True,overexpression,,,,
ecded636-8864-4e2e-bc01-b7de6a6d0a42,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"A type 3 reaction, or immune complex reaction (table 8.1), is the result of an immune complex forming either locally or circulating from elsewhere and then depositing itself in tissue; the immune complex then instigates an immune system attack that involves the tissue. Pulmonary vasculitis can be caused by type 3 immune disorders.",True,overexpression,,,,
fadbb58c-ba27-41aa-a219-2148de5e68ee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Lastly, a type 4 reaction, or cell-mediated hypersensitivity (table 8.1), is caused by a population of hypersensitive T cells whose response to an antigen is exaggerated and leads to the proliferation of that cell population and the release of lymphokines to induce an inflammatory response. While this pattern is the same as the normal response to many infections, the magnitude of the response is inappropriate and can lead to pathological changes, such as allergic alveolitis.",True,overexpression,,,,
cc18c6f4-da00-49e1-8ade-6b079c139b8e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Table 8.1: Types of immune mechanisms involved in lung tissue injury.,True,overexpression,,,,
5a3578ba-82c1-4463-b782-2ce0d7d29268,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"With those mechanisms defined, let us look at some specific disorders.",True,overexpression,,,,
40036861-22c1-4534-b623-29887a1f8e25,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Hypersensitivity Pneumonitis,False,Hypersensitivity Pneumonitis,,,,
513c66e1-b30f-47a0-804e-ced6ad9b3808,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
513c66e1-b30f-47a0-804e-ced6ad9b3808,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
513c66e1-b30f-47a0-804e-ced6ad9b3808,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
513c66e1-b30f-47a0-804e-ced6ad9b3808,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
513c66e1-b30f-47a0-804e-ced6ad9b3808,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
da5f7d98-82bc-43e0-a76b-cdd2a83989b1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
da5f7d98-82bc-43e0-a76b-cdd2a83989b1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
da5f7d98-82bc-43e0-a76b-cdd2a83989b1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
da5f7d98-82bc-43e0-a76b-cdd2a83989b1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
da5f7d98-82bc-43e0-a76b-cdd2a83989b1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
7b3bd5e9-a454-42b0-8a3f-997b89d1dd59,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Clinical signs,False,Clinical signs,,,,
82e72dd8-37aa-46e6-9f8e-d4af6a758814,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,How hypersensitivity pneumonitis presents is somewhat dependent on the form of exposure the patient had.,True,Clinical signs,,,,
e2f9d8e0-f40a-4675-87b5-a9ce46016902,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"With brief but heavy exposure, an acute presentation of pneumonitis will present with fever, malaise, cough, and dyspnea. Physical exam confirms the fever and tachypnea and cyanosis can reflect the severity of the response. Bibasilar rales are often present, but unless a type 1 hypersensitivity arises then wheeze is usually absent (but you might note here that concurrent allergenic asthma is not beyond the realms of possibility). This acute form usually resolves within a couple of days, but can reoccur when the patient is exposed to the causal agent again.",True,Clinical signs,,,,
9534c8bf-8a47-49c8-b624-35f5e7524840,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"When exposure is light but prolonged, the onset of hypersensitivity pneumonitis is more insidious and clinically challenging. The patient will describe a slowly progressive cough and developing dyspnea, also weakness and weight loss. This form of onset is common with continuous exposure to organic dust. With this longer time line the patient is not usually aware of the symptom’s relation to occupation and exposure persists until diffuse pulmonary fibrosis is established. At this point the signs and symptoms are related to respiratory insufficiency.",True,Clinical signs,,,,
27dbb277-bd31-4765-9a3e-5c8992135f0b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Goodpasture’s Syndrome,False,Goodpasture’s Syndrome,,,,
83c774e0-247f-4160-9fe3-318fedde43a7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Systemic Diseases Affecting the Lung,False,Systemic Diseases Affecting the Lung,,,,
f01ffebf-2ee9-4d93-b8d6-bf2ba343025e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Systemic Lupus Erythematosus (SLE),False,Systemic Lupus Erythematosus (SLE),,,,
92c213eb-a541-4823-8fdd-39f460143f1e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Lupus erythematosus is a type 3 reaction. Autoantibodies are formed against cell components, particularly the nucleus and its associated proteins. The most common antibodies found are against single– or double–stranded DNA. About 70 percent of SLE patients have lung involvement that can be either acute or chronic.",True,Systemic Lupus Erythematosus (SLE),,,,
7a8cf594-b20f-4214-bffe-fd844c13ac11,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Acute SLE,False,Acute SLE,,,,
a4e79593-235f-4368-8a83-505add623aa5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"The acute form is referred to as lupus pneumonitis, and its signs and symptoms mimic bacterial pneumonia. It can have a rapidly progressive course with acute pleuritic chest pain and can lead to respiratory failure. The inflammation it involves can disrupt pulmonary capillaries and lead to hemorrhage. Patients with SLE are highly susceptible to infection, so diagnosis of an SLE patient should distinguish between respiratory tract infection and changes directly related to lupus. Changes in lupus come as flares followed by remission, and there are a number of triggers for flares including:",True,Acute SLE,,,,
4f1b2da3-f763-4146-b69b-7eb32711c318,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Chronic SLE,False,Chronic SLE,,,,
a963a7f7-ee87-4a98-b028-be212f62d59d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
a963a7f7-ee87-4a98-b028-be212f62d59d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
a963a7f7-ee87-4a98-b028-be212f62d59d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
a963a7f7-ee87-4a98-b028-be212f62d59d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
a963a7f7-ee87-4a98-b028-be212f62d59d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
edd02594-cd35-4eb2-bab1-9ede2016b8bc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Rheumatoid Disease,False,Rheumatoid Disease,,,,
c48b9516-2cb6-4fe5-92f6-604b85200655,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"More famous for its effect on the joints, rheumatoid disease can also affect the lungs and pleura. Rheumatoid factors that generate rheumatoid disease continue to be investigated, but in brief, they are antibodies generated against gamma globulins. Pleural and pulmonary lesions are probably the result of local immune complex–mediated reactions associated with high levels of circulating rheumatoid factors.",True,Rheumatoid Disease,,,,
04d7b4aa-886a-4536-98ed-070284e4bd95,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
04d7b4aa-886a-4536-98ed-070284e4bd95,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
04d7b4aa-886a-4536-98ed-070284e4bd95,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
04d7b4aa-886a-4536-98ed-070284e4bd95,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
04d7b4aa-886a-4536-98ed-070284e4bd95,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
ede6027d-fb5a-4e30-9117-95507266dd44,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
ede6027d-fb5a-4e30-9117-95507266dd44,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
ede6027d-fb5a-4e30-9117-95507266dd44,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
ede6027d-fb5a-4e30-9117-95507266dd44,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
ede6027d-fb5a-4e30-9117-95507266dd44,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
42a08419-43ef-4114-bb9f-0f12c3b4dfa6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"It should be noted here that some drugs used to treat difficult rheumatoid arthritis, such as gold preparations, methotrexate, and penicillamine, are toxic to the lung and can produce their own pulmonary lesions.",True,Rheumatoid Disease,,,,
e7f48fa1-4602-4de2-8883-60fec43a7b9d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Progressive Systemic Sclerosis,False,Progressive Systemic Sclerosis,,,,
cb8e1a9f-2a82-4a89-b17c-a1610c12363b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Also known as scleroderma, progressive systemic sclerosis primarily affects the blood vessels and connective tissue and likely has an autoimmune mechanism. The result is dysregulation of fibroblasts and uncontrolled collagen formation. The disease can affect many organs and tissues, and pulmonary manifestations are common.",True,Progressive Systemic Sclerosis,,,,
1c381b39-cda0-46b1-83e7-0ef197c5085c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"The most common pulmonary findings are interstitial fibrosis, bronchiolar dilation, and pleural fibrosis, as well as the vascular changes that are seen in other organs. These changes produce dyspnea, cough, and basilar rales. The vascular changes can produce pulmonary hypertension that may lead to cor pulmonale.",True,Progressive Systemic Sclerosis,,,,
46f49161-5bd8-4b1a-bce3-e07a1097b217,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
46f49161-5bd8-4b1a-bce3-e07a1097b217,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
46f49161-5bd8-4b1a-bce3-e07a1097b217,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
46f49161-5bd8-4b1a-bce3-e07a1097b217,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
46f49161-5bd8-4b1a-bce3-e07a1097b217,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
bad4aa7c-1e8e-4856-8aa1-fb7482b6cff6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Polymyositis,False,Polymyositis,,,,
bdc02467-c4ab-42d3-959c-6b0c22fd235a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Polymyositis is an autoimmune disease that attacks striated muscle through a cell-mediated mechanism, but can also affect other organ systems, including the lung.",True,Polymyositis,,,,
3b291a83-50c1-498a-a5ca-d3ec4c152236,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,There is some direct involvement with development of bronchiolitis obliterans organizing pneumonia (BOOP) and chronic interstitial pneumonitis and fibrosis. But the most frequent respiratory complications are a result of the respiratory muscles and muscles involved with swallowing becoming affected. Poor control of swallowing and inability to generate effective cough promote aspiration and retention of airway secretions. This is a recipe for bronchopneumonia—and this ends up being the most common form of death. Infection risk is often increased by the patient taking large doses of corticosteroids or immunosuppressive drugs to address the disease.,True,Polymyositis,,,,
4f4a4536-cbad-4d81-be35-34a42cdbea76,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Summary,False,Summary,,,,
18cc338a-ebb8-4172-ab25-10a0067cd924,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"To summarize, the immunological responses to inhaled particles, localized immune responses, and systemic immunological disease can produce pulmonary manifestations that are generally related to acute and then chronic inflammatory responses. The distinguishing features and pulmonary manifestations are summarized in table 8.2.",True,Summary,,,,
8e232397-5b37-4af4-ad5a-bcf6c313532f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Table 8.2: Summary of immune and systemic disorders that affect the lung.,True,Summary,,,,
78bb4df6-b309-415c-bc1c-7d8273042111,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,Text,False,Text,,,,
c95fa1fa-f9e3-450e-b56a-ad2feb79761c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapters 13–14.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
57da44ae-a71b-473a-ade7-099d35c54c0a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
46cbc4df-cf41-4ebf-99e9-0d40ac274b65,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
46cbc4df-cf41-4ebf-99e9-0d40ac274b65,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
46cbc4df-cf41-4ebf-99e9-0d40ac274b65,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
46cbc4df-cf41-4ebf-99e9-0d40ac274b65,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
46cbc4df-cf41-4ebf-99e9-0d40ac274b65,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-4,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
515cac81-2046-4f5f-a7f0-9e4bd782cd7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"The lung is no different from any other organ in that it is susceptible to disorders of the immune system. One might argue that it is surprising that the lung does not encounter more problems, given the lung’s exposure to the environment and the myriad antigens it encounters. Before we start looking at a few specific disorders, let us quickly review the four mechanisms through which the immune system might disrupt lung tissue.",True,Text,,,,
33f1f249-01d5-4412-ac59-4f26defa869f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"A type 1 reaction, or immediate hypersensitivity (table 8.1), is a result of overexpression of IgE (table 8.1). When an antigen binds to the overexpressed IgE on the surface of mast cells, the cell releases histamine and leukotrienes that in turn induce an inappropriate or exaggerated inflammatory response. Allergic asthma is an example of a type 1 reaction.",True,Text,,,,
022381fc-053f-4cdf-992d-920c55438de8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,overexpression,False,overexpression,,,,
6288ad1f-6b80-43b1-83b5-1af560662661,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"A type 2 reaction, or antibody-dependent cytotoxic reaction (table 8.1), is the result of a circulating antibody reacting with a component of a cell or tissue. The formation of this inappropriate immune complex results in the cell or tissue being flagged for attack by the immune system. Goodpasture’s syndrome is an example of a type 2 reaction.",True,overexpression,,,,
aaa53f29-56e0-465c-8e64-746e6fc930b7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"A type 3 reaction, or immune complex reaction (table 8.1), is the result of an immune complex forming either locally or circulating from elsewhere and then depositing itself in tissue; the immune complex then instigates an immune system attack that involves the tissue. Pulmonary vasculitis can be caused by type 3 immune disorders.",True,overexpression,,,,
bec1523a-b121-4e00-85cd-a7077528d386,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Lastly, a type 4 reaction, or cell-mediated hypersensitivity (table 8.1), is caused by a population of hypersensitive T cells whose response to an antigen is exaggerated and leads to the proliferation of that cell population and the release of lymphokines to induce an inflammatory response. While this pattern is the same as the normal response to many infections, the magnitude of the response is inappropriate and can lead to pathological changes, such as allergic alveolitis.",True,overexpression,,,,
3dcdb785-9097-466f-a8a4-7585189f2c81,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Table 8.1: Types of immune mechanisms involved in lung tissue injury.,True,overexpression,,,,
6bb40ff3-c7db-4df7-a84b-492a39655b33,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"With those mechanisms defined, let us look at some specific disorders.",True,overexpression,,,,
462585cd-1964-4d92-a40b-02b777093c41,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Hypersensitivity Pneumonitis,False,Hypersensitivity Pneumonitis,,,,
36f80c3b-e8b2-4074-898f-4c143767916c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
36f80c3b-e8b2-4074-898f-4c143767916c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
36f80c3b-e8b2-4074-898f-4c143767916c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
36f80c3b-e8b2-4074-898f-4c143767916c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
36f80c3b-e8b2-4074-898f-4c143767916c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
bcd867e4-4c92-4e33-8999-a4bc69eb76d8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
bcd867e4-4c92-4e33-8999-a4bc69eb76d8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
bcd867e4-4c92-4e33-8999-a4bc69eb76d8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
bcd867e4-4c92-4e33-8999-a4bc69eb76d8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
bcd867e4-4c92-4e33-8999-a4bc69eb76d8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
734c04c6-7598-470e-9ed9-6f75dba7f10d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Clinical signs,False,Clinical signs,,,,
8ee8e6d1-32c4-4d0e-acde-421ad106424a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,How hypersensitivity pneumonitis presents is somewhat dependent on the form of exposure the patient had.,True,Clinical signs,,,,
98e69265-b9e2-4c9f-81ff-84deb2c75190,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"With brief but heavy exposure, an acute presentation of pneumonitis will present with fever, malaise, cough, and dyspnea. Physical exam confirms the fever and tachypnea and cyanosis can reflect the severity of the response. Bibasilar rales are often present, but unless a type 1 hypersensitivity arises then wheeze is usually absent (but you might note here that concurrent allergenic asthma is not beyond the realms of possibility). This acute form usually resolves within a couple of days, but can reoccur when the patient is exposed to the causal agent again.",True,Clinical signs,,,,
7ab6bb34-d61c-4c2d-b3e1-f56a8f869fd6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"When exposure is light but prolonged, the onset of hypersensitivity pneumonitis is more insidious and clinically challenging. The patient will describe a slowly progressive cough and developing dyspnea, also weakness and weight loss. This form of onset is common with continuous exposure to organic dust. With this longer time line the patient is not usually aware of the symptom’s relation to occupation and exposure persists until diffuse pulmonary fibrosis is established. At this point the signs and symptoms are related to respiratory insufficiency.",True,Clinical signs,,,,
d775756d-8af5-4b3c-a806-4f2a99f37475,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Goodpasture’s Syndrome,False,Goodpasture’s Syndrome,,,,
ef25fe47-d278-4f22-a1c5-1e5c4f08365d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Systemic Diseases Affecting the Lung,False,Systemic Diseases Affecting the Lung,,,,
bbd63212-c660-4cef-a2eb-cdcc349a9fcc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Systemic Lupus Erythematosus (SLE),False,Systemic Lupus Erythematosus (SLE),,,,
15edc5bc-bb82-47d5-beb0-1fa7ca1395c6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Lupus erythematosus is a type 3 reaction. Autoantibodies are formed against cell components, particularly the nucleus and its associated proteins. The most common antibodies found are against single– or double–stranded DNA. About 70 percent of SLE patients have lung involvement that can be either acute or chronic.",True,Systemic Lupus Erythematosus (SLE),,,,
744d9255-01e0-45fa-85bf-cf1d3e3411a3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Acute SLE,False,Acute SLE,,,,
688b8b2c-6cc7-43b3-9bec-b360057e065f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"The acute form is referred to as lupus pneumonitis, and its signs and symptoms mimic bacterial pneumonia. It can have a rapidly progressive course with acute pleuritic chest pain and can lead to respiratory failure. The inflammation it involves can disrupt pulmonary capillaries and lead to hemorrhage. Patients with SLE are highly susceptible to infection, so diagnosis of an SLE patient should distinguish between respiratory tract infection and changes directly related to lupus. Changes in lupus come as flares followed by remission, and there are a number of triggers for flares including:",True,Acute SLE,,,,
bd30652e-94fe-4d88-9d76-185c7e8c4f45,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Chronic SLE,False,Chronic SLE,,,,
b7dd12f6-fd52-4779-a1a3-0d6c49120c20,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
b7dd12f6-fd52-4779-a1a3-0d6c49120c20,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
b7dd12f6-fd52-4779-a1a3-0d6c49120c20,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
b7dd12f6-fd52-4779-a1a3-0d6c49120c20,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
b7dd12f6-fd52-4779-a1a3-0d6c49120c20,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
ab7d96b8-d386-40fa-80f9-aae30e9b4c74,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Rheumatoid Disease,False,Rheumatoid Disease,,,,
1b0b2578-35ca-4a0c-88e2-192d56cc74f7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"More famous for its effect on the joints, rheumatoid disease can also affect the lungs and pleura. Rheumatoid factors that generate rheumatoid disease continue to be investigated, but in brief, they are antibodies generated against gamma globulins. Pleural and pulmonary lesions are probably the result of local immune complex–mediated reactions associated with high levels of circulating rheumatoid factors.",True,Rheumatoid Disease,,,,
b7631bb9-8279-4136-a635-490326e0c438,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
b7631bb9-8279-4136-a635-490326e0c438,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
b7631bb9-8279-4136-a635-490326e0c438,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
b7631bb9-8279-4136-a635-490326e0c438,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
b7631bb9-8279-4136-a635-490326e0c438,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
8adcf6a0-0295-48bb-bb29-09d849f32ebb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
8adcf6a0-0295-48bb-bb29-09d849f32ebb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
8adcf6a0-0295-48bb-bb29-09d849f32ebb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
8adcf6a0-0295-48bb-bb29-09d849f32ebb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
8adcf6a0-0295-48bb-bb29-09d849f32ebb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
ccf29aac-5da4-4dbf-8f60-df9faa759592,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"It should be noted here that some drugs used to treat difficult rheumatoid arthritis, such as gold preparations, methotrexate, and penicillamine, are toxic to the lung and can produce their own pulmonary lesions.",True,Rheumatoid Disease,,,,
c5561212-d29d-46a0-b3c4-8f62569ad932,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Progressive Systemic Sclerosis,False,Progressive Systemic Sclerosis,,,,
4a0968af-74cc-454f-9a61-8fc328025641,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Also known as scleroderma, progressive systemic sclerosis primarily affects the blood vessels and connective tissue and likely has an autoimmune mechanism. The result is dysregulation of fibroblasts and uncontrolled collagen formation. The disease can affect many organs and tissues, and pulmonary manifestations are common.",True,Progressive Systemic Sclerosis,,,,
eb5bd118-7d1a-42d9-ad8d-fca511812685,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"The most common pulmonary findings are interstitial fibrosis, bronchiolar dilation, and pleural fibrosis, as well as the vascular changes that are seen in other organs. These changes produce dyspnea, cough, and basilar rales. The vascular changes can produce pulmonary hypertension that may lead to cor pulmonale.",True,Progressive Systemic Sclerosis,,,,
f45166c2-68ba-4950-8225-127da8f088f3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
f45166c2-68ba-4950-8225-127da8f088f3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
f45166c2-68ba-4950-8225-127da8f088f3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
f45166c2-68ba-4950-8225-127da8f088f3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
f45166c2-68ba-4950-8225-127da8f088f3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
13a1824c-90aa-4ad4-9a0e-4808f6d62f3a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Polymyositis,False,Polymyositis,,,,
f739a21d-58d0-4a86-b32f-0ade55453fe5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Polymyositis is an autoimmune disease that attacks striated muscle through a cell-mediated mechanism, but can also affect other organ systems, including the lung.",True,Polymyositis,,,,
9a1ec5fa-76bb-42ef-b4db-486186adbd23,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,There is some direct involvement with development of bronchiolitis obliterans organizing pneumonia (BOOP) and chronic interstitial pneumonitis and fibrosis. But the most frequent respiratory complications are a result of the respiratory muscles and muscles involved with swallowing becoming affected. Poor control of swallowing and inability to generate effective cough promote aspiration and retention of airway secretions. This is a recipe for bronchopneumonia—and this ends up being the most common form of death. Infection risk is often increased by the patient taking large doses of corticosteroids or immunosuppressive drugs to address the disease.,True,Polymyositis,,,,
3073c249-8bd1-4757-b567-3fc065566aec,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Summary,False,Summary,,,,
0048dc63-20ae-47d1-809e-52750ba90e67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"To summarize, the immunological responses to inhaled particles, localized immune responses, and systemic immunological disease can produce pulmonary manifestations that are generally related to acute and then chronic inflammatory responses. The distinguishing features and pulmonary manifestations are summarized in table 8.2.",True,Summary,,,,
8b4da1cb-c699-49c6-ab11-9a254af096c1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Table 8.2: Summary of immune and systemic disorders that affect the lung.,True,Summary,,,,
feb7f448-bd39-4a58-8815-a729111cc419,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,Text,False,Text,,,,
e610e448-9e17-4a1f-b07c-e4b828308df8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapters 13–14.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
c74bed75-36b6-4fa0-acb6-b2227257fd44,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
8fd5c13e-7fce-480e-8809-dd7a07063301,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
8fd5c13e-7fce-480e-8809-dd7a07063301,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
8fd5c13e-7fce-480e-8809-dd7a07063301,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
8fd5c13e-7fce-480e-8809-dd7a07063301,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
8fd5c13e-7fce-480e-8809-dd7a07063301,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-3,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
20f82048-c070-46e6-84ae-98cd919b6732,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"The lung is no different from any other organ in that it is susceptible to disorders of the immune system. One might argue that it is surprising that the lung does not encounter more problems, given the lung’s exposure to the environment and the myriad antigens it encounters. Before we start looking at a few specific disorders, let us quickly review the four mechanisms through which the immune system might disrupt lung tissue.",True,Text,,,,
8840efd5-8379-4551-8bff-187bb331ae68,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"A type 1 reaction, or immediate hypersensitivity (table 8.1), is a result of overexpression of IgE (table 8.1). When an antigen binds to the overexpressed IgE on the surface of mast cells, the cell releases histamine and leukotrienes that in turn induce an inappropriate or exaggerated inflammatory response. Allergic asthma is an example of a type 1 reaction.",True,Text,,,,
c9a52c51-f867-4bc2-851a-990961ce4bfd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,overexpression,False,overexpression,,,,
de5a0418-bb9d-4c8c-afda-1f23566168e6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"A type 2 reaction, or antibody-dependent cytotoxic reaction (table 8.1), is the result of a circulating antibody reacting with a component of a cell or tissue. The formation of this inappropriate immune complex results in the cell or tissue being flagged for attack by the immune system. Goodpasture’s syndrome is an example of a type 2 reaction.",True,overexpression,,,,
fb135fac-dc7d-4a2f-86ef-965c781e511a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"A type 3 reaction, or immune complex reaction (table 8.1), is the result of an immune complex forming either locally or circulating from elsewhere and then depositing itself in tissue; the immune complex then instigates an immune system attack that involves the tissue. Pulmonary vasculitis can be caused by type 3 immune disorders.",True,overexpression,,,,
60b8e92e-3d3d-47db-b3f7-127160ff034d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Lastly, a type 4 reaction, or cell-mediated hypersensitivity (table 8.1), is caused by a population of hypersensitive T cells whose response to an antigen is exaggerated and leads to the proliferation of that cell population and the release of lymphokines to induce an inflammatory response. While this pattern is the same as the normal response to many infections, the magnitude of the response is inappropriate and can lead to pathological changes, such as allergic alveolitis.",True,overexpression,,,,
0a04b876-e8a7-41d7-be46-b23d853f4b5f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Table 8.1: Types of immune mechanisms involved in lung tissue injury.,True,overexpression,,,,
f3ac78f0-9bed-46fd-be3d-12979fd60e12,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"With those mechanisms defined, let us look at some specific disorders.",True,overexpression,,,,
5e97ef62-ff14-45fd-a4c9-2103786bbe17,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Hypersensitivity Pneumonitis,False,Hypersensitivity Pneumonitis,,,,
9b6081d5-1b95-416d-82ec-914d6aae68f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
9b6081d5-1b95-416d-82ec-914d6aae68f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
9b6081d5-1b95-416d-82ec-914d6aae68f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
9b6081d5-1b95-416d-82ec-914d6aae68f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
9b6081d5-1b95-416d-82ec-914d6aae68f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
158ee26b-e373-4fc2-a386-418d6143296b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
158ee26b-e373-4fc2-a386-418d6143296b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
158ee26b-e373-4fc2-a386-418d6143296b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
158ee26b-e373-4fc2-a386-418d6143296b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
158ee26b-e373-4fc2-a386-418d6143296b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
0de4837a-57d7-48a9-af19-23c18ce05b8f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Clinical signs,False,Clinical signs,,,,
c4a2d478-d71b-4d9b-a7e6-caa70cf6d368,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,How hypersensitivity pneumonitis presents is somewhat dependent on the form of exposure the patient had.,True,Clinical signs,,,,
0a161a16-b907-4f64-a0dd-01abc379f7fb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"With brief but heavy exposure, an acute presentation of pneumonitis will present with fever, malaise, cough, and dyspnea. Physical exam confirms the fever and tachypnea and cyanosis can reflect the severity of the response. Bibasilar rales are often present, but unless a type 1 hypersensitivity arises then wheeze is usually absent (but you might note here that concurrent allergenic asthma is not beyond the realms of possibility). This acute form usually resolves within a couple of days, but can reoccur when the patient is exposed to the causal agent again.",True,Clinical signs,,,,
ffb041aa-c8bd-4330-8947-edb85dc71724,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"When exposure is light but prolonged, the onset of hypersensitivity pneumonitis is more insidious and clinically challenging. The patient will describe a slowly progressive cough and developing dyspnea, also weakness and weight loss. This form of onset is common with continuous exposure to organic dust. With this longer time line the patient is not usually aware of the symptom’s relation to occupation and exposure persists until diffuse pulmonary fibrosis is established. At this point the signs and symptoms are related to respiratory insufficiency.",True,Clinical signs,,,,
c829ce6f-f1a1-43d5-a662-b015d526be14,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Goodpasture’s Syndrome,False,Goodpasture’s Syndrome,,,,
863b424d-dd3d-4f29-ba85-58c521540d6c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Systemic Diseases Affecting the Lung,False,Systemic Diseases Affecting the Lung,,,,
9cb1b89b-020d-4009-8f76-15f7e34f2d75,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Systemic Lupus Erythematosus (SLE),False,Systemic Lupus Erythematosus (SLE),,,,
b57799b5-9bb9-4da9-ad28-e094ba32647c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Lupus erythematosus is a type 3 reaction. Autoantibodies are formed against cell components, particularly the nucleus and its associated proteins. The most common antibodies found are against single– or double–stranded DNA. About 70 percent of SLE patients have lung involvement that can be either acute or chronic.",True,Systemic Lupus Erythematosus (SLE),,,,
4d5ebce7-6489-4762-9d66-b4f544fc10c5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Acute SLE,False,Acute SLE,,,,
be9f0d04-6eb6-43a5-8720-8c3c2999f787,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"The acute form is referred to as lupus pneumonitis, and its signs and symptoms mimic bacterial pneumonia. It can have a rapidly progressive course with acute pleuritic chest pain and can lead to respiratory failure. The inflammation it involves can disrupt pulmonary capillaries and lead to hemorrhage. Patients with SLE are highly susceptible to infection, so diagnosis of an SLE patient should distinguish between respiratory tract infection and changes directly related to lupus. Changes in lupus come as flares followed by remission, and there are a number of triggers for flares including:",True,Acute SLE,,,,
68271364-7b72-43c0-a24a-299d123c1266,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Chronic SLE,False,Chronic SLE,,,,
2b9aff0e-298d-4628-bcf4-3c50f278345b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
2b9aff0e-298d-4628-bcf4-3c50f278345b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
2b9aff0e-298d-4628-bcf4-3c50f278345b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
2b9aff0e-298d-4628-bcf4-3c50f278345b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
2b9aff0e-298d-4628-bcf4-3c50f278345b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
0df04f96-cb4e-4e08-b338-1fd87383e1be,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Rheumatoid Disease,False,Rheumatoid Disease,,,,
076a564e-7fa3-451b-911e-0b79e0982013,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"More famous for its effect on the joints, rheumatoid disease can also affect the lungs and pleura. Rheumatoid factors that generate rheumatoid disease continue to be investigated, but in brief, they are antibodies generated against gamma globulins. Pleural and pulmonary lesions are probably the result of local immune complex–mediated reactions associated with high levels of circulating rheumatoid factors.",True,Rheumatoid Disease,,,,
460b13a3-ee07-4aeb-a5c0-be873b1f8ee1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
460b13a3-ee07-4aeb-a5c0-be873b1f8ee1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
460b13a3-ee07-4aeb-a5c0-be873b1f8ee1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
460b13a3-ee07-4aeb-a5c0-be873b1f8ee1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
460b13a3-ee07-4aeb-a5c0-be873b1f8ee1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
d629e75c-477b-4285-bef6-2a4f2b55e49a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
d629e75c-477b-4285-bef6-2a4f2b55e49a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
d629e75c-477b-4285-bef6-2a4f2b55e49a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
d629e75c-477b-4285-bef6-2a4f2b55e49a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
d629e75c-477b-4285-bef6-2a4f2b55e49a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
febe7c9d-61fd-464f-ab78-a1b45eca613b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"It should be noted here that some drugs used to treat difficult rheumatoid arthritis, such as gold preparations, methotrexate, and penicillamine, are toxic to the lung and can produce their own pulmonary lesions.",True,Rheumatoid Disease,,,,
c0f06096-7aa6-4484-86c0-467b13bf8f7d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Progressive Systemic Sclerosis,False,Progressive Systemic Sclerosis,,,,
3674e159-7108-42d4-b953-27976e452e26,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Also known as scleroderma, progressive systemic sclerosis primarily affects the blood vessels and connective tissue and likely has an autoimmune mechanism. The result is dysregulation of fibroblasts and uncontrolled collagen formation. The disease can affect many organs and tissues, and pulmonary manifestations are common.",True,Progressive Systemic Sclerosis,,,,
8c3f3bcf-089b-4f17-bfce-7db98c404de4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"The most common pulmonary findings are interstitial fibrosis, bronchiolar dilation, and pleural fibrosis, as well as the vascular changes that are seen in other organs. These changes produce dyspnea, cough, and basilar rales. The vascular changes can produce pulmonary hypertension that may lead to cor pulmonale.",True,Progressive Systemic Sclerosis,,,,
575f2258-2044-48d6-ade2-9c79b14c3a32,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
575f2258-2044-48d6-ade2-9c79b14c3a32,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
575f2258-2044-48d6-ade2-9c79b14c3a32,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
575f2258-2044-48d6-ade2-9c79b14c3a32,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
575f2258-2044-48d6-ade2-9c79b14c3a32,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
720ffa12-49f0-4d54-b0ca-3d9e5ea59934,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Polymyositis,False,Polymyositis,,,,
897cd928-85cd-4cab-b5aa-19a61ecd8840,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Polymyositis is an autoimmune disease that attacks striated muscle through a cell-mediated mechanism, but can also affect other organ systems, including the lung.",True,Polymyositis,,,,
7ad559c5-12b7-4b87-8925-17203e89ce19,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,There is some direct involvement with development of bronchiolitis obliterans organizing pneumonia (BOOP) and chronic interstitial pneumonitis and fibrosis. But the most frequent respiratory complications are a result of the respiratory muscles and muscles involved with swallowing becoming affected. Poor control of swallowing and inability to generate effective cough promote aspiration and retention of airway secretions. This is a recipe for bronchopneumonia—and this ends up being the most common form of death. Infection risk is often increased by the patient taking large doses of corticosteroids or immunosuppressive drugs to address the disease.,True,Polymyositis,,,,
913282ff-b0a1-4705-904a-70675811c9ad,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Summary,False,Summary,,,,
66877aa0-0a4c-49ed-b605-d9db5a888e3e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"To summarize, the immunological responses to inhaled particles, localized immune responses, and systemic immunological disease can produce pulmonary manifestations that are generally related to acute and then chronic inflammatory responses. The distinguishing features and pulmonary manifestations are summarized in table 8.2.",True,Summary,,,,
3d907671-a457-43fa-ab94-93ce2ddeb0ee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Table 8.2: Summary of immune and systemic disorders that affect the lung.,True,Summary,,,,
1e5204a9-c240-4e1d-a492-4e3dc66f483e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,Text,False,Text,,,,
de8a7e9c-88bc-46db-9da2-dd574da2766f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapters 13–14.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
1b585647-1c2a-4c04-be1e-6cbeb1c8b219,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
db5c056c-93ce-4f5a-8d2b-82896a8fdd83,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
db5c056c-93ce-4f5a-8d2b-82896a8fdd83,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
db5c056c-93ce-4f5a-8d2b-82896a8fdd83,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
db5c056c-93ce-4f5a-8d2b-82896a8fdd83,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
db5c056c-93ce-4f5a-8d2b-82896a8fdd83,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-2,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
2d7ed15f-b002-4b92-9043-3bd4b042f08b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"The lung is no different from any other organ in that it is susceptible to disorders of the immune system. One might argue that it is surprising that the lung does not encounter more problems, given the lung’s exposure to the environment and the myriad antigens it encounters. Before we start looking at a few specific disorders, let us quickly review the four mechanisms through which the immune system might disrupt lung tissue.",True,Text,,,,
29ef0e7b-6f5b-4d35-9af2-ab2dc3df0e3b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"A type 1 reaction, or immediate hypersensitivity (table 8.1), is a result of overexpression of IgE (table 8.1). When an antigen binds to the overexpressed IgE on the surface of mast cells, the cell releases histamine and leukotrienes that in turn induce an inappropriate or exaggerated inflammatory response. Allergic asthma is an example of a type 1 reaction.",True,Text,,,,
0b281461-6044-4a2d-b454-bd511c635a0d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,overexpression,False,overexpression,,,,
d1f8393a-52d1-4c87-ad54-919edcb5ff9a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"A type 2 reaction, or antibody-dependent cytotoxic reaction (table 8.1), is the result of a circulating antibody reacting with a component of a cell or tissue. The formation of this inappropriate immune complex results in the cell or tissue being flagged for attack by the immune system. Goodpasture’s syndrome is an example of a type 2 reaction.",True,overexpression,,,,
b523a6c0-9df9-402c-aedc-bea73f81d2c5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"A type 3 reaction, or immune complex reaction (table 8.1), is the result of an immune complex forming either locally or circulating from elsewhere and then depositing itself in tissue; the immune complex then instigates an immune system attack that involves the tissue. Pulmonary vasculitis can be caused by type 3 immune disorders.",True,overexpression,,,,
6fb18c2e-1d5a-4c86-8f9a-ecb62429318d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Lastly, a type 4 reaction, or cell-mediated hypersensitivity (table 8.1), is caused by a population of hypersensitive T cells whose response to an antigen is exaggerated and leads to the proliferation of that cell population and the release of lymphokines to induce an inflammatory response. While this pattern is the same as the normal response to many infections, the magnitude of the response is inappropriate and can lead to pathological changes, such as allergic alveolitis.",True,overexpression,,,,
a9d7f28d-4a84-4495-8503-7571e1bef029,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Table 8.1: Types of immune mechanisms involved in lung tissue injury.,True,overexpression,,,,
8777df5c-21c5-47b1-a8ee-038af28c4a9c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"With those mechanisms defined, let us look at some specific disorders.",True,overexpression,,,,
0689872b-9c85-40ec-ada6-57623bbbfe9c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Hypersensitivity Pneumonitis,False,Hypersensitivity Pneumonitis,,,,
5507d2b4-22e2-4303-97ec-3768b9a24ebd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
5507d2b4-22e2-4303-97ec-3768b9a24ebd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
5507d2b4-22e2-4303-97ec-3768b9a24ebd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
5507d2b4-22e2-4303-97ec-3768b9a24ebd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
5507d2b4-22e2-4303-97ec-3768b9a24ebd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
8bb1c47e-2dad-46c2-b6d5-74a638754815,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
8bb1c47e-2dad-46c2-b6d5-74a638754815,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
8bb1c47e-2dad-46c2-b6d5-74a638754815,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
8bb1c47e-2dad-46c2-b6d5-74a638754815,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
8bb1c47e-2dad-46c2-b6d5-74a638754815,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
fbb80f8e-103f-484a-a193-1f0581196df0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Clinical signs,False,Clinical signs,,,,
0fe8c33f-b025-44ac-be17-7a1dd12f4ad9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,How hypersensitivity pneumonitis presents is somewhat dependent on the form of exposure the patient had.,True,Clinical signs,,,,
458dbf92-5d05-47a8-bc91-90727f1bc9d1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"With brief but heavy exposure, an acute presentation of pneumonitis will present with fever, malaise, cough, and dyspnea. Physical exam confirms the fever and tachypnea and cyanosis can reflect the severity of the response. Bibasilar rales are often present, but unless a type 1 hypersensitivity arises then wheeze is usually absent (but you might note here that concurrent allergenic asthma is not beyond the realms of possibility). This acute form usually resolves within a couple of days, but can reoccur when the patient is exposed to the causal agent again.",True,Clinical signs,,,,
53211beb-83ae-4f26-8b17-aa499b54375b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"When exposure is light but prolonged, the onset of hypersensitivity pneumonitis is more insidious and clinically challenging. The patient will describe a slowly progressive cough and developing dyspnea, also weakness and weight loss. This form of onset is common with continuous exposure to organic dust. With this longer time line the patient is not usually aware of the symptom’s relation to occupation and exposure persists until diffuse pulmonary fibrosis is established. At this point the signs and symptoms are related to respiratory insufficiency.",True,Clinical signs,,,,
bfeb0912-f574-4b7c-9540-c1e89218b74b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Goodpasture’s Syndrome,False,Goodpasture’s Syndrome,,,,
94ef95c5-8625-4a01-9377-bfbc01bd5bbe,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Systemic Diseases Affecting the Lung,False,Systemic Diseases Affecting the Lung,,,,
1a77b398-de9f-4665-aed8-64ef0a1f3829,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Systemic Lupus Erythematosus (SLE),False,Systemic Lupus Erythematosus (SLE),,,,
9687e61a-e1d8-4e9f-8920-9e54b85e19f0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Lupus erythematosus is a type 3 reaction. Autoantibodies are formed against cell components, particularly the nucleus and its associated proteins. The most common antibodies found are against single– or double–stranded DNA. About 70 percent of SLE patients have lung involvement that can be either acute or chronic.",True,Systemic Lupus Erythematosus (SLE),,,,
dcd0f7f1-a7cb-4cab-8d0a-c3a50d481485,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Acute SLE,False,Acute SLE,,,,
e210a8e9-8290-49b7-9642-4353d80f8513,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"The acute form is referred to as lupus pneumonitis, and its signs and symptoms mimic bacterial pneumonia. It can have a rapidly progressive course with acute pleuritic chest pain and can lead to respiratory failure. The inflammation it involves can disrupt pulmonary capillaries and lead to hemorrhage. Patients with SLE are highly susceptible to infection, so diagnosis of an SLE patient should distinguish between respiratory tract infection and changes directly related to lupus. Changes in lupus come as flares followed by remission, and there are a number of triggers for flares including:",True,Acute SLE,,,,
df5b2c72-7db7-4cfe-9e51-839978961085,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Chronic SLE,False,Chronic SLE,,,,
f89715ce-3320-4303-a32b-889701277a83,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
f89715ce-3320-4303-a32b-889701277a83,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
f89715ce-3320-4303-a32b-889701277a83,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
f89715ce-3320-4303-a32b-889701277a83,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
f89715ce-3320-4303-a32b-889701277a83,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
8cd4250d-b001-42df-a851-7c7b17765c44,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Rheumatoid Disease,False,Rheumatoid Disease,,,,
84b2f58c-f002-49af-bad8-6a1b7b0ed5c7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"More famous for its effect on the joints, rheumatoid disease can also affect the lungs and pleura. Rheumatoid factors that generate rheumatoid disease continue to be investigated, but in brief, they are antibodies generated against gamma globulins. Pleural and pulmonary lesions are probably the result of local immune complex–mediated reactions associated with high levels of circulating rheumatoid factors.",True,Rheumatoid Disease,,,,
2a29d633-28e4-49d4-bf52-af9b46bfa576,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
2a29d633-28e4-49d4-bf52-af9b46bfa576,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
2a29d633-28e4-49d4-bf52-af9b46bfa576,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
2a29d633-28e4-49d4-bf52-af9b46bfa576,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
2a29d633-28e4-49d4-bf52-af9b46bfa576,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
06ac20e4-8f53-42a2-a3e4-2f7ad65ce726,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
06ac20e4-8f53-42a2-a3e4-2f7ad65ce726,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
06ac20e4-8f53-42a2-a3e4-2f7ad65ce726,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
06ac20e4-8f53-42a2-a3e4-2f7ad65ce726,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
06ac20e4-8f53-42a2-a3e4-2f7ad65ce726,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
724d85ac-5dfa-4adc-bbd6-076e12386c09,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"It should be noted here that some drugs used to treat difficult rheumatoid arthritis, such as gold preparations, methotrexate, and penicillamine, are toxic to the lung and can produce their own pulmonary lesions.",True,Rheumatoid Disease,,,,
0cdfd236-f97a-4bb5-b8d8-3a00b05990bd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Progressive Systemic Sclerosis,False,Progressive Systemic Sclerosis,,,,
b0d4ae08-32c1-4375-8191-8f244908c793,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Also known as scleroderma, progressive systemic sclerosis primarily affects the blood vessels and connective tissue and likely has an autoimmune mechanism. The result is dysregulation of fibroblasts and uncontrolled collagen formation. The disease can affect many organs and tissues, and pulmonary manifestations are common.",True,Progressive Systemic Sclerosis,,,,
1e021861-5180-4928-bcdd-1d855553e7ed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"The most common pulmonary findings are interstitial fibrosis, bronchiolar dilation, and pleural fibrosis, as well as the vascular changes that are seen in other organs. These changes produce dyspnea, cough, and basilar rales. The vascular changes can produce pulmonary hypertension that may lead to cor pulmonale.",True,Progressive Systemic Sclerosis,,,,
b8abdd0a-c6a3-462c-a2bd-d6483247053f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
b8abdd0a-c6a3-462c-a2bd-d6483247053f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
b8abdd0a-c6a3-462c-a2bd-d6483247053f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
b8abdd0a-c6a3-462c-a2bd-d6483247053f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
b8abdd0a-c6a3-462c-a2bd-d6483247053f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
b9d3bed9-9019-4f9f-bd4d-7ffe53c75209,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Polymyositis,False,Polymyositis,,,,
40f782e6-619e-4512-8dd2-d77cdd4f1f0c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Polymyositis is an autoimmune disease that attacks striated muscle through a cell-mediated mechanism, but can also affect other organ systems, including the lung.",True,Polymyositis,,,,
3064599a-f9a2-4af3-981e-8f66c68caa52,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,There is some direct involvement with development of bronchiolitis obliterans organizing pneumonia (BOOP) and chronic interstitial pneumonitis and fibrosis. But the most frequent respiratory complications are a result of the respiratory muscles and muscles involved with swallowing becoming affected. Poor control of swallowing and inability to generate effective cough promote aspiration and retention of airway secretions. This is a recipe for bronchopneumonia—and this ends up being the most common form of death. Infection risk is often increased by the patient taking large doses of corticosteroids or immunosuppressive drugs to address the disease.,True,Polymyositis,,,,
449d6db5-07f5-4385-b83a-e462ebb33132,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Summary,False,Summary,,,,
506071eb-6bd9-41da-8a4d-55a934b02f4e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"To summarize, the immunological responses to inhaled particles, localized immune responses, and systemic immunological disease can produce pulmonary manifestations that are generally related to acute and then chronic inflammatory responses. The distinguishing features and pulmonary manifestations are summarized in table 8.2.",True,Summary,,,,
8c5cd1b6-62a0-4345-be86-257d7f62aa54,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Table 8.2: Summary of immune and systemic disorders that affect the lung.,True,Summary,,,,
7ecf4e8f-afec-4ac8-9d39-f5c97d981660,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,Text,False,Text,,,,
527b4692-fed6-4ee3-a05e-3ad17b8da0d9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapters 13–14.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
6a58da6c-5c86-4d92-ad09-0b9723caca7a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
fe275498-4810-43c2-8f42-ea5973e60722,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
fe275498-4810-43c2-8f42-ea5973e60722,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
fe275498-4810-43c2-8f42-ea5973e60722,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
fe275498-4810-43c2-8f42-ea5973e60722,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
fe275498-4810-43c2-8f42-ea5973e60722,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/#chapter-39-section-1,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
67402f87-6d85-4bb2-b678-f8a5b61fe326,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"The lung is no different from any other organ in that it is susceptible to disorders of the immune system. One might argue that it is surprising that the lung does not encounter more problems, given the lung’s exposure to the environment and the myriad antigens it encounters. Before we start looking at a few specific disorders, let us quickly review the four mechanisms through which the immune system might disrupt lung tissue.",True,Text,,,,
f21874cd-2529-4ba6-b4d0-df0ddf7beb34,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"A type 1 reaction, or immediate hypersensitivity (table 8.1), is a result of overexpression of IgE (table 8.1). When an antigen binds to the overexpressed IgE on the surface of mast cells, the cell releases histamine and leukotrienes that in turn induce an inappropriate or exaggerated inflammatory response. Allergic asthma is an example of a type 1 reaction.",True,Text,,,,
e55b3aa7-ce84-46c1-a88b-8671f0d1f24a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,overexpression,False,overexpression,,,,
a2a99c01-3dca-4e42-a1c4-e7d3e4426d75,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"A type 2 reaction, or antibody-dependent cytotoxic reaction (table 8.1), is the result of a circulating antibody reacting with a component of a cell or tissue. The formation of this inappropriate immune complex results in the cell or tissue being flagged for attack by the immune system. Goodpasture’s syndrome is an example of a type 2 reaction.",True,overexpression,,,,
18a6b529-efc2-44b6-8990-ce4e97ec4892,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"A type 3 reaction, or immune complex reaction (table 8.1), is the result of an immune complex forming either locally or circulating from elsewhere and then depositing itself in tissue; the immune complex then instigates an immune system attack that involves the tissue. Pulmonary vasculitis can be caused by type 3 immune disorders.",True,overexpression,,,,
951aac0d-6825-488d-85fc-8b2338476d1b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Lastly, a type 4 reaction, or cell-mediated hypersensitivity (table 8.1), is caused by a population of hypersensitive T cells whose response to an antigen is exaggerated and leads to the proliferation of that cell population and the release of lymphokines to induce an inflammatory response. While this pattern is the same as the normal response to many infections, the magnitude of the response is inappropriate and can lead to pathological changes, such as allergic alveolitis.",True,overexpression,,,,
e8b42c29-a68c-4be8-9947-59667eba76ec,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Table 8.1: Types of immune mechanisms involved in lung tissue injury.,True,overexpression,,,,
2b40c73c-1aa0-44fe-8581-0d8352b09f4c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"With those mechanisms defined, let us look at some specific disorders.",True,overexpression,,,,
2644ae75-2011-4d4f-b554-6270975f35cf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Hypersensitivity Pneumonitis,False,Hypersensitivity Pneumonitis,,,,
089ac754-fa75-45a3-a1fd-6950d7265866,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
089ac754-fa75-45a3-a1fd-6950d7265866,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
089ac754-fa75-45a3-a1fd-6950d7265866,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
089ac754-fa75-45a3-a1fd-6950d7265866,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
089ac754-fa75-45a3-a1fd-6950d7265866,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"In the acute phase, lymphocytes and macrophages infiltrate the alveolar walls and loose granulomas can form. The presence of multi-nucleated giant cells (figure 8.2), are helpful in diagnosis, but more typical is a dramatic rise in lymphocyte count in BAL fluid, particularly CD8+ cells.",True,Hypersensitivity Pneumonitis,Figure 8.2,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.2.png,Figure 8.2: Chronic phase of hypersensitivity pneumonitis with established fibrosis.
e93afe82-ed49-4091-94e5-15ad5465d044,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
e93afe82-ed49-4091-94e5-15ad5465d044,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
e93afe82-ed49-4091-94e5-15ad5465d044,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
e93afe82-ed49-4091-94e5-15ad5465d044,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
e93afe82-ed49-4091-94e5-15ad5465d044,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"In the subacute phase there is evidence of interstitial thickening and the onset of fibrosis can be seen. Involvement of the bronchioles is seen with evidence of chronic bronchiolitis. The chronic form is marked by significant fibrosis (figure 8.3), to the extent it is indistinguishable from pulmonary fibrosis with distinctive fibrotic patterns and all the hallmarks of restrictive lung disease.",True,Hypersensitivity Pneumonitis,Figure 8.3,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.3.jpeg,Figure 8.3: Patchy airspace consolidation associated with Goodpasture’s syndrome.
49c7ea83-c392-4400-a58a-e600494800b6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Clinical signs,False,Clinical signs,,,,
ad1f1d3a-a82c-4fd1-928a-e0f008ddc251,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,How hypersensitivity pneumonitis presents is somewhat dependent on the form of exposure the patient had.,True,Clinical signs,,,,
e6af496b-1a94-4378-98f3-9881c5910f90,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"With brief but heavy exposure, an acute presentation of pneumonitis will present with fever, malaise, cough, and dyspnea. Physical exam confirms the fever and tachypnea and cyanosis can reflect the severity of the response. Bibasilar rales are often present, but unless a type 1 hypersensitivity arises then wheeze is usually absent (but you might note here that concurrent allergenic asthma is not beyond the realms of possibility). This acute form usually resolves within a couple of days, but can reoccur when the patient is exposed to the causal agent again.",True,Clinical signs,,,,
fbf14dfb-93d3-4ae5-9053-5e7a5021cc34,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"When exposure is light but prolonged, the onset of hypersensitivity pneumonitis is more insidious and clinically challenging. The patient will describe a slowly progressive cough and developing dyspnea, also weakness and weight loss. This form of onset is common with continuous exposure to organic dust. With this longer time line the patient is not usually aware of the symptom’s relation to occupation and exposure persists until diffuse pulmonary fibrosis is established. At this point the signs and symptoms are related to respiratory insufficiency.",True,Clinical signs,,,,
075c0eac-86ae-430c-9d08-c53008e663dc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Goodpasture’s Syndrome,False,Goodpasture’s Syndrome,,,,
7373c3fc-1b30-49b6-a90a-ecc5f80beda2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Systemic Diseases Affecting the Lung,False,Systemic Diseases Affecting the Lung,,,,
d8ff2de4-1562-48c3-9f6b-fe11d788c590,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Systemic Lupus Erythematosus (SLE),False,Systemic Lupus Erythematosus (SLE),,,,
2d2db0f4-2351-4211-905e-24123d3a602f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Lupus erythematosus is a type 3 reaction. Autoantibodies are formed against cell components, particularly the nucleus and its associated proteins. The most common antibodies found are against single– or double–stranded DNA. About 70 percent of SLE patients have lung involvement that can be either acute or chronic.",True,Systemic Lupus Erythematosus (SLE),,,,
60b5ca50-6cc5-4f15-9d22-cd618621d223,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Acute SLE,False,Acute SLE,,,,
cb38473f-fe20-4aa4-8b15-8974a67ee620,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"The acute form is referred to as lupus pneumonitis, and its signs and symptoms mimic bacterial pneumonia. It can have a rapidly progressive course with acute pleuritic chest pain and can lead to respiratory failure. The inflammation it involves can disrupt pulmonary capillaries and lead to hemorrhage. Patients with SLE are highly susceptible to infection, so diagnosis of an SLE patient should distinguish between respiratory tract infection and changes directly related to lupus. Changes in lupus come as flares followed by remission, and there are a number of triggers for flares including:",True,Acute SLE,,,,
f3abd725-8750-423d-b248-4af57b2070fd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Chronic SLE,False,Chronic SLE,,,,
f8076864-37a8-4114-bab8-ce667322326b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
f8076864-37a8-4114-bab8-ce667322326b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
f8076864-37a8-4114-bab8-ce667322326b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
f8076864-37a8-4114-bab8-ce667322326b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
f8076864-37a8-4114-bab8-ce667322326b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"The chronic form can progress insidiously with no symptoms or physical findings, and so it frequently it goes unrecognized until later stages of the disease. The later stages are marked with the appearance of progressive fibrosis. This is evident in the chest x-rays in figure 8.4 showing the appearance of diffuse fibrosis over a twenty-month period in a young SLE patient. The fibrosis produces reduced lung volumes and basilar atelectasis may also occur. The increased recoil of the lung can also produce an elevated and weakened diaphragm. There may also be pleural involvement with effusions arising that are normally bilateral and small.",True,Chronic SLE,Figure 8.4,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
d63d0773-0ab6-42c1-afb3-934cb1a853c6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Rheumatoid Disease,False,Rheumatoid Disease,,,,
97dd2c60-4e2f-40d9-b62d-0a829fb487da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"More famous for its effect on the joints, rheumatoid disease can also affect the lungs and pleura. Rheumatoid factors that generate rheumatoid disease continue to be investigated, but in brief, they are antibodies generated against gamma globulins. Pleural and pulmonary lesions are probably the result of local immune complex–mediated reactions associated with high levels of circulating rheumatoid factors.",True,Rheumatoid Disease,,,,
ed67bd6d-82f4-4a75-a8b9-bfda51aad307,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
ed67bd6d-82f4-4a75-a8b9-bfda51aad307,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
ed67bd6d-82f4-4a75-a8b9-bfda51aad307,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
ed67bd6d-82f4-4a75-a8b9-bfda51aad307,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
ed67bd6d-82f4-4a75-a8b9-bfda51aad307,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Up to 50 percent of rheumatoid patients show pulmonary or pleural manifestations, with pleural involvement being more common and most frequently manifested as pleural effusion (figure 8.5). The effusate tends to have low glucose, and this finding is useful for diagnosis. Pleural and pulmonary manifestations of rheumatoid disease are more common in male patients.",True,Rheumatoid Disease,Figure 8.5,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
91b19f77-c42d-4e27-b528-b8be06e81d58,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
91b19f77-c42d-4e27-b528-b8be06e81d58,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
91b19f77-c42d-4e27-b528-b8be06e81d58,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
91b19f77-c42d-4e27-b528-b8be06e81d58,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
91b19f77-c42d-4e27-b528-b8be06e81d58,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Pulmonary involvement shows as either diffuse or nodular lesions (figure 8.6). The diffuse lesions are similar to those seen in idiopathic pulmonary fibrosis. The nodular lesions are variable in size and number and usually do not cause symptoms. They are known as necrobiotic nodules and are capable of cavitating. Bronchiolitis obliterans organizing pneumonia and bronchiectasis have also been seen in rheumatoid disease.,True,Rheumatoid Disease,Figure 8.6,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.6.jpg,Figure 8.6: A nodular lesion (arrow) associated with rheumatoid disease.
5859458b-e18a-4539-b3b3-4a887893c9ec,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"It should be noted here that some drugs used to treat difficult rheumatoid arthritis, such as gold preparations, methotrexate, and penicillamine, are toxic to the lung and can produce their own pulmonary lesions.",True,Rheumatoid Disease,,,,
16872369-f896-486a-bb4f-125c258aad1b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Progressive Systemic Sclerosis,False,Progressive Systemic Sclerosis,,,,
08f79fc8-ebf6-4a6b-84cf-11a4471dd4c9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Also known as scleroderma, progressive systemic sclerosis primarily affects the blood vessels and connective tissue and likely has an autoimmune mechanism. The result is dysregulation of fibroblasts and uncontrolled collagen formation. The disease can affect many organs and tissues, and pulmonary manifestations are common.",True,Progressive Systemic Sclerosis,,,,
4770442e-a326-47d3-a3e4-87b6d626cfc8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"The most common pulmonary findings are interstitial fibrosis, bronchiolar dilation, and pleural fibrosis, as well as the vascular changes that are seen in other organs. These changes produce dyspnea, cough, and basilar rales. The vascular changes can produce pulmonary hypertension that may lead to cor pulmonale.",True,Progressive Systemic Sclerosis,,,,
02189255-be20-467c-92cd-59b284aa5e46,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
02189255-be20-467c-92cd-59b284aa5e46,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
02189255-be20-467c-92cd-59b284aa5e46,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
02189255-be20-467c-92cd-59b284aa5e46,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
02189255-be20-467c-92cd-59b284aa5e46,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"The radiographic findings are similar to pulmonary fibrosis with the early stage of the disease showing fine reticular patterning that progresses to honeycombing in the late stage of the disease (figure 8.7). These changes are mostly found in the lower lung fields. As you might expect, the disease has restrictive characteristics along with diffusion abnormalities that produce hypoxemia during exercise.",True,Progressive Systemic Sclerosis,Figure 8.7,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.7.png,Figure 8.7: Fine reticular fibrosis in lower lung fields (upper CT image) progressing to honeycombing (lower CT image).
2a93137c-1a67-4d0d-8531-c0c3b5c1e45c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Polymyositis,False,Polymyositis,,,,
cdcb0ead-4167-41a6-aad3-f53cb42aa475,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Polymyositis is an autoimmune disease that attacks striated muscle through a cell-mediated mechanism, but can also affect other organ systems, including the lung.",True,Polymyositis,,,,
05b84cde-672f-4141-ba18-41a34b9a9eae,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,There is some direct involvement with development of bronchiolitis obliterans organizing pneumonia (BOOP) and chronic interstitial pneumonitis and fibrosis. But the most frequent respiratory complications are a result of the respiratory muscles and muscles involved with swallowing becoming affected. Poor control of swallowing and inability to generate effective cough promote aspiration and retention of airway secretions. This is a recipe for bronchopneumonia—and this ends up being the most common form of death. Infection risk is often increased by the patient taking large doses of corticosteroids or immunosuppressive drugs to address the disease.,True,Polymyositis,,,,
3fcb1324-44d9-4bc6-a51c-44080715fa00,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Summary,False,Summary,,,,
1173c116-6ede-4700-85d7-63ffc19c9e83,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"To summarize, the immunological responses to inhaled particles, localized immune responses, and systemic immunological disease can produce pulmonary manifestations that are generally related to acute and then chronic inflammatory responses. The distinguishing features and pulmonary manifestations are summarized in table 8.2.",True,Summary,,,,
cbc9153c-a588-47b9-8550-9a3432b5133b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Table 8.2: Summary of immune and systemic disorders that affect the lung.,True,Summary,,,,
05de69da-6f6f-4aa4-b556-cdc95d11f1a9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,Text,False,Text,,,,
80ca904c-c4a1-47a2-8306-6be17009950a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapters 13–14.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
a8218eee-d0fd-434d-aae3-b500888c3c9d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
0f262f0f-79f9-4a09-a294-120ca337a99c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
0f262f0f-79f9-4a09-a294-120ca337a99c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Systemic Diseases Affecting the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
0f262f0f-79f9-4a09-a294-120ca337a99c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Goodpasture’s Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
0f262f0f-79f9-4a09-a294-120ca337a99c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,Hypersensitivity Pneumonitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
0f262f0f-79f9-4a09-a294-120ca337a99c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/immunological-diseases-of-the-lung/,"Table 8.1: Types of immune mechanisms involved in lung tissue injury. Includes Immune mechanism – type 1 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 2 by Kindred Grey from Internet archive (CC BY 4.0), Immune mechanism – type 3 by Kindred Grey from Internet archive (CC BY 4.0), and Immune mechanism – type 4 by Kindred Grey from Internet archive (CC BY 4.0).Figure 8.1: Acute phase of hypersensitivity pneumonitis. Mutleysmith. 2012. CC BY-SA 3.0. From WikimediaCommons.",True,Text,Figure 8.1,8. Immunological Diseases of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.1-scaled.jpeg,"Figure 8.1: Acute phase of hypersensitivity pneumonitis. Note presence of giant cells in the alveolar septum on the center, right-hand side of field of view."
135b6718-449f-4a77-b8d5-731b7a7b5b9c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"About 90 percent of PEs are caused by deep vein thrombi, but at least one of three main predisposing factors (Virchow’s triad) are present in a case of PE:",True,Text,,,,
aef45487-2615-4be4-a797-d111df99f816,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,PEs,False,PEs,,,,
128585f5-b225-4d9f-9d7e-0936c134ceaf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,Abnormal vessel walls: Damage to the inner wall of veins causes adherence of blood platelets and activation of clotting factors. Similarly inflammation or trauma of the vein or surrounding area can lead to a risk of local clotting.,True,PEs,,,,
55e13d6c-43b2-49b5-b0d3-5960b0cf3b6d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"Venous stasis: Venous stasis appears to be the most important factor in thrombus formation, and cases of PE are often preceded by periods of immobility (top tip: a USMLE question with a long-haul flight in the stem should raise the PE flag). But other causes of disrupted venous blood flow can elevate the risk.",True,PEs,,,,
0505343e-efa3-4401-8511-7e73ec43f5b9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,USMLE,False,USMLE,,,,
1bd5b401-9a57-4794-9b36-57eae7a373c0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"Hypercoagulability: Any condition that increases coagulability elevates the risk of PE, and most are due to trauma of some form or another or an elevated inflammatory state such as cancer or the postsurgery state. Birth control pills predispose the patient to thromboembolic disease so thereby also increase the risk of PE.",True,USMLE,,,,
d27d2d5c-e52c-4fe9-8300-893c2131ccb1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,Pathophysiology of PE,False,Pathophysiology of PE,,,,
6a3a9432-5ad0-4334-a824-8d3ad6ddd2f8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"The pathophysiology and clinical severity of PE depend on the number and size of the emboli, so clinical manifestations can be highly variable. In fact, PE is suspected to be much more common than previously thought because of improved detection techniques revealing more small and asymptomatic cases.",True,Pathophysiology of PE,,,,
4d0d3628-5138-4854-a44d-ba58dcd8838c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"Small emboli that can travel further into the vasculature may cause occlusion of relatively small areas of the lung, but with these areas receiving no perfusion and still being ventilated V/Q becomes inappropriately high. Not being able to pass the occlusion, blood will be diverted to other areas of the lung, and consequently cause them to be overperfused, lowering V/Q.",True,Pathophysiology of PE,,,,
d640376a-ecdb-4c83-8343-613efd368b53,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"Depending on the size and number of emboli, these V/Q mismatches can produce a widening alveolar–arterial PO2 difference and lead to hypoxemia.",True,Pathophysiology of PE,,,,
6a590143-e548-4a81-9811-77266509fd09,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,Clinical Signs of PE,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
6a590143-e548-4a81-9811-77266509fd09,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,Pathophysiology of PE,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
6a590143-e548-4a81-9811-77266509fd09,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
6a590143-e548-4a81-9811-77266509fd09,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
b6c06c73-33d6-4676-a8a9-9d5c8ec1bf3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"Pulmonary infarction, however, is rare, occurring in only 10 percent of PE cases. The lung tissue is supplied by the bronchial circulation so can usually survive the embolism in the pulmonary circulation unless there is preexisting cardiac disease.",True,Pathophysiology of PE,,,,
c67c20a9-6db0-4f5e-9ac3-41b7a49866de,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,Clinical Signs of PE,False,Clinical Signs of PE,,,,
d0ce662e-8d5d-405f-8e7d-b7f8d24379a4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"The clinical manifestations of PE vary widely, from asymptomatic when emboli are small or few, to sudden death when they are large or numerous.",True,Clinical Signs of PE,,,,
b6c9dbed-4067-4944-a3a9-3f53dbf12971,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"Signs of DVT may precede PE cases, such as leg pain, venous swelling, or warm skin over the thrombus site, but these are present in less than half of patients. Once instigated, the presenting symptom of PE is usually dyspnea but can also include chest pain. There can be clinical clues in the dyspnea as it has a rapid onset and is disproportionate to any initial clinical findings. The nature of its onset also tends to generate significant anxiety. Chest pain can start as anginal but then become more pleuritic.",True,Clinical Signs of PE,,,,
a83aa3ad-12e5-42ec-88f7-9ec3557150fe,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"Hemoptysis is less common but an important symptom. In severe cases involving massive PE tachypnea, tachycardia and cyanosis are usually present.",True,Clinical Signs of PE,,,,
c57159d5-62f7-43e4-8af9-290d57a70f62,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"Because of the mechanical and metabolic strain on the heart, cardiac manifestations, including arrhythmia, acute cor pulmonale, or signs of cardiac failure or shock, may be detected with an increased difference between alveolar and arterial PO2s.",True,Clinical Signs of PE,,,,
1893bfc2-8422-4729-a3ed-19ebc7de8e7d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"The chest x-ray will appear normal, unless there are complications such as pleural effusion, atelectasis, or pulmonary infarction. CT angiography is used to detect the presence of a PE when suspicion is high. When suspicion is lower, labs will include a D-dimer test (a protein fragment produced by a dissolving clot), which, if negative, can help rule out the presence of a PE, but if positive would require further investigation (e.g., CT angiography) for confirmation.",True,Clinical Signs of PE,,,,
7ea8cb48-2a09-42c4-a0ac-299c32c58b60,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,Text,False,Text,,,,
682f75a3-5287-4893-b258-f8c47679450f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 21.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
e7d61d76-6502-4961-ba1a-2ff1d43c325c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
99ef9463-cb8b-4725-b750-3a5bfddf0607,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-3,"West, John B. “Chapter 6: Vascular Diseases.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Text,,,,
08b0c6ff-b81a-458d-b890-f5c99ae67ca4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"About 90 percent of PEs are caused by deep vein thrombi, but at least one of three main predisposing factors (Virchow’s triad) are present in a case of PE:",True,Text,,,,
01ffa567-50c7-44e2-827d-fcb6d100fb5e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,PEs,False,PEs,,,,
3bfa5c95-e7d5-408c-bd0c-e7c3fba4414c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,Abnormal vessel walls: Damage to the inner wall of veins causes adherence of blood platelets and activation of clotting factors. Similarly inflammation or trauma of the vein or surrounding area can lead to a risk of local clotting.,True,PEs,,,,
7503120b-eb1c-4cf9-8970-573de3f93bf8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"Venous stasis: Venous stasis appears to be the most important factor in thrombus formation, and cases of PE are often preceded by periods of immobility (top tip: a USMLE question with a long-haul flight in the stem should raise the PE flag). But other causes of disrupted venous blood flow can elevate the risk.",True,PEs,,,,
742f9d9a-28be-46c3-8d12-3eb3b4ed8925,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,USMLE,False,USMLE,,,,
25de5ac1-5129-40eb-9a05-6924d4786e56,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"Hypercoagulability: Any condition that increases coagulability elevates the risk of PE, and most are due to trauma of some form or another or an elevated inflammatory state such as cancer or the postsurgery state. Birth control pills predispose the patient to thromboembolic disease so thereby also increase the risk of PE.",True,USMLE,,,,
863b27ba-2459-4662-930d-25a81b7d4b41,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,Pathophysiology of PE,False,Pathophysiology of PE,,,,
a662a59f-045a-4d35-b4e7-4cdc4eb74ab0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"The pathophysiology and clinical severity of PE depend on the number and size of the emboli, so clinical manifestations can be highly variable. In fact, PE is suspected to be much more common than previously thought because of improved detection techniques revealing more small and asymptomatic cases.",True,Pathophysiology of PE,,,,
39ef382d-cf6c-4a48-bff7-33490642448b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"Small emboli that can travel further into the vasculature may cause occlusion of relatively small areas of the lung, but with these areas receiving no perfusion and still being ventilated V/Q becomes inappropriately high. Not being able to pass the occlusion, blood will be diverted to other areas of the lung, and consequently cause them to be overperfused, lowering V/Q.",True,Pathophysiology of PE,,,,
5db02f5e-e544-4c2f-88eb-0f02a2d79d5d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"Depending on the size and number of emboli, these V/Q mismatches can produce a widening alveolar–arterial PO2 difference and lead to hypoxemia.",True,Pathophysiology of PE,,,,
5c282c8f-be50-4b31-a118-ddbed5916939,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,Clinical Signs of PE,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
5c282c8f-be50-4b31-a118-ddbed5916939,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,Pathophysiology of PE,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
5c282c8f-be50-4b31-a118-ddbed5916939,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
5c282c8f-be50-4b31-a118-ddbed5916939,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
17044bc1-42c6-4c68-a736-b846fc154ecb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"Pulmonary infarction, however, is rare, occurring in only 10 percent of PE cases. The lung tissue is supplied by the bronchial circulation so can usually survive the embolism in the pulmonary circulation unless there is preexisting cardiac disease.",True,Pathophysiology of PE,,,,
8b210f30-fbec-488b-959f-0b66f1cb3185,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,Clinical Signs of PE,False,Clinical Signs of PE,,,,
df76c9b5-043b-412e-bb6f-74089e293b64,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"The clinical manifestations of PE vary widely, from asymptomatic when emboli are small or few, to sudden death when they are large or numerous.",True,Clinical Signs of PE,,,,
9fdbd10b-b2ac-4461-99d0-226a4486c82b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"Signs of DVT may precede PE cases, such as leg pain, venous swelling, or warm skin over the thrombus site, but these are present in less than half of patients. Once instigated, the presenting symptom of PE is usually dyspnea but can also include chest pain. There can be clinical clues in the dyspnea as it has a rapid onset and is disproportionate to any initial clinical findings. The nature of its onset also tends to generate significant anxiety. Chest pain can start as anginal but then become more pleuritic.",True,Clinical Signs of PE,,,,
dfd46621-00c4-45b1-b18b-8a646796b6b9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"Hemoptysis is less common but an important symptom. In severe cases involving massive PE tachypnea, tachycardia and cyanosis are usually present.",True,Clinical Signs of PE,,,,
0895aace-bea7-4e80-a5df-213373944da2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"Because of the mechanical and metabolic strain on the heart, cardiac manifestations, including arrhythmia, acute cor pulmonale, or signs of cardiac failure or shock, may be detected with an increased difference between alveolar and arterial PO2s.",True,Clinical Signs of PE,,,,
87c7b016-e7ff-4965-873b-703e2dd7cea0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"The chest x-ray will appear normal, unless there are complications such as pleural effusion, atelectasis, or pulmonary infarction. CT angiography is used to detect the presence of a PE when suspicion is high. When suspicion is lower, labs will include a D-dimer test (a protein fragment produced by a dissolving clot), which, if negative, can help rule out the presence of a PE, but if positive would require further investigation (e.g., CT angiography) for confirmation.",True,Clinical Signs of PE,,,,
27f4961b-87f6-420b-b6aa-1c7c94055f31,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,Text,False,Text,,,,
7a09098c-e6bb-4c5c-bc0d-1464cdfad19a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 21.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
aed7f074-5eb3-43ce-a901-46e97d090d22,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
43ad4ae9-8454-4996-9aa8-a7d03cacc1fa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathophysiology of PE,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-2,"West, John B. “Chapter 6: Vascular Diseases.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Text,,,,
1a1cf12e-6e79-48fc-bcdb-7d8b19848e75,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"About 90 percent of PEs are caused by deep vein thrombi, but at least one of three main predisposing factors (Virchow’s triad) are present in a case of PE:",True,Text,,,,
12e88dfd-ec5f-4f2d-bc20-a2d3d245e93f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,PEs,False,PEs,,,,
15b8aaae-c92e-4cff-a67d-260414d6e613,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,Abnormal vessel walls: Damage to the inner wall of veins causes adherence of blood platelets and activation of clotting factors. Similarly inflammation or trauma of the vein or surrounding area can lead to a risk of local clotting.,True,PEs,,,,
61368b09-70ee-4059-89a6-218e8d0b23ec,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"Venous stasis: Venous stasis appears to be the most important factor in thrombus formation, and cases of PE are often preceded by periods of immobility (top tip: a USMLE question with a long-haul flight in the stem should raise the PE flag). But other causes of disrupted venous blood flow can elevate the risk.",True,PEs,,,,
2762c8ff-9ae5-47d1-91ec-0e8382d6d854,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,USMLE,False,USMLE,,,,
a16709f4-fc05-4ba3-bc9b-f04154cad623,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"Hypercoagulability: Any condition that increases coagulability elevates the risk of PE, and most are due to trauma of some form or another or an elevated inflammatory state such as cancer or the postsurgery state. Birth control pills predispose the patient to thromboembolic disease so thereby also increase the risk of PE.",True,USMLE,,,,
2ceb8445-b1d8-4af7-afb6-cf81385a35ac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,Pathophysiology of PE,False,Pathophysiology of PE,,,,
fae8cf7f-ddfd-4b6c-9177-eb4d3d1993ca,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"The pathophysiology and clinical severity of PE depend on the number and size of the emboli, so clinical manifestations can be highly variable. In fact, PE is suspected to be much more common than previously thought because of improved detection techniques revealing more small and asymptomatic cases.",True,Pathophysiology of PE,,,,
3d777661-bc39-4d76-be5a-2b83664ce162,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"Small emboli that can travel further into the vasculature may cause occlusion of relatively small areas of the lung, but with these areas receiving no perfusion and still being ventilated V/Q becomes inappropriately high. Not being able to pass the occlusion, blood will be diverted to other areas of the lung, and consequently cause them to be overperfused, lowering V/Q.",True,Pathophysiology of PE,,,,
9b60cba8-aa1b-483d-ade6-89162ddb1300,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"Depending on the size and number of emboli, these V/Q mismatches can produce a widening alveolar–arterial PO2 difference and lead to hypoxemia.",True,Pathophysiology of PE,,,,
1f73bdb4-53a6-45bc-9513-eda27526af28,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,Clinical Signs of PE,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
1f73bdb4-53a6-45bc-9513-eda27526af28,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,Pathophysiology of PE,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
1f73bdb4-53a6-45bc-9513-eda27526af28,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
1f73bdb4-53a6-45bc-9513-eda27526af28,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
377bdfc7-7a5d-449c-9e0f-7133b3d939fe,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"Pulmonary infarction, however, is rare, occurring in only 10 percent of PE cases. The lung tissue is supplied by the bronchial circulation so can usually survive the embolism in the pulmonary circulation unless there is preexisting cardiac disease.",True,Pathophysiology of PE,,,,
1b199ddc-a97f-47c6-a0e1-67a3089959c0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,Clinical Signs of PE,False,Clinical Signs of PE,,,,
f5c22f58-53a8-42a2-ad73-5867791ef381,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"The clinical manifestations of PE vary widely, from asymptomatic when emboli are small or few, to sudden death when they are large or numerous.",True,Clinical Signs of PE,,,,
780160cb-9049-4e57-93fe-3171a368aaa4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"Signs of DVT may precede PE cases, such as leg pain, venous swelling, or warm skin over the thrombus site, but these are present in less than half of patients. Once instigated, the presenting symptom of PE is usually dyspnea but can also include chest pain. There can be clinical clues in the dyspnea as it has a rapid onset and is disproportionate to any initial clinical findings. The nature of its onset also tends to generate significant anxiety. Chest pain can start as anginal but then become more pleuritic.",True,Clinical Signs of PE,,,,
cf41c8f1-5222-442e-b9d8-3956d1af9d1e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"Hemoptysis is less common but an important symptom. In severe cases involving massive PE tachypnea, tachycardia and cyanosis are usually present.",True,Clinical Signs of PE,,,,
ce8c9951-e422-43d5-a0b7-199e79df3ba7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"Because of the mechanical and metabolic strain on the heart, cardiac manifestations, including arrhythmia, acute cor pulmonale, or signs of cardiac failure or shock, may be detected with an increased difference between alveolar and arterial PO2s.",True,Clinical Signs of PE,,,,
1a980974-dbf8-4d79-99df-9a5240e4f6cd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"The chest x-ray will appear normal, unless there are complications such as pleural effusion, atelectasis, or pulmonary infarction. CT angiography is used to detect the presence of a PE when suspicion is high. When suspicion is lower, labs will include a D-dimer test (a protein fragment produced by a dissolving clot), which, if negative, can help rule out the presence of a PE, but if positive would require further investigation (e.g., CT angiography) for confirmation.",True,Clinical Signs of PE,,,,
49bab002-9225-416b-8ace-d1f8b26d048e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,Text,False,Text,,,,
93768787-4bd1-4055-8add-fea55eed2da1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 21.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
e82cba39-57bf-47db-a7f5-01f721ad25fb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
a11f1bab-ba4d-4ccf-8a8d-7018bd410a17,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/#chapter-37-section-1,"West, John B. “Chapter 6: Vascular Diseases.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Text,,,,
98a62b5e-fc1c-4922-97a4-e4f71ff912f6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"About 90 percent of PEs are caused by deep vein thrombi, but at least one of three main predisposing factors (Virchow’s triad) are present in a case of PE:",True,Text,,,,
db353fae-edc5-4408-925a-fad3a98d7eaa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,PEs,False,PEs,,,,
4f4ee0ba-50c2-49aa-a5e2-9328f874c901,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,Abnormal vessel walls: Damage to the inner wall of veins causes adherence of blood platelets and activation of clotting factors. Similarly inflammation or trauma of the vein or surrounding area can lead to a risk of local clotting.,True,PEs,,,,
40ff3ead-1a14-459c-b650-3c6ec882d0d6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"Venous stasis: Venous stasis appears to be the most important factor in thrombus formation, and cases of PE are often preceded by periods of immobility (top tip: a USMLE question with a long-haul flight in the stem should raise the PE flag). But other causes of disrupted venous blood flow can elevate the risk.",True,PEs,,,,
e93e6310-b410-4fb4-a993-2e29cc06622b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,USMLE,False,USMLE,,,,
95f115dd-9345-4e88-84a2-6711fbe8a0c1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"Hypercoagulability: Any condition that increases coagulability elevates the risk of PE, and most are due to trauma of some form or another or an elevated inflammatory state such as cancer or the postsurgery state. Birth control pills predispose the patient to thromboembolic disease so thereby also increase the risk of PE.",True,USMLE,,,,
9ae00c7b-1d28-4ca1-8dc0-f69bace83155,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,Pathophysiology of PE,False,Pathophysiology of PE,,,,
e572be09-4e9e-42ee-ac92-ef662bd38a09,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"The pathophysiology and clinical severity of PE depend on the number and size of the emboli, so clinical manifestations can be highly variable. In fact, PE is suspected to be much more common than previously thought because of improved detection techniques revealing more small and asymptomatic cases.",True,Pathophysiology of PE,,,,
b7ea2c26-1c87-488b-afe2-1a514737a0c4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"Small emboli that can travel further into the vasculature may cause occlusion of relatively small areas of the lung, but with these areas receiving no perfusion and still being ventilated V/Q becomes inappropriately high. Not being able to pass the occlusion, blood will be diverted to other areas of the lung, and consequently cause them to be overperfused, lowering V/Q.",True,Pathophysiology of PE,,,,
88e8b996-92af-4e35-8a30-4a3c9d7b8e26,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"Depending on the size and number of emboli, these V/Q mismatches can produce a widening alveolar–arterial PO2 difference and lead to hypoxemia.",True,Pathophysiology of PE,,,,
b1fa406b-ddce-4694-9477-0a5fd088e4b3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,Clinical Signs of PE,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
b1fa406b-ddce-4694-9477-0a5fd088e4b3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,Pathophysiology of PE,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
b1fa406b-ddce-4694-9477-0a5fd088e4b3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,Pathology of Pulmonary Embolism (PE),https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
b1fa406b-ddce-4694-9477-0a5fd088e4b3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"With larger emboli that occlude larger vessels there will not only be a larger impact on gas exchange, but also a more increase in pulmonary vascular resistance. The extreme  (and thankfully rare) case is a “saddle” embolus that is large enough to straddle the bifurcation of the pulmonary trunk, obstruct the left and right pulmonary arteries, and lead to immediate hemodynamic collapse. In lesser cases, pulmonary hypertension will overwhelm the thin myocardium of the right ventricle, and as pulmonary arterial pressure approaches right ventricle pressure then cardiac output will fall. This will exaggerate the hypoxemia and cause the pulmonary vasculature to perform its normal vasoconstrictive response to low oxygen tensions that in turn worsens the pulmonary hypertension (summarized in figure 7.1).",True,Pathophysiology of PE,Figure 7.1,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/7.1.png,Figure 7.1: Pathophysiology of pulmonary embolism.
1fee3cc5-555f-4f03-a101-006503aa6b59,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"Pulmonary infarction, however, is rare, occurring in only 10 percent of PE cases. The lung tissue is supplied by the bronchial circulation so can usually survive the embolism in the pulmonary circulation unless there is preexisting cardiac disease.",True,Pathophysiology of PE,,,,
876f71db-4c61-4bc9-877a-11aee95dbc03,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,Clinical Signs of PE,False,Clinical Signs of PE,,,,
36ec913d-ea1c-427f-9d5f-01f95ea7a0b4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"The clinical manifestations of PE vary widely, from asymptomatic when emboli are small or few, to sudden death when they are large or numerous.",True,Clinical Signs of PE,,,,
05703eee-a6cf-4255-abcf-37f6a8ebc602,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"Signs of DVT may precede PE cases, such as leg pain, venous swelling, or warm skin over the thrombus site, but these are present in less than half of patients. Once instigated, the presenting symptom of PE is usually dyspnea but can also include chest pain. There can be clinical clues in the dyspnea as it has a rapid onset and is disproportionate to any initial clinical findings. The nature of its onset also tends to generate significant anxiety. Chest pain can start as anginal but then become more pleuritic.",True,Clinical Signs of PE,,,,
5122943d-8d23-4a41-9cb1-87b01bba1545,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"Hemoptysis is less common but an important symptom. In severe cases involving massive PE tachypnea, tachycardia and cyanosis are usually present.",True,Clinical Signs of PE,,,,
e6eb1d17-5234-4780-9c4c-e00fbbfcfeb7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"Because of the mechanical and metabolic strain on the heart, cardiac manifestations, including arrhythmia, acute cor pulmonale, or signs of cardiac failure or shock, may be detected with an increased difference between alveolar and arterial PO2s.",True,Clinical Signs of PE,,,,
72e5ed54-2f43-4820-a75f-931cf5943191,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"The chest x-ray will appear normal, unless there are complications such as pleural effusion, atelectasis, or pulmonary infarction. CT angiography is used to detect the presence of a PE when suspicion is high. When suspicion is lower, labs will include a D-dimer test (a protein fragment produced by a dissolving clot), which, if negative, can help rule out the presence of a PE, but if positive would require further investigation (e.g., CT angiography) for confirmation.",True,Clinical Signs of PE,,,,
dc20bc1a-2d8b-48ad-9841-35e1a9fd9055,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,Text,False,Text,,,,
b4cdcc5d-d0a7-474f-a7e9-76e9ef53fa7d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 21.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
4c9b41b5-875f-4d87-bcbc-2576d2dec30f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
923edfcc-3ec1-48f2-9443-d35aaea4ffa7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,7. Pulmonary Embolism,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/pulmonary-embolism/,"West, John B. “Chapter 6: Vascular Diseases.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Text,,,,
cc05c711-e485-49f6-b7d0-98f4edb46105,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Four major types of bronchogenic carcinoma can be distinguished by histology, epidemiology, clinical features, and prognosis. They are:",True,Text,,,,
046f1ecf-3b74-4390-bea9-b69b3dda0bfa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,Let us look at the features of each.,False,Let us look at the features of each.,,,,
9a306b09-6db0-463b-9cb9-10788b53dde6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,Squamous Cell,False,Squamous Cell,,,,
2c4b095c-1962-4a38-bb39-11b4df914910,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Squamous cell cancer accounts for about one-third of all lung cancers and is more common in men. It is pathologically characterized by keratin formation between cells and the development of large, well-outlined islands of cancer cells. It is usually centrally located and associated with the main bronchi. Metastasis tends to be local, affecting the surrounding areas and lymph nodes.",True,Squamous Cell,,,,
6b852530-6e48-49ff-a901-bd5e60dd3029,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,Adenocarcinoma,False,Adenocarcinoma,,,,
642f8c65-9e6d-4e5e-b739-5d8733fdee5c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,Adenocarcinoma also accounts for about one-third of cases but is the most common lung cancer in women. The lesion has a glandular structure and may produce mucin. This is usually a peripheral lesion and distant metastasis is common.,True,Adenocarcinoma,,,,
0712d162-582e-4737-b2dd-bab1cfa038df,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,Large Cell,False,Large Cell,,,,
837940c9-02fc-4c10-87a0-f1b1d8a03509,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Large cell is less common and is seen in about 10 percent of cases, most of whom are male. The diagnosis is made by cell size, which is large and easily distinguished from squamous cell cancer or adenocarcinoma. The lesions can be anywhere in the lung but are often found in the periphery. This is a fast-growing cancer and so is frequently diagnosed at a later disease stage.",True,Large Cell,,,,
36b0b4d7-4991-4f22-8732-9bc79c6f0f2d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,Small Cell,False,Small Cell,,,,
a57a9a27-05f6-41c2-b9e1-cd5de525f8d1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"The previous three types of cancer are collectively known as non-small cell lung cancer. Alternatively, small cell cancer is found in about 15 percent of cases. It is less predominant in men, and incidence in women is rising. The small cells have an oat-like appearance, and the most common small cell cancer is known as oat cell carcinoma and the lesions frequently have endocrine function. Originating in the main bronchi this cancer spreads very quickly into other thoracic and extrathoracic sites, and this form carries a very poor prognosis.",True,Small Cell,,,,
57fec407-a47f-41cf-a8a1-5e48c3670f1a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,The characteristics of these forms of lung cancer are summarized in table 6.1.,True,Small Cell,,,,
56b5f3ed-7941-4317-9144-71ab189085ac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,Table 6.1: Summary of forms of lung cancer.,True,Small Cell,,,,
cdddcce6-bc5d-4326-accf-7d8161eea481,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,Clinical Signs,False,Clinical Signs,,,,
d34dcb43-d5bb-43a5-a675-20a43c43d204,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"The signs and symptoms can be variable and diverse depending on the location, type, size, and rapidity of growth. Patients may even be asymptomatic when the lesion is found on chest x-ray or with bronchoscope.",True,Clinical Signs,,,,
51c38948-4396-4f5a-b997-bb40f22f0dc6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"The most common symptom is cough, but unfortunately the patient, likely being a smoker, may be accustomed to cough and not think anything of it. Bloody sputum occurs in only about half of patients and is a frequent cause for them seeking medical advice, and severe hemoptysis is uncommon.",True,Clinical Signs,,,,
6ff06d00-15aa-4d3a-9574-871ab4f18cb5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Chest pain is fairly common and ranges from a mild ache or feeling of heaviness, to severe and unremitting. Pain does not necessarily indicate pleural or chest wall involvement, although significant steady pain is more indicative of this complication.",True,Clinical Signs,,,,
4edb3231-5a6a-4444-9c9b-b8e352550942,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Dyspnea may arise as the tumor obstructs a major airway or causes a large pleural effusion, but it can also be due to underlying bronchopulmonary disease.",True,Clinical Signs,,,,
e4bfe82d-3803-4ffe-919f-997f2394bc42,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Physical exam is likely to be normal in the early stages of the disease, but as the cancer progresses the exam usually reveals signs associated with either bronchial obstruction or a consequence of metastasis. Bronchial obstruction can lead to wheeze or other modified breath sounds, atelectasis, down-stream pneumonia, or pleural effusion. Paraneoplastic syndromes associated with the cancer can cause disruption to other systems and lead to characteristic weight loss, muscle wasting, and digital clubbing.",True,Clinical Signs,,,,
92f391cb-397f-42ca-8027-6aeabc48b471,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Clinical Signs,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
92f391cb-397f-42ca-8027-6aeabc48b471,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Small Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
92f391cb-397f-42ca-8027-6aeabc48b471,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Large Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
92f391cb-397f-42ca-8027-6aeabc48b471,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Adenocarcinoma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
92f391cb-397f-42ca-8027-6aeabc48b471,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Squamous Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
92f391cb-397f-42ca-8027-6aeabc48b471,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,6. Lung Cancer,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
702c58ed-93b8-41cb-a3c6-f03db2418ff2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,Text,False,Text,,,,
d412e5db-7af7-4ded-98bd-d3838d618392,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 20.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
6339e04b-8509-4e9e-970b-bb8cc0ec57ff,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
5b90a401-f907-458e-acb6-06e6ef81186f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical Signs,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-5,"Table 6.1: Summary of forms of lung cancer. Includes Squamous Cell Carcinoma Lung 40x by Calicut Medical College from WikimediaCommons (CC BY-SA 4.0), Papillary adenocarcinoma of the lung — intermed mag by Nephron from WikimediaCommons (CC BY-SA 3.0), Large cell carcinoma of the lung by The Armed Forces Institute of Pathology (AFIP) from WikimediaCommons (Public domain), and Lung small cell carcinoma (1) by core needle biopsy by KGH from WikimediaCommons (CC BY-SA 3.0).",True,Text,,,,
e77dcb15-e7ff-4096-b531-0a46609eab48,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Four major types of bronchogenic carcinoma can be distinguished by histology, epidemiology, clinical features, and prognosis. They are:",True,Text,,,,
3de8e983-5015-427f-bd94-ef47501bddda,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,Let us look at the features of each.,False,Let us look at the features of each.,,,,
b152bfbd-ca08-47d8-a3b3-dd926cddd8ea,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,Squamous Cell,False,Squamous Cell,,,,
339ac9f3-b226-412e-8908-d413adbc7e6e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Squamous cell cancer accounts for about one-third of all lung cancers and is more common in men. It is pathologically characterized by keratin formation between cells and the development of large, well-outlined islands of cancer cells. It is usually centrally located and associated with the main bronchi. Metastasis tends to be local, affecting the surrounding areas and lymph nodes.",True,Squamous Cell,,,,
e255b5a6-b8d0-4fcf-9948-5e04f387f858,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,Adenocarcinoma,False,Adenocarcinoma,,,,
20c81271-32c4-464d-b78f-b6947c1c0081,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,Adenocarcinoma also accounts for about one-third of cases but is the most common lung cancer in women. The lesion has a glandular structure and may produce mucin. This is usually a peripheral lesion and distant metastasis is common.,True,Adenocarcinoma,,,,
7523d2b1-20cc-4f5e-a6a6-014223e48a1a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,Large Cell,False,Large Cell,,,,
f3df5d60-c895-4cfe-ace6-bd8beaf88033,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Large cell is less common and is seen in about 10 percent of cases, most of whom are male. The diagnosis is made by cell size, which is large and easily distinguished from squamous cell cancer or adenocarcinoma. The lesions can be anywhere in the lung but are often found in the periphery. This is a fast-growing cancer and so is frequently diagnosed at a later disease stage.",True,Large Cell,,,,
a6eb8250-ac55-491d-b697-2bdf603017ec,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,Small Cell,False,Small Cell,,,,
c5e8a378-8962-4239-9ce6-47b94b81d98f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"The previous three types of cancer are collectively known as non-small cell lung cancer. Alternatively, small cell cancer is found in about 15 percent of cases. It is less predominant in men, and incidence in women is rising. The small cells have an oat-like appearance, and the most common small cell cancer is known as oat cell carcinoma and the lesions frequently have endocrine function. Originating in the main bronchi this cancer spreads very quickly into other thoracic and extrathoracic sites, and this form carries a very poor prognosis.",True,Small Cell,,,,
222cc4a1-ab37-46d8-9b33-06b9006bef04,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,The characteristics of these forms of lung cancer are summarized in table 6.1.,True,Small Cell,,,,
515bc113-a4dc-4bce-8ce0-a665643362f6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,Table 6.1: Summary of forms of lung cancer.,True,Small Cell,,,,
5d7c2762-f0d3-4d87-8213-90474ca6e413,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,Clinical Signs,False,Clinical Signs,,,,
70c5a132-2245-47d3-937d-481b974e4fac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"The signs and symptoms can be variable and diverse depending on the location, type, size, and rapidity of growth. Patients may even be asymptomatic when the lesion is found on chest x-ray or with bronchoscope.",True,Clinical Signs,,,,
19577736-06eb-4c07-8643-2551891a97be,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"The most common symptom is cough, but unfortunately the patient, likely being a smoker, may be accustomed to cough and not think anything of it. Bloody sputum occurs in only about half of patients and is a frequent cause for them seeking medical advice, and severe hemoptysis is uncommon.",True,Clinical Signs,,,,
8bb42193-3c1b-46e8-8b70-e8d8e3f18b2c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Chest pain is fairly common and ranges from a mild ache or feeling of heaviness, to severe and unremitting. Pain does not necessarily indicate pleural or chest wall involvement, although significant steady pain is more indicative of this complication.",True,Clinical Signs,,,,
1cf1ea55-fbf6-4320-8322-762a3062617d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Dyspnea may arise as the tumor obstructs a major airway or causes a large pleural effusion, but it can also be due to underlying bronchopulmonary disease.",True,Clinical Signs,,,,
7e574517-98bd-40a7-82a4-695ea64f668c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Physical exam is likely to be normal in the early stages of the disease, but as the cancer progresses the exam usually reveals signs associated with either bronchial obstruction or a consequence of metastasis. Bronchial obstruction can lead to wheeze or other modified breath sounds, atelectasis, down-stream pneumonia, or pleural effusion. Paraneoplastic syndromes associated with the cancer can cause disruption to other systems and lead to characteristic weight loss, muscle wasting, and digital clubbing.",True,Clinical Signs,,,,
c6468308-b180-430b-99d7-8bb77693ae77,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Clinical Signs,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
c6468308-b180-430b-99d7-8bb77693ae77,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Small Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
c6468308-b180-430b-99d7-8bb77693ae77,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Large Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
c6468308-b180-430b-99d7-8bb77693ae77,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Adenocarcinoma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
c6468308-b180-430b-99d7-8bb77693ae77,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Squamous Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
c6468308-b180-430b-99d7-8bb77693ae77,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,6. Lung Cancer,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
f7b80fec-ead2-40ff-a366-993b461997d7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,Text,False,Text,,,,
534aae6e-3da6-48a8-bb44-f6098b52d051,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 20.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
1a16e4f8-e65b-469c-a859-794a19a4796d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
09cc65a7-7403-41ce-8787-785552dbd523,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Small Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-4,"Table 6.1: Summary of forms of lung cancer. Includes Squamous Cell Carcinoma Lung 40x by Calicut Medical College from WikimediaCommons (CC BY-SA 4.0), Papillary adenocarcinoma of the lung — intermed mag by Nephron from WikimediaCommons (CC BY-SA 3.0), Large cell carcinoma of the lung by The Armed Forces Institute of Pathology (AFIP) from WikimediaCommons (Public domain), and Lung small cell carcinoma (1) by core needle biopsy by KGH from WikimediaCommons (CC BY-SA 3.0).",True,Text,,,,
6bd6fba9-c15e-4f09-bae8-c6547ef51bc1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Four major types of bronchogenic carcinoma can be distinguished by histology, epidemiology, clinical features, and prognosis. They are:",True,Text,,,,
e502421e-e6e1-4001-a20d-7627b97f00ee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,Let us look at the features of each.,False,Let us look at the features of each.,,,,
42ca258c-53e2-4fbc-ae27-6ddb04934aca,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,Squamous Cell,False,Squamous Cell,,,,
db991609-ebdc-44d3-a4c1-4a81a9145baa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Squamous cell cancer accounts for about one-third of all lung cancers and is more common in men. It is pathologically characterized by keratin formation between cells and the development of large, well-outlined islands of cancer cells. It is usually centrally located and associated with the main bronchi. Metastasis tends to be local, affecting the surrounding areas and lymph nodes.",True,Squamous Cell,,,,
594ee9b9-a3da-454c-9dd6-8e959d3deff5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,Adenocarcinoma,False,Adenocarcinoma,,,,
eda462b4-9cc5-4172-b7aa-50916e77affe,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,Adenocarcinoma also accounts for about one-third of cases but is the most common lung cancer in women. The lesion has a glandular structure and may produce mucin. This is usually a peripheral lesion and distant metastasis is common.,True,Adenocarcinoma,,,,
feba4ef6-4481-4527-a737-5d5830a5c16e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,Large Cell,False,Large Cell,,,,
82d83e46-d738-4378-adac-9b5037117453,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Large cell is less common and is seen in about 10 percent of cases, most of whom are male. The diagnosis is made by cell size, which is large and easily distinguished from squamous cell cancer or adenocarcinoma. The lesions can be anywhere in the lung but are often found in the periphery. This is a fast-growing cancer and so is frequently diagnosed at a later disease stage.",True,Large Cell,,,,
5c8d5635-a209-4414-84ae-1aa8f3c96a7d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,Small Cell,False,Small Cell,,,,
452fdec1-c966-4004-8078-c10143b418ce,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"The previous three types of cancer are collectively known as non-small cell lung cancer. Alternatively, small cell cancer is found in about 15 percent of cases. It is less predominant in men, and incidence in women is rising. The small cells have an oat-like appearance, and the most common small cell cancer is known as oat cell carcinoma and the lesions frequently have endocrine function. Originating in the main bronchi this cancer spreads very quickly into other thoracic and extrathoracic sites, and this form carries a very poor prognosis.",True,Small Cell,,,,
005df045-62d0-4509-84c8-44b7c1ec939f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,The characteristics of these forms of lung cancer are summarized in table 6.1.,True,Small Cell,,,,
dba758e7-9791-48c0-a31f-d03ffba147be,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,Table 6.1: Summary of forms of lung cancer.,True,Small Cell,,,,
d92ce170-95cf-4a5e-8e43-b6baadba7ebf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,Clinical Signs,False,Clinical Signs,,,,
ef2b95f4-4695-46e3-9c74-b9b3a95c5e4d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"The signs and symptoms can be variable and diverse depending on the location, type, size, and rapidity of growth. Patients may even be asymptomatic when the lesion is found on chest x-ray or with bronchoscope.",True,Clinical Signs,,,,
e5f9c9cd-5e05-4344-a563-d7221b3bd54c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"The most common symptom is cough, but unfortunately the patient, likely being a smoker, may be accustomed to cough and not think anything of it. Bloody sputum occurs in only about half of patients and is a frequent cause for them seeking medical advice, and severe hemoptysis is uncommon.",True,Clinical Signs,,,,
8c6a5f82-73ca-4151-adb7-40ab2800bb3e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Chest pain is fairly common and ranges from a mild ache or feeling of heaviness, to severe and unremitting. Pain does not necessarily indicate pleural or chest wall involvement, although significant steady pain is more indicative of this complication.",True,Clinical Signs,,,,
86f3a818-2c7c-425e-b335-637117d97811,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Dyspnea may arise as the tumor obstructs a major airway or causes a large pleural effusion, but it can also be due to underlying bronchopulmonary disease.",True,Clinical Signs,,,,
07eb7e8e-51a7-4069-a893-158e9435831a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Physical exam is likely to be normal in the early stages of the disease, but as the cancer progresses the exam usually reveals signs associated with either bronchial obstruction or a consequence of metastasis. Bronchial obstruction can lead to wheeze or other modified breath sounds, atelectasis, down-stream pneumonia, or pleural effusion. Paraneoplastic syndromes associated with the cancer can cause disruption to other systems and lead to characteristic weight loss, muscle wasting, and digital clubbing.",True,Clinical Signs,,,,
cf4df749-f021-44ae-81d7-ab7fffaf2244,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Clinical Signs,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
cf4df749-f021-44ae-81d7-ab7fffaf2244,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Small Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
cf4df749-f021-44ae-81d7-ab7fffaf2244,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Large Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
cf4df749-f021-44ae-81d7-ab7fffaf2244,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Adenocarcinoma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
cf4df749-f021-44ae-81d7-ab7fffaf2244,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Squamous Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
cf4df749-f021-44ae-81d7-ab7fffaf2244,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,6. Lung Cancer,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
f5b6e5c3-efb1-4278-852f-de280b6e9403,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,Text,False,Text,,,,
6a696ddc-136f-4d02-8df8-538c70607e8e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 20.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
8fa46f15-5d1a-4e3c-b740-e87eddac0341,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
7891345b-e643-4bbb-85c5-0e7332cd627a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Large Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-3,"Table 6.1: Summary of forms of lung cancer. Includes Squamous Cell Carcinoma Lung 40x by Calicut Medical College from WikimediaCommons (CC BY-SA 4.0), Papillary adenocarcinoma of the lung — intermed mag by Nephron from WikimediaCommons (CC BY-SA 3.0), Large cell carcinoma of the lung by The Armed Forces Institute of Pathology (AFIP) from WikimediaCommons (Public domain), and Lung small cell carcinoma (1) by core needle biopsy by KGH from WikimediaCommons (CC BY-SA 3.0).",True,Text,,,,
2a8e260a-1294-4b23-8214-91497da17806,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Four major types of bronchogenic carcinoma can be distinguished by histology, epidemiology, clinical features, and prognosis. They are:",True,Text,,,,
225c18ab-f65b-4606-956c-dbaa281bd28f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,Let us look at the features of each.,False,Let us look at the features of each.,,,,
b4eb73c3-ea68-4528-9ed0-483dbc079eec,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,Squamous Cell,False,Squamous Cell,,,,
b2e05322-cda7-43bc-876a-eb21dbe22486,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Squamous cell cancer accounts for about one-third of all lung cancers and is more common in men. It is pathologically characterized by keratin formation between cells and the development of large, well-outlined islands of cancer cells. It is usually centrally located and associated with the main bronchi. Metastasis tends to be local, affecting the surrounding areas and lymph nodes.",True,Squamous Cell,,,,
a30fdf9b-7baa-4ad3-b4a5-cd1f95fd874c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,Adenocarcinoma,False,Adenocarcinoma,,,,
543ed3d1-c0b1-4fa8-95d7-20a09a360dcc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,Adenocarcinoma also accounts for about one-third of cases but is the most common lung cancer in women. The lesion has a glandular structure and may produce mucin. This is usually a peripheral lesion and distant metastasis is common.,True,Adenocarcinoma,,,,
b9b5129e-c085-4898-b04e-23ca79e72b94,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,Large Cell,False,Large Cell,,,,
540722a1-eacb-40c4-bff8-f2e69463a8ea,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Large cell is less common and is seen in about 10 percent of cases, most of whom are male. The diagnosis is made by cell size, which is large and easily distinguished from squamous cell cancer or adenocarcinoma. The lesions can be anywhere in the lung but are often found in the periphery. This is a fast-growing cancer and so is frequently diagnosed at a later disease stage.",True,Large Cell,,,,
b5c9c030-bba6-4f1c-8532-5bf7b0e9d20d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,Small Cell,False,Small Cell,,,,
d6493f5f-8f3f-4f27-a8a2-ac29e43fac9d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"The previous three types of cancer are collectively known as non-small cell lung cancer. Alternatively, small cell cancer is found in about 15 percent of cases. It is less predominant in men, and incidence in women is rising. The small cells have an oat-like appearance, and the most common small cell cancer is known as oat cell carcinoma and the lesions frequently have endocrine function. Originating in the main bronchi this cancer spreads very quickly into other thoracic and extrathoracic sites, and this form carries a very poor prognosis.",True,Small Cell,,,,
f66edce9-d9b3-4b2b-86a4-b260956fa7ae,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,The characteristics of these forms of lung cancer are summarized in table 6.1.,True,Small Cell,,,,
083ebf56-3397-4827-b4eb-1a6b94f659f4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,Table 6.1: Summary of forms of lung cancer.,True,Small Cell,,,,
60ff49b7-162d-49d3-93ba-2bd20fcdea3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,Clinical Signs,False,Clinical Signs,,,,
a72142f6-8bc1-44bd-a4ec-1549c24ea6ab,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"The signs and symptoms can be variable and diverse depending on the location, type, size, and rapidity of growth. Patients may even be asymptomatic when the lesion is found on chest x-ray or with bronchoscope.",True,Clinical Signs,,,,
ad926822-2abe-42dc-81f4-d3050a882cc2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"The most common symptom is cough, but unfortunately the patient, likely being a smoker, may be accustomed to cough and not think anything of it. Bloody sputum occurs in only about half of patients and is a frequent cause for them seeking medical advice, and severe hemoptysis is uncommon.",True,Clinical Signs,,,,
c3b7b945-64ec-4546-a849-fd27803b64be,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Chest pain is fairly common and ranges from a mild ache or feeling of heaviness, to severe and unremitting. Pain does not necessarily indicate pleural or chest wall involvement, although significant steady pain is more indicative of this complication.",True,Clinical Signs,,,,
8a152a3f-8fff-4cf4-9973-5abb9fcf1984,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Dyspnea may arise as the tumor obstructs a major airway or causes a large pleural effusion, but it can also be due to underlying bronchopulmonary disease.",True,Clinical Signs,,,,
61725136-6350-4298-af0e-496aafee1638,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Physical exam is likely to be normal in the early stages of the disease, but as the cancer progresses the exam usually reveals signs associated with either bronchial obstruction or a consequence of metastasis. Bronchial obstruction can lead to wheeze or other modified breath sounds, atelectasis, down-stream pneumonia, or pleural effusion. Paraneoplastic syndromes associated with the cancer can cause disruption to other systems and lead to characteristic weight loss, muscle wasting, and digital clubbing.",True,Clinical Signs,,,,
926b240b-c7e2-496b-93cd-b8c58edb09f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Clinical Signs,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
926b240b-c7e2-496b-93cd-b8c58edb09f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Small Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
926b240b-c7e2-496b-93cd-b8c58edb09f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Large Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
926b240b-c7e2-496b-93cd-b8c58edb09f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Adenocarcinoma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
926b240b-c7e2-496b-93cd-b8c58edb09f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Squamous Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
926b240b-c7e2-496b-93cd-b8c58edb09f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,6. Lung Cancer,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
23d3d3aa-298a-4eda-9471-0cb678881d8d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,Text,False,Text,,,,
c1158385-8149-4bf9-b472-469ceb7cb6bb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 20.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
78078075-c7e3-4a52-95b1-a88c1d48b6e6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
ecfd2b43-da35-4d9d-aa19-85bb3e733478,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Adenocarcinoma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-2,"Table 6.1: Summary of forms of lung cancer. Includes Squamous Cell Carcinoma Lung 40x by Calicut Medical College from WikimediaCommons (CC BY-SA 4.0), Papillary adenocarcinoma of the lung — intermed mag by Nephron from WikimediaCommons (CC BY-SA 3.0), Large cell carcinoma of the lung by The Armed Forces Institute of Pathology (AFIP) from WikimediaCommons (Public domain), and Lung small cell carcinoma (1) by core needle biopsy by KGH from WikimediaCommons (CC BY-SA 3.0).",True,Text,,,,
8a5eb963-6a5e-45d5-b1ec-7a49a5728953,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Four major types of bronchogenic carcinoma can be distinguished by histology, epidemiology, clinical features, and prognosis. They are:",True,Text,,,,
a646a7cb-e552-464c-bd52-fce0233ddcb5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,Let us look at the features of each.,False,Let us look at the features of each.,,,,
e05be771-e468-4227-ae7d-2886c676938b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,Squamous Cell,False,Squamous Cell,,,,
d69626f6-3fcf-442c-9f14-c94ea569e207,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Squamous cell cancer accounts for about one-third of all lung cancers and is more common in men. It is pathologically characterized by keratin formation between cells and the development of large, well-outlined islands of cancer cells. It is usually centrally located and associated with the main bronchi. Metastasis tends to be local, affecting the surrounding areas and lymph nodes.",True,Squamous Cell,,,,
2c629440-8eb6-4a52-8492-9a441f96b07a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,Adenocarcinoma,False,Adenocarcinoma,,,,
962d6820-f7ee-4be5-b055-7300b1f18032,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,Adenocarcinoma also accounts for about one-third of cases but is the most common lung cancer in women. The lesion has a glandular structure and may produce mucin. This is usually a peripheral lesion and distant metastasis is common.,True,Adenocarcinoma,,,,
94c98c98-a34e-4ddf-ac4f-a392a7890d87,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,Large Cell,False,Large Cell,,,,
8b7de282-fd62-45ba-bf5a-1ecd8f27ce8c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Large cell is less common and is seen in about 10 percent of cases, most of whom are male. The diagnosis is made by cell size, which is large and easily distinguished from squamous cell cancer or adenocarcinoma. The lesions can be anywhere in the lung but are often found in the periphery. This is a fast-growing cancer and so is frequently diagnosed at a later disease stage.",True,Large Cell,,,,
98d360b5-b185-4f8b-a42d-5a1bb233c06b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,Small Cell,False,Small Cell,,,,
86b45b90-9f3e-4eb2-97e4-700d92b6d257,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"The previous three types of cancer are collectively known as non-small cell lung cancer. Alternatively, small cell cancer is found in about 15 percent of cases. It is less predominant in men, and incidence in women is rising. The small cells have an oat-like appearance, and the most common small cell cancer is known as oat cell carcinoma and the lesions frequently have endocrine function. Originating in the main bronchi this cancer spreads very quickly into other thoracic and extrathoracic sites, and this form carries a very poor prognosis.",True,Small Cell,,,,
6511ed99-1ca3-4284-bd99-d57f3a01c371,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,The characteristics of these forms of lung cancer are summarized in table 6.1.,True,Small Cell,,,,
9f791ff2-6a20-4761-b2dc-36386c4c37ff,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,Table 6.1: Summary of forms of lung cancer.,True,Small Cell,,,,
c8ea04f3-17bf-45b7-8d90-6121e2f7fa0e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,Clinical Signs,False,Clinical Signs,,,,
9b05a4d4-10c4-4845-b7f4-3d41f3c4a308,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"The signs and symptoms can be variable and diverse depending on the location, type, size, and rapidity of growth. Patients may even be asymptomatic when the lesion is found on chest x-ray or with bronchoscope.",True,Clinical Signs,,,,
60cc29f9-c4bb-4306-b27f-f0785068a9f2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"The most common symptom is cough, but unfortunately the patient, likely being a smoker, may be accustomed to cough and not think anything of it. Bloody sputum occurs in only about half of patients and is a frequent cause for them seeking medical advice, and severe hemoptysis is uncommon.",True,Clinical Signs,,,,
aacb7acd-1df1-40b6-b908-d0155e3e2cd7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Chest pain is fairly common and ranges from a mild ache or feeling of heaviness, to severe and unremitting. Pain does not necessarily indicate pleural or chest wall involvement, although significant steady pain is more indicative of this complication.",True,Clinical Signs,,,,
9eee058f-28d9-403e-ab83-19a0556e8c99,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Dyspnea may arise as the tumor obstructs a major airway or causes a large pleural effusion, but it can also be due to underlying bronchopulmonary disease.",True,Clinical Signs,,,,
19fa9dbe-c040-47d2-a949-7c72fdc9c1ca,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Physical exam is likely to be normal in the early stages of the disease, but as the cancer progresses the exam usually reveals signs associated with either bronchial obstruction or a consequence of metastasis. Bronchial obstruction can lead to wheeze or other modified breath sounds, atelectasis, down-stream pneumonia, or pleural effusion. Paraneoplastic syndromes associated with the cancer can cause disruption to other systems and lead to characteristic weight loss, muscle wasting, and digital clubbing.",True,Clinical Signs,,,,
640ed150-6fc8-4f83-841b-4bbc79773c6d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Clinical Signs,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
640ed150-6fc8-4f83-841b-4bbc79773c6d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Small Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
640ed150-6fc8-4f83-841b-4bbc79773c6d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Large Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
640ed150-6fc8-4f83-841b-4bbc79773c6d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Adenocarcinoma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
640ed150-6fc8-4f83-841b-4bbc79773c6d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Squamous Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
640ed150-6fc8-4f83-841b-4bbc79773c6d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,6. Lung Cancer,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
469686d4-0c3e-4cfd-a2f5-4a91ea6cd9ee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,Text,False,Text,,,,
b449f681-cb54-4f2d-86c4-9b9a8fc20c3a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 20.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
be73ba2e-b6a7-498b-9815-ffd1a9836d91,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
785759c8-0761-4040-8372-40147aee22f7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Squamous Cell,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/#chapter-35-section-1,"Table 6.1: Summary of forms of lung cancer. Includes Squamous Cell Carcinoma Lung 40x by Calicut Medical College from WikimediaCommons (CC BY-SA 4.0), Papillary adenocarcinoma of the lung — intermed mag by Nephron from WikimediaCommons (CC BY-SA 3.0), Large cell carcinoma of the lung by The Armed Forces Institute of Pathology (AFIP) from WikimediaCommons (Public domain), and Lung small cell carcinoma (1) by core needle biopsy by KGH from WikimediaCommons (CC BY-SA 3.0).",True,Text,,,,
b5b0b219-085c-450e-b09f-5b3db170fde0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Four major types of bronchogenic carcinoma can be distinguished by histology, epidemiology, clinical features, and prognosis. They are:",True,Text,,,,
21b586c4-40ed-4428-946c-ee17f2136515,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,Let us look at the features of each.,False,Let us look at the features of each.,,,,
f3acda00-b0e6-4b2b-a962-32708166e1cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,Squamous Cell,False,Squamous Cell,,,,
6b718c22-3ad8-4b46-8b5c-a56a0235a5ac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Squamous cell cancer accounts for about one-third of all lung cancers and is more common in men. It is pathologically characterized by keratin formation between cells and the development of large, well-outlined islands of cancer cells. It is usually centrally located and associated with the main bronchi. Metastasis tends to be local, affecting the surrounding areas and lymph nodes.",True,Squamous Cell,,,,
aeed0a1d-470f-4b11-9063-e61901c7cdd0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,Adenocarcinoma,False,Adenocarcinoma,,,,
e2fb6d79-0d7a-4e40-852b-f76468610260,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,Adenocarcinoma also accounts for about one-third of cases but is the most common lung cancer in women. The lesion has a glandular structure and may produce mucin. This is usually a peripheral lesion and distant metastasis is common.,True,Adenocarcinoma,,,,
3fa47f0e-53e7-404e-8892-7633437b4613,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,Large Cell,False,Large Cell,,,,
c495d6fd-3d50-4e1a-9119-80efc2668f84,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Large cell is less common and is seen in about 10 percent of cases, most of whom are male. The diagnosis is made by cell size, which is large and easily distinguished from squamous cell cancer or adenocarcinoma. The lesions can be anywhere in the lung but are often found in the periphery. This is a fast-growing cancer and so is frequently diagnosed at a later disease stage.",True,Large Cell,,,,
fc585bbd-845d-43c8-8b22-f0dea2364330,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,Small Cell,False,Small Cell,,,,
0fc22ffa-c99f-47e1-93e9-257e39d9f538,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"The previous three types of cancer are collectively known as non-small cell lung cancer. Alternatively, small cell cancer is found in about 15 percent of cases. It is less predominant in men, and incidence in women is rising. The small cells have an oat-like appearance, and the most common small cell cancer is known as oat cell carcinoma and the lesions frequently have endocrine function. Originating in the main bronchi this cancer spreads very quickly into other thoracic and extrathoracic sites, and this form carries a very poor prognosis.",True,Small Cell,,,,
723327cf-bd70-4cde-8dfb-5078652473c8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,The characteristics of these forms of lung cancer are summarized in table 6.1.,True,Small Cell,,,,
53fa73ed-c0bc-4a64-8bbd-ec78276f5657,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,Table 6.1: Summary of forms of lung cancer.,True,Small Cell,,,,
2bce9f32-0985-4cea-b83b-3c04a730aa5a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,Clinical Signs,False,Clinical Signs,,,,
285ddc76-3255-43f9-8aea-75ba82d0b066,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"The signs and symptoms can be variable and diverse depending on the location, type, size, and rapidity of growth. Patients may even be asymptomatic when the lesion is found on chest x-ray or with bronchoscope.",True,Clinical Signs,,,,
1d1242a7-cd01-4507-aaa5-5c5d72d87331,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"The most common symptom is cough, but unfortunately the patient, likely being a smoker, may be accustomed to cough and not think anything of it. Bloody sputum occurs in only about half of patients and is a frequent cause for them seeking medical advice, and severe hemoptysis is uncommon.",True,Clinical Signs,,,,
92ead256-eb6a-492b-94c7-49e25fc185b3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Chest pain is fairly common and ranges from a mild ache or feeling of heaviness, to severe and unremitting. Pain does not necessarily indicate pleural or chest wall involvement, although significant steady pain is more indicative of this complication.",True,Clinical Signs,,,,
da839d63-8739-4fa9-a1be-8d13ddf67319,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Dyspnea may arise as the tumor obstructs a major airway or causes a large pleural effusion, but it can also be due to underlying bronchopulmonary disease.",True,Clinical Signs,,,,
0830e379-9dd4-423c-bb9f-d75c078878ee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Physical exam is likely to be normal in the early stages of the disease, but as the cancer progresses the exam usually reveals signs associated with either bronchial obstruction or a consequence of metastasis. Bronchial obstruction can lead to wheeze or other modified breath sounds, atelectasis, down-stream pneumonia, or pleural effusion. Paraneoplastic syndromes associated with the cancer can cause disruption to other systems and lead to characteristic weight loss, muscle wasting, and digital clubbing.",True,Clinical Signs,,,,
40ebe9d6-bbe8-4c4a-a70c-7dd076adaed4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Clinical Signs,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
40ebe9d6-bbe8-4c4a-a70c-7dd076adaed4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Small Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
40ebe9d6-bbe8-4c4a-a70c-7dd076adaed4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Large Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
40ebe9d6-bbe8-4c4a-a70c-7dd076adaed4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Adenocarcinoma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
40ebe9d6-bbe8-4c4a-a70c-7dd076adaed4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,Squamous Cell,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
40ebe9d6-bbe8-4c4a-a70c-7dd076adaed4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Chest x-ray is usually only capable of detecting advanced cancer stages, and therefore is not the best screening tool. Low-dose CT screening can be used to detect early stages of disease before symptoms arise and is advised for patients between fifty to eighty years old with a twenty-pack-per-year smoking history or who have quit smoking in the past fifteen years. Once the disease is established, however, the x-ray’s findings can either be direct detection of a mass, or a secondary consequence of the mass; therefore they are quite variable (figure 6.1).",True,Clinical Signs,Figure 6.1,6. Lung Cancer,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/6.1.png,Figure 6.1: Potential radiographic findings in lung cancer.
4f2fba6d-4d0b-4f04-8864-4c27183b6de3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,Text,False,Text,,,,
da554a6f-3d6f-4f95-9b4f-a5a108542eea,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 20.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
7b7c024b-24c3-4be5-8e64-0c3184e97c3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
60fc0e81-792d-469a-b1a8-36d8610c6b87,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,6. Lung Cancer,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lung-cancer/,"Table 6.1: Summary of forms of lung cancer. Includes Squamous Cell Carcinoma Lung 40x by Calicut Medical College from WikimediaCommons (CC BY-SA 4.0), Papillary adenocarcinoma of the lung — intermed mag by Nephron from WikimediaCommons (CC BY-SA 3.0), Large cell carcinoma of the lung by The Armed Forces Institute of Pathology (AFIP) from WikimediaCommons (Public domain), and Lung small cell carcinoma (1) by core needle biopsy by KGH from WikimediaCommons (CC BY-SA 3.0).",True,Text,,,,
56cdcda8-5410-4a9a-b9e0-4b3903d27c1a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"There are about two hundred thousand cases of ARDS in the United States each year. Each case starts with an initial insult to the lung parenchyma and there are numerous examples of this instigating event, but the most common of these (and therefore worth remembering) are sepsis, pulmonary aspiration, and thoracic trauma. The insult can arrive from the airway, such as in pulmonary aspiration or smoke inhalation, or can arrive from the bloodstream, as in a fat embolism or blood-born pathogen.",True,Text,,,,
01bbc814-2276-4901-bc9f-9f07e914f0f3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"Regardless of the insult’s route or indeed form, the ensuing pathological events are similar and lead to the same alteration of the lungs. What is initiated is a defensive inflammatory response, and what results is vascular endothelial and alveolar epithelial damage and a leaky alveolar capillary membrane.",True,Text,,,,
b2a8a37a-8535-47d2-acfe-ff7ef390f4cb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,Let us look at the process step-by-step.,False,Let us look at the process step-by-step.,,,,
b002921a-3855-45f1-bd5a-3d96e9e69018,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
b002921a-3855-45f1-bd5a-3d96e9e69018,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
b002921a-3855-45f1-bd5a-3d96e9e69018,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
b002921a-3855-45f1-bd5a-3d96e9e69018,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
b002921a-3855-45f1-bd5a-3d96e9e69018,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
2794a745-20cb-4acf-b405-e536c3706482,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,Stages of ARDS,False,Stages of ARDS,,,,
e54ba1f2-811d-4479-8f6a-356829aa4914,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,There are three defined stages for the progression of ARDS.,False,There are three defined stages for the progression of ARDS.,,,,
81fd3fe0-f6b1-4b2f-8f8b-91243a4d8699,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
81fd3fe0-f6b1-4b2f-8f8b-91243a4d8699,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
81fd3fe0-f6b1-4b2f-8f8b-91243a4d8699,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
81fd3fe0-f6b1-4b2f-8f8b-91243a4d8699,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
81fd3fe0-f6b1-4b2f-8f8b-91243a4d8699,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
d97bee38-539e-41c2-88f9-d40dec596de6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
d97bee38-539e-41c2-88f9-d40dec596de6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
d97bee38-539e-41c2-88f9-d40dec596de6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
d97bee38-539e-41c2-88f9-d40dec596de6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
d97bee38-539e-41c2-88f9-d40dec596de6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
b43019e3-eb73-4f55-8900-49b4367dafee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
b43019e3-eb73-4f55-8900-49b4367dafee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
b43019e3-eb73-4f55-8900-49b4367dafee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
b43019e3-eb73-4f55-8900-49b4367dafee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
b43019e3-eb73-4f55-8900-49b4367dafee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
eb8b7084-b786-4bf2-a726-f9174f2d84aa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,Systemic pathophysiology of ARDS,False,Systemic pathophysiology of ARDS,,,,
bca299ce-c242-4db3-a09d-fe0e59b21c40,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"We start with initial lung injury leading to alveolarcapillary leaking. As we have seen, this leads to the airspace edema and hyaline membrane formation.",True,Systemic pathophysiology of ARDS,,,,
b87eec7f-9f61-4c00-838d-5a163aebf10b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"The lack of gas exchange from affected areas produces a right–left shunt and hypoxemia will result. This produces dyspnea, the major symptom of ARDS.",True,Systemic pathophysiology of ARDS,,,,
b1e93c93-2590-4e21-8d02-3e16493195df,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"But the disruption caused by the inflammatory process also leads to other pathophysiological issues. The loss of type II cells causes surfactant production to decline. This of course reduces lung compliance, and the resultant increase in the work of breathing contributes to the patient’s dyspnea.",True,Systemic pathophysiology of ARDS,,,,
7136c68b-396a-4e35-9b14-9e06025e19e2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"But we are still not done. The fibrin clots forming obstructions in the lung microvasculature lead to V/Q mismatches, and these contribute to the hypoxemia. The obstructed vasculature also produces pulmonary hypertension, which is exacerbated by the vasculature’s response to the hypoxia.",True,Systemic pathophysiology of ARDS,,,,
2ecfaf5b-8efb-465b-b22d-a058379b6da2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,These mechanisms are reflected in the clinical manifestations of ARDS.,False,These mechanisms are reflected in the clinical manifestations of ARDS.,,,,
851fb10a-bdf8-4c87-9475-7ac2afe90723,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,Clinical signs of ARDS,False,Clinical signs of ARDS,,,,
4d0fb6e4-a76c-4d8b-a501-8e8dd45920f3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"The onset of dyspnea usually occurs within one to two days after the initial injury, and as tachypnea arises, this symptom progressively worsens. Cough is common and may produce blood-tinged sputum. Findings on chest exam may be surprisingly scant, but some bronchial breath sounds and crackles may be heard.",True,Clinical signs of ARDS,,,,
899da8e7-7c71-4f23-9158-a61a1da39096,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"As cyanosis becomes apparent, minute ventilation and dyspnea continue to increase and the patient will likely become distressed.",True,Clinical signs of ARDS,,,,
ce745529-8ee6-4ec7-8b21-bd5fce8cf006,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"A high ventilatory rate driven by the hypoxemia can produce hypocapnia and a respiratory alkalosis. The arterial pH can be complicated by the underlying disorder, and it is not uncommon for a mixed acid–base disorder to occur with concurrent respiratory alkalosis and metabolic acidosis. At the onset of respiratory failure arterial CO2 will rise and produce a respiratory acidosis.",True,Clinical signs of ARDS,,,,
f8616bb2-6c63-4fc9-bf8a-9bcd12f1a732,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
f8616bb2-6c63-4fc9-bf8a-9bcd12f1a732,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
f8616bb2-6c63-4fc9-bf8a-9bcd12f1a732,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
f8616bb2-6c63-4fc9-bf8a-9bcd12f1a732,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
f8616bb2-6c63-4fc9-bf8a-9bcd12f1a732,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
b66d19ed-4bac-409b-900e-56e1916f41a5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,So now you should have a clear understanding that after an initial insult to the lung an exaggerated and perpetual inflammatory response leads to the destruction of the alveolar–capillary interface. The resulting edema and hyaline membrane formation produces severe hypoxemia and a critically ill patient.,True,Clinical signs of ARDS,,,,
2b893c3e-06dd-4978-b4f6-bfdced1fc2f3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,Text,False,Text,,,,
a657cac1-87c9-4a34-a8b2-a3d673f6934b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 27.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
1ad22479-cf9b-4964-acac-6b7570cbc5c6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
5351bcef-c613-420f-a998-817912cb0590,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-4,"West, John B. “Chapter 8: Respiratory Failure.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Text,,,,
2a833e60-fca6-4369-a5bc-716fc52b636c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"There are about two hundred thousand cases of ARDS in the United States each year. Each case starts with an initial insult to the lung parenchyma and there are numerous examples of this instigating event, but the most common of these (and therefore worth remembering) are sepsis, pulmonary aspiration, and thoracic trauma. The insult can arrive from the airway, such as in pulmonary aspiration or smoke inhalation, or can arrive from the bloodstream, as in a fat embolism or blood-born pathogen.",True,Text,,,,
83f2ecf0-6ccd-46cc-90b7-010c67264cd8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"Regardless of the insult’s route or indeed form, the ensuing pathological events are similar and lead to the same alteration of the lungs. What is initiated is a defensive inflammatory response, and what results is vascular endothelial and alveolar epithelial damage and a leaky alveolar capillary membrane.",True,Text,,,,
8ed8b4ce-1c6e-4a95-b1b3-9e32bed8cbb4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,Let us look at the process step-by-step.,False,Let us look at the process step-by-step.,,,,
c593c726-2c75-4b57-8b66-843a79eafc8b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
c593c726-2c75-4b57-8b66-843a79eafc8b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
c593c726-2c75-4b57-8b66-843a79eafc8b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
c593c726-2c75-4b57-8b66-843a79eafc8b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
c593c726-2c75-4b57-8b66-843a79eafc8b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
225e88f8-95ec-4407-a660-506cf84b6e2d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,Stages of ARDS,False,Stages of ARDS,,,,
f6d35331-bc09-463e-8dde-d5f61c8e2df8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,There are three defined stages for the progression of ARDS.,False,There are three defined stages for the progression of ARDS.,,,,
f164df64-01a2-452f-8a5c-cad904117b3f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
f164df64-01a2-452f-8a5c-cad904117b3f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
f164df64-01a2-452f-8a5c-cad904117b3f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
f164df64-01a2-452f-8a5c-cad904117b3f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
f164df64-01a2-452f-8a5c-cad904117b3f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
4d8e5507-4921-4d4d-bbfc-5fde235670e5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
4d8e5507-4921-4d4d-bbfc-5fde235670e5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
4d8e5507-4921-4d4d-bbfc-5fde235670e5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
4d8e5507-4921-4d4d-bbfc-5fde235670e5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
4d8e5507-4921-4d4d-bbfc-5fde235670e5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
794e7da2-9073-46d6-8c46-00074b80d384,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
794e7da2-9073-46d6-8c46-00074b80d384,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
794e7da2-9073-46d6-8c46-00074b80d384,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
794e7da2-9073-46d6-8c46-00074b80d384,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
794e7da2-9073-46d6-8c46-00074b80d384,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
4a20a4d1-cb2f-4e92-8b47-26b0280be5d0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,Systemic pathophysiology of ARDS,False,Systemic pathophysiology of ARDS,,,,
09c2a108-87c1-4ab4-b6f2-5319e698a48e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"We start with initial lung injury leading to alveolarcapillary leaking. As we have seen, this leads to the airspace edema and hyaline membrane formation.",True,Systemic pathophysiology of ARDS,,,,
77a85949-b1d2-44fb-91a1-1aa7969fb4e9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"The lack of gas exchange from affected areas produces a right–left shunt and hypoxemia will result. This produces dyspnea, the major symptom of ARDS.",True,Systemic pathophysiology of ARDS,,,,
39efb9bc-eaf2-4b05-93a1-04764c7e0593,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"But the disruption caused by the inflammatory process also leads to other pathophysiological issues. The loss of type II cells causes surfactant production to decline. This of course reduces lung compliance, and the resultant increase in the work of breathing contributes to the patient’s dyspnea.",True,Systemic pathophysiology of ARDS,,,,
d8865174-4a60-4d88-b7a4-f0796f715965,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"But we are still not done. The fibrin clots forming obstructions in the lung microvasculature lead to V/Q mismatches, and these contribute to the hypoxemia. The obstructed vasculature also produces pulmonary hypertension, which is exacerbated by the vasculature’s response to the hypoxia.",True,Systemic pathophysiology of ARDS,,,,
50d4e331-458a-40f2-867a-5059859e6b3a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,These mechanisms are reflected in the clinical manifestations of ARDS.,False,These mechanisms are reflected in the clinical manifestations of ARDS.,,,,
c1e481a6-582a-4aa9-bf42-41d1cf4eaad8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,Clinical signs of ARDS,False,Clinical signs of ARDS,,,,
5a56aad1-86ee-4533-8cae-aeb1a54afee0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"The onset of dyspnea usually occurs within one to two days after the initial injury, and as tachypnea arises, this symptom progressively worsens. Cough is common and may produce blood-tinged sputum. Findings on chest exam may be surprisingly scant, but some bronchial breath sounds and crackles may be heard.",True,Clinical signs of ARDS,,,,
b25a35fc-9e94-458b-aeee-3c762fad26e8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"As cyanosis becomes apparent, minute ventilation and dyspnea continue to increase and the patient will likely become distressed.",True,Clinical signs of ARDS,,,,
de8975df-b307-4e7f-a858-4ff42f62ca08,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"A high ventilatory rate driven by the hypoxemia can produce hypocapnia and a respiratory alkalosis. The arterial pH can be complicated by the underlying disorder, and it is not uncommon for a mixed acid–base disorder to occur with concurrent respiratory alkalosis and metabolic acidosis. At the onset of respiratory failure arterial CO2 will rise and produce a respiratory acidosis.",True,Clinical signs of ARDS,,,,
926fa2d0-eea2-45e2-adf5-5d3b0a42de41,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
926fa2d0-eea2-45e2-adf5-5d3b0a42de41,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
926fa2d0-eea2-45e2-adf5-5d3b0a42de41,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
926fa2d0-eea2-45e2-adf5-5d3b0a42de41,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
926fa2d0-eea2-45e2-adf5-5d3b0a42de41,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
8a92e673-88b3-4b38-b57d-9a39005fd3b8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,So now you should have a clear understanding that after an initial insult to the lung an exaggerated and perpetual inflammatory response leads to the destruction of the alveolar–capillary interface. The resulting edema and hyaline membrane formation produces severe hypoxemia and a critically ill patient.,True,Clinical signs of ARDS,,,,
def3f426-9277-408f-a238-179c20f15893,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,Text,False,Text,,,,
4f39b8ad-70fb-43ce-a637-45f6a6d66bee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 27.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
c017d08c-0829-4750-a353-eae2de6c3133,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
c8eaf83b-5ecd-4c40-9486-a9c65ed55c52,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-3,"West, John B. “Chapter 8: Respiratory Failure.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Text,,,,
f0f5f419-a889-4176-a98f-7f70ab8791c6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"There are about two hundred thousand cases of ARDS in the United States each year. Each case starts with an initial insult to the lung parenchyma and there are numerous examples of this instigating event, but the most common of these (and therefore worth remembering) are sepsis, pulmonary aspiration, and thoracic trauma. The insult can arrive from the airway, such as in pulmonary aspiration or smoke inhalation, or can arrive from the bloodstream, as in a fat embolism or blood-born pathogen.",True,Text,,,,
72c9c6c9-4e3a-4301-a0a1-ae87a8490809,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"Regardless of the insult’s route or indeed form, the ensuing pathological events are similar and lead to the same alteration of the lungs. What is initiated is a defensive inflammatory response, and what results is vascular endothelial and alveolar epithelial damage and a leaky alveolar capillary membrane.",True,Text,,,,
efe04f16-095f-4c1c-90ad-ed71d1ddee43,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,Let us look at the process step-by-step.,False,Let us look at the process step-by-step.,,,,
945abe34-56b6-42b1-a990-baa0370bda3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
945abe34-56b6-42b1-a990-baa0370bda3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
945abe34-56b6-42b1-a990-baa0370bda3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
945abe34-56b6-42b1-a990-baa0370bda3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
945abe34-56b6-42b1-a990-baa0370bda3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
d017bc7d-8443-4383-a970-2e1d8207309b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,Stages of ARDS,False,Stages of ARDS,,,,
7c53a68e-dc71-4a23-bba0-75b1194b3df2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,There are three defined stages for the progression of ARDS.,False,There are three defined stages for the progression of ARDS.,,,,
9095213c-11ce-4a2f-8c53-ac4cdc09f192,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
9095213c-11ce-4a2f-8c53-ac4cdc09f192,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
9095213c-11ce-4a2f-8c53-ac4cdc09f192,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
9095213c-11ce-4a2f-8c53-ac4cdc09f192,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
9095213c-11ce-4a2f-8c53-ac4cdc09f192,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
075b3558-c15a-40e9-b9b8-92b1baba48b9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
075b3558-c15a-40e9-b9b8-92b1baba48b9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
075b3558-c15a-40e9-b9b8-92b1baba48b9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
075b3558-c15a-40e9-b9b8-92b1baba48b9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
075b3558-c15a-40e9-b9b8-92b1baba48b9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
e31fe05e-5d34-4c2c-92c5-6915a0befe39,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
e31fe05e-5d34-4c2c-92c5-6915a0befe39,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
e31fe05e-5d34-4c2c-92c5-6915a0befe39,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
e31fe05e-5d34-4c2c-92c5-6915a0befe39,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
e31fe05e-5d34-4c2c-92c5-6915a0befe39,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
017be6c3-28d6-4d7d-85fe-906d447ecc44,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,Systemic pathophysiology of ARDS,False,Systemic pathophysiology of ARDS,,,,
94a56487-68ed-4cbe-99d9-573fe37a84dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"We start with initial lung injury leading to alveolarcapillary leaking. As we have seen, this leads to the airspace edema and hyaline membrane formation.",True,Systemic pathophysiology of ARDS,,,,
28caf3f9-536e-47f8-9c4f-96b84e4675ef,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"The lack of gas exchange from affected areas produces a right–left shunt and hypoxemia will result. This produces dyspnea, the major symptom of ARDS.",True,Systemic pathophysiology of ARDS,,,,
37167f0b-71cf-44f3-bfde-73675b62498c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"But the disruption caused by the inflammatory process also leads to other pathophysiological issues. The loss of type II cells causes surfactant production to decline. This of course reduces lung compliance, and the resultant increase in the work of breathing contributes to the patient’s dyspnea.",True,Systemic pathophysiology of ARDS,,,,
834b5655-52c3-490a-857e-63ede77c799e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"But we are still not done. The fibrin clots forming obstructions in the lung microvasculature lead to V/Q mismatches, and these contribute to the hypoxemia. The obstructed vasculature also produces pulmonary hypertension, which is exacerbated by the vasculature’s response to the hypoxia.",True,Systemic pathophysiology of ARDS,,,,
78953acc-2727-464c-93b3-6f2bed511899,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,These mechanisms are reflected in the clinical manifestations of ARDS.,False,These mechanisms are reflected in the clinical manifestations of ARDS.,,,,
dd5e3e21-813c-48a4-ae63-2de8951fe792,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,Clinical signs of ARDS,False,Clinical signs of ARDS,,,,
8ab5698f-b2c8-4384-87b1-fc5aa1e0b322,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"The onset of dyspnea usually occurs within one to two days after the initial injury, and as tachypnea arises, this symptom progressively worsens. Cough is common and may produce blood-tinged sputum. Findings on chest exam may be surprisingly scant, but some bronchial breath sounds and crackles may be heard.",True,Clinical signs of ARDS,,,,
50873ff6-5053-4478-a1d7-305658107666,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"As cyanosis becomes apparent, minute ventilation and dyspnea continue to increase and the patient will likely become distressed.",True,Clinical signs of ARDS,,,,
dec49d3c-dcb9-4dab-9041-1d0d9f2c25c3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"A high ventilatory rate driven by the hypoxemia can produce hypocapnia and a respiratory alkalosis. The arterial pH can be complicated by the underlying disorder, and it is not uncommon for a mixed acid–base disorder to occur with concurrent respiratory alkalosis and metabolic acidosis. At the onset of respiratory failure arterial CO2 will rise and produce a respiratory acidosis.",True,Clinical signs of ARDS,,,,
e3503de6-923b-4720-9683-bd5980b890da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
e3503de6-923b-4720-9683-bd5980b890da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
e3503de6-923b-4720-9683-bd5980b890da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
e3503de6-923b-4720-9683-bd5980b890da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
e3503de6-923b-4720-9683-bd5980b890da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
67839ead-0ef8-41de-a432-8aca96daf31f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,So now you should have a clear understanding that after an initial insult to the lung an exaggerated and perpetual inflammatory response leads to the destruction of the alveolar–capillary interface. The resulting edema and hyaline membrane formation produces severe hypoxemia and a critically ill patient.,True,Clinical signs of ARDS,,,,
59cb90d8-63ed-47eb-b560-7c3a710e7625,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,Text,False,Text,,,,
0785dfc8-c747-4bba-ba53-97e7e95d60e2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 27.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
252425ef-76cd-48bb-911a-d0413bad4c42,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
0091bbb9-8d97-4127-ac9b-290c7678a458,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Stages of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-2,"West, John B. “Chapter 8: Respiratory Failure.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Text,,,,
b2455f7b-ac46-41d9-8fd6-b5f35cd5dbb7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"There are about two hundred thousand cases of ARDS in the United States each year. Each case starts with an initial insult to the lung parenchyma and there are numerous examples of this instigating event, but the most common of these (and therefore worth remembering) are sepsis, pulmonary aspiration, and thoracic trauma. The insult can arrive from the airway, such as in pulmonary aspiration or smoke inhalation, or can arrive from the bloodstream, as in a fat embolism or blood-born pathogen.",True,Text,,,,
5c1a8236-1108-4b21-8cdf-d5e3fa7875f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"Regardless of the insult’s route or indeed form, the ensuing pathological events are similar and lead to the same alteration of the lungs. What is initiated is a defensive inflammatory response, and what results is vascular endothelial and alveolar epithelial damage and a leaky alveolar capillary membrane.",True,Text,,,,
480e05bb-96f9-442b-bdc6-da9278caca98,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,Let us look at the process step-by-step.,False,Let us look at the process step-by-step.,,,,
48b56010-1d3c-4ce7-8a04-df89fe76a920,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
48b56010-1d3c-4ce7-8a04-df89fe76a920,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
48b56010-1d3c-4ce7-8a04-df89fe76a920,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
48b56010-1d3c-4ce7-8a04-df89fe76a920,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
48b56010-1d3c-4ce7-8a04-df89fe76a920,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
4749a5fd-bd97-47e3-ada0-d77a273ee4dc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,Stages of ARDS,False,Stages of ARDS,,,,
fc10a7e1-1340-41dd-b992-746fcf4041d9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,There are three defined stages for the progression of ARDS.,False,There are three defined stages for the progression of ARDS.,,,,
ce8d9f8d-1ae5-4a3c-abb2-cad48d4eebde,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
ce8d9f8d-1ae5-4a3c-abb2-cad48d4eebde,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
ce8d9f8d-1ae5-4a3c-abb2-cad48d4eebde,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
ce8d9f8d-1ae5-4a3c-abb2-cad48d4eebde,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
ce8d9f8d-1ae5-4a3c-abb2-cad48d4eebde,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
f91fd127-67cb-42e3-b520-6fdac63ec871,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
f91fd127-67cb-42e3-b520-6fdac63ec871,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
f91fd127-67cb-42e3-b520-6fdac63ec871,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
f91fd127-67cb-42e3-b520-6fdac63ec871,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
f91fd127-67cb-42e3-b520-6fdac63ec871,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
cdfc821b-e48d-4636-a71f-d1e640d4f065,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
cdfc821b-e48d-4636-a71f-d1e640d4f065,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
cdfc821b-e48d-4636-a71f-d1e640d4f065,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
cdfc821b-e48d-4636-a71f-d1e640d4f065,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
cdfc821b-e48d-4636-a71f-d1e640d4f065,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
1a6348c4-4d0d-414c-930a-ffefacb65604,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,Systemic pathophysiology of ARDS,False,Systemic pathophysiology of ARDS,,,,
2b1fc29d-577e-49c7-8256-c830e12c3a44,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"We start with initial lung injury leading to alveolarcapillary leaking. As we have seen, this leads to the airspace edema and hyaline membrane formation.",True,Systemic pathophysiology of ARDS,,,,
f7fdb203-176b-4afb-adcf-3de0e3bb2e8c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"The lack of gas exchange from affected areas produces a right–left shunt and hypoxemia will result. This produces dyspnea, the major symptom of ARDS.",True,Systemic pathophysiology of ARDS,,,,
92de044f-15a8-44e6-ae4f-58935bd6e339,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"But the disruption caused by the inflammatory process also leads to other pathophysiological issues. The loss of type II cells causes surfactant production to decline. This of course reduces lung compliance, and the resultant increase in the work of breathing contributes to the patient’s dyspnea.",True,Systemic pathophysiology of ARDS,,,,
38e3bff4-088d-44d6-a214-302315556215,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"But we are still not done. The fibrin clots forming obstructions in the lung microvasculature lead to V/Q mismatches, and these contribute to the hypoxemia. The obstructed vasculature also produces pulmonary hypertension, which is exacerbated by the vasculature’s response to the hypoxia.",True,Systemic pathophysiology of ARDS,,,,
fa6fec1a-6b48-47bd-bc49-724ff5c04cd7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,These mechanisms are reflected in the clinical manifestations of ARDS.,False,These mechanisms are reflected in the clinical manifestations of ARDS.,,,,
175ea06b-bd3b-4f6a-bd4d-d53c0793dd61,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,Clinical signs of ARDS,False,Clinical signs of ARDS,,,,
ef028dce-b8db-4dc6-b04b-0b67bf8e73f6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"The onset of dyspnea usually occurs within one to two days after the initial injury, and as tachypnea arises, this symptom progressively worsens. Cough is common and may produce blood-tinged sputum. Findings on chest exam may be surprisingly scant, but some bronchial breath sounds and crackles may be heard.",True,Clinical signs of ARDS,,,,
80bcb22c-f2fb-4cf4-bd76-3ed065f5dc0b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"As cyanosis becomes apparent, minute ventilation and dyspnea continue to increase and the patient will likely become distressed.",True,Clinical signs of ARDS,,,,
572dd8a9-6583-4f9c-b9bb-5d00c7d3e784,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"A high ventilatory rate driven by the hypoxemia can produce hypocapnia and a respiratory alkalosis. The arterial pH can be complicated by the underlying disorder, and it is not uncommon for a mixed acid–base disorder to occur with concurrent respiratory alkalosis and metabolic acidosis. At the onset of respiratory failure arterial CO2 will rise and produce a respiratory acidosis.",True,Clinical signs of ARDS,,,,
618e936a-70aa-46ba-abd3-4c48e1bd864a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
618e936a-70aa-46ba-abd3-4c48e1bd864a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
618e936a-70aa-46ba-abd3-4c48e1bd864a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
618e936a-70aa-46ba-abd3-4c48e1bd864a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
618e936a-70aa-46ba-abd3-4c48e1bd864a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
ccf69ca5-600c-4f1d-8ad3-4bef78465f44,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,So now you should have a clear understanding that after an initial insult to the lung an exaggerated and perpetual inflammatory response leads to the destruction of the alveolar–capillary interface. The resulting edema and hyaline membrane formation produces severe hypoxemia and a critically ill patient.,True,Clinical signs of ARDS,,,,
07b44bb4-b5ff-43f3-9439-d8fa069160fb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,Text,False,Text,,,,
8dae0b3c-4a71-449b-8ec5-ddd28f969495,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 27.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
09cec6c7-731f-43e9-b400-a06b3920ab7b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
a6b6c3a9-9bbb-4ec2-a75f-11925b630eb5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pathology of ARDS,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/#chapter-33-section-1,"West, John B. “Chapter 8: Respiratory Failure.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Text,,,,
bae20b6d-84ce-4060-869e-8338c62193bf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"There are about two hundred thousand cases of ARDS in the United States each year. Each case starts with an initial insult to the lung parenchyma and there are numerous examples of this instigating event, but the most common of these (and therefore worth remembering) are sepsis, pulmonary aspiration, and thoracic trauma. The insult can arrive from the airway, such as in pulmonary aspiration or smoke inhalation, or can arrive from the bloodstream, as in a fat embolism or blood-born pathogen.",True,Text,,,,
21e86ca0-7e6c-4afe-b2f9-b27841857448,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"Regardless of the insult’s route or indeed form, the ensuing pathological events are similar and lead to the same alteration of the lungs. What is initiated is a defensive inflammatory response, and what results is vascular endothelial and alveolar epithelial damage and a leaky alveolar capillary membrane.",True,Text,,,,
5b1a1487-490e-4469-92a8-c468a5215cb2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,Let us look at the process step-by-step.,False,Let us look at the process step-by-step.,,,,
39b67833-ad47-425c-a8f2-6409c3fd1896,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
39b67833-ad47-425c-a8f2-6409c3fd1896,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
39b67833-ad47-425c-a8f2-6409c3fd1896,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
39b67833-ad47-425c-a8f2-6409c3fd1896,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
39b67833-ad47-425c-a8f2-6409c3fd1896,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,The process is summarized in figure 5.2.,True,Let us look at the process step-by-step.,Figure 5.2,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.2.png,Figure 5.2: Pathophysiological events of ARDS. ROS = reactive oxygen species.
3dbb2fad-a0de-41e0-a52e-4ba43a9da898,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,Stages of ARDS,False,Stages of ARDS,,,,
2a1ed0f5-8f95-457d-abc1-ebb0b20a0f26,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,There are three defined stages for the progression of ARDS.,False,There are three defined stages for the progression of ARDS.,,,,
c144f286-2a5b-4eb6-83bc-efca610a8f46,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
c144f286-2a5b-4eb6-83bc-efca610a8f46,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
c144f286-2a5b-4eb6-83bc-efca610a8f46,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
c144f286-2a5b-4eb6-83bc-efca610a8f46,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
c144f286-2a5b-4eb6-83bc-efca610a8f46,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"1. Exudative: The first six to seven days comprise the exudative phase that begins with edema appearing in the interstitial walls seen here by the widened alveolar septum. Cellular debris can also be seen in the airspaces, and this can continue with the formation of the hyaline membranes that coat the alveolar surface (figure 5.3).",True,There are three defined stages for the progression of ARDS.,Figure 5.3,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.3.jpg,Figure 5.3: Alveolar wall edema and onset of hyaline membrane formation during the exudative phase of ARDS. The debris inside the airspace is the result of the inflammatory response and the beginning of a hyaline membrane made of “cellular debris.”
e5cf8f7b-01ba-45a6-8637-72bd06f34a1c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
e5cf8f7b-01ba-45a6-8637-72bd06f34a1c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
e5cf8f7b-01ba-45a6-8637-72bd06f34a1c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
e5cf8f7b-01ba-45a6-8637-72bd06f34a1c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
e5cf8f7b-01ba-45a6-8637-72bd06f34a1c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"2. Proliferative: In the early proliferative stage, there is increased cell infiltration and squamous metaplasia with proliferation of type II cells (figure 5.4), and these mitotic type II cells have a “hob-nail” like appearance over a time line of weeks. The infiltrating cells include fibroblasts that begin laying down collagen.",True,There are three defined stages for the progression of ARDS.,Figure 5.4,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.4.jpg,Figure 5.4: Proliferation of type II cells and infiltration of fibroblasts in the proliferative phase of ARDS. A clear amount of debris in the airspace can be seen and forms a hyaline membrane that will impede gas exchange.
3e4a917c-fcb9-4781-897a-4cf12da80498,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
3e4a917c-fcb9-4781-897a-4cf12da80498,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
3e4a917c-fcb9-4781-897a-4cf12da80498,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
3e4a917c-fcb9-4781-897a-4cf12da80498,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
3e4a917c-fcb9-4781-897a-4cf12da80498,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"3. Fibrotic: Without resolution the patient may enter the third stage, fibrotic stage, that occurs over months (figure 5.5). This stage occurs much later and is a consequence of unresolved chronic inflammation. Diffuse fibrosis permanently obliterates normal lung architecture and may form cysts.",True,There are three defined stages for the progression of ARDS.,Figure 5.5,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage of ARDS.
6749b95a-2735-4a1e-9d36-16a2dd7dc5a0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,Systemic pathophysiology of ARDS,False,Systemic pathophysiology of ARDS,,,,
2febd2fa-ad5c-4883-98cd-ec76ab6ce02e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"We start with initial lung injury leading to alveolarcapillary leaking. As we have seen, this leads to the airspace edema and hyaline membrane formation.",True,Systemic pathophysiology of ARDS,,,,
127b0e7b-a295-4c9d-900c-73d2855e4123,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"The lack of gas exchange from affected areas produces a right–left shunt and hypoxemia will result. This produces dyspnea, the major symptom of ARDS.",True,Systemic pathophysiology of ARDS,,,,
9017c164-c0a8-4b44-a1bf-2f36f90cf1a8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"But the disruption caused by the inflammatory process also leads to other pathophysiological issues. The loss of type II cells causes surfactant production to decline. This of course reduces lung compliance, and the resultant increase in the work of breathing contributes to the patient’s dyspnea.",True,Systemic pathophysiology of ARDS,,,,
e6d55e1c-2940-476e-9837-1027341ea5ae,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"But we are still not done. The fibrin clots forming obstructions in the lung microvasculature lead to V/Q mismatches, and these contribute to the hypoxemia. The obstructed vasculature also produces pulmonary hypertension, which is exacerbated by the vasculature’s response to the hypoxia.",True,Systemic pathophysiology of ARDS,,,,
733b919d-e7d9-4187-8971-633e7638078d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,These mechanisms are reflected in the clinical manifestations of ARDS.,False,These mechanisms are reflected in the clinical manifestations of ARDS.,,,,
a0bb1f26-f648-4732-9313-0e875e213c89,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,Clinical signs of ARDS,False,Clinical signs of ARDS,,,,
cc8f3b4a-1744-4a8d-a969-08cc05a20f28,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"The onset of dyspnea usually occurs within one to two days after the initial injury, and as tachypnea arises, this symptom progressively worsens. Cough is common and may produce blood-tinged sputum. Findings on chest exam may be surprisingly scant, but some bronchial breath sounds and crackles may be heard.",True,Clinical signs of ARDS,,,,
700cd787-37a2-42bd-bac2-944732ba751a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"As cyanosis becomes apparent, minute ventilation and dyspnea continue to increase and the patient will likely become distressed.",True,Clinical signs of ARDS,,,,
7fff5bf5-a09d-4e36-ac61-1fb52a40bd1f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"A high ventilatory rate driven by the hypoxemia can produce hypocapnia and a respiratory alkalosis. The arterial pH can be complicated by the underlying disorder, and it is not uncommon for a mixed acid–base disorder to occur with concurrent respiratory alkalosis and metabolic acidosis. At the onset of respiratory failure arterial CO2 will rise and produce a respiratory acidosis.",True,Clinical signs of ARDS,,,,
e772717b-10be-453e-8f2c-260a435044e4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Clinical signs of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
e772717b-10be-453e-8f2c-260a435044e4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Systemic pathophysiology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
e772717b-10be-453e-8f2c-260a435044e4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Stages of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
e772717b-10be-453e-8f2c-260a435044e4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,Pathology of ARDS,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
e772717b-10be-453e-8f2c-260a435044e4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"Radiographic findings are an essential part of diagnosing the ARDS patient and will show diffuse bilateral interstitial and airspace densities caused by the edema (figure 5.7). Normal heart and vessel size and absence of pleural effusion distinguish ARDS from cardiogenic pulmonary edema. Although the x-ray gives the appearance of diffuse edema, high-resolution CT often shows that the process is heterogeneous and patchy. This heterogeneity is reflected by remnant patchy fibrosis if the patient recovers; however, the mortality rate for ARDS is around 50 percent.",True,Clinical signs of ARDS,Figure 5.7,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.7.jpeg,Figure 5.7: Diffuse bilateral densities associated with ARDS.
c037a52c-4137-4689-aabe-d29005643492,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,So now you should have a clear understanding that after an initial insult to the lung an exaggerated and perpetual inflammatory response leads to the destruction of the alveolar–capillary interface. The resulting edema and hyaline membrane formation produces severe hypoxemia and a critically ill patient.,True,Clinical signs of ARDS,,,,
d85d45fa-ee11-4a15-aea9-f808c408f342,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,Text,False,Text,,,,
e2bbb43c-806e-4bc3-9b4e-dd37cd729bcd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 27.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
361fbb0e-478b-4ac8-be97-4498c7dabab2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
06bdae96-1e91-4a85-b3fd-9c91fa6a2bc8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,5. Acute Respiratory Distress Syndrome,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/acute-respiratory-distress-syndrome/,"West, John B. “Chapter 8: Respiratory Failure.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Text,,,,
2bf2097e-c952-4e61-bdc7-c018fed73a0c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Before we start taking about diseases affecting the lung interstitium, let us remind ourselves of what it is.",True,Text,,,,
5a2ecb16-7483-4ecc-9625-a5985a2879c5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The interstitial tissue, sometimes referred to as parenchyma, surrounds the alveolar and capillary structures and contributes to the mechanical behavior of the lungs. The interstitium is extremely thin between the alveoli and capillaries, and forms the basement membrane through which gas exchange occurs. On the parenchymal side of the capillaries the interstitium is more substantial and is more involved in fluid exchange. There is also substantial amounts of interstitial tissue in the spaces around major vessels and airways, and it also makes up the interlobular septa.",True,Text,,,,
a74b942f-6009-491d-a057-817dbfa4d4d1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Mechanisms of ILD,False,Mechanisms of ILD,,,,
485f64ad-fa63-4fbf-8b74-59c779f369f8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Now we will look at the generalized mechanism of interstitial lung disease (figure 4.1). It is worth noting that the numerous conditions that the term ILD encompasses have subtle differences in mechanism and manifestations, and these differences are what we will deal with elsewhere.",True,Mechanisms of ILD,Figure 4.1,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
485f64ad-fa63-4fbf-8b74-59c779f369f8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Now we will look at the generalized mechanism of interstitial lung disease (figure 4.1). It is worth noting that the numerous conditions that the term ILD encompasses have subtle differences in mechanism and manifestations, and these differences are what we will deal with elsewhere.",True,Mechanisms of ILD,Figure 4.1,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
485f64ad-fa63-4fbf-8b74-59c779f369f8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Now we will look at the generalized mechanism of interstitial lung disease (figure 4.1). It is worth noting that the numerous conditions that the term ILD encompasses have subtle differences in mechanism and manifestations, and these differences are what we will deal with elsewhere.",True,Mechanisms of ILD,Figure 4.1,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
d93f40ad-2e9a-4561-aa97-f98e78ac26cd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,ILD,False,ILD,,,,
6288be73-5e03-483d-8f33-eb75f593ae7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Generally though, ILD starts with an initial insult to the lung (#1, figure 4.1); the type of insult is a major contributor to the different ILD conditions. (It probably will not be what is depicted in figure 4.1, but if it was, it might lead to the inflammatory condition of tiefitis.)",True,ILD,Figure 4.1,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
6288be73-5e03-483d-8f33-eb75f593ae7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Generally though, ILD starts with an initial insult to the lung (#1, figure 4.1); the type of insult is a major contributor to the different ILD conditions. (It probably will not be what is depicted in figure 4.1, but if it was, it might lead to the inflammatory condition of tiefitis.)",True,ILD,Figure 4.1,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
6288be73-5e03-483d-8f33-eb75f593ae7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Generally though, ILD starts with an initial insult to the lung (#1, figure 4.1); the type of insult is a major contributor to the different ILD conditions. (It probably will not be what is depicted in figure 4.1, but if it was, it might lead to the inflammatory condition of tiefitis.)",True,ILD,Figure 4.1,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
2704353f-3a9a-48a2-a80a-787c5aa914ee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,tiefitis,False,tiefitis,,,,
0d6d0d01-0c63-4bba-ae16-38598ec0bebd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"There is then a response by neutrophils and alveolar macrophages (#2, figure 4.1). The macrophage response seems particularly important to the development of ILD. Release of cytokines (#3, figure 4.1) attracts other inflammatory cells, and the arrival of polymorphonuclear leukocytes and lymphocytes play an important role in disease instigation. These cells release cytokines, enzymes, and toxic oxygen radicals that damage and destroy local tissue. Released growth factors, such as TGF-Beta, instigate the transition of mesenchymal cells to fibroblasts.",True,tiefitis,Figure 4.1,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
0d6d0d01-0c63-4bba-ae16-38598ec0bebd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"There is then a response by neutrophils and alveolar macrophages (#2, figure 4.1). The macrophage response seems particularly important to the development of ILD. Release of cytokines (#3, figure 4.1) attracts other inflammatory cells, and the arrival of polymorphonuclear leukocytes and lymphocytes play an important role in disease instigation. These cells release cytokines, enzymes, and toxic oxygen radicals that damage and destroy local tissue. Released growth factors, such as TGF-Beta, instigate the transition of mesenchymal cells to fibroblasts.",True,tiefitis,Figure 4.1,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
0d6d0d01-0c63-4bba-ae16-38598ec0bebd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"There is then a response by neutrophils and alveolar macrophages (#2, figure 4.1). The macrophage response seems particularly important to the development of ILD. Release of cytokines (#3, figure 4.1) attracts other inflammatory cells, and the arrival of polymorphonuclear leukocytes and lymphocytes play an important role in disease instigation. These cells release cytokines, enzymes, and toxic oxygen radicals that damage and destroy local tissue. Released growth factors, such as TGF-Beta, instigate the transition of mesenchymal cells to fibroblasts.",True,tiefitis,Figure 4.1,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
0930cfa0-06e6-4970-8ec3-ce8ab0031868,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"It is worth noting at this point that some forms of ILD are caused by an exaggerated immune reaction—either through an allergic-like response, or a direct immune disorder.",True,tiefitis,,,,
b95bc8bc-346f-4fba-875a-8acf17538a8e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The destruction of tissue and activity of a growing number of fibroblasts results in the inflamed interstitium becoming fibrosed with excess connective tissue, particularly collagen (#4, figure 4.1).",True,tiefitis,Figure 4.1,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
b95bc8bc-346f-4fba-875a-8acf17538a8e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The destruction of tissue and activity of a growing number of fibroblasts results in the inflamed interstitium becoming fibrosed with excess connective tissue, particularly collagen (#4, figure 4.1).",True,tiefitis,Figure 4.1,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
b95bc8bc-346f-4fba-875a-8acf17538a8e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The destruction of tissue and activity of a growing number of fibroblasts results in the inflamed interstitium becoming fibrosed with excess connective tissue, particularly collagen (#4, figure 4.1).",True,tiefitis,Figure 4.1,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
e29f4123-018e-437d-9f4e-375e9361e180,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Pathology of ILD,False,Pathology of ILD,,,,
0c71ff29-d3ba-42a8-8fce-844052080d90,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"These changes in structure dramatically change the functional and mechanical properties of the tissue. The changes also tend to follow a characteristic pattern, although, as you might imagine, different conditions have subtle differences in pattern.",True,Pathology of ILD,,,,
2f7dba2a-3d57-4504-8aab-3a738a53efd2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The action of fibroblasts laying down connective tissue, combined with the destruction of alveolar and capillary structures, leads to a widening of airspaces with thick collagenous and infiltrated walls (figure 4.2A and 4.2B), which are a functionally significant departure from the ideal structure for gas exchange.",True,Pathology of ILD,Figure 4.2,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
2f7dba2a-3d57-4504-8aab-3a738a53efd2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The action of fibroblasts laying down connective tissue, combined with the destruction of alveolar and capillary structures, leads to a widening of airspaces with thick collagenous and infiltrated walls (figure 4.2A and 4.2B), which are a functionally significant departure from the ideal structure for gas exchange.",True,Pathology of ILD,Figure 4.2,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
2f7dba2a-3d57-4504-8aab-3a738a53efd2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The action of fibroblasts laying down connective tissue, combined with the destruction of alveolar and capillary structures, leads to a widening of airspaces with thick collagenous and infiltrated walls (figure 4.2A and 4.2B), which are a functionally significant departure from the ideal structure for gas exchange.",True,Pathology of ILD,Figure 4.2,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
6ca2500b-8328-4fa4-8dff-737e70c8af8d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The thickened basement membrane poses a significant obstacle to the transfer of gases, and the dense connective tissue stiffens the lung and thereby reduces its compliance. Combined with loss of capillary beds and airspace surface area, gas exchange is reduced.",True,Pathology of ILD,,,,
caac64f9-dba5-4e86-981f-0c9bc3eb92d9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"At the end of the disease the lung takes on a characteristic honeycomb appearance, and “ground glass opacities” are a hallmark sign on CT images (figure 4.2C). These morphological changes lead to pathophysiological consequences that are shared by most forms of the disease, as all cause varying degrees of interstitial inflammation and connective tissue deposition.",True,Pathology of ILD,Figure 4.2,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
caac64f9-dba5-4e86-981f-0c9bc3eb92d9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"At the end of the disease the lung takes on a characteristic honeycomb appearance, and “ground glass opacities” are a hallmark sign on CT images (figure 4.2C). These morphological changes lead to pathophysiological consequences that are shared by most forms of the disease, as all cause varying degrees of interstitial inflammation and connective tissue deposition.",True,Pathology of ILD,Figure 4.2,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
caac64f9-dba5-4e86-981f-0c9bc3eb92d9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"At the end of the disease the lung takes on a characteristic honeycomb appearance, and “ground glass opacities” are a hallmark sign on CT images (figure 4.2C). These morphological changes lead to pathophysiological consequences that are shared by most forms of the disease, as all cause varying degrees of interstitial inflammation and connective tissue deposition.",True,Pathology of ILD,Figure 4.2,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
960fed43-8f50-48f9-a402-66f313f86cbf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Pathophysiology of ILD,False,Pathophysiology of ILD,,,,
3c042458-99fe-4f55-985d-09fb29fe1eae,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The first major issue is the reduced diffusion capacity of the involved areas, and all ILD patients demonstrate a reduced transfer factor, or DLCO (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
3c042458-99fe-4f55-985d-09fb29fe1eae,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The first major issue is the reduced diffusion capacity of the involved areas, and all ILD patients demonstrate a reduced transfer factor, or DLCO (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
3c042458-99fe-4f55-985d-09fb29fe1eae,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The first major issue is the reduced diffusion capacity of the involved areas, and all ILD patients demonstrate a reduced transfer factor, or DLCO (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
34939227-a8c9-4d82-8cdf-b7a470753c69,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Because of the heterogenous distribution of the disease, and the involvement of the pulmonary circulation, severe V/Q abnormalities arise throughout the lung. This and the reduced diffusion capacity result in hypoxemia. In the chronic disease state this may lead to cor pulmonale (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
34939227-a8c9-4d82-8cdf-b7a470753c69,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Because of the heterogenous distribution of the disease, and the involvement of the pulmonary circulation, severe V/Q abnormalities arise throughout the lung. This and the reduced diffusion capacity result in hypoxemia. In the chronic disease state this may lead to cor pulmonale (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
34939227-a8c9-4d82-8cdf-b7a470753c69,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Because of the heterogenous distribution of the disease, and the involvement of the pulmonary circulation, severe V/Q abnormalities arise throughout the lung. This and the reduced diffusion capacity result in hypoxemia. In the chronic disease state this may lead to cor pulmonale (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
5f0a5066-7816-41f8-bb4b-d3e9611df59f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The reduction in lung compliance leads to a reduced lung volume. This is easily detected with spirometry as shown by the inner plot of the flow-volume loop in figure 4.3. Because FEV1 and FVC are both reduced, the ratio frequently remains the same or may even rise; as such FEV1/FVC is a poor indicator of restrictive disease.",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
5f0a5066-7816-41f8-bb4b-d3e9611df59f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The reduction in lung compliance leads to a reduced lung volume. This is easily detected with spirometry as shown by the inner plot of the flow-volume loop in figure 4.3. Because FEV1 and FVC are both reduced, the ratio frequently remains the same or may even rise; as such FEV1/FVC is a poor indicator of restrictive disease.",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
5f0a5066-7816-41f8-bb4b-d3e9611df59f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The reduction in lung compliance leads to a reduced lung volume. This is easily detected with spirometry as shown by the inner plot of the flow-volume loop in figure 4.3. Because FEV1 and FVC are both reduced, the ratio frequently remains the same or may even rise; as such FEV1/FVC is a poor indicator of restrictive disease.",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
f1ec629d-7d66-4592-a222-c5466b6cea6d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The reduced lung volume and compliance results in a characteristic rapid, shallow breathing pattern as the patient tries to maintain alveolar ventilation (figure 4.3). However, while avoiding unnecessary increases in the work of breathing by not trying to over-expand the noncompliant lung, the rapid shallow breathing proportionally increases dead space ventilation.",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
f1ec629d-7d66-4592-a222-c5466b6cea6d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The reduced lung volume and compliance results in a characteristic rapid, shallow breathing pattern as the patient tries to maintain alveolar ventilation (figure 4.3). However, while avoiding unnecessary increases in the work of breathing by not trying to over-expand the noncompliant lung, the rapid shallow breathing proportionally increases dead space ventilation.",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
f1ec629d-7d66-4592-a222-c5466b6cea6d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The reduced lung volume and compliance results in a characteristic rapid, shallow breathing pattern as the patient tries to maintain alveolar ventilation (figure 4.3). However, while avoiding unnecessary increases in the work of breathing by not trying to over-expand the noncompliant lung, the rapid shallow breathing proportionally increases dead space ventilation.",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
c60ff515-57cc-465c-890f-8733b6745c07,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The reduction in tidal volume, combined with a raised hypoxic drive to breathe, results in the cardinal symptom of ILD, which is dyspnea (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
c60ff515-57cc-465c-890f-8733b6745c07,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The reduction in tidal volume, combined with a raised hypoxic drive to breathe, results in the cardinal symptom of ILD, which is dyspnea (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
c60ff515-57cc-465c-890f-8733b6745c07,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The reduction in tidal volume, combined with a raised hypoxic drive to breathe, results in the cardinal symptom of ILD, which is dyspnea (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
60c964f5-e704-431d-80fb-b1fea82c3126,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Clinical Signs of ILD,False,Clinical Signs of ILD,,,,
5e1f063f-f1c0-4dae-8e69-7164d4942037,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The correlation of dyspnea and disease stage is closer in ILD than any other respiratory disease. The onset is insidious, appearing first during exercise, and it likely contributes to the other major complaints of weakness and fatigue. The dyspnea gets progressively worse until it can be debilitating.",True,Clinical Signs of ILD,,,,
f791e25d-b16b-4201-94be-727765967b11,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Inflammation and excitation of pulmonary receptors leads to a nonproductive and persistent cough, and upon examination patients will have limited chest expansion and demonstrate the characteristic breathing pattern of restrictive lung disease.",True,Clinical Signs of ILD,,,,
359b4715-62df-4b4d-8d03-da46801bf029,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Hallmark lung sounds are fine crackles, commonly found at the base of the lung, and may appear louder than expected because of increased transmission through denser than normal tissue.",True,Clinical Signs of ILD,,,,
a577d412-0202-4478-96a2-acb4b15fac20,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,At later stages of the disease the patient shows signs of the prolonged hypoxemia with digital clubbing and cyanosis.,True,Clinical Signs of ILD,,,,
44188d5b-669b-47b4-8767-749f6d2f8aa7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Forms of Interstitial Lung Disease,False,Forms of Interstitial Lung Disease,,,,
ed9376b6-c726-4557-947d-0005c1a4e3cf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Our major subcategory is idiopathic interstitial pneumonia (figure 4.4), or IIP, and this is divided again into six more useful categories that can be distinguished by history, time line, and histological changes. We will deal with these categories in this section, but it might be noted that usual interstitial pneumonia, still frequently called idiopathic pulmonary fibrosis, is the only one that remains untreatable, and early differentiation from the other forms is critical (figure 4.4).",True,Forms of Interstitial Lung Disease,Figure 4.4,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
ed9376b6-c726-4557-947d-0005c1a4e3cf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Our major subcategory is idiopathic interstitial pneumonia (figure 4.4), or IIP, and this is divided again into six more useful categories that can be distinguished by history, time line, and histological changes. We will deal with these categories in this section, but it might be noted that usual interstitial pneumonia, still frequently called idiopathic pulmonary fibrosis, is the only one that remains untreatable, and early differentiation from the other forms is critical (figure 4.4).",True,Forms of Interstitial Lung Disease,Figure 4.4,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
ed9376b6-c726-4557-947d-0005c1a4e3cf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Our major subcategory is idiopathic interstitial pneumonia (figure 4.4), or IIP, and this is divided again into six more useful categories that can be distinguished by history, time line, and histological changes. We will deal with these categories in this section, but it might be noted that usual interstitial pneumonia, still frequently called idiopathic pulmonary fibrosis, is the only one that remains untreatable, and early differentiation from the other forms is critical (figure 4.4).",True,Forms of Interstitial Lung Disease,Figure 4.4,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
08ab9220-0913-4a7d-8109-9a3caba0c7a8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Interstitial lung diseases can also be induced by numerous different environmental causes that produce nuanced conditions that are distinguishable by environmental and social history (figure 4.4) as well as specific histological features.,True,Forms of Interstitial Lung Disease,Figure 4.4,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
08ab9220-0913-4a7d-8109-9a3caba0c7a8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Interstitial lung diseases can also be induced by numerous different environmental causes that produce nuanced conditions that are distinguishable by environmental and social history (figure 4.4) as well as specific histological features.,True,Forms of Interstitial Lung Disease,Figure 4.4,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
08ab9220-0913-4a7d-8109-9a3caba0c7a8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Interstitial lung diseases can also be induced by numerous different environmental causes that produce nuanced conditions that are distinguishable by environmental and social history (figure 4.4) as well as specific histological features.,True,Forms of Interstitial Lung Disease,Figure 4.4,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
27ff98b6-20f0-436a-8d91-d312ab01dd09,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The characteristics of usual interstitial pneumonia have been covered in the “Basis of ILD” section, so let us start looking at the pathophysiological and clinical features of the other broader disease categories.",True,Forms of Interstitial Lung Disease,,,,
45be8f70-d29b-4b56-a748-8855baf5f736,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,False,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,,,,
50787a16-ae6e-4bba-a29d-10236766ba20,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,We can deal with the first two together as both share common characteristics and are potentially the same disease occurring in different anatomical locations. Desquamative interstitial pneumonia and respiratory bronchiolitis–associated ILD are both smoking related and are relatively uncommon.,True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,,,,
91e53081-b90c-49bc-a7fb-9984fb280b67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The histological hallmark is accumulation of numerous smoker’s macrophages in the airspaces (figure 4.5) or the first- and second-order respiratory bronchioles. These macrophages have a characteristic brown pigmentation. In desquamative interstitial pneumonia the airspaces are the primary site of involvement, whereas a respiratory bronchiolitis–associated ILD sees more involvement of the bronchioles (as the name suggests). The alveolar septum may be thickened with infiltrate and there may be mild peribronchilor or alveolar fibrosis, but this does not result in a honeycomb pattern seen in usual interstitial pneumonia.",True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,Figure 4.5,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.5.jpeg,Figure 4.5: Smoker’s macrophages occupying an airspace.
91e53081-b90c-49bc-a7fb-9984fb280b67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The histological hallmark is accumulation of numerous smoker’s macrophages in the airspaces (figure 4.5) or the first- and second-order respiratory bronchioles. These macrophages have a characteristic brown pigmentation. In desquamative interstitial pneumonia the airspaces are the primary site of involvement, whereas a respiratory bronchiolitis–associated ILD sees more involvement of the bronchioles (as the name suggests). The alveolar septum may be thickened with infiltrate and there may be mild peribronchilor or alveolar fibrosis, but this does not result in a honeycomb pattern seen in usual interstitial pneumonia.",True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,Figure 4.5,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.5.jpeg,Figure 4.5: Smoker’s macrophages occupying an airspace.
91e53081-b90c-49bc-a7fb-9984fb280b67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The histological hallmark is accumulation of numerous smoker’s macrophages in the airspaces (figure 4.5) or the first- and second-order respiratory bronchioles. These macrophages have a characteristic brown pigmentation. In desquamative interstitial pneumonia the airspaces are the primary site of involvement, whereas a respiratory bronchiolitis–associated ILD sees more involvement of the bronchioles (as the name suggests). The alveolar septum may be thickened with infiltrate and there may be mild peribronchilor or alveolar fibrosis, but this does not result in a honeycomb pattern seen in usual interstitial pneumonia.",True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,Figure 4.5,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.5.jpeg,Figure 4.5: Smoker’s macrophages occupying an airspace.
59bb848d-4092-487d-adf4-e5a25c7cadcf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"These ILDs are more prevalent in men, and are usually found in the fifth decade of life and after thirty-pack years. They are marked by the gradual and insidious onset of dyspnea, but lung reductions are usually minimal with both forms. The response to corticosteroid therapy and smoking cessation is good in about 80 percent of patients who remain stable or improve.",True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,,,,
528cdcc2-f2a4-4a6f-9060-f58645483422,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Diffuse Alveolar Damage (DAD),False,Diffuse Alveolar Damage (DAD),,,,
17bb1651-8d8a-4b45-afc2-efd30c082a87,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"While the development of most interstitial lung diseases is slow and insidious, the hallmark of diffuse alveolar damage is rapid, occurring in a matter of days and often in previously healthy individuals. The manifestation of the disease is similar to acute respiratory distress syndrome, and in fact it has been suggested that DAD is a form of ARDS.",True,Diffuse Alveolar Damage (DAD),,,,
c57682e2-8ace-4639-8dc6-8b0d318ccbd1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The start is marked by a brief exudative phase with fluid entering the airspaces, but the following organizing or proliferative phase is what is usually seen by the time a biopsy is taken and where the similarities to ARDS are seen. The alveolar septa are thickened due to the interstitial edema and the septa may collapse or appose each other (figure 4.7). There is marked infiltration of the interstitial and airspaces by inflammatory cells, and type II cells proliferate. The destruction of the alveolar structure leaves a sludgy hyaline membrane of debris. Thrombi in small arteries may also be apparent.",True,Diffuse Alveolar Damage (DAD),Figure 4.7,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.7.jpeg,Figure 4.7: Diffuse alveolar damage.
c57682e2-8ace-4639-8dc6-8b0d318ccbd1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The start is marked by a brief exudative phase with fluid entering the airspaces, but the following organizing or proliferative phase is what is usually seen by the time a biopsy is taken and where the similarities to ARDS are seen. The alveolar septa are thickened due to the interstitial edema and the septa may collapse or appose each other (figure 4.7). There is marked infiltration of the interstitial and airspaces by inflammatory cells, and type II cells proliferate. The destruction of the alveolar structure leaves a sludgy hyaline membrane of debris. Thrombi in small arteries may also be apparent.",True,Diffuse Alveolar Damage (DAD),Figure 4.7,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.7.jpeg,Figure 4.7: Diffuse alveolar damage.
c57682e2-8ace-4639-8dc6-8b0d318ccbd1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The start is marked by a brief exudative phase with fluid entering the airspaces, but the following organizing or proliferative phase is what is usually seen by the time a biopsy is taken and where the similarities to ARDS are seen. The alveolar septa are thickened due to the interstitial edema and the septa may collapse or appose each other (figure 4.7). There is marked infiltration of the interstitial and airspaces by inflammatory cells, and type II cells proliferate. The destruction of the alveolar structure leaves a sludgy hyaline membrane of debris. Thrombi in small arteries may also be apparent.",True,Diffuse Alveolar Damage (DAD),Figure 4.7,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.7.jpeg,Figure 4.7: Diffuse alveolar damage.
686812e2-4e59-41f6-b99c-c0510409912e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Should the patient survive (about 50 percent do not) the healing phase can show recovery of the alveolar structure with varying degrees of fibrosis. Many patients return to normal lung function, but a few show a progressive fibrotic process that resembles idiopathic pulmonary fibrosis.",True,Diffuse Alveolar Damage (DAD),,,,
85e07c4e-5535-4942-9ac3-4df19764c6c7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Without biopsy, DAD is usually differentiated from other forms of interstitial disease by its rapid onset, but this can be confused with acute exacerbations of other diseases. However, the uniform pattern of damage in real DAD is representative of a single time line.",True,Diffuse Alveolar Damage (DAD),,,,
69d4d3b4-7a30-4e8c-9373-8785cf6ec1bf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Nonspecific Interstitial Pneumonia,False,Nonspecific Interstitial Pneumonia,,,,
4f4b5176-7c16-47a4-b394-6d43d48321aa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Our next disease is at least courteous enough to only have one name, nonspecific interstitial pneumonia (NSIP), but irritatingly, it has three groups that are determined by the degree of either interstitial inflammation or fibrosis. Group 1 is primarily inflammation, group 2 involves inflammation and fibrosis, and group 3 is primarily fibrosis. The differences in groups are most clearly seen looking at the extremes—group 1 shows the puffy alveolar septa infiltrated with lymphocytes (left panel, figure 4.8), whereas group 3 shows a matrix of fibrosis that can be distinguished from usual interstitial pneumonia by the absence of fibroblastic foci and a homogenous onset and distribution (right panel, figure 4.8). As its name suggests, the distinguishing feature of nonspecific interstitial pneumonia is the lack of features that determine it to be something else. If that sounds a bit wishy-washy, take solace in the fact that even experts argue over its classification.",True,Nonspecific Interstitial Pneumonia,Figure 4.8,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.8.png,Figure 4.8: Extremes of nonspecific interstitial pneumonia.
4f4b5176-7c16-47a4-b394-6d43d48321aa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Our next disease is at least courteous enough to only have one name, nonspecific interstitial pneumonia (NSIP), but irritatingly, it has three groups that are determined by the degree of either interstitial inflammation or fibrosis. Group 1 is primarily inflammation, group 2 involves inflammation and fibrosis, and group 3 is primarily fibrosis. The differences in groups are most clearly seen looking at the extremes—group 1 shows the puffy alveolar septa infiltrated with lymphocytes (left panel, figure 4.8), whereas group 3 shows a matrix of fibrosis that can be distinguished from usual interstitial pneumonia by the absence of fibroblastic foci and a homogenous onset and distribution (right panel, figure 4.8). As its name suggests, the distinguishing feature of nonspecific interstitial pneumonia is the lack of features that determine it to be something else. If that sounds a bit wishy-washy, take solace in the fact that even experts argue over its classification.",True,Nonspecific Interstitial Pneumonia,Figure 4.8,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.8.png,Figure 4.8: Extremes of nonspecific interstitial pneumonia.
4f4b5176-7c16-47a4-b394-6d43d48321aa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Our next disease is at least courteous enough to only have one name, nonspecific interstitial pneumonia (NSIP), but irritatingly, it has three groups that are determined by the degree of either interstitial inflammation or fibrosis. Group 1 is primarily inflammation, group 2 involves inflammation and fibrosis, and group 3 is primarily fibrosis. The differences in groups are most clearly seen looking at the extremes—group 1 shows the puffy alveolar septa infiltrated with lymphocytes (left panel, figure 4.8), whereas group 3 shows a matrix of fibrosis that can be distinguished from usual interstitial pneumonia by the absence of fibroblastic foci and a homogenous onset and distribution (right panel, figure 4.8). As its name suggests, the distinguishing feature of nonspecific interstitial pneumonia is the lack of features that determine it to be something else. If that sounds a bit wishy-washy, take solace in the fact that even experts argue over its classification.",True,Nonspecific Interstitial Pneumonia,Figure 4.8,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.8.png,Figure 4.8: Extremes of nonspecific interstitial pneumonia.
f2b66fec-7e69-4784-9992-536c85ba1f51,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The presence of lymphocytes in biopsy and bronchoalveolar lavage fluid suggests the involvement of the immune system in the pathogenesis of nonspecific interstitial pneumonia. This is supported by the occurrence of NSIP in immune diseases such as HIV infection and several connective tissue disorders including polymyositis, rheumatoid arthritis, and systemic sclerosis. Our understanding of the pathological mechanisms is still evolving.",True,Nonspecific Interstitial Pneumonia,,,,
450cb617-af94-48cb-8873-d86d84015ccd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Cryptogenic Organizing Pneumonia,False,Cryptogenic Organizing Pneumonia,,,,
94cbfa4e-dc95-405c-9469-5c5a0ac83543,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Our final major classification is cryptogenic organizing pneumonia (COP). This form of interstitial disease affects the distal bronchioles, respiratory bronchioles, and alveoli, but the primary site of injury is usually the alveolar walls.",True,Cryptogenic Organizing Pneumonia,,,,
474b1b0f-a8b8-4fca-b7ce-0b84ca99c8dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The hallmark of COP is an excessive proliferation of granulation tissue made of collagen-embedded fibroblasts and myofibroblasts that starts in the alveolar space. These plugs of fibrotic tissue may extend from one alveolus to another via the pores of Kohn and give rise to a characteristic butterfly pattern. The pathogenesis is an initial alveolar injury, with plasma proteins leaking into the alveolar lumen that is followed by recruited fibroblasts depositing connective tissue with the lumen itself. These fibrotic lesions show a homogenous time line and movement to the distal airways, but are actually reversible, which is in contrast of the lesions seen in usual interstitial pneumonia. In COP the lung architecture is maintained, probably through more thorough regulation of angiogenesis and apoptosis than that seen in usual interstitial pneumonia (UIP).",True,Cryptogenic Organizing Pneumonia,,,,
78dd4afc-a302-48c5-9219-af147740fc68,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The onset of COP is marked with dyspnea and dry cough (as with most ILDs), and it has a moderate time line of a couple of months, after which symptoms subside. History is again important to determine the initial insult, and potential culprits include connective tissue disease, new medications, or exposure to therapeutic radiation, fumes, or dusts.",True,Cryptogenic Organizing Pneumonia,,,,
52a62519-6f4a-47dd-bd95-b2522a1ee01c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Environment-Induced ILDs,False,Environment-Induced ILDs,,,,
7aabfb20-1e7d-4953-a924-49592b48b60f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Now we will look at several specific forms of interstitial disease that are related to occupational exposure. While these forms of ILD have some distinguishing factors, the importance of taking a good history cannot be understated.",True,Environment-Induced ILDs,,,,
e084c3f6-8c00-4e69-9860-478637301b42,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Silicosis,False,Silicosis,,,,
32228d49-8d1c-4271-8ef0-75cbf93cb15f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Silicosis is related to exposure to silica that occurs frequently in occupations such as stone cutting, foundry work, and mining. Cutting or breaking stone can produce crystalline silica, and when less than 5 microns in diameter, it becomes respirable. When particle size is between 1 and 3 microns, it can reach the alveoli.",True,Silicosis,,,,
b52f3881-27ab-47c1-bb26-ec221d70d180,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The formation of silicosis can be acute with heavy brief exposure (often seen in sandblasters), or chronic and insidious with more prolonged lighter exposures. The process is initiated with alveolar macrophages engulfing the crystals. In response they release cytokines to attract lymphocytes, neutrophils, and fibroblasts—and a familiar story of tissue destruction and laying down of collagen begins. (You might note at this point that engulfing silica in vitro has been shown to damage macrophages, causing them to release their intracellular enzymes, which may contribute to the destructive mechanism in vivo.)",True,Silicosis,,,,
f072a2a0-20f4-4d5a-9f7a-84901c47f894,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The pattern of collagen deposition is distinct, with silicotic nodules forming with concentric fibers producing a whirled pattern (figure 4.10). These nodules are distributed throughout the lung but are more common in the upper lobes and perihilar area (figure 4.11). They tend to be surrounded by distorted lung tissue that may show emphysematous changes. Ongoing disease coalescence of the nodules produces irregular masses of noncaseating granulomas. This progressive massive fibrosis can be helped with concurrent TB or atypical mycobacterial disease where caseating granulomas may also be present. Likewise silicosis may impair the macrophage response to TB. It causes contraction of the upper lobes and may lead to emphysema in the lower lobes, sometimes with large bullous changes. The pathophysiology of silicosis is summarized in figure 4.12.",True,Silicosis,Figure 4.10,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.10.jpeg,Figure 4.10: Silicotic nodule in the parenchyma of the lung.
f072a2a0-20f4-4d5a-9f7a-84901c47f894,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The pattern of collagen deposition is distinct, with silicotic nodules forming with concentric fibers producing a whirled pattern (figure 4.10). These nodules are distributed throughout the lung but are more common in the upper lobes and perihilar area (figure 4.11). They tend to be surrounded by distorted lung tissue that may show emphysematous changes. Ongoing disease coalescence of the nodules produces irregular masses of noncaseating granulomas. This progressive massive fibrosis can be helped with concurrent TB or atypical mycobacterial disease where caseating granulomas may also be present. Likewise silicosis may impair the macrophage response to TB. It causes contraction of the upper lobes and may lead to emphysema in the lower lobes, sometimes with large bullous changes. The pathophysiology of silicosis is summarized in figure 4.12.",True,Silicosis,Figure 4.10,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.10.jpeg,Figure 4.10: Silicotic nodule in the parenchyma of the lung.
f072a2a0-20f4-4d5a-9f7a-84901c47f894,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The pattern of collagen deposition is distinct, with silicotic nodules forming with concentric fibers producing a whirled pattern (figure 4.10). These nodules are distributed throughout the lung but are more common in the upper lobes and perihilar area (figure 4.11). They tend to be surrounded by distorted lung tissue that may show emphysematous changes. Ongoing disease coalescence of the nodules produces irregular masses of noncaseating granulomas. This progressive massive fibrosis can be helped with concurrent TB or atypical mycobacterial disease where caseating granulomas may also be present. Likewise silicosis may impair the macrophage response to TB. It causes contraction of the upper lobes and may lead to emphysema in the lower lobes, sometimes with large bullous changes. The pathophysiology of silicosis is summarized in figure 4.12.",True,Silicosis,Figure 4.10,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.10.jpeg,Figure 4.10: Silicotic nodule in the parenchyma of the lung.
db3a7449-a665-414c-9338-2d9268f62327,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"After an insidious, asymptomatic beginning, the main symptom of silicosis is dyspnea, with or without cough (cough is likely generated by concurrent smoking). The dyspnea is progressive but other symptoms that occur are often due to secondary, superimposed infection making repeated bacteriological studies important.",True,Silicosis,,,,
c2584430-2397-44fb-b8f1-d1715a340a30,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,The pathophysiology of silicosis is summarized in figure 4.12.,True,Silicosis,Figure 4.12,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.12.png,Figure 4.12: The pathophysiology of silicosis.
c2584430-2397-44fb-b8f1-d1715a340a30,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,The pathophysiology of silicosis is summarized in figure 4.12.,True,Silicosis,Figure 4.12,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.12.png,Figure 4.12: The pathophysiology of silicosis.
c2584430-2397-44fb-b8f1-d1715a340a30,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,The pathophysiology of silicosis is summarized in figure 4.12.,True,Silicosis,Figure 4.12,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.12.png,Figure 4.12: The pathophysiology of silicosis.
8d39b7cb-1ef4-416d-b135-6a8805e33116,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Asbestosis,False,Asbestosis,,,,
2ab10898-0cbd-4b8b-a680-b16e2a09947a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"There are a number of pulmonary manifestations arising from exposure to asbestos. Previously used in the construction and manufacturing industries, the occurrence of related illness led to legislation to restrict its use. However, demolition or renovation of asbestos-containing buildings can still lead to air-born asbestos exposure. The pulmonary manifestations include pulmonary fibrosis, bronchogenic carcinoma, pleural effusion, pleural fibrosis, and mesothelioma. We will deal with the pulmonary fibrosis here and what is known as asbestosis.",True,Asbestosis,,,,
9164de85-0de6-4f9f-a42d-86c789adf3cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The disease course (summarized in figure 4.13) is similar to that described for silicosis. Asbestos fibers arrive in the alveoli and macrophages initiate an inflammatory response. Note that the arrival of neutrophilic leukocytes and their release of cytokines and oxygen radicals seem to play a significant role. Short fibers can be phagocytized and removed, but larger fibers persist in the airway and perpetuate the inflammatory reaction, promoting fibrosis.",True,Asbestosis,Figure 4.13,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.13.png,Figure 4.13: Pathophysiology of asbestosis.
9164de85-0de6-4f9f-a42d-86c789adf3cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The disease course (summarized in figure 4.13) is similar to that described for silicosis. Asbestos fibers arrive in the alveoli and macrophages initiate an inflammatory response. Note that the arrival of neutrophilic leukocytes and their release of cytokines and oxygen radicals seem to play a significant role. Short fibers can be phagocytized and removed, but larger fibers persist in the airway and perpetuate the inflammatory reaction, promoting fibrosis.",True,Asbestosis,Figure 4.13,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.13.png,Figure 4.13: Pathophysiology of asbestosis.
9164de85-0de6-4f9f-a42d-86c789adf3cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The disease course (summarized in figure 4.13) is similar to that described for silicosis. Asbestos fibers arrive in the alveoli and macrophages initiate an inflammatory response. Note that the arrival of neutrophilic leukocytes and their release of cytokines and oxygen radicals seem to play a significant role. Short fibers can be phagocytized and removed, but larger fibers persist in the airway and perpetuate the inflammatory reaction, promoting fibrosis.",True,Asbestosis,Figure 4.13,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.13.png,Figure 4.13: Pathophysiology of asbestosis.
20b818f5-a04d-473e-a4cf-a17b43be300c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Histologically, these fibers can been seen as asbestos bodies, or ferruginous bodies, as they are coated with iron-containing protein (figure 4.14).",True,Asbestosis,Figure 4.14,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.14-scaled.jpg,Figure 4.14: Ferruginous bodies associated with asbestosis.
20b818f5-a04d-473e-a4cf-a17b43be300c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Histologically, these fibers can been seen as asbestos bodies, or ferruginous bodies, as they are coated with iron-containing protein (figure 4.14).",True,Asbestosis,Figure 4.14,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.14-scaled.jpg,Figure 4.14: Ferruginous bodies associated with asbestosis.
20b818f5-a04d-473e-a4cf-a17b43be300c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Histologically, these fibers can been seen as asbestos bodies, or ferruginous bodies, as they are coated with iron-containing protein (figure 4.14).",True,Asbestosis,Figure 4.14,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.14-scaled.jpg,Figure 4.14: Ferruginous bodies associated with asbestosis.
7d14e285-f52b-478d-a30d-2ae3074fbc5a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Fibrosis ensues, but in contrast to silicosis, asbestos-related fibrosis is nonnodular and mostly involves the lower lung fields and frequently includes pleural thickening.",True,Asbestosis,,,,
60ca387f-32f1-45fc-9f1e-42ea6f6a1e59,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The extent of fibrosis is highly variable, from thickened alveolar septum to complete destruction of the alveolar spaces. In the advanced disease honeycomb lung can be observed with CT. Radiography of later-stage disease shows reticular interstitial markings in the lower lung fields (left panel, figure 4.15). Pleural changes are also more common. Rounded atelectasis may occur after a pleural effusion has been reabsorbed and caused a section of the airway to become trapped. A rounded atelectasis is indicated by the arrow in figure 4.15, and care should be taken not to mistake this for a neoplasm. Abestosis is a risk factor for the development of mesothelioma and should be considered for patients working in “at-risk” environments or occupations.",True,Asbestosis,Figure 4.15,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.15.jpeg,Figure 4.15: Radiographic findings in asbestosis.
60ca387f-32f1-45fc-9f1e-42ea6f6a1e59,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The extent of fibrosis is highly variable, from thickened alveolar septum to complete destruction of the alveolar spaces. In the advanced disease honeycomb lung can be observed with CT. Radiography of later-stage disease shows reticular interstitial markings in the lower lung fields (left panel, figure 4.15). Pleural changes are also more common. Rounded atelectasis may occur after a pleural effusion has been reabsorbed and caused a section of the airway to become trapped. A rounded atelectasis is indicated by the arrow in figure 4.15, and care should be taken not to mistake this for a neoplasm. Abestosis is a risk factor for the development of mesothelioma and should be considered for patients working in “at-risk” environments or occupations.",True,Asbestosis,Figure 4.15,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.15.jpeg,Figure 4.15: Radiographic findings in asbestosis.
60ca387f-32f1-45fc-9f1e-42ea6f6a1e59,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The extent of fibrosis is highly variable, from thickened alveolar septum to complete destruction of the alveolar spaces. In the advanced disease honeycomb lung can be observed with CT. Radiography of later-stage disease shows reticular interstitial markings in the lower lung fields (left panel, figure 4.15). Pleural changes are also more common. Rounded atelectasis may occur after a pleural effusion has been reabsorbed and caused a section of the airway to become trapped. A rounded atelectasis is indicated by the arrow in figure 4.15, and care should be taken not to mistake this for a neoplasm. Abestosis is a risk factor for the development of mesothelioma and should be considered for patients working in “at-risk” environments or occupations.",True,Asbestosis,Figure 4.15,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.15.jpeg,Figure 4.15: Radiographic findings in asbestosis.
c32bacc1-2601-4dfd-b866-69c682c56bc3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Coal worker’s pneumoconiosis (CWP),False,Coal worker’s pneumoconiosis (CWP),,,,
57b439a5-0b86-4157-85f8-33afd87605ff,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"CWP arises after prolonged exposure to coal dust. While drilling through rock the miner may be susceptible to silicosis, but prolonged and heavy exposure to aerosolized carbon (that is not usually fibrogenic in lesser exposures) can result in its own distinct condition. Even then it can take ten to twelve years of underground exposure to develop.",True,Coal worker’s pneumoconiosis (CWP),,,,
830ca7d1-c3ed-4807-978c-783dda3ba844,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Again we see the process start with phagocytosis of the coal dust by macrophages after the mucocillary escalator is overwhelmed. The macrophages launch their inflammatory process, and tissue damage is caused by the resultant cytokine bloom and oxygen radical and enzyme release. Fibroblasts form reticulin networks, but there is no significant collagen deposition. Aggregates of reticulin fibers, macrophages, and dust form coal macules (figure 4.16). The coal macules appear as black spots in lung sections and give rise to the condition’s nickname of “black lung.”",True,Coal worker’s pneumoconiosis (CWP),Figure 4.16,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.16.jpeg,Figure 4.16: Example of coal macules in simple CWP showing fibrosis and coal macules.
830ca7d1-c3ed-4807-978c-783dda3ba844,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Again we see the process start with phagocytosis of the coal dust by macrophages after the mucocillary escalator is overwhelmed. The macrophages launch their inflammatory process, and tissue damage is caused by the resultant cytokine bloom and oxygen radical and enzyme release. Fibroblasts form reticulin networks, but there is no significant collagen deposition. Aggregates of reticulin fibers, macrophages, and dust form coal macules (figure 4.16). The coal macules appear as black spots in lung sections and give rise to the condition’s nickname of “black lung.”",True,Coal worker’s pneumoconiosis (CWP),Figure 4.16,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.16.jpeg,Figure 4.16: Example of coal macules in simple CWP showing fibrosis and coal macules.
830ca7d1-c3ed-4807-978c-783dda3ba844,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Again we see the process start with phagocytosis of the coal dust by macrophages after the mucocillary escalator is overwhelmed. The macrophages launch their inflammatory process, and tissue damage is caused by the resultant cytokine bloom and oxygen radical and enzyme release. Fibroblasts form reticulin networks, but there is no significant collagen deposition. Aggregates of reticulin fibers, macrophages, and dust form coal macules (figure 4.16). The coal macules appear as black spots in lung sections and give rise to the condition’s nickname of “black lung.”",True,Coal worker’s pneumoconiosis (CWP),Figure 4.16,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.16.jpeg,Figure 4.16: Example of coal macules in simple CWP showing fibrosis and coal macules.
486e98a7-1b80-4b9d-8880-2ac7031ec1ac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The coal macules are associated with dilation of the respiratory bronchioles that can manifest as focal centrilobar emphysema (figure 4.16). This is referred to as simple CWP, whereas the less common, complicated form involves progressive massive fibrosis, usually in the upper lobes, as in silicosis. However, in CWP these lesions are black and relatively homogenous, where as in silicosis they are a conglomeration of intersecting nodules. Figure 4.17 shows a large black fibrotic lesion destroying the perihilar lung parenchyma.",True,Coal worker’s pneumoconiosis (CWP),Figure 4.17,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.17.jpeg,Figure 4.17: Large perihilar lesion in complicated CWP.
486e98a7-1b80-4b9d-8880-2ac7031ec1ac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The coal macules are associated with dilation of the respiratory bronchioles that can manifest as focal centrilobar emphysema (figure 4.16). This is referred to as simple CWP, whereas the less common, complicated form involves progressive massive fibrosis, usually in the upper lobes, as in silicosis. However, in CWP these lesions are black and relatively homogenous, where as in silicosis they are a conglomeration of intersecting nodules. Figure 4.17 shows a large black fibrotic lesion destroying the perihilar lung parenchyma.",True,Coal worker’s pneumoconiosis (CWP),Figure 4.17,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.17.jpeg,Figure 4.17: Large perihilar lesion in complicated CWP.
486e98a7-1b80-4b9d-8880-2ac7031ec1ac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The coal macules are associated with dilation of the respiratory bronchioles that can manifest as focal centrilobar emphysema (figure 4.16). This is referred to as simple CWP, whereas the less common, complicated form involves progressive massive fibrosis, usually in the upper lobes, as in silicosis. However, in CWP these lesions are black and relatively homogenous, where as in silicosis they are a conglomeration of intersecting nodules. Figure 4.17 shows a large black fibrotic lesion destroying the perihilar lung parenchyma.",True,Coal worker’s pneumoconiosis (CWP),Figure 4.17,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.17.jpeg,Figure 4.17: Large perihilar lesion in complicated CWP.
5e78f8d0-ca02-4c2d-8811-44c02d710618,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Clinical manifestations are often complicated by concurrent cigarette smoking that may alone explain the frequency of chronic bronchitis in CWP patients. The simple form can be asymptomatic, but the complicated form produces dyspnea and signs of respiratory failures, pulmonary hypertension, and cor pulmonale.",True,Coal worker’s pneumoconiosis (CWP),,,,
2889a80a-7fdb-4eed-917f-8af14ca7ddd6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Berylliosis,False,Berylliosis,,,,
18d67239-f8dd-44ba-a54a-bd7b25e8113a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"The last occupational disorder we will look at is berylliosis, or chronic beryllium disease (CBD), that occurs after exposure to beryllium, a metal used in manufacturing. Here the start to our story is a little different. Beryllium arrives in the airway and there is a hypersensitization of T cells. On subsequent exposures the T cells proliferate—the bronchoalveolar lavage (BAL) fluid of berylliosis patients is rich in sensitized CD4+ cells.",True,Berylliosis,,,,
a71e1a5a-4ba3-4599-97ec-a55e8d32aa1e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Now we return to our pattern: the abundant CD4+ cells release proinflammatory cytokines and granulomatous fibrosis occurs (figure 4.18). The granulomas (figure 4.19) are indistinguishable from those caused by sarcoidosis (which are also caused by CD4+ cells), and many CBD patients may be misdiagnosed as sarcoidosis cases, so appropriate history taking is paramount. Usually CBD involves greater interstitial inflammation, but the most definitive diagnosis comes from the beryllium lymphocyte proliferation test. The test involves exposing lymphocytes from the patient’s blood or BAL fluid to different concentrations of beryllium and assaying their proliferation.",True,Berylliosis,Figure 4.18,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.18.png,Figure 4.18: Pathophysiology of berylliosis.
a71e1a5a-4ba3-4599-97ec-a55e8d32aa1e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Now we return to our pattern: the abundant CD4+ cells release proinflammatory cytokines and granulomatous fibrosis occurs (figure 4.18). The granulomas (figure 4.19) are indistinguishable from those caused by sarcoidosis (which are also caused by CD4+ cells), and many CBD patients may be misdiagnosed as sarcoidosis cases, so appropriate history taking is paramount. Usually CBD involves greater interstitial inflammation, but the most definitive diagnosis comes from the beryllium lymphocyte proliferation test. The test involves exposing lymphocytes from the patient’s blood or BAL fluid to different concentrations of beryllium and assaying their proliferation.",True,Berylliosis,Figure 4.18,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.18.png,Figure 4.18: Pathophysiology of berylliosis.
a71e1a5a-4ba3-4599-97ec-a55e8d32aa1e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Now we return to our pattern: the abundant CD4+ cells release proinflammatory cytokines and granulomatous fibrosis occurs (figure 4.18). The granulomas (figure 4.19) are indistinguishable from those caused by sarcoidosis (which are also caused by CD4+ cells), and many CBD patients may be misdiagnosed as sarcoidosis cases, so appropriate history taking is paramount. Usually CBD involves greater interstitial inflammation, but the most definitive diagnosis comes from the beryllium lymphocyte proliferation test. The test involves exposing lymphocytes from the patient’s blood or BAL fluid to different concentrations of beryllium and assaying their proliferation.",True,Berylliosis,Figure 4.18,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.18.png,Figure 4.18: Pathophysiology of berylliosis.
793e99c6-587d-4319-b0be-1b2bd3dbae63,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Susceptibility to becoming hypersensitized appears to have a significant genetic component. Why the process continues after exposure has stopped is unclear, but possibilities include a fundamental T cell disorder, or the fact that the insoluble beryllium causes apoptosis of macrophages, leading them to release a previously phagocytized beryllium load.",True,Berylliosis,,,,
be30c734-8a28-4d0d-9a91-b90bf3f61f50,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"As the disease progresses, radiographic findings show that the granuoles can become more organized to produce fibrous nodules that may begin to impact lung function. The immune system involvement can produce hilar lymphadenopathy, and common later signs include interstital fibrosis and pleural thickening.",True,Berylliosis,,,,
209d8456-2dd6-4030-a28d-b0f9b9bd3b6c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Summary,False,Summary,,,,
d740c2b8-6c64-41b1-b581-e7cb38c70dc9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"So there is a selection of interstitial lung diseases that, while sharing the pathophysiological manifestations of restrictive lung disease, can be distinguished through good history taking or identifying distinct histological features.",True,Summary,,,,
cc2a6bb7-bf42-4ea1-bdb6-932c1a322b02,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"References, Resources, and Further Reading",False,"References, Resources, and Further Reading",,,,
47a3e1a9-57fd-43f8-9f42-14020684c220,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,Text,False,Text,,,,
99cfc116-0672-4e5d-a968-44f58a5d1a46,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapters 12–15.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
e5ffe90d-7521-41b9-baff-f2a2890e989e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-2,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
8fd4c0d0-4808-49c3-8d73-76da8aff9ad2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Before we start taking about diseases affecting the lung interstitium, let us remind ourselves of what it is.",True,Text,,,,
ad2932a0-3b6e-45fd-9952-53dba8611503,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The interstitial tissue, sometimes referred to as parenchyma, surrounds the alveolar and capillary structures and contributes to the mechanical behavior of the lungs. The interstitium is extremely thin between the alveoli and capillaries, and forms the basement membrane through which gas exchange occurs. On the parenchymal side of the capillaries the interstitium is more substantial and is more involved in fluid exchange. There is also substantial amounts of interstitial tissue in the spaces around major vessels and airways, and it also makes up the interlobular septa.",True,Text,,,,
b41976e2-026c-42f2-afef-c7aa821ffca8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Mechanisms of ILD,False,Mechanisms of ILD,,,,
f2561f14-ef9e-414d-ba04-a9f1c1e9ccee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Now we will look at the generalized mechanism of interstitial lung disease (figure 4.1). It is worth noting that the numerous conditions that the term ILD encompasses have subtle differences in mechanism and manifestations, and these differences are what we will deal with elsewhere.",True,Mechanisms of ILD,Figure 4.1,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
f2561f14-ef9e-414d-ba04-a9f1c1e9ccee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Now we will look at the generalized mechanism of interstitial lung disease (figure 4.1). It is worth noting that the numerous conditions that the term ILD encompasses have subtle differences in mechanism and manifestations, and these differences are what we will deal with elsewhere.",True,Mechanisms of ILD,Figure 4.1,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
f2561f14-ef9e-414d-ba04-a9f1c1e9ccee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Now we will look at the generalized mechanism of interstitial lung disease (figure 4.1). It is worth noting that the numerous conditions that the term ILD encompasses have subtle differences in mechanism and manifestations, and these differences are what we will deal with elsewhere.",True,Mechanisms of ILD,Figure 4.1,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
308c6c54-e015-406b-8dad-9d75d4b12752,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,ILD,False,ILD,,,,
193f08d7-ec7e-4109-ac74-37317dd4152f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Generally though, ILD starts with an initial insult to the lung (#1, figure 4.1); the type of insult is a major contributor to the different ILD conditions. (It probably will not be what is depicted in figure 4.1, but if it was, it might lead to the inflammatory condition of tiefitis.)",True,ILD,Figure 4.1,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
193f08d7-ec7e-4109-ac74-37317dd4152f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Generally though, ILD starts with an initial insult to the lung (#1, figure 4.1); the type of insult is a major contributor to the different ILD conditions. (It probably will not be what is depicted in figure 4.1, but if it was, it might lead to the inflammatory condition of tiefitis.)",True,ILD,Figure 4.1,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
193f08d7-ec7e-4109-ac74-37317dd4152f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Generally though, ILD starts with an initial insult to the lung (#1, figure 4.1); the type of insult is a major contributor to the different ILD conditions. (It probably will not be what is depicted in figure 4.1, but if it was, it might lead to the inflammatory condition of tiefitis.)",True,ILD,Figure 4.1,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
55f53f3f-9443-49cd-97a0-fd34cdab7484,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,tiefitis,False,tiefitis,,,,
a3ed3e77-e95c-439d-a8ab-691c0f1d9487,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"There is then a response by neutrophils and alveolar macrophages (#2, figure 4.1). The macrophage response seems particularly important to the development of ILD. Release of cytokines (#3, figure 4.1) attracts other inflammatory cells, and the arrival of polymorphonuclear leukocytes and lymphocytes play an important role in disease instigation. These cells release cytokines, enzymes, and toxic oxygen radicals that damage and destroy local tissue. Released growth factors, such as TGF-Beta, instigate the transition of mesenchymal cells to fibroblasts.",True,tiefitis,Figure 4.1,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
a3ed3e77-e95c-439d-a8ab-691c0f1d9487,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"There is then a response by neutrophils and alveolar macrophages (#2, figure 4.1). The macrophage response seems particularly important to the development of ILD. Release of cytokines (#3, figure 4.1) attracts other inflammatory cells, and the arrival of polymorphonuclear leukocytes and lymphocytes play an important role in disease instigation. These cells release cytokines, enzymes, and toxic oxygen radicals that damage and destroy local tissue. Released growth factors, such as TGF-Beta, instigate the transition of mesenchymal cells to fibroblasts.",True,tiefitis,Figure 4.1,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
a3ed3e77-e95c-439d-a8ab-691c0f1d9487,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"There is then a response by neutrophils and alveolar macrophages (#2, figure 4.1). The macrophage response seems particularly important to the development of ILD. Release of cytokines (#3, figure 4.1) attracts other inflammatory cells, and the arrival of polymorphonuclear leukocytes and lymphocytes play an important role in disease instigation. These cells release cytokines, enzymes, and toxic oxygen radicals that damage and destroy local tissue. Released growth factors, such as TGF-Beta, instigate the transition of mesenchymal cells to fibroblasts.",True,tiefitis,Figure 4.1,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
828792d4-28dd-4366-9a47-7d623eec5ea2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"It is worth noting at this point that some forms of ILD are caused by an exaggerated immune reaction—either through an allergic-like response, or a direct immune disorder.",True,tiefitis,,,,
ce35fc0f-9b3c-4a78-91ab-3547429abfb7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The destruction of tissue and activity of a growing number of fibroblasts results in the inflamed interstitium becoming fibrosed with excess connective tissue, particularly collagen (#4, figure 4.1).",True,tiefitis,Figure 4.1,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
ce35fc0f-9b3c-4a78-91ab-3547429abfb7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The destruction of tissue and activity of a growing number of fibroblasts results in the inflamed interstitium becoming fibrosed with excess connective tissue, particularly collagen (#4, figure 4.1).",True,tiefitis,Figure 4.1,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
ce35fc0f-9b3c-4a78-91ab-3547429abfb7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The destruction of tissue and activity of a growing number of fibroblasts results in the inflamed interstitium becoming fibrosed with excess connective tissue, particularly collagen (#4, figure 4.1).",True,tiefitis,Figure 4.1,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
0bb63ec1-dc1f-42f2-a5db-d946d8706532,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Pathology of ILD,False,Pathology of ILD,,,,
1cbd9f73-8f97-4f8b-92b3-e7cd73b568dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"These changes in structure dramatically change the functional and mechanical properties of the tissue. The changes also tend to follow a characteristic pattern, although, as you might imagine, different conditions have subtle differences in pattern.",True,Pathology of ILD,,,,
55537f61-6bb2-4685-8035-cdee543b3899,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The action of fibroblasts laying down connective tissue, combined with the destruction of alveolar and capillary structures, leads to a widening of airspaces with thick collagenous and infiltrated walls (figure 4.2A and 4.2B), which are a functionally significant departure from the ideal structure for gas exchange.",True,Pathology of ILD,Figure 4.2,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
55537f61-6bb2-4685-8035-cdee543b3899,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The action of fibroblasts laying down connective tissue, combined with the destruction of alveolar and capillary structures, leads to a widening of airspaces with thick collagenous and infiltrated walls (figure 4.2A and 4.2B), which are a functionally significant departure from the ideal structure for gas exchange.",True,Pathology of ILD,Figure 4.2,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
55537f61-6bb2-4685-8035-cdee543b3899,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The action of fibroblasts laying down connective tissue, combined with the destruction of alveolar and capillary structures, leads to a widening of airspaces with thick collagenous and infiltrated walls (figure 4.2A and 4.2B), which are a functionally significant departure from the ideal structure for gas exchange.",True,Pathology of ILD,Figure 4.2,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
ea364bdb-80ff-4d50-bcc0-fa373279f18c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The thickened basement membrane poses a significant obstacle to the transfer of gases, and the dense connective tissue stiffens the lung and thereby reduces its compliance. Combined with loss of capillary beds and airspace surface area, gas exchange is reduced.",True,Pathology of ILD,,,,
2c4bfea6-114e-4109-bcd1-eb7d20fa0529,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"At the end of the disease the lung takes on a characteristic honeycomb appearance, and “ground glass opacities” are a hallmark sign on CT images (figure 4.2C). These morphological changes lead to pathophysiological consequences that are shared by most forms of the disease, as all cause varying degrees of interstitial inflammation and connective tissue deposition.",True,Pathology of ILD,Figure 4.2,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
2c4bfea6-114e-4109-bcd1-eb7d20fa0529,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"At the end of the disease the lung takes on a characteristic honeycomb appearance, and “ground glass opacities” are a hallmark sign on CT images (figure 4.2C). These morphological changes lead to pathophysiological consequences that are shared by most forms of the disease, as all cause varying degrees of interstitial inflammation and connective tissue deposition.",True,Pathology of ILD,Figure 4.2,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
2c4bfea6-114e-4109-bcd1-eb7d20fa0529,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"At the end of the disease the lung takes on a characteristic honeycomb appearance, and “ground glass opacities” are a hallmark sign on CT images (figure 4.2C). These morphological changes lead to pathophysiological consequences that are shared by most forms of the disease, as all cause varying degrees of interstitial inflammation and connective tissue deposition.",True,Pathology of ILD,Figure 4.2,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
ce83f6a6-5dec-4b10-8b47-7d8f38f1d664,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Pathophysiology of ILD,False,Pathophysiology of ILD,,,,
0cf3a5a5-ecab-4725-80e7-1b4d83b48fd3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The first major issue is the reduced diffusion capacity of the involved areas, and all ILD patients demonstrate a reduced transfer factor, or DLCO (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
0cf3a5a5-ecab-4725-80e7-1b4d83b48fd3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The first major issue is the reduced diffusion capacity of the involved areas, and all ILD patients demonstrate a reduced transfer factor, or DLCO (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
0cf3a5a5-ecab-4725-80e7-1b4d83b48fd3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The first major issue is the reduced diffusion capacity of the involved areas, and all ILD patients demonstrate a reduced transfer factor, or DLCO (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
49e2eb4d-7e95-4b89-882d-6858ebfd4515,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Because of the heterogenous distribution of the disease, and the involvement of the pulmonary circulation, severe V/Q abnormalities arise throughout the lung. This and the reduced diffusion capacity result in hypoxemia. In the chronic disease state this may lead to cor pulmonale (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
49e2eb4d-7e95-4b89-882d-6858ebfd4515,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Because of the heterogenous distribution of the disease, and the involvement of the pulmonary circulation, severe V/Q abnormalities arise throughout the lung. This and the reduced diffusion capacity result in hypoxemia. In the chronic disease state this may lead to cor pulmonale (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
49e2eb4d-7e95-4b89-882d-6858ebfd4515,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Because of the heterogenous distribution of the disease, and the involvement of the pulmonary circulation, severe V/Q abnormalities arise throughout the lung. This and the reduced diffusion capacity result in hypoxemia. In the chronic disease state this may lead to cor pulmonale (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
a9fe3d72-50a8-4d44-aa6e-02af2ed8e064,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The reduction in lung compliance leads to a reduced lung volume. This is easily detected with spirometry as shown by the inner plot of the flow-volume loop in figure 4.3. Because FEV1 and FVC are both reduced, the ratio frequently remains the same or may even rise; as such FEV1/FVC is a poor indicator of restrictive disease.",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
a9fe3d72-50a8-4d44-aa6e-02af2ed8e064,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The reduction in lung compliance leads to a reduced lung volume. This is easily detected with spirometry as shown by the inner plot of the flow-volume loop in figure 4.3. Because FEV1 and FVC are both reduced, the ratio frequently remains the same or may even rise; as such FEV1/FVC is a poor indicator of restrictive disease.",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
a9fe3d72-50a8-4d44-aa6e-02af2ed8e064,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The reduction in lung compliance leads to a reduced lung volume. This is easily detected with spirometry as shown by the inner plot of the flow-volume loop in figure 4.3. Because FEV1 and FVC are both reduced, the ratio frequently remains the same or may even rise; as such FEV1/FVC is a poor indicator of restrictive disease.",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
e0c6b8be-76c8-453e-bbaa-6603affa133d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The reduced lung volume and compliance results in a characteristic rapid, shallow breathing pattern as the patient tries to maintain alveolar ventilation (figure 4.3). However, while avoiding unnecessary increases in the work of breathing by not trying to over-expand the noncompliant lung, the rapid shallow breathing proportionally increases dead space ventilation.",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
e0c6b8be-76c8-453e-bbaa-6603affa133d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The reduced lung volume and compliance results in a characteristic rapid, shallow breathing pattern as the patient tries to maintain alveolar ventilation (figure 4.3). However, while avoiding unnecessary increases in the work of breathing by not trying to over-expand the noncompliant lung, the rapid shallow breathing proportionally increases dead space ventilation.",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
e0c6b8be-76c8-453e-bbaa-6603affa133d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The reduced lung volume and compliance results in a characteristic rapid, shallow breathing pattern as the patient tries to maintain alveolar ventilation (figure 4.3). However, while avoiding unnecessary increases in the work of breathing by not trying to over-expand the noncompliant lung, the rapid shallow breathing proportionally increases dead space ventilation.",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
29c7e7bc-8aa0-4d1c-8b05-22a7bbb88beb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The reduction in tidal volume, combined with a raised hypoxic drive to breathe, results in the cardinal symptom of ILD, which is dyspnea (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
29c7e7bc-8aa0-4d1c-8b05-22a7bbb88beb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The reduction in tidal volume, combined with a raised hypoxic drive to breathe, results in the cardinal symptom of ILD, which is dyspnea (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
29c7e7bc-8aa0-4d1c-8b05-22a7bbb88beb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The reduction in tidal volume, combined with a raised hypoxic drive to breathe, results in the cardinal symptom of ILD, which is dyspnea (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
1a2db67f-5e61-4cc7-a4ed-7c8ebc2cd6f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Clinical Signs of ILD,False,Clinical Signs of ILD,,,,
4838e0e7-ee30-40db-934a-aacaed2a4902,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The correlation of dyspnea and disease stage is closer in ILD than any other respiratory disease. The onset is insidious, appearing first during exercise, and it likely contributes to the other major complaints of weakness and fatigue. The dyspnea gets progressively worse until it can be debilitating.",True,Clinical Signs of ILD,,,,
c1c518e7-19be-47c7-bfbb-a8c9f5b2d4b2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Inflammation and excitation of pulmonary receptors leads to a nonproductive and persistent cough, and upon examination patients will have limited chest expansion and demonstrate the characteristic breathing pattern of restrictive lung disease.",True,Clinical Signs of ILD,,,,
dd0a1291-e61c-4abc-a998-658deeed981f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Hallmark lung sounds are fine crackles, commonly found at the base of the lung, and may appear louder than expected because of increased transmission through denser than normal tissue.",True,Clinical Signs of ILD,,,,
3a685164-bcd3-45c3-a37d-a0d9957a3162,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,At later stages of the disease the patient shows signs of the prolonged hypoxemia with digital clubbing and cyanosis.,True,Clinical Signs of ILD,,,,
e87d3ff1-c702-4689-8062-ec3275574fdf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Forms of Interstitial Lung Disease,False,Forms of Interstitial Lung Disease,,,,
2bed441f-4445-48dc-8531-b527d6e40fc5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Our major subcategory is idiopathic interstitial pneumonia (figure 4.4), or IIP, and this is divided again into six more useful categories that can be distinguished by history, time line, and histological changes. We will deal with these categories in this section, but it might be noted that usual interstitial pneumonia, still frequently called idiopathic pulmonary fibrosis, is the only one that remains untreatable, and early differentiation from the other forms is critical (figure 4.4).",True,Forms of Interstitial Lung Disease,Figure 4.4,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
2bed441f-4445-48dc-8531-b527d6e40fc5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Our major subcategory is idiopathic interstitial pneumonia (figure 4.4), or IIP, and this is divided again into six more useful categories that can be distinguished by history, time line, and histological changes. We will deal with these categories in this section, but it might be noted that usual interstitial pneumonia, still frequently called idiopathic pulmonary fibrosis, is the only one that remains untreatable, and early differentiation from the other forms is critical (figure 4.4).",True,Forms of Interstitial Lung Disease,Figure 4.4,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
2bed441f-4445-48dc-8531-b527d6e40fc5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Our major subcategory is idiopathic interstitial pneumonia (figure 4.4), or IIP, and this is divided again into six more useful categories that can be distinguished by history, time line, and histological changes. We will deal with these categories in this section, but it might be noted that usual interstitial pneumonia, still frequently called idiopathic pulmonary fibrosis, is the only one that remains untreatable, and early differentiation from the other forms is critical (figure 4.4).",True,Forms of Interstitial Lung Disease,Figure 4.4,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
b984068a-46ee-42b6-bd19-7498b55afdff,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Interstitial lung diseases can also be induced by numerous different environmental causes that produce nuanced conditions that are distinguishable by environmental and social history (figure 4.4) as well as specific histological features.,True,Forms of Interstitial Lung Disease,Figure 4.4,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
b984068a-46ee-42b6-bd19-7498b55afdff,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Interstitial lung diseases can also be induced by numerous different environmental causes that produce nuanced conditions that are distinguishable by environmental and social history (figure 4.4) as well as specific histological features.,True,Forms of Interstitial Lung Disease,Figure 4.4,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
b984068a-46ee-42b6-bd19-7498b55afdff,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Interstitial lung diseases can also be induced by numerous different environmental causes that produce nuanced conditions that are distinguishable by environmental and social history (figure 4.4) as well as specific histological features.,True,Forms of Interstitial Lung Disease,Figure 4.4,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
8f6e3814-81c6-4f79-a065-b08620587f31,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The characteristics of usual interstitial pneumonia have been covered in the “Basis of ILD” section, so let us start looking at the pathophysiological and clinical features of the other broader disease categories.",True,Forms of Interstitial Lung Disease,,,,
17171256-5843-421f-b915-3fba76ff3769,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,False,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,,,,
7b7bf10c-6290-4c99-b4dc-c56a474a0982,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,We can deal with the first two together as both share common characteristics and are potentially the same disease occurring in different anatomical locations. Desquamative interstitial pneumonia and respiratory bronchiolitis–associated ILD are both smoking related and are relatively uncommon.,True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,,,,
7a58c5b8-29d9-4fda-8d35-888b1d8ce1b1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The histological hallmark is accumulation of numerous smoker’s macrophages in the airspaces (figure 4.5) or the first- and second-order respiratory bronchioles. These macrophages have a characteristic brown pigmentation. In desquamative interstitial pneumonia the airspaces are the primary site of involvement, whereas a respiratory bronchiolitis–associated ILD sees more involvement of the bronchioles (as the name suggests). The alveolar septum may be thickened with infiltrate and there may be mild peribronchilor or alveolar fibrosis, but this does not result in a honeycomb pattern seen in usual interstitial pneumonia.",True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,Figure 4.5,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.5.jpeg,Figure 4.5: Smoker’s macrophages occupying an airspace.
7a58c5b8-29d9-4fda-8d35-888b1d8ce1b1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The histological hallmark is accumulation of numerous smoker’s macrophages in the airspaces (figure 4.5) or the first- and second-order respiratory bronchioles. These macrophages have a characteristic brown pigmentation. In desquamative interstitial pneumonia the airspaces are the primary site of involvement, whereas a respiratory bronchiolitis–associated ILD sees more involvement of the bronchioles (as the name suggests). The alveolar septum may be thickened with infiltrate and there may be mild peribronchilor or alveolar fibrosis, but this does not result in a honeycomb pattern seen in usual interstitial pneumonia.",True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,Figure 4.5,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.5.jpeg,Figure 4.5: Smoker’s macrophages occupying an airspace.
7a58c5b8-29d9-4fda-8d35-888b1d8ce1b1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The histological hallmark is accumulation of numerous smoker’s macrophages in the airspaces (figure 4.5) or the first- and second-order respiratory bronchioles. These macrophages have a characteristic brown pigmentation. In desquamative interstitial pneumonia the airspaces are the primary site of involvement, whereas a respiratory bronchiolitis–associated ILD sees more involvement of the bronchioles (as the name suggests). The alveolar septum may be thickened with infiltrate and there may be mild peribronchilor or alveolar fibrosis, but this does not result in a honeycomb pattern seen in usual interstitial pneumonia.",True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,Figure 4.5,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.5.jpeg,Figure 4.5: Smoker’s macrophages occupying an airspace.
01f3ce77-6f24-48ec-867e-2ffa45a9cda9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"These ILDs are more prevalent in men, and are usually found in the fifth decade of life and after thirty-pack years. They are marked by the gradual and insidious onset of dyspnea, but lung reductions are usually minimal with both forms. The response to corticosteroid therapy and smoking cessation is good in about 80 percent of patients who remain stable or improve.",True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,,,,
20716092-b92b-49f3-b1a9-e663fd54d3c8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Diffuse Alveolar Damage (DAD),False,Diffuse Alveolar Damage (DAD),,,,
2b80788b-78ed-4268-8614-6b6963fc16aa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"While the development of most interstitial lung diseases is slow and insidious, the hallmark of diffuse alveolar damage is rapid, occurring in a matter of days and often in previously healthy individuals. The manifestation of the disease is similar to acute respiratory distress syndrome, and in fact it has been suggested that DAD is a form of ARDS.",True,Diffuse Alveolar Damage (DAD),,,,
68a2fde3-0ef7-4ac5-846a-adc43ecd7d86,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The start is marked by a brief exudative phase with fluid entering the airspaces, but the following organizing or proliferative phase is what is usually seen by the time a biopsy is taken and where the similarities to ARDS are seen. The alveolar septa are thickened due to the interstitial edema and the septa may collapse or appose each other (figure 4.7). There is marked infiltration of the interstitial and airspaces by inflammatory cells, and type II cells proliferate. The destruction of the alveolar structure leaves a sludgy hyaline membrane of debris. Thrombi in small arteries may also be apparent.",True,Diffuse Alveolar Damage (DAD),Figure 4.7,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.7.jpeg,Figure 4.7: Diffuse alveolar damage.
68a2fde3-0ef7-4ac5-846a-adc43ecd7d86,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The start is marked by a brief exudative phase with fluid entering the airspaces, but the following organizing or proliferative phase is what is usually seen by the time a biopsy is taken and where the similarities to ARDS are seen. The alveolar septa are thickened due to the interstitial edema and the septa may collapse or appose each other (figure 4.7). There is marked infiltration of the interstitial and airspaces by inflammatory cells, and type II cells proliferate. The destruction of the alveolar structure leaves a sludgy hyaline membrane of debris. Thrombi in small arteries may also be apparent.",True,Diffuse Alveolar Damage (DAD),Figure 4.7,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.7.jpeg,Figure 4.7: Diffuse alveolar damage.
68a2fde3-0ef7-4ac5-846a-adc43ecd7d86,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The start is marked by a brief exudative phase with fluid entering the airspaces, but the following organizing or proliferative phase is what is usually seen by the time a biopsy is taken and where the similarities to ARDS are seen. The alveolar septa are thickened due to the interstitial edema and the septa may collapse or appose each other (figure 4.7). There is marked infiltration of the interstitial and airspaces by inflammatory cells, and type II cells proliferate. The destruction of the alveolar structure leaves a sludgy hyaline membrane of debris. Thrombi in small arteries may also be apparent.",True,Diffuse Alveolar Damage (DAD),Figure 4.7,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.7.jpeg,Figure 4.7: Diffuse alveolar damage.
0267cee8-65de-40a7-bdc5-62476ba9ccf4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Should the patient survive (about 50 percent do not) the healing phase can show recovery of the alveolar structure with varying degrees of fibrosis. Many patients return to normal lung function, but a few show a progressive fibrotic process that resembles idiopathic pulmonary fibrosis.",True,Diffuse Alveolar Damage (DAD),,,,
4dd77f9a-01bf-4059-9eb8-be53e47f3ff6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Without biopsy, DAD is usually differentiated from other forms of interstitial disease by its rapid onset, but this can be confused with acute exacerbations of other diseases. However, the uniform pattern of damage in real DAD is representative of a single time line.",True,Diffuse Alveolar Damage (DAD),,,,
18332b4e-a325-43f4-b726-e9916d5d12fa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Nonspecific Interstitial Pneumonia,False,Nonspecific Interstitial Pneumonia,,,,
10164504-ab87-43e5-a75e-852f4ad42b69,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Our next disease is at least courteous enough to only have one name, nonspecific interstitial pneumonia (NSIP), but irritatingly, it has three groups that are determined by the degree of either interstitial inflammation or fibrosis. Group 1 is primarily inflammation, group 2 involves inflammation and fibrosis, and group 3 is primarily fibrosis. The differences in groups are most clearly seen looking at the extremes—group 1 shows the puffy alveolar septa infiltrated with lymphocytes (left panel, figure 4.8), whereas group 3 shows a matrix of fibrosis that can be distinguished from usual interstitial pneumonia by the absence of fibroblastic foci and a homogenous onset and distribution (right panel, figure 4.8). As its name suggests, the distinguishing feature of nonspecific interstitial pneumonia is the lack of features that determine it to be something else. If that sounds a bit wishy-washy, take solace in the fact that even experts argue over its classification.",True,Nonspecific Interstitial Pneumonia,Figure 4.8,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.8.png,Figure 4.8: Extremes of nonspecific interstitial pneumonia.
10164504-ab87-43e5-a75e-852f4ad42b69,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Our next disease is at least courteous enough to only have one name, nonspecific interstitial pneumonia (NSIP), but irritatingly, it has three groups that are determined by the degree of either interstitial inflammation or fibrosis. Group 1 is primarily inflammation, group 2 involves inflammation and fibrosis, and group 3 is primarily fibrosis. The differences in groups are most clearly seen looking at the extremes—group 1 shows the puffy alveolar septa infiltrated with lymphocytes (left panel, figure 4.8), whereas group 3 shows a matrix of fibrosis that can be distinguished from usual interstitial pneumonia by the absence of fibroblastic foci and a homogenous onset and distribution (right panel, figure 4.8). As its name suggests, the distinguishing feature of nonspecific interstitial pneumonia is the lack of features that determine it to be something else. If that sounds a bit wishy-washy, take solace in the fact that even experts argue over its classification.",True,Nonspecific Interstitial Pneumonia,Figure 4.8,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.8.png,Figure 4.8: Extremes of nonspecific interstitial pneumonia.
10164504-ab87-43e5-a75e-852f4ad42b69,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Our next disease is at least courteous enough to only have one name, nonspecific interstitial pneumonia (NSIP), but irritatingly, it has three groups that are determined by the degree of either interstitial inflammation or fibrosis. Group 1 is primarily inflammation, group 2 involves inflammation and fibrosis, and group 3 is primarily fibrosis. The differences in groups are most clearly seen looking at the extremes—group 1 shows the puffy alveolar septa infiltrated with lymphocytes (left panel, figure 4.8), whereas group 3 shows a matrix of fibrosis that can be distinguished from usual interstitial pneumonia by the absence of fibroblastic foci and a homogenous onset and distribution (right panel, figure 4.8). As its name suggests, the distinguishing feature of nonspecific interstitial pneumonia is the lack of features that determine it to be something else. If that sounds a bit wishy-washy, take solace in the fact that even experts argue over its classification.",True,Nonspecific Interstitial Pneumonia,Figure 4.8,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.8.png,Figure 4.8: Extremes of nonspecific interstitial pneumonia.
51643476-51ec-41bc-87bd-4dc25910ca52,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The presence of lymphocytes in biopsy and bronchoalveolar lavage fluid suggests the involvement of the immune system in the pathogenesis of nonspecific interstitial pneumonia. This is supported by the occurrence of NSIP in immune diseases such as HIV infection and several connective tissue disorders including polymyositis, rheumatoid arthritis, and systemic sclerosis. Our understanding of the pathological mechanisms is still evolving.",True,Nonspecific Interstitial Pneumonia,,,,
91d86721-86d1-40d3-bd43-f5c0c0b0cfcf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Cryptogenic Organizing Pneumonia,False,Cryptogenic Organizing Pneumonia,,,,
db36a5a1-065e-466d-8899-deac54c83cb1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Our final major classification is cryptogenic organizing pneumonia (COP). This form of interstitial disease affects the distal bronchioles, respiratory bronchioles, and alveoli, but the primary site of injury is usually the alveolar walls.",True,Cryptogenic Organizing Pneumonia,,,,
f0c06a02-341d-4284-8f74-0c8790060a7f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The hallmark of COP is an excessive proliferation of granulation tissue made of collagen-embedded fibroblasts and myofibroblasts that starts in the alveolar space. These plugs of fibrotic tissue may extend from one alveolus to another via the pores of Kohn and give rise to a characteristic butterfly pattern. The pathogenesis is an initial alveolar injury, with plasma proteins leaking into the alveolar lumen that is followed by recruited fibroblasts depositing connective tissue with the lumen itself. These fibrotic lesions show a homogenous time line and movement to the distal airways, but are actually reversible, which is in contrast of the lesions seen in usual interstitial pneumonia. In COP the lung architecture is maintained, probably through more thorough regulation of angiogenesis and apoptosis than that seen in usual interstitial pneumonia (UIP).",True,Cryptogenic Organizing Pneumonia,,,,
7deb323c-7cf5-4ec3-bc57-43d2dd013c47,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The onset of COP is marked with dyspnea and dry cough (as with most ILDs), and it has a moderate time line of a couple of months, after which symptoms subside. History is again important to determine the initial insult, and potential culprits include connective tissue disease, new medications, or exposure to therapeutic radiation, fumes, or dusts.",True,Cryptogenic Organizing Pneumonia,,,,
cf7d9bf0-2ce4-4d9a-ad7a-932bebc12801,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Environment-Induced ILDs,False,Environment-Induced ILDs,,,,
13af9b26-58a9-4ce9-b667-352e7f110ef7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Now we will look at several specific forms of interstitial disease that are related to occupational exposure. While these forms of ILD have some distinguishing factors, the importance of taking a good history cannot be understated.",True,Environment-Induced ILDs,,,,
1d5171fc-a615-41eb-8074-631e4eaa5680,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Silicosis,False,Silicosis,,,,
29db701b-78d3-4c0e-9508-b1c578a09680,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Silicosis is related to exposure to silica that occurs frequently in occupations such as stone cutting, foundry work, and mining. Cutting or breaking stone can produce crystalline silica, and when less than 5 microns in diameter, it becomes respirable. When particle size is between 1 and 3 microns, it can reach the alveoli.",True,Silicosis,,,,
8521f140-d191-4f47-89af-281a112a0f12,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The formation of silicosis can be acute with heavy brief exposure (often seen in sandblasters), or chronic and insidious with more prolonged lighter exposures. The process is initiated with alveolar macrophages engulfing the crystals. In response they release cytokines to attract lymphocytes, neutrophils, and fibroblasts—and a familiar story of tissue destruction and laying down of collagen begins. (You might note at this point that engulfing silica in vitro has been shown to damage macrophages, causing them to release their intracellular enzymes, which may contribute to the destructive mechanism in vivo.)",True,Silicosis,,,,
2798569c-c5f0-45a8-924c-68dc54320327,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The pattern of collagen deposition is distinct, with silicotic nodules forming with concentric fibers producing a whirled pattern (figure 4.10). These nodules are distributed throughout the lung but are more common in the upper lobes and perihilar area (figure 4.11). They tend to be surrounded by distorted lung tissue that may show emphysematous changes. Ongoing disease coalescence of the nodules produces irregular masses of noncaseating granulomas. This progressive massive fibrosis can be helped with concurrent TB or atypical mycobacterial disease where caseating granulomas may also be present. Likewise silicosis may impair the macrophage response to TB. It causes contraction of the upper lobes and may lead to emphysema in the lower lobes, sometimes with large bullous changes. The pathophysiology of silicosis is summarized in figure 4.12.",True,Silicosis,Figure 4.10,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.10.jpeg,Figure 4.10: Silicotic nodule in the parenchyma of the lung.
2798569c-c5f0-45a8-924c-68dc54320327,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The pattern of collagen deposition is distinct, with silicotic nodules forming with concentric fibers producing a whirled pattern (figure 4.10). These nodules are distributed throughout the lung but are more common in the upper lobes and perihilar area (figure 4.11). They tend to be surrounded by distorted lung tissue that may show emphysematous changes. Ongoing disease coalescence of the nodules produces irregular masses of noncaseating granulomas. This progressive massive fibrosis can be helped with concurrent TB or atypical mycobacterial disease where caseating granulomas may also be present. Likewise silicosis may impair the macrophage response to TB. It causes contraction of the upper lobes and may lead to emphysema in the lower lobes, sometimes with large bullous changes. The pathophysiology of silicosis is summarized in figure 4.12.",True,Silicosis,Figure 4.10,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.10.jpeg,Figure 4.10: Silicotic nodule in the parenchyma of the lung.
2798569c-c5f0-45a8-924c-68dc54320327,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The pattern of collagen deposition is distinct, with silicotic nodules forming with concentric fibers producing a whirled pattern (figure 4.10). These nodules are distributed throughout the lung but are more common in the upper lobes and perihilar area (figure 4.11). They tend to be surrounded by distorted lung tissue that may show emphysematous changes. Ongoing disease coalescence of the nodules produces irregular masses of noncaseating granulomas. This progressive massive fibrosis can be helped with concurrent TB or atypical mycobacterial disease where caseating granulomas may also be present. Likewise silicosis may impair the macrophage response to TB. It causes contraction of the upper lobes and may lead to emphysema in the lower lobes, sometimes with large bullous changes. The pathophysiology of silicosis is summarized in figure 4.12.",True,Silicosis,Figure 4.10,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.10.jpeg,Figure 4.10: Silicotic nodule in the parenchyma of the lung.
9d5b90d3-9729-4fd4-b0aa-dec9fdbf13cf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"After an insidious, asymptomatic beginning, the main symptom of silicosis is dyspnea, with or without cough (cough is likely generated by concurrent smoking). The dyspnea is progressive but other symptoms that occur are often due to secondary, superimposed infection making repeated bacteriological studies important.",True,Silicosis,,,,
5b38886c-9a9b-45a9-9782-9d22dae28801,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,The pathophysiology of silicosis is summarized in figure 4.12.,True,Silicosis,Figure 4.12,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.12.png,Figure 4.12: The pathophysiology of silicosis.
5b38886c-9a9b-45a9-9782-9d22dae28801,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,The pathophysiology of silicosis is summarized in figure 4.12.,True,Silicosis,Figure 4.12,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.12.png,Figure 4.12: The pathophysiology of silicosis.
5b38886c-9a9b-45a9-9782-9d22dae28801,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,The pathophysiology of silicosis is summarized in figure 4.12.,True,Silicosis,Figure 4.12,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.12.png,Figure 4.12: The pathophysiology of silicosis.
bc68c31c-d3a2-42ad-81b8-e99fa14cc6b2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Asbestosis,False,Asbestosis,,,,
1d7b0885-57e4-4abb-af75-8099ab638571,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"There are a number of pulmonary manifestations arising from exposure to asbestos. Previously used in the construction and manufacturing industries, the occurrence of related illness led to legislation to restrict its use. However, demolition or renovation of asbestos-containing buildings can still lead to air-born asbestos exposure. The pulmonary manifestations include pulmonary fibrosis, bronchogenic carcinoma, pleural effusion, pleural fibrosis, and mesothelioma. We will deal with the pulmonary fibrosis here and what is known as asbestosis.",True,Asbestosis,,,,
6fdaca7e-52b0-482b-9106-65a3b5eba8a3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The disease course (summarized in figure 4.13) is similar to that described for silicosis. Asbestos fibers arrive in the alveoli and macrophages initiate an inflammatory response. Note that the arrival of neutrophilic leukocytes and their release of cytokines and oxygen radicals seem to play a significant role. Short fibers can be phagocytized and removed, but larger fibers persist in the airway and perpetuate the inflammatory reaction, promoting fibrosis.",True,Asbestosis,Figure 4.13,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.13.png,Figure 4.13: Pathophysiology of asbestosis.
6fdaca7e-52b0-482b-9106-65a3b5eba8a3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The disease course (summarized in figure 4.13) is similar to that described for silicosis. Asbestos fibers arrive in the alveoli and macrophages initiate an inflammatory response. Note that the arrival of neutrophilic leukocytes and their release of cytokines and oxygen radicals seem to play a significant role. Short fibers can be phagocytized and removed, but larger fibers persist in the airway and perpetuate the inflammatory reaction, promoting fibrosis.",True,Asbestosis,Figure 4.13,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.13.png,Figure 4.13: Pathophysiology of asbestosis.
6fdaca7e-52b0-482b-9106-65a3b5eba8a3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The disease course (summarized in figure 4.13) is similar to that described for silicosis. Asbestos fibers arrive in the alveoli and macrophages initiate an inflammatory response. Note that the arrival of neutrophilic leukocytes and their release of cytokines and oxygen radicals seem to play a significant role. Short fibers can be phagocytized and removed, but larger fibers persist in the airway and perpetuate the inflammatory reaction, promoting fibrosis.",True,Asbestosis,Figure 4.13,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.13.png,Figure 4.13: Pathophysiology of asbestosis.
e73180c7-3bba-4838-b5f6-37fd203cb5eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Histologically, these fibers can been seen as asbestos bodies, or ferruginous bodies, as they are coated with iron-containing protein (figure 4.14).",True,Asbestosis,Figure 4.14,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.14-scaled.jpg,Figure 4.14: Ferruginous bodies associated with asbestosis.
e73180c7-3bba-4838-b5f6-37fd203cb5eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Histologically, these fibers can been seen as asbestos bodies, or ferruginous bodies, as they are coated with iron-containing protein (figure 4.14).",True,Asbestosis,Figure 4.14,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.14-scaled.jpg,Figure 4.14: Ferruginous bodies associated with asbestosis.
e73180c7-3bba-4838-b5f6-37fd203cb5eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Histologically, these fibers can been seen as asbestos bodies, or ferruginous bodies, as they are coated with iron-containing protein (figure 4.14).",True,Asbestosis,Figure 4.14,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.14-scaled.jpg,Figure 4.14: Ferruginous bodies associated with asbestosis.
234b74d2-de1b-41cb-a0c4-ce0fea40097e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Fibrosis ensues, but in contrast to silicosis, asbestos-related fibrosis is nonnodular and mostly involves the lower lung fields and frequently includes pleural thickening.",True,Asbestosis,,,,
7a435aa6-667d-4eea-a54a-f8db68b0a3b5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The extent of fibrosis is highly variable, from thickened alveolar septum to complete destruction of the alveolar spaces. In the advanced disease honeycomb lung can be observed with CT. Radiography of later-stage disease shows reticular interstitial markings in the lower lung fields (left panel, figure 4.15). Pleural changes are also more common. Rounded atelectasis may occur after a pleural effusion has been reabsorbed and caused a section of the airway to become trapped. A rounded atelectasis is indicated by the arrow in figure 4.15, and care should be taken not to mistake this for a neoplasm. Abestosis is a risk factor for the development of mesothelioma and should be considered for patients working in “at-risk” environments or occupations.",True,Asbestosis,Figure 4.15,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.15.jpeg,Figure 4.15: Radiographic findings in asbestosis.
7a435aa6-667d-4eea-a54a-f8db68b0a3b5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The extent of fibrosis is highly variable, from thickened alveolar septum to complete destruction of the alveolar spaces. In the advanced disease honeycomb lung can be observed with CT. Radiography of later-stage disease shows reticular interstitial markings in the lower lung fields (left panel, figure 4.15). Pleural changes are also more common. Rounded atelectasis may occur after a pleural effusion has been reabsorbed and caused a section of the airway to become trapped. A rounded atelectasis is indicated by the arrow in figure 4.15, and care should be taken not to mistake this for a neoplasm. Abestosis is a risk factor for the development of mesothelioma and should be considered for patients working in “at-risk” environments or occupations.",True,Asbestosis,Figure 4.15,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.15.jpeg,Figure 4.15: Radiographic findings in asbestosis.
7a435aa6-667d-4eea-a54a-f8db68b0a3b5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The extent of fibrosis is highly variable, from thickened alveolar septum to complete destruction of the alveolar spaces. In the advanced disease honeycomb lung can be observed with CT. Radiography of later-stage disease shows reticular interstitial markings in the lower lung fields (left panel, figure 4.15). Pleural changes are also more common. Rounded atelectasis may occur after a pleural effusion has been reabsorbed and caused a section of the airway to become trapped. A rounded atelectasis is indicated by the arrow in figure 4.15, and care should be taken not to mistake this for a neoplasm. Abestosis is a risk factor for the development of mesothelioma and should be considered for patients working in “at-risk” environments or occupations.",True,Asbestosis,Figure 4.15,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.15.jpeg,Figure 4.15: Radiographic findings in asbestosis.
c0eaf213-b6b2-41ec-be20-0a3c50fbbd6d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Coal worker’s pneumoconiosis (CWP),False,Coal worker’s pneumoconiosis (CWP),,,,
fc6f34db-49eb-4691-88be-a23e0f4edd07,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"CWP arises after prolonged exposure to coal dust. While drilling through rock the miner may be susceptible to silicosis, but prolonged and heavy exposure to aerosolized carbon (that is not usually fibrogenic in lesser exposures) can result in its own distinct condition. Even then it can take ten to twelve years of underground exposure to develop.",True,Coal worker’s pneumoconiosis (CWP),,,,
c2150c08-e875-4149-ae94-9bcf8df39364,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Again we see the process start with phagocytosis of the coal dust by macrophages after the mucocillary escalator is overwhelmed. The macrophages launch their inflammatory process, and tissue damage is caused by the resultant cytokine bloom and oxygen radical and enzyme release. Fibroblasts form reticulin networks, but there is no significant collagen deposition. Aggregates of reticulin fibers, macrophages, and dust form coal macules (figure 4.16). The coal macules appear as black spots in lung sections and give rise to the condition’s nickname of “black lung.”",True,Coal worker’s pneumoconiosis (CWP),Figure 4.16,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.16.jpeg,Figure 4.16: Example of coal macules in simple CWP showing fibrosis and coal macules.
c2150c08-e875-4149-ae94-9bcf8df39364,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Again we see the process start with phagocytosis of the coal dust by macrophages after the mucocillary escalator is overwhelmed. The macrophages launch their inflammatory process, and tissue damage is caused by the resultant cytokine bloom and oxygen radical and enzyme release. Fibroblasts form reticulin networks, but there is no significant collagen deposition. Aggregates of reticulin fibers, macrophages, and dust form coal macules (figure 4.16). The coal macules appear as black spots in lung sections and give rise to the condition’s nickname of “black lung.”",True,Coal worker’s pneumoconiosis (CWP),Figure 4.16,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.16.jpeg,Figure 4.16: Example of coal macules in simple CWP showing fibrosis and coal macules.
c2150c08-e875-4149-ae94-9bcf8df39364,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Again we see the process start with phagocytosis of the coal dust by macrophages after the mucocillary escalator is overwhelmed. The macrophages launch their inflammatory process, and tissue damage is caused by the resultant cytokine bloom and oxygen radical and enzyme release. Fibroblasts form reticulin networks, but there is no significant collagen deposition. Aggregates of reticulin fibers, macrophages, and dust form coal macules (figure 4.16). The coal macules appear as black spots in lung sections and give rise to the condition’s nickname of “black lung.”",True,Coal worker’s pneumoconiosis (CWP),Figure 4.16,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.16.jpeg,Figure 4.16: Example of coal macules in simple CWP showing fibrosis and coal macules.
85695151-9386-4052-8317-d0e371b5d1e8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The coal macules are associated with dilation of the respiratory bronchioles that can manifest as focal centrilobar emphysema (figure 4.16). This is referred to as simple CWP, whereas the less common, complicated form involves progressive massive fibrosis, usually in the upper lobes, as in silicosis. However, in CWP these lesions are black and relatively homogenous, where as in silicosis they are a conglomeration of intersecting nodules. Figure 4.17 shows a large black fibrotic lesion destroying the perihilar lung parenchyma.",True,Coal worker’s pneumoconiosis (CWP),Figure 4.17,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.17.jpeg,Figure 4.17: Large perihilar lesion in complicated CWP.
85695151-9386-4052-8317-d0e371b5d1e8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The coal macules are associated with dilation of the respiratory bronchioles that can manifest as focal centrilobar emphysema (figure 4.16). This is referred to as simple CWP, whereas the less common, complicated form involves progressive massive fibrosis, usually in the upper lobes, as in silicosis. However, in CWP these lesions are black and relatively homogenous, where as in silicosis they are a conglomeration of intersecting nodules. Figure 4.17 shows a large black fibrotic lesion destroying the perihilar lung parenchyma.",True,Coal worker’s pneumoconiosis (CWP),Figure 4.17,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.17.jpeg,Figure 4.17: Large perihilar lesion in complicated CWP.
85695151-9386-4052-8317-d0e371b5d1e8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The coal macules are associated with dilation of the respiratory bronchioles that can manifest as focal centrilobar emphysema (figure 4.16). This is referred to as simple CWP, whereas the less common, complicated form involves progressive massive fibrosis, usually in the upper lobes, as in silicosis. However, in CWP these lesions are black and relatively homogenous, where as in silicosis they are a conglomeration of intersecting nodules. Figure 4.17 shows a large black fibrotic lesion destroying the perihilar lung parenchyma.",True,Coal worker’s pneumoconiosis (CWP),Figure 4.17,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.17.jpeg,Figure 4.17: Large perihilar lesion in complicated CWP.
c3453903-5d64-4566-8b34-6af61a54d1f2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Clinical manifestations are often complicated by concurrent cigarette smoking that may alone explain the frequency of chronic bronchitis in CWP patients. The simple form can be asymptomatic, but the complicated form produces dyspnea and signs of respiratory failures, pulmonary hypertension, and cor pulmonale.",True,Coal worker’s pneumoconiosis (CWP),,,,
8245131a-bab9-4a92-8560-e4c7ca357e04,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Berylliosis,False,Berylliosis,,,,
92aa3fb2-27e6-4577-b223-11aab7a33465,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"The last occupational disorder we will look at is berylliosis, or chronic beryllium disease (CBD), that occurs after exposure to beryllium, a metal used in manufacturing. Here the start to our story is a little different. Beryllium arrives in the airway and there is a hypersensitization of T cells. On subsequent exposures the T cells proliferate—the bronchoalveolar lavage (BAL) fluid of berylliosis patients is rich in sensitized CD4+ cells.",True,Berylliosis,,,,
aed885db-c582-46bf-93c1-5d8ee8de63fc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Now we return to our pattern: the abundant CD4+ cells release proinflammatory cytokines and granulomatous fibrosis occurs (figure 4.18). The granulomas (figure 4.19) are indistinguishable from those caused by sarcoidosis (which are also caused by CD4+ cells), and many CBD patients may be misdiagnosed as sarcoidosis cases, so appropriate history taking is paramount. Usually CBD involves greater interstitial inflammation, but the most definitive diagnosis comes from the beryllium lymphocyte proliferation test. The test involves exposing lymphocytes from the patient’s blood or BAL fluid to different concentrations of beryllium and assaying their proliferation.",True,Berylliosis,Figure 4.18,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.18.png,Figure 4.18: Pathophysiology of berylliosis.
aed885db-c582-46bf-93c1-5d8ee8de63fc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Now we return to our pattern: the abundant CD4+ cells release proinflammatory cytokines and granulomatous fibrosis occurs (figure 4.18). The granulomas (figure 4.19) are indistinguishable from those caused by sarcoidosis (which are also caused by CD4+ cells), and many CBD patients may be misdiagnosed as sarcoidosis cases, so appropriate history taking is paramount. Usually CBD involves greater interstitial inflammation, but the most definitive diagnosis comes from the beryllium lymphocyte proliferation test. The test involves exposing lymphocytes from the patient’s blood or BAL fluid to different concentrations of beryllium and assaying their proliferation.",True,Berylliosis,Figure 4.18,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.18.png,Figure 4.18: Pathophysiology of berylliosis.
aed885db-c582-46bf-93c1-5d8ee8de63fc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Now we return to our pattern: the abundant CD4+ cells release proinflammatory cytokines and granulomatous fibrosis occurs (figure 4.18). The granulomas (figure 4.19) are indistinguishable from those caused by sarcoidosis (which are also caused by CD4+ cells), and many CBD patients may be misdiagnosed as sarcoidosis cases, so appropriate history taking is paramount. Usually CBD involves greater interstitial inflammation, but the most definitive diagnosis comes from the beryllium lymphocyte proliferation test. The test involves exposing lymphocytes from the patient’s blood or BAL fluid to different concentrations of beryllium and assaying their proliferation.",True,Berylliosis,Figure 4.18,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.18.png,Figure 4.18: Pathophysiology of berylliosis.
4a709bfe-a99d-49a2-9909-cf50048e610f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Susceptibility to becoming hypersensitized appears to have a significant genetic component. Why the process continues after exposure has stopped is unclear, but possibilities include a fundamental T cell disorder, or the fact that the insoluble beryllium causes apoptosis of macrophages, leading them to release a previously phagocytized beryllium load.",True,Berylliosis,,,,
325062af-2802-44fd-a467-f8a7df71e82b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"As the disease progresses, radiographic findings show that the granuoles can become more organized to produce fibrous nodules that may begin to impact lung function. The immune system involvement can produce hilar lymphadenopathy, and common later signs include interstital fibrosis and pleural thickening.",True,Berylliosis,,,,
9f031a0c-652a-4d55-982f-d001172b0242,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Summary,False,Summary,,,,
a87a5f49-1e07-4993-a633-9baab2602c7a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"So there is a selection of interstitial lung diseases that, while sharing the pathophysiological manifestations of restrictive lung disease, can be distinguished through good history taking or identifying distinct histological features.",True,Summary,,,,
c3046aa0-6f97-4412-b7a7-14b0cf08698c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"References, Resources, and Further Reading",False,"References, Resources, and Further Reading",,,,
dccb896a-bd46-4de9-9f42-21de2da3df7b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,Text,False,Text,,,,
31109643-c191-45e9-b983-23ac1703b3ba,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapters 12–15.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
3487393a-fa5f-4ec9-a9c3-9e5ce29eff3a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/#chapter-31-section-1,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
af8688d9-352e-45f1-98a2-928153074b72,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Before we start taking about diseases affecting the lung interstitium, let us remind ourselves of what it is.",True,Text,,,,
40c85026-d4b9-48cd-8da6-1ed8606e2969,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The interstitial tissue, sometimes referred to as parenchyma, surrounds the alveolar and capillary structures and contributes to the mechanical behavior of the lungs. The interstitium is extremely thin between the alveoli and capillaries, and forms the basement membrane through which gas exchange occurs. On the parenchymal side of the capillaries the interstitium is more substantial and is more involved in fluid exchange. There is also substantial amounts of interstitial tissue in the spaces around major vessels and airways, and it also makes up the interlobular septa.",True,Text,,,,
56814a5f-9831-4a3e-85f2-49e93b51504f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Mechanisms of ILD,False,Mechanisms of ILD,,,,
39301e72-0cf1-4860-8826-ed81517866b2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Now we will look at the generalized mechanism of interstitial lung disease (figure 4.1). It is worth noting that the numerous conditions that the term ILD encompasses have subtle differences in mechanism and manifestations, and these differences are what we will deal with elsewhere.",True,Mechanisms of ILD,Figure 4.1,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
39301e72-0cf1-4860-8826-ed81517866b2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Now we will look at the generalized mechanism of interstitial lung disease (figure 4.1). It is worth noting that the numerous conditions that the term ILD encompasses have subtle differences in mechanism and manifestations, and these differences are what we will deal with elsewhere.",True,Mechanisms of ILD,Figure 4.1,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
39301e72-0cf1-4860-8826-ed81517866b2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Now we will look at the generalized mechanism of interstitial lung disease (figure 4.1). It is worth noting that the numerous conditions that the term ILD encompasses have subtle differences in mechanism and manifestations, and these differences are what we will deal with elsewhere.",True,Mechanisms of ILD,Figure 4.1,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
c96ed0d3-f91f-4085-8dc3-7da7b766b43d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,ILD,False,ILD,,,,
bdb02940-0b25-4619-b856-77169eb65bbd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Generally though, ILD starts with an initial insult to the lung (#1, figure 4.1); the type of insult is a major contributor to the different ILD conditions. (It probably will not be what is depicted in figure 4.1, but if it was, it might lead to the inflammatory condition of tiefitis.)",True,ILD,Figure 4.1,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
bdb02940-0b25-4619-b856-77169eb65bbd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Generally though, ILD starts with an initial insult to the lung (#1, figure 4.1); the type of insult is a major contributor to the different ILD conditions. (It probably will not be what is depicted in figure 4.1, but if it was, it might lead to the inflammatory condition of tiefitis.)",True,ILD,Figure 4.1,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
bdb02940-0b25-4619-b856-77169eb65bbd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Generally though, ILD starts with an initial insult to the lung (#1, figure 4.1); the type of insult is a major contributor to the different ILD conditions. (It probably will not be what is depicted in figure 4.1, but if it was, it might lead to the inflammatory condition of tiefitis.)",True,ILD,Figure 4.1,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
199644ee-7aac-43de-a63f-4e86db069575,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,tiefitis,False,tiefitis,,,,
2d171b66-00c1-431a-974e-aba3d6db69ea,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"There is then a response by neutrophils and alveolar macrophages (#2, figure 4.1). The macrophage response seems particularly important to the development of ILD. Release of cytokines (#3, figure 4.1) attracts other inflammatory cells, and the arrival of polymorphonuclear leukocytes and lymphocytes play an important role in disease instigation. These cells release cytokines, enzymes, and toxic oxygen radicals that damage and destroy local tissue. Released growth factors, such as TGF-Beta, instigate the transition of mesenchymal cells to fibroblasts.",True,tiefitis,Figure 4.1,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
2d171b66-00c1-431a-974e-aba3d6db69ea,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"There is then a response by neutrophils and alveolar macrophages (#2, figure 4.1). The macrophage response seems particularly important to the development of ILD. Release of cytokines (#3, figure 4.1) attracts other inflammatory cells, and the arrival of polymorphonuclear leukocytes and lymphocytes play an important role in disease instigation. These cells release cytokines, enzymes, and toxic oxygen radicals that damage and destroy local tissue. Released growth factors, such as TGF-Beta, instigate the transition of mesenchymal cells to fibroblasts.",True,tiefitis,Figure 4.1,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
2d171b66-00c1-431a-974e-aba3d6db69ea,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"There is then a response by neutrophils and alveolar macrophages (#2, figure 4.1). The macrophage response seems particularly important to the development of ILD. Release of cytokines (#3, figure 4.1) attracts other inflammatory cells, and the arrival of polymorphonuclear leukocytes and lymphocytes play an important role in disease instigation. These cells release cytokines, enzymes, and toxic oxygen radicals that damage and destroy local tissue. Released growth factors, such as TGF-Beta, instigate the transition of mesenchymal cells to fibroblasts.",True,tiefitis,Figure 4.1,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
f84f545b-7dfc-476f-b25f-960aa972f50c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"It is worth noting at this point that some forms of ILD are caused by an exaggerated immune reaction—either through an allergic-like response, or a direct immune disorder.",True,tiefitis,,,,
a5277444-04d7-4162-828c-3d3e687f37da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The destruction of tissue and activity of a growing number of fibroblasts results in the inflamed interstitium becoming fibrosed with excess connective tissue, particularly collagen (#4, figure 4.1).",True,tiefitis,Figure 4.1,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
a5277444-04d7-4162-828c-3d3e687f37da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The destruction of tissue and activity of a growing number of fibroblasts results in the inflamed interstitium becoming fibrosed with excess connective tissue, particularly collagen (#4, figure 4.1).",True,tiefitis,Figure 4.1,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
a5277444-04d7-4162-828c-3d3e687f37da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The destruction of tissue and activity of a growing number of fibroblasts results in the inflamed interstitium becoming fibrosed with excess connective tissue, particularly collagen (#4, figure 4.1).",True,tiefitis,Figure 4.1,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
c3bc57c6-1be3-4b1b-b0f9-82345c2f0588,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Pathology of ILD,False,Pathology of ILD,,,,
cbc065a8-fdd2-4bc8-95de-51a1bbe604fc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"These changes in structure dramatically change the functional and mechanical properties of the tissue. The changes also tend to follow a characteristic pattern, although, as you might imagine, different conditions have subtle differences in pattern.",True,Pathology of ILD,,,,
6c914af9-ff0f-496b-aa40-f18a39b50d04,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The action of fibroblasts laying down connective tissue, combined with the destruction of alveolar and capillary structures, leads to a widening of airspaces with thick collagenous and infiltrated walls (figure 4.2A and 4.2B), which are a functionally significant departure from the ideal structure for gas exchange.",True,Pathology of ILD,Figure 4.2,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
6c914af9-ff0f-496b-aa40-f18a39b50d04,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The action of fibroblasts laying down connective tissue, combined with the destruction of alveolar and capillary structures, leads to a widening of airspaces with thick collagenous and infiltrated walls (figure 4.2A and 4.2B), which are a functionally significant departure from the ideal structure for gas exchange.",True,Pathology of ILD,Figure 4.2,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
6c914af9-ff0f-496b-aa40-f18a39b50d04,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The action of fibroblasts laying down connective tissue, combined with the destruction of alveolar and capillary structures, leads to a widening of airspaces with thick collagenous and infiltrated walls (figure 4.2A and 4.2B), which are a functionally significant departure from the ideal structure for gas exchange.",True,Pathology of ILD,Figure 4.2,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
ef092c7b-d2c6-4956-80f5-84fae32e843f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The thickened basement membrane poses a significant obstacle to the transfer of gases, and the dense connective tissue stiffens the lung and thereby reduces its compliance. Combined with loss of capillary beds and airspace surface area, gas exchange is reduced.",True,Pathology of ILD,,,,
826f48f0-5124-4474-8137-e2fff32c5ea7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"At the end of the disease the lung takes on a characteristic honeycomb appearance, and “ground glass opacities” are a hallmark sign on CT images (figure 4.2C). These morphological changes lead to pathophysiological consequences that are shared by most forms of the disease, as all cause varying degrees of interstitial inflammation and connective tissue deposition.",True,Pathology of ILD,Figure 4.2,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
826f48f0-5124-4474-8137-e2fff32c5ea7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"At the end of the disease the lung takes on a characteristic honeycomb appearance, and “ground glass opacities” are a hallmark sign on CT images (figure 4.2C). These morphological changes lead to pathophysiological consequences that are shared by most forms of the disease, as all cause varying degrees of interstitial inflammation and connective tissue deposition.",True,Pathology of ILD,Figure 4.2,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
826f48f0-5124-4474-8137-e2fff32c5ea7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"At the end of the disease the lung takes on a characteristic honeycomb appearance, and “ground glass opacities” are a hallmark sign on CT images (figure 4.2C). These morphological changes lead to pathophysiological consequences that are shared by most forms of the disease, as all cause varying degrees of interstitial inflammation and connective tissue deposition.",True,Pathology of ILD,Figure 4.2,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.2.png,"Figure 4.2: Changes in pulmonary histology (A, B) and gross anatomy (C) with interstitial lung disease."
24c6d49f-201e-46d0-b14f-eb7b51bacf09,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Pathophysiology of ILD,False,Pathophysiology of ILD,,,,
e955b13a-6fe4-4b45-b619-83d9816ce49e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The first major issue is the reduced diffusion capacity of the involved areas, and all ILD patients demonstrate a reduced transfer factor, or DLCO (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
e955b13a-6fe4-4b45-b619-83d9816ce49e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The first major issue is the reduced diffusion capacity of the involved areas, and all ILD patients demonstrate a reduced transfer factor, or DLCO (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
e955b13a-6fe4-4b45-b619-83d9816ce49e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The first major issue is the reduced diffusion capacity of the involved areas, and all ILD patients demonstrate a reduced transfer factor, or DLCO (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
a112f31f-d3ff-42b4-afa9-2940b0abc62b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Because of the heterogenous distribution of the disease, and the involvement of the pulmonary circulation, severe V/Q abnormalities arise throughout the lung. This and the reduced diffusion capacity result in hypoxemia. In the chronic disease state this may lead to cor pulmonale (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
a112f31f-d3ff-42b4-afa9-2940b0abc62b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Because of the heterogenous distribution of the disease, and the involvement of the pulmonary circulation, severe V/Q abnormalities arise throughout the lung. This and the reduced diffusion capacity result in hypoxemia. In the chronic disease state this may lead to cor pulmonale (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
a112f31f-d3ff-42b4-afa9-2940b0abc62b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Because of the heterogenous distribution of the disease, and the involvement of the pulmonary circulation, severe V/Q abnormalities arise throughout the lung. This and the reduced diffusion capacity result in hypoxemia. In the chronic disease state this may lead to cor pulmonale (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
7c786e2a-4e8f-4581-98ca-8ce47231a1b7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The reduction in lung compliance leads to a reduced lung volume. This is easily detected with spirometry as shown by the inner plot of the flow-volume loop in figure 4.3. Because FEV1 and FVC are both reduced, the ratio frequently remains the same or may even rise; as such FEV1/FVC is a poor indicator of restrictive disease.",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
7c786e2a-4e8f-4581-98ca-8ce47231a1b7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The reduction in lung compliance leads to a reduced lung volume. This is easily detected with spirometry as shown by the inner plot of the flow-volume loop in figure 4.3. Because FEV1 and FVC are both reduced, the ratio frequently remains the same or may even rise; as such FEV1/FVC is a poor indicator of restrictive disease.",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
7c786e2a-4e8f-4581-98ca-8ce47231a1b7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The reduction in lung compliance leads to a reduced lung volume. This is easily detected with spirometry as shown by the inner plot of the flow-volume loop in figure 4.3. Because FEV1 and FVC are both reduced, the ratio frequently remains the same or may even rise; as such FEV1/FVC is a poor indicator of restrictive disease.",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
8a616845-f60d-4824-be7f-6202a38e985e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The reduced lung volume and compliance results in a characteristic rapid, shallow breathing pattern as the patient tries to maintain alveolar ventilation (figure 4.3). However, while avoiding unnecessary increases in the work of breathing by not trying to over-expand the noncompliant lung, the rapid shallow breathing proportionally increases dead space ventilation.",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
8a616845-f60d-4824-be7f-6202a38e985e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The reduced lung volume and compliance results in a characteristic rapid, shallow breathing pattern as the patient tries to maintain alveolar ventilation (figure 4.3). However, while avoiding unnecessary increases in the work of breathing by not trying to over-expand the noncompliant lung, the rapid shallow breathing proportionally increases dead space ventilation.",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
8a616845-f60d-4824-be7f-6202a38e985e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The reduced lung volume and compliance results in a characteristic rapid, shallow breathing pattern as the patient tries to maintain alveolar ventilation (figure 4.3). However, while avoiding unnecessary increases in the work of breathing by not trying to over-expand the noncompliant lung, the rapid shallow breathing proportionally increases dead space ventilation.",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
8495f4ec-338b-4c06-af82-3ec58a5b152c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The reduction in tidal volume, combined with a raised hypoxic drive to breathe, results in the cardinal symptom of ILD, which is dyspnea (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
8495f4ec-338b-4c06-af82-3ec58a5b152c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The reduction in tidal volume, combined with a raised hypoxic drive to breathe, results in the cardinal symptom of ILD, which is dyspnea (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
8495f4ec-338b-4c06-af82-3ec58a5b152c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The reduction in tidal volume, combined with a raised hypoxic drive to breathe, results in the cardinal symptom of ILD, which is dyspnea (figure 4.3).",True,Pathophysiology of ILD,Figure 4.3,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
fa7bdec3-a66e-4cdc-adf8-ce21b89f18f6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Clinical Signs of ILD,False,Clinical Signs of ILD,,,,
989b3c2b-de3c-4421-9d86-de4262c0193a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The correlation of dyspnea and disease stage is closer in ILD than any other respiratory disease. The onset is insidious, appearing first during exercise, and it likely contributes to the other major complaints of weakness and fatigue. The dyspnea gets progressively worse until it can be debilitating.",True,Clinical Signs of ILD,,,,
28448d38-7e62-462a-be19-26569f85c7a3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Inflammation and excitation of pulmonary receptors leads to a nonproductive and persistent cough, and upon examination patients will have limited chest expansion and demonstrate the characteristic breathing pattern of restrictive lung disease.",True,Clinical Signs of ILD,,,,
f3240f27-312d-4847-83e8-3d0c91ed90cf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Hallmark lung sounds are fine crackles, commonly found at the base of the lung, and may appear louder than expected because of increased transmission through denser than normal tissue.",True,Clinical Signs of ILD,,,,
bb549cf4-de32-4e59-a3d5-273d6f3edc1d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,At later stages of the disease the patient shows signs of the prolonged hypoxemia with digital clubbing and cyanosis.,True,Clinical Signs of ILD,,,,
e8b1639f-9336-4151-8581-068bad0ef379,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Forms of Interstitial Lung Disease,False,Forms of Interstitial Lung Disease,,,,
1b77f56b-0a85-4f54-af5b-b8a186a45f7b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Our major subcategory is idiopathic interstitial pneumonia (figure 4.4), or IIP, and this is divided again into six more useful categories that can be distinguished by history, time line, and histological changes. We will deal with these categories in this section, but it might be noted that usual interstitial pneumonia, still frequently called idiopathic pulmonary fibrosis, is the only one that remains untreatable, and early differentiation from the other forms is critical (figure 4.4).",True,Forms of Interstitial Lung Disease,Figure 4.4,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
1b77f56b-0a85-4f54-af5b-b8a186a45f7b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Our major subcategory is idiopathic interstitial pneumonia (figure 4.4), or IIP, and this is divided again into six more useful categories that can be distinguished by history, time line, and histological changes. We will deal with these categories in this section, but it might be noted that usual interstitial pneumonia, still frequently called idiopathic pulmonary fibrosis, is the only one that remains untreatable, and early differentiation from the other forms is critical (figure 4.4).",True,Forms of Interstitial Lung Disease,Figure 4.4,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
1b77f56b-0a85-4f54-af5b-b8a186a45f7b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Our major subcategory is idiopathic interstitial pneumonia (figure 4.4), or IIP, and this is divided again into six more useful categories that can be distinguished by history, time line, and histological changes. We will deal with these categories in this section, but it might be noted that usual interstitial pneumonia, still frequently called idiopathic pulmonary fibrosis, is the only one that remains untreatable, and early differentiation from the other forms is critical (figure 4.4).",True,Forms of Interstitial Lung Disease,Figure 4.4,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
d1e4d7a9-e092-4767-acd4-4f3c6279cb84,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Interstitial lung diseases can also be induced by numerous different environmental causes that produce nuanced conditions that are distinguishable by environmental and social history (figure 4.4) as well as specific histological features.,True,Forms of Interstitial Lung Disease,Figure 4.4,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
d1e4d7a9-e092-4767-acd4-4f3c6279cb84,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Interstitial lung diseases can also be induced by numerous different environmental causes that produce nuanced conditions that are distinguishable by environmental and social history (figure 4.4) as well as specific histological features.,True,Forms of Interstitial Lung Disease,Figure 4.4,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
d1e4d7a9-e092-4767-acd4-4f3c6279cb84,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Interstitial lung diseases can also be induced by numerous different environmental causes that produce nuanced conditions that are distinguishable by environmental and social history (figure 4.4) as well as specific histological features.,True,Forms of Interstitial Lung Disease,Figure 4.4,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.4-1024x680.png,Figure 4.4: Classifications of ILD.
24f233eb-6a8e-4d96-8db8-f1a334c2f9bc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The characteristics of usual interstitial pneumonia have been covered in the “Basis of ILD” section, so let us start looking at the pathophysiological and clinical features of the other broader disease categories.",True,Forms of Interstitial Lung Disease,,,,
ba560354-7e46-4230-bcdb-0ac7cbbc2270,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,False,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,,,,
f53fd6f5-ea86-413c-9418-91a10c400182,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,We can deal with the first two together as both share common characteristics and are potentially the same disease occurring in different anatomical locations. Desquamative interstitial pneumonia and respiratory bronchiolitis–associated ILD are both smoking related and are relatively uncommon.,True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,,,,
db2d21d9-b10a-4da9-87f8-76e4791d9843,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The histological hallmark is accumulation of numerous smoker’s macrophages in the airspaces (figure 4.5) or the first- and second-order respiratory bronchioles. These macrophages have a characteristic brown pigmentation. In desquamative interstitial pneumonia the airspaces are the primary site of involvement, whereas a respiratory bronchiolitis–associated ILD sees more involvement of the bronchioles (as the name suggests). The alveolar septum may be thickened with infiltrate and there may be mild peribronchilor or alveolar fibrosis, but this does not result in a honeycomb pattern seen in usual interstitial pneumonia.",True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,Figure 4.5,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.5.jpeg,Figure 4.5: Smoker’s macrophages occupying an airspace.
db2d21d9-b10a-4da9-87f8-76e4791d9843,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The histological hallmark is accumulation of numerous smoker’s macrophages in the airspaces (figure 4.5) or the first- and second-order respiratory bronchioles. These macrophages have a characteristic brown pigmentation. In desquamative interstitial pneumonia the airspaces are the primary site of involvement, whereas a respiratory bronchiolitis–associated ILD sees more involvement of the bronchioles (as the name suggests). The alveolar septum may be thickened with infiltrate and there may be mild peribronchilor or alveolar fibrosis, but this does not result in a honeycomb pattern seen in usual interstitial pneumonia.",True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,Figure 4.5,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.5.jpeg,Figure 4.5: Smoker’s macrophages occupying an airspace.
db2d21d9-b10a-4da9-87f8-76e4791d9843,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The histological hallmark is accumulation of numerous smoker’s macrophages in the airspaces (figure 4.5) or the first- and second-order respiratory bronchioles. These macrophages have a characteristic brown pigmentation. In desquamative interstitial pneumonia the airspaces are the primary site of involvement, whereas a respiratory bronchiolitis–associated ILD sees more involvement of the bronchioles (as the name suggests). The alveolar septum may be thickened with infiltrate and there may be mild peribronchilor or alveolar fibrosis, but this does not result in a honeycomb pattern seen in usual interstitial pneumonia.",True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,Figure 4.5,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.5.jpeg,Figure 4.5: Smoker’s macrophages occupying an airspace.
316bf996-7eaa-427b-8878-38829492f47b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"These ILDs are more prevalent in men, and are usually found in the fifth decade of life and after thirty-pack years. They are marked by the gradual and insidious onset of dyspnea, but lung reductions are usually minimal with both forms. The response to corticosteroid therapy and smoking cessation is good in about 80 percent of patients who remain stable or improve.",True,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,,,,
14b8c92a-ce26-4c0e-a68c-4df1921732e2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Diffuse Alveolar Damage (DAD),False,Diffuse Alveolar Damage (DAD),,,,
48469a26-f087-470a-b762-d4ee7962ea05,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"While the development of most interstitial lung diseases is slow and insidious, the hallmark of diffuse alveolar damage is rapid, occurring in a matter of days and often in previously healthy individuals. The manifestation of the disease is similar to acute respiratory distress syndrome, and in fact it has been suggested that DAD is a form of ARDS.",True,Diffuse Alveolar Damage (DAD),,,,
f038f67c-2055-403d-90b3-bfcec6ec1af9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The start is marked by a brief exudative phase with fluid entering the airspaces, but the following organizing or proliferative phase is what is usually seen by the time a biopsy is taken and where the similarities to ARDS are seen. The alveolar septa are thickened due to the interstitial edema and the septa may collapse or appose each other (figure 4.7). There is marked infiltration of the interstitial and airspaces by inflammatory cells, and type II cells proliferate. The destruction of the alveolar structure leaves a sludgy hyaline membrane of debris. Thrombi in small arteries may also be apparent.",True,Diffuse Alveolar Damage (DAD),Figure 4.7,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.7.jpeg,Figure 4.7: Diffuse alveolar damage.
f038f67c-2055-403d-90b3-bfcec6ec1af9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The start is marked by a brief exudative phase with fluid entering the airspaces, but the following organizing or proliferative phase is what is usually seen by the time a biopsy is taken and where the similarities to ARDS are seen. The alveolar septa are thickened due to the interstitial edema and the septa may collapse or appose each other (figure 4.7). There is marked infiltration of the interstitial and airspaces by inflammatory cells, and type II cells proliferate. The destruction of the alveolar structure leaves a sludgy hyaline membrane of debris. Thrombi in small arteries may also be apparent.",True,Diffuse Alveolar Damage (DAD),Figure 4.7,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.7.jpeg,Figure 4.7: Diffuse alveolar damage.
f038f67c-2055-403d-90b3-bfcec6ec1af9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The start is marked by a brief exudative phase with fluid entering the airspaces, but the following organizing or proliferative phase is what is usually seen by the time a biopsy is taken and where the similarities to ARDS are seen. The alveolar septa are thickened due to the interstitial edema and the septa may collapse or appose each other (figure 4.7). There is marked infiltration of the interstitial and airspaces by inflammatory cells, and type II cells proliferate. The destruction of the alveolar structure leaves a sludgy hyaline membrane of debris. Thrombi in small arteries may also be apparent.",True,Diffuse Alveolar Damage (DAD),Figure 4.7,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.7.jpeg,Figure 4.7: Diffuse alveolar damage.
31bc9d91-43ea-4b6e-bfa5-bd0281436a45,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Should the patient survive (about 50 percent do not) the healing phase can show recovery of the alveolar structure with varying degrees of fibrosis. Many patients return to normal lung function, but a few show a progressive fibrotic process that resembles idiopathic pulmonary fibrosis.",True,Diffuse Alveolar Damage (DAD),,,,
74283dea-769f-4c21-ae91-ae6dc9039d09,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Without biopsy, DAD is usually differentiated from other forms of interstitial disease by its rapid onset, but this can be confused with acute exacerbations of other diseases. However, the uniform pattern of damage in real DAD is representative of a single time line.",True,Diffuse Alveolar Damage (DAD),,,,
753b7bdb-772a-4705-864e-408c76232106,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Nonspecific Interstitial Pneumonia,False,Nonspecific Interstitial Pneumonia,,,,
6795f0eb-fe27-4be3-bf73-2976caea075e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Our next disease is at least courteous enough to only have one name, nonspecific interstitial pneumonia (NSIP), but irritatingly, it has three groups that are determined by the degree of either interstitial inflammation or fibrosis. Group 1 is primarily inflammation, group 2 involves inflammation and fibrosis, and group 3 is primarily fibrosis. The differences in groups are most clearly seen looking at the extremes—group 1 shows the puffy alveolar septa infiltrated with lymphocytes (left panel, figure 4.8), whereas group 3 shows a matrix of fibrosis that can be distinguished from usual interstitial pneumonia by the absence of fibroblastic foci and a homogenous onset and distribution (right panel, figure 4.8). As its name suggests, the distinguishing feature of nonspecific interstitial pneumonia is the lack of features that determine it to be something else. If that sounds a bit wishy-washy, take solace in the fact that even experts argue over its classification.",True,Nonspecific Interstitial Pneumonia,Figure 4.8,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.8.png,Figure 4.8: Extremes of nonspecific interstitial pneumonia.
6795f0eb-fe27-4be3-bf73-2976caea075e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Our next disease is at least courteous enough to only have one name, nonspecific interstitial pneumonia (NSIP), but irritatingly, it has three groups that are determined by the degree of either interstitial inflammation or fibrosis. Group 1 is primarily inflammation, group 2 involves inflammation and fibrosis, and group 3 is primarily fibrosis. The differences in groups are most clearly seen looking at the extremes—group 1 shows the puffy alveolar septa infiltrated with lymphocytes (left panel, figure 4.8), whereas group 3 shows a matrix of fibrosis that can be distinguished from usual interstitial pneumonia by the absence of fibroblastic foci and a homogenous onset and distribution (right panel, figure 4.8). As its name suggests, the distinguishing feature of nonspecific interstitial pneumonia is the lack of features that determine it to be something else. If that sounds a bit wishy-washy, take solace in the fact that even experts argue over its classification.",True,Nonspecific Interstitial Pneumonia,Figure 4.8,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.8.png,Figure 4.8: Extremes of nonspecific interstitial pneumonia.
6795f0eb-fe27-4be3-bf73-2976caea075e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Our next disease is at least courteous enough to only have one name, nonspecific interstitial pneumonia (NSIP), but irritatingly, it has three groups that are determined by the degree of either interstitial inflammation or fibrosis. Group 1 is primarily inflammation, group 2 involves inflammation and fibrosis, and group 3 is primarily fibrosis. The differences in groups are most clearly seen looking at the extremes—group 1 shows the puffy alveolar septa infiltrated with lymphocytes (left panel, figure 4.8), whereas group 3 shows a matrix of fibrosis that can be distinguished from usual interstitial pneumonia by the absence of fibroblastic foci and a homogenous onset and distribution (right panel, figure 4.8). As its name suggests, the distinguishing feature of nonspecific interstitial pneumonia is the lack of features that determine it to be something else. If that sounds a bit wishy-washy, take solace in the fact that even experts argue over its classification.",True,Nonspecific Interstitial Pneumonia,Figure 4.8,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.8.png,Figure 4.8: Extremes of nonspecific interstitial pneumonia.
cf1f83d5-b121-4c02-ae67-16098dcc5b44,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The presence of lymphocytes in biopsy and bronchoalveolar lavage fluid suggests the involvement of the immune system in the pathogenesis of nonspecific interstitial pneumonia. This is supported by the occurrence of NSIP in immune diseases such as HIV infection and several connective tissue disorders including polymyositis, rheumatoid arthritis, and systemic sclerosis. Our understanding of the pathological mechanisms is still evolving.",True,Nonspecific Interstitial Pneumonia,,,,
886264db-feee-451d-b487-7710bad40a0c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Cryptogenic Organizing Pneumonia,False,Cryptogenic Organizing Pneumonia,,,,
77e2d4c2-ac28-41fe-91ad-32343acbf4b4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Our final major classification is cryptogenic organizing pneumonia (COP). This form of interstitial disease affects the distal bronchioles, respiratory bronchioles, and alveoli, but the primary site of injury is usually the alveolar walls.",True,Cryptogenic Organizing Pneumonia,,,,
3a41dcc6-2d77-4e85-ab4e-614deff6414d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The hallmark of COP is an excessive proliferation of granulation tissue made of collagen-embedded fibroblasts and myofibroblasts that starts in the alveolar space. These plugs of fibrotic tissue may extend from one alveolus to another via the pores of Kohn and give rise to a characteristic butterfly pattern. The pathogenesis is an initial alveolar injury, with plasma proteins leaking into the alveolar lumen that is followed by recruited fibroblasts depositing connective tissue with the lumen itself. These fibrotic lesions show a homogenous time line and movement to the distal airways, but are actually reversible, which is in contrast of the lesions seen in usual interstitial pneumonia. In COP the lung architecture is maintained, probably through more thorough regulation of angiogenesis and apoptosis than that seen in usual interstitial pneumonia (UIP).",True,Cryptogenic Organizing Pneumonia,,,,
d7b09b2f-b5f6-4a55-986f-3d5a24fb2cc6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The onset of COP is marked with dyspnea and dry cough (as with most ILDs), and it has a moderate time line of a couple of months, after which symptoms subside. History is again important to determine the initial insult, and potential culprits include connective tissue disease, new medications, or exposure to therapeutic radiation, fumes, or dusts.",True,Cryptogenic Organizing Pneumonia,,,,
d097ed23-aba0-446f-85c4-674e8da9e456,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Environment-Induced ILDs,False,Environment-Induced ILDs,,,,
7f624963-8d39-42f3-9bef-515c283b6293,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Now we will look at several specific forms of interstitial disease that are related to occupational exposure. While these forms of ILD have some distinguishing factors, the importance of taking a good history cannot be understated.",True,Environment-Induced ILDs,,,,
ac0186a1-fdcd-48e1-ba82-651c77925233,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Silicosis,False,Silicosis,,,,
4600a659-1918-44bb-b7eb-a43416a6af20,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Silicosis is related to exposure to silica that occurs frequently in occupations such as stone cutting, foundry work, and mining. Cutting or breaking stone can produce crystalline silica, and when less than 5 microns in diameter, it becomes respirable. When particle size is between 1 and 3 microns, it can reach the alveoli.",True,Silicosis,,,,
754e6def-2b5f-4a78-9a7b-55496aeaf102,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The formation of silicosis can be acute with heavy brief exposure (often seen in sandblasters), or chronic and insidious with more prolonged lighter exposures. The process is initiated with alveolar macrophages engulfing the crystals. In response they release cytokines to attract lymphocytes, neutrophils, and fibroblasts—and a familiar story of tissue destruction and laying down of collagen begins. (You might note at this point that engulfing silica in vitro has been shown to damage macrophages, causing them to release their intracellular enzymes, which may contribute to the destructive mechanism in vivo.)",True,Silicosis,,,,
2b14f638-9e4b-4095-8aa0-edff4db87fa2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The pattern of collagen deposition is distinct, with silicotic nodules forming with concentric fibers producing a whirled pattern (figure 4.10). These nodules are distributed throughout the lung but are more common in the upper lobes and perihilar area (figure 4.11). They tend to be surrounded by distorted lung tissue that may show emphysematous changes. Ongoing disease coalescence of the nodules produces irregular masses of noncaseating granulomas. This progressive massive fibrosis can be helped with concurrent TB or atypical mycobacterial disease where caseating granulomas may also be present. Likewise silicosis may impair the macrophage response to TB. It causes contraction of the upper lobes and may lead to emphysema in the lower lobes, sometimes with large bullous changes. The pathophysiology of silicosis is summarized in figure 4.12.",True,Silicosis,Figure 4.10,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.10.jpeg,Figure 4.10: Silicotic nodule in the parenchyma of the lung.
2b14f638-9e4b-4095-8aa0-edff4db87fa2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The pattern of collagen deposition is distinct, with silicotic nodules forming with concentric fibers producing a whirled pattern (figure 4.10). These nodules are distributed throughout the lung but are more common in the upper lobes and perihilar area (figure 4.11). They tend to be surrounded by distorted lung tissue that may show emphysematous changes. Ongoing disease coalescence of the nodules produces irregular masses of noncaseating granulomas. This progressive massive fibrosis can be helped with concurrent TB or atypical mycobacterial disease where caseating granulomas may also be present. Likewise silicosis may impair the macrophage response to TB. It causes contraction of the upper lobes and may lead to emphysema in the lower lobes, sometimes with large bullous changes. The pathophysiology of silicosis is summarized in figure 4.12.",True,Silicosis,Figure 4.10,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.10.jpeg,Figure 4.10: Silicotic nodule in the parenchyma of the lung.
2b14f638-9e4b-4095-8aa0-edff4db87fa2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The pattern of collagen deposition is distinct, with silicotic nodules forming with concentric fibers producing a whirled pattern (figure 4.10). These nodules are distributed throughout the lung but are more common in the upper lobes and perihilar area (figure 4.11). They tend to be surrounded by distorted lung tissue that may show emphysematous changes. Ongoing disease coalescence of the nodules produces irregular masses of noncaseating granulomas. This progressive massive fibrosis can be helped with concurrent TB or atypical mycobacterial disease where caseating granulomas may also be present. Likewise silicosis may impair the macrophage response to TB. It causes contraction of the upper lobes and may lead to emphysema in the lower lobes, sometimes with large bullous changes. The pathophysiology of silicosis is summarized in figure 4.12.",True,Silicosis,Figure 4.10,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.10.jpeg,Figure 4.10: Silicotic nodule in the parenchyma of the lung.
1bf14a9f-1b74-4088-80bb-56e5eb74fc7f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"After an insidious, asymptomatic beginning, the main symptom of silicosis is dyspnea, with or without cough (cough is likely generated by concurrent smoking). The dyspnea is progressive but other symptoms that occur are often due to secondary, superimposed infection making repeated bacteriological studies important.",True,Silicosis,,,,
a51fc1c1-e61c-460f-a2a3-f5779989cf3b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,The pathophysiology of silicosis is summarized in figure 4.12.,True,Silicosis,Figure 4.12,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.12.png,Figure 4.12: The pathophysiology of silicosis.
a51fc1c1-e61c-460f-a2a3-f5779989cf3b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,The pathophysiology of silicosis is summarized in figure 4.12.,True,Silicosis,Figure 4.12,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.12.png,Figure 4.12: The pathophysiology of silicosis.
a51fc1c1-e61c-460f-a2a3-f5779989cf3b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,The pathophysiology of silicosis is summarized in figure 4.12.,True,Silicosis,Figure 4.12,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.12.png,Figure 4.12: The pathophysiology of silicosis.
22149512-6bd8-4cfa-a4b3-d0f2a64b8e37,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Asbestosis,False,Asbestosis,,,,
bbdbefe8-3ae0-4de0-aa3a-a0cabfa44df7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"There are a number of pulmonary manifestations arising from exposure to asbestos. Previously used in the construction and manufacturing industries, the occurrence of related illness led to legislation to restrict its use. However, demolition or renovation of asbestos-containing buildings can still lead to air-born asbestos exposure. The pulmonary manifestations include pulmonary fibrosis, bronchogenic carcinoma, pleural effusion, pleural fibrosis, and mesothelioma. We will deal with the pulmonary fibrosis here and what is known as asbestosis.",True,Asbestosis,,,,
1444487e-27f2-4fcd-b15f-dfa7abfab1b4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The disease course (summarized in figure 4.13) is similar to that described for silicosis. Asbestos fibers arrive in the alveoli and macrophages initiate an inflammatory response. Note that the arrival of neutrophilic leukocytes and their release of cytokines and oxygen radicals seem to play a significant role. Short fibers can be phagocytized and removed, but larger fibers persist in the airway and perpetuate the inflammatory reaction, promoting fibrosis.",True,Asbestosis,Figure 4.13,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.13.png,Figure 4.13: Pathophysiology of asbestosis.
1444487e-27f2-4fcd-b15f-dfa7abfab1b4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The disease course (summarized in figure 4.13) is similar to that described for silicosis. Asbestos fibers arrive in the alveoli and macrophages initiate an inflammatory response. Note that the arrival of neutrophilic leukocytes and their release of cytokines and oxygen radicals seem to play a significant role. Short fibers can be phagocytized and removed, but larger fibers persist in the airway and perpetuate the inflammatory reaction, promoting fibrosis.",True,Asbestosis,Figure 4.13,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.13.png,Figure 4.13: Pathophysiology of asbestosis.
1444487e-27f2-4fcd-b15f-dfa7abfab1b4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The disease course (summarized in figure 4.13) is similar to that described for silicosis. Asbestos fibers arrive in the alveoli and macrophages initiate an inflammatory response. Note that the arrival of neutrophilic leukocytes and their release of cytokines and oxygen radicals seem to play a significant role. Short fibers can be phagocytized and removed, but larger fibers persist in the airway and perpetuate the inflammatory reaction, promoting fibrosis.",True,Asbestosis,Figure 4.13,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.13.png,Figure 4.13: Pathophysiology of asbestosis.
13c6fabc-f8e9-49cc-8c3a-9e948c4c7350,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Histologically, these fibers can been seen as asbestos bodies, or ferruginous bodies, as they are coated with iron-containing protein (figure 4.14).",True,Asbestosis,Figure 4.14,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.14-scaled.jpg,Figure 4.14: Ferruginous bodies associated with asbestosis.
13c6fabc-f8e9-49cc-8c3a-9e948c4c7350,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Histologically, these fibers can been seen as asbestos bodies, or ferruginous bodies, as they are coated with iron-containing protein (figure 4.14).",True,Asbestosis,Figure 4.14,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.14-scaled.jpg,Figure 4.14: Ferruginous bodies associated with asbestosis.
13c6fabc-f8e9-49cc-8c3a-9e948c4c7350,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Histologically, these fibers can been seen as asbestos bodies, or ferruginous bodies, as they are coated with iron-containing protein (figure 4.14).",True,Asbestosis,Figure 4.14,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.14-scaled.jpg,Figure 4.14: Ferruginous bodies associated with asbestosis.
ffd316fa-f283-4d3d-a327-4a73424b47ac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Fibrosis ensues, but in contrast to silicosis, asbestos-related fibrosis is nonnodular and mostly involves the lower lung fields and frequently includes pleural thickening.",True,Asbestosis,,,,
25c6883f-a686-4c12-be6a-d94332a4edaf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The extent of fibrosis is highly variable, from thickened alveolar septum to complete destruction of the alveolar spaces. In the advanced disease honeycomb lung can be observed with CT. Radiography of later-stage disease shows reticular interstitial markings in the lower lung fields (left panel, figure 4.15). Pleural changes are also more common. Rounded atelectasis may occur after a pleural effusion has been reabsorbed and caused a section of the airway to become trapped. A rounded atelectasis is indicated by the arrow in figure 4.15, and care should be taken not to mistake this for a neoplasm. Abestosis is a risk factor for the development of mesothelioma and should be considered for patients working in “at-risk” environments or occupations.",True,Asbestosis,Figure 4.15,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.15.jpeg,Figure 4.15: Radiographic findings in asbestosis.
25c6883f-a686-4c12-be6a-d94332a4edaf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The extent of fibrosis is highly variable, from thickened alveolar septum to complete destruction of the alveolar spaces. In the advanced disease honeycomb lung can be observed with CT. Radiography of later-stage disease shows reticular interstitial markings in the lower lung fields (left panel, figure 4.15). Pleural changes are also more common. Rounded atelectasis may occur after a pleural effusion has been reabsorbed and caused a section of the airway to become trapped. A rounded atelectasis is indicated by the arrow in figure 4.15, and care should be taken not to mistake this for a neoplasm. Abestosis is a risk factor for the development of mesothelioma and should be considered for patients working in “at-risk” environments or occupations.",True,Asbestosis,Figure 4.15,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.15.jpeg,Figure 4.15: Radiographic findings in asbestosis.
25c6883f-a686-4c12-be6a-d94332a4edaf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The extent of fibrosis is highly variable, from thickened alveolar septum to complete destruction of the alveolar spaces. In the advanced disease honeycomb lung can be observed with CT. Radiography of later-stage disease shows reticular interstitial markings in the lower lung fields (left panel, figure 4.15). Pleural changes are also more common. Rounded atelectasis may occur after a pleural effusion has been reabsorbed and caused a section of the airway to become trapped. A rounded atelectasis is indicated by the arrow in figure 4.15, and care should be taken not to mistake this for a neoplasm. Abestosis is a risk factor for the development of mesothelioma and should be considered for patients working in “at-risk” environments or occupations.",True,Asbestosis,Figure 4.15,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.15.jpeg,Figure 4.15: Radiographic findings in asbestosis.
af9d1cc8-8e45-44c9-8458-4f2291f40efd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Coal worker’s pneumoconiosis (CWP),False,Coal worker’s pneumoconiosis (CWP),,,,
c7b025bf-6811-43f3-9a11-61a6aea32427,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"CWP arises after prolonged exposure to coal dust. While drilling through rock the miner may be susceptible to silicosis, but prolonged and heavy exposure to aerosolized carbon (that is not usually fibrogenic in lesser exposures) can result in its own distinct condition. Even then it can take ten to twelve years of underground exposure to develop.",True,Coal worker’s pneumoconiosis (CWP),,,,
740c464e-8deb-434b-a019-3343e9fd9bdf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Again we see the process start with phagocytosis of the coal dust by macrophages after the mucocillary escalator is overwhelmed. The macrophages launch their inflammatory process, and tissue damage is caused by the resultant cytokine bloom and oxygen radical and enzyme release. Fibroblasts form reticulin networks, but there is no significant collagen deposition. Aggregates of reticulin fibers, macrophages, and dust form coal macules (figure 4.16). The coal macules appear as black spots in lung sections and give rise to the condition’s nickname of “black lung.”",True,Coal worker’s pneumoconiosis (CWP),Figure 4.16,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.16.jpeg,Figure 4.16: Example of coal macules in simple CWP showing fibrosis and coal macules.
740c464e-8deb-434b-a019-3343e9fd9bdf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Again we see the process start with phagocytosis of the coal dust by macrophages after the mucocillary escalator is overwhelmed. The macrophages launch their inflammatory process, and tissue damage is caused by the resultant cytokine bloom and oxygen radical and enzyme release. Fibroblasts form reticulin networks, but there is no significant collagen deposition. Aggregates of reticulin fibers, macrophages, and dust form coal macules (figure 4.16). The coal macules appear as black spots in lung sections and give rise to the condition’s nickname of “black lung.”",True,Coal worker’s pneumoconiosis (CWP),Figure 4.16,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.16.jpeg,Figure 4.16: Example of coal macules in simple CWP showing fibrosis and coal macules.
740c464e-8deb-434b-a019-3343e9fd9bdf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Again we see the process start with phagocytosis of the coal dust by macrophages after the mucocillary escalator is overwhelmed. The macrophages launch their inflammatory process, and tissue damage is caused by the resultant cytokine bloom and oxygen radical and enzyme release. Fibroblasts form reticulin networks, but there is no significant collagen deposition. Aggregates of reticulin fibers, macrophages, and dust form coal macules (figure 4.16). The coal macules appear as black spots in lung sections and give rise to the condition’s nickname of “black lung.”",True,Coal worker’s pneumoconiosis (CWP),Figure 4.16,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.16.jpeg,Figure 4.16: Example of coal macules in simple CWP showing fibrosis and coal macules.
769bd611-fd0a-4e7d-a485-b5c986bf0ebb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The coal macules are associated with dilation of the respiratory bronchioles that can manifest as focal centrilobar emphysema (figure 4.16). This is referred to as simple CWP, whereas the less common, complicated form involves progressive massive fibrosis, usually in the upper lobes, as in silicosis. However, in CWP these lesions are black and relatively homogenous, where as in silicosis they are a conglomeration of intersecting nodules. Figure 4.17 shows a large black fibrotic lesion destroying the perihilar lung parenchyma.",True,Coal worker’s pneumoconiosis (CWP),Figure 4.17,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.17.jpeg,Figure 4.17: Large perihilar lesion in complicated CWP.
769bd611-fd0a-4e7d-a485-b5c986bf0ebb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The coal macules are associated with dilation of the respiratory bronchioles that can manifest as focal centrilobar emphysema (figure 4.16). This is referred to as simple CWP, whereas the less common, complicated form involves progressive massive fibrosis, usually in the upper lobes, as in silicosis. However, in CWP these lesions are black and relatively homogenous, where as in silicosis they are a conglomeration of intersecting nodules. Figure 4.17 shows a large black fibrotic lesion destroying the perihilar lung parenchyma.",True,Coal worker’s pneumoconiosis (CWP),Figure 4.17,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.17.jpeg,Figure 4.17: Large perihilar lesion in complicated CWP.
769bd611-fd0a-4e7d-a485-b5c986bf0ebb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The coal macules are associated with dilation of the respiratory bronchioles that can manifest as focal centrilobar emphysema (figure 4.16). This is referred to as simple CWP, whereas the less common, complicated form involves progressive massive fibrosis, usually in the upper lobes, as in silicosis. However, in CWP these lesions are black and relatively homogenous, where as in silicosis they are a conglomeration of intersecting nodules. Figure 4.17 shows a large black fibrotic lesion destroying the perihilar lung parenchyma.",True,Coal worker’s pneumoconiosis (CWP),Figure 4.17,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.17.jpeg,Figure 4.17: Large perihilar lesion in complicated CWP.
8af560b4-a4e3-4ddf-9788-85c873d8514e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Clinical manifestations are often complicated by concurrent cigarette smoking that may alone explain the frequency of chronic bronchitis in CWP patients. The simple form can be asymptomatic, but the complicated form produces dyspnea and signs of respiratory failures, pulmonary hypertension, and cor pulmonale.",True,Coal worker’s pneumoconiosis (CWP),,,,
abd8d54e-ce31-4fc2-a7a8-563694da0b75,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Berylliosis,False,Berylliosis,,,,
2aa90f18-6ef1-4b4d-b700-b9cfbbebf021,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"The last occupational disorder we will look at is berylliosis, or chronic beryllium disease (CBD), that occurs after exposure to beryllium, a metal used in manufacturing. Here the start to our story is a little different. Beryllium arrives in the airway and there is a hypersensitization of T cells. On subsequent exposures the T cells proliferate—the bronchoalveolar lavage (BAL) fluid of berylliosis patients is rich in sensitized CD4+ cells.",True,Berylliosis,,,,
5af7dfe9-f54b-45db-9ac2-01dcc5e997dc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Now we return to our pattern: the abundant CD4+ cells release proinflammatory cytokines and granulomatous fibrosis occurs (figure 4.18). The granulomas (figure 4.19) are indistinguishable from those caused by sarcoidosis (which are also caused by CD4+ cells), and many CBD patients may be misdiagnosed as sarcoidosis cases, so appropriate history taking is paramount. Usually CBD involves greater interstitial inflammation, but the most definitive diagnosis comes from the beryllium lymphocyte proliferation test. The test involves exposing lymphocytes from the patient’s blood or BAL fluid to different concentrations of beryllium and assaying their proliferation.",True,Berylliosis,Figure 4.18,Forms of Interstitial Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.18.png,Figure 4.18: Pathophysiology of berylliosis.
5af7dfe9-f54b-45db-9ac2-01dcc5e997dc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Now we return to our pattern: the abundant CD4+ cells release proinflammatory cytokines and granulomatous fibrosis occurs (figure 4.18). The granulomas (figure 4.19) are indistinguishable from those caused by sarcoidosis (which are also caused by CD4+ cells), and many CBD patients may be misdiagnosed as sarcoidosis cases, so appropriate history taking is paramount. Usually CBD involves greater interstitial inflammation, but the most definitive diagnosis comes from the beryllium lymphocyte proliferation test. The test involves exposing lymphocytes from the patient’s blood or BAL fluid to different concentrations of beryllium and assaying their proliferation.",True,Berylliosis,Figure 4.18,Basis of Restrictive Lung Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.18.png,Figure 4.18: Pathophysiology of berylliosis.
5af7dfe9-f54b-45db-9ac2-01dcc5e997dc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Now we return to our pattern: the abundant CD4+ cells release proinflammatory cytokines and granulomatous fibrosis occurs (figure 4.18). The granulomas (figure 4.19) are indistinguishable from those caused by sarcoidosis (which are also caused by CD4+ cells), and many CBD patients may be misdiagnosed as sarcoidosis cases, so appropriate history taking is paramount. Usually CBD involves greater interstitial inflammation, but the most definitive diagnosis comes from the beryllium lymphocyte proliferation test. The test involves exposing lymphocytes from the patient’s blood or BAL fluid to different concentrations of beryllium and assaying their proliferation.",True,Berylliosis,Figure 4.18,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.18.png,Figure 4.18: Pathophysiology of berylliosis.
8d7110b2-14c8-4d10-aa24-7933720e2ca8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Susceptibility to becoming hypersensitized appears to have a significant genetic component. Why the process continues after exposure has stopped is unclear, but possibilities include a fundamental T cell disorder, or the fact that the insoluble beryllium causes apoptosis of macrophages, leading them to release a previously phagocytized beryllium load.",True,Berylliosis,,,,
88916f17-83c8-45d5-8093-6face88dd809,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"As the disease progresses, radiographic findings show that the granuoles can become more organized to produce fibrous nodules that may begin to impact lung function. The immune system involvement can produce hilar lymphadenopathy, and common later signs include interstital fibrosis and pleural thickening.",True,Berylliosis,,,,
bf551e28-c545-49c0-acdb-d2bf33166d9e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Summary,False,Summary,,,,
14765492-a7f6-4ca6-8343-517133e9765c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"So there is a selection of interstitial lung diseases that, while sharing the pathophysiological manifestations of restrictive lung disease, can be distinguished through good history taking or identifying distinct histological features.",True,Summary,,,,
d5a025a1-12d3-47f6-9c18-4115675e5fc5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"References, Resources, and Further Reading",False,"References, Resources, and Further Reading",,,,
63bb18c7-24da-4a89-a07f-3176abf2d806,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,Text,False,Text,,,,
53439acb-6ba1-4685-8076-6d74cbf320cd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapters 12–15.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
3ef58e99-051b-4e85-a9b2-70fef7654ac9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,4. The Restrictive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/the-restrictive-lung-diseases/,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
507964a7-1d6e-4de0-8c65-12ad6bac428d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,Acute Bronchitis,False,Acute Bronchitis,,,,
e61c8ba1-f3e6-4190-862a-754314aecd49,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
e61c8ba1-f3e6-4190-862a-754314aecd49,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
e61c8ba1-f3e6-4190-862a-754314aecd49,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
e61c8ba1-f3e6-4190-862a-754314aecd49,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
21f621b2-758a-44b4-b393-a22b8bf3f997,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"First the bronchial mucus membranes become inflamed. Taking a careful history can help you distinguish infectious causes from other instigators of airway inflammation, such as physical or chemical insults or an allergic response. The inflammation will initially produce a dry cough, but within two to three days bronchial secretions will be established, the cough will become productive, and rales can be heard over the site of the infection, which constitutes the clinical diagnosis.",True,Acute Bronchitis,,,,
6038d957-953a-4829-b401-c34b0d6d4459,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
6038d957-953a-4829-b401-c34b0d6d4459,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
6038d957-953a-4829-b401-c34b0d6d4459,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
6038d957-953a-4829-b401-c34b0d6d4459,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
7830c754-3d28-4507-8175-340511b09acb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,Infectious Bronchiolitis,False,Infectious Bronchiolitis,,,,
1de3847d-9228-4391-8a1e-61fb82d789a5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Penetrating deeper into the airway a pathogen can cause acute infectious bronchiolitis. By far the most common culprit is respiratory syncytial virus (RSV). This is the most common cause of lower airway infection in children under one year old and is estimated to cause more infant deaths than any other pathogen with the exception of malaria. While it can affect adults, it usually occurs only in the elderly and immunosuppressed patients.",True,Infectious Bronchiolitis,,,,
97215dbd-07f2-492e-a63c-bbcefb6af430,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
97215dbd-07f2-492e-a63c-bbcefb6af430,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
97215dbd-07f2-492e-a63c-bbcefb6af430,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
97215dbd-07f2-492e-a63c-bbcefb6af430,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
bd8e5ef5-b7b4-44f2-a158-2026b0e84aba,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"The young patient will likely present with a recent history of cough and hallmarks of shortness of breath such as use of accessory muscles. A scattered wheeze is likely, and in severe cases the child develops an expiratory grunt.",True,Infectious Bronchiolitis,,,,
ee55f954-65e9-4b0a-b623-926f13541b01,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Unresolved the RSV can spread to type 1 and 2 pneumocytes through cell-to-cell transmission. There is a high incidence of apnea associated with RSV infection, presumably due to the virus activating defensive reflexes associated with the larynx.",True,Infectious Bronchiolitis,,,,
8d5ab566-67bb-4e46-99dc-70c169ed78d2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,Pneumonia,False,Pneumonia,,,,
fba594d9-9875-4ed1-bfdf-0b867f9bafbe,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Now we will look at the consequences of infection of the terminal airways and what is referred to as pneumonia. Although pneumonia can result from infection by one of any number of pathogens, we will first look at a generalized pathophysiological mechanism.",True,Pneumonia,,,,
ecb4cda9-73d9-465b-a415-9e0b6f0a0216,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
ecb4cda9-73d9-465b-a415-9e0b6f0a0216,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
ecb4cda9-73d9-465b-a415-9e0b6f0a0216,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
ecb4cda9-73d9-465b-a415-9e0b6f0a0216,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
86998207-255c-4311-928a-b83dfc103fff,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"The infection may not be retained by the airway structure and can penetrate the pleural space, in which case an effusion is likely.",True,Pneumonia,,,,
505daa00-9d90-4d25-8a91-46ff01fb9606,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"The pneumonia-causing pathogen can often be found in blood analysis but the patient remains asymptomatic, but if the infection becomes more established significant signs and symptoms of bacteremia arise.",True,Pneumonia,,,,
ac6216e8-fbc9-4370-bd3e-fa476d4658c9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
ac6216e8-fbc9-4370-bd3e-fa476d4658c9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
ac6216e8-fbc9-4370-bd3e-fa476d4658c9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
ac6216e8-fbc9-4370-bd3e-fa476d4658c9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
e97cf051-8598-45bd-b0aa-4a62ae4c5e56,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,Classification of Pneumonia,False,Classification of Pneumonia,,,,
95934a74-2855-452b-a2a3-432867c22907,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"The causes of pneumonia are many, but so are the ways in which they are classified. Pneumonias are distinguished by:",True,Classification of Pneumonia,,,,
438437fe-a071-4091-80c8-08aa789c5d34,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Typical or atypical pneumonia: We can start at arguably the least clinically helpful classification, the microscopic location. Pneumonias can be either typical or atypical. Typical pneumonium involves the presence of pathogens and immune cells in the airspace, whereas atypical has the pathogen and inflammatory response within the alveolar walls and interstitium (table 3.1). The site is usually dictated by the mode of the pathogen, with typical pneumonia being bacterial and atypical being caused by virus or mycobacterium that are capable of entering cells.",True,Classification of Pneumonia,,,,
7477bdfc-7b61-4dd0-8ac9-02a4d17ba85a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"The two forms can have different signs and symptoms with typical pneumonia having a more rapid onset and atypical being more gradual. Both can be associated with fever, but extrapulmonary features such as headache, joint and muscle pain, and nausea are more characteristic of atypical pneumonia. Because of the location of the pathogen; typical pneumonia is associated with a productive cough, whereas the cough of atypical pneumonia is dry, as summarized in table 3.1.",True,Classification of Pneumonia,,,,
713d6958-5764-43d4-a923-64346f755f53,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"On x-ray the atypical pneumonia shows more diffuse patchy markings associated with the infiltrated interstitium, whereas an x-ray of typical pneumonia shows lobar opacities caused by consolidated airspaces (table 3.1).",True,Classification of Pneumonia,,,,
5a6ebf85-4f36-4a26-a717-15cc3f95e5f6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,Table 3.1: Comparison of typical and atypical pneumonia.,True,Classification of Pneumonia,,,,
0f23faf8-323b-4cd4-a086-1dd7be010e57,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Bronchopneumonia or lobar pneumonia: The next classification is based on the infection’s gross location—whether it occurs in a bronchiolocentric pattern to produce bronchopneumonia, or whether the consolidation occurs in continuous airspaces to occupy a lobe to produce lobar pneumonia. Bronchopneumonia will produce distinct areas of infiltrate, and the chest x-ray will reflect this with opacities following the effected airways (table 3.2). Lobar pneumonia will involve dense consolidation outlining the whole lobe and the possibility of air brochograms as air-filled bronchi are surrounded by the infiltrated, more dense alveoli (table 3.2). Bronchopneumonia is usually bilateral, whereas lobar pneumonia tends to be unilateral. However, both can exist in the same patient, as is the case in the example x-ray in table 3.2.",True,Classification of Pneumonia,,,,
294ad406-c7b4-453e-bd20-61bb68dc8f51,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,Table 3.2: Comparison of bronchopneumonia and lobar pneumonia.,True,Classification of Pneumonia,,,,
f58ce162-f3dc-48b1-b302-4c9c8ca5e5f4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Hospital-acquired or community-acquired pneumonia: The last classification relates to the setting in which the infection was acquired, either out in the community or during hospitalization. This classification can provide clues to identifying the pathogen involved. By far the most common cause of community-acquired pneumonia is Streptococcus pneumoniae. Other pathogens can be responsible but tend to affect only those with an underlying condition or characteristic; they are listed in table 3.3 with the usual instigating issue in parentheses. Legionella-related pneumonia requires exposure to laced water droplets, and mycoplasma infection tends to affect young adults living in close quarters, such as military barracks or college dorms. Lastly, and more uncommonly, the pneumonia may be caused by a viral infection.",True,Classification of Pneumonia,,,,
cccfb2b1-fc1f-4bcd-a743-378ffee040c7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Hospital-acquired pneumonia is defined as occurring at least three days after hospitalization. Unlike community-acquired pneumonias the pathogen is frequently a gram-negative bacteria or staphylococci that normally would not be able to become established in the lung. However, the hospitalized patient’s weakened state of health, state of consciousness, exposure to poor sterile technique for intubation, or antibiotic therapy can provide these listed pathogens an opportunity (table 3.3).",True,Classification of Pneumonia,,,,
0eee94c8-8250-407c-8983-8b44a16ee7c7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,Table 3.3: Comparison of community- and hospital-acquired pneumonias.,True,Classification of Pneumonia,,,,
83b3ceb3-e457-48ce-ba75-7d3d5192c12b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,Clinical Findings of Pneumonia,False,Clinical Findings of Pneumonia,,,,
44ac7006-eea1-4c80-bcbc-e9f4d17676a1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"The clinical findings depend on the severity of the infection and underlying cause. Onset can be abrupt or gradual, and is often preceded by upper airway symptoms and associated with malaise, fever, or chills. As the infection progresses cough is established and chest pain and dyspnea can develop.",True,Clinical Findings of Pneumonia,,,,
d866b20e-d26c-4af9-8875-a2252d6ed55e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,As the infection progresses expectoration increases and can be purulent or even blood tinged. Mental confusion can arise particularly in elderly or alcoholic patients. If there is multiple lobe involvement then dyspnea can become severe and cyanosis may arise as intrapulmonary shunts become established and more significant. The hypoxemia can be accompanied by hypocapnia as the patient hyperventilates due to the hypoxic drive to breathe.,True,Clinical Findings of Pneumonia,,,,
716a2dfa-d8d8-4d23-9414-09f8dc804adf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,Chest exams can have variable findings but may include poor respiratory excursion. The consolidated lung fields result in dullness to percussion and a reduction in breath sounds and increase in tactile fremitus. Inspiratory crackles may be heard. With continued progression arterial hypoxia worsens and arterial CO2 falls due to hyperventilation.,True,Clinical Findings of Pneumonia,,,,
c3db54b1-55df-4ecf-ada2-dbb18f992feb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Chest x-ray allows the areas of consolidation to be seen, but typically there is no volume loss, which allows pneumonia to be distinguished from atelectasis (although pneumonia and atelectasis can co-occur). Particularly in the case of a typical pneumonia the complete blood count (CBC) panel will show an elevated white blood cell count. See table 3.4 for summary.",True,Clinical Findings of Pneumonia,,,,
426b3711-f442-4cbd-befa-21ac65108c0c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,Table 3.4: Summary of the clinical findings of pneumonia.,True,Clinical Findings of Pneumonia,,,,
3ca33f96-1120-4b54-a7fc-8358271c0d09,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,Text,False,Text,,,,
643821d1-ed82-48c7-93e1-ebc504ed1987,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 3.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
5b82ef18-50e8-4834-8732-0e514bf449af,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
85c596d0-c0f5-467f-b2ce-39e772dc507b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Table 3.1: Comparison of typical and atypical pneumonia. Includes Case 1 by Bell, D., Hacking, C., et al. from https://doi.org/10.53347/rID-68496 (CC BY-NC-SA 3.0), Acute pneumonia – i — low mag by Nephron from WikimediaCommons (CC BY-SA 3.0), Case 2 by Paks, M., Knipe, H., et al. from https://doi.org/10.53347/rID-27535 (CC BY-NC-SA 3.0), and image 1 by Dr Patsy Lill from University of South Carolina School of Medicine’s Microbiologybook.org (Fair use).",True,Text,,,,
b3d33b15-a961-4fcf-90af-d04139c33ca5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pneumonia,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-3,"Table 3.2: Comparison of bronchopneumonia and lobar pneumonia. Includes Bronchopneumonia by Kindred Grey from Internet archive (CC BY 4.0), Lobar pneumonia by Kindred Grey from Internet archive (CC BY 4.0), X-ray of bronchopneumonia by Franquet T., Chung J.H. from WikimediaCommons (CC BY 4.0), Case 3 by Paks, M., Knipe, H., et al. from https://doi.org/10.53347/rID-26886 (CC BY-NC-SA 3.0).",True,Text,,,,
5eb8a692-eff2-4c3b-ad3f-2277a98f101a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,Acute Bronchitis,False,Acute Bronchitis,,,,
ceec6382-be12-4e01-b731-7380f19f410a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
ceec6382-be12-4e01-b731-7380f19f410a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
ceec6382-be12-4e01-b731-7380f19f410a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
ceec6382-be12-4e01-b731-7380f19f410a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
0347437a-93aa-4843-9033-258f931cad97,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"First the bronchial mucus membranes become inflamed. Taking a careful history can help you distinguish infectious causes from other instigators of airway inflammation, such as physical or chemical insults or an allergic response. The inflammation will initially produce a dry cough, but within two to three days bronchial secretions will be established, the cough will become productive, and rales can be heard over the site of the infection, which constitutes the clinical diagnosis.",True,Acute Bronchitis,,,,
3b883493-300d-4b86-b0c9-e0b065aab4ea,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
3b883493-300d-4b86-b0c9-e0b065aab4ea,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
3b883493-300d-4b86-b0c9-e0b065aab4ea,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
3b883493-300d-4b86-b0c9-e0b065aab4ea,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
599758e7-cf3d-40eb-a20e-4d569705dfc2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,Infectious Bronchiolitis,False,Infectious Bronchiolitis,,,,
212146b6-5da0-4d6c-9f70-398e3c45e11c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Penetrating deeper into the airway a pathogen can cause acute infectious bronchiolitis. By far the most common culprit is respiratory syncytial virus (RSV). This is the most common cause of lower airway infection in children under one year old and is estimated to cause more infant deaths than any other pathogen with the exception of malaria. While it can affect adults, it usually occurs only in the elderly and immunosuppressed patients.",True,Infectious Bronchiolitis,,,,
69655e19-ad1b-4b58-9d95-30958e5e7553,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
69655e19-ad1b-4b58-9d95-30958e5e7553,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
69655e19-ad1b-4b58-9d95-30958e5e7553,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
69655e19-ad1b-4b58-9d95-30958e5e7553,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
d36ef1b5-e6f0-479d-ab69-a486857d2feb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"The young patient will likely present with a recent history of cough and hallmarks of shortness of breath such as use of accessory muscles. A scattered wheeze is likely, and in severe cases the child develops an expiratory grunt.",True,Infectious Bronchiolitis,,,,
bf836b0c-225e-4d88-9eff-beac33785e61,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Unresolved the RSV can spread to type 1 and 2 pneumocytes through cell-to-cell transmission. There is a high incidence of apnea associated with RSV infection, presumably due to the virus activating defensive reflexes associated with the larynx.",True,Infectious Bronchiolitis,,,,
6abf11c0-00be-439c-aadd-32184a73d9e7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,Pneumonia,False,Pneumonia,,,,
8e3cb9a7-4430-4ade-becd-26e23d9d1e04,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Now we will look at the consequences of infection of the terminal airways and what is referred to as pneumonia. Although pneumonia can result from infection by one of any number of pathogens, we will first look at a generalized pathophysiological mechanism.",True,Pneumonia,,,,
fecd7003-41ee-4948-8aba-fe1115ba5124,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
fecd7003-41ee-4948-8aba-fe1115ba5124,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
fecd7003-41ee-4948-8aba-fe1115ba5124,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
fecd7003-41ee-4948-8aba-fe1115ba5124,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
b49c5b3f-a9ec-4465-a274-673741d9da91,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"The infection may not be retained by the airway structure and can penetrate the pleural space, in which case an effusion is likely.",True,Pneumonia,,,,
a05ba775-2acf-49eb-8570-1256b14ec85b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"The pneumonia-causing pathogen can often be found in blood analysis but the patient remains asymptomatic, but if the infection becomes more established significant signs and symptoms of bacteremia arise.",True,Pneumonia,,,,
a922f603-097e-4f90-94d5-ef66414e807a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
a922f603-097e-4f90-94d5-ef66414e807a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
a922f603-097e-4f90-94d5-ef66414e807a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
a922f603-097e-4f90-94d5-ef66414e807a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
57670ecf-4fa6-4fec-b352-74e746f881cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,Classification of Pneumonia,False,Classification of Pneumonia,,,,
f92324fd-00c8-43a7-9f89-a684eff5dbdf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"The causes of pneumonia are many, but so are the ways in which they are classified. Pneumonias are distinguished by:",True,Classification of Pneumonia,,,,
ce3a29e9-991f-4a30-ad29-6d071e89e024,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Typical or atypical pneumonia: We can start at arguably the least clinically helpful classification, the microscopic location. Pneumonias can be either typical or atypical. Typical pneumonium involves the presence of pathogens and immune cells in the airspace, whereas atypical has the pathogen and inflammatory response within the alveolar walls and interstitium (table 3.1). The site is usually dictated by the mode of the pathogen, with typical pneumonia being bacterial and atypical being caused by virus or mycobacterium that are capable of entering cells.",True,Classification of Pneumonia,,,,
56cb5046-a357-4a3c-8848-13257622c6d8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"The two forms can have different signs and symptoms with typical pneumonia having a more rapid onset and atypical being more gradual. Both can be associated with fever, but extrapulmonary features such as headache, joint and muscle pain, and nausea are more characteristic of atypical pneumonia. Because of the location of the pathogen; typical pneumonia is associated with a productive cough, whereas the cough of atypical pneumonia is dry, as summarized in table 3.1.",True,Classification of Pneumonia,,,,
39d7df0e-6b9e-4012-966f-122d24749402,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"On x-ray the atypical pneumonia shows more diffuse patchy markings associated with the infiltrated interstitium, whereas an x-ray of typical pneumonia shows lobar opacities caused by consolidated airspaces (table 3.1).",True,Classification of Pneumonia,,,,
f017bdd0-61a9-4ac8-8aea-c35934242c0c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,Table 3.1: Comparison of typical and atypical pneumonia.,True,Classification of Pneumonia,,,,
1248cf26-0379-4989-9a26-ae86bb46dfdd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Bronchopneumonia or lobar pneumonia: The next classification is based on the infection’s gross location—whether it occurs in a bronchiolocentric pattern to produce bronchopneumonia, or whether the consolidation occurs in continuous airspaces to occupy a lobe to produce lobar pneumonia. Bronchopneumonia will produce distinct areas of infiltrate, and the chest x-ray will reflect this with opacities following the effected airways (table 3.2). Lobar pneumonia will involve dense consolidation outlining the whole lobe and the possibility of air brochograms as air-filled bronchi are surrounded by the infiltrated, more dense alveoli (table 3.2). Bronchopneumonia is usually bilateral, whereas lobar pneumonia tends to be unilateral. However, both can exist in the same patient, as is the case in the example x-ray in table 3.2.",True,Classification of Pneumonia,,,,
a1c60280-87ae-4d4c-9a88-04836fa53d4b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,Table 3.2: Comparison of bronchopneumonia and lobar pneumonia.,True,Classification of Pneumonia,,,,
ee636b61-fa7d-4356-a5a7-1868254dfa66,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Hospital-acquired or community-acquired pneumonia: The last classification relates to the setting in which the infection was acquired, either out in the community or during hospitalization. This classification can provide clues to identifying the pathogen involved. By far the most common cause of community-acquired pneumonia is Streptococcus pneumoniae. Other pathogens can be responsible but tend to affect only those with an underlying condition or characteristic; they are listed in table 3.3 with the usual instigating issue in parentheses. Legionella-related pneumonia requires exposure to laced water droplets, and mycoplasma infection tends to affect young adults living in close quarters, such as military barracks or college dorms. Lastly, and more uncommonly, the pneumonia may be caused by a viral infection.",True,Classification of Pneumonia,,,,
b5706476-f986-45cd-a7ea-137fb669b927,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Hospital-acquired pneumonia is defined as occurring at least three days after hospitalization. Unlike community-acquired pneumonias the pathogen is frequently a gram-negative bacteria or staphylococci that normally would not be able to become established in the lung. However, the hospitalized patient’s weakened state of health, state of consciousness, exposure to poor sterile technique for intubation, or antibiotic therapy can provide these listed pathogens an opportunity (table 3.3).",True,Classification of Pneumonia,,,,
ab83f3d9-b830-47d2-8ce8-cc6b33de1f70,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,Table 3.3: Comparison of community- and hospital-acquired pneumonias.,True,Classification of Pneumonia,,,,
88487560-eec4-4560-8cd2-be71413dbd9b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,Clinical Findings of Pneumonia,False,Clinical Findings of Pneumonia,,,,
1e1e0fc1-b6ae-4c56-8334-877899627b0e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"The clinical findings depend on the severity of the infection and underlying cause. Onset can be abrupt or gradual, and is often preceded by upper airway symptoms and associated with malaise, fever, or chills. As the infection progresses cough is established and chest pain and dyspnea can develop.",True,Clinical Findings of Pneumonia,,,,
1e61ac55-0595-4275-9d4d-dfe4b0505bfb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,As the infection progresses expectoration increases and can be purulent or even blood tinged. Mental confusion can arise particularly in elderly or alcoholic patients. If there is multiple lobe involvement then dyspnea can become severe and cyanosis may arise as intrapulmonary shunts become established and more significant. The hypoxemia can be accompanied by hypocapnia as the patient hyperventilates due to the hypoxic drive to breathe.,True,Clinical Findings of Pneumonia,,,,
bc761779-7096-4a59-b927-8f0c77a040e9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,Chest exams can have variable findings but may include poor respiratory excursion. The consolidated lung fields result in dullness to percussion and a reduction in breath sounds and increase in tactile fremitus. Inspiratory crackles may be heard. With continued progression arterial hypoxia worsens and arterial CO2 falls due to hyperventilation.,True,Clinical Findings of Pneumonia,,,,
4fc32fa9-1026-495d-83d7-bf4c7e906369,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Chest x-ray allows the areas of consolidation to be seen, but typically there is no volume loss, which allows pneumonia to be distinguished from atelectasis (although pneumonia and atelectasis can co-occur). Particularly in the case of a typical pneumonia the complete blood count (CBC) panel will show an elevated white blood cell count. See table 3.4 for summary.",True,Clinical Findings of Pneumonia,,,,
22c16505-47ef-4766-95f7-368d868e15d0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,Table 3.4: Summary of the clinical findings of pneumonia.,True,Clinical Findings of Pneumonia,,,,
d2c673a2-622a-4779-85f3-e2f4fa0d2aa8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,Text,False,Text,,,,
894073f7-cc5a-4474-892c-0037c868eaf8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 3.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
6773be8e-41cb-4099-99b9-347c9c9150ba,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
9c7e6f81-474c-4a6b-8436-6d0f6c14d529,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Table 3.1: Comparison of typical and atypical pneumonia. Includes Case 1 by Bell, D., Hacking, C., et al. from https://doi.org/10.53347/rID-68496 (CC BY-NC-SA 3.0), Acute pneumonia – i — low mag by Nephron from WikimediaCommons (CC BY-SA 3.0), Case 2 by Paks, M., Knipe, H., et al. from https://doi.org/10.53347/rID-27535 (CC BY-NC-SA 3.0), and image 1 by Dr Patsy Lill from University of South Carolina School of Medicine’s Microbiologybook.org (Fair use).",True,Text,,,,
ea306d74-a9cc-4bd8-8953-daf4520569af,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-2,"Table 3.2: Comparison of bronchopneumonia and lobar pneumonia. Includes Bronchopneumonia by Kindred Grey from Internet archive (CC BY 4.0), Lobar pneumonia by Kindred Grey from Internet archive (CC BY 4.0), X-ray of bronchopneumonia by Franquet T., Chung J.H. from WikimediaCommons (CC BY 4.0), Case 3 by Paks, M., Knipe, H., et al. from https://doi.org/10.53347/rID-26886 (CC BY-NC-SA 3.0).",True,Text,,,,
12341e38-e40e-40e1-8325-069078286c53,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,Acute Bronchitis,False,Acute Bronchitis,,,,
db8360ab-7fd4-4cd8-bcd6-6926cf583eec,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
db8360ab-7fd4-4cd8-bcd6-6926cf583eec,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
db8360ab-7fd4-4cd8-bcd6-6926cf583eec,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
db8360ab-7fd4-4cd8-bcd6-6926cf583eec,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
d5dbc954-eca1-4086-8085-5d439b1bd212,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"First the bronchial mucus membranes become inflamed. Taking a careful history can help you distinguish infectious causes from other instigators of airway inflammation, such as physical or chemical insults or an allergic response. The inflammation will initially produce a dry cough, but within two to three days bronchial secretions will be established, the cough will become productive, and rales can be heard over the site of the infection, which constitutes the clinical diagnosis.",True,Acute Bronchitis,,,,
60baa1ed-e85e-46da-960d-6c6db5b4e4ac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
60baa1ed-e85e-46da-960d-6c6db5b4e4ac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
60baa1ed-e85e-46da-960d-6c6db5b4e4ac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
60baa1ed-e85e-46da-960d-6c6db5b4e4ac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
75bc709b-049c-4d7e-877f-0d8bcf00230c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,Infectious Bronchiolitis,False,Infectious Bronchiolitis,,,,
5229c466-3cd4-467d-a29c-ec5a6fb00e7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Penetrating deeper into the airway a pathogen can cause acute infectious bronchiolitis. By far the most common culprit is respiratory syncytial virus (RSV). This is the most common cause of lower airway infection in children under one year old and is estimated to cause more infant deaths than any other pathogen with the exception of malaria. While it can affect adults, it usually occurs only in the elderly and immunosuppressed patients.",True,Infectious Bronchiolitis,,,,
cd7ba502-a07e-4cc9-a18a-182f6a16ef5c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
cd7ba502-a07e-4cc9-a18a-182f6a16ef5c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
cd7ba502-a07e-4cc9-a18a-182f6a16ef5c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
cd7ba502-a07e-4cc9-a18a-182f6a16ef5c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
f33aac49-2d43-440c-97b5-29e8f91832a5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"The young patient will likely present with a recent history of cough and hallmarks of shortness of breath such as use of accessory muscles. A scattered wheeze is likely, and in severe cases the child develops an expiratory grunt.",True,Infectious Bronchiolitis,,,,
415fa064-8531-4807-8048-901c6d89b5d5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Unresolved the RSV can spread to type 1 and 2 pneumocytes through cell-to-cell transmission. There is a high incidence of apnea associated with RSV infection, presumably due to the virus activating defensive reflexes associated with the larynx.",True,Infectious Bronchiolitis,,,,
89122eef-ff17-4cc3-becc-9168de4ac76a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,Pneumonia,False,Pneumonia,,,,
9b1611b4-a823-4af7-82fa-0dbc3cabaa68,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Now we will look at the consequences of infection of the terminal airways and what is referred to as pneumonia. Although pneumonia can result from infection by one of any number of pathogens, we will first look at a generalized pathophysiological mechanism.",True,Pneumonia,,,,
96f02299-c2c9-427b-a06b-403ec157552e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
96f02299-c2c9-427b-a06b-403ec157552e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
96f02299-c2c9-427b-a06b-403ec157552e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
96f02299-c2c9-427b-a06b-403ec157552e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
2fcb0ef8-2057-490a-9f10-4438f2cf31d7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"The infection may not be retained by the airway structure and can penetrate the pleural space, in which case an effusion is likely.",True,Pneumonia,,,,
3085509c-8d00-4509-a869-25157093c2d7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"The pneumonia-causing pathogen can often be found in blood analysis but the patient remains asymptomatic, but if the infection becomes more established significant signs and symptoms of bacteremia arise.",True,Pneumonia,,,,
cd970edb-bce9-4124-8e3c-9466a8793060,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
cd970edb-bce9-4124-8e3c-9466a8793060,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
cd970edb-bce9-4124-8e3c-9466a8793060,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
cd970edb-bce9-4124-8e3c-9466a8793060,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
08b05c40-7f2d-495f-8540-64e723b48a91,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,Classification of Pneumonia,False,Classification of Pneumonia,,,,
279c3a76-5513-47ff-9a56-5d0dfafadba5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"The causes of pneumonia are many, but so are the ways in which they are classified. Pneumonias are distinguished by:",True,Classification of Pneumonia,,,,
83ed3d23-0e6e-402c-aba9-1b435b162f38,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Typical or atypical pneumonia: We can start at arguably the least clinically helpful classification, the microscopic location. Pneumonias can be either typical or atypical. Typical pneumonium involves the presence of pathogens and immune cells in the airspace, whereas atypical has the pathogen and inflammatory response within the alveolar walls and interstitium (table 3.1). The site is usually dictated by the mode of the pathogen, with typical pneumonia being bacterial and atypical being caused by virus or mycobacterium that are capable of entering cells.",True,Classification of Pneumonia,,,,
131e4ff6-1726-4ff5-a175-1787867438a0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"The two forms can have different signs and symptoms with typical pneumonia having a more rapid onset and atypical being more gradual. Both can be associated with fever, but extrapulmonary features such as headache, joint and muscle pain, and nausea are more characteristic of atypical pneumonia. Because of the location of the pathogen; typical pneumonia is associated with a productive cough, whereas the cough of atypical pneumonia is dry, as summarized in table 3.1.",True,Classification of Pneumonia,,,,
48267d31-0810-4290-85a1-026ea8eeab27,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"On x-ray the atypical pneumonia shows more diffuse patchy markings associated with the infiltrated interstitium, whereas an x-ray of typical pneumonia shows lobar opacities caused by consolidated airspaces (table 3.1).",True,Classification of Pneumonia,,,,
017e958e-a3c5-41f0-8356-823f33ccf303,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,Table 3.1: Comparison of typical and atypical pneumonia.,True,Classification of Pneumonia,,,,
64a6be7b-eb16-452e-8871-4f4ba84a0a5f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Bronchopneumonia or lobar pneumonia: The next classification is based on the infection’s gross location—whether it occurs in a bronchiolocentric pattern to produce bronchopneumonia, or whether the consolidation occurs in continuous airspaces to occupy a lobe to produce lobar pneumonia. Bronchopneumonia will produce distinct areas of infiltrate, and the chest x-ray will reflect this with opacities following the effected airways (table 3.2). Lobar pneumonia will involve dense consolidation outlining the whole lobe and the possibility of air brochograms as air-filled bronchi are surrounded by the infiltrated, more dense alveoli (table 3.2). Bronchopneumonia is usually bilateral, whereas lobar pneumonia tends to be unilateral. However, both can exist in the same patient, as is the case in the example x-ray in table 3.2.",True,Classification of Pneumonia,,,,
a7b12296-7c4a-4669-bdd4-8df8a0609c61,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,Table 3.2: Comparison of bronchopneumonia and lobar pneumonia.,True,Classification of Pneumonia,,,,
fae23d6b-8a53-4a9c-9671-575524ad4b0d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Hospital-acquired or community-acquired pneumonia: The last classification relates to the setting in which the infection was acquired, either out in the community or during hospitalization. This classification can provide clues to identifying the pathogen involved. By far the most common cause of community-acquired pneumonia is Streptococcus pneumoniae. Other pathogens can be responsible but tend to affect only those with an underlying condition or characteristic; they are listed in table 3.3 with the usual instigating issue in parentheses. Legionella-related pneumonia requires exposure to laced water droplets, and mycoplasma infection tends to affect young adults living in close quarters, such as military barracks or college dorms. Lastly, and more uncommonly, the pneumonia may be caused by a viral infection.",True,Classification of Pneumonia,,,,
1d666638-21d8-42b0-a289-3e8b8288fd4e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Hospital-acquired pneumonia is defined as occurring at least three days after hospitalization. Unlike community-acquired pneumonias the pathogen is frequently a gram-negative bacteria or staphylococci that normally would not be able to become established in the lung. However, the hospitalized patient’s weakened state of health, state of consciousness, exposure to poor sterile technique for intubation, or antibiotic therapy can provide these listed pathogens an opportunity (table 3.3).",True,Classification of Pneumonia,,,,
f0651cf3-da25-4d72-aaf7-0da561177237,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,Table 3.3: Comparison of community- and hospital-acquired pneumonias.,True,Classification of Pneumonia,,,,
ced04e78-80a3-4aef-82e6-f199eb9f6646,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,Clinical Findings of Pneumonia,False,Clinical Findings of Pneumonia,,,,
45aa65e4-ff7d-4d52-bbf6-656b708597b6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"The clinical findings depend on the severity of the infection and underlying cause. Onset can be abrupt or gradual, and is often preceded by upper airway symptoms and associated with malaise, fever, or chills. As the infection progresses cough is established and chest pain and dyspnea can develop.",True,Clinical Findings of Pneumonia,,,,
b9504de8-4df2-4488-8a9b-6979b4b5ec23,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,As the infection progresses expectoration increases and can be purulent or even blood tinged. Mental confusion can arise particularly in elderly or alcoholic patients. If there is multiple lobe involvement then dyspnea can become severe and cyanosis may arise as intrapulmonary shunts become established and more significant. The hypoxemia can be accompanied by hypocapnia as the patient hyperventilates due to the hypoxic drive to breathe.,True,Clinical Findings of Pneumonia,,,,
1741ea43-d0f2-4fd0-86e5-50902f7b7651,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,Chest exams can have variable findings but may include poor respiratory excursion. The consolidated lung fields result in dullness to percussion and a reduction in breath sounds and increase in tactile fremitus. Inspiratory crackles may be heard. With continued progression arterial hypoxia worsens and arterial CO2 falls due to hyperventilation.,True,Clinical Findings of Pneumonia,,,,
9d4cd3c6-f474-49c9-95a0-b6e794811292,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Chest x-ray allows the areas of consolidation to be seen, but typically there is no volume loss, which allows pneumonia to be distinguished from atelectasis (although pneumonia and atelectasis can co-occur). Particularly in the case of a typical pneumonia the complete blood count (CBC) panel will show an elevated white blood cell count. See table 3.4 for summary.",True,Clinical Findings of Pneumonia,,,,
0a948180-94e8-4b49-a261-628128dc503b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,Table 3.4: Summary of the clinical findings of pneumonia.,True,Clinical Findings of Pneumonia,,,,
4ed75111-3279-453c-9142-4c77c158ab60,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,Text,False,Text,,,,
dcfcdec3-4f2a-470a-aa70-0321091d20f8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 3.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
b55e20fa-dec5-4f53-a8d1-7a7f90fce88c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
2fb47bc9-04d6-4fd4-afa1-5d386136fe09,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Table 3.1: Comparison of typical and atypical pneumonia. Includes Case 1 by Bell, D., Hacking, C., et al. from https://doi.org/10.53347/rID-68496 (CC BY-NC-SA 3.0), Acute pneumonia – i — low mag by Nephron from WikimediaCommons (CC BY-SA 3.0), Case 2 by Paks, M., Knipe, H., et al. from https://doi.org/10.53347/rID-27535 (CC BY-NC-SA 3.0), and image 1 by Dr Patsy Lill from University of South Carolina School of Medicine’s Microbiologybook.org (Fair use).",True,Text,,,,
1fe1ce0d-e3d6-48fa-8fa5-ed1f793ef8b1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Acute Bronchitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/#chapter-29-section-1,"Table 3.2: Comparison of bronchopneumonia and lobar pneumonia. Includes Bronchopneumonia by Kindred Grey from Internet archive (CC BY 4.0), Lobar pneumonia by Kindred Grey from Internet archive (CC BY 4.0), X-ray of bronchopneumonia by Franquet T., Chung J.H. from WikimediaCommons (CC BY 4.0), Case 3 by Paks, M., Knipe, H., et al. from https://doi.org/10.53347/rID-26886 (CC BY-NC-SA 3.0).",True,Text,,,,
75be82c0-7fbb-4a02-974f-6d97cac90091,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,Acute Bronchitis,False,Acute Bronchitis,,,,
56571a44-2e2c-4b99-a6fa-4eda0364021f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
56571a44-2e2c-4b99-a6fa-4eda0364021f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
56571a44-2e2c-4b99-a6fa-4eda0364021f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
56571a44-2e2c-4b99-a6fa-4eda0364021f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Acute bronchitis often originates from a migrating upper airway infection, and hence the usual candidates for a URI are the pathogens associated with acute bronchitis, and most are viral but can include mycoplasma infection. Acute bronchitis can be caused by bacteria, but it is usually an opportunistic secondary infection by resident bacteria taking advantage of a weakened airway. Regardless of the pathogen, let us look at the sequence of pathophysiological events in acute bronchitis (figure 3.1).",True,Acute Bronchitis,Figure 3.1,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
e5a2aed9-149b-4188-b129-6fd08e64ef76,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"First the bronchial mucus membranes become inflamed. Taking a careful history can help you distinguish infectious causes from other instigators of airway inflammation, such as physical or chemical insults or an allergic response. The inflammation will initially produce a dry cough, but within two to three days bronchial secretions will be established, the cough will become productive, and rales can be heard over the site of the infection, which constitutes the clinical diagnosis.",True,Acute Bronchitis,,,,
23b901db-7d4a-412e-8403-e85899bfc38e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
23b901db-7d4a-412e-8403-e85899bfc38e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
23b901db-7d4a-412e-8403-e85899bfc38e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
23b901db-7d4a-412e-8403-e85899bfc38e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"The inflamed airways may also become hyperreactive, and this may compound any concurrent allergic response or existing asthma resulting in bronchospasm and wheeze. See figure 3.1 for a summary.",True,Acute Bronchitis,Figure 3.1,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.1.png,Figure 3.1: Pathophysiology of acute bronchitis.
2e5c6c06-4c9c-46f8-a674-a43f61cc8cfe,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,Infectious Bronchiolitis,False,Infectious Bronchiolitis,,,,
000d8510-2198-49f0-9a7b-644c12ebb244,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Penetrating deeper into the airway a pathogen can cause acute infectious bronchiolitis. By far the most common culprit is respiratory syncytial virus (RSV). This is the most common cause of lower airway infection in children under one year old and is estimated to cause more infant deaths than any other pathogen with the exception of malaria. While it can affect adults, it usually occurs only in the elderly and immunosuppressed patients.",True,Infectious Bronchiolitis,,,,
8c6cb2b3-d48c-483d-8589-ab086de76ad5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
8c6cb2b3-d48c-483d-8589-ab086de76ad5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
8c6cb2b3-d48c-483d-8589-ab086de76ad5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
8c6cb2b3-d48c-483d-8589-ab086de76ad5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Infection starts in the nasopharynx and then progresses to the epithelium of the bronchioles that appears particularly susceptible to RSV infection. Immune cells are called to the area, but the predominant feature of the infection is the sloughing of the bronchiolar epithelium and the appearance of syncytial giant cells in the airway lumen, as seen in the insert of the histology slide in figure 3.2. With anatomically smaller bronchioles, infants are susceptible to this epithelial sludge blocking the airway. The hallmark of the infection reflects the obstructive nature of the disease with hyperinflation.",True,Infectious Bronchiolitis,Figure 3.2,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.2.png,Figure 3.2: Histological and radiographic findings for an RSV infection. The left panel shows syncytial giant cells (circled). The right panel shows an x-ray of a child with RSV where densities folow bronchi and a flattened diaphragm.
f1f5e2ee-ee9b-4731-9d39-73a79b92f10c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"The young patient will likely present with a recent history of cough and hallmarks of shortness of breath such as use of accessory muscles. A scattered wheeze is likely, and in severe cases the child develops an expiratory grunt.",True,Infectious Bronchiolitis,,,,
18aeb702-e387-4e70-934f-758661cbae5e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Unresolved the RSV can spread to type 1 and 2 pneumocytes through cell-to-cell transmission. There is a high incidence of apnea associated with RSV infection, presumably due to the virus activating defensive reflexes associated with the larynx.",True,Infectious Bronchiolitis,,,,
10b14ef4-e428-49de-9191-786a8ddac150,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,Pneumonia,False,Pneumonia,,,,
2e403652-2144-41da-8683-e8674d45e2b8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Now we will look at the consequences of infection of the terminal airways and what is referred to as pneumonia. Although pneumonia can result from infection by one of any number of pathogens, we will first look at a generalized pathophysiological mechanism.",True,Pneumonia,,,,
895aa625-684a-43d0-ad7a-ee66058b2592,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
895aa625-684a-43d0-ad7a-ee66058b2592,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
895aa625-684a-43d0-ad7a-ee66058b2592,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
895aa625-684a-43d0-ad7a-ee66058b2592,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"The pathogen arrives in the alveolar space causing activation of alveolar macrophages and recruitment of neutrophils from the bloodstream. These first responder cells release cytokines to attract more neutrophils and hyperpermeabilize the vasculature. Consequently the airspace becomes congested with pathogens, neutrophils, and exudate and incapable of being ventilated (figure 3.3). This produces V/Q mismatching in the effected area and the potential for the establishing of intrapulmonary shunts.",True,Pneumonia,Figure 3.3,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.3.jpeg,"Figure 3.3: Neutrophils, bacteria, and exudate occupy airspaces in a typical pneumonia."
4566b159-165f-461e-b8e3-8a62546e8dc0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"The infection may not be retained by the airway structure and can penetrate the pleural space, in which case an effusion is likely.",True,Pneumonia,,,,
0cfbc2cc-812e-4608-9380-4371a9ebdb7f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"The pneumonia-causing pathogen can often be found in blood analysis but the patient remains asymptomatic, but if the infection becomes more established significant signs and symptoms of bacteremia arise.",True,Pneumonia,,,,
a99a62f5-e7d5-4608-b48e-e2393c98cf47,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
a99a62f5-e7d5-4608-b48e-e2393c98cf47,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,Infectious Bronchiolitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
a99a62f5-e7d5-4608-b48e-e2393c98cf47,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,Acute Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
a99a62f5-e7d5-4608-b48e-e2393c98cf47,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"An infection may lead to necrotized tissue and formation of an abscess in the lung. The prevalence of this is mostly dependent on the pathogen; for example, a tuberculosis infection is famous for causing walled-off abscesses (or granuloma) that try to contain the mycobacterium. These processes are summarized in figure 3.4.",True,Pneumonia,Figure 3.4,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/3.4.png,Figure 3.4: General pathophysiology of pneumonia.
ba3b7f12-4fd3-44b1-890a-f2e201e8056f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,Classification of Pneumonia,False,Classification of Pneumonia,,,,
0b1cf2f3-4bfb-4352-97e6-b792fb420aa6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"The causes of pneumonia are many, but so are the ways in which they are classified. Pneumonias are distinguished by:",True,Classification of Pneumonia,,,,
9973b1bf-ccd1-4066-b124-6bfe4d4de2f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Typical or atypical pneumonia: We can start at arguably the least clinically helpful classification, the microscopic location. Pneumonias can be either typical or atypical. Typical pneumonium involves the presence of pathogens and immune cells in the airspace, whereas atypical has the pathogen and inflammatory response within the alveolar walls and interstitium (table 3.1). The site is usually dictated by the mode of the pathogen, with typical pneumonia being bacterial and atypical being caused by virus or mycobacterium that are capable of entering cells.",True,Classification of Pneumonia,,,,
e4ab16d8-112e-43c2-825a-255c04d589ef,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"The two forms can have different signs and symptoms with typical pneumonia having a more rapid onset and atypical being more gradual. Both can be associated with fever, but extrapulmonary features such as headache, joint and muscle pain, and nausea are more characteristic of atypical pneumonia. Because of the location of the pathogen; typical pneumonia is associated with a productive cough, whereas the cough of atypical pneumonia is dry, as summarized in table 3.1.",True,Classification of Pneumonia,,,,
e1fe8c9b-e75c-42a0-b734-411f6ab3d59b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"On x-ray the atypical pneumonia shows more diffuse patchy markings associated with the infiltrated interstitium, whereas an x-ray of typical pneumonia shows lobar opacities caused by consolidated airspaces (table 3.1).",True,Classification of Pneumonia,,,,
d5f883e1-ea19-4e67-a971-ef2e6fe43ed9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,Table 3.1: Comparison of typical and atypical pneumonia.,True,Classification of Pneumonia,,,,
cf95665c-6abe-4fb1-b4fd-14be5e13ee3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Bronchopneumonia or lobar pneumonia: The next classification is based on the infection’s gross location—whether it occurs in a bronchiolocentric pattern to produce bronchopneumonia, or whether the consolidation occurs in continuous airspaces to occupy a lobe to produce lobar pneumonia. Bronchopneumonia will produce distinct areas of infiltrate, and the chest x-ray will reflect this with opacities following the effected airways (table 3.2). Lobar pneumonia will involve dense consolidation outlining the whole lobe and the possibility of air brochograms as air-filled bronchi are surrounded by the infiltrated, more dense alveoli (table 3.2). Bronchopneumonia is usually bilateral, whereas lobar pneumonia tends to be unilateral. However, both can exist in the same patient, as is the case in the example x-ray in table 3.2.",True,Classification of Pneumonia,,,,
06d73b6a-d6e8-4098-82ef-0b48aeea821c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,Table 3.2: Comparison of bronchopneumonia and lobar pneumonia.,True,Classification of Pneumonia,,,,
c9cd91cf-a768-4839-897d-f00d5351d669,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Hospital-acquired or community-acquired pneumonia: The last classification relates to the setting in which the infection was acquired, either out in the community or during hospitalization. This classification can provide clues to identifying the pathogen involved. By far the most common cause of community-acquired pneumonia is Streptococcus pneumoniae. Other pathogens can be responsible but tend to affect only those with an underlying condition or characteristic; they are listed in table 3.3 with the usual instigating issue in parentheses. Legionella-related pneumonia requires exposure to laced water droplets, and mycoplasma infection tends to affect young adults living in close quarters, such as military barracks or college dorms. Lastly, and more uncommonly, the pneumonia may be caused by a viral infection.",True,Classification of Pneumonia,,,,
7d11dea4-399b-4f31-adac-206ef9fb1f1a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Hospital-acquired pneumonia is defined as occurring at least three days after hospitalization. Unlike community-acquired pneumonias the pathogen is frequently a gram-negative bacteria or staphylococci that normally would not be able to become established in the lung. However, the hospitalized patient’s weakened state of health, state of consciousness, exposure to poor sterile technique for intubation, or antibiotic therapy can provide these listed pathogens an opportunity (table 3.3).",True,Classification of Pneumonia,,,,
031ae06f-edac-4fe8-a96e-b192f235e5c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,Table 3.3: Comparison of community- and hospital-acquired pneumonias.,True,Classification of Pneumonia,,,,
8fab24c3-fe3e-4b9a-b7bd-1c5830cc7dc4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,Clinical Findings of Pneumonia,False,Clinical Findings of Pneumonia,,,,
a32bcaf9-2aaa-4157-9b76-97540a98110f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"The clinical findings depend on the severity of the infection and underlying cause. Onset can be abrupt or gradual, and is often preceded by upper airway symptoms and associated with malaise, fever, or chills. As the infection progresses cough is established and chest pain and dyspnea can develop.",True,Clinical Findings of Pneumonia,,,,
5fb8864e-cb12-4ae4-a7ba-02d4b491d8b3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,As the infection progresses expectoration increases and can be purulent or even blood tinged. Mental confusion can arise particularly in elderly or alcoholic patients. If there is multiple lobe involvement then dyspnea can become severe and cyanosis may arise as intrapulmonary shunts become established and more significant. The hypoxemia can be accompanied by hypocapnia as the patient hyperventilates due to the hypoxic drive to breathe.,True,Clinical Findings of Pneumonia,,,,
b1c65ed6-69c7-45e6-b0c8-c77eea8ed9a1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,Chest exams can have variable findings but may include poor respiratory excursion. The consolidated lung fields result in dullness to percussion and a reduction in breath sounds and increase in tactile fremitus. Inspiratory crackles may be heard. With continued progression arterial hypoxia worsens and arterial CO2 falls due to hyperventilation.,True,Clinical Findings of Pneumonia,,,,
0cdf3285-50d3-4c28-abb0-bd9cc718a4cd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Chest x-ray allows the areas of consolidation to be seen, but typically there is no volume loss, which allows pneumonia to be distinguished from atelectasis (although pneumonia and atelectasis can co-occur). Particularly in the case of a typical pneumonia the complete blood count (CBC) panel will show an elevated white blood cell count. See table 3.4 for summary.",True,Clinical Findings of Pneumonia,,,,
f1a19e3b-ab9b-4f8e-b2a7-ff29625f6d92,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,Table 3.4: Summary of the clinical findings of pneumonia.,True,Clinical Findings of Pneumonia,,,,
fb87d48c-e2e3-4979-b59d-2d324b98a9c1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,Text,False,Text,,,,
7f57aff3-e4cb-43f3-bd90-f560fb548677,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapter 3.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
bae2fdef-e32b-47f4-aa83-57115d974439,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
9c7cd85e-4c0d-4050-9e29-769bb05cae6e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Table 3.1: Comparison of typical and atypical pneumonia. Includes Case 1 by Bell, D., Hacking, C., et al. from https://doi.org/10.53347/rID-68496 (CC BY-NC-SA 3.0), Acute pneumonia – i — low mag by Nephron from WikimediaCommons (CC BY-SA 3.0), Case 2 by Paks, M., Knipe, H., et al. from https://doi.org/10.53347/rID-27535 (CC BY-NC-SA 3.0), and image 1 by Dr Patsy Lill from University of South Carolina School of Medicine’s Microbiologybook.org (Fair use).",True,Text,,,,
2f5984c8-5f69-48bb-bf52-1ecb4aa606a9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,3. Lower Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/lower-airway-infections/,"Table 3.2: Comparison of bronchopneumonia and lobar pneumonia. Includes Bronchopneumonia by Kindred Grey from Internet archive (CC BY 4.0), Lobar pneumonia by Kindred Grey from Internet archive (CC BY 4.0), X-ray of bronchopneumonia by Franquet T., Chung J.H. from WikimediaCommons (CC BY 4.0), Case 3 by Paks, M., Knipe, H., et al. from https://doi.org/10.53347/rID-26886 (CC BY-NC-SA 3.0).",True,Text,,,,
7d48f651-5ec9-4c8c-8c1d-f8ac28654b61,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"As with most URIs the common cold is caused by a viral infection, and although there are several different viral candidates for causing a common cold, the pathophysiological mechanism and symptoms are the same regardless of the type. This is because it is the innate immune response, rather than the direct infection, that is responsible for most of the symptoms.",True,Text,,,,
8366273b-f54a-4656-950c-0e1f56f2c1db,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,URIs,False,URIs,,,,
93234398-69a1-4864-9f54-5418cb35f91b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
93234398-69a1-4864-9f54-5418cb35f91b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
93234398-69a1-4864-9f54-5418cb35f91b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
93234398-69a1-4864-9f54-5418cb35f91b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
93234398-69a1-4864-9f54-5418cb35f91b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
93234398-69a1-4864-9f54-5418cb35f91b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
d37b6aa6-f48f-4625-b3a4-2ecdb13824d4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Once in the upper airway, and if the pathogen can breach the innate defenses here (mucus and the mucociliary escalator), the virus attaches to, and then enters, the epithelial cells. In response, the invaded epithelial cells release cytokines to instigate an immune response. The primary cytokine released in this scenario is IL-8, which causes the attraction and accumulation of polymorphonuclear cells (PMN).",True,URIs,,,,
c2e4bd97-d89a-432b-bfb7-ebacb05d761c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"It is the substantial increase in PMN cells that is responsible for most of the symptoms of a common cold—runny nose, postnasal drip, and other signs of epithelial inflammation.",True,URIs,,,,
88424554-821d-4fd4-a30b-408bce446a9b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"By far the most common cause of the common cold is the rhinovirus, followed by coronavirus and influenza, then less frequently by parainfluenza respiratory syncytial virus (RSV), and then rarely by adenovirus or enterovirus (table 2.1).",True,URIs,,,,
3569c1e2-50a7-4653-83e2-246fef266886,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,Table 2.1: The viral pathogens.,True,URIs,,,,
e77d6cb6-3b21-4d89-afcf-f5d3ac3b7693,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Seasonal differences (table 2.1) in the prevalence of these pathogens might help you identify the causal agent, but as the viral infections are self-limiting it is more important to ensure there is no bacterial involvement.",True,URIs,,,,
9beb875c-6f9f-4efd-ba79-b48cb3ecb649,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"A viral infection can progress and cause more specific conditions than a cold, and these are identified by their location.",True,URIs,,,,
68cb27b9-bd5f-425c-a9ff-b1c0d53a8967,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,Rhinosinusitis,False,Rhinosinusitis,,,,
24c1986f-c27f-4396-9450-53a6f5faec95,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Rhinosinusitis is most commonly caused by a viral infection, and despite popular belief is only rarely associated with a concurrent bacterial infection in adults. The lining of the nasal and sinus cavities becomes inflamed, again as a result of the immune response rather than a direct effect of the virus. The congestion can be painful, but symptoms can be treated with over-the-counter analgesics. Like the common cold, the condition is self-limiting and normally resolves in seven to ten days.",True,Rhinosinusitis,,,,
4bf82c37-fde3-4792-945b-2a91892fa019,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,Pharyngitis,False,Pharyngitis,,,,
710ca630-de22-4dc6-8c76-46bd170c4ab2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"When the pharynx is involved the local inflammation will cause the patient to present with a sore throat and a hoarse voice. Pharyngitis is most commonly caused by viral infection, but more serious bacterial infections (e.g., Streptococcus) should be considered. The two infection types are easily distinguished with tonsillar exudate and petechial mottling of the soft palate being present in a bacterial infection, but absent in a viral infection. Treatment of viral pharyngitis is limited to symptom relief, and antibiotics should be avoided.",True,Pharyngitis,,,,
cf725991-52d5-4701-bb60-adef0d49cd62,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,Viral Croup,False,Viral Croup,,,,
52964135-ef76-4376-b7cf-88a0dbf15328,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
52964135-ef76-4376-b7cf-88a0dbf15328,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
52964135-ef76-4376-b7cf-88a0dbf15328,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
52964135-ef76-4376-b7cf-88a0dbf15328,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
52964135-ef76-4376-b7cf-88a0dbf15328,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
52964135-ef76-4376-b7cf-88a0dbf15328,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
209014bb-63b4-4118-8464-97c1cdc00faa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,Bacterial Infection of the Upper Airway,False,Bacterial Infection of the Upper Airway,,,,
64087e6b-fc24-4968-804b-febccb8669fb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"The induction of upper airway infection by bacteria is similar to that by virus with droplet inhalation or hand-to-mouth or nose contact. Cell adherence is usually promoted by bacterial properties, but it is bacterial toxins that instigate the signs and symptoms of infection rather than the innate immune system. We will now cover four bacteria that are capable of causing an upper airway infection.",True,Bacterial Infection of the Upper Airway,,,,
9a7f5e73-c25c-4f37-87d7-565dcf9c55c3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,Group A Streptococcus,False,Group A Streptococcus,,,,
ebfbe95b-bedd-4fac-ac1f-5c74fd78055d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"The pathogenic mechanisms of Group A Streptococcus are poorly understood—partly because of the numerous and complex ways it interacts with its human host. Its coat protects it from phagocytosis, antibody binding, and opsonization. It is capable of releasing a cocktail of cell-lysing toxins as well as pyrogenic exotoxins that:",True,Group A Streptococcus,,,,
22b5f3a0-0ae4-4e40-ad22-f6114b7ea720,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
22b5f3a0-0ae4-4e40-ad22-f6114b7ea720,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
22b5f3a0-0ae4-4e40-ad22-f6114b7ea720,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
22b5f3a0-0ae4-4e40-ad22-f6114b7ea720,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
22b5f3a0-0ae4-4e40-ad22-f6114b7ea720,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
22b5f3a0-0ae4-4e40-ad22-f6114b7ea720,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
71d6e409-0047-4551-b772-dc1d7281ecdf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,Corynebacterium diphtheriae,False,Corynebacterium diphtheriae,,,,
eb7578ba-a236-4c00-a201-cbae2fe28bd9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
eb7578ba-a236-4c00-a201-cbae2fe28bd9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
eb7578ba-a236-4c00-a201-cbae2fe28bd9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
eb7578ba-a236-4c00-a201-cbae2fe28bd9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
eb7578ba-a236-4c00-a201-cbae2fe28bd9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
eb7578ba-a236-4c00-a201-cbae2fe28bd9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
6ab77704-04f8-4f13-bf71-52db4f633233,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,Bordetella pertussis,False,Bordetella pertussis,,,,
aeb4da5c-5a33-4f95-b93b-47cae4dd7543,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"After inhalation, B. pertussis attaches to airway cells through a variety of adhesion molecules. The organism then releases cytotoxins that cause loss of protective respiratory cells and promote microaspiration and a distinct and prolonged cough. Pertussis’s nickname of whooping cough comes from the distinct inspiratory noise. The paroxysmal stage of pertussis (that involving cough) can last between two and ten weeks, and this prolongation is likely due to the bacteria penetrating deeper regions of the lung (the cytotoxins have been found in alveolar macrophages). The disease can be life threatening to infants, but widespread vaccinations started in the forties dramatically reduced its incidence.",True,Bordetella pertussis,,,,
5357f402-18f9-4d82-9694-3d472c184804,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,Haemophilus influenzae,False,Haemophilus influenzae,,,,
92187996-cc71-4081-aaa9-5aeafdc2f8e2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"The outer coat of the H. influenzae contains several proteins that attach to upper airway cells and specifically promote pharyngeal and the middle ear colonization. The outer coat also acts as an endotoxin and elicits a potent inflammatory response to produce the symptoms of the infection. Prior to routine vaccination, vascular invasion by the pathogen could produce metastatic foci including meningitis, septic arthritis, osteomyelitis, and cellulitis. Today, while upper airway infection can lead to pneumonia, the incidence of bacteremia is low.",True,Haemophilus influenzae,,,,
8b07893a-38c6-4b3a-b198-fcef38f83f09,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,Text,False,Text,,,,
c9d5fd5e-55d3-44b1-94eb-4c180bbf3596,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-5,"Thomas, Micah, and Paul A. Bomar. Upper Respiratory Tract Infection. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532961, CC BY 4.0.",True,Text,,,,
0b0ab6da-f7f4-4a75-a902-60b54a1d6646,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"As with most URIs the common cold is caused by a viral infection, and although there are several different viral candidates for causing a common cold, the pathophysiological mechanism and symptoms are the same regardless of the type. This is because it is the innate immune response, rather than the direct infection, that is responsible for most of the symptoms.",True,Text,,,,
44cf6308-581a-4c50-8d20-e690b992e03f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,URIs,False,URIs,,,,
74ff0123-f2d5-4d60-ab0d-8918c4a82090,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
74ff0123-f2d5-4d60-ab0d-8918c4a82090,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
74ff0123-f2d5-4d60-ab0d-8918c4a82090,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
74ff0123-f2d5-4d60-ab0d-8918c4a82090,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
74ff0123-f2d5-4d60-ab0d-8918c4a82090,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
74ff0123-f2d5-4d60-ab0d-8918c4a82090,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
db76bc6c-068f-4581-b258-9695744daace,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Once in the upper airway, and if the pathogen can breach the innate defenses here (mucus and the mucociliary escalator), the virus attaches to, and then enters, the epithelial cells. In response, the invaded epithelial cells release cytokines to instigate an immune response. The primary cytokine released in this scenario is IL-8, which causes the attraction and accumulation of polymorphonuclear cells (PMN).",True,URIs,,,,
17b51591-63fa-4581-9729-35aa633b73ad,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"It is the substantial increase in PMN cells that is responsible for most of the symptoms of a common cold—runny nose, postnasal drip, and other signs of epithelial inflammation.",True,URIs,,,,
53ee4060-85cd-429b-809e-6b77e649611f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"By far the most common cause of the common cold is the rhinovirus, followed by coronavirus and influenza, then less frequently by parainfluenza respiratory syncytial virus (RSV), and then rarely by adenovirus or enterovirus (table 2.1).",True,URIs,,,,
ccc85396-8ff8-49ef-977d-defa803944cf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,Table 2.1: The viral pathogens.,True,URIs,,,,
32890754-6c5b-4d1f-95f7-461b16dab331,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Seasonal differences (table 2.1) in the prevalence of these pathogens might help you identify the causal agent, but as the viral infections are self-limiting it is more important to ensure there is no bacterial involvement.",True,URIs,,,,
5ff1c604-bdfd-4024-b46a-645ac300defc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"A viral infection can progress and cause more specific conditions than a cold, and these are identified by their location.",True,URIs,,,,
57185055-064e-4d73-9a7a-d59ec87afd9a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,Rhinosinusitis,False,Rhinosinusitis,,,,
94d40008-3be6-431d-b141-e46251dab713,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Rhinosinusitis is most commonly caused by a viral infection, and despite popular belief is only rarely associated with a concurrent bacterial infection in adults. The lining of the nasal and sinus cavities becomes inflamed, again as a result of the immune response rather than a direct effect of the virus. The congestion can be painful, but symptoms can be treated with over-the-counter analgesics. Like the common cold, the condition is self-limiting and normally resolves in seven to ten days.",True,Rhinosinusitis,,,,
2ad3afce-db94-4f0e-a1dc-ff806508d8be,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,Pharyngitis,False,Pharyngitis,,,,
52c1b376-74ab-4e64-8ac6-f57c45fe97d1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"When the pharynx is involved the local inflammation will cause the patient to present with a sore throat and a hoarse voice. Pharyngitis is most commonly caused by viral infection, but more serious bacterial infections (e.g., Streptococcus) should be considered. The two infection types are easily distinguished with tonsillar exudate and petechial mottling of the soft palate being present in a bacterial infection, but absent in a viral infection. Treatment of viral pharyngitis is limited to symptom relief, and antibiotics should be avoided.",True,Pharyngitis,,,,
121bb0b4-7b51-4edc-8225-c6e9938631d4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,Viral Croup,False,Viral Croup,,,,
739e60cb-cd59-4856-8b0b-12c613e9be54,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
739e60cb-cd59-4856-8b0b-12c613e9be54,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
739e60cb-cd59-4856-8b0b-12c613e9be54,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
739e60cb-cd59-4856-8b0b-12c613e9be54,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
739e60cb-cd59-4856-8b0b-12c613e9be54,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
739e60cb-cd59-4856-8b0b-12c613e9be54,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
25578212-9ee4-4df4-9a38-41c1bfe37de3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,Bacterial Infection of the Upper Airway,False,Bacterial Infection of the Upper Airway,,,,
05cd8e7a-8220-4ba9-a9ce-09452f5e5c20,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"The induction of upper airway infection by bacteria is similar to that by virus with droplet inhalation or hand-to-mouth or nose contact. Cell adherence is usually promoted by bacterial properties, but it is bacterial toxins that instigate the signs and symptoms of infection rather than the innate immune system. We will now cover four bacteria that are capable of causing an upper airway infection.",True,Bacterial Infection of the Upper Airway,,,,
30f145ae-157d-42c0-b961-eb5e93926d15,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,Group A Streptococcus,False,Group A Streptococcus,,,,
f9d1bd2d-6311-44a4-a46e-a2a5e3cc7cab,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"The pathogenic mechanisms of Group A Streptococcus are poorly understood—partly because of the numerous and complex ways it interacts with its human host. Its coat protects it from phagocytosis, antibody binding, and opsonization. It is capable of releasing a cocktail of cell-lysing toxins as well as pyrogenic exotoxins that:",True,Group A Streptococcus,,,,
498b65ef-b145-4f1d-bb6f-3987e3aced31,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
498b65ef-b145-4f1d-bb6f-3987e3aced31,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
498b65ef-b145-4f1d-bb6f-3987e3aced31,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
498b65ef-b145-4f1d-bb6f-3987e3aced31,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
498b65ef-b145-4f1d-bb6f-3987e3aced31,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
498b65ef-b145-4f1d-bb6f-3987e3aced31,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
18d337ba-5001-4972-8110-630caac88c35,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,Corynebacterium diphtheriae,False,Corynebacterium diphtheriae,,,,
e5706453-bcbd-4847-9c4b-46a09a8bdeb4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
e5706453-bcbd-4847-9c4b-46a09a8bdeb4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
e5706453-bcbd-4847-9c4b-46a09a8bdeb4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
e5706453-bcbd-4847-9c4b-46a09a8bdeb4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
e5706453-bcbd-4847-9c4b-46a09a8bdeb4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
e5706453-bcbd-4847-9c4b-46a09a8bdeb4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
e4c06a39-aea7-439b-a32c-fde57d06ab54,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,Bordetella pertussis,False,Bordetella pertussis,,,,
9bff81d0-1251-4a41-93c2-68980e5741a8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"After inhalation, B. pertussis attaches to airway cells through a variety of adhesion molecules. The organism then releases cytotoxins that cause loss of protective respiratory cells and promote microaspiration and a distinct and prolonged cough. Pertussis’s nickname of whooping cough comes from the distinct inspiratory noise. The paroxysmal stage of pertussis (that involving cough) can last between two and ten weeks, and this prolongation is likely due to the bacteria penetrating deeper regions of the lung (the cytotoxins have been found in alveolar macrophages). The disease can be life threatening to infants, but widespread vaccinations started in the forties dramatically reduced its incidence.",True,Bordetella pertussis,,,,
42d174f8-afd9-417d-aa09-b667639dad7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,Haemophilus influenzae,False,Haemophilus influenzae,,,,
2f5bfd7d-e59c-4e37-84ce-ba8babcb013d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"The outer coat of the H. influenzae contains several proteins that attach to upper airway cells and specifically promote pharyngeal and the middle ear colonization. The outer coat also acts as an endotoxin and elicits a potent inflammatory response to produce the symptoms of the infection. Prior to routine vaccination, vascular invasion by the pathogen could produce metastatic foci including meningitis, septic arthritis, osteomyelitis, and cellulitis. Today, while upper airway infection can lead to pneumonia, the incidence of bacteremia is low.",True,Haemophilus influenzae,,,,
63ed94aa-c81d-45e5-abde-c9f746efef1d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,Text,False,Text,,,,
25b5e613-2b4b-4da3-8be4-7edad2c88a4f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Viral Croup,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-4,"Thomas, Micah, and Paul A. Bomar. Upper Respiratory Tract Infection. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532961, CC BY 4.0.",True,Text,,,,
3582811d-3c54-4828-9b1e-275f829165de,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"As with most URIs the common cold is caused by a viral infection, and although there are several different viral candidates for causing a common cold, the pathophysiological mechanism and symptoms are the same regardless of the type. This is because it is the innate immune response, rather than the direct infection, that is responsible for most of the symptoms.",True,Text,,,,
320c857a-e11e-4600-b7df-fbca925bad2b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,URIs,False,URIs,,,,
66e612fd-27ed-47bb-a60e-42ae9f663b4a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
66e612fd-27ed-47bb-a60e-42ae9f663b4a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
66e612fd-27ed-47bb-a60e-42ae9f663b4a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
66e612fd-27ed-47bb-a60e-42ae9f663b4a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
66e612fd-27ed-47bb-a60e-42ae9f663b4a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
66e612fd-27ed-47bb-a60e-42ae9f663b4a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
d8e17cee-f804-4e0d-8c2a-b2b9f8edf318,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Once in the upper airway, and if the pathogen can breach the innate defenses here (mucus and the mucociliary escalator), the virus attaches to, and then enters, the epithelial cells. In response, the invaded epithelial cells release cytokines to instigate an immune response. The primary cytokine released in this scenario is IL-8, which causes the attraction and accumulation of polymorphonuclear cells (PMN).",True,URIs,,,,
f34d5e0f-5637-44be-ba2d-5118c29aedc4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"It is the substantial increase in PMN cells that is responsible for most of the symptoms of a common cold—runny nose, postnasal drip, and other signs of epithelial inflammation.",True,URIs,,,,
ced069b5-ad7f-49ed-86c7-3238c7f6c184,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"By far the most common cause of the common cold is the rhinovirus, followed by coronavirus and influenza, then less frequently by parainfluenza respiratory syncytial virus (RSV), and then rarely by adenovirus or enterovirus (table 2.1).",True,URIs,,,,
f92c32a3-d0dd-4f3a-bd21-a40f00fca40a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,Table 2.1: The viral pathogens.,True,URIs,,,,
76a12771-d1c6-46ba-854b-6d7de02d5fb9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Seasonal differences (table 2.1) in the prevalence of these pathogens might help you identify the causal agent, but as the viral infections are self-limiting it is more important to ensure there is no bacterial involvement.",True,URIs,,,,
cfc140ab-a084-4a4f-b6b4-7b76832eeaed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"A viral infection can progress and cause more specific conditions than a cold, and these are identified by their location.",True,URIs,,,,
fa4f1e31-e2cb-4a27-9dc9-593ddfb13b2b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,Rhinosinusitis,False,Rhinosinusitis,,,,
b1c9f693-4801-4d1c-b0cd-1dd2cbb7c914,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Rhinosinusitis is most commonly caused by a viral infection, and despite popular belief is only rarely associated with a concurrent bacterial infection in adults. The lining of the nasal and sinus cavities becomes inflamed, again as a result of the immune response rather than a direct effect of the virus. The congestion can be painful, but symptoms can be treated with over-the-counter analgesics. Like the common cold, the condition is self-limiting and normally resolves in seven to ten days.",True,Rhinosinusitis,,,,
c84d74b9-e85b-4a08-be2a-45b9acd72383,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,Pharyngitis,False,Pharyngitis,,,,
3b05a25d-8fb0-4944-9201-e83ee99b5d57,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"When the pharynx is involved the local inflammation will cause the patient to present with a sore throat and a hoarse voice. Pharyngitis is most commonly caused by viral infection, but more serious bacterial infections (e.g., Streptococcus) should be considered. The two infection types are easily distinguished with tonsillar exudate and petechial mottling of the soft palate being present in a bacterial infection, but absent in a viral infection. Treatment of viral pharyngitis is limited to symptom relief, and antibiotics should be avoided.",True,Pharyngitis,,,,
610097bb-d38d-4a4d-b5d0-d955a2a42cda,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,Viral Croup,False,Viral Croup,,,,
93f11255-d692-4fe1-b9de-84cf9da06abd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
93f11255-d692-4fe1-b9de-84cf9da06abd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
93f11255-d692-4fe1-b9de-84cf9da06abd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
93f11255-d692-4fe1-b9de-84cf9da06abd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
93f11255-d692-4fe1-b9de-84cf9da06abd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
93f11255-d692-4fe1-b9de-84cf9da06abd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
e827b12f-7918-4c95-8d32-abaf05cefe44,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,Bacterial Infection of the Upper Airway,False,Bacterial Infection of the Upper Airway,,,,
1f17ed98-9eb8-4861-b75b-35d9610ad8fa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"The induction of upper airway infection by bacteria is similar to that by virus with droplet inhalation or hand-to-mouth or nose contact. Cell adherence is usually promoted by bacterial properties, but it is bacterial toxins that instigate the signs and symptoms of infection rather than the innate immune system. We will now cover four bacteria that are capable of causing an upper airway infection.",True,Bacterial Infection of the Upper Airway,,,,
35e4e74b-aa5c-4aa8-870f-1b8a78041a34,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,Group A Streptococcus,False,Group A Streptococcus,,,,
beb48e55-cc63-4c34-8b7d-26ed8c672b78,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"The pathogenic mechanisms of Group A Streptococcus are poorly understood—partly because of the numerous and complex ways it interacts with its human host. Its coat protects it from phagocytosis, antibody binding, and opsonization. It is capable of releasing a cocktail of cell-lysing toxins as well as pyrogenic exotoxins that:",True,Group A Streptococcus,,,,
7f5abd21-56f7-492c-8b0c-3f431ffb8858,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
7f5abd21-56f7-492c-8b0c-3f431ffb8858,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
7f5abd21-56f7-492c-8b0c-3f431ffb8858,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
7f5abd21-56f7-492c-8b0c-3f431ffb8858,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
7f5abd21-56f7-492c-8b0c-3f431ffb8858,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
7f5abd21-56f7-492c-8b0c-3f431ffb8858,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
132e2421-f3ff-4e00-a1a9-22856a99ff4a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,Corynebacterium diphtheriae,False,Corynebacterium diphtheriae,,,,
b5794183-fd8e-4e7a-affa-a8abb07840c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
b5794183-fd8e-4e7a-affa-a8abb07840c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
b5794183-fd8e-4e7a-affa-a8abb07840c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
b5794183-fd8e-4e7a-affa-a8abb07840c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
b5794183-fd8e-4e7a-affa-a8abb07840c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
b5794183-fd8e-4e7a-affa-a8abb07840c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
3a96b32a-5c2f-406b-8760-5d86f0af0b57,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,Bordetella pertussis,False,Bordetella pertussis,,,,
4c39d2e5-fbb1-43eb-bf99-916258ebd5ac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"After inhalation, B. pertussis attaches to airway cells through a variety of adhesion molecules. The organism then releases cytotoxins that cause loss of protective respiratory cells and promote microaspiration and a distinct and prolonged cough. Pertussis’s nickname of whooping cough comes from the distinct inspiratory noise. The paroxysmal stage of pertussis (that involving cough) can last between two and ten weeks, and this prolongation is likely due to the bacteria penetrating deeper regions of the lung (the cytotoxins have been found in alveolar macrophages). The disease can be life threatening to infants, but widespread vaccinations started in the forties dramatically reduced its incidence.",True,Bordetella pertussis,,,,
347ebcb0-0ce2-4446-8d96-34cc696e3f3c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,Haemophilus influenzae,False,Haemophilus influenzae,,,,
16f44c4e-c22e-46a0-b2e1-632a8cd8d046,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"The outer coat of the H. influenzae contains several proteins that attach to upper airway cells and specifically promote pharyngeal and the middle ear colonization. The outer coat also acts as an endotoxin and elicits a potent inflammatory response to produce the symptoms of the infection. Prior to routine vaccination, vascular invasion by the pathogen could produce metastatic foci including meningitis, septic arthritis, osteomyelitis, and cellulitis. Today, while upper airway infection can lead to pneumonia, the incidence of bacteremia is low.",True,Haemophilus influenzae,,,,
de184c02-a9ed-44dc-aaf7-aaa0d7477c46,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,Text,False,Text,,,,
4ef17b05-a401-4274-ab34-04356b02b5bc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Pharyngitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-3,"Thomas, Micah, and Paul A. Bomar. Upper Respiratory Tract Infection. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532961, CC BY 4.0.",True,Text,,,,
b41592f1-2ddf-4352-b52b-0f4a4166c059,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"As with most URIs the common cold is caused by a viral infection, and although there are several different viral candidates for causing a common cold, the pathophysiological mechanism and symptoms are the same regardless of the type. This is because it is the innate immune response, rather than the direct infection, that is responsible for most of the symptoms.",True,Text,,,,
b5a77618-d079-456e-99ad-e48fc1d0cd4c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,URIs,False,URIs,,,,
c6db294a-559e-4780-bc18-5e2b7ea1a7eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
c6db294a-559e-4780-bc18-5e2b7ea1a7eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
c6db294a-559e-4780-bc18-5e2b7ea1a7eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
c6db294a-559e-4780-bc18-5e2b7ea1a7eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
c6db294a-559e-4780-bc18-5e2b7ea1a7eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
c6db294a-559e-4780-bc18-5e2b7ea1a7eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
7db74434-f457-40c9-8bd3-fe54cef7c0c6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Once in the upper airway, and if the pathogen can breach the innate defenses here (mucus and the mucociliary escalator), the virus attaches to, and then enters, the epithelial cells. In response, the invaded epithelial cells release cytokines to instigate an immune response. The primary cytokine released in this scenario is IL-8, which causes the attraction and accumulation of polymorphonuclear cells (PMN).",True,URIs,,,,
94299437-65ea-4490-bb61-d07923b6177e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"It is the substantial increase in PMN cells that is responsible for most of the symptoms of a common cold—runny nose, postnasal drip, and other signs of epithelial inflammation.",True,URIs,,,,
4ab2201c-bcda-48ec-bb3a-0df56ebcb49f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"By far the most common cause of the common cold is the rhinovirus, followed by coronavirus and influenza, then less frequently by parainfluenza respiratory syncytial virus (RSV), and then rarely by adenovirus or enterovirus (table 2.1).",True,URIs,,,,
dd98a37b-9e64-421d-9986-6352f4b32b53,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,Table 2.1: The viral pathogens.,True,URIs,,,,
57fc6b16-0564-4d12-9664-2fe6344c1487,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Seasonal differences (table 2.1) in the prevalence of these pathogens might help you identify the causal agent, but as the viral infections are self-limiting it is more important to ensure there is no bacterial involvement.",True,URIs,,,,
b145d71b-8bfc-413b-a253-764d535ee0db,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"A viral infection can progress and cause more specific conditions than a cold, and these are identified by their location.",True,URIs,,,,
78087952-a718-4a52-adae-b35e24a7e459,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,Rhinosinusitis,False,Rhinosinusitis,,,,
8689a02f-f56b-46a1-8ba4-4ce1b2566a6d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Rhinosinusitis is most commonly caused by a viral infection, and despite popular belief is only rarely associated with a concurrent bacterial infection in adults. The lining of the nasal and sinus cavities becomes inflamed, again as a result of the immune response rather than a direct effect of the virus. The congestion can be painful, but symptoms can be treated with over-the-counter analgesics. Like the common cold, the condition is self-limiting and normally resolves in seven to ten days.",True,Rhinosinusitis,,,,
3c27d6da-cb07-4758-acb6-51790613a183,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,Pharyngitis,False,Pharyngitis,,,,
c0363a2a-554f-4722-ba69-0817bf3eae82,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"When the pharynx is involved the local inflammation will cause the patient to present with a sore throat and a hoarse voice. Pharyngitis is most commonly caused by viral infection, but more serious bacterial infections (e.g., Streptococcus) should be considered. The two infection types are easily distinguished with tonsillar exudate and petechial mottling of the soft palate being present in a bacterial infection, but absent in a viral infection. Treatment of viral pharyngitis is limited to symptom relief, and antibiotics should be avoided.",True,Pharyngitis,,,,
2106ed23-7a09-49df-a9e3-3cf84623b6ee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,Viral Croup,False,Viral Croup,,,,
9b122515-1947-48fc-8da9-5c1bc6012858,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
9b122515-1947-48fc-8da9-5c1bc6012858,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
9b122515-1947-48fc-8da9-5c1bc6012858,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
9b122515-1947-48fc-8da9-5c1bc6012858,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
9b122515-1947-48fc-8da9-5c1bc6012858,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
9b122515-1947-48fc-8da9-5c1bc6012858,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
e60bcfe9-4f7c-4c39-a679-8ca4f636a78d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,Bacterial Infection of the Upper Airway,False,Bacterial Infection of the Upper Airway,,,,
28209f40-ed1a-4df3-beb7-57c6854e96fd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"The induction of upper airway infection by bacteria is similar to that by virus with droplet inhalation or hand-to-mouth or nose contact. Cell adherence is usually promoted by bacterial properties, but it is bacterial toxins that instigate the signs and symptoms of infection rather than the innate immune system. We will now cover four bacteria that are capable of causing an upper airway infection.",True,Bacterial Infection of the Upper Airway,,,,
4858b6ed-2861-461c-abba-02525b837d43,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,Group A Streptococcus,False,Group A Streptococcus,,,,
5e61b96b-88a2-404b-80c1-70f98463514d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"The pathogenic mechanisms of Group A Streptococcus are poorly understood—partly because of the numerous and complex ways it interacts with its human host. Its coat protects it from phagocytosis, antibody binding, and opsonization. It is capable of releasing a cocktail of cell-lysing toxins as well as pyrogenic exotoxins that:",True,Group A Streptococcus,,,,
d6f7b46d-b805-4477-9a11-0612adba9a1b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
d6f7b46d-b805-4477-9a11-0612adba9a1b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
d6f7b46d-b805-4477-9a11-0612adba9a1b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
d6f7b46d-b805-4477-9a11-0612adba9a1b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
d6f7b46d-b805-4477-9a11-0612adba9a1b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
d6f7b46d-b805-4477-9a11-0612adba9a1b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
b470ff4b-bd5b-4607-aa00-a43bb7405065,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,Corynebacterium diphtheriae,False,Corynebacterium diphtheriae,,,,
fd489ea4-9e6e-43db-bf6d-e19ebfc74f66,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
fd489ea4-9e6e-43db-bf6d-e19ebfc74f66,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
fd489ea4-9e6e-43db-bf6d-e19ebfc74f66,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
fd489ea4-9e6e-43db-bf6d-e19ebfc74f66,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
fd489ea4-9e6e-43db-bf6d-e19ebfc74f66,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
fd489ea4-9e6e-43db-bf6d-e19ebfc74f66,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
b2046990-ec07-41e3-9e5f-f7eb9e8e47fe,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,Bordetella pertussis,False,Bordetella pertussis,,,,
5e6a6077-111c-4b39-aa4b-8ffe422a021d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"After inhalation, B. pertussis attaches to airway cells through a variety of adhesion molecules. The organism then releases cytotoxins that cause loss of protective respiratory cells and promote microaspiration and a distinct and prolonged cough. Pertussis’s nickname of whooping cough comes from the distinct inspiratory noise. The paroxysmal stage of pertussis (that involving cough) can last between two and ten weeks, and this prolongation is likely due to the bacteria penetrating deeper regions of the lung (the cytotoxins have been found in alveolar macrophages). The disease can be life threatening to infants, but widespread vaccinations started in the forties dramatically reduced its incidence.",True,Bordetella pertussis,,,,
5be6b37f-aeb1-4c74-8626-4d637c70734c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,Haemophilus influenzae,False,Haemophilus influenzae,,,,
6e2be9ef-d521-4edf-98e0-caaad9f70c27,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"The outer coat of the H. influenzae contains several proteins that attach to upper airway cells and specifically promote pharyngeal and the middle ear colonization. The outer coat also acts as an endotoxin and elicits a potent inflammatory response to produce the symptoms of the infection. Prior to routine vaccination, vascular invasion by the pathogen could produce metastatic foci including meningitis, septic arthritis, osteomyelitis, and cellulitis. Today, while upper airway infection can lead to pneumonia, the incidence of bacteremia is low.",True,Haemophilus influenzae,,,,
7ecde184-4b70-490e-9b4b-fa88625164d2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,Text,False,Text,,,,
75ceb77c-3c0d-4e7c-8ae2-cb4301a103db,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Rhinosinusitis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-2,"Thomas, Micah, and Paul A. Bomar. Upper Respiratory Tract Infection. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532961, CC BY 4.0.",True,Text,,,,
1dda4c96-acdd-4287-be17-43e851131ca7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"As with most URIs the common cold is caused by a viral infection, and although there are several different viral candidates for causing a common cold, the pathophysiological mechanism and symptoms are the same regardless of the type. This is because it is the innate immune response, rather than the direct infection, that is responsible for most of the symptoms.",True,Text,,,,
b5ca4dd7-2fba-4928-8a64-4917639ee1cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,URIs,False,URIs,,,,
02d36acc-1e1d-4755-800c-0efac5d38e4a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
02d36acc-1e1d-4755-800c-0efac5d38e4a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
02d36acc-1e1d-4755-800c-0efac5d38e4a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
02d36acc-1e1d-4755-800c-0efac5d38e4a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
02d36acc-1e1d-4755-800c-0efac5d38e4a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
02d36acc-1e1d-4755-800c-0efac5d38e4a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
eb833318-f806-416a-9329-7ab81ad1a896,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Once in the upper airway, and if the pathogen can breach the innate defenses here (mucus and the mucociliary escalator), the virus attaches to, and then enters, the epithelial cells. In response, the invaded epithelial cells release cytokines to instigate an immune response. The primary cytokine released in this scenario is IL-8, which causes the attraction and accumulation of polymorphonuclear cells (PMN).",True,URIs,,,,
7d2b8024-22fd-43a3-aa5d-1a7a7ecb6756,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"It is the substantial increase in PMN cells that is responsible for most of the symptoms of a common cold—runny nose, postnasal drip, and other signs of epithelial inflammation.",True,URIs,,,,
ffdc4d16-2b58-4673-85fd-ae1416093f6b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"By far the most common cause of the common cold is the rhinovirus, followed by coronavirus and influenza, then less frequently by parainfluenza respiratory syncytial virus (RSV), and then rarely by adenovirus or enterovirus (table 2.1).",True,URIs,,,,
57ced738-df6a-4399-a92a-da8700cdf533,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,Table 2.1: The viral pathogens.,True,URIs,,,,
418f0b10-45f9-4bec-8bc6-71c20ed4d1b4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Seasonal differences (table 2.1) in the prevalence of these pathogens might help you identify the causal agent, but as the viral infections are self-limiting it is more important to ensure there is no bacterial involvement.",True,URIs,,,,
a8a50f05-1658-4838-b00b-da9735f12273,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"A viral infection can progress and cause more specific conditions than a cold, and these are identified by their location.",True,URIs,,,,
8201c553-392c-406a-99d4-152186ebe35a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,Rhinosinusitis,False,Rhinosinusitis,,,,
90c8aca6-399b-4407-828d-0a62d09ed78d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Rhinosinusitis is most commonly caused by a viral infection, and despite popular belief is only rarely associated with a concurrent bacterial infection in adults. The lining of the nasal and sinus cavities becomes inflamed, again as a result of the immune response rather than a direct effect of the virus. The congestion can be painful, but symptoms can be treated with over-the-counter analgesics. Like the common cold, the condition is self-limiting and normally resolves in seven to ten days.",True,Rhinosinusitis,,,,
843f80fe-aeb6-4d90-b58e-78a9567b9836,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,Pharyngitis,False,Pharyngitis,,,,
0816e8c6-fc2a-4532-8fa9-ec574a252498,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"When the pharynx is involved the local inflammation will cause the patient to present with a sore throat and a hoarse voice. Pharyngitis is most commonly caused by viral infection, but more serious bacterial infections (e.g., Streptococcus) should be considered. The two infection types are easily distinguished with tonsillar exudate and petechial mottling of the soft palate being present in a bacterial infection, but absent in a viral infection. Treatment of viral pharyngitis is limited to symptom relief, and antibiotics should be avoided.",True,Pharyngitis,,,,
1aa34789-7e37-4db5-848b-c60ab5bd4c7a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,Viral Croup,False,Viral Croup,,,,
e3efa4da-f782-49c6-ad3e-0b7e9afdbc07,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
e3efa4da-f782-49c6-ad3e-0b7e9afdbc07,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
e3efa4da-f782-49c6-ad3e-0b7e9afdbc07,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
e3efa4da-f782-49c6-ad3e-0b7e9afdbc07,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
e3efa4da-f782-49c6-ad3e-0b7e9afdbc07,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
e3efa4da-f782-49c6-ad3e-0b7e9afdbc07,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
7a0962e2-e933-4225-934c-d48acdc8ac9a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,Bacterial Infection of the Upper Airway,False,Bacterial Infection of the Upper Airway,,,,
639c16f9-2cce-4ee3-98d5-3c0f285c74f0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"The induction of upper airway infection by bacteria is similar to that by virus with droplet inhalation or hand-to-mouth or nose contact. Cell adherence is usually promoted by bacterial properties, but it is bacterial toxins that instigate the signs and symptoms of infection rather than the innate immune system. We will now cover four bacteria that are capable of causing an upper airway infection.",True,Bacterial Infection of the Upper Airway,,,,
0ad4e1d5-27f3-4a57-bf0d-8bfa046e3595,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,Group A Streptococcus,False,Group A Streptococcus,,,,
294e79f2-e202-4220-b0f5-3e20519eead1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"The pathogenic mechanisms of Group A Streptococcus are poorly understood—partly because of the numerous and complex ways it interacts with its human host. Its coat protects it from phagocytosis, antibody binding, and opsonization. It is capable of releasing a cocktail of cell-lysing toxins as well as pyrogenic exotoxins that:",True,Group A Streptococcus,,,,
d9a5328c-3c8e-42c5-acd6-a0473d17e477,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
d9a5328c-3c8e-42c5-acd6-a0473d17e477,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
d9a5328c-3c8e-42c5-acd6-a0473d17e477,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
d9a5328c-3c8e-42c5-acd6-a0473d17e477,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
d9a5328c-3c8e-42c5-acd6-a0473d17e477,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
d9a5328c-3c8e-42c5-acd6-a0473d17e477,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
e9eef841-3877-4952-b254-d15353cb1740,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,Corynebacterium diphtheriae,False,Corynebacterium diphtheriae,,,,
544d4638-86e2-4c3f-ab03-88f83dfe66fb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
544d4638-86e2-4c3f-ab03-88f83dfe66fb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
544d4638-86e2-4c3f-ab03-88f83dfe66fb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
544d4638-86e2-4c3f-ab03-88f83dfe66fb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
544d4638-86e2-4c3f-ab03-88f83dfe66fb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
544d4638-86e2-4c3f-ab03-88f83dfe66fb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
9298c38c-1bbc-44a8-89ee-583609e8935a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,Bordetella pertussis,False,Bordetella pertussis,,,,
697e1cab-af8f-4692-830e-e08f5a987f66,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"After inhalation, B. pertussis attaches to airway cells through a variety of adhesion molecules. The organism then releases cytotoxins that cause loss of protective respiratory cells and promote microaspiration and a distinct and prolonged cough. Pertussis’s nickname of whooping cough comes from the distinct inspiratory noise. The paroxysmal stage of pertussis (that involving cough) can last between two and ten weeks, and this prolongation is likely due to the bacteria penetrating deeper regions of the lung (the cytotoxins have been found in alveolar macrophages). The disease can be life threatening to infants, but widespread vaccinations started in the forties dramatically reduced its incidence.",True,Bordetella pertussis,,,,
691424c3-6548-4842-93d8-4e0e62ed7281,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,Haemophilus influenzae,False,Haemophilus influenzae,,,,
1604379b-56da-48de-9954-2e8597a74fb0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"The outer coat of the H. influenzae contains several proteins that attach to upper airway cells and specifically promote pharyngeal and the middle ear colonization. The outer coat also acts as an endotoxin and elicits a potent inflammatory response to produce the symptoms of the infection. Prior to routine vaccination, vascular invasion by the pathogen could produce metastatic foci including meningitis, septic arthritis, osteomyelitis, and cellulitis. Today, while upper airway infection can lead to pneumonia, the incidence of bacteremia is low.",True,Haemophilus influenzae,,,,
79de9648-1100-4419-90eb-519338424e47,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,Text,False,Text,,,,
6514bc9f-0432-4666-9947-a645e726e6a2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,The Common Cold,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/#chapter-27-section-1,"Thomas, Micah, and Paul A. Bomar. Upper Respiratory Tract Infection. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532961, CC BY 4.0.",True,Text,,,,
5864f6ba-a43f-492d-8f04-3eb1da68e425,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"As with most URIs the common cold is caused by a viral infection, and although there are several different viral candidates for causing a common cold, the pathophysiological mechanism and symptoms are the same regardless of the type. This is because it is the innate immune response, rather than the direct infection, that is responsible for most of the symptoms.",True,Text,,,,
0e748548-4f2d-487c-9fec-d2d546e6264b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,URIs,False,URIs,,,,
3325d695-1b49-4c2c-bd61-f6bd5a061e1e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
3325d695-1b49-4c2c-bd61-f6bd5a061e1e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
3325d695-1b49-4c2c-bd61-f6bd5a061e1e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
3325d695-1b49-4c2c-bd61-f6bd5a061e1e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
3325d695-1b49-4c2c-bd61-f6bd5a061e1e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
3325d695-1b49-4c2c-bd61-f6bd5a061e1e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Looking at the sequence of events involved in “getting a cold” (figure 2.2), we start with delivery of the pathogen to the upper airway and inoculation. The most common modes of delivery are hand-to-nose or hand-to-mouth contact or inhalation of aerosolized nasal fluid produced from a sneeze of an infected person. The causal virus is rarely found in saliva, so infection is spread from snot not spit.",True,URIs,Figure 2.2,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
0f56d278-9f15-4a2b-b6ed-bca3b4d46b3e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Once in the upper airway, and if the pathogen can breach the innate defenses here (mucus and the mucociliary escalator), the virus attaches to, and then enters, the epithelial cells. In response, the invaded epithelial cells release cytokines to instigate an immune response. The primary cytokine released in this scenario is IL-8, which causes the attraction and accumulation of polymorphonuclear cells (PMN).",True,URIs,,,,
5ce6875b-c6a8-4c48-8e1d-c0debf63d54a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"It is the substantial increase in PMN cells that is responsible for most of the symptoms of a common cold—runny nose, postnasal drip, and other signs of epithelial inflammation.",True,URIs,,,,
89dc9dee-e665-4d1b-a33b-364be45f6b26,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"By far the most common cause of the common cold is the rhinovirus, followed by coronavirus and influenza, then less frequently by parainfluenza respiratory syncytial virus (RSV), and then rarely by adenovirus or enterovirus (table 2.1).",True,URIs,,,,
58c21548-13d8-4808-8a43-75bb2d483035,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,Table 2.1: The viral pathogens.,True,URIs,,,,
d3f9ee0b-679a-49fd-b1d5-b5b27bac2221,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Seasonal differences (table 2.1) in the prevalence of these pathogens might help you identify the causal agent, but as the viral infections are self-limiting it is more important to ensure there is no bacterial involvement.",True,URIs,,,,
f285f099-4f4f-44da-967e-aad9c363ba68,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"A viral infection can progress and cause more specific conditions than a cold, and these are identified by their location.",True,URIs,,,,
4e77d7a7-1218-48c4-9a63-d7f298747151,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,Rhinosinusitis,False,Rhinosinusitis,,,,
91cc7cca-8a38-4690-a53e-3974a3cdab8a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Rhinosinusitis is most commonly caused by a viral infection, and despite popular belief is only rarely associated with a concurrent bacterial infection in adults. The lining of the nasal and sinus cavities becomes inflamed, again as a result of the immune response rather than a direct effect of the virus. The congestion can be painful, but symptoms can be treated with over-the-counter analgesics. Like the common cold, the condition is self-limiting and normally resolves in seven to ten days.",True,Rhinosinusitis,,,,
06ca6888-1290-4b98-9756-464b6832d9b9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,Pharyngitis,False,Pharyngitis,,,,
0cbf7737-cd80-416e-86d4-b76c4e1f368d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"When the pharynx is involved the local inflammation will cause the patient to present with a sore throat and a hoarse voice. Pharyngitis is most commonly caused by viral infection, but more serious bacterial infections (e.g., Streptococcus) should be considered. The two infection types are easily distinguished with tonsillar exudate and petechial mottling of the soft palate being present in a bacterial infection, but absent in a viral infection. Treatment of viral pharyngitis is limited to symptom relief, and antibiotics should be avoided.",True,Pharyngitis,,,,
80785ef1-ae2f-4f4b-a0a0-c0adc82c88e1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,Viral Croup,False,Viral Croup,,,,
f66311a8-5cfe-422c-8c81-16863d4d3b3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
f66311a8-5cfe-422c-8c81-16863d4d3b3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
f66311a8-5cfe-422c-8c81-16863d4d3b3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
f66311a8-5cfe-422c-8c81-16863d4d3b3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
f66311a8-5cfe-422c-8c81-16863d4d3b3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
f66311a8-5cfe-422c-8c81-16863d4d3b3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Involvement of the larynx and subglottic airway will produce croup. There are numerous causes of croup and subclassifications depending on the region involved. Viral croup, like other forms, involves inflammation of the larynx that causes the airway to narrow. Edematous airway walls form an upper airway obstruction that produces stridor. Stridor is a crow-like airway sound, and the phase of breathing that it appears in can be helpful in determining the site of obstruction. Stridor during inspiration is indicative of airway collapse above the vocal cords (i.e., extrathoracic), and expiratory stridor suggests a tracheal or bronchial obstruction (i.e., intrathoracic). The constriction of the airway can be seen on x-ray when severe and the narrowing produces a characteristic “steeple” sign in the trachea (see figure 2.3).",True,Viral Croup,Figure 2.3,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.3.jpeg,Figure 2.3: An x-ray of the upper airway of a child suffering from tracheal croup. The arrow points to a narrowing of the trachea that produces a characteristic “steeple” sign as the constriction looks like the pointed steeple of a church building.
85f5e01d-f446-479b-894c-b51fd49fa836,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,Bacterial Infection of the Upper Airway,False,Bacterial Infection of the Upper Airway,,,,
b9a54d70-9cea-40af-9b01-3c7b6165b65a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"The induction of upper airway infection by bacteria is similar to that by virus with droplet inhalation or hand-to-mouth or nose contact. Cell adherence is usually promoted by bacterial properties, but it is bacterial toxins that instigate the signs and symptoms of infection rather than the innate immune system. We will now cover four bacteria that are capable of causing an upper airway infection.",True,Bacterial Infection of the Upper Airway,,,,
443464d0-7f0e-4c5a-a31d-c16a9f9d4ef6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,Group A Streptococcus,False,Group A Streptococcus,,,,
deffae4a-fe49-4cf7-bec9-3a7f82c84ba5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"The pathogenic mechanisms of Group A Streptococcus are poorly understood—partly because of the numerous and complex ways it interacts with its human host. Its coat protects it from phagocytosis, antibody binding, and opsonization. It is capable of releasing a cocktail of cell-lysing toxins as well as pyrogenic exotoxins that:",True,Group A Streptococcus,,,,
24a9f237-cb6c-4927-bd4d-a44dbe073f32,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
24a9f237-cb6c-4927-bd4d-a44dbe073f32,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
24a9f237-cb6c-4927-bd4d-a44dbe073f32,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
24a9f237-cb6c-4927-bd4d-a44dbe073f32,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
24a9f237-cb6c-4927-bd4d-a44dbe073f32,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
24a9f237-cb6c-4927-bd4d-a44dbe073f32,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"In terms of the upper airway it is the leading cause of tonsillopharyngitis in both adults and children. A sore throat may be accompanied by fever, headache, and vomiting. Inflamed tonsils and uvula may be coated in exudates, and palatal petechiae (figure 2.4) may be be present as well as a scarlatiniform rash. Symptoms resolve in three to five days, but antibiotic therapy should be used to reduce the risk of complications that include peritonsillar cellulitis, otitis media, sinusitis, and even acute rheumatic fever.",True,Group A Streptococcus,Figure 2.4,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
5d79bad9-6a54-4941-8e13-4d26c2e1c60c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,Corynebacterium diphtheriae,False,Corynebacterium diphtheriae,,,,
36fde283-5d2a-4d1e-a90c-c6c633ee1afc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Bacterial Infection of the Upper Airway,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
36fde283-5d2a-4d1e-a90c-c6c633ee1afc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Viral Croup,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
36fde283-5d2a-4d1e-a90c-c6c633ee1afc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Pharyngitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
36fde283-5d2a-4d1e-a90c-c6c633ee1afc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,Rhinosinusitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
36fde283-5d2a-4d1e-a90c-c6c633ee1afc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,The Common Cold,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
36fde283-5d2a-4d1e-a90c-c6c633ee1afc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"After inoculation, C. diphtheriae releases diphtheria exotoxin and enters the cell by exploiting a membrane receptor. Once inside, the exotoxin inactivates elongation factor 2, halting protein production and causing cell death. Occurrence of diphtheria is now rare in developed countries because of vaccination programs, but infection produces sore throat, swelling of cervical lymph glands, and low-grade fever. Most cases are tonsillopharyngeal where a pseudomembrane and exudate (figure 2.5) is produced that can spread to other areas. In severe cases the spread can lead to the bull neck of diphtheria (figure 2.5) as swelling and pseudomembranes accumulate and swallowing can become difficult. If the infection becomes systemic, cardiac, neural, and renal issues may arise, including myocarditis, local neuropathies, and in severe cases renal failure.",True,Corynebacterium diphtheriae,Figure 2.5,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.5.png,Figure 2.5: Clinical signs of C. diphtheriae: pseudomembrane exudate (left) and bull neck (right).
dc29832d-bddd-43fb-9cea-534992a4eeac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,Bordetella pertussis,False,Bordetella pertussis,,,,
838c0e9a-6b32-4d80-96e1-6ca7e4220e9a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"After inhalation, B. pertussis attaches to airway cells through a variety of adhesion molecules. The organism then releases cytotoxins that cause loss of protective respiratory cells and promote microaspiration and a distinct and prolonged cough. Pertussis’s nickname of whooping cough comes from the distinct inspiratory noise. The paroxysmal stage of pertussis (that involving cough) can last between two and ten weeks, and this prolongation is likely due to the bacteria penetrating deeper regions of the lung (the cytotoxins have been found in alveolar macrophages). The disease can be life threatening to infants, but widespread vaccinations started in the forties dramatically reduced its incidence.",True,Bordetella pertussis,,,,
3b505ce6-468d-4cad-9cc9-0d348a7c32bc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,Haemophilus influenzae,False,Haemophilus influenzae,,,,
acb1420d-5844-4f97-9aab-145604b59e9a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"The outer coat of the H. influenzae contains several proteins that attach to upper airway cells and specifically promote pharyngeal and the middle ear colonization. The outer coat also acts as an endotoxin and elicits a potent inflammatory response to produce the symptoms of the infection. Prior to routine vaccination, vascular invasion by the pathogen could produce metastatic foci including meningitis, septic arthritis, osteomyelitis, and cellulitis. Today, while upper airway infection can lead to pneumonia, the incidence of bacteremia is low.",True,Haemophilus influenzae,,,,
99467da9-1291-42e4-a602-bbefd08ebb61,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,Text,False,Text,,,,
a7ead140-9bb9-4ea4-ad0a-334f96b8ea5e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,2. Upper Airway Infections,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/upper-airway-infections/,"Thomas, Micah, and Paul A. Bomar. Upper Respiratory Tract Infection. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532961, CC BY 4.0.",True,Text,,,,
fc7ec5d0-c678-4556-971c-1fdf56177f67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
fc7ec5d0-c678-4556-971c-1fdf56177f67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
fc7ec5d0-c678-4556-971c-1fdf56177f67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
fc7ec5d0-c678-4556-971c-1fdf56177f67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
fc7ec5d0-c678-4556-971c-1fdf56177f67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
5257cee7-51ab-414b-b5ce-f379a71ee95f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,We will also look at how exercise and certain pharmacological agents can produce asthma.,True,Text,,,,
fbf759df-934f-4ba5-9987-deb818c57280,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
fbf759df-934f-4ba5-9987-deb818c57280,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
fbf759df-934f-4ba5-9987-deb818c57280,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
fbf759df-934f-4ba5-9987-deb818c57280,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
fbf759df-934f-4ba5-9987-deb818c57280,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
599e5a4c-1511-40fc-b5e3-7a46fd760407,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,proinflammatory,False,proinflammatory,,,,
9403cfd2-ebde-42f9-a224-89717149c0c8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,The results of this cocktail’s release are the hallmarks of asthma:,True,proinflammatory,,,,
63c4f3fd-ee46-4636-86bd-254ef135edf6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The timeline from the exposure to the antigen to asthmatic response is not straightforward. A response may occur within minutes (“early response”), or hours later (“late response”). Some patients show only an early response, some only a late one, and some show both in a “dual” response. The late response may correspond to the arrival of leucocytes in response to the initial release of cytokines. It may also be due to a mild stimulus arriving later in an airway that was sensitized earlier.",True,proinflammatory,,,,
5ae6e870-08ae-4364-8f65-65722fd3bbf1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
5ae6e870-08ae-4364-8f65-65722fd3bbf1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
5ae6e870-08ae-4364-8f65-65722fd3bbf1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
5ae6e870-08ae-4364-8f65-65722fd3bbf1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
5ae6e870-08ae-4364-8f65-65722fd3bbf1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
302d3114-64ae-41b8-8183-aca19772daa3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
302d3114-64ae-41b8-8183-aca19772daa3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
302d3114-64ae-41b8-8183-aca19772daa3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
302d3114-64ae-41b8-8183-aca19772daa3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
302d3114-64ae-41b8-8183-aca19772daa3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
3fd37337-9e1e-405b-a12d-12309bb29ada,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The cholinergic response may help produce an asthmatic response to another stimulus that normally would not have produced one (i.e., it may play a part in the hypersensitivity of the asthmatic airways). Likewise, the presence of an infection, particularly a viral infection, may place the airway in a proinflammatory state.",True,proinflammatory,,,,
8a63cccf-ca7b-410b-a20c-45c4d45b3743,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
8a63cccf-ca7b-410b-a20c-45c4d45b3743,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
8a63cccf-ca7b-410b-a20c-45c4d45b3743,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
8a63cccf-ca7b-410b-a20c-45c4d45b3743,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
8a63cccf-ca7b-410b-a20c-45c4d45b3743,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
7fb4e653-c7a8-4681-b61d-029242e94098,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Exercise-induced asthma: Although exercise is associated with increased airway caliber, it can also induce asthma. Increased airway flow to meet the increased metabolic demand of exercise results in loss of fluid and heat from airway surfaces. This leaves the peribronchial fluid in a hypertonic state and causes excitation of the irritant airway receptors, which leads to release of the mast cells’ cocktail.",True,proinflammatory,,,,
65f28ac8-49a8-498c-b6bb-2bfa734c1f6e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Exercise-induced asthma is more prevalent in cold (i.e. dry air) where water loss will be higher, so occurs more in sports such as cross-country skiing than swimming in a warm humid environment. Bronchoconstriction usually occurs when exercise stops—when the protective effect of sympathetic activity to the airway smooth muscles ceases.",True,proinflammatory,,,,
a09ded15-2746-415c-a59c-bbbda3c9bb0e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Drug-induced asthma: There are several pharmaceutical and food products that can promote asthma, including tartrazine (a yellow food coloring) and sulfides used as food preservatives. Additionally, 10 to 20 percent of asthmatics are sensitive to aspirin.",True,proinflammatory,,,,
210444a3-7639-4c7d-a3c6-2ccacaada374,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
210444a3-7639-4c7d-a3c6-2ccacaada374,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
210444a3-7639-4c7d-a3c6-2ccacaada374,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
210444a3-7639-4c7d-a3c6-2ccacaada374,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
210444a3-7639-4c7d-a3c6-2ccacaada374,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
6455b9cb-3f00-467a-9e70-4d28360886e5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Environmental/occupational asthma: As the airway is open to the environment, it is susceptible to inhaled substances that can cause sensitization; there are over two hundred substances known to cause asthma, both organic and inorganic. Some common ones are listed below.",True,proinflammatory,,,,
047df8a3-3958-4a52-a01f-7b69cc7475ff,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Table 1.1: Some of the most common environmental causes of asthma. Taking a pulmonary history should include asking about potential environmental exposures.,True,proinflammatory,,,,
5b3bd0da-eb35-4624-b0a3-d90f9074bb62,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Determining whether airway hypersensitivity is due to environmental factors is complicated by widely varying latency periods. Short latency periods can be as brief as twenty-four hours and are associated with vapor or smoke exposure that does not cause an immunological response. Longer latency periods that may last years are more commonly associated with an immunological response to large particles that act like antigens.,True,proinflammatory,,,,
e0159ef2-2eec-4bae-836c-8c9b1b80a7dc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The situation is further confused by occupation-related responses, which often cause the airway to become more sensitive to some of the other causes of asthma covered here. This makes the role of an environmental factor more difficult to determine.",True,proinflammatory,,,,
ad756858-ab3a-4120-8722-def595ee09a5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Pathophysiology of Asthma,False,Pathophysiology of Asthma,,,,
097ec5df-dd0e-408e-a729-5850a903e263,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
097ec5df-dd0e-408e-a729-5850a903e263,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
097ec5df-dd0e-408e-a729-5850a903e263,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
097ec5df-dd0e-408e-a729-5850a903e263,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
097ec5df-dd0e-408e-a729-5850a903e263,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
c47f79de-4ee0-4513-8306-9f155e88c752,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
c47f79de-4ee0-4513-8306-9f155e88c752,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
c47f79de-4ee0-4513-8306-9f155e88c752,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
c47f79de-4ee0-4513-8306-9f155e88c752,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
c47f79de-4ee0-4513-8306-9f155e88c752,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
65a1b979-d155-41e2-9cca-a8018cbe9cb8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
65a1b979-d155-41e2-9cca-a8018cbe9cb8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
65a1b979-d155-41e2-9cca-a8018cbe9cb8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
65a1b979-d155-41e2-9cca-a8018cbe9cb8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
65a1b979-d155-41e2-9cca-a8018cbe9cb8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
92854127-014f-41fd-a517-c1814b0aafbb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
92854127-014f-41fd-a517-c1814b0aafbb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
92854127-014f-41fd-a517-c1814b0aafbb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
92854127-014f-41fd-a517-c1814b0aafbb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
92854127-014f-41fd-a517-c1814b0aafbb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
ec813426-d647-4b36-8367-04d914eec7ec,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Clinical Presentation of Asthma,False,Clinical Presentation of Asthma,,,,
4580d001-127d-4038-bcb0-87a588b04fb0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"One useful diagnostic element of asthma is its episodic or acute behavior. However, as patients may be asymptomatic between attacks, the severity of asthma can be difficult to determine without performing bronchial challenge tests.",True,Clinical Presentation of Asthma,,,,
9749b941-584e-42d8-944a-ef58e9aff4ed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
9749b941-584e-42d8-944a-ef58e9aff4ed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
9749b941-584e-42d8-944a-ef58e9aff4ed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
9749b941-584e-42d8-944a-ef58e9aff4ed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
9749b941-584e-42d8-944a-ef58e9aff4ed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
48ac981b-61b0-4a77-b2f4-33fd1bcebd77,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"As airway resistance increases, the accessory muscles are deployed to maintain sufficient airflow through the narrowing airways, and the patient experiences an increased effort to breathe. Increased expiratory efforts produce dynamic airway collapse and lead to hyperinflation. Further decreases in airway caliber result in insufficient alveolar ventilation and deranged blood gases. The sensation reported at this point is air hunger. Once the patient is severely bronchoconstricted, delivery of inhaled therapies is much more difficult, and mechanical ventilation to support the respiratory muscles becomes complicated. Other signs present during a severe attack are raised heart (tachycardia) and breathing (tachypnea) rates as well as a paradoxical pulse (i.e., a rise in blood pressure during expiration).",True,Clinical Presentation of Asthma,,,,
663afe60-899e-40ce-a85c-3fca6c6c6eb1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
663afe60-899e-40ce-a85c-3fca6c6c6eb1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
663afe60-899e-40ce-a85c-3fca6c6c6eb1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
663afe60-899e-40ce-a85c-3fca6c6c6eb1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
663afe60-899e-40ce-a85c-3fca6c6c6eb1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
9a382f8f-4157-4d04-8714-04868c4b5bc6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Chronic Obstructive Pulmonary Disease,False,Chronic Obstructive Pulmonary Disease,,,,
2c66bf8c-8e8b-48d9-b6b6-1f58a75dc8bf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Although chronic bronchitis and emphysema have different underlying pathologies, they frequently have the same root cause and are often found together in a patient. In brief, chronic bronchitis is associated with an increase in mucus production, while emphysema involves disruption of the lung structure.",True,Chronic Obstructive Pulmonary Disease,,,,
a71a0984-5f66-4bcf-b5f3-2dbcfcdd20dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The relative role of chronic bronchitis in COPD has diminished since the Clean Air Act reduced atmospheric sulphur dioxide, but with 90 percent of COPD caused by cigarette smoking there is still plenty of bronchitis and emphysema to treat—at enormous cost to the health system from over eight million hospitalizations a year that are mostly paid for by Medicare. The COPD patient tends to be older and poorer and will likely have comorbidities, the most common of which is hypertension. What is perhaps more disturbing is that of the most common causes of death, COPD is the only one whose incidence continues to rise.",True,Chronic Obstructive Pulmonary Disease,,,,
5388bea8-f0ed-4ba6-ae0f-cdc4a122d9af,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"We will now look at the underlying mechanisms of COPD. Despite the fact it is usually composed of some elements of both chronic bronchitis and emphysema, we will deal with each separately for the sake of simplicity.",True,Chronic Obstructive Pulmonary Disease,,,,
00227ab3-84b1-4041-bea4-4567cacb37e0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Chronic Bronchitis,False,Chronic Bronchitis,,,,
c7b77aef-bf23-437e-9c38-10f3e5de0d04,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Chronic bronchitis is clinically defined as a persistent and productive cough that lasts for at least three months per year for two consecutive years.,True,Chronic Bronchitis,,,,
416a3eeb-8aba-4a5b-b5d7-0ca3490bffeb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
416a3eeb-8aba-4a5b-b5d7-0ca3490bffeb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
416a3eeb-8aba-4a5b-b5d7-0ca3490bffeb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
416a3eeb-8aba-4a5b-b5d7-0ca3490bffeb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
416a3eeb-8aba-4a5b-b5d7-0ca3490bffeb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
ba022a1a-fb87-493e-bdf6-facc52b46271,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Neutrophils, lymphocytes, and macrophages are attracted to the irritated airway, and their presence is maintained through increased expression of cell adhesion molecules on the airway walls. These immune cells lead to acute airway wall inflammation that narrows the airway, and if chronic, can lead to tissue damage. The cytokines released by these cells also sensitize airway irritant receptors, which exacerbates the response to future irritant exposure.",True,Chronic Bronchitis,,,,
b5129469-dd40-4ea7-9332-cf7ed356411a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Mucus production increases, and the glands themselves may also release cytokines that further exacerbate the inflammatory response. The mucus also contributes to airway narrowing, and mucus plugs may form that completely block bronchioles.",True,Chronic Bronchitis,,,,
25da24f2-ae7b-400c-9da9-c66259b49f04,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Mesenchymal cells transition into fibroblasts as part of the inflammatory response, and their chronic presence leads to the deposition of fibrotic tissue.",True,Chronic Bronchitis,,,,
4f1e1d33-20b5-47bb-a322-14f0cda5f106,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Collectively these responses to the irritants result in a narrowed airway that is (1) hypersensitive, (2) fibrosed, and (3) blocked by excessive secretions.",True,Chronic Bronchitis,,,,
54cd4ac6-6907-4268-9406-ca5c0f5c7c9d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
54cd4ac6-6907-4268-9406-ca5c0f5c7c9d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
54cd4ac6-6907-4268-9406-ca5c0f5c7c9d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
54cd4ac6-6907-4268-9406-ca5c0f5c7c9d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
54cd4ac6-6907-4268-9406-ca5c0f5c7c9d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
ad01645b-127f-4836-9e86-73e40913b9dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
ad01645b-127f-4836-9e86-73e40913b9dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
ad01645b-127f-4836-9e86-73e40913b9dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
ad01645b-127f-4836-9e86-73e40913b9dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
ad01645b-127f-4836-9e86-73e40913b9dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
d7cd9b07-d0a5-4899-bcc0-30d05cabb18e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"These changes result in an airway that produces more mucus and is less capable of removing it. The static mucus not only causes airway plugging, but can also promote infections that lead to episodic and characteristic exacerbation of COPD symptoms.",True,Chronic Bronchitis,,,,
bbfd4ab4-546f-40e2-97c2-f5f2f54438f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Clinical Presentation of Chronic Bronchitis,False,Clinical Presentation of Chronic Bronchitis,,,,
d0fdcfa1-6dc9-494a-b681-9e5ac098fbed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
d0fdcfa1-6dc9-494a-b681-9e5ac098fbed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
d0fdcfa1-6dc9-494a-b681-9e5ac098fbed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
d0fdcfa1-6dc9-494a-b681-9e5ac098fbed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
d0fdcfa1-6dc9-494a-b681-9e5ac098fbed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
2954d908-e93e-4674-b0c9-0975d6cf9fb2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"As with many pulmonary diseases, the onset can be insidious. Small airway damage may be present but undetectable with normal spirometry, while the patient becomes accustomed to and tolerates a persistent productive cough. However, with continued irritant exposure, this initial simple bronchitis progresses.",True,Clinical Presentation of Chronic Bronchitis,,,,
08a74477-a8f1-4b48-ab90-84cbe7259665,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Secretions continue to worsen and peribronchiolar fibrosis marks the onset of obstructive bronchitis that is reflected by significant expiratory airflow limitation. At this point the patient may have tolerated years of productive cough and experienced frequent chest infections related to poor mucus clearance. COPDers are particularly susceptible to Haemophilus influenza and Streptococcus pneumoniae. The sputum is abundant and capable of plugging significant numbers of airways and may be blood tinged; COPD is the most common cause of hemoptysis. Airways may demonstrate hyperreactivity and mimic an asthmatic response.,True,Clinical Presentation of Chronic Bronchitis,,,,
27931927-1824-4817-a27b-c32536ca3786,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The onset of dyspnea is insidious and is usually first experienced during exertion—leading the patient to avoid exercise, which in turn leads to deconditioning and a worsening of the symptom. Lung sounds include wheezes and rales, the rales often clearing after cough.",True,Clinical Presentation of Chronic Bronchitis,,,,
2d83191b-b693-4cca-b87f-54e3eaed3a93,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,With worsening airway flow limitation expiration becomes prolonged and may be incomplete due to airway collapse that leads to characteristic hyperinflation.,True,Clinical Presentation of Chronic Bronchitis,,,,
0fa93e3c-8ee7-41c9-9d8d-e1eb7473e407,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Mucus plugging and airway closure leads to areas of V/Q abnormalities through the lung, and localized areas of hypoxia can lead to pulmonary vasoconstriction. When significant regions of the lung are vasoconstricted, pulmonary vascular resistance can rise enough to induce right-sided heart failure.",True,Clinical Presentation of Chronic Bronchitis,,,,
e05298ae-d73f-4d8e-ac5c-1a8da3dd5ecf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"With continued progression of the disease, blood gases become deranged as insufficient alveolar ventilation is achieved. As the disease approaches its end stage, the patient experiences dyspnea at rest until respiratory failure occurs and the patient is hypoxemic and hypercarbic.",True,Clinical Presentation of Chronic Bronchitis,,,,
963c92c0-a40d-4cd8-a5d1-3a6339951f85,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Emphysema,False,Emphysema,,,,
3f0a580f-86e2-435d-b0e4-caa5108fb91d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
3f0a580f-86e2-435d-b0e4-caa5108fb91d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
3f0a580f-86e2-435d-b0e4-caa5108fb91d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
3f0a580f-86e2-435d-b0e4-caa5108fb91d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
3f0a580f-86e2-435d-b0e4-caa5108fb91d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
92d7a511-da4d-461c-abdb-666c0aea2745,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
92d7a511-da4d-461c-abdb-666c0aea2745,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
92d7a511-da4d-461c-abdb-666c0aea2745,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
92d7a511-da4d-461c-abdb-666c0aea2745,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
92d7a511-da4d-461c-abdb-666c0aea2745,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
693063c9-85f7-4633-8cb5-7d1b00c1cbcf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
693063c9-85f7-4633-8cb5-7d1b00c1cbcf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
693063c9-85f7-4633-8cb5-7d1b00c1cbcf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
693063c9-85f7-4633-8cb5-7d1b00c1cbcf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
693063c9-85f7-4633-8cb5-7d1b00c1cbcf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
a390d983-31fe-4f9e-a25a-8c31c79eb96b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
a390d983-31fe-4f9e-a25a-8c31c79eb96b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
a390d983-31fe-4f9e-a25a-8c31c79eb96b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
a390d983-31fe-4f9e-a25a-8c31c79eb96b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
a390d983-31fe-4f9e-a25a-8c31c79eb96b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
e21ed96a-346e-493e-986c-6f00e6c6eb04,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"So having seen the morphology of emphysema, we will look at how this damage occurs.",True,Emphysema,,,,
d1a82a18-b452-46c8-a6d9-2495e0259472,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Pathophysiology of Emphysema,False,Pathophysiology of Emphysema,,,,
b097a932-7fa1-4947-8e11-bafa3186560d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,The normal structure of alveoli and respiratory ducts consists of type 1 and type 2 pneumocytes with elastic fibers that contribute to the structure’s mechanical behavior. Emphysema involves the loss of these parenchymal fibers.,True,Pathophysiology of Emphysema,,,,
0fa0b53b-3f87-4efd-b6a0-387c8245a5ae,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The presence of irritants, such as cigarette smoke, causes oxidization and the dysfunction of antiprotease enzymes. Without their inhibitory action, the activity of proteases increases and causes the destruction of local tissue. One of these proteases is elastase, whose elevated activity leads to irreparable loss of parenchymal fibers.",True,Pathophysiology of Emphysema,,,,
459fd924-7a3d-4a28-81ac-df7382c9d225,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Elastase is also released by neutrophils and macrophages that arrive in response to the inflammatory cascade caused by the inhaled smoke. This causes further destruction of elastin fibers.,True,Pathophysiology of Emphysema,,,,
dc111024-3189-4be2-ad9d-918c626fa685,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
dc111024-3189-4be2-ad9d-918c626fa685,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
dc111024-3189-4be2-ad9d-918c626fa685,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
dc111024-3189-4be2-ad9d-918c626fa685,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
dc111024-3189-4be2-ad9d-918c626fa685,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
881ad255-a783-48fa-994c-2231712d0f30,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
881ad255-a783-48fa-994c-2231712d0f30,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
881ad255-a783-48fa-994c-2231712d0f30,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
881ad255-a783-48fa-994c-2231712d0f30,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
881ad255-a783-48fa-994c-2231712d0f30,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
0e44cc30-7e48-4ce3-b0b4-d2e00966239a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,The loss of the elastic tissue and alveolar structure produces several pathophysiological changes in lung mechanics and function that result in typical clinical signs.,True,Pathophysiology of Emphysema,,,,
a2044916-d978-4967-ba49-0dbd0bd4e69e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Clinical Presentation of Emphysema,False,Clinical Presentation of Emphysema,,,,
7d8c96ce-9924-4387-94a1-80d055ee2d40,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
7d8c96ce-9924-4387-94a1-80d055ee2d40,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
7d8c96ce-9924-4387-94a1-80d055ee2d40,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
7d8c96ce-9924-4387-94a1-80d055ee2d40,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
7d8c96ce-9924-4387-94a1-80d055ee2d40,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
87a017cc-f379-4643-98f9-aa8f53dbf94b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
87a017cc-f379-4643-98f9-aa8f53dbf94b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
87a017cc-f379-4643-98f9-aa8f53dbf94b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
87a017cc-f379-4643-98f9-aa8f53dbf94b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
87a017cc-f379-4643-98f9-aa8f53dbf94b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
5742c7ee-8ee9-444a-9662-df0710c7f307,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
5742c7ee-8ee9-444a-9662-df0710c7f307,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
5742c7ee-8ee9-444a-9662-df0710c7f307,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
5742c7ee-8ee9-444a-9662-df0710c7f307,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
5742c7ee-8ee9-444a-9662-df0710c7f307,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
871edbd3-de1f-4969-ac90-c77d04e4fc7d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The deterioration of gas exchange and lung mechanics worsens as more lung becomes involved, and the stage of the disease, and any concurrent chronic bronchitis, is classified by the level of airway flow limitation (e.g., FEV1/FVC).",True,Clinical Presentation of Emphysema,,,,
048065e5-22d3-4ca8-acae-021631ba02ca,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"It might also be worth noting here that COPD can produce or be associated with a number of comorbidities; we have already mentioned hypertension, but pulmonary artery disease, coronary heart disease, heart failure, lung cancer, and malnutrition may contribute to a low quality of life that is typically associated with COPD. This in turn may contribute to the high incidence of anxiety disorders and depression experienced by COPD patients.",True,Clinical Presentation of Emphysema,,,,
107fd696-fc65-4daf-b86d-7e9ffad6a981,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Cystic Fibrosis,False,Cystic Fibrosis,,,,
446ba93b-2d1f-45e0-9927-2200ddcc767c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Cystic fibrosis (CF) is an inherited disorder that affects the exocrine glands of not only the lungs, but also the pancreas, intestines, and bile ducts. We will focus only on the pulmonary aspects here and see how CF produces an obstructive lung disease.",True,Cystic Fibrosis,,,,
cc3aa53a-178f-4cde-88eb-5fa08e0edb7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Cystic fibrosis affects the composition of the fluid lining the airways. Changes in this fluid lead to serious sequelae that dramatically shorten life expectancy. Even with modern therapy, many CF patients only live until their thirties or early forties, and some still die in infancy.",True,Cystic Fibrosis,,,,
fe7d98ff-0733-4afe-8ed2-012c4841b697,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,There are two hypotheses about the pathophysiological mechanism of CF: the low volume and the high salt. We will focus only on the low volume hypothesis as there is increasing evidence to support this and emerging evidence against the high salt hypothesis.,True,Cystic Fibrosis,,,,
320fbdd4-4262-4fb7-8ee1-d6d7f6d14c86,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Pathophysiology of Cystic Fibrosis,False,Pathophysiology of Cystic Fibrosis,,,,
436e0f88-184e-4ef8-83a7-8ff24e16d8aa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
436e0f88-184e-4ef8-83a7-8ff24e16d8aa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
436e0f88-184e-4ef8-83a7-8ff24e16d8aa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
436e0f88-184e-4ef8-83a7-8ff24e16d8aa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
436e0f88-184e-4ef8-83a7-8ff24e16d8aa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
c51b2b76-808f-4c22-b6ae-ca302afcd512,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,ENaC,False,ENaC,,,,
92c3a7db-46c2-4254-a908-437e66526269,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
92c3a7db-46c2-4254-a908-437e66526269,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
92c3a7db-46c2-4254-a908-437e66526269,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
92c3a7db-46c2-4254-a908-437e66526269,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
92c3a7db-46c2-4254-a908-437e66526269,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
db961fb6-7ee8-42ad-9b6a-50252109c9f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"There are numerous mutations that are known to produce a dysfunctional CFTR channel, but 70 percent of CF cases are due to the delta-F-508 mutation (so named as the mutation leads to a deletion of phenylalanine at position 508 of the CFTR protein). This is a Mendelian recessive trait, and CF occurrence is 1 in 2,500 live births.",True,ENaC,,,,
db063a96-38f8-483f-b708-339a80edfada,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
db063a96-38f8-483f-b708-339a80edfada,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
db063a96-38f8-483f-b708-339a80edfada,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
db063a96-38f8-483f-b708-339a80edfada,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
db063a96-38f8-483f-b708-339a80edfada,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
a720ab5f-669c-4f95-9082-c5872f7f154a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"This combination severely impacts mucus clearance (thicker, heavier mucus with compromised cillary escalator). The defective CFTR channel therefore results in mucus retention and airway obstruction. This in turn leads to reduced alveolar ventilation and repeated infections. The two most common culprits for infection in CF are Staphylococcus aureus and Pseudomonsa aeruginosa. Normal functional CFTR appears to suppress P. aeruginosa, perhaps explaining its prevalence in cystic fibrosis where it can be found in the sputum of almost all CF patients.",True,ENaC,,,,
a25dfe12-9f4b-4756-b788-94c791e655c9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,cillary,False,cillary,,,,
86a21e75-3242-4576-80c5-2a3511c93234,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Pseudomonsa,False,Pseudomonsa,,,,
abc7971b-13c4-4067-9a5a-7665cfa7f8e2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
abc7971b-13c4-4067-9a5a-7665cfa7f8e2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
abc7971b-13c4-4067-9a5a-7665cfa7f8e2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
abc7971b-13c4-4067-9a5a-7665cfa7f8e2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
abc7971b-13c4-4067-9a5a-7665cfa7f8e2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
0d167435-239a-41d7-9361-89ba1424b20c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The findings of CF obviously include the results of other effected organs, such as the pancreas. But nowadays these are more easily addressed, and it is pulmonary involvement that still proves critical. The onset of pulmonary involvement is variable and may be weeks or years after birth.",True,Pseudomonsa,,,,
6dc18b65-ea6a-40e3-9641-bbad580a78ec,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Clinical Presentation of Cystic Fibrosis,False,Clinical Presentation of Cystic Fibrosis,,,,
1dd450c4-c78b-4e97-aae4-77b0aeec4455,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
1dd450c4-c78b-4e97-aae4-77b0aeec4455,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
1dd450c4-c78b-4e97-aae4-77b0aeec4455,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
1dd450c4-c78b-4e97-aae4-77b0aeec4455,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
1dd450c4-c78b-4e97-aae4-77b0aeec4455,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
6d6d09c5-8305-4eb8-9cb4-2713e9900058,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,CF patients usually have an abnormal sinus x-ray and evidence of chronic sinusitis as well as a high occurrence of nasal polyps.,True,Clinical Presentation of Cystic Fibrosis,,,,
8f15251e-c619-47d8-b829-86276075121b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"With increasing and irreversible airway damage, the patients begins to experience dyspnea, and the damage may lead to hemoptysis, spontaneous pneumothorax, and a barrel chested appearance. Signs of prolonged pulmonary dysfunction appear as the disease progresses, such as finger clubbing, cyanosis, and cor pulmonale (right-sided heart failure caused by lung disease). As the patient approaches respiratory failure the accessory muscles are deployed. Patients succumb to the respiratory failure or an overwhelming infection.",True,Clinical Presentation of Cystic Fibrosis,,,,
65d7b0a8-11a4-4885-af6f-25d2bf1e9767,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Because CF also affects sweat gland function, the sweat test remains a standard diagnostic with a chloride level greater than 60 mEq/L being indicative of CF. This test is more reliable in children than adults, who may have developed other conditions that affect the composition of sweat.",True,Clinical Presentation of Cystic Fibrosis,,,,
9f26e820-60de-49c3-bf18-3b819e96857d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
9f26e820-60de-49c3-bf18-3b819e96857d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
9f26e820-60de-49c3-bf18-3b819e96857d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
9f26e820-60de-49c3-bf18-3b819e96857d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
9f26e820-60de-49c3-bf18-3b819e96857d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
b23a55bf-50a0-48a9-930e-2c99087daa92,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Spirometry detects the airway obstruction and hyperinflation that produce a low vital capacity and high residual volume.,True,Clinical Presentation of Cystic Fibrosis,,,,
be8d4b9f-383c-46a1-ad8b-8db539f1cd1e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Bronchiectasis,False,Bronchiectasis,,,,
63e29543-59b0-4f8e-a93b-d4dd2a24df97,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"This section will address bronchiectasis, a form of airway obstruction that is often a manifestation of chronic airway inflammation. Bronchiectasis involves a permanent dilation of a bronchi or bronchiole—think of bronchiectasis as the airway equivalent of an aneurysm.",True,Bronchiectasis,,,,
5087adaa-b775-4acc-b424-fac0e5a412c4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
5087adaa-b775-4acc-b424-fac0e5a412c4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
5087adaa-b775-4acc-b424-fac0e5a412c4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
5087adaa-b775-4acc-b424-fac0e5a412c4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
5087adaa-b775-4acc-b424-fac0e5a412c4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
72b427b6-7cf6-41a2-a298-ee8f69387133,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
72b427b6-7cf6-41a2-a298-ee8f69387133,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
72b427b6-7cf6-41a2-a298-ee8f69387133,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
72b427b6-7cf6-41a2-a298-ee8f69387133,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
72b427b6-7cf6-41a2-a298-ee8f69387133,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
3b0e3f15-bb01-4e8b-9eb4-5a773362a5ae,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The establishing of a bronchiectasis has an initial phase leading to persistent inflammation, desquamation (which worsens the mucus clearance), and the ulceration. In what is probably a familiar story, the continued inflammation leads to fibrosis in the chronic phase of development, and this can lead to airway destruction and perhaps the condition of bronchiolitis obliterans.",True,Bronchiectasis,,,,
a5320adc-ab03-4bae-9409-fc5390366aaa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Let us look at how this process can get started.,False,Let us look at how this process can get started.,,,,
245d0174-f290-48c4-9075-03e670e83e13,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Pathogenesis of Bronchiectasis,False,Pathogenesis of Bronchiectasis,,,,
f428b662-610b-4f62-8621-6d3f4a454180,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
f428b662-610b-4f62-8621-6d3f4a454180,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
f428b662-610b-4f62-8621-6d3f4a454180,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
f428b662-610b-4f62-8621-6d3f4a454180,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
f428b662-610b-4f62-8621-6d3f4a454180,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
1eadf609-f7b9-4fd9-a3d2-599321b3bb81,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"About 50 percent of bronchiectasis cases are associated with cystic fibrosis where the genetic condition causes production of copious, thick mucus that is difficult to clear and often results in infection (commonly caused by Staphylococcus aureus).",True,Pathogenesis of Bronchiectasis,,,,
21b1bf7f-bbf0-4bb6-92c1-c5a3b2272546,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Conditions causing cillary dyskinesia, as seen in Kartagener’s syndrome, also disrupt the mucocillary escalator.",True,Pathogenesis of Bronchiectasis,,,,
e79bcd0f-909c-4162-a204-1814d026d215,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,mucocillary,False,mucocillary,,,,
81114ed9-a389-4422-9698-34946e4a2b4c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Another common cause of bronchiectasis is an allergy to Aspergillus fumigatus, a common fungus. In hypersensitive or immune-compromised individuals, chronic exposure can lead to allergic bronchopulmonary aspiragillosis.",True,mucocillary,,,,
f53be8d8-093c-4f44-8a54-75b91e51a664,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,aspiragillosis,False,aspiragillosis,,,,
d35443aa-6694-4620-9ecf-6c8d4a9eb6c4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Bronchiectasis can be initiated in the vicinity of tuberculosis or other necrotizing infections that damage and weaken airway walls.,True,aspiragillosis,,,,
952f8828-37b3-4834-a902-a380893228f9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Obstruction of the bronchioles or bronchi by inhaled foreign objects, tumors, or compacted mucus can also initiate bronchiectasis through local inflammation and by preventing mucus clearance. The dilation of the airway can be worsened further by distal atelectasis that produces a negative pressure around the affected airway.",True,aspiragillosis,,,,
ac939b98-dff5-4043-9842-1069b2af1ff1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"As you might have gather by now, repeated local infection or inflammation has the potential to initiate bronchiectasis, so it is perhaps not surprising that with the advent of high resolution computed tomography (CT) imaging, bronchiectasis has also been found in association with AIDS, transplant rejection, and rheumatoid lung disease.",True,aspiragillosis,,,,
24b36b6e-9f47-4d43-b379-0ab403d4d606,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,We will now examine the results of these instigating factors.,False,We will now examine the results of these instigating factors.,,,,
39454d4c-cbdf-4474-9829-118f5f384c0c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Pathology of Bronchiectasis,False,Pathology of Bronchiectasis,,,,
04f9aefe-9a2e-4d2a-87d6-5f8b1b94232f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
04f9aefe-9a2e-4d2a-87d6-5f8b1b94232f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
04f9aefe-9a2e-4d2a-87d6-5f8b1b94232f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
04f9aefe-9a2e-4d2a-87d6-5f8b1b94232f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
04f9aefe-9a2e-4d2a-87d6-5f8b1b94232f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
aa4b374a-8833-4dd4-8069-844da9e21e7a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
aa4b374a-8833-4dd4-8069-844da9e21e7a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
aa4b374a-8833-4dd4-8069-844da9e21e7a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
aa4b374a-8833-4dd4-8069-844da9e21e7a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
aa4b374a-8833-4dd4-8069-844da9e21e7a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
ee2a56dd-bf2a-4bec-846d-e142501aa5a8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
ee2a56dd-bf2a-4bec-846d-e142501aa5a8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
ee2a56dd-bf2a-4bec-846d-e142501aa5a8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
ee2a56dd-bf2a-4bec-846d-e142501aa5a8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
ee2a56dd-bf2a-4bec-846d-e142501aa5a8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
6fbaaa0c-eb4e-4a4f-af24-e98089ffce9c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"A bronchiectasis can be cylindrical, varicose (also known as fusiform), or cystic (also known as saccular). The shape is relevant to their effect on the efficacy of coughing; cylindrical form has very little effect on cough’s ability to clear mucus, whereas varicose and cystic forms tend to disproportionately collapse during cough and reduce its effectiveness at moving mucus up the airway.",True,Pathology of Bronchiectasis,,,,
9b95f1a0-8db6-4189-993e-9db465dcd585,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
9b95f1a0-8db6-4189-993e-9db465dcd585,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
9b95f1a0-8db6-4189-993e-9db465dcd585,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
9b95f1a0-8db6-4189-993e-9db465dcd585,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
9b95f1a0-8db6-4189-993e-9db465dcd585,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
40cf67f9-f2f5-4f16-9935-fbb7f928762f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
40cf67f9-f2f5-4f16-9935-fbb7f928762f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
40cf67f9-f2f5-4f16-9935-fbb7f928762f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
40cf67f9-f2f5-4f16-9935-fbb7f928762f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
40cf67f9-f2f5-4f16-9935-fbb7f928762f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
d5c4f82c-5276-4294-802a-0338ebfbb119,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"So, how does bronchiectasis present, and what are the results of diagnostic tests?",True,Pathology of Bronchiectasis,,,,
864e8077-5058-493e-b661-921959e477bb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Clinical Presentation of Bronchiectasis,False,Clinical Presentation of Bronchiectasis,,,,
5e65bc8e-27c1-4d20-b621-19cbb49f66bf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The initial complaint is usually a persistent cough with copious expectoration. The amount of mucus the cough produces varies and can be as high as several hundred milliliters per day, particular when the dependent airways are involved. However, it is worth noting here that bronchiectasis in the upper lobes (usually associated with infection) may be dry with little or no mucus expectoration.",True,Clinical Presentation of Bronchiectasis,,,,
937f0cac-75b1-4750-b24a-1102b5b8155a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Generally though there is mucopurulent expectorate, and if it is associated with an anerobic infection it will likely have a foul odor. Sputum smears are loaded with white blood cells and can contain both gram-positive and -negative organisms.",True,Clinical Presentation of Bronchiectasis,,,,
a107792c-c797-481e-aa49-75245f1a3990,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The patient will likely have a history of recurrent pneumonia, the site of the pneumonia being consistent with locality of the bronchiectasis.",True,Clinical Presentation of Bronchiectasis,,,,
625e0746-b32e-4849-bf71-4250bb7116a0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The expectorate may also contain blood. The degree and frequency of hemoptysis is variable and unpredictable, but occasionally it can be massive and life threatening.",True,Clinical Presentation of Bronchiectasis,,,,
cf6b7f64-2bf3-4cc9-8ff1-0ff2a604ccd0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"The standard diagnostic tests may not be helpful in early stages, but typical signs appear with worsening airway involvement. In the early stages the patient will likely appear normal on a physical exam and have normal spirometry and arterial blood gas values. With more significant bronchiectasis, rales and rhonchi over the affected site can be heard.",True,Clinical Presentation of Bronchiectasis,,,,
c3d3baf9-f5f9-45b0-92f5-3092c6460159,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Later signs with long-standing bronchiectasis include finger clubbing, but this is not exclusive to the condition.",True,Clinical Presentation of Bronchiectasis,,,,
32463f67-8faa-40ef-b65c-da948ae39c76,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"A chest x-ray will show the peribronchial fibrosis and any atelectasis. But, as mentioned earlier, a high-resolution CT is much more effective at determining the degree and type of airway changes.",True,Clinical Presentation of Bronchiectasis,,,,
1d80c3c1-1b09-4e81-95ea-0b5a00c94ab7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"References, Resources, and Further Reading",False,"References, Resources, and Further Reading",,,,
e2d74c48-6f60-43ae-9d7c-8c0b9e8ee9fd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,Text,False,Text,,,,
cbb9aaad-105e-4a3e-ac67-3afc2bac6e48,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapters 8–11.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
829c19b6-1a42-40a8-8731-523e040541e9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
2fae69a4-a520-4df1-b51b-916b71d658bf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Bronchiectasis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-4,"West, John B. “Chapter 4: Obstructive Diseases.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Text,,,,
98186909-99b3-4463-bbbd-edf3c7471b71,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
98186909-99b3-4463-bbbd-edf3c7471b71,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
98186909-99b3-4463-bbbd-edf3c7471b71,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
98186909-99b3-4463-bbbd-edf3c7471b71,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
98186909-99b3-4463-bbbd-edf3c7471b71,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
c484cede-c606-4fe2-8d97-ffb821525f56,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,We will also look at how exercise and certain pharmacological agents can produce asthma.,True,Text,,,,
41bb0bb4-f200-41ec-acb6-263bf97812c5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
41bb0bb4-f200-41ec-acb6-263bf97812c5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
41bb0bb4-f200-41ec-acb6-263bf97812c5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
41bb0bb4-f200-41ec-acb6-263bf97812c5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
41bb0bb4-f200-41ec-acb6-263bf97812c5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
314c16fa-822d-4f1b-80f8-95580fe8b43a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,proinflammatory,False,proinflammatory,,,,
37b8de65-664a-4df9-8232-a3f0f809f049,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,The results of this cocktail’s release are the hallmarks of asthma:,True,proinflammatory,,,,
d81cca6a-70c3-4266-a8f3-11e98f4748f6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The timeline from the exposure to the antigen to asthmatic response is not straightforward. A response may occur within minutes (“early response”), or hours later (“late response”). Some patients show only an early response, some only a late one, and some show both in a “dual” response. The late response may correspond to the arrival of leucocytes in response to the initial release of cytokines. It may also be due to a mild stimulus arriving later in an airway that was sensitized earlier.",True,proinflammatory,,,,
400f6fd1-1a16-4fd0-b88a-9a754d71d9b8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
400f6fd1-1a16-4fd0-b88a-9a754d71d9b8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
400f6fd1-1a16-4fd0-b88a-9a754d71d9b8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
400f6fd1-1a16-4fd0-b88a-9a754d71d9b8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
400f6fd1-1a16-4fd0-b88a-9a754d71d9b8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
d399844a-5615-4b57-a2f4-392743f71b63,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
d399844a-5615-4b57-a2f4-392743f71b63,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
d399844a-5615-4b57-a2f4-392743f71b63,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
d399844a-5615-4b57-a2f4-392743f71b63,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
d399844a-5615-4b57-a2f4-392743f71b63,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
a890fd94-0d8f-43f6-ab5c-96025b0b549e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The cholinergic response may help produce an asthmatic response to another stimulus that normally would not have produced one (i.e., it may play a part in the hypersensitivity of the asthmatic airways). Likewise, the presence of an infection, particularly a viral infection, may place the airway in a proinflammatory state.",True,proinflammatory,,,,
a11ef751-24da-493c-b0fc-836f4a335b00,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
a11ef751-24da-493c-b0fc-836f4a335b00,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
a11ef751-24da-493c-b0fc-836f4a335b00,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
a11ef751-24da-493c-b0fc-836f4a335b00,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
a11ef751-24da-493c-b0fc-836f4a335b00,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
839f8f72-356b-4076-bfa5-c2810d2211db,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Exercise-induced asthma: Although exercise is associated with increased airway caliber, it can also induce asthma. Increased airway flow to meet the increased metabolic demand of exercise results in loss of fluid and heat from airway surfaces. This leaves the peribronchial fluid in a hypertonic state and causes excitation of the irritant airway receptors, which leads to release of the mast cells’ cocktail.",True,proinflammatory,,,,
3a87cc83-ff48-4d3b-8258-6e6bedb76ce3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Exercise-induced asthma is more prevalent in cold (i.e. dry air) where water loss will be higher, so occurs more in sports such as cross-country skiing than swimming in a warm humid environment. Bronchoconstriction usually occurs when exercise stops—when the protective effect of sympathetic activity to the airway smooth muscles ceases.",True,proinflammatory,,,,
9b6fdeba-42c2-4fb7-984b-4415a7575c2d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Drug-induced asthma: There are several pharmaceutical and food products that can promote asthma, including tartrazine (a yellow food coloring) and sulfides used as food preservatives. Additionally, 10 to 20 percent of asthmatics are sensitive to aspirin.",True,proinflammatory,,,,
43b5e481-554c-49e6-83b3-e31d4e251663,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
43b5e481-554c-49e6-83b3-e31d4e251663,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
43b5e481-554c-49e6-83b3-e31d4e251663,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
43b5e481-554c-49e6-83b3-e31d4e251663,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
43b5e481-554c-49e6-83b3-e31d4e251663,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
58dd2796-c290-474d-98e9-c90fdfae62a4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Environmental/occupational asthma: As the airway is open to the environment, it is susceptible to inhaled substances that can cause sensitization; there are over two hundred substances known to cause asthma, both organic and inorganic. Some common ones are listed below.",True,proinflammatory,,,,
13a145f7-cc29-450d-aad5-2f26626fab6b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Table 1.1: Some of the most common environmental causes of asthma. Taking a pulmonary history should include asking about potential environmental exposures.,True,proinflammatory,,,,
01a3ca23-3bc5-46e1-a0c2-ba00024cbf4e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Determining whether airway hypersensitivity is due to environmental factors is complicated by widely varying latency periods. Short latency periods can be as brief as twenty-four hours and are associated with vapor or smoke exposure that does not cause an immunological response. Longer latency periods that may last years are more commonly associated with an immunological response to large particles that act like antigens.,True,proinflammatory,,,,
3704593b-5050-4d3f-b8e4-0cae547634e0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The situation is further confused by occupation-related responses, which often cause the airway to become more sensitive to some of the other causes of asthma covered here. This makes the role of an environmental factor more difficult to determine.",True,proinflammatory,,,,
188d14fc-da82-459d-8066-454fc3737705,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Pathophysiology of Asthma,False,Pathophysiology of Asthma,,,,
e11d0192-ec9e-4b48-9326-9b13cdc8bdb9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
e11d0192-ec9e-4b48-9326-9b13cdc8bdb9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
e11d0192-ec9e-4b48-9326-9b13cdc8bdb9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
e11d0192-ec9e-4b48-9326-9b13cdc8bdb9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
e11d0192-ec9e-4b48-9326-9b13cdc8bdb9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
cdccc8c0-3466-454e-a068-a4260e9e0f52,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
cdccc8c0-3466-454e-a068-a4260e9e0f52,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
cdccc8c0-3466-454e-a068-a4260e9e0f52,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
cdccc8c0-3466-454e-a068-a4260e9e0f52,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
cdccc8c0-3466-454e-a068-a4260e9e0f52,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
c406a8a9-6b8e-4a14-ac82-f0590827e099,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
c406a8a9-6b8e-4a14-ac82-f0590827e099,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
c406a8a9-6b8e-4a14-ac82-f0590827e099,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
c406a8a9-6b8e-4a14-ac82-f0590827e099,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
c406a8a9-6b8e-4a14-ac82-f0590827e099,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
71667aa9-9c03-4c2e-9b6f-8935f026eb02,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
71667aa9-9c03-4c2e-9b6f-8935f026eb02,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
71667aa9-9c03-4c2e-9b6f-8935f026eb02,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
71667aa9-9c03-4c2e-9b6f-8935f026eb02,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
71667aa9-9c03-4c2e-9b6f-8935f026eb02,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
fad98cd2-0cb7-447b-8185-1612ab26c8f5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Clinical Presentation of Asthma,False,Clinical Presentation of Asthma,,,,
33c24201-f138-4557-897a-c497fb1a4b3c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"One useful diagnostic element of asthma is its episodic or acute behavior. However, as patients may be asymptomatic between attacks, the severity of asthma can be difficult to determine without performing bronchial challenge tests.",True,Clinical Presentation of Asthma,,,,
795d94a2-5c1a-499c-9d39-8f42fa3114ad,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
795d94a2-5c1a-499c-9d39-8f42fa3114ad,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
795d94a2-5c1a-499c-9d39-8f42fa3114ad,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
795d94a2-5c1a-499c-9d39-8f42fa3114ad,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
795d94a2-5c1a-499c-9d39-8f42fa3114ad,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
ced438f5-0f50-4ea2-ab26-ff0fa6cd3f51,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"As airway resistance increases, the accessory muscles are deployed to maintain sufficient airflow through the narrowing airways, and the patient experiences an increased effort to breathe. Increased expiratory efforts produce dynamic airway collapse and lead to hyperinflation. Further decreases in airway caliber result in insufficient alveolar ventilation and deranged blood gases. The sensation reported at this point is air hunger. Once the patient is severely bronchoconstricted, delivery of inhaled therapies is much more difficult, and mechanical ventilation to support the respiratory muscles becomes complicated. Other signs present during a severe attack are raised heart (tachycardia) and breathing (tachypnea) rates as well as a paradoxical pulse (i.e., a rise in blood pressure during expiration).",True,Clinical Presentation of Asthma,,,,
0a06c82f-a218-4e7a-ad30-a1c3d33176e3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
0a06c82f-a218-4e7a-ad30-a1c3d33176e3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
0a06c82f-a218-4e7a-ad30-a1c3d33176e3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
0a06c82f-a218-4e7a-ad30-a1c3d33176e3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
0a06c82f-a218-4e7a-ad30-a1c3d33176e3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
0ae06c4d-76d5-45d0-aa65-a6ba32591dde,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Chronic Obstructive Pulmonary Disease,False,Chronic Obstructive Pulmonary Disease,,,,
4ffa5592-cd59-4484-828b-d46fb7a10a9a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Although chronic bronchitis and emphysema have different underlying pathologies, they frequently have the same root cause and are often found together in a patient. In brief, chronic bronchitis is associated with an increase in mucus production, while emphysema involves disruption of the lung structure.",True,Chronic Obstructive Pulmonary Disease,,,,
3654e6cb-baaa-4e5c-acfa-43a24620fd0b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The relative role of chronic bronchitis in COPD has diminished since the Clean Air Act reduced atmospheric sulphur dioxide, but with 90 percent of COPD caused by cigarette smoking there is still plenty of bronchitis and emphysema to treat—at enormous cost to the health system from over eight million hospitalizations a year that are mostly paid for by Medicare. The COPD patient tends to be older and poorer and will likely have comorbidities, the most common of which is hypertension. What is perhaps more disturbing is that of the most common causes of death, COPD is the only one whose incidence continues to rise.",True,Chronic Obstructive Pulmonary Disease,,,,
973cf02e-2e26-4891-9b61-5bd59329c96a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"We will now look at the underlying mechanisms of COPD. Despite the fact it is usually composed of some elements of both chronic bronchitis and emphysema, we will deal with each separately for the sake of simplicity.",True,Chronic Obstructive Pulmonary Disease,,,,
b735a833-a521-4e28-9545-42e65a412ae8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Chronic Bronchitis,False,Chronic Bronchitis,,,,
de24d61d-42ff-499c-8d3a-89050f0c3a20,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Chronic bronchitis is clinically defined as a persistent and productive cough that lasts for at least three months per year for two consecutive years.,True,Chronic Bronchitis,,,,
1fdb0c9b-4420-4442-b0fb-0c7fe5fe4505,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
1fdb0c9b-4420-4442-b0fb-0c7fe5fe4505,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
1fdb0c9b-4420-4442-b0fb-0c7fe5fe4505,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
1fdb0c9b-4420-4442-b0fb-0c7fe5fe4505,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
1fdb0c9b-4420-4442-b0fb-0c7fe5fe4505,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
96c50cf6-5b41-4d67-97fe-311ed03da122,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Neutrophils, lymphocytes, and macrophages are attracted to the irritated airway, and their presence is maintained through increased expression of cell adhesion molecules on the airway walls. These immune cells lead to acute airway wall inflammation that narrows the airway, and if chronic, can lead to tissue damage. The cytokines released by these cells also sensitize airway irritant receptors, which exacerbates the response to future irritant exposure.",True,Chronic Bronchitis,,,,
0813df04-33a4-4223-8f01-61d0918f055d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Mucus production increases, and the glands themselves may also release cytokines that further exacerbate the inflammatory response. The mucus also contributes to airway narrowing, and mucus plugs may form that completely block bronchioles.",True,Chronic Bronchitis,,,,
409588ad-2a31-4559-b364-edc777ce2385,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Mesenchymal cells transition into fibroblasts as part of the inflammatory response, and their chronic presence leads to the deposition of fibrotic tissue.",True,Chronic Bronchitis,,,,
3e7e5820-b367-49f7-b502-26a43d40d4da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Collectively these responses to the irritants result in a narrowed airway that is (1) hypersensitive, (2) fibrosed, and (3) blocked by excessive secretions.",True,Chronic Bronchitis,,,,
efaf4e1b-170a-40b5-9e8c-1b64fd8220ab,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
efaf4e1b-170a-40b5-9e8c-1b64fd8220ab,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
efaf4e1b-170a-40b5-9e8c-1b64fd8220ab,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
efaf4e1b-170a-40b5-9e8c-1b64fd8220ab,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
efaf4e1b-170a-40b5-9e8c-1b64fd8220ab,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
7e0862e4-22ba-4ed0-a229-49161e3f0c7b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
7e0862e4-22ba-4ed0-a229-49161e3f0c7b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
7e0862e4-22ba-4ed0-a229-49161e3f0c7b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
7e0862e4-22ba-4ed0-a229-49161e3f0c7b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
7e0862e4-22ba-4ed0-a229-49161e3f0c7b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
a379e277-fa29-4b6c-bd50-efc15830b1f0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"These changes result in an airway that produces more mucus and is less capable of removing it. The static mucus not only causes airway plugging, but can also promote infections that lead to episodic and characteristic exacerbation of COPD symptoms.",True,Chronic Bronchitis,,,,
ffe71c69-1726-4966-99b5-035648e82f11,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Clinical Presentation of Chronic Bronchitis,False,Clinical Presentation of Chronic Bronchitis,,,,
b5f61d3c-7180-4553-b059-8b217bf9f466,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
b5f61d3c-7180-4553-b059-8b217bf9f466,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
b5f61d3c-7180-4553-b059-8b217bf9f466,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
b5f61d3c-7180-4553-b059-8b217bf9f466,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
b5f61d3c-7180-4553-b059-8b217bf9f466,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
9ed7da85-3a41-44d1-b30c-f6df4af5f0c3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"As with many pulmonary diseases, the onset can be insidious. Small airway damage may be present but undetectable with normal spirometry, while the patient becomes accustomed to and tolerates a persistent productive cough. However, with continued irritant exposure, this initial simple bronchitis progresses.",True,Clinical Presentation of Chronic Bronchitis,,,,
9bc887ea-80ff-491c-b7e7-0ab0b2f70a1c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Secretions continue to worsen and peribronchiolar fibrosis marks the onset of obstructive bronchitis that is reflected by significant expiratory airflow limitation. At this point the patient may have tolerated years of productive cough and experienced frequent chest infections related to poor mucus clearance. COPDers are particularly susceptible to Haemophilus influenza and Streptococcus pneumoniae. The sputum is abundant and capable of plugging significant numbers of airways and may be blood tinged; COPD is the most common cause of hemoptysis. Airways may demonstrate hyperreactivity and mimic an asthmatic response.,True,Clinical Presentation of Chronic Bronchitis,,,,
86378570-154d-45a9-a7dd-422d462d9593,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The onset of dyspnea is insidious and is usually first experienced during exertion—leading the patient to avoid exercise, which in turn leads to deconditioning and a worsening of the symptom. Lung sounds include wheezes and rales, the rales often clearing after cough.",True,Clinical Presentation of Chronic Bronchitis,,,,
03b17268-2acc-472e-acda-46989943adb1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,With worsening airway flow limitation expiration becomes prolonged and may be incomplete due to airway collapse that leads to characteristic hyperinflation.,True,Clinical Presentation of Chronic Bronchitis,,,,
bd490a1d-7b40-4463-bd96-3fe5cacbb753,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Mucus plugging and airway closure leads to areas of V/Q abnormalities through the lung, and localized areas of hypoxia can lead to pulmonary vasoconstriction. When significant regions of the lung are vasoconstricted, pulmonary vascular resistance can rise enough to induce right-sided heart failure.",True,Clinical Presentation of Chronic Bronchitis,,,,
aa31cfcc-2b62-40fb-8151-9f68dc79c548,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"With continued progression of the disease, blood gases become deranged as insufficient alveolar ventilation is achieved. As the disease approaches its end stage, the patient experiences dyspnea at rest until respiratory failure occurs and the patient is hypoxemic and hypercarbic.",True,Clinical Presentation of Chronic Bronchitis,,,,
019efe28-d63a-49b6-beb9-48b7b2195279,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Emphysema,False,Emphysema,,,,
67ea3608-4061-463b-87fb-99d7fda8da14,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
67ea3608-4061-463b-87fb-99d7fda8da14,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
67ea3608-4061-463b-87fb-99d7fda8da14,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
67ea3608-4061-463b-87fb-99d7fda8da14,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
67ea3608-4061-463b-87fb-99d7fda8da14,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
6810fa68-62f6-4784-b06c-5bd81ad4fc65,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
6810fa68-62f6-4784-b06c-5bd81ad4fc65,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
6810fa68-62f6-4784-b06c-5bd81ad4fc65,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
6810fa68-62f6-4784-b06c-5bd81ad4fc65,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
6810fa68-62f6-4784-b06c-5bd81ad4fc65,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
d9039f21-9453-49ab-843c-f9e6d433d923,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
d9039f21-9453-49ab-843c-f9e6d433d923,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
d9039f21-9453-49ab-843c-f9e6d433d923,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
d9039f21-9453-49ab-843c-f9e6d433d923,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
d9039f21-9453-49ab-843c-f9e6d433d923,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
59482d9a-2e57-4e61-8bd6-1c39ad6d606e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
59482d9a-2e57-4e61-8bd6-1c39ad6d606e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
59482d9a-2e57-4e61-8bd6-1c39ad6d606e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
59482d9a-2e57-4e61-8bd6-1c39ad6d606e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
59482d9a-2e57-4e61-8bd6-1c39ad6d606e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
b4a3a278-0082-4615-8c6f-e8ac2e0531f4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"So having seen the morphology of emphysema, we will look at how this damage occurs.",True,Emphysema,,,,
df47e449-e03b-4135-99c8-66d36e54803e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Pathophysiology of Emphysema,False,Pathophysiology of Emphysema,,,,
4f39a877-0c3d-420e-aa73-c5c8b2563eeb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,The normal structure of alveoli and respiratory ducts consists of type 1 and type 2 pneumocytes with elastic fibers that contribute to the structure’s mechanical behavior. Emphysema involves the loss of these parenchymal fibers.,True,Pathophysiology of Emphysema,,,,
a5bb75de-ea10-4787-8ed3-1ff992ef849e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The presence of irritants, such as cigarette smoke, causes oxidization and the dysfunction of antiprotease enzymes. Without their inhibitory action, the activity of proteases increases and causes the destruction of local tissue. One of these proteases is elastase, whose elevated activity leads to irreparable loss of parenchymal fibers.",True,Pathophysiology of Emphysema,,,,
9d208083-4115-4a1a-b987-adf236fcfcdf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Elastase is also released by neutrophils and macrophages that arrive in response to the inflammatory cascade caused by the inhaled smoke. This causes further destruction of elastin fibers.,True,Pathophysiology of Emphysema,,,,
da7cc003-5855-4b03-99dd-d8b2dd4b7f5b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
da7cc003-5855-4b03-99dd-d8b2dd4b7f5b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
da7cc003-5855-4b03-99dd-d8b2dd4b7f5b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
da7cc003-5855-4b03-99dd-d8b2dd4b7f5b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
da7cc003-5855-4b03-99dd-d8b2dd4b7f5b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
4f8a5ebd-4f4a-4baf-a042-937f0e3950f9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
4f8a5ebd-4f4a-4baf-a042-937f0e3950f9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
4f8a5ebd-4f4a-4baf-a042-937f0e3950f9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
4f8a5ebd-4f4a-4baf-a042-937f0e3950f9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
4f8a5ebd-4f4a-4baf-a042-937f0e3950f9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
a0cfd88c-928d-4794-a6d8-41e9df582f15,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,The loss of the elastic tissue and alveolar structure produces several pathophysiological changes in lung mechanics and function that result in typical clinical signs.,True,Pathophysiology of Emphysema,,,,
8dae09d8-a709-488d-b648-9964748af63c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Clinical Presentation of Emphysema,False,Clinical Presentation of Emphysema,,,,
b6760764-4dc7-4092-a3f4-2ace35b51f9f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
b6760764-4dc7-4092-a3f4-2ace35b51f9f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
b6760764-4dc7-4092-a3f4-2ace35b51f9f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
b6760764-4dc7-4092-a3f4-2ace35b51f9f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
b6760764-4dc7-4092-a3f4-2ace35b51f9f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
3978a689-f2c1-49cd-a439-05b3d407c10c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
3978a689-f2c1-49cd-a439-05b3d407c10c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
3978a689-f2c1-49cd-a439-05b3d407c10c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
3978a689-f2c1-49cd-a439-05b3d407c10c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
3978a689-f2c1-49cd-a439-05b3d407c10c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
b9105354-53f1-4710-ac91-2e2e9ecb8501,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
b9105354-53f1-4710-ac91-2e2e9ecb8501,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
b9105354-53f1-4710-ac91-2e2e9ecb8501,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
b9105354-53f1-4710-ac91-2e2e9ecb8501,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
b9105354-53f1-4710-ac91-2e2e9ecb8501,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
90817f7d-b664-4081-8297-a9ab5c53f3cb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The deterioration of gas exchange and lung mechanics worsens as more lung becomes involved, and the stage of the disease, and any concurrent chronic bronchitis, is classified by the level of airway flow limitation (e.g., FEV1/FVC).",True,Clinical Presentation of Emphysema,,,,
07c322aa-53b2-40dd-b63f-25c2dae12338,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"It might also be worth noting here that COPD can produce or be associated with a number of comorbidities; we have already mentioned hypertension, but pulmonary artery disease, coronary heart disease, heart failure, lung cancer, and malnutrition may contribute to a low quality of life that is typically associated with COPD. This in turn may contribute to the high incidence of anxiety disorders and depression experienced by COPD patients.",True,Clinical Presentation of Emphysema,,,,
b73c2f65-9fd9-4ae9-b4f0-39c7d189844d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Cystic Fibrosis,False,Cystic Fibrosis,,,,
172d16f9-5ff8-4619-aa51-cef43bcc76fa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Cystic fibrosis (CF) is an inherited disorder that affects the exocrine glands of not only the lungs, but also the pancreas, intestines, and bile ducts. We will focus only on the pulmonary aspects here and see how CF produces an obstructive lung disease.",True,Cystic Fibrosis,,,,
9a3cddfa-519c-47bb-97dc-f4bc89b0f092,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Cystic fibrosis affects the composition of the fluid lining the airways. Changes in this fluid lead to serious sequelae that dramatically shorten life expectancy. Even with modern therapy, many CF patients only live until their thirties or early forties, and some still die in infancy.",True,Cystic Fibrosis,,,,
54977102-022d-419f-afea-62186a5a3707,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,There are two hypotheses about the pathophysiological mechanism of CF: the low volume and the high salt. We will focus only on the low volume hypothesis as there is increasing evidence to support this and emerging evidence against the high salt hypothesis.,True,Cystic Fibrosis,,,,
d02b78cc-63e7-4c2b-a0d9-0e2125bb0f60,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Pathophysiology of Cystic Fibrosis,False,Pathophysiology of Cystic Fibrosis,,,,
af36007a-f34d-42b5-8428-c0b348ab6089,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
af36007a-f34d-42b5-8428-c0b348ab6089,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
af36007a-f34d-42b5-8428-c0b348ab6089,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
af36007a-f34d-42b5-8428-c0b348ab6089,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
af36007a-f34d-42b5-8428-c0b348ab6089,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
7e8dca34-3ffe-4d84-bbf7-8b07e4fff914,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,ENaC,False,ENaC,,,,
6206a844-77a3-42ef-a761-be3b1da99a02,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
6206a844-77a3-42ef-a761-be3b1da99a02,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
6206a844-77a3-42ef-a761-be3b1da99a02,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
6206a844-77a3-42ef-a761-be3b1da99a02,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
6206a844-77a3-42ef-a761-be3b1da99a02,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
51fb8e1a-ca40-4a95-82ef-23ef2d7a6b7d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"There are numerous mutations that are known to produce a dysfunctional CFTR channel, but 70 percent of CF cases are due to the delta-F-508 mutation (so named as the mutation leads to a deletion of phenylalanine at position 508 of the CFTR protein). This is a Mendelian recessive trait, and CF occurrence is 1 in 2,500 live births.",True,ENaC,,,,
4aff4a0b-de32-4260-a117-082fa03bc711,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
4aff4a0b-de32-4260-a117-082fa03bc711,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
4aff4a0b-de32-4260-a117-082fa03bc711,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
4aff4a0b-de32-4260-a117-082fa03bc711,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
4aff4a0b-de32-4260-a117-082fa03bc711,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
07c5dc45-c252-46a3-a637-3f3a01c5f501,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"This combination severely impacts mucus clearance (thicker, heavier mucus with compromised cillary escalator). The defective CFTR channel therefore results in mucus retention and airway obstruction. This in turn leads to reduced alveolar ventilation and repeated infections. The two most common culprits for infection in CF are Staphylococcus aureus and Pseudomonsa aeruginosa. Normal functional CFTR appears to suppress P. aeruginosa, perhaps explaining its prevalence in cystic fibrosis where it can be found in the sputum of almost all CF patients.",True,ENaC,,,,
2966ab9a-f801-4ef5-9554-893357cb5796,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,cillary,False,cillary,,,,
4fd173af-356b-4719-a09a-027337a677ed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Pseudomonsa,False,Pseudomonsa,,,,
685664f7-5f47-4a23-ae77-5f4aa8933eb6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
685664f7-5f47-4a23-ae77-5f4aa8933eb6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
685664f7-5f47-4a23-ae77-5f4aa8933eb6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
685664f7-5f47-4a23-ae77-5f4aa8933eb6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
685664f7-5f47-4a23-ae77-5f4aa8933eb6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
7e9bed9b-e30f-452b-9132-5bff8841ed30,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The findings of CF obviously include the results of other effected organs, such as the pancreas. But nowadays these are more easily addressed, and it is pulmonary involvement that still proves critical. The onset of pulmonary involvement is variable and may be weeks or years after birth.",True,Pseudomonsa,,,,
21be7e88-c313-4bab-8005-6a5f6505faab,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Clinical Presentation of Cystic Fibrosis,False,Clinical Presentation of Cystic Fibrosis,,,,
057a664d-e28f-4832-9b68-c536606f2607,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
057a664d-e28f-4832-9b68-c536606f2607,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
057a664d-e28f-4832-9b68-c536606f2607,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
057a664d-e28f-4832-9b68-c536606f2607,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
057a664d-e28f-4832-9b68-c536606f2607,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
4759f02d-fedc-44fb-ad93-c226d46e50ce,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,CF patients usually have an abnormal sinus x-ray and evidence of chronic sinusitis as well as a high occurrence of nasal polyps.,True,Clinical Presentation of Cystic Fibrosis,,,,
94b5cd9c-2bfc-419f-a2e0-17bd0a849ac8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"With increasing and irreversible airway damage, the patients begins to experience dyspnea, and the damage may lead to hemoptysis, spontaneous pneumothorax, and a barrel chested appearance. Signs of prolonged pulmonary dysfunction appear as the disease progresses, such as finger clubbing, cyanosis, and cor pulmonale (right-sided heart failure caused by lung disease). As the patient approaches respiratory failure the accessory muscles are deployed. Patients succumb to the respiratory failure or an overwhelming infection.",True,Clinical Presentation of Cystic Fibrosis,,,,
4335451f-2494-4e88-b4ec-94a641a5fdff,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Because CF also affects sweat gland function, the sweat test remains a standard diagnostic with a chloride level greater than 60 mEq/L being indicative of CF. This test is more reliable in children than adults, who may have developed other conditions that affect the composition of sweat.",True,Clinical Presentation of Cystic Fibrosis,,,,
6260091c-03ed-41a3-963d-51235f96ffb3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
6260091c-03ed-41a3-963d-51235f96ffb3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
6260091c-03ed-41a3-963d-51235f96ffb3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
6260091c-03ed-41a3-963d-51235f96ffb3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
6260091c-03ed-41a3-963d-51235f96ffb3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
63d3d699-9efa-4924-ade2-6ab6059e5227,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Spirometry detects the airway obstruction and hyperinflation that produce a low vital capacity and high residual volume.,True,Clinical Presentation of Cystic Fibrosis,,,,
8c62913d-ea3e-4082-afd4-4806efcada93,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Bronchiectasis,False,Bronchiectasis,,,,
c268c198-157a-431e-a453-ec77e81f491a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"This section will address bronchiectasis, a form of airway obstruction that is often a manifestation of chronic airway inflammation. Bronchiectasis involves a permanent dilation of a bronchi or bronchiole—think of bronchiectasis as the airway equivalent of an aneurysm.",True,Bronchiectasis,,,,
d3a158f3-33a9-429d-b50c-c91812fc4e0f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
d3a158f3-33a9-429d-b50c-c91812fc4e0f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
d3a158f3-33a9-429d-b50c-c91812fc4e0f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
d3a158f3-33a9-429d-b50c-c91812fc4e0f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
d3a158f3-33a9-429d-b50c-c91812fc4e0f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
81b9ddd6-cf7f-4046-b752-7f2f8151d60f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
81b9ddd6-cf7f-4046-b752-7f2f8151d60f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
81b9ddd6-cf7f-4046-b752-7f2f8151d60f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
81b9ddd6-cf7f-4046-b752-7f2f8151d60f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
81b9ddd6-cf7f-4046-b752-7f2f8151d60f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
610bc4d6-e804-488d-8882-c97e2fdc9293,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The establishing of a bronchiectasis has an initial phase leading to persistent inflammation, desquamation (which worsens the mucus clearance), and the ulceration. In what is probably a familiar story, the continued inflammation leads to fibrosis in the chronic phase of development, and this can lead to airway destruction and perhaps the condition of bronchiolitis obliterans.",True,Bronchiectasis,,,,
f0d247cb-d0d3-4cf8-a5bb-288c1bdec4e5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Let us look at how this process can get started.,False,Let us look at how this process can get started.,,,,
1d9c0cb5-c28b-4303-af1a-ce7fd2ca0d74,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Pathogenesis of Bronchiectasis,False,Pathogenesis of Bronchiectasis,,,,
163d3e9c-0a93-4634-a74a-e427363d12f7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
163d3e9c-0a93-4634-a74a-e427363d12f7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
163d3e9c-0a93-4634-a74a-e427363d12f7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
163d3e9c-0a93-4634-a74a-e427363d12f7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
163d3e9c-0a93-4634-a74a-e427363d12f7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
cc32fbf6-dc2b-4fae-8f1f-c6e307d3c29b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"About 50 percent of bronchiectasis cases are associated with cystic fibrosis where the genetic condition causes production of copious, thick mucus that is difficult to clear and often results in infection (commonly caused by Staphylococcus aureus).",True,Pathogenesis of Bronchiectasis,,,,
5b99d39f-333f-48b4-84cb-7dc905fecadd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Conditions causing cillary dyskinesia, as seen in Kartagener’s syndrome, also disrupt the mucocillary escalator.",True,Pathogenesis of Bronchiectasis,,,,
d5120138-2951-44dd-8027-69f063c01e0f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,mucocillary,False,mucocillary,,,,
e1793262-fad6-4a03-89d6-40c47e446ca5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Another common cause of bronchiectasis is an allergy to Aspergillus fumigatus, a common fungus. In hypersensitive or immune-compromised individuals, chronic exposure can lead to allergic bronchopulmonary aspiragillosis.",True,mucocillary,,,,
dd64c69a-37e5-406d-bc7a-b27842740e8f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,aspiragillosis,False,aspiragillosis,,,,
f54b08b0-5a59-43f7-ae05-f5cef72fdbf2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Bronchiectasis can be initiated in the vicinity of tuberculosis or other necrotizing infections that damage and weaken airway walls.,True,aspiragillosis,,,,
056104bf-4ac9-410e-848a-a9c7aeeb1005,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Obstruction of the bronchioles or bronchi by inhaled foreign objects, tumors, or compacted mucus can also initiate bronchiectasis through local inflammation and by preventing mucus clearance. The dilation of the airway can be worsened further by distal atelectasis that produces a negative pressure around the affected airway.",True,aspiragillosis,,,,
5894deac-f34a-4477-ba78-e2e9e1f2439b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"As you might have gather by now, repeated local infection or inflammation has the potential to initiate bronchiectasis, so it is perhaps not surprising that with the advent of high resolution computed tomography (CT) imaging, bronchiectasis has also been found in association with AIDS, transplant rejection, and rheumatoid lung disease.",True,aspiragillosis,,,,
00b795db-d46a-442e-b728-e31bcdb0acc8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,We will now examine the results of these instigating factors.,False,We will now examine the results of these instigating factors.,,,,
bef38b02-ea2e-46c2-8d3a-c8952814695f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Pathology of Bronchiectasis,False,Pathology of Bronchiectasis,,,,
e1ef6836-5659-4eb2-8635-888f738742b5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
e1ef6836-5659-4eb2-8635-888f738742b5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
e1ef6836-5659-4eb2-8635-888f738742b5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
e1ef6836-5659-4eb2-8635-888f738742b5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
e1ef6836-5659-4eb2-8635-888f738742b5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
d7832658-a0f8-4ae4-8dfb-0b64e496d5d7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
d7832658-a0f8-4ae4-8dfb-0b64e496d5d7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
d7832658-a0f8-4ae4-8dfb-0b64e496d5d7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
d7832658-a0f8-4ae4-8dfb-0b64e496d5d7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
d7832658-a0f8-4ae4-8dfb-0b64e496d5d7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
825fb1f6-269e-41d9-a162-851541e9bf78,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
825fb1f6-269e-41d9-a162-851541e9bf78,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
825fb1f6-269e-41d9-a162-851541e9bf78,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
825fb1f6-269e-41d9-a162-851541e9bf78,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
825fb1f6-269e-41d9-a162-851541e9bf78,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
214e85cf-6789-4d13-9a25-9d1dadd8deaa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"A bronchiectasis can be cylindrical, varicose (also known as fusiform), or cystic (also known as saccular). The shape is relevant to their effect on the efficacy of coughing; cylindrical form has very little effect on cough’s ability to clear mucus, whereas varicose and cystic forms tend to disproportionately collapse during cough and reduce its effectiveness at moving mucus up the airway.",True,Pathology of Bronchiectasis,,,,
1ca80deb-a10d-4211-9f61-ff7bc907df7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
1ca80deb-a10d-4211-9f61-ff7bc907df7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
1ca80deb-a10d-4211-9f61-ff7bc907df7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
1ca80deb-a10d-4211-9f61-ff7bc907df7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
1ca80deb-a10d-4211-9f61-ff7bc907df7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
2fefcac4-837c-4f15-8b01-f4f85cb1c748,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
2fefcac4-837c-4f15-8b01-f4f85cb1c748,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
2fefcac4-837c-4f15-8b01-f4f85cb1c748,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
2fefcac4-837c-4f15-8b01-f4f85cb1c748,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
2fefcac4-837c-4f15-8b01-f4f85cb1c748,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
a0f2d932-3e59-4374-97e4-3a9bc799b18b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"So, how does bronchiectasis present, and what are the results of diagnostic tests?",True,Pathology of Bronchiectasis,,,,
23f94ecf-aa36-4528-aadc-638a4711f5f2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Clinical Presentation of Bronchiectasis,False,Clinical Presentation of Bronchiectasis,,,,
8177954f-4d57-4202-94ef-ca02f3638f1e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The initial complaint is usually a persistent cough with copious expectoration. The amount of mucus the cough produces varies and can be as high as several hundred milliliters per day, particular when the dependent airways are involved. However, it is worth noting here that bronchiectasis in the upper lobes (usually associated with infection) may be dry with little or no mucus expectoration.",True,Clinical Presentation of Bronchiectasis,,,,
f4be8cf7-0479-45a1-a676-436c0bab4a57,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Generally though there is mucopurulent expectorate, and if it is associated with an anerobic infection it will likely have a foul odor. Sputum smears are loaded with white blood cells and can contain both gram-positive and -negative organisms.",True,Clinical Presentation of Bronchiectasis,,,,
b98fb766-4611-454f-855b-6e935d27b68a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The patient will likely have a history of recurrent pneumonia, the site of the pneumonia being consistent with locality of the bronchiectasis.",True,Clinical Presentation of Bronchiectasis,,,,
650bd405-610e-4d7e-b204-c32594335dc7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The expectorate may also contain blood. The degree and frequency of hemoptysis is variable and unpredictable, but occasionally it can be massive and life threatening.",True,Clinical Presentation of Bronchiectasis,,,,
a94286a0-8b1a-4c29-b8d4-f5d6ff3a5f2a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"The standard diagnostic tests may not be helpful in early stages, but typical signs appear with worsening airway involvement. In the early stages the patient will likely appear normal on a physical exam and have normal spirometry and arterial blood gas values. With more significant bronchiectasis, rales and rhonchi over the affected site can be heard.",True,Clinical Presentation of Bronchiectasis,,,,
ac24803c-6393-4041-ba95-509144a05804,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Later signs with long-standing bronchiectasis include finger clubbing, but this is not exclusive to the condition.",True,Clinical Presentation of Bronchiectasis,,,,
c10e01ad-edac-4f4b-98d7-b76b9eace4a8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"A chest x-ray will show the peribronchial fibrosis and any atelectasis. But, as mentioned earlier, a high-resolution CT is much more effective at determining the degree and type of airway changes.",True,Clinical Presentation of Bronchiectasis,,,,
8a7f7f35-7455-4a65-b345-b2fdff9ad9d8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"References, Resources, and Further Reading",False,"References, Resources, and Further Reading",,,,
846b7acd-af11-4008-bc41-e78da85d3592,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,Text,False,Text,,,,
15add341-5700-4724-8b0a-4ce3d9014a2a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapters 8–11.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
1193d138-64bd-4a9e-b1c5-367039609bcd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
cc812a3a-5704-4b99-a6a9-18337825abc1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Cystic Fibrosis,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-3,"West, John B. “Chapter 4: Obstructive Diseases.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Text,,,,
2d6ce0d2-2f2b-43e4-95f7-7c002b233562,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
2d6ce0d2-2f2b-43e4-95f7-7c002b233562,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
2d6ce0d2-2f2b-43e4-95f7-7c002b233562,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
2d6ce0d2-2f2b-43e4-95f7-7c002b233562,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
2d6ce0d2-2f2b-43e4-95f7-7c002b233562,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
a50786ae-0d73-4132-b047-3b37ba6a1e27,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,We will also look at how exercise and certain pharmacological agents can produce asthma.,True,Text,,,,
f1cd6894-df65-4760-a43a-30b580b41caf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
f1cd6894-df65-4760-a43a-30b580b41caf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
f1cd6894-df65-4760-a43a-30b580b41caf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
f1cd6894-df65-4760-a43a-30b580b41caf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
f1cd6894-df65-4760-a43a-30b580b41caf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
d41604cb-c831-435f-ae87-bc966fd5e86d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,proinflammatory,False,proinflammatory,,,,
b7e83193-398a-44cf-abe4-19f01636e708,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,The results of this cocktail’s release are the hallmarks of asthma:,True,proinflammatory,,,,
0881643c-daf5-40ec-8555-38a1b5bea5ce,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The timeline from the exposure to the antigen to asthmatic response is not straightforward. A response may occur within minutes (“early response”), or hours later (“late response”). Some patients show only an early response, some only a late one, and some show both in a “dual” response. The late response may correspond to the arrival of leucocytes in response to the initial release of cytokines. It may also be due to a mild stimulus arriving later in an airway that was sensitized earlier.",True,proinflammatory,,,,
3a0c39fd-e995-4973-949a-582ebf606573,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
3a0c39fd-e995-4973-949a-582ebf606573,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
3a0c39fd-e995-4973-949a-582ebf606573,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
3a0c39fd-e995-4973-949a-582ebf606573,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
3a0c39fd-e995-4973-949a-582ebf606573,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
5710d39a-f0a4-4860-b827-f3695b36b448,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
5710d39a-f0a4-4860-b827-f3695b36b448,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
5710d39a-f0a4-4860-b827-f3695b36b448,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
5710d39a-f0a4-4860-b827-f3695b36b448,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
5710d39a-f0a4-4860-b827-f3695b36b448,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
a86d7a19-0f1a-4af1-b46c-fe9f4cd01716,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The cholinergic response may help produce an asthmatic response to another stimulus that normally would not have produced one (i.e., it may play a part in the hypersensitivity of the asthmatic airways). Likewise, the presence of an infection, particularly a viral infection, may place the airway in a proinflammatory state.",True,proinflammatory,,,,
604a2e5d-e37a-4cad-a964-a55db9986ba9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
604a2e5d-e37a-4cad-a964-a55db9986ba9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
604a2e5d-e37a-4cad-a964-a55db9986ba9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
604a2e5d-e37a-4cad-a964-a55db9986ba9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
604a2e5d-e37a-4cad-a964-a55db9986ba9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
f87dc5bb-da56-4bf1-83f6-5c22c4caeadc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Exercise-induced asthma: Although exercise is associated with increased airway caliber, it can also induce asthma. Increased airway flow to meet the increased metabolic demand of exercise results in loss of fluid and heat from airway surfaces. This leaves the peribronchial fluid in a hypertonic state and causes excitation of the irritant airway receptors, which leads to release of the mast cells’ cocktail.",True,proinflammatory,,,,
0846ec4a-6945-4c3e-bc14-d3e46195b70d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Exercise-induced asthma is more prevalent in cold (i.e. dry air) where water loss will be higher, so occurs more in sports such as cross-country skiing than swimming in a warm humid environment. Bronchoconstriction usually occurs when exercise stops—when the protective effect of sympathetic activity to the airway smooth muscles ceases.",True,proinflammatory,,,,
9b5957d6-03ba-4030-bb0f-4cfb83361138,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Drug-induced asthma: There are several pharmaceutical and food products that can promote asthma, including tartrazine (a yellow food coloring) and sulfides used as food preservatives. Additionally, 10 to 20 percent of asthmatics are sensitive to aspirin.",True,proinflammatory,,,,
365af580-3495-431d-a2f6-350d8a5ca91c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
365af580-3495-431d-a2f6-350d8a5ca91c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
365af580-3495-431d-a2f6-350d8a5ca91c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
365af580-3495-431d-a2f6-350d8a5ca91c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
365af580-3495-431d-a2f6-350d8a5ca91c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
246c5080-e04d-496e-902a-f0a8d05b00a3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Environmental/occupational asthma: As the airway is open to the environment, it is susceptible to inhaled substances that can cause sensitization; there are over two hundred substances known to cause asthma, both organic and inorganic. Some common ones are listed below.",True,proinflammatory,,,,
82b7c192-523f-42e0-85db-41d5067c158a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Table 1.1: Some of the most common environmental causes of asthma. Taking a pulmonary history should include asking about potential environmental exposures.,True,proinflammatory,,,,
c07d9cde-d40b-44fc-b229-e1ef94f86bce,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Determining whether airway hypersensitivity is due to environmental factors is complicated by widely varying latency periods. Short latency periods can be as brief as twenty-four hours and are associated with vapor or smoke exposure that does not cause an immunological response. Longer latency periods that may last years are more commonly associated with an immunological response to large particles that act like antigens.,True,proinflammatory,,,,
074d1b4f-77e6-4dae-8170-cc842a15bfee,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The situation is further confused by occupation-related responses, which often cause the airway to become more sensitive to some of the other causes of asthma covered here. This makes the role of an environmental factor more difficult to determine.",True,proinflammatory,,,,
f52d55a9-c3ec-4b20-956c-a09f9f71ca98,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Pathophysiology of Asthma,False,Pathophysiology of Asthma,,,,
c914cbe2-bf45-4505-b8bc-d9ca066ee345,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
c914cbe2-bf45-4505-b8bc-d9ca066ee345,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
c914cbe2-bf45-4505-b8bc-d9ca066ee345,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
c914cbe2-bf45-4505-b8bc-d9ca066ee345,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
c914cbe2-bf45-4505-b8bc-d9ca066ee345,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
e6833bb8-4fe2-4015-9432-78cfaec8c030,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
e6833bb8-4fe2-4015-9432-78cfaec8c030,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
e6833bb8-4fe2-4015-9432-78cfaec8c030,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
e6833bb8-4fe2-4015-9432-78cfaec8c030,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
e6833bb8-4fe2-4015-9432-78cfaec8c030,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
a2fca22b-ec69-484d-81af-21a1960b455b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
a2fca22b-ec69-484d-81af-21a1960b455b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
a2fca22b-ec69-484d-81af-21a1960b455b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
a2fca22b-ec69-484d-81af-21a1960b455b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
a2fca22b-ec69-484d-81af-21a1960b455b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
804119e8-ccad-498d-8725-280b1a6b89cb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
804119e8-ccad-498d-8725-280b1a6b89cb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
804119e8-ccad-498d-8725-280b1a6b89cb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
804119e8-ccad-498d-8725-280b1a6b89cb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
804119e8-ccad-498d-8725-280b1a6b89cb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
5e0a623d-fe5f-4949-a005-9d48ccd85bd1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Clinical Presentation of Asthma,False,Clinical Presentation of Asthma,,,,
45d697f9-bb1f-417e-ad78-97a81ca06ae9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"One useful diagnostic element of asthma is its episodic or acute behavior. However, as patients may be asymptomatic between attacks, the severity of asthma can be difficult to determine without performing bronchial challenge tests.",True,Clinical Presentation of Asthma,,,,
ee73400a-0d3b-4a52-98e9-e3ed5e6005c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
ee73400a-0d3b-4a52-98e9-e3ed5e6005c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
ee73400a-0d3b-4a52-98e9-e3ed5e6005c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
ee73400a-0d3b-4a52-98e9-e3ed5e6005c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
ee73400a-0d3b-4a52-98e9-e3ed5e6005c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
be8de91c-6051-4f37-bdda-6adaa35d3c5a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"As airway resistance increases, the accessory muscles are deployed to maintain sufficient airflow through the narrowing airways, and the patient experiences an increased effort to breathe. Increased expiratory efforts produce dynamic airway collapse and lead to hyperinflation. Further decreases in airway caliber result in insufficient alveolar ventilation and deranged blood gases. The sensation reported at this point is air hunger. Once the patient is severely bronchoconstricted, delivery of inhaled therapies is much more difficult, and mechanical ventilation to support the respiratory muscles becomes complicated. Other signs present during a severe attack are raised heart (tachycardia) and breathing (tachypnea) rates as well as a paradoxical pulse (i.e., a rise in blood pressure during expiration).",True,Clinical Presentation of Asthma,,,,
c5f2ec9d-3159-4422-9227-7ae1c555d479,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
c5f2ec9d-3159-4422-9227-7ae1c555d479,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
c5f2ec9d-3159-4422-9227-7ae1c555d479,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
c5f2ec9d-3159-4422-9227-7ae1c555d479,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
c5f2ec9d-3159-4422-9227-7ae1c555d479,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
3d3d6adb-0f96-4c3d-90d4-b39f6b7a1fbc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Chronic Obstructive Pulmonary Disease,False,Chronic Obstructive Pulmonary Disease,,,,
9966e7f9-a015-439c-b25a-679f4c55e733,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Although chronic bronchitis and emphysema have different underlying pathologies, they frequently have the same root cause and are often found together in a patient. In brief, chronic bronchitis is associated with an increase in mucus production, while emphysema involves disruption of the lung structure.",True,Chronic Obstructive Pulmonary Disease,,,,
9aadf755-28bd-4d53-a3dd-adcb1cf40331,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The relative role of chronic bronchitis in COPD has diminished since the Clean Air Act reduced atmospheric sulphur dioxide, but with 90 percent of COPD caused by cigarette smoking there is still plenty of bronchitis and emphysema to treat—at enormous cost to the health system from over eight million hospitalizations a year that are mostly paid for by Medicare. The COPD patient tends to be older and poorer and will likely have comorbidities, the most common of which is hypertension. What is perhaps more disturbing is that of the most common causes of death, COPD is the only one whose incidence continues to rise.",True,Chronic Obstructive Pulmonary Disease,,,,
3286077f-4b4c-49cc-87ac-2382830af996,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"We will now look at the underlying mechanisms of COPD. Despite the fact it is usually composed of some elements of both chronic bronchitis and emphysema, we will deal with each separately for the sake of simplicity.",True,Chronic Obstructive Pulmonary Disease,,,,
b7119f01-410f-48cf-b6a2-a64e33e3a6d4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Chronic Bronchitis,False,Chronic Bronchitis,,,,
bd191e7d-2ea8-443f-94d6-7c0fe781557e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Chronic bronchitis is clinically defined as a persistent and productive cough that lasts for at least three months per year for two consecutive years.,True,Chronic Bronchitis,,,,
6ee8324d-ce41-4d07-b285-f30ca720d4c1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
6ee8324d-ce41-4d07-b285-f30ca720d4c1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
6ee8324d-ce41-4d07-b285-f30ca720d4c1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
6ee8324d-ce41-4d07-b285-f30ca720d4c1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
6ee8324d-ce41-4d07-b285-f30ca720d4c1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
3b669743-edcf-4bf2-a3d3-a7dc20787b3f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Neutrophils, lymphocytes, and macrophages are attracted to the irritated airway, and their presence is maintained through increased expression of cell adhesion molecules on the airway walls. These immune cells lead to acute airway wall inflammation that narrows the airway, and if chronic, can lead to tissue damage. The cytokines released by these cells also sensitize airway irritant receptors, which exacerbates the response to future irritant exposure.",True,Chronic Bronchitis,,,,
d46d20e4-b0ad-494f-abf8-e1cca7f3a3c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Mucus production increases, and the glands themselves may also release cytokines that further exacerbate the inflammatory response. The mucus also contributes to airway narrowing, and mucus plugs may form that completely block bronchioles.",True,Chronic Bronchitis,,,,
d48251cb-8525-4a63-b5d7-2c6641ad459b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Mesenchymal cells transition into fibroblasts as part of the inflammatory response, and their chronic presence leads to the deposition of fibrotic tissue.",True,Chronic Bronchitis,,,,
a44e92df-fdce-4928-8c2e-fc9575a41307,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Collectively these responses to the irritants result in a narrowed airway that is (1) hypersensitive, (2) fibrosed, and (3) blocked by excessive secretions.",True,Chronic Bronchitis,,,,
043fbfd7-a06a-44b0-b85d-9fa311f3bcb4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
043fbfd7-a06a-44b0-b85d-9fa311f3bcb4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
043fbfd7-a06a-44b0-b85d-9fa311f3bcb4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
043fbfd7-a06a-44b0-b85d-9fa311f3bcb4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
043fbfd7-a06a-44b0-b85d-9fa311f3bcb4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
51c11cd3-21a2-45dc-be3b-85cc535d41bc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
51c11cd3-21a2-45dc-be3b-85cc535d41bc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
51c11cd3-21a2-45dc-be3b-85cc535d41bc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
51c11cd3-21a2-45dc-be3b-85cc535d41bc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
51c11cd3-21a2-45dc-be3b-85cc535d41bc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
d5b62bd5-5092-4b32-a934-ffdb54356cc8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"These changes result in an airway that produces more mucus and is less capable of removing it. The static mucus not only causes airway plugging, but can also promote infections that lead to episodic and characteristic exacerbation of COPD symptoms.",True,Chronic Bronchitis,,,,
8913a274-87d7-45b6-b676-a472f5394603,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Clinical Presentation of Chronic Bronchitis,False,Clinical Presentation of Chronic Bronchitis,,,,
004d7d90-5188-4e07-ac07-7a7362c8451e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
004d7d90-5188-4e07-ac07-7a7362c8451e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
004d7d90-5188-4e07-ac07-7a7362c8451e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
004d7d90-5188-4e07-ac07-7a7362c8451e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
004d7d90-5188-4e07-ac07-7a7362c8451e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
f4d96d9d-a4ab-42c7-b890-b759d0b15929,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"As with many pulmonary diseases, the onset can be insidious. Small airway damage may be present but undetectable with normal spirometry, while the patient becomes accustomed to and tolerates a persistent productive cough. However, with continued irritant exposure, this initial simple bronchitis progresses.",True,Clinical Presentation of Chronic Bronchitis,,,,
ff09b567-db41-41aa-9c0e-62c33509e3da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Secretions continue to worsen and peribronchiolar fibrosis marks the onset of obstructive bronchitis that is reflected by significant expiratory airflow limitation. At this point the patient may have tolerated years of productive cough and experienced frequent chest infections related to poor mucus clearance. COPDers are particularly susceptible to Haemophilus influenza and Streptococcus pneumoniae. The sputum is abundant and capable of plugging significant numbers of airways and may be blood tinged; COPD is the most common cause of hemoptysis. Airways may demonstrate hyperreactivity and mimic an asthmatic response.,True,Clinical Presentation of Chronic Bronchitis,,,,
f39c1be4-3523-4726-a2ad-f4f4651aca1a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The onset of dyspnea is insidious and is usually first experienced during exertion—leading the patient to avoid exercise, which in turn leads to deconditioning and a worsening of the symptom. Lung sounds include wheezes and rales, the rales often clearing after cough.",True,Clinical Presentation of Chronic Bronchitis,,,,
eeaae1d1-52ac-4c44-895e-9d1e70d755b2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,With worsening airway flow limitation expiration becomes prolonged and may be incomplete due to airway collapse that leads to characteristic hyperinflation.,True,Clinical Presentation of Chronic Bronchitis,,,,
92532c08-f65c-4d60-b3ac-64463ff16518,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Mucus plugging and airway closure leads to areas of V/Q abnormalities through the lung, and localized areas of hypoxia can lead to pulmonary vasoconstriction. When significant regions of the lung are vasoconstricted, pulmonary vascular resistance can rise enough to induce right-sided heart failure.",True,Clinical Presentation of Chronic Bronchitis,,,,
537b5d17-3800-4ec9-bd3d-5ac9083238a2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"With continued progression of the disease, blood gases become deranged as insufficient alveolar ventilation is achieved. As the disease approaches its end stage, the patient experiences dyspnea at rest until respiratory failure occurs and the patient is hypoxemic and hypercarbic.",True,Clinical Presentation of Chronic Bronchitis,,,,
d65a4271-2b59-4616-b5cd-1006be494987,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Emphysema,False,Emphysema,,,,
919e0f57-91e7-47ed-b362-1e79b2836bcb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
919e0f57-91e7-47ed-b362-1e79b2836bcb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
919e0f57-91e7-47ed-b362-1e79b2836bcb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
919e0f57-91e7-47ed-b362-1e79b2836bcb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
919e0f57-91e7-47ed-b362-1e79b2836bcb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
e6fa5a8b-b831-40f7-a9cc-de4b4abcc160,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
e6fa5a8b-b831-40f7-a9cc-de4b4abcc160,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
e6fa5a8b-b831-40f7-a9cc-de4b4abcc160,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
e6fa5a8b-b831-40f7-a9cc-de4b4abcc160,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
e6fa5a8b-b831-40f7-a9cc-de4b4abcc160,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
f75b0fab-3f66-474c-b771-2ea6372fbc11,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
f75b0fab-3f66-474c-b771-2ea6372fbc11,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
f75b0fab-3f66-474c-b771-2ea6372fbc11,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
f75b0fab-3f66-474c-b771-2ea6372fbc11,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
f75b0fab-3f66-474c-b771-2ea6372fbc11,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
4618b584-e154-4a4e-a641-4ea1bf2b8e98,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
4618b584-e154-4a4e-a641-4ea1bf2b8e98,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
4618b584-e154-4a4e-a641-4ea1bf2b8e98,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
4618b584-e154-4a4e-a641-4ea1bf2b8e98,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
4618b584-e154-4a4e-a641-4ea1bf2b8e98,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
bf5621e8-b905-4363-abd0-f59ae87eda3a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"So having seen the morphology of emphysema, we will look at how this damage occurs.",True,Emphysema,,,,
3d7b16a7-c5c0-4ab4-bd20-e3db509ba6f5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Pathophysiology of Emphysema,False,Pathophysiology of Emphysema,,,,
885c9b2d-c2ed-47ac-a8c6-34905d685d3d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,The normal structure of alveoli and respiratory ducts consists of type 1 and type 2 pneumocytes with elastic fibers that contribute to the structure’s mechanical behavior. Emphysema involves the loss of these parenchymal fibers.,True,Pathophysiology of Emphysema,,,,
3d0b10b3-2c5a-4463-873d-750881e3203e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The presence of irritants, such as cigarette smoke, causes oxidization and the dysfunction of antiprotease enzymes. Without their inhibitory action, the activity of proteases increases and causes the destruction of local tissue. One of these proteases is elastase, whose elevated activity leads to irreparable loss of parenchymal fibers.",True,Pathophysiology of Emphysema,,,,
dc5d5b67-0180-4cf1-adc2-a9c1a2549a73,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Elastase is also released by neutrophils and macrophages that arrive in response to the inflammatory cascade caused by the inhaled smoke. This causes further destruction of elastin fibers.,True,Pathophysiology of Emphysema,,,,
efecc2fb-d022-4120-8201-1cf64a3c5ae8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
efecc2fb-d022-4120-8201-1cf64a3c5ae8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
efecc2fb-d022-4120-8201-1cf64a3c5ae8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
efecc2fb-d022-4120-8201-1cf64a3c5ae8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
efecc2fb-d022-4120-8201-1cf64a3c5ae8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
22259f2e-64fc-41fe-be23-4aa545981b7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
22259f2e-64fc-41fe-be23-4aa545981b7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
22259f2e-64fc-41fe-be23-4aa545981b7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
22259f2e-64fc-41fe-be23-4aa545981b7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
22259f2e-64fc-41fe-be23-4aa545981b7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
d508e7ad-13bf-4fe4-a4e8-db078f423958,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,The loss of the elastic tissue and alveolar structure produces several pathophysiological changes in lung mechanics and function that result in typical clinical signs.,True,Pathophysiology of Emphysema,,,,
a000f1d8-89c2-4978-8bc4-4a6681c96f35,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Clinical Presentation of Emphysema,False,Clinical Presentation of Emphysema,,,,
38733dfd-a741-4bb0-ba27-7ba77f15b6f8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
38733dfd-a741-4bb0-ba27-7ba77f15b6f8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
38733dfd-a741-4bb0-ba27-7ba77f15b6f8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
38733dfd-a741-4bb0-ba27-7ba77f15b6f8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
38733dfd-a741-4bb0-ba27-7ba77f15b6f8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
a4f1ee65-d600-49bf-85e0-6eaa80129ec6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
a4f1ee65-d600-49bf-85e0-6eaa80129ec6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
a4f1ee65-d600-49bf-85e0-6eaa80129ec6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
a4f1ee65-d600-49bf-85e0-6eaa80129ec6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
a4f1ee65-d600-49bf-85e0-6eaa80129ec6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
905e6810-3122-4f2f-b628-07cc4e289c54,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
905e6810-3122-4f2f-b628-07cc4e289c54,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
905e6810-3122-4f2f-b628-07cc4e289c54,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
905e6810-3122-4f2f-b628-07cc4e289c54,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
905e6810-3122-4f2f-b628-07cc4e289c54,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
396f8fcf-42e0-402c-8fe0-68c5acb61cae,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The deterioration of gas exchange and lung mechanics worsens as more lung becomes involved, and the stage of the disease, and any concurrent chronic bronchitis, is classified by the level of airway flow limitation (e.g., FEV1/FVC).",True,Clinical Presentation of Emphysema,,,,
a72ccf2f-146f-48ed-8d62-b5a9b987f5bd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"It might also be worth noting here that COPD can produce or be associated with a number of comorbidities; we have already mentioned hypertension, but pulmonary artery disease, coronary heart disease, heart failure, lung cancer, and malnutrition may contribute to a low quality of life that is typically associated with COPD. This in turn may contribute to the high incidence of anxiety disorders and depression experienced by COPD patients.",True,Clinical Presentation of Emphysema,,,,
349dda59-23f8-4773-bfcf-c32b1ecc699b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Cystic Fibrosis,False,Cystic Fibrosis,,,,
88ce7113-f46b-417c-9c18-0043d924a6b2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Cystic fibrosis (CF) is an inherited disorder that affects the exocrine glands of not only the lungs, but also the pancreas, intestines, and bile ducts. We will focus only on the pulmonary aspects here and see how CF produces an obstructive lung disease.",True,Cystic Fibrosis,,,,
fe41f267-9ad3-4451-88c4-bef9654d5529,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Cystic fibrosis affects the composition of the fluid lining the airways. Changes in this fluid lead to serious sequelae that dramatically shorten life expectancy. Even with modern therapy, many CF patients only live until their thirties or early forties, and some still die in infancy.",True,Cystic Fibrosis,,,,
fb13c669-2214-43e1-a497-9f38bf322df7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,There are two hypotheses about the pathophysiological mechanism of CF: the low volume and the high salt. We will focus only on the low volume hypothesis as there is increasing evidence to support this and emerging evidence against the high salt hypothesis.,True,Cystic Fibrosis,,,,
a24d7979-9b20-4293-8d00-be6a9defeb56,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Pathophysiology of Cystic Fibrosis,False,Pathophysiology of Cystic Fibrosis,,,,
c74af52b-49b0-47fa-a5d1-de0147b2ca5a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
c74af52b-49b0-47fa-a5d1-de0147b2ca5a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
c74af52b-49b0-47fa-a5d1-de0147b2ca5a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
c74af52b-49b0-47fa-a5d1-de0147b2ca5a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
c74af52b-49b0-47fa-a5d1-de0147b2ca5a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
f01d49d4-b4be-407b-8791-871a588eadb8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,ENaC,False,ENaC,,,,
99043551-0b8d-496a-a9c2-8501dbaa5bd7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
99043551-0b8d-496a-a9c2-8501dbaa5bd7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
99043551-0b8d-496a-a9c2-8501dbaa5bd7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
99043551-0b8d-496a-a9c2-8501dbaa5bd7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
99043551-0b8d-496a-a9c2-8501dbaa5bd7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
ee93a55d-2b7d-4e58-8bd6-c0fe716275bf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"There are numerous mutations that are known to produce a dysfunctional CFTR channel, but 70 percent of CF cases are due to the delta-F-508 mutation (so named as the mutation leads to a deletion of phenylalanine at position 508 of the CFTR protein). This is a Mendelian recessive trait, and CF occurrence is 1 in 2,500 live births.",True,ENaC,,,,
4ab0f26a-5aa9-45df-a466-5ffa1e7db7b1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
4ab0f26a-5aa9-45df-a466-5ffa1e7db7b1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
4ab0f26a-5aa9-45df-a466-5ffa1e7db7b1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
4ab0f26a-5aa9-45df-a466-5ffa1e7db7b1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
4ab0f26a-5aa9-45df-a466-5ffa1e7db7b1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
9d5a952e-dcbd-482c-99b5-cdaa8ad573c3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"This combination severely impacts mucus clearance (thicker, heavier mucus with compromised cillary escalator). The defective CFTR channel therefore results in mucus retention and airway obstruction. This in turn leads to reduced alveolar ventilation and repeated infections. The two most common culprits for infection in CF are Staphylococcus aureus and Pseudomonsa aeruginosa. Normal functional CFTR appears to suppress P. aeruginosa, perhaps explaining its prevalence in cystic fibrosis where it can be found in the sputum of almost all CF patients.",True,ENaC,,,,
cc2eb8f8-16e6-41a4-8e77-43e6d4184a0a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,cillary,False,cillary,,,,
8c3960b4-69c1-4125-9537-6f5bb57ca66d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Pseudomonsa,False,Pseudomonsa,,,,
d196c8d0-fb96-4d0a-a69e-f60250ddb6c9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
d196c8d0-fb96-4d0a-a69e-f60250ddb6c9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
d196c8d0-fb96-4d0a-a69e-f60250ddb6c9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
d196c8d0-fb96-4d0a-a69e-f60250ddb6c9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
d196c8d0-fb96-4d0a-a69e-f60250ddb6c9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
b60b0892-b39d-4f82-bb12-9fdcd96df4fb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The findings of CF obviously include the results of other effected organs, such as the pancreas. But nowadays these are more easily addressed, and it is pulmonary involvement that still proves critical. The onset of pulmonary involvement is variable and may be weeks or years after birth.",True,Pseudomonsa,,,,
10adf1aa-176a-4748-a45c-a9c3fa5bdc12,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Clinical Presentation of Cystic Fibrosis,False,Clinical Presentation of Cystic Fibrosis,,,,
2c16d761-01e6-464e-b905-8bc8dfbd3abe,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
2c16d761-01e6-464e-b905-8bc8dfbd3abe,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
2c16d761-01e6-464e-b905-8bc8dfbd3abe,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
2c16d761-01e6-464e-b905-8bc8dfbd3abe,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
2c16d761-01e6-464e-b905-8bc8dfbd3abe,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
6afbaae1-6b2a-43fd-93d8-3a6e16a19dbf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,CF patients usually have an abnormal sinus x-ray and evidence of chronic sinusitis as well as a high occurrence of nasal polyps.,True,Clinical Presentation of Cystic Fibrosis,,,,
4fa644bd-92e2-48b1-922e-e3848a765b47,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"With increasing and irreversible airway damage, the patients begins to experience dyspnea, and the damage may lead to hemoptysis, spontaneous pneumothorax, and a barrel chested appearance. Signs of prolonged pulmonary dysfunction appear as the disease progresses, such as finger clubbing, cyanosis, and cor pulmonale (right-sided heart failure caused by lung disease). As the patient approaches respiratory failure the accessory muscles are deployed. Patients succumb to the respiratory failure or an overwhelming infection.",True,Clinical Presentation of Cystic Fibrosis,,,,
db91437d-d5a9-4024-a181-c0715bce2ad9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Because CF also affects sweat gland function, the sweat test remains a standard diagnostic with a chloride level greater than 60 mEq/L being indicative of CF. This test is more reliable in children than adults, who may have developed other conditions that affect the composition of sweat.",True,Clinical Presentation of Cystic Fibrosis,,,,
5ed56e71-05e1-459b-afec-6a63c50fbf8f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
5ed56e71-05e1-459b-afec-6a63c50fbf8f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
5ed56e71-05e1-459b-afec-6a63c50fbf8f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
5ed56e71-05e1-459b-afec-6a63c50fbf8f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
5ed56e71-05e1-459b-afec-6a63c50fbf8f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
8284da3b-ff73-4c8d-84d1-b08599f3591f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Spirometry detects the airway obstruction and hyperinflation that produce a low vital capacity and high residual volume.,True,Clinical Presentation of Cystic Fibrosis,,,,
e25001bd-9574-459f-b870-55e9b1990d68,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Bronchiectasis,False,Bronchiectasis,,,,
c6e5cf2f-4808-45b1-b518-74ddcc792024,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"This section will address bronchiectasis, a form of airway obstruction that is often a manifestation of chronic airway inflammation. Bronchiectasis involves a permanent dilation of a bronchi or bronchiole—think of bronchiectasis as the airway equivalent of an aneurysm.",True,Bronchiectasis,,,,
377eb215-7b4b-4966-a51d-1488927a9402,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
377eb215-7b4b-4966-a51d-1488927a9402,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
377eb215-7b4b-4966-a51d-1488927a9402,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
377eb215-7b4b-4966-a51d-1488927a9402,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
377eb215-7b4b-4966-a51d-1488927a9402,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
806346bf-e245-4084-8c94-a5f32ed12d23,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
806346bf-e245-4084-8c94-a5f32ed12d23,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
806346bf-e245-4084-8c94-a5f32ed12d23,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
806346bf-e245-4084-8c94-a5f32ed12d23,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
806346bf-e245-4084-8c94-a5f32ed12d23,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
d90ef04b-8cf7-48d8-adae-859d5cd01111,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The establishing of a bronchiectasis has an initial phase leading to persistent inflammation, desquamation (which worsens the mucus clearance), and the ulceration. In what is probably a familiar story, the continued inflammation leads to fibrosis in the chronic phase of development, and this can lead to airway destruction and perhaps the condition of bronchiolitis obliterans.",True,Bronchiectasis,,,,
261ce61e-92d5-4391-bbd9-b8d30168f869,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Let us look at how this process can get started.,False,Let us look at how this process can get started.,,,,
be52a1f4-c518-4f8f-941b-1a5629e760a7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Pathogenesis of Bronchiectasis,False,Pathogenesis of Bronchiectasis,,,,
2c43a175-ff3d-466f-bd84-39d7b0de1484,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
2c43a175-ff3d-466f-bd84-39d7b0de1484,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
2c43a175-ff3d-466f-bd84-39d7b0de1484,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
2c43a175-ff3d-466f-bd84-39d7b0de1484,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
2c43a175-ff3d-466f-bd84-39d7b0de1484,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
3800a58d-e42d-40bc-a4b0-10a1f34a5199,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"About 50 percent of bronchiectasis cases are associated with cystic fibrosis where the genetic condition causes production of copious, thick mucus that is difficult to clear and often results in infection (commonly caused by Staphylococcus aureus).",True,Pathogenesis of Bronchiectasis,,,,
07e58338-2f16-4abc-a400-aa0cfd7cfecd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Conditions causing cillary dyskinesia, as seen in Kartagener’s syndrome, also disrupt the mucocillary escalator.",True,Pathogenesis of Bronchiectasis,,,,
c8f43023-ded7-46c3-9581-4b255c27c008,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,mucocillary,False,mucocillary,,,,
7e73de42-db2d-4365-ab47-1378113eaad4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Another common cause of bronchiectasis is an allergy to Aspergillus fumigatus, a common fungus. In hypersensitive or immune-compromised individuals, chronic exposure can lead to allergic bronchopulmonary aspiragillosis.",True,mucocillary,,,,
671f0f3a-1d25-4f1a-b355-e7b65aa3d836,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,aspiragillosis,False,aspiragillosis,,,,
35566538-a4f1-4ea9-8315-032d4a9396af,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Bronchiectasis can be initiated in the vicinity of tuberculosis or other necrotizing infections that damage and weaken airway walls.,True,aspiragillosis,,,,
fbed82d0-344a-4b64-8704-4badb9530448,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Obstruction of the bronchioles or bronchi by inhaled foreign objects, tumors, or compacted mucus can also initiate bronchiectasis through local inflammation and by preventing mucus clearance. The dilation of the airway can be worsened further by distal atelectasis that produces a negative pressure around the affected airway.",True,aspiragillosis,,,,
aac54638-401c-4877-b6ed-e32780bc9dc2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"As you might have gather by now, repeated local infection or inflammation has the potential to initiate bronchiectasis, so it is perhaps not surprising that with the advent of high resolution computed tomography (CT) imaging, bronchiectasis has also been found in association with AIDS, transplant rejection, and rheumatoid lung disease.",True,aspiragillosis,,,,
ab0e0c36-77dc-4954-be47-4e4cb45cc283,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,We will now examine the results of these instigating factors.,False,We will now examine the results of these instigating factors.,,,,
b7fe630a-ab01-4165-a629-06f36f673cf9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Pathology of Bronchiectasis,False,Pathology of Bronchiectasis,,,,
8f11de79-d768-4986-a276-4bc228a55234,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
8f11de79-d768-4986-a276-4bc228a55234,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
8f11de79-d768-4986-a276-4bc228a55234,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
8f11de79-d768-4986-a276-4bc228a55234,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
8f11de79-d768-4986-a276-4bc228a55234,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
a9cce0e0-dc47-45f9-8d17-1bf93cbf37ae,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
a9cce0e0-dc47-45f9-8d17-1bf93cbf37ae,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
a9cce0e0-dc47-45f9-8d17-1bf93cbf37ae,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
a9cce0e0-dc47-45f9-8d17-1bf93cbf37ae,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
a9cce0e0-dc47-45f9-8d17-1bf93cbf37ae,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
598e05b7-a6be-4d1f-8413-95199e2fcef4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
598e05b7-a6be-4d1f-8413-95199e2fcef4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
598e05b7-a6be-4d1f-8413-95199e2fcef4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
598e05b7-a6be-4d1f-8413-95199e2fcef4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
598e05b7-a6be-4d1f-8413-95199e2fcef4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
e607f22e-8573-4b1f-8e49-c5fd1dd1cc23,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"A bronchiectasis can be cylindrical, varicose (also known as fusiform), or cystic (also known as saccular). The shape is relevant to their effect on the efficacy of coughing; cylindrical form has very little effect on cough’s ability to clear mucus, whereas varicose and cystic forms tend to disproportionately collapse during cough and reduce its effectiveness at moving mucus up the airway.",True,Pathology of Bronchiectasis,,,,
a13da9ce-d61d-4441-a8b5-a3158e33aba7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
a13da9ce-d61d-4441-a8b5-a3158e33aba7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
a13da9ce-d61d-4441-a8b5-a3158e33aba7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
a13da9ce-d61d-4441-a8b5-a3158e33aba7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
a13da9ce-d61d-4441-a8b5-a3158e33aba7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
e0bac35a-cf16-47de-8c48-4d8328672fd0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
e0bac35a-cf16-47de-8c48-4d8328672fd0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
e0bac35a-cf16-47de-8c48-4d8328672fd0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
e0bac35a-cf16-47de-8c48-4d8328672fd0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
e0bac35a-cf16-47de-8c48-4d8328672fd0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
234e2b2c-27b0-4923-a8c9-24aec5e9e0a7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"So, how does bronchiectasis present, and what are the results of diagnostic tests?",True,Pathology of Bronchiectasis,,,,
7e27d5cc-829e-434c-b2cd-be7cff82cf97,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Clinical Presentation of Bronchiectasis,False,Clinical Presentation of Bronchiectasis,,,,
cda0a252-fc63-4f83-a0e1-327dbcc50c0a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The initial complaint is usually a persistent cough with copious expectoration. The amount of mucus the cough produces varies and can be as high as several hundred milliliters per day, particular when the dependent airways are involved. However, it is worth noting here that bronchiectasis in the upper lobes (usually associated with infection) may be dry with little or no mucus expectoration.",True,Clinical Presentation of Bronchiectasis,,,,
14d76669-9672-4b15-8fe4-3025bceba6e1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Generally though there is mucopurulent expectorate, and if it is associated with an anerobic infection it will likely have a foul odor. Sputum smears are loaded with white blood cells and can contain both gram-positive and -negative organisms.",True,Clinical Presentation of Bronchiectasis,,,,
95830ccb-187b-4b9c-9651-3030fe356a41,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The patient will likely have a history of recurrent pneumonia, the site of the pneumonia being consistent with locality of the bronchiectasis.",True,Clinical Presentation of Bronchiectasis,,,,
2313e93d-4b94-4312-a5a3-1c37cc38ae54,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The expectorate may also contain blood. The degree and frequency of hemoptysis is variable and unpredictable, but occasionally it can be massive and life threatening.",True,Clinical Presentation of Bronchiectasis,,,,
549696df-7798-42c1-a3e9-6f6f3b002d25,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"The standard diagnostic tests may not be helpful in early stages, but typical signs appear with worsening airway involvement. In the early stages the patient will likely appear normal on a physical exam and have normal spirometry and arterial blood gas values. With more significant bronchiectasis, rales and rhonchi over the affected site can be heard.",True,Clinical Presentation of Bronchiectasis,,,,
b4ea13fe-7f72-45bf-a215-641ffb1bf362,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Later signs with long-standing bronchiectasis include finger clubbing, but this is not exclusive to the condition.",True,Clinical Presentation of Bronchiectasis,,,,
9412ffb5-47a5-4876-98dd-62335a668c30,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"A chest x-ray will show the peribronchial fibrosis and any atelectasis. But, as mentioned earlier, a high-resolution CT is much more effective at determining the degree and type of airway changes.",True,Clinical Presentation of Bronchiectasis,,,,
5aa74418-60be-4d01-a56b-54e6ab2d3c02,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"References, Resources, and Further Reading",False,"References, Resources, and Further Reading",,,,
ea8d0877-9ac0-4ec6-a047-b17aa9b4c2c5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,Text,False,Text,,,,
93684652-6fbf-4dcc-8968-e6be933aaa61,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapters 8–11.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
b90e7a50-50cc-4d59-aceb-80490fc5f3b6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
09e8c497-4dc4-47c2-a344-8251bdbf34a6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-2,"West, John B. “Chapter 4: Obstructive Diseases.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Text,,,,
a51efe54-a0bc-4422-813f-a15a73002a5d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
a51efe54-a0bc-4422-813f-a15a73002a5d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
a51efe54-a0bc-4422-813f-a15a73002a5d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
a51efe54-a0bc-4422-813f-a15a73002a5d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
a51efe54-a0bc-4422-813f-a15a73002a5d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
020cff74-2fd1-48cb-9de8-612ce5da7de5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,We will also look at how exercise and certain pharmacological agents can produce asthma.,True,Text,,,,
e0ffe090-ce24-4fbc-b005-59738d8316ed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
e0ffe090-ce24-4fbc-b005-59738d8316ed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
e0ffe090-ce24-4fbc-b005-59738d8316ed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
e0ffe090-ce24-4fbc-b005-59738d8316ed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
e0ffe090-ce24-4fbc-b005-59738d8316ed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
c74f18a0-d2b9-4ef8-bdf5-ca6f83de46b0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,proinflammatory,False,proinflammatory,,,,
f34d0f88-dea8-4b62-a445-c9dbdcb2a70e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,The results of this cocktail’s release are the hallmarks of asthma:,True,proinflammatory,,,,
dd25f421-f369-4ab7-b8ba-549417ecc0dc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The timeline from the exposure to the antigen to asthmatic response is not straightforward. A response may occur within minutes (“early response”), or hours later (“late response”). Some patients show only an early response, some only a late one, and some show both in a “dual” response. The late response may correspond to the arrival of leucocytes in response to the initial release of cytokines. It may also be due to a mild stimulus arriving later in an airway that was sensitized earlier.",True,proinflammatory,,,,
bbb40cbe-684c-42dc-b6b4-f74f03433271,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
bbb40cbe-684c-42dc-b6b4-f74f03433271,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
bbb40cbe-684c-42dc-b6b4-f74f03433271,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
bbb40cbe-684c-42dc-b6b4-f74f03433271,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
bbb40cbe-684c-42dc-b6b4-f74f03433271,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
5424bd59-0dde-420f-a254-b47056970829,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
5424bd59-0dde-420f-a254-b47056970829,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
5424bd59-0dde-420f-a254-b47056970829,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
5424bd59-0dde-420f-a254-b47056970829,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
5424bd59-0dde-420f-a254-b47056970829,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
90c81ddf-9a85-4411-a12c-8d4e7aa5b47e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The cholinergic response may help produce an asthmatic response to another stimulus that normally would not have produced one (i.e., it may play a part in the hypersensitivity of the asthmatic airways). Likewise, the presence of an infection, particularly a viral infection, may place the airway in a proinflammatory state.",True,proinflammatory,,,,
973bc55c-d8c8-4726-a1c7-daa82d35789d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
973bc55c-d8c8-4726-a1c7-daa82d35789d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
973bc55c-d8c8-4726-a1c7-daa82d35789d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
973bc55c-d8c8-4726-a1c7-daa82d35789d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
973bc55c-d8c8-4726-a1c7-daa82d35789d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
493a2bd2-32da-4dff-aec2-77910211076b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Exercise-induced asthma: Although exercise is associated with increased airway caliber, it can also induce asthma. Increased airway flow to meet the increased metabolic demand of exercise results in loss of fluid and heat from airway surfaces. This leaves the peribronchial fluid in a hypertonic state and causes excitation of the irritant airway receptors, which leads to release of the mast cells’ cocktail.",True,proinflammatory,,,,
d52138d6-6232-4937-92b6-4560e258313d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Exercise-induced asthma is more prevalent in cold (i.e. dry air) where water loss will be higher, so occurs more in sports such as cross-country skiing than swimming in a warm humid environment. Bronchoconstriction usually occurs when exercise stops—when the protective effect of sympathetic activity to the airway smooth muscles ceases.",True,proinflammatory,,,,
4ea46e38-9f8d-4bbd-a7bf-0ba450924e84,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Drug-induced asthma: There are several pharmaceutical and food products that can promote asthma, including tartrazine (a yellow food coloring) and sulfides used as food preservatives. Additionally, 10 to 20 percent of asthmatics are sensitive to aspirin.",True,proinflammatory,,,,
0e9a5003-add8-44d2-bf0d-261e86d237c0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
0e9a5003-add8-44d2-bf0d-261e86d237c0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
0e9a5003-add8-44d2-bf0d-261e86d237c0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
0e9a5003-add8-44d2-bf0d-261e86d237c0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
0e9a5003-add8-44d2-bf0d-261e86d237c0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
60f7b0de-abb3-4a19-83d3-8948fbf1d482,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Environmental/occupational asthma: As the airway is open to the environment, it is susceptible to inhaled substances that can cause sensitization; there are over two hundred substances known to cause asthma, both organic and inorganic. Some common ones are listed below.",True,proinflammatory,,,,
e83d5428-5d36-4199-92cd-72611a320e4c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Table 1.1: Some of the most common environmental causes of asthma. Taking a pulmonary history should include asking about potential environmental exposures.,True,proinflammatory,,,,
2ec95dba-edba-4160-b02d-7fcd9764b2f6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Determining whether airway hypersensitivity is due to environmental factors is complicated by widely varying latency periods. Short latency periods can be as brief as twenty-four hours and are associated with vapor or smoke exposure that does not cause an immunological response. Longer latency periods that may last years are more commonly associated with an immunological response to large particles that act like antigens.,True,proinflammatory,,,,
16fc924f-9ba5-44f4-91dc-167823806dbf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The situation is further confused by occupation-related responses, which often cause the airway to become more sensitive to some of the other causes of asthma covered here. This makes the role of an environmental factor more difficult to determine.",True,proinflammatory,,,,
7da9cced-7649-4837-8ed0-167d194cc53b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Pathophysiology of Asthma,False,Pathophysiology of Asthma,,,,
75e21075-e651-40c6-a12d-c60c6047d075,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
75e21075-e651-40c6-a12d-c60c6047d075,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
75e21075-e651-40c6-a12d-c60c6047d075,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
75e21075-e651-40c6-a12d-c60c6047d075,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
75e21075-e651-40c6-a12d-c60c6047d075,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
f5ae5f2a-a020-446c-8b4f-6929f0e43ea6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
f5ae5f2a-a020-446c-8b4f-6929f0e43ea6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
f5ae5f2a-a020-446c-8b4f-6929f0e43ea6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
f5ae5f2a-a020-446c-8b4f-6929f0e43ea6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
f5ae5f2a-a020-446c-8b4f-6929f0e43ea6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
0ec7d20e-5c3a-4828-9da5-e7e3b1aab56c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
0ec7d20e-5c3a-4828-9da5-e7e3b1aab56c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
0ec7d20e-5c3a-4828-9da5-e7e3b1aab56c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
0ec7d20e-5c3a-4828-9da5-e7e3b1aab56c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
0ec7d20e-5c3a-4828-9da5-e7e3b1aab56c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
47c75763-598b-490f-8d09-fb5d2ecf3049,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
47c75763-598b-490f-8d09-fb5d2ecf3049,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
47c75763-598b-490f-8d09-fb5d2ecf3049,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
47c75763-598b-490f-8d09-fb5d2ecf3049,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
47c75763-598b-490f-8d09-fb5d2ecf3049,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
e5887185-a7be-4174-a32d-bb80444057e2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Clinical Presentation of Asthma,False,Clinical Presentation of Asthma,,,,
9f2852ed-9682-4a33-92a2-0b9a04c36004,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"One useful diagnostic element of asthma is its episodic or acute behavior. However, as patients may be asymptomatic between attacks, the severity of asthma can be difficult to determine without performing bronchial challenge tests.",True,Clinical Presentation of Asthma,,,,
14992fcd-36c4-461f-b6f3-bea1e1f44afa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
14992fcd-36c4-461f-b6f3-bea1e1f44afa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
14992fcd-36c4-461f-b6f3-bea1e1f44afa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
14992fcd-36c4-461f-b6f3-bea1e1f44afa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
14992fcd-36c4-461f-b6f3-bea1e1f44afa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
76492549-fec0-464f-82ee-bcd0acf10a1c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"As airway resistance increases, the accessory muscles are deployed to maintain sufficient airflow through the narrowing airways, and the patient experiences an increased effort to breathe. Increased expiratory efforts produce dynamic airway collapse and lead to hyperinflation. Further decreases in airway caliber result in insufficient alveolar ventilation and deranged blood gases. The sensation reported at this point is air hunger. Once the patient is severely bronchoconstricted, delivery of inhaled therapies is much more difficult, and mechanical ventilation to support the respiratory muscles becomes complicated. Other signs present during a severe attack are raised heart (tachycardia) and breathing (tachypnea) rates as well as a paradoxical pulse (i.e., a rise in blood pressure during expiration).",True,Clinical Presentation of Asthma,,,,
9b7df993-2c02-4280-9a8c-fc47ce1ffd80,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
9b7df993-2c02-4280-9a8c-fc47ce1ffd80,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
9b7df993-2c02-4280-9a8c-fc47ce1ffd80,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
9b7df993-2c02-4280-9a8c-fc47ce1ffd80,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
9b7df993-2c02-4280-9a8c-fc47ce1ffd80,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
9428ebee-9a83-40c0-b52d-eb39f809144e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Chronic Obstructive Pulmonary Disease,False,Chronic Obstructive Pulmonary Disease,,,,
c9280022-aed1-43e8-bf3e-8506407d2c61,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Although chronic bronchitis and emphysema have different underlying pathologies, they frequently have the same root cause and are often found together in a patient. In brief, chronic bronchitis is associated with an increase in mucus production, while emphysema involves disruption of the lung structure.",True,Chronic Obstructive Pulmonary Disease,,,,
b522fbe3-1bfa-4e94-bf09-d95aadd9deb5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The relative role of chronic bronchitis in COPD has diminished since the Clean Air Act reduced atmospheric sulphur dioxide, but with 90 percent of COPD caused by cigarette smoking there is still plenty of bronchitis and emphysema to treat—at enormous cost to the health system from over eight million hospitalizations a year that are mostly paid for by Medicare. The COPD patient tends to be older and poorer and will likely have comorbidities, the most common of which is hypertension. What is perhaps more disturbing is that of the most common causes of death, COPD is the only one whose incidence continues to rise.",True,Chronic Obstructive Pulmonary Disease,,,,
26dd9ca6-40be-4ae8-8964-8008fe880602,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"We will now look at the underlying mechanisms of COPD. Despite the fact it is usually composed of some elements of both chronic bronchitis and emphysema, we will deal with each separately for the sake of simplicity.",True,Chronic Obstructive Pulmonary Disease,,,,
cb1bd1bf-203a-451c-b082-90924e0660e1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Chronic Bronchitis,False,Chronic Bronchitis,,,,
492d6a9f-e9dc-41da-b1de-252c0778461e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Chronic bronchitis is clinically defined as a persistent and productive cough that lasts for at least three months per year for two consecutive years.,True,Chronic Bronchitis,,,,
469bdcb6-8c20-4d9f-90c3-59cc4dabb7c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
469bdcb6-8c20-4d9f-90c3-59cc4dabb7c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
469bdcb6-8c20-4d9f-90c3-59cc4dabb7c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
469bdcb6-8c20-4d9f-90c3-59cc4dabb7c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
469bdcb6-8c20-4d9f-90c3-59cc4dabb7c2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
358ed86a-83a2-40f1-b7d9-83e09e05f8f1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Neutrophils, lymphocytes, and macrophages are attracted to the irritated airway, and their presence is maintained through increased expression of cell adhesion molecules on the airway walls. These immune cells lead to acute airway wall inflammation that narrows the airway, and if chronic, can lead to tissue damage. The cytokines released by these cells also sensitize airway irritant receptors, which exacerbates the response to future irritant exposure.",True,Chronic Bronchitis,,,,
7337d6fa-f837-434b-89f2-fad625f88fa5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Mucus production increases, and the glands themselves may also release cytokines that further exacerbate the inflammatory response. The mucus also contributes to airway narrowing, and mucus plugs may form that completely block bronchioles.",True,Chronic Bronchitis,,,,
068dbe55-6314-4a0d-a525-fadf669088c6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Mesenchymal cells transition into fibroblasts as part of the inflammatory response, and their chronic presence leads to the deposition of fibrotic tissue.",True,Chronic Bronchitis,,,,
ee54dcc1-8d58-4a92-baef-64fbcaaae697,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Collectively these responses to the irritants result in a narrowed airway that is (1) hypersensitive, (2) fibrosed, and (3) blocked by excessive secretions.",True,Chronic Bronchitis,,,,
69867d4b-e143-45d9-96c6-1ac6c7c7fd16,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
69867d4b-e143-45d9-96c6-1ac6c7c7fd16,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
69867d4b-e143-45d9-96c6-1ac6c7c7fd16,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
69867d4b-e143-45d9-96c6-1ac6c7c7fd16,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
69867d4b-e143-45d9-96c6-1ac6c7c7fd16,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
0b56c024-ef77-42be-bb52-77bb38a123dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
0b56c024-ef77-42be-bb52-77bb38a123dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
0b56c024-ef77-42be-bb52-77bb38a123dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
0b56c024-ef77-42be-bb52-77bb38a123dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
0b56c024-ef77-42be-bb52-77bb38a123dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
a87f7cfa-8a93-4a68-a46c-6def86ef68fb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"These changes result in an airway that produces more mucus and is less capable of removing it. The static mucus not only causes airway plugging, but can also promote infections that lead to episodic and characteristic exacerbation of COPD symptoms.",True,Chronic Bronchitis,,,,
65ecb559-e586-4b91-a734-4af1d2b1fa71,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Clinical Presentation of Chronic Bronchitis,False,Clinical Presentation of Chronic Bronchitis,,,,
7ab18f1b-73a8-4c56-ac6b-e3780005c893,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
7ab18f1b-73a8-4c56-ac6b-e3780005c893,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
7ab18f1b-73a8-4c56-ac6b-e3780005c893,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
7ab18f1b-73a8-4c56-ac6b-e3780005c893,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
7ab18f1b-73a8-4c56-ac6b-e3780005c893,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
be870f32-4aba-4857-8b90-a14768898947,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"As with many pulmonary diseases, the onset can be insidious. Small airway damage may be present but undetectable with normal spirometry, while the patient becomes accustomed to and tolerates a persistent productive cough. However, with continued irritant exposure, this initial simple bronchitis progresses.",True,Clinical Presentation of Chronic Bronchitis,,,,
fafd1cf2-66ad-4833-aea6-2255226b3d99,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Secretions continue to worsen and peribronchiolar fibrosis marks the onset of obstructive bronchitis that is reflected by significant expiratory airflow limitation. At this point the patient may have tolerated years of productive cough and experienced frequent chest infections related to poor mucus clearance. COPDers are particularly susceptible to Haemophilus influenza and Streptococcus pneumoniae. The sputum is abundant and capable of plugging significant numbers of airways and may be blood tinged; COPD is the most common cause of hemoptysis. Airways may demonstrate hyperreactivity and mimic an asthmatic response.,True,Clinical Presentation of Chronic Bronchitis,,,,
58a5266e-69d2-463c-b498-49d8be2004e4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The onset of dyspnea is insidious and is usually first experienced during exertion—leading the patient to avoid exercise, which in turn leads to deconditioning and a worsening of the symptom. Lung sounds include wheezes and rales, the rales often clearing after cough.",True,Clinical Presentation of Chronic Bronchitis,,,,
a20a1bb2-77a0-4bc7-8725-36aa2e895edc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,With worsening airway flow limitation expiration becomes prolonged and may be incomplete due to airway collapse that leads to characteristic hyperinflation.,True,Clinical Presentation of Chronic Bronchitis,,,,
f68843d5-3367-4378-a144-2c92db6b9d04,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Mucus plugging and airway closure leads to areas of V/Q abnormalities through the lung, and localized areas of hypoxia can lead to pulmonary vasoconstriction. When significant regions of the lung are vasoconstricted, pulmonary vascular resistance can rise enough to induce right-sided heart failure.",True,Clinical Presentation of Chronic Bronchitis,,,,
ff39b6b7-7eee-4e70-934b-bfe83b5db668,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"With continued progression of the disease, blood gases become deranged as insufficient alveolar ventilation is achieved. As the disease approaches its end stage, the patient experiences dyspnea at rest until respiratory failure occurs and the patient is hypoxemic and hypercarbic.",True,Clinical Presentation of Chronic Bronchitis,,,,
ddc4b051-5a3e-47fa-b151-961b48ca2a75,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Emphysema,False,Emphysema,,,,
e83cf318-3852-4816-976c-e5e441dad502,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
e83cf318-3852-4816-976c-e5e441dad502,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
e83cf318-3852-4816-976c-e5e441dad502,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
e83cf318-3852-4816-976c-e5e441dad502,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
e83cf318-3852-4816-976c-e5e441dad502,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
9379398c-7945-4fed-a2cb-b5ec425fd255,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
9379398c-7945-4fed-a2cb-b5ec425fd255,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
9379398c-7945-4fed-a2cb-b5ec425fd255,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
9379398c-7945-4fed-a2cb-b5ec425fd255,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
9379398c-7945-4fed-a2cb-b5ec425fd255,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
0716d8b3-66e7-4c58-b185-296e09e93c71,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
0716d8b3-66e7-4c58-b185-296e09e93c71,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
0716d8b3-66e7-4c58-b185-296e09e93c71,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
0716d8b3-66e7-4c58-b185-296e09e93c71,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
0716d8b3-66e7-4c58-b185-296e09e93c71,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
d990608c-9585-44af-9c20-7e94a4dbf8f3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
d990608c-9585-44af-9c20-7e94a4dbf8f3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
d990608c-9585-44af-9c20-7e94a4dbf8f3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
d990608c-9585-44af-9c20-7e94a4dbf8f3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
d990608c-9585-44af-9c20-7e94a4dbf8f3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
724acc9f-052c-4343-8f39-63ad9bfb1e0a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"So having seen the morphology of emphysema, we will look at how this damage occurs.",True,Emphysema,,,,
fd2c7c65-cfdc-4060-9a45-7d3ffc2f7cef,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Pathophysiology of Emphysema,False,Pathophysiology of Emphysema,,,,
6d839056-3a6d-40bd-88db-949daf25bdcd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,The normal structure of alveoli and respiratory ducts consists of type 1 and type 2 pneumocytes with elastic fibers that contribute to the structure’s mechanical behavior. Emphysema involves the loss of these parenchymal fibers.,True,Pathophysiology of Emphysema,,,,
b78712de-14fe-42bb-9568-a173b61e0f6d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The presence of irritants, such as cigarette smoke, causes oxidization and the dysfunction of antiprotease enzymes. Without their inhibitory action, the activity of proteases increases and causes the destruction of local tissue. One of these proteases is elastase, whose elevated activity leads to irreparable loss of parenchymal fibers.",True,Pathophysiology of Emphysema,,,,
dc119042-7d5b-4435-be04-27d7729336d7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Elastase is also released by neutrophils and macrophages that arrive in response to the inflammatory cascade caused by the inhaled smoke. This causes further destruction of elastin fibers.,True,Pathophysiology of Emphysema,,,,
b459d212-67a7-4b7c-89ef-a271c8d3099b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
b459d212-67a7-4b7c-89ef-a271c8d3099b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
b459d212-67a7-4b7c-89ef-a271c8d3099b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
b459d212-67a7-4b7c-89ef-a271c8d3099b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
b459d212-67a7-4b7c-89ef-a271c8d3099b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
10f97d96-2a1f-4354-b570-8cf2271f44da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
10f97d96-2a1f-4354-b570-8cf2271f44da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
10f97d96-2a1f-4354-b570-8cf2271f44da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
10f97d96-2a1f-4354-b570-8cf2271f44da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
10f97d96-2a1f-4354-b570-8cf2271f44da,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
3bda9f84-3004-4c01-a284-408f86dc91a8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,The loss of the elastic tissue and alveolar structure produces several pathophysiological changes in lung mechanics and function that result in typical clinical signs.,True,Pathophysiology of Emphysema,,,,
ba0f0359-a836-423e-8f70-99938c597048,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Clinical Presentation of Emphysema,False,Clinical Presentation of Emphysema,,,,
91619c3d-d486-4527-857a-76c24f21b066,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
91619c3d-d486-4527-857a-76c24f21b066,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
91619c3d-d486-4527-857a-76c24f21b066,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
91619c3d-d486-4527-857a-76c24f21b066,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
91619c3d-d486-4527-857a-76c24f21b066,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
944ab828-b202-463e-8579-17647203b581,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
944ab828-b202-463e-8579-17647203b581,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
944ab828-b202-463e-8579-17647203b581,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
944ab828-b202-463e-8579-17647203b581,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
944ab828-b202-463e-8579-17647203b581,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
9812e73b-7838-43ab-be96-c4453d3f7d51,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
9812e73b-7838-43ab-be96-c4453d3f7d51,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
9812e73b-7838-43ab-be96-c4453d3f7d51,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
9812e73b-7838-43ab-be96-c4453d3f7d51,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
9812e73b-7838-43ab-be96-c4453d3f7d51,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
b68977a3-213a-4d58-acff-dd7e0ddcd74b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The deterioration of gas exchange and lung mechanics worsens as more lung becomes involved, and the stage of the disease, and any concurrent chronic bronchitis, is classified by the level of airway flow limitation (e.g., FEV1/FVC).",True,Clinical Presentation of Emphysema,,,,
a3472fa5-fcfa-4f3e-8930-1a25dc55d7e0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"It might also be worth noting here that COPD can produce or be associated with a number of comorbidities; we have already mentioned hypertension, but pulmonary artery disease, coronary heart disease, heart failure, lung cancer, and malnutrition may contribute to a low quality of life that is typically associated with COPD. This in turn may contribute to the high incidence of anxiety disorders and depression experienced by COPD patients.",True,Clinical Presentation of Emphysema,,,,
a68f2bde-c0f7-40e0-bb09-085f56ae0bb3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Cystic Fibrosis,False,Cystic Fibrosis,,,,
c282394a-1e4e-4e7d-b8be-a13516566676,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Cystic fibrosis (CF) is an inherited disorder that affects the exocrine glands of not only the lungs, but also the pancreas, intestines, and bile ducts. We will focus only on the pulmonary aspects here and see how CF produces an obstructive lung disease.",True,Cystic Fibrosis,,,,
d4c965ae-bf64-43ec-882b-3f0b3e1354f0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Cystic fibrosis affects the composition of the fluid lining the airways. Changes in this fluid lead to serious sequelae that dramatically shorten life expectancy. Even with modern therapy, many CF patients only live until their thirties or early forties, and some still die in infancy.",True,Cystic Fibrosis,,,,
43f22cc3-5821-44f3-8042-e2f5361813a6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,There are two hypotheses about the pathophysiological mechanism of CF: the low volume and the high salt. We will focus only on the low volume hypothesis as there is increasing evidence to support this and emerging evidence against the high salt hypothesis.,True,Cystic Fibrosis,,,,
6a24ee64-8a18-4a28-972d-eac4a607de1c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Pathophysiology of Cystic Fibrosis,False,Pathophysiology of Cystic Fibrosis,,,,
b898370b-26b0-4c3c-a932-9f4e7dc6f810,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
b898370b-26b0-4c3c-a932-9f4e7dc6f810,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
b898370b-26b0-4c3c-a932-9f4e7dc6f810,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
b898370b-26b0-4c3c-a932-9f4e7dc6f810,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
b898370b-26b0-4c3c-a932-9f4e7dc6f810,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
638a4e52-ca9d-4d4f-8426-32aeda74f808,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,ENaC,False,ENaC,,,,
661b5935-754e-45f0-8140-ff9e3dabdb9b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
661b5935-754e-45f0-8140-ff9e3dabdb9b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
661b5935-754e-45f0-8140-ff9e3dabdb9b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
661b5935-754e-45f0-8140-ff9e3dabdb9b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
661b5935-754e-45f0-8140-ff9e3dabdb9b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
822b7c7e-5005-4f61-9441-ef0c3aa8d511,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"There are numerous mutations that are known to produce a dysfunctional CFTR channel, but 70 percent of CF cases are due to the delta-F-508 mutation (so named as the mutation leads to a deletion of phenylalanine at position 508 of the CFTR protein). This is a Mendelian recessive trait, and CF occurrence is 1 in 2,500 live births.",True,ENaC,,,,
a4eab559-090e-44a3-818a-de447dc2073e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
a4eab559-090e-44a3-818a-de447dc2073e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
a4eab559-090e-44a3-818a-de447dc2073e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
a4eab559-090e-44a3-818a-de447dc2073e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
a4eab559-090e-44a3-818a-de447dc2073e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
c3036ef3-0a27-4d24-934b-9e214160593c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"This combination severely impacts mucus clearance (thicker, heavier mucus with compromised cillary escalator). The defective CFTR channel therefore results in mucus retention and airway obstruction. This in turn leads to reduced alveolar ventilation and repeated infections. The two most common culprits for infection in CF are Staphylococcus aureus and Pseudomonsa aeruginosa. Normal functional CFTR appears to suppress P. aeruginosa, perhaps explaining its prevalence in cystic fibrosis where it can be found in the sputum of almost all CF patients.",True,ENaC,,,,
87a25992-0d6a-4d84-bcb1-3db0f9dff299,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,cillary,False,cillary,,,,
2f12a7c9-09c0-4bde-a0d5-2c3819799cdb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Pseudomonsa,False,Pseudomonsa,,,,
70f72e7f-3280-4dcf-8275-f6798cd2be9f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
70f72e7f-3280-4dcf-8275-f6798cd2be9f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
70f72e7f-3280-4dcf-8275-f6798cd2be9f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
70f72e7f-3280-4dcf-8275-f6798cd2be9f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
70f72e7f-3280-4dcf-8275-f6798cd2be9f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
f1102b42-8914-449c-9c3c-ab215e71737c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The findings of CF obviously include the results of other effected organs, such as the pancreas. But nowadays these are more easily addressed, and it is pulmonary involvement that still proves critical. The onset of pulmonary involvement is variable and may be weeks or years after birth.",True,Pseudomonsa,,,,
1134c5e3-9432-453e-80e0-7e5dab309b1b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Clinical Presentation of Cystic Fibrosis,False,Clinical Presentation of Cystic Fibrosis,,,,
ab29f869-022c-41a8-b145-d959b2182341,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
ab29f869-022c-41a8-b145-d959b2182341,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
ab29f869-022c-41a8-b145-d959b2182341,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
ab29f869-022c-41a8-b145-d959b2182341,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
ab29f869-022c-41a8-b145-d959b2182341,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
dc10315b-1a6b-4b0e-a7db-976e7c286b62,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,CF patients usually have an abnormal sinus x-ray and evidence of chronic sinusitis as well as a high occurrence of nasal polyps.,True,Clinical Presentation of Cystic Fibrosis,,,,
65ce6119-577c-448c-bbc8-c803856b3487,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"With increasing and irreversible airway damage, the patients begins to experience dyspnea, and the damage may lead to hemoptysis, spontaneous pneumothorax, and a barrel chested appearance. Signs of prolonged pulmonary dysfunction appear as the disease progresses, such as finger clubbing, cyanosis, and cor pulmonale (right-sided heart failure caused by lung disease). As the patient approaches respiratory failure the accessory muscles are deployed. Patients succumb to the respiratory failure or an overwhelming infection.",True,Clinical Presentation of Cystic Fibrosis,,,,
3a09e040-325b-438c-a6cc-4c1d976da0d1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Because CF also affects sweat gland function, the sweat test remains a standard diagnostic with a chloride level greater than 60 mEq/L being indicative of CF. This test is more reliable in children than adults, who may have developed other conditions that affect the composition of sweat.",True,Clinical Presentation of Cystic Fibrosis,,,,
e4d6b9ce-f966-4641-b5f7-6e4baa67d8eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
e4d6b9ce-f966-4641-b5f7-6e4baa67d8eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
e4d6b9ce-f966-4641-b5f7-6e4baa67d8eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
e4d6b9ce-f966-4641-b5f7-6e4baa67d8eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
e4d6b9ce-f966-4641-b5f7-6e4baa67d8eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
f5da88b8-be33-4532-bb1d-73c71ebec8c6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Spirometry detects the airway obstruction and hyperinflation that produce a low vital capacity and high residual volume.,True,Clinical Presentation of Cystic Fibrosis,,,,
874d75e2-b337-45f5-af75-1a45620358c6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Bronchiectasis,False,Bronchiectasis,,,,
049c56ca-7d74-412b-81db-d7223dfc701a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"This section will address bronchiectasis, a form of airway obstruction that is often a manifestation of chronic airway inflammation. Bronchiectasis involves a permanent dilation of a bronchi or bronchiole—think of bronchiectasis as the airway equivalent of an aneurysm.",True,Bronchiectasis,,,,
a92b8fb9-1559-4f0e-b212-43d15ef6f89d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
a92b8fb9-1559-4f0e-b212-43d15ef6f89d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
a92b8fb9-1559-4f0e-b212-43d15ef6f89d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
a92b8fb9-1559-4f0e-b212-43d15ef6f89d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
a92b8fb9-1559-4f0e-b212-43d15ef6f89d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
98750071-4849-4f09-8da0-9953aabf03a3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
98750071-4849-4f09-8da0-9953aabf03a3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
98750071-4849-4f09-8da0-9953aabf03a3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
98750071-4849-4f09-8da0-9953aabf03a3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
98750071-4849-4f09-8da0-9953aabf03a3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
2659ec78-37a8-41ce-bf92-44a34e82170e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The establishing of a bronchiectasis has an initial phase leading to persistent inflammation, desquamation (which worsens the mucus clearance), and the ulceration. In what is probably a familiar story, the continued inflammation leads to fibrosis in the chronic phase of development, and this can lead to airway destruction and perhaps the condition of bronchiolitis obliterans.",True,Bronchiectasis,,,,
febdd837-dccb-4f29-82fd-64b67f833234,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Let us look at how this process can get started.,False,Let us look at how this process can get started.,,,,
a40f651f-4bd5-49d9-8aeb-9877de9e8245,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Pathogenesis of Bronchiectasis,False,Pathogenesis of Bronchiectasis,,,,
230bd8dc-b685-4fa9-858d-ea72a4e46cf0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
230bd8dc-b685-4fa9-858d-ea72a4e46cf0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
230bd8dc-b685-4fa9-858d-ea72a4e46cf0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
230bd8dc-b685-4fa9-858d-ea72a4e46cf0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
230bd8dc-b685-4fa9-858d-ea72a4e46cf0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
c551498c-5124-4049-873e-2225bcb01299,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"About 50 percent of bronchiectasis cases are associated with cystic fibrosis where the genetic condition causes production of copious, thick mucus that is difficult to clear and often results in infection (commonly caused by Staphylococcus aureus).",True,Pathogenesis of Bronchiectasis,,,,
1be611d2-90ba-41c0-bab2-fdb8266c0f3e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Conditions causing cillary dyskinesia, as seen in Kartagener’s syndrome, also disrupt the mucocillary escalator.",True,Pathogenesis of Bronchiectasis,,,,
b5e6760c-ab4a-46fa-8dde-97c0e3559e10,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,mucocillary,False,mucocillary,,,,
aade988f-41c2-46a3-a0b9-f8b61f48ce45,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Another common cause of bronchiectasis is an allergy to Aspergillus fumigatus, a common fungus. In hypersensitive or immune-compromised individuals, chronic exposure can lead to allergic bronchopulmonary aspiragillosis.",True,mucocillary,,,,
6cd1231d-ae05-47ff-aa43-527b29427898,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,aspiragillosis,False,aspiragillosis,,,,
8877aced-2bea-4786-990d-cb1e17266883,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Bronchiectasis can be initiated in the vicinity of tuberculosis or other necrotizing infections that damage and weaken airway walls.,True,aspiragillosis,,,,
9753f6f5-072f-4988-ad8b-c83b4ae92467,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Obstruction of the bronchioles or bronchi by inhaled foreign objects, tumors, or compacted mucus can also initiate bronchiectasis through local inflammation and by preventing mucus clearance. The dilation of the airway can be worsened further by distal atelectasis that produces a negative pressure around the affected airway.",True,aspiragillosis,,,,
c9bbf1b2-5463-4156-8020-a05fc7c5517d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"As you might have gather by now, repeated local infection or inflammation has the potential to initiate bronchiectasis, so it is perhaps not surprising that with the advent of high resolution computed tomography (CT) imaging, bronchiectasis has also been found in association with AIDS, transplant rejection, and rheumatoid lung disease.",True,aspiragillosis,,,,
e91c6077-477e-4d2d-9d22-0ac860bd8ff4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,We will now examine the results of these instigating factors.,False,We will now examine the results of these instigating factors.,,,,
dcf2ace1-b8db-4f76-aaf7-34dd591bb9cf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Pathology of Bronchiectasis,False,Pathology of Bronchiectasis,,,,
67b37a14-0469-4a50-9c1c-9853fb0cf986,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
67b37a14-0469-4a50-9c1c-9853fb0cf986,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
67b37a14-0469-4a50-9c1c-9853fb0cf986,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
67b37a14-0469-4a50-9c1c-9853fb0cf986,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
67b37a14-0469-4a50-9c1c-9853fb0cf986,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
6a21cd22-7cea-444b-8b82-0cceb0bcd3c8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
6a21cd22-7cea-444b-8b82-0cceb0bcd3c8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
6a21cd22-7cea-444b-8b82-0cceb0bcd3c8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
6a21cd22-7cea-444b-8b82-0cceb0bcd3c8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
6a21cd22-7cea-444b-8b82-0cceb0bcd3c8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
9d6d6e9e-9b5d-4dc9-b706-26f64b1ea5c3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
9d6d6e9e-9b5d-4dc9-b706-26f64b1ea5c3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
9d6d6e9e-9b5d-4dc9-b706-26f64b1ea5c3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
9d6d6e9e-9b5d-4dc9-b706-26f64b1ea5c3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
9d6d6e9e-9b5d-4dc9-b706-26f64b1ea5c3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
355f5d5f-29ec-45fe-98cc-ca77f4c9fead,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"A bronchiectasis can be cylindrical, varicose (also known as fusiform), or cystic (also known as saccular). The shape is relevant to their effect on the efficacy of coughing; cylindrical form has very little effect on cough’s ability to clear mucus, whereas varicose and cystic forms tend to disproportionately collapse during cough and reduce its effectiveness at moving mucus up the airway.",True,Pathology of Bronchiectasis,,,,
c70c6d14-f998-4f79-abbc-12c8c321da7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
c70c6d14-f998-4f79-abbc-12c8c321da7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
c70c6d14-f998-4f79-abbc-12c8c321da7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
c70c6d14-f998-4f79-abbc-12c8c321da7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
c70c6d14-f998-4f79-abbc-12c8c321da7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
2be1e07c-4e8a-43dc-99cd-835dfec4a008,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
2be1e07c-4e8a-43dc-99cd-835dfec4a008,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
2be1e07c-4e8a-43dc-99cd-835dfec4a008,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
2be1e07c-4e8a-43dc-99cd-835dfec4a008,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
2be1e07c-4e8a-43dc-99cd-835dfec4a008,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
c31f74c2-31c1-4745-8b41-74a1b62912b8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"So, how does bronchiectasis present, and what are the results of diagnostic tests?",True,Pathology of Bronchiectasis,,,,
ecd29361-00ea-4571-a5a6-7685767636bf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Clinical Presentation of Bronchiectasis,False,Clinical Presentation of Bronchiectasis,,,,
d63896b0-4d6e-4e31-9197-75abcf3e1f03,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The initial complaint is usually a persistent cough with copious expectoration. The amount of mucus the cough produces varies and can be as high as several hundred milliliters per day, particular when the dependent airways are involved. However, it is worth noting here that bronchiectasis in the upper lobes (usually associated with infection) may be dry with little or no mucus expectoration.",True,Clinical Presentation of Bronchiectasis,,,,
06d6e613-3d38-4e94-918a-92ea513e94df,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Generally though there is mucopurulent expectorate, and if it is associated with an anerobic infection it will likely have a foul odor. Sputum smears are loaded with white blood cells and can contain both gram-positive and -negative organisms.",True,Clinical Presentation of Bronchiectasis,,,,
68444ff1-bd65-4893-96ff-a679de35b6d6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The patient will likely have a history of recurrent pneumonia, the site of the pneumonia being consistent with locality of the bronchiectasis.",True,Clinical Presentation of Bronchiectasis,,,,
4c4bc299-746f-4bf5-8952-6270d579f228,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The expectorate may also contain blood. The degree and frequency of hemoptysis is variable and unpredictable, but occasionally it can be massive and life threatening.",True,Clinical Presentation of Bronchiectasis,,,,
7d47358c-4087-4e34-9ccb-748e22a51c79,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"The standard diagnostic tests may not be helpful in early stages, but typical signs appear with worsening airway involvement. In the early stages the patient will likely appear normal on a physical exam and have normal spirometry and arterial blood gas values. With more significant bronchiectasis, rales and rhonchi over the affected site can be heard.",True,Clinical Presentation of Bronchiectasis,,,,
b6350fe5-ccd4-4bca-8f09-a16d31f162bd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Later signs with long-standing bronchiectasis include finger clubbing, but this is not exclusive to the condition.",True,Clinical Presentation of Bronchiectasis,,,,
696bbeb7-1b4a-4993-a37e-19dcd4945aa5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"A chest x-ray will show the peribronchial fibrosis and any atelectasis. But, as mentioned earlier, a high-resolution CT is much more effective at determining the degree and type of airway changes.",True,Clinical Presentation of Bronchiectasis,,,,
bb84508c-adab-49aa-abe1-574456c9cd40,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"References, Resources, and Further Reading",False,"References, Resources, and Further Reading",,,,
f9fdd4ec-56f5-4055-b0ff-3a97c49e4085,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,Text,False,Text,,,,
3c8984f3-200d-452d-b3c1-bf1802677b83,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapters 8–11.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
6e3d9856-830f-4cff-86cb-d97d0b4ef2e1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
9ef4d7f0-9596-4eef-9ae4-9915e995f344,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,Asthma,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/#chapter-5-section-1,"West, John B. “Chapter 4: Obstructive Diseases.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Text,,,,
7c63d289-66e0-45f5-b2d5-e2f71c7c4e84,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
7c63d289-66e0-45f5-b2d5-e2f71c7c4e84,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
7c63d289-66e0-45f5-b2d5-e2f71c7c4e84,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
7c63d289-66e0-45f5-b2d5-e2f71c7c4e84,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
7c63d289-66e0-45f5-b2d5-e2f71c7c4e84,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"There are numerous underlying mechanisms of asthma (figure 1.1), and they may not be exclusive or independent within the same patient.",True,Text,Figure 1.1,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
c94b7852-0ec6-4d8f-a5ad-59458c31c429,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,We will also look at how exercise and certain pharmacological agents can produce asthma.,True,Text,,,,
47daab75-1cbf-498c-90be-902986e6dc41,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
47daab75-1cbf-498c-90be-902986e6dc41,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
47daab75-1cbf-498c-90be-902986e6dc41,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
47daab75-1cbf-498c-90be-902986e6dc41,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
47daab75-1cbf-498c-90be-902986e6dc41,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Allergenic asthma: Most allergic asthma is caused by the presence of an excessive amount of IgE (the hallmark antibody of an allergy). Formation of an immune complex between the antigen and the overexpressed IgE results in binding to surface receptors on mast cells and basophilic granulocytes, of which there are plenty in the lung. The IgE receptor binding results in the release of a cocktail of proinflammatory and airway-active substances. Some of these, including histamine and cytokines that attract eosinophils and neutrophils, are stored in vesicles of mast cells shown in figure 1.2. Others are produced on demand, including leukotrienes, and are derivatives of arachidonic acid (we will return to this later).",True,Text,Figure 1.2,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.2.png,Figure 1.2: Example of a mast cell loaded with secretory granules.
1e32b98e-1c05-4c94-94fe-3c41360b3f05,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,proinflammatory,False,proinflammatory,,,,
b93e9051-db12-49ce-a30e-551d9a47d147,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,The results of this cocktail’s release are the hallmarks of asthma:,True,proinflammatory,,,,
7942f1ca-5184-4400-84be-0a53790bb6c0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The timeline from the exposure to the antigen to asthmatic response is not straightforward. A response may occur within minutes (“early response”), or hours later (“late response”). Some patients show only an early response, some only a late one, and some show both in a “dual” response. The late response may correspond to the arrival of leucocytes in response to the initial release of cytokines. It may also be due to a mild stimulus arriving later in an airway that was sensitized earlier.",True,proinflammatory,,,,
9f3b0a43-9d8d-4253-8327-a667a33b2dab,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
9f3b0a43-9d8d-4253-8327-a667a33b2dab,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
9f3b0a43-9d8d-4253-8327-a667a33b2dab,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
9f3b0a43-9d8d-4253-8327-a667a33b2dab,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
9f3b0a43-9d8d-4253-8327-a667a33b2dab,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Cholinergic asthma: Because it is open to the external environment, the airway has defensive, vagal reflexes (figure 1.3). An inappropriate exaggeration of some of these may lead to asthma. The basic reflex arch that ends with a cholinergic response begins with stimulation of airway irritant receptors in the epithelium. An afferent signal to the brainstem instigates an efferent signal to cause airway smooth muscle contraction and mucus secretion by glandular cells. The reflex also stimulates mast cells to release their cocktail, which includes histamine.",True,proinflammatory,Figure 1.3,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
a9e35db5-d668-4d34-b6f4-25195fed0c8c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
a9e35db5-d668-4d34-b6f4-25195fed0c8c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
a9e35db5-d668-4d34-b6f4-25195fed0c8c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
a9e35db5-d668-4d34-b6f4-25195fed0c8c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
a9e35db5-d668-4d34-b6f4-25195fed0c8c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The released histamine stimulates the airway receptors, setting up the potential for a positive feedback loop and perpetuating the cycle of bronchoconstriction and secretion. The histamine also stimulates bronchoconstriction through its direct action on the smooth muscle as well as sensitizing the smooth muscle to further vagal stimulation. These processes are summarized in figure 1.3.",True,proinflammatory,Figure 1.3,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.3.png,Figure 1.3: Vagal reflex of irritant airway receptors and the onset of asthma.
b9ae0b7a-fcbf-404f-af0f-b20f6a463ee3,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The cholinergic response may help produce an asthmatic response to another stimulus that normally would not have produced one (i.e., it may play a part in the hypersensitivity of the asthmatic airways). Likewise, the presence of an infection, particularly a viral infection, may place the airway in a proinflammatory state.",True,proinflammatory,,,,
aae7eea9-dcef-4315-90f5-618e2c11e6f6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
aae7eea9-dcef-4315-90f5-618e2c11e6f6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
aae7eea9-dcef-4315-90f5-618e2c11e6f6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
aae7eea9-dcef-4315-90f5-618e2c11e6f6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
aae7eea9-dcef-4315-90f5-618e2c11e6f6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Neural airway control may also contribute to the high prevalence of nocturnal asthma, as during rest when the airways are predominantly under parasympathetic control. But other factors (summarized in figure 1.4) may contribute:",True,proinflammatory,Figure 1.4,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
243be2ae-337e-4a0c-be33-b8691280a48a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Exercise-induced asthma: Although exercise is associated with increased airway caliber, it can also induce asthma. Increased airway flow to meet the increased metabolic demand of exercise results in loss of fluid and heat from airway surfaces. This leaves the peribronchial fluid in a hypertonic state and causes excitation of the irritant airway receptors, which leads to release of the mast cells’ cocktail.",True,proinflammatory,,,,
1b835241-40b3-465f-9f02-4b35dc840a2d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Exercise-induced asthma is more prevalent in cold (i.e. dry air) where water loss will be higher, so occurs more in sports such as cross-country skiing than swimming in a warm humid environment. Bronchoconstriction usually occurs when exercise stops—when the protective effect of sympathetic activity to the airway smooth muscles ceases.",True,proinflammatory,,,,
cbe47a16-704b-4cbc-909b-e5992ae74aa2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Drug-induced asthma: There are several pharmaceutical and food products that can promote asthma, including tartrazine (a yellow food coloring) and sulfides used as food preservatives. Additionally, 10 to 20 percent of asthmatics are sensitive to aspirin.",True,proinflammatory,,,,
a55082cd-be14-495e-9917-cf5d68cf563b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
a55082cd-be14-495e-9917-cf5d68cf563b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
a55082cd-be14-495e-9917-cf5d68cf563b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
a55082cd-be14-495e-9917-cf5d68cf563b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
a55082cd-be14-495e-9917-cf5d68cf563b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Recall that some of the on-demand components of the mast cell’s cocktail were derived from arachidonic acid. There are two pertinent pathways in which arachidonic acid is used: the lipoxygenase pathway and the cyclooxygenase pathway (figure 1.5). The first leads to the production of leukotrienes, which are potent bronchoconstrictors. The second leads to the production of prostaglandins and thromboxane. Normally the distribution of arachidonic acid down these pathways is balanced to meet demand. However, NSAIDS such as aspirin are COX 2 inhibitors and block the cyclooxygenase route, leaving more substrate for the lipoxygenase pathway and production of leukotrienes (figure 1.5) with their bronchoconstrictive effect.",True,proinflammatory,Figure 1.5,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.5.png,"Figure 1.5: NSAIDS, including aspirin, shift metabolism of arachidonic acid toward bronchoconstrictive leukotrienes."
247ebad4-9aa7-4626-b9c5-798afaa6f6dd,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Environmental/occupational asthma: As the airway is open to the environment, it is susceptible to inhaled substances that can cause sensitization; there are over two hundred substances known to cause asthma, both organic and inorganic. Some common ones are listed below.",True,proinflammatory,,,,
aa3116a3-7318-4cb5-bb9e-1dbf1eaa694f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Table 1.1: Some of the most common environmental causes of asthma. Taking a pulmonary history should include asking about potential environmental exposures.,True,proinflammatory,,,,
67d185dc-5757-42f1-814b-85c1f84b2af0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Determining whether airway hypersensitivity is due to environmental factors is complicated by widely varying latency periods. Short latency periods can be as brief as twenty-four hours and are associated with vapor or smoke exposure that does not cause an immunological response. Longer latency periods that may last years are more commonly associated with an immunological response to large particles that act like antigens.,True,proinflammatory,,,,
7a4f86be-f621-4060-a5f8-7ae75a53c7cc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The situation is further confused by occupation-related responses, which often cause the airway to become more sensitive to some of the other causes of asthma covered here. This makes the role of an environmental factor more difficult to determine.",True,proinflammatory,,,,
7921192e-cdbc-4bdf-bc0c-d9c816cf1b28,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Pathophysiology of Asthma,False,Pathophysiology of Asthma,,,,
515bdac9-f642-4f32-926f-31302a37f9e8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
515bdac9-f642-4f32-926f-31302a37f9e8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
515bdac9-f642-4f32-926f-31302a37f9e8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
515bdac9-f642-4f32-926f-31302a37f9e8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
515bdac9-f642-4f32-926f-31302a37f9e8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"With numerous and maybe concurrent mechanisms, what does asthma look like in the airway? The normal lumen of the airway has a relatively lower resistance, as depicted in panel A of figure 1.6, but in mild asthma the lumen is narrowed (thereby raising resistance to airflow) through swelling of the airway wall, contraction of airway smooth muscle, and blockage (or plugging) of the airway by increased mucus secretion (figure 1.6B). This worsens in more severe asthma until the lumen can be extremely narrow (figure 1.6C) or even completely blocked.",True,Pathophysiology of Asthma,Figure 1.6,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.6.png,"Figure 1.6: Illustrations of normal (A), mildly asthmatic (B), and severely asthmatic (C) airways."
7cdd5627-44a1-448e-9884-992553becb67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
7cdd5627-44a1-448e-9884-992553becb67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
7cdd5627-44a1-448e-9884-992553becb67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
7cdd5627-44a1-448e-9884-992553becb67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
7cdd5627-44a1-448e-9884-992553becb67,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Other characteristics of asthma include the presence of eosinophillic that infiltrate into the airway walls. The eosinophil enzymes also leave a telltale sign: Charcot–Leyden crystals, as shown in the circled area of figure 1.7A.",True,Pathophysiology of Asthma,Figure 1.7,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
ef2b3542-fddd-4d46-bd87-3c45df55df50,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
ef2b3542-fddd-4d46-bd87-3c45df55df50,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
ef2b3542-fddd-4d46-bd87-3c45df55df50,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
ef2b3542-fddd-4d46-bd87-3c45df55df50,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
ef2b3542-fddd-4d46-bd87-3c45df55df50,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The sputum of the asthmatic may also contain Curshman’s spirals (figure 1.7B), which are casts of small bronchioles consisting of mucus and shed epithelial cells. However, Curshman’s spirals are not exclusive to asthma.",True,Pathophysiology of Asthma,Figure 1.7,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.7.png,"Figure 1.7: Histological signs of asthma: A = Charcot–Leyden crystals, B = Curshman’s spirals."
5e210160-148e-4c07-a742-14a4a59068b7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
5e210160-148e-4c07-a742-14a4a59068b7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
5e210160-148e-4c07-a742-14a4a59068b7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
5e210160-148e-4c07-a742-14a4a59068b7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
5e210160-148e-4c07-a742-14a4a59068b7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"With persistent asthma the airway undergoes remodeling (figure 1.8), with thickening of the airway wall and basement membrane, enlarged submucosal glands, and hypertrophy and hyperplasia of airway smooth muscle.",True,Pathophysiology of Asthma,Figure 1.8,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.9.png,"Figure 1.8: Components of airway remodeling in persistent asthma. The epithelium in asthma shows mucous hyperplasia and hypersecretion (gray), and significant basement membrane thickening. Smooth muscle volume is also increased in asthma."
4f8eb667-0ece-403c-a734-6451d7f95e93,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Clinical Presentation of Asthma,False,Clinical Presentation of Asthma,,,,
2c135cfa-b24e-4f13-87ad-646db714ddf5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"One useful diagnostic element of asthma is its episodic or acute behavior. However, as patients may be asymptomatic between attacks, the severity of asthma can be difficult to determine without performing bronchial challenge tests.",True,Clinical Presentation of Asthma,,,,
aa26303d-18f8-4e40-88bc-5f1b6c7ccff1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
aa26303d-18f8-4e40-88bc-5f1b6c7ccff1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
aa26303d-18f8-4e40-88bc-5f1b6c7ccff1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
aa26303d-18f8-4e40-88bc-5f1b6c7ccff1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
aa26303d-18f8-4e40-88bc-5f1b6c7ccff1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The characteristic signs of asthma progress and vary with declining FEV1 (summarized in figure 1.9). Most attacks start with mild wheezing and coughing, which progress with the severity of attack. The location and form of sensations vary between patients, but most asthmatics complain of chest tightness. This sensation is more commonly reported by asthmatics than other pulmonary patients, so it is a useful diagnostic sign.",True,Clinical Presentation of Asthma,Figure 1.9,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
8af2c366-56c6-4673-b64d-e8476f4a8f32,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"As airway resistance increases, the accessory muscles are deployed to maintain sufficient airflow through the narrowing airways, and the patient experiences an increased effort to breathe. Increased expiratory efforts produce dynamic airway collapse and lead to hyperinflation. Further decreases in airway caliber result in insufficient alveolar ventilation and deranged blood gases. The sensation reported at this point is air hunger. Once the patient is severely bronchoconstricted, delivery of inhaled therapies is much more difficult, and mechanical ventilation to support the respiratory muscles becomes complicated. Other signs present during a severe attack are raised heart (tachycardia) and breathing (tachypnea) rates as well as a paradoxical pulse (i.e., a rise in blood pressure during expiration).",True,Clinical Presentation of Asthma,,,,
86cb5661-20b6-4b9b-a4eb-2e9af19c2441,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
86cb5661-20b6-4b9b-a4eb-2e9af19c2441,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
86cb5661-20b6-4b9b-a4eb-2e9af19c2441,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
86cb5661-20b6-4b9b-a4eb-2e9af19c2441,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
86cb5661-20b6-4b9b-a4eb-2e9af19c2441,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The typical chest x-ray of an asthmatic (figure 1.10) shows hyperlucent lung fields, evidence of hyperinflation and peribronchial infiltrate, and perhaps areas of atelectasis. However, the chest x-ray is not particularly effective at distinguishing asthma from some other obstructive disorders.",True,Clinical Presentation of Asthma,Figure 1.10,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.10.jpeg,Figure 1.10: Typical chest x-ray of an asthmatic patient showing hyperlucent fields and hyperinflation. Notice the flattened diaphragm and the number of ribs that are visible; more than six anterior ribs or ten posterior ribs being visible is indicative of hyperinflation.
3dc80a8b-63b8-4e62-bfad-162dd36439d8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Chronic Obstructive Pulmonary Disease,False,Chronic Obstructive Pulmonary Disease,,,,
172772d0-48e0-466b-b6c5-68ea0df6ceba,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Although chronic bronchitis and emphysema have different underlying pathologies, they frequently have the same root cause and are often found together in a patient. In brief, chronic bronchitis is associated with an increase in mucus production, while emphysema involves disruption of the lung structure.",True,Chronic Obstructive Pulmonary Disease,,,,
8e7c0bd9-58d4-4be2-86d2-05d01c3aed62,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The relative role of chronic bronchitis in COPD has diminished since the Clean Air Act reduced atmospheric sulphur dioxide, but with 90 percent of COPD caused by cigarette smoking there is still plenty of bronchitis and emphysema to treat—at enormous cost to the health system from over eight million hospitalizations a year that are mostly paid for by Medicare. The COPD patient tends to be older and poorer and will likely have comorbidities, the most common of which is hypertension. What is perhaps more disturbing is that of the most common causes of death, COPD is the only one whose incidence continues to rise.",True,Chronic Obstructive Pulmonary Disease,,,,
1e0bcf6f-49cf-4fde-a723-9053ac5a42e1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"We will now look at the underlying mechanisms of COPD. Despite the fact it is usually composed of some elements of both chronic bronchitis and emphysema, we will deal with each separately for the sake of simplicity.",True,Chronic Obstructive Pulmonary Disease,,,,
3e2d3cb4-126b-4fc2-859d-5bf1c2b5f377,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Chronic Bronchitis,False,Chronic Bronchitis,,,,
5264caff-e41e-4911-aab6-20d1543b9c12,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Chronic bronchitis is clinically defined as a persistent and productive cough that lasts for at least three months per year for two consecutive years.,True,Chronic Bronchitis,,,,
2e71adcd-aea8-4373-8f87-1c0aadb0c2e9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
2e71adcd-aea8-4373-8f87-1c0aadb0c2e9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
2e71adcd-aea8-4373-8f87-1c0aadb0c2e9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
2e71adcd-aea8-4373-8f87-1c0aadb0c2e9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
2e71adcd-aea8-4373-8f87-1c0aadb0c2e9,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Chronic bronchitis arises from chronic exposure to bronchial irritants, the most common of which is tobacco smoke. These irritants initiate the release of cytokines from airway epithelial cells and macrophages that result in a cascade of responses (summarized in figure 1.11).",True,Chronic Bronchitis,Figure 1.11,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
b21985de-ea7f-49e7-9a53-d2e2f4d78e27,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Neutrophils, lymphocytes, and macrophages are attracted to the irritated airway, and their presence is maintained through increased expression of cell adhesion molecules on the airway walls. These immune cells lead to acute airway wall inflammation that narrows the airway, and if chronic, can lead to tissue damage. The cytokines released by these cells also sensitize airway irritant receptors, which exacerbates the response to future irritant exposure.",True,Chronic Bronchitis,,,,
f99e5e72-85b3-464e-8a07-8ab803a1e3f8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Mucus production increases, and the glands themselves may also release cytokines that further exacerbate the inflammatory response. The mucus also contributes to airway narrowing, and mucus plugs may form that completely block bronchioles.",True,Chronic Bronchitis,,,,
d885634f-7b28-4599-8e6c-e1cfc4438d37,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Mesenchymal cells transition into fibroblasts as part of the inflammatory response, and their chronic presence leads to the deposition of fibrotic tissue.",True,Chronic Bronchitis,,,,
a4aec5f7-2ea0-4c35-b409-d91953ee9891,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Collectively these responses to the irritants result in a narrowed airway that is (1) hypersensitive, (2) fibrosed, and (3) blocked by excessive secretions.",True,Chronic Bronchitis,,,,
c8aa286f-27ec-45a1-aa6f-978bd072ef38,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
c8aa286f-27ec-45a1-aa6f-978bd072ef38,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
c8aa286f-27ec-45a1-aa6f-978bd072ef38,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
c8aa286f-27ec-45a1-aa6f-978bd072ef38,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
c8aa286f-27ec-45a1-aa6f-978bd072ef38,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Continued exposure to irritants leads to other chronic changes beyond fibrosis. With excessive stimulation, the size and number of mucus glands increases. The size of mucosal glands is used as a diagnostic test, and the Reid index describes what proportion of the submucosa is spanned by a gland—in the normal airway a normal gland spans less than 40 percent of the submucosa’s depth, but in chronic bronchitis this exceeds 50 percent (figure 1.12).",True,Chronic Bronchitis,Figure 1.12,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.12-1024x669.png,Figure 1.12: The Reid index compares the width of mucus glands to the width of the submucosal layer of airways.
58c65ac9-615b-4c1f-a828-0748046b1110,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
58c65ac9-615b-4c1f-a828-0748046b1110,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
58c65ac9-615b-4c1f-a828-0748046b1110,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
58c65ac9-615b-4c1f-a828-0748046b1110,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
58c65ac9-615b-4c1f-a828-0748046b1110,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"In conjunction with an increased mucus production capacity, the airway has a reduced mucus clearance capability with airway remodeling, including squamous metaplasia replacing normal ciliated columnar epithelium (figure 1.13). The mucus escalator is also compromised by a decline in function of the remaining cilia with exposure to cigarette smoke.",True,Chronic Bronchitis,Figure 1.13,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.13.png,Figure 1.13: Prolonged irritant exposure can lead to airway remodeling with loss of normal ciliated epithelium.
d08f934c-477a-4809-a009-da4149f0a0eb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"These changes result in an airway that produces more mucus and is less capable of removing it. The static mucus not only causes airway plugging, but can also promote infections that lead to episodic and characteristic exacerbation of COPD symptoms.",True,Chronic Bronchitis,,,,
379a3569-f178-4c75-9dcf-5627b9431ef4,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Clinical Presentation of Chronic Bronchitis,False,Clinical Presentation of Chronic Bronchitis,,,,
ae9a42d4-408b-4f44-96aa-f5b52dee941d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
ae9a42d4-408b-4f44-96aa-f5b52dee941d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
ae9a42d4-408b-4f44-96aa-f5b52dee941d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
ae9a42d4-408b-4f44-96aa-f5b52dee941d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
ae9a42d4-408b-4f44-96aa-f5b52dee941d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,The signs and symptoms of chronic bronchitis depend on the level of airway obstruction and the consequent decline in lung function (summarized in figure 1.14).,True,Clinical Presentation of Chronic Bronchitis,Figure 1.14,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.14-914x1024.png,Figure 1.14: The pathophysiological and clinical events as chronic bronchitis progresses.
4396a991-937d-4a0d-ba46-5c838d85ee68,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"As with many pulmonary diseases, the onset can be insidious. Small airway damage may be present but undetectable with normal spirometry, while the patient becomes accustomed to and tolerates a persistent productive cough. However, with continued irritant exposure, this initial simple bronchitis progresses.",True,Clinical Presentation of Chronic Bronchitis,,,,
e65afcfc-0b58-45e4-880c-9574b223be79,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Secretions continue to worsen and peribronchiolar fibrosis marks the onset of obstructive bronchitis that is reflected by significant expiratory airflow limitation. At this point the patient may have tolerated years of productive cough and experienced frequent chest infections related to poor mucus clearance. COPDers are particularly susceptible to Haemophilus influenza and Streptococcus pneumoniae. The sputum is abundant and capable of plugging significant numbers of airways and may be blood tinged; COPD is the most common cause of hemoptysis. Airways may demonstrate hyperreactivity and mimic an asthmatic response.,True,Clinical Presentation of Chronic Bronchitis,,,,
1373416e-6f43-4e8f-ac42-4bab22bdea88,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The onset of dyspnea is insidious and is usually first experienced during exertion—leading the patient to avoid exercise, which in turn leads to deconditioning and a worsening of the symptom. Lung sounds include wheezes and rales, the rales often clearing after cough.",True,Clinical Presentation of Chronic Bronchitis,,,,
94057993-8db8-4904-95c9-e71444c8c16d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,With worsening airway flow limitation expiration becomes prolonged and may be incomplete due to airway collapse that leads to characteristic hyperinflation.,True,Clinical Presentation of Chronic Bronchitis,,,,
a323d457-233d-4a4b-bd39-b91fedd58b8d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Mucus plugging and airway closure leads to areas of V/Q abnormalities through the lung, and localized areas of hypoxia can lead to pulmonary vasoconstriction. When significant regions of the lung are vasoconstricted, pulmonary vascular resistance can rise enough to induce right-sided heart failure.",True,Clinical Presentation of Chronic Bronchitis,,,,
91aa09d0-333a-4ca2-9918-5ca73e76675e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"With continued progression of the disease, blood gases become deranged as insufficient alveolar ventilation is achieved. As the disease approaches its end stage, the patient experiences dyspnea at rest until respiratory failure occurs and the patient is hypoxemic and hypercarbic.",True,Clinical Presentation of Chronic Bronchitis,,,,
e9bc9237-1a47-4bad-987b-9e781d679d36,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Emphysema,False,Emphysema,,,,
c5164549-8527-4dcb-968b-54f2e6c2dbaa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
c5164549-8527-4dcb-968b-54f2e6c2dbaa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
c5164549-8527-4dcb-968b-54f2e6c2dbaa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
c5164549-8527-4dcb-968b-54f2e6c2dbaa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
c5164549-8527-4dcb-968b-54f2e6c2dbaa,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Emphysema, a possible second component to COPD, involves permanent enlargement of airspaces distal to the terminal bronchioles and destruction of alveolar walls, as is evident in figure 1.15.",True,Emphysema,Figure 1.15,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
38263cf2-32b0-4772-8d0a-7af435aa1be8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
38263cf2-32b0-4772-8d0a-7af435aa1be8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
38263cf2-32b0-4772-8d0a-7af435aa1be8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
38263cf2-32b0-4772-8d0a-7af435aa1be8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
38263cf2-32b0-4772-8d0a-7af435aa1be8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The pattern of airspace destruction varies with underlying cause and revolves around the acinus (figure 1.16), the functional unit of the lung comprised of the terminal airways and the alveoli that collectively make up the respiratory zone of the lung. In its broadest classification, emphysema can take on either a centriacinar or panacinar distribution (figure 1.16). In centriacinar emphysema, the respiratory duct is affected while the distal alveoli are mostly unaffected. This is more commonly found in the upper lung fields and associated with smoking and the concurrent presence of chronic bronchitis.",True,Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
1c4fdcf2-b903-4b0f-b7d6-df2a8b34ffb7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
1c4fdcf2-b903-4b0f-b7d6-df2a8b34ffb7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
1c4fdcf2-b903-4b0f-b7d6-df2a8b34ffb7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
1c4fdcf2-b903-4b0f-b7d6-df2a8b34ffb7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
1c4fdcf2-b903-4b0f-b7d6-df2a8b34ffb7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"This pathology slide in figure 1.15 illustrates this pattern of tissue destruction with isolated areas of damage, surrounded by relatively normal alveolar structure.",True,Emphysema,Figure 1.15,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.15-300x132.png,Figure 1.15: Histological comparison of normal (left) and emphysematous (right) lung tissue.
e09ef9f9-479c-4d28-8a7f-9b3a8dbb37a7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
e09ef9f9-479c-4d28-8a7f-9b3a8dbb37a7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
e09ef9f9-479c-4d28-8a7f-9b3a8dbb37a7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
e09ef9f9-479c-4d28-8a7f-9b3a8dbb37a7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
e09ef9f9-479c-4d28-8a7f-9b3a8dbb37a7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Panacinar emphysema, as the name suggests, involves the entire acinus (figure 1.16), and the alveolar structure is more involved creating large airspaces that occur throughout the lung. This is evident in the pathology slide in figure 1.16 that shows much more uniform damage than the centriacinar example. Panacinar emphysema is much less common and is the pattern of destruction associated with alpha-1 antitrypsin deficiency, which we will deal with in a moment.",True,Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
f5ad977f-f6e0-479e-b69d-a1a59982bcc7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"So having seen the morphology of emphysema, we will look at how this damage occurs.",True,Emphysema,,,,
f1972a34-8969-44f8-a823-b6104f6ec47e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Pathophysiology of Emphysema,False,Pathophysiology of Emphysema,,,,
8efbb221-7b61-4132-9024-5e0521e842c8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,The normal structure of alveoli and respiratory ducts consists of type 1 and type 2 pneumocytes with elastic fibers that contribute to the structure’s mechanical behavior. Emphysema involves the loss of these parenchymal fibers.,True,Pathophysiology of Emphysema,,,,
1f15e17f-150c-403f-9dc9-b12e2c28b868,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The presence of irritants, such as cigarette smoke, causes oxidization and the dysfunction of antiprotease enzymes. Without their inhibitory action, the activity of proteases increases and causes the destruction of local tissue. One of these proteases is elastase, whose elevated activity leads to irreparable loss of parenchymal fibers.",True,Pathophysiology of Emphysema,,,,
97e5a121-8bf9-4f97-ab8d-4bc3de3bc186,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Elastase is also released by neutrophils and macrophages that arrive in response to the inflammatory cascade caused by the inhaled smoke. This causes further destruction of elastin fibers.,True,Pathophysiology of Emphysema,,,,
0bb287a6-c405-42f9-a944-b05c373c361c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
0bb287a6-c405-42f9-a944-b05c373c361c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
0bb287a6-c405-42f9-a944-b05c373c361c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
0bb287a6-c405-42f9-a944-b05c373c361c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
0bb287a6-c405-42f9-a944-b05c373c361c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The pathogenesis of emphysema (figure 1.17) might be summarized as an imbalance between the activities of antiproteases and proteases. Antiproteases are suppressed, and proteases are elevated.",True,Pathophysiology of Emphysema,Figure 1.17,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
07b8c3ec-1c4d-41c9-966e-3ad8663e6533,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
07b8c3ec-1c4d-41c9-966e-3ad8663e6533,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
07b8c3ec-1c4d-41c9-966e-3ad8663e6533,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
07b8c3ec-1c4d-41c9-966e-3ad8663e6533,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
07b8c3ec-1c4d-41c9-966e-3ad8663e6533,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The emphysema in about 1 percent of COPD patients is caused by a genetic lack of alpha-1 anti-trypsin. Even without tobacco use, these patients have an antiprotease/protease imbalance that results in loss of elastin and collagen and produces the panacinar emphysema shown previously (figure 1.16). If an alpha1-anti-trypsin patient does smoke, this imbalance is worsened and emphysema may develop by their late twenties.",True,Pathophysiology of Emphysema,Figure 1.16,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
65f1a01c-d659-40a5-be88-755719b71f9e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,The loss of the elastic tissue and alveolar structure produces several pathophysiological changes in lung mechanics and function that result in typical clinical signs.,True,Pathophysiology of Emphysema,,,,
be0b85e8-980d-4673-a685-1754e41a1895,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Clinical Presentation of Emphysema,False,Clinical Presentation of Emphysema,,,,
cfa2c530-747c-4b46-8ec3-603a7eeae292,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
cfa2c530-747c-4b46-8ec3-603a7eeae292,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
cfa2c530-747c-4b46-8ec3-603a7eeae292,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
cfa2c530-747c-4b46-8ec3-603a7eeae292,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
cfa2c530-747c-4b46-8ec3-603a7eeae292,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Lung recoil is the opposing force to the chest wall’s tendency to spring outward. The loss of elastin reduces lung recoil and the chest wall can move outward, producing a characteristic “barrel-chest” (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
7a9b8cfa-c028-43e1-a858-1fae5b7f2990,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
7a9b8cfa-c028-43e1-a858-1fae5b7f2990,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
7a9b8cfa-c028-43e1-a858-1fae5b7f2990,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
7a9b8cfa-c028-43e1-a858-1fae5b7f2990,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
7a9b8cfa-c028-43e1-a858-1fae5b7f2990,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The lack of recoil also means that passive expiration is ineffective and active expiration must be employed. The positive pleural pressure associated with active expiration enhances dynamic airway collapse that leads to gas trapping and characteristic hyperinflation (figure 1.18). To prevent this, the emphysema patient may adopt pursed lip breathing to maintain airway pressure during expiration that props open the airways.",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
2ce5a771-36f5-4fae-a455-b7ff82217f0e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
2ce5a771-36f5-4fae-a455-b7ff82217f0e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
2ce5a771-36f5-4fae-a455-b7ff82217f0e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
2ce5a771-36f5-4fae-a455-b7ff82217f0e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
2ce5a771-36f5-4fae-a455-b7ff82217f0e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The hyperinflation and nonuniform tissue damage can lead to a heterogenous distribution of ventilation and V/Q abnormalities that diminish gas exchange. Gas exchange will also be diminished by the enlargement of airspaces, reducing available surface area (figure 1.18).",True,Clinical Presentation of Emphysema,Figure 1.18,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.18.png,Figure 1.18: The pathophysiological events that lead to the clinical signs of emphysema.
1b9c05df-3ece-48c0-9b25-0391892c1b7e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The deterioration of gas exchange and lung mechanics worsens as more lung becomes involved, and the stage of the disease, and any concurrent chronic bronchitis, is classified by the level of airway flow limitation (e.g., FEV1/FVC).",True,Clinical Presentation of Emphysema,,,,
2263eb8e-25cf-4842-ba17-ce86b44f826f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"It might also be worth noting here that COPD can produce or be associated with a number of comorbidities; we have already mentioned hypertension, but pulmonary artery disease, coronary heart disease, heart failure, lung cancer, and malnutrition may contribute to a low quality of life that is typically associated with COPD. This in turn may contribute to the high incidence of anxiety disorders and depression experienced by COPD patients.",True,Clinical Presentation of Emphysema,,,,
b968e2c8-4f36-4d49-b393-701d8197e8e5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Cystic Fibrosis,False,Cystic Fibrosis,,,,
35367137-e4e6-4a4e-8dfa-3fd5fd424ec8,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Cystic fibrosis (CF) is an inherited disorder that affects the exocrine glands of not only the lungs, but also the pancreas, intestines, and bile ducts. We will focus only on the pulmonary aspects here and see how CF produces an obstructive lung disease.",True,Cystic Fibrosis,,,,
e9453d18-aef1-4874-9ccf-191944df285e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Cystic fibrosis affects the composition of the fluid lining the airways. Changes in this fluid lead to serious sequelae that dramatically shorten life expectancy. Even with modern therapy, many CF patients only live until their thirties or early forties, and some still die in infancy.",True,Cystic Fibrosis,,,,
ad5f1452-ec5d-4082-8c7f-0fd114f8e6a0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,There are two hypotheses about the pathophysiological mechanism of CF: the low volume and the high salt. We will focus only on the low volume hypothesis as there is increasing evidence to support this and emerging evidence against the high salt hypothesis.,True,Cystic Fibrosis,,,,
28818233-f925-4080-8800-a734b473c60c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Pathophysiology of Cystic Fibrosis,False,Pathophysiology of Cystic Fibrosis,,,,
29bd932b-a0b6-4f10-b882-f5d47767c79f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
29bd932b-a0b6-4f10-b882-f5d47767c79f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
29bd932b-a0b6-4f10-b882-f5d47767c79f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
29bd932b-a0b6-4f10-b882-f5d47767c79f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
29bd932b-a0b6-4f10-b882-f5d47767c79f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Control of the airway fluid relies on the action of ion channels in the apical membranes of epithelial cells, and there are two channels to focus on: CFTR and ENaC. The CFTR channels let chloride out of the cell, while the ENaC lets sodium in (top panel, figure 1.19).",True,Pathophysiology of Cystic Fibrosis,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
3d55bdf7-3c45-4e70-b082-da69e93269ec,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,ENaC,False,ENaC,,,,
581fb044-fa26-4ea5-a702-27ad0a67549a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
581fb044-fa26-4ea5-a702-27ad0a67549a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
581fb044-fa26-4ea5-a702-27ad0a67549a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
581fb044-fa26-4ea5-a702-27ad0a67549a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
581fb044-fa26-4ea5-a702-27ad0a67549a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"This exchange helps maintain a healthy fluid layer in the airway, but fails in CF because of a nonfunctioning CFTR channel (right panel, figure 1.19).",True,ENaC,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
96e70f38-d11f-497a-a35c-d3f8153d2af1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"There are numerous mutations that are known to produce a dysfunctional CFTR channel, but 70 percent of CF cases are due to the delta-F-508 mutation (so named as the mutation leads to a deletion of phenylalanine at position 508 of the CFTR protein). This is a Mendelian recessive trait, and CF occurrence is 1 in 2,500 live births.",True,ENaC,,,,
8d186bee-e8c0-44a5-84b9-8bf9a88fde60,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
8d186bee-e8c0-44a5-84b9-8bf9a88fde60,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
8d186bee-e8c0-44a5-84b9-8bf9a88fde60,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
8d186bee-e8c0-44a5-84b9-8bf9a88fde60,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
8d186bee-e8c0-44a5-84b9-8bf9a88fde60,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"So what are the consequences of CFTR dysfunction? Chloride ends up being trapped inside the cell (bottom panel, figure 1.19), and this leads to a greater influx of sodium through the ENaC down its electrochemical gradient, leaving a higher concentration of salt inside the cells that pulls water in from the airway lumen. The low fluid volume in the airway results in:",True,ENaC,Figure 1.19,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.19.png,Figure 1.19: The impact of ion currents in normal and CF cells on fluid layer and cilia.
859136f9-623d-4d21-ad59-f81c485de693,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"This combination severely impacts mucus clearance (thicker, heavier mucus with compromised cillary escalator). The defective CFTR channel therefore results in mucus retention and airway obstruction. This in turn leads to reduced alveolar ventilation and repeated infections. The two most common culprits for infection in CF are Staphylococcus aureus and Pseudomonsa aeruginosa. Normal functional CFTR appears to suppress P. aeruginosa, perhaps explaining its prevalence in cystic fibrosis where it can be found in the sputum of almost all CF patients.",True,ENaC,,,,
209c47c9-14c5-4418-8833-5dece19a404c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,cillary,False,cillary,,,,
99b9fb58-9796-421b-9cd4-91c252b399e2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Pseudomonsa,False,Pseudomonsa,,,,
a26233d3-4117-4414-92f8-a01634ba89b2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
a26233d3-4117-4414-92f8-a01634ba89b2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
a26233d3-4117-4414-92f8-a01634ba89b2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
a26233d3-4117-4414-92f8-a01634ba89b2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
a26233d3-4117-4414-92f8-a01634ba89b2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The consequences of repeated infection are a mixture of serious conditions and pathologies including atelectasis, pneumonia, bronchiectasis, and other structural abnormalities of the airways (figure 1.20).",True,Pseudomonsa,Figure 1.20,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
6e0878ff-e800-4981-ae33-012245b6272e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The findings of CF obviously include the results of other effected organs, such as the pancreas. But nowadays these are more easily addressed, and it is pulmonary involvement that still proves critical. The onset of pulmonary involvement is variable and may be weeks or years after birth.",True,Pseudomonsa,,,,
d4e61183-fe51-4e7f-8343-1e6d18b85ab0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Clinical Presentation of Cystic Fibrosis,False,Clinical Presentation of Cystic Fibrosis,,,,
77d7256e-7796-4db3-9a33-710dd7469421,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
77d7256e-7796-4db3-9a33-710dd7469421,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
77d7256e-7796-4db3-9a33-710dd7469421,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
77d7256e-7796-4db3-9a33-710dd7469421,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
77d7256e-7796-4db3-9a33-710dd7469421,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Findings progress with progressive airway damage (figure 1.21), but start with cough that may be dry at first but transitions to productive to expel the copious, viscous mucus. With poor mucus clearance, the patient experiences repeated infections that exacerbate symptoms at each stage of the disease.",True,Clinical Presentation of Cystic Fibrosis,Figure 1.21,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.21.png,Figure 1.21: Clinical signs of the pulmonary progression of CF.
21898d41-96fb-433c-95c6-f7ca010dce31,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,CF patients usually have an abnormal sinus x-ray and evidence of chronic sinusitis as well as a high occurrence of nasal polyps.,True,Clinical Presentation of Cystic Fibrosis,,,,
664202c5-5124-465a-9eee-df20e5d53f60,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"With increasing and irreversible airway damage, the patients begins to experience dyspnea, and the damage may lead to hemoptysis, spontaneous pneumothorax, and a barrel chested appearance. Signs of prolonged pulmonary dysfunction appear as the disease progresses, such as finger clubbing, cyanosis, and cor pulmonale (right-sided heart failure caused by lung disease). As the patient approaches respiratory failure the accessory muscles are deployed. Patients succumb to the respiratory failure or an overwhelming infection.",True,Clinical Presentation of Cystic Fibrosis,,,,
85bf77ce-381a-49db-8241-691f5e9706bf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Because CF also affects sweat gland function, the sweat test remains a standard diagnostic with a chloride level greater than 60 mEq/L being indicative of CF. This test is more reliable in children than adults, who may have developed other conditions that affect the composition of sweat.",True,Clinical Presentation of Cystic Fibrosis,,,,
e924c5e2-ae4d-40e1-81a3-9c8a56217594,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
e924c5e2-ae4d-40e1-81a3-9c8a56217594,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
e924c5e2-ae4d-40e1-81a3-9c8a56217594,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
e924c5e2-ae4d-40e1-81a3-9c8a56217594,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
e924c5e2-ae4d-40e1-81a3-9c8a56217594,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Chest x-rays show (figure 1.22) signs of hyperinflation associated with gas trapping and the hallmarks of any other complications that the CF has induced. These are viewed more clearly with the common use of high-resolution computed tomography (HRCT)(figure 1.23) to determine the type and extent of damage that may include bronchiectasis and mucus impactions.,True,Clinical Presentation of Cystic Fibrosis,Figure 1.22,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.22.png,Figure 1.22: Typical chest x-ray findings of CF.
22b55f64-ba1d-4783-8d5c-54ef6ccb2c4a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Spirometry detects the airway obstruction and hyperinflation that produce a low vital capacity and high residual volume.,True,Clinical Presentation of Cystic Fibrosis,,,,
ec6bc2a8-2e1d-474d-9d14-9bd4c29c4ebc,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Bronchiectasis,False,Bronchiectasis,,,,
7b7c575e-6357-4a7c-9748-e07e72fa5928,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"This section will address bronchiectasis, a form of airway obstruction that is often a manifestation of chronic airway inflammation. Bronchiectasis involves a permanent dilation of a bronchi or bronchiole—think of bronchiectasis as the airway equivalent of an aneurysm.",True,Bronchiectasis,,,,
40369011-159e-43b1-9782-0766716a7341,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
40369011-159e-43b1-9782-0766716a7341,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
40369011-159e-43b1-9782-0766716a7341,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
40369011-159e-43b1-9782-0766716a7341,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
40369011-159e-43b1-9782-0766716a7341,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"A bronchiectasis starts with a section of airway wall becoming inflamed (figure 1.24), disrupting and weakening its structure. This weakening leads to a permanent dilation of the airway that impairs the clearance of secretion. Because the airway is inflamed, the amount of secretion may be significant and it begins to accumulate.",True,Bronchiectasis,Figure 1.24,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
8abb41ed-d5f4-4a8a-8ddc-ded4d7997d8e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
8abb41ed-d5f4-4a8a-8ddc-ded4d7997d8e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
8abb41ed-d5f4-4a8a-8ddc-ded4d7997d8e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
8abb41ed-d5f4-4a8a-8ddc-ded4d7997d8e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
8abb41ed-d5f4-4a8a-8ddc-ded4d7997d8e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The stagnant secretion promotes a secondary infection that leads to further inflammation, wall disruption, and dilation. Thus the airway has entered a vicious cycle that causes the dilation and retention of mucus to perpetuate (figure 1.24).",True,Bronchiectasis,Figure 1.24,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
89f6a314-597c-4c25-bf8d-68102c2ccd70,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The establishing of a bronchiectasis has an initial phase leading to persistent inflammation, desquamation (which worsens the mucus clearance), and the ulceration. In what is probably a familiar story, the continued inflammation leads to fibrosis in the chronic phase of development, and this can lead to airway destruction and perhaps the condition of bronchiolitis obliterans.",True,Bronchiectasis,,,,
c086040c-3c23-4824-b4c2-7700f2842284,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Let us look at how this process can get started.,False,Let us look at how this process can get started.,,,,
ac042d75-927e-40bf-bf28-776ef676fd4f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Pathogenesis of Bronchiectasis,False,Pathogenesis of Bronchiectasis,,,,
dce5201a-3f5e-42ad-85b4-b4bd02d9fddb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
dce5201a-3f5e-42ad-85b4-b4bd02d9fddb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
dce5201a-3f5e-42ad-85b4-b4bd02d9fddb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
dce5201a-3f5e-42ad-85b4-b4bd02d9fddb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
dce5201a-3f5e-42ad-85b4-b4bd02d9fddb,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,There are some common culprits for initiating bronchiectasis (figure 1.25). Most start with either a decline in mucus clearance and the associated inflammation or damage to the airway wall.,True,Pathogenesis of Bronchiectasis,Figure 1.25,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
ed1ac42a-c710-45c4-a01c-18ba3c769d29,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"About 50 percent of bronchiectasis cases are associated with cystic fibrosis where the genetic condition causes production of copious, thick mucus that is difficult to clear and often results in infection (commonly caused by Staphylococcus aureus).",True,Pathogenesis of Bronchiectasis,,,,
e81e71ed-e40a-42d8-a956-22209eb1692e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Conditions causing cillary dyskinesia, as seen in Kartagener’s syndrome, also disrupt the mucocillary escalator.",True,Pathogenesis of Bronchiectasis,,,,
6da56a38-c93e-4fc4-bd05-21b4c83354f0,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,mucocillary,False,mucocillary,,,,
5a735abd-336e-4836-b84a-8d2521ff7e28,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Another common cause of bronchiectasis is an allergy to Aspergillus fumigatus, a common fungus. In hypersensitive or immune-compromised individuals, chronic exposure can lead to allergic bronchopulmonary aspiragillosis.",True,mucocillary,,,,
5210ce05-8c3f-4fda-904d-ff8b464d4ee1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,aspiragillosis,False,aspiragillosis,,,,
292ce5fc-4847-47f9-a345-c2a7e14977a1,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Bronchiectasis can be initiated in the vicinity of tuberculosis or other necrotizing infections that damage and weaken airway walls.,True,aspiragillosis,,,,
0397c030-2947-4d7a-9133-724e79ecea86,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Obstruction of the bronchioles or bronchi by inhaled foreign objects, tumors, or compacted mucus can also initiate bronchiectasis through local inflammation and by preventing mucus clearance. The dilation of the airway can be worsened further by distal atelectasis that produces a negative pressure around the affected airway.",True,aspiragillosis,,,,
2cc4061f-ec41-42e7-b057-1bb7d58a812b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"As you might have gather by now, repeated local infection or inflammation has the potential to initiate bronchiectasis, so it is perhaps not surprising that with the advent of high resolution computed tomography (CT) imaging, bronchiectasis has also been found in association with AIDS, transplant rejection, and rheumatoid lung disease.",True,aspiragillosis,,,,
4504d36b-77e1-4d10-a6c4-d474d8b82941,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,We will now examine the results of these instigating factors.,False,We will now examine the results of these instigating factors.,,,,
c0ca8d41-40b3-4304-9058-2d9392902e8c,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Pathology of Bronchiectasis,False,Pathology of Bronchiectasis,,,,
a19d01fe-bb53-40d8-bd1a-6474972dd372,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
a19d01fe-bb53-40d8-bd1a-6474972dd372,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
a19d01fe-bb53-40d8-bd1a-6474972dd372,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
a19d01fe-bb53-40d8-bd1a-6474972dd372,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
a19d01fe-bb53-40d8-bd1a-6474972dd372,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The outcomes of bronchiectasis are seen in the histology slide in figure 1.26, with the affected airway lumen filled with mucus and pus, and the airway walls exhibiting fibroglandular tissue and infiltration by inflammatory cells (outer red circle).",True,Pathology of Bronchiectasis,Figure 1.26,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
06c14211-0457-4c24-90a6-de790d1b6486,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
06c14211-0457-4c24-90a6-de790d1b6486,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
06c14211-0457-4c24-90a6-de790d1b6486,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
06c14211-0457-4c24-90a6-de790d1b6486,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
06c14211-0457-4c24-90a6-de790d1b6486,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The gross view (right panel, figure 1.26) shows severely dilated bronchi and noticeable thickening of their walls.",True,Pathology of Bronchiectasis,Figure 1.26,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.26.png,Figure 1.26: Histological and gross changes associated with severe bronchiectasis.
ce1c4bcb-1608-4a8f-8cf2-6cbdc0cdb8f7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
ce1c4bcb-1608-4a8f-8cf2-6cbdc0cdb8f7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
ce1c4bcb-1608-4a8f-8cf2-6cbdc0cdb8f7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
ce1c4bcb-1608-4a8f-8cf2-6cbdc0cdb8f7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
ce1c4bcb-1608-4a8f-8cf2-6cbdc0cdb8f7,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,There are different forms of bronchiectasis; these are classified by their shape (figure 1.27).,True,Pathology of Bronchiectasis,Figure 1.27,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
40d89d36-bf6f-49fa-b14e-7d622b1d0f27,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"A bronchiectasis can be cylindrical, varicose (also known as fusiform), or cystic (also known as saccular). The shape is relevant to their effect on the efficacy of coughing; cylindrical form has very little effect on cough’s ability to clear mucus, whereas varicose and cystic forms tend to disproportionately collapse during cough and reduce its effectiveness at moving mucus up the airway.",True,Pathology of Bronchiectasis,,,,
648a2b3b-5213-48ef-b52d-31e34d17a3b6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
648a2b3b-5213-48ef-b52d-31e34d17a3b6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
648a2b3b-5213-48ef-b52d-31e34d17a3b6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
648a2b3b-5213-48ef-b52d-31e34d17a3b6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
648a2b3b-5213-48ef-b52d-31e34d17a3b6,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"As shown in figure 1.28 an x-ray shows the presence of bronchiectasis, but it can be difficult to ascertain the form. High resolution CT (figure 1.28) is better at determining the form and has all but replaced the much more invasive bronchography, which involves instillation of radiopaque medium into the tracheobronchial tree.",True,Pathology of Bronchiectasis,Figure 1.28,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.28.png,Figure 1.28: Chest x-ray and CT of severe bronchiectasis. In the x-ray there are clear markings in the right lung that follow the path of affected bronchi. The distinctly widened airways on the right of the CT are consistent with severe bronchiectasis.
1917c678-f68f-4748-8968-92bac3212adf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
1917c678-f68f-4748-8968-92bac3212adf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Cystic Fibrosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
1917c678-f68f-4748-8968-92bac3212adf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Chronic Obstructive Pulmonary Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
1917c678-f68f-4748-8968-92bac3212adf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
1917c678-f68f-4748-8968-92bac3212adf,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Where the bronchiectasis occurs in the lung is somewhat dependent on the cause. The segmental and subsegmental bronchi are the airway types most commonly affected, and the basilar segments of the lower lobes are the most frequent region in the lung. The second most common locations are the right middle lobe and lingual segments, while bronchiectasis caused by primary tuberculosis (TB) and other infections tend to occur in the upper lung fields where the infection is located (see figure 1.29).",True,Pathology of Bronchiectasis,Figure 1.29,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.29.png,Figure 1.29: Common locations of the segmental and subsegmental broncho affected by bronchiectasis.
d84f2d1a-1a68-4db4-9752-7e1f0b81eeed,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"So, how does bronchiectasis present, and what are the results of diagnostic tests?",True,Pathology of Bronchiectasis,,,,
e62c8926-4cae-429b-bc4a-87a094d5815d,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Clinical Presentation of Bronchiectasis,False,Clinical Presentation of Bronchiectasis,,,,
db6eaeed-5dd7-4693-b155-c6c4a93ff80e,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The initial complaint is usually a persistent cough with copious expectoration. The amount of mucus the cough produces varies and can be as high as several hundred milliliters per day, particular when the dependent airways are involved. However, it is worth noting here that bronchiectasis in the upper lobes (usually associated with infection) may be dry with little or no mucus expectoration.",True,Clinical Presentation of Bronchiectasis,,,,
9bb40485-fd5d-4756-b344-d7289ec958a5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Generally though there is mucopurulent expectorate, and if it is associated with an anerobic infection it will likely have a foul odor. Sputum smears are loaded with white blood cells and can contain both gram-positive and -negative organisms.",True,Clinical Presentation of Bronchiectasis,,,,
21574d0e-5f9a-4107-bcdc-53870939e00a,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The patient will likely have a history of recurrent pneumonia, the site of the pneumonia being consistent with locality of the bronchiectasis.",True,Clinical Presentation of Bronchiectasis,,,,
2f70de5e-1483-44e1-b87d-68910b5fbdac,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The expectorate may also contain blood. The degree and frequency of hemoptysis is variable and unpredictable, but occasionally it can be massive and life threatening.",True,Clinical Presentation of Bronchiectasis,,,,
29fb4724-9c59-4982-97e2-0809be46d891,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"The standard diagnostic tests may not be helpful in early stages, but typical signs appear with worsening airway involvement. In the early stages the patient will likely appear normal on a physical exam and have normal spirometry and arterial blood gas values. With more significant bronchiectasis, rales and rhonchi over the affected site can be heard.",True,Clinical Presentation of Bronchiectasis,,,,
43f72bbe-f585-4774-b249-2150a28225a5,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Later signs with long-standing bronchiectasis include finger clubbing, but this is not exclusive to the condition.",True,Clinical Presentation of Bronchiectasis,,,,
1a7744f2-e417-4d26-863b-7be6beba611f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"A chest x-ray will show the peribronchial fibrosis and any atelectasis. But, as mentioned earlier, a high-resolution CT is much more effective at determining the degree and type of airway changes.",True,Clinical Presentation of Bronchiectasis,,,,
e9b38d7b-0281-49c4-9b09-f981b8b26c28,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"References, Resources, and Further Reading",False,"References, Resources, and Further Reading",,,,
a7d95d7d-6f8b-4db3-b64b-3ee5647d2ec2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,Text,False,Text,,,,
d272d383-5389-409b-ab99-753448d1b31b,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Farzan, Sattar, with Doris L. Hunsinger and Mary L. Phillips. “Chapters 8–11.” In A Concise Handbook of Respiratory Diseases. Reston, VA: Reston Publishing Company, 1978.",True,Text,,,,
94dc5bd4-fa3a-4982-8ef3-9f0b4e6c69b2,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"Husain, Aliya N. “Chapter 15: The Lung.” In Robbins and Cotran Pathologic Basis of Disease, 9th ed., edited by Vinay Kumar, Abul K. Abbas, and John C. Aster. Philadelphia: Saunders, an imprint of Elsevier Inc., 2015.",True,Text,,,,
4c059fff-39e8-4284-b4cd-dcc25bfe343f,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/,1. The Obstructive Lung Diseases,https://pressbooks.lib.vt.edu/pulmonarypathophysiology/chapter/chapter-1/,"West, John B. “Chapter 4: Obstructive Diseases.” In Pulmonary Pathophysiology: The Essentials, 7th ed. Baltimore: Lippincott Williams & Wilkins, a Wolters Kluwer business, 2008.",True,Text,,,,