pulmonary/queries.csv

fig_num,sub_section_headings,images-src,image_caption
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.
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.
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."
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.
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
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.
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.
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.
Figure 8.4,Chronic SLE,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.4.jpeg,Figure 8.4: Progression of diffuse fibrosis in chronic SLE.
Figure 8.5,Rheumatoid Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/8.5.jpeg,Figure 8.5: Pleural effusion in a rheumatoid patient.
Figure 8.6,Rheumatoid Disease,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.
Figure 8.7,Progressive Systemic Sclerosis,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).
Figure 8.1,Text,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."
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.
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.
Figure 5.2,Let us look at the process step-by-step.,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.
Figure 5.3,There are three defined stages for the progression 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.”
Figure 5.4,There are three defined stages for the progression 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.
Figure 5.5,There are three defined stages for the progression of ARDS.,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/5.5.jpg,Figure 5.5: Fibrotic stage 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.
Figure 4.1,Mechanisms of ILD,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
Figure 4.1,ILD,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
Figure 4.1,tiefitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.1.png,Figure 4.1: Basic mechanism of interstitial lung disease.
Figure 4.2,Pathology of ILD,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."
Figure 4.3,Pathophysiology of ILD,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.3.png,Figure 4.3: Pathophysiological consequences of ILD.
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.
Figure 4.5,Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis–Associated ILD,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.5.jpeg,Figure 4.5: Smoker’s macrophages occupying an airspace.
Figure 4.7,Diffuse Alveolar Damage (DAD),https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.7.jpeg,Figure 4.7: Diffuse alveolar damage.
Figure 4.8,Nonspecific Interstitial Pneumonia,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.8.png,Figure 4.8: Extremes of nonspecific interstitial pneumonia.
Figure 4.10,Silicosis,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.
Figure 4.12,Silicosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.12.png,Figure 4.12: The pathophysiology of silicosis.
Figure 4.13,Asbestosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.13.png,Figure 4.13: Pathophysiology of asbestosis.
Figure 4.14,Asbestosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.14-scaled.jpg,Figure 4.14: Ferruginous bodies associated with asbestosis.
Figure 4.15,Asbestosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.15.jpeg,Figure 4.15: Radiographic findings in asbestosis.
Figure 4.16,Coal worker’s pneumoconiosis (CWP),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.
Figure 4.17,Coal worker’s pneumoconiosis (CWP),https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.17.jpeg,Figure 4.17: Large perihilar lesion in complicated CWP.
Figure 4.18,Berylliosis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/4.18.png,Figure 4.18: Pathophysiology of berylliosis.
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.
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.
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."
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.
Figure 2.2,URIs,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.2.png,Figure 2.2: Pathophysiology of the common cold.
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.
Figure 2.4,Group A Streptococcus,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/2.4.jpeg,Figure 2.4: Typical signs of “strep throat.”
Figure 2.5,Corynebacterium diphtheriae,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).
Figure 1.1,Text,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/02/1.1.png,Figure 1.1: Forms and prevalence of asthma.
Figure 1.2,Text,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.
Figure 1.3,proinflammatory,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.
Figure 1.4,proinflammatory,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.4.png,Figure 1.4: Factors promoting asthma at night.
Figure 1.5,proinflammatory,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."
Figure 1.6,Pathophysiology of 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."
Figure 1.7,Pathophysiology of 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."
Figure 1.8,Pathophysiology of 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."
Figure 1.9,Clinical Presentation of Asthma,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.8.png,Figure 1.9: The progression of an asthma “attack.”
Figure 1.10,Clinical Presentation of 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.
Figure 1.11,Chronic Bronchitis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.11-1024x602.png,Figure 1.11: Pathophysiology of chronic bronchitis.
Figure 1.12,Chronic Bronchitis,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.
Figure 1.13,Chronic Bronchitis,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.
Figure 1.14,Clinical Presentation of Chronic Bronchitis,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.
Figure 1.15,Emphysema,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.
Figure 1.16,Emphysema,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
Figure 1.17,Pathophysiology of Emphysema,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.17.png,Figure 1.17: Pathological process of emphysema.
Figure 1.16,Pathophysiology of Emphysema,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.16.png,Figure 1.16: Characteristic patterns of emphysema.
Figure 1.18,Clinical Presentation of Emphysema,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.
Figure 1.19,Pathophysiology of 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.
Figure 1.19,ENaC,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.
Figure 1.20,Pseudomonsa,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.20.png,Figure 1.20: Pulmonary consequences of CF.
Figure 1.21,Clinical Presentation of 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.
Figure 1.22,Clinical Presentation of 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.
Figure 1.24,Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.24.png,Figure 1.24: Pathophysiology of bronchiectasis.
Figure 1.25,Pathogenesis of Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.25.png,Figure 1.25: Instigating factors for bronchiectasis.
Figure 1.26,Pathology of 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.
Figure 1.27,Pathology of Bronchiectasis,https://pressbooks.lib.vt.edu/app/uploads/sites/72/2022/05/1.27.png,Figure 1.27: Forms of bronchiectasis.
Figure 1.28,Pathology of 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.
Figure 1.29,Pathology of 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.