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Camurati-Engelmann Disease (CED) is a is a form of dysplasia and a very rare autosomal dominant genetic disorder that causes characteristic anomalies in the skeleton. Patients typically have heavily-thickened bones, especially along the shafts of the long bones (called diaphyseal dysplasia). The skull bones may be thickened so that the passages through the skull that carry nerves and blood vessels become narrowed, possibly leading to sensory deficits, blindness, or deafness. This disease often appears in childhood and is considered to be inherited, however some patients have no previous history of Camurati Engelmanns Disease within their family. There are approximately 200 cases worldwide. The disease is slowly progressive and, while there is no cure, there is treatment. The most common mutation causing Camurati-Engelmann Disease is in the gene encoding for the TGF-β2 receptor.	What does Camurati-Engelmann disease mean?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What does Camurati-Engelmann disease mean? [/INST] \n Camurati-Engelmann Disease (CED) is a is a form of dysplasia and a very rare autosomal dominant genetic disorder that causes characteristic anomalies in the skeleton. Patients typically have heavily-thickened bones, especially along the shafts of the long bones (called diaphyseal dysplasia). The skull bones may be thickened so that the passages through the skull that carry nerves and blood vessels become narrowed, possibly leading to sensory deficits, blindness, or deafness. This disease often appears in childhood and is considered to be inherited, however some patients have no previous history of Camurati Engelmanns Disease within their family. There are approximately 200 cases worldwide. The disease is slowly progressive and, while there is no cure, there is treatment. The most common mutation causing Camurati-Engelmann Disease is in the gene encoding for the TGF-β2 receptor.</s>
Vomiting blood - NIH/Medline Template:WikiDoc Sources	What is the explanation for Hematemesis and External Links?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the explanation for Hematemesis and External Links? [/INST] \n Vomiting blood - NIH/Medline Template:WikiDoc Sources</s>
The diagnosis of polycythemia vera is based on the World Health Organization criteria, which was initially proposed in 2008 then revised in 2016. In general, the diagnosis of polycythemia vera requires a combination of elevated hemoglobin, which include high levels of hemoglobin, presence of JAK2 V617F mutation, hypercellularity on bone marrow biopsy, low serum erythropoietin level, and endogenous erythroid colony formation in vitro. THe 2016 WHO criteria more accurately reflect the disease biology of polycythemia vera.	What criteria are used to diagnose Polycythemia Vera?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What criteria are used to diagnose Polycythemia Vera? [/INST] \n The diagnosis of polycythemia vera is based on the World Health Organization criteria, which was initially proposed in 2008 then revised in 2016. In general, the diagnosis of polycythemia vera requires a combination of elevated hemoglobin, which include high levels of hemoglobin, presence of JAK2 V617F mutation, hypercellularity on bone marrow biopsy, low serum erythropoietin level, and endogenous erythroid colony formation in vitro. THe 2016 WHO criteria more accurately reflect the disease biology of polycythemia vera.</s>
It has been described in two brothers.	What is the Sohval-Soffer syndrome?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the Sohval-Soffer syndrome? [/INST] \n It has been described in two brothers.</s>
Dermatitis herpetiformis is an autoimmune disease. In case of diagnosing DH, tests should be done to rule out other autoimmune diseases .	What other diagnostic tests can be done to diagnose Dermatitis Herpetiformis?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What other diagnostic tests can be done to diagnose Dermatitis Herpetiformis? [/INST] \n Dermatitis herpetiformis is an autoimmune disease. In case of diagnosing DH, tests should be done to rule out other autoimmune diseases .</s>
The prevalence of rheumatic (the main cause of MS) mitral stenosis is approximately 1 per 100,000 in developed countries. The prevalence of mitral stenosis continues to decline as the prevalence of rheumatic fever declines. Currently, the estimated incidence in the United States is 1:100,000. The incidence in higher in developing countries. Rheumatic fever is a disease of childhood. Mitral stenosis usually becomes symptomatic in the third or fourth decade of life. Although rheumatic fever occurs in equal numbers in males and females, two thirds of all patients with rheumatic mitral stenosis are females. Despite a decline in rheumatic fever, rheumatic disease remains the major cause of mitral valve stenosis. The prevalence of rheumatic disease in developed nations is steadily declining. In United States the prevalence rate is less than 5 per 100,000 persons. This could be attributed to the introduction of penicillin or a change in the virulence of the Streptococcus. In countries with low prevalence of rheumatic disease, mitral stenosis may be congenital. Though the incidence is low, these patients have high mortality rates. Developing countries have higher rates of rheumatic fever and consequently higher rates of mitral stenosis with prevalence of more than 10 cases per 1,000 in India and 4-10 cases per 1,000 in China, Russia, Africa, and Australia.	What are the epidemiology and demographics of mitral stenosis?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What are the epidemiology and demographics of mitral stenosis? [/INST] \n The prevalence of rheumatic (the main cause of MS) mitral stenosis is approximately 1 per 100,000 in developed countries. The prevalence of mitral stenosis continues to decline as the prevalence of rheumatic fever declines. Currently, the estimated incidence in the United States is 1:100,000. The incidence in higher in developing countries. Rheumatic fever is a disease of childhood. Mitral stenosis usually becomes symptomatic in the third or fourth decade of life. Although rheumatic fever occurs in equal numbers in males and females, two thirds of all patients with rheumatic mitral stenosis are females. Despite a decline in rheumatic fever, rheumatic disease remains the major cause of mitral valve stenosis. The prevalence of rheumatic disease in developed nations is steadily declining. In United States the prevalence rate is less than 5 per 100,000 persons. This could be attributed to the introduction of penicillin or a change in the virulence of the Streptococcus. In countries with low prevalence of rheumatic disease, mitral stenosis may be congenital. Though the incidence is low, these patients have high mortality rates. Developing countries have higher rates of rheumatic fever and consequently higher rates of mitral stenosis with prevalence of more than 10 cases per 1,000 in India and 4-10 cases per 1,000 in China, Russia, Africa, and Australia.</s>
In 1886, Fränkel made the first description of a patient with pheochromocytoma. In 1912, Ludwig Pick formulated the term pheochromocytoma.1912. In 1926, the first surgical removal of pheochromocytoma in the Military Medical Academy in Yugoslavia was performed by Professor Isidor Papo.	Can you provide a summary of Pheochromocytoma?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Can you provide a summary of Pheochromocytoma? [/INST] \n In 1886, Fränkel made the first description of a patient with pheochromocytoma. In 1912, Ludwig Pick formulated the term pheochromocytoma.1912. In 1926, the first surgical removal of pheochromocytoma in the Military Medical Academy in Yugoslavia was performed by Professor Isidor Papo.</s>
Myocardial ischemia is a substrate for sustained polymorphic VT, or VF. Revascularization is a treatment of choice for myocardial ischemia. Survival after CABG in patients with life-threatening ventricular arrhythmia was reasonable. For patients with ischemic heart disease and reduced LVEF undergoing CABG, the risk of sudden cardiac death lessened compared with medical therapy. Among survival of SCD, the risk of death reduced by revascularization procedure including PCI or CABG. Ischemic heart disease is responsible for 24% to 55% of SCD cases in young patients <35 years of age. Anomalous aortic origin of the coronary arteries detected in 10% to 17% of patients in postmortem studies, is an important cause of SCD in the young. Revascularization is recommended for treating ischemia leading life-threatening ventricular arrhythmia due to anomalous aortic origin of the coronary arteries. Cardiac surgery is rarely performed for treating ventricular tachycardia in case of highly symptomatic patients with failed antiarrhythmic medications or unsuccessful ventricular ablation. Inaccessible sites for ventricular ablation including area deep in the myocardium, beneath epicardial fat, or near the coronary arteries may lead to unsuccessful ablation. Surgical ablation of ventricular arrhythmia can be done during other surgical intervention such as placement of LVAD or at the time of left ventricular aneurysectomy which is a substrate for VT. VT or VF maybe provoked by Sympathetic activation and maybe inhibited by parasympathetic activity. Prevention of ventricular arrhythmia can be done by interruption of sympathetic outflow to the heart, pharmacological beta-blockade, or through stimulation of the parasympathetic pathway (vagal nerve stimulators, spinal cord stimulators). Autonomic modulation is effective in conditions such as long QT syndrome and catecholaminergic polymorphic ventricular tachycardia. Efficacy for ventricular tachycardia is under investigation. Atenolol was effective for controlling symptomatic ventricular tachycardia in patients without structural heart disease.	What does the surgery for ventricular tachycardia involve?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What does the surgery for ventricular tachycardia involve? [/INST] \n Myocardial ischemia is a substrate for sustained polymorphic VT, or VF. Revascularization is a treatment of choice for myocardial ischemia. Survival after CABG in patients with life-threatening ventricular arrhythmia was reasonable. For patients with ischemic heart disease and reduced LVEF undergoing CABG, the risk of sudden cardiac death lessened compared with medical therapy. Among survival of SCD, the risk of death reduced by revascularization procedure including PCI or CABG. Ischemic heart disease is responsible for 24% to 55% of SCD cases in young patients <35 years of age. Anomalous aortic origin of the coronary arteries detected in 10% to 17% of patients in postmortem studies, is an important cause of SCD in the young. Revascularization is recommended for treating ischemia leading life-threatening ventricular arrhythmia due to anomalous aortic origin of the coronary arteries. Cardiac surgery is rarely performed for treating ventricular tachycardia in case of highly symptomatic patients with failed antiarrhythmic medications or unsuccessful ventricular ablation. Inaccessible sites for ventricular ablation including area deep in the myocardium, beneath epicardial fat, or near the coronary arteries may lead to unsuccessful ablation. Surgical ablation of ventricular arrhythmia can be done during other surgical intervention such as placement of LVAD or at the time of left ventricular aneurysectomy which is a substrate for VT. VT or VF maybe provoked by Sympathetic activation and maybe inhibited by parasympathetic activity. Prevention of ventricular arrhythmia can be done by interruption of sympathetic outflow to the heart, pharmacological beta-blockade, or through stimulation of the parasympathetic pathway (vagal nerve stimulators, spinal cord stimulators). Autonomic modulation is effective in conditions such as long QT syndrome and catecholaminergic polymorphic ventricular tachycardia. Efficacy for ventricular tachycardia is under investigation. Atenolol was effective for controlling symptomatic ventricular tachycardia in patients without structural heart disease.</s>
There are no ultrasound findings associated with brain tumors.	Which imaging technique is utilized for the detection of a brain tumor: echocardiography or ultrasound?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Which imaging technique is utilized for the detection of a brain tumor: echocardiography or ultrasound? [/INST] \n There are no ultrasound findings associated with brain tumors.</s>
Differential diagnosis of vomiting may be a result of a range of causes, including GI (obstructive and inflammatory) etiologies, CNS disease, pulmonary problems, renal disease, endocrine/metabolic disorders, drugs (either as side effects or in over dosages), psychiatric disorders, strep throat, pregnancy or stress.	What is the definition of nausea and vomiting?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the definition of nausea and vomiting? [/INST] \n Differential diagnosis of vomiting may be a result of a range of causes, including GI (obstructive and inflammatory) etiologies, CNS disease, pulmonary problems, renal disease, endocrine/metabolic disorders, drugs (either as side effects or in over dosages), psychiatric disorders, strep throat, pregnancy or stress.</s>
Anthrax lesions at any site are characterized by extensive necrosis and confluent exudate, containing macrophages and neutrophils. In histopathological specimens or culture media, the presence of large boxcar-shaped Gram-positive bacilli in chains suggests the diagnosis. Histologic examination of skin lesions caused by cutaneous anthrax reveals: Tissue necrosis Edema Lymphocytic infiltrates No liquefaction No abscess formation (lesion is not suppurative) Focal points of hemorrhage Thrombosis Bacilli in subcutaneous tissue, revealed by Gram staining Histologic evaluation of affected tissues reveals: Numerous necrotic foci of hemorrhage in the mediastinum or hilar and peribronchial lymph nodes Pulmonary infection may also result in interstitial pneumonia associated with: Vasculitis Edema Infiltrating macrophages and neutrophils Bacilli are most likely to be observed in the alveolar capillaries and venules and, to a lesser degree, within the alveolar space and draining lymph nodes Histologic evaluation of affected tissues revealed: Edema Mucosal necrosis Inflammatory infiltrates Peritoneal fluid may reveal gram-positive bacilli Occasionally mediastinal widening	What is the explanation of the pathophysiological process of anthrax?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the explanation of the pathophysiological process of anthrax? [/INST] \n Anthrax lesions at any site are characterized by extensive necrosis and confluent exudate, containing macrophages and neutrophils. In histopathological specimens or culture media, the presence of large boxcar-shaped Gram-positive bacilli in chains suggests the diagnosis. Histologic examination of skin lesions caused by cutaneous anthrax reveals: Tissue necrosis Edema Lymphocytic infiltrates No liquefaction No abscess formation (lesion is not suppurative) Focal points of hemorrhage Thrombosis Bacilli in subcutaneous tissue, revealed by Gram staining Histologic evaluation of affected tissues reveals: Numerous necrotic foci of hemorrhage in the mediastinum or hilar and peribronchial lymph nodes Pulmonary infection may also result in interstitial pneumonia associated with: Vasculitis Edema Infiltrating macrophages and neutrophils Bacilli are most likely to be observed in the alveolar capillaries and venules and, to a lesser degree, within the alveolar space and draining lymph nodes Histologic evaluation of affected tissues revealed: Edema Mucosal necrosis Inflammatory infiltrates Peritoneal fluid may reveal gram-positive bacilli Occasionally mediastinal widening</s>
Pulmonary edema is fluid accumulation in the lungs. This fluid accumulation leads to impaired gas exchange and hypoxia. Management of patients with pulmonary edema Oxygen (Class I) or ventilatory support (Class IIa) Systolic blood pressure ≥110 mmHg Yes NO Loop diuretics (Class I) and/or vasodilators (Class IIb) Signs of hypoperfusion Yes NO Loop diuretics (Class I) and inotropes / vasopressors (Class IIb) Loop diuretics (Class I) Congestion relief Yes NO Optimized medical therapy Renal replacement therapy Mechanical circulatory support Palliative therapy Acute pulmonary edema is related to lung congestion. Clinical characteristics include dyspnea with orthopnea, respiratory failure (hypoxemia - hypercapnia), tachypnea >25 breaths/min, and increased work of breathing. Treatment including as follows: Oxygen, given as continuous positive airway pressure, non-invasive positive pressure- ventilation and/or high-flow nasal cannula Diuretics Vasodilators if systolic BP (SBP) is high, to reduce LV afterload In the setting of acute pulmonary edema with low cardiac output state, inotropes, vasopressors, and/or MCS are indicated to restore organ perfusion.	What is the appropriate pharmacotherapy for the acute management of congestive heart failure?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the appropriate pharmacotherapy for the acute management of congestive heart failure? [/INST] \n Pulmonary edema is fluid accumulation in the lungs. This fluid accumulation leads to impaired gas exchange and hypoxia. Management of patients with pulmonary edema Oxygen (Class I) or ventilatory support (Class IIa) Systolic blood pressure ≥110 mmHg Yes NO Loop diuretics (Class I) and/or vasodilators (Class IIb) Signs of hypoperfusion Yes NO Loop diuretics (Class I) and inotropes / vasopressors (Class IIb) Loop diuretics (Class I) Congestion relief Yes NO Optimized medical therapy Renal replacement therapy Mechanical circulatory support Palliative therapy Acute pulmonary edema is related to lung congestion. Clinical characteristics include dyspnea with orthopnea, respiratory failure (hypoxemia - hypercapnia), tachypnea >25 breaths/min, and increased work of breathing. Treatment including as follows: Oxygen, given as continuous positive airway pressure, non-invasive positive pressure- ventilation and/or high-flow nasal cannula Diuretics Vasodilators if systolic BP (SBP) is high, to reduce LV afterload In the setting of acute pulmonary edema with low cardiac output state, inotropes, vasopressors, and/or MCS are indicated to restore organ perfusion.</s>
Supports: Bengali, Devanagari, Gujarati, Gurmukhi, Kannada, Malayalam, Oriya, Sinhala, Tamil, Telugu, Tibetan Complex text support is automatically enabled. You do not need to do anything to enable viewing of Indic text. Windows Vista like Windows XP have inbuilt InScript Keyboards for nearly all Indian languages. You can add them via Control Panel. For Phonetic typing BarahaIME is suggested and for Remington typing IndicIME is suggested.	What is the meaning of "Multilingual: support Indic"?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the meaning of "Multilingual: support Indic"? [/INST] \n Supports: Bengali, Devanagari, Gujarati, Gurmukhi, Kannada, Malayalam, Oriya, Sinhala, Tamil, Telugu, Tibetan Complex text support is automatically enabled. You do not need to do anything to enable viewing of Indic text. Windows Vista like Windows XP have inbuilt InScript Keyboards for nearly all Indian languages. You can add them via Control Panel. For Phonetic typing BarahaIME is suggested and for Remington typing IndicIME is suggested.</s>
A. lumbricoides, a roundworm, infects humans when an ingested fertilised egg becomes a larval worm that penetrates the wall of the duodenum and enters the blood stream. From there, it is carried to the liver and heart, and enters pulmonary circulation to break free in the alveoli, where it grows and molts. In three weeks, the larva passes from the respiratory system to be coughed up, swallowed, and thus returned to the small intestine, where it matures to an adult male or female worm. Fertilization can now occur and the female produces as many as 200,000 eggs per day for a year. These fertilized eggs become infectious after two weeks in soil; they can persist in soil for 10 years or more. The eggs have a lipid layer which makes them resistant to the effects of acids and alkalis, as well as other chemicals. This resilience helps to explain why this nematode is such a ubiquitous parasite.	What are the factors responsible for causing Ascariasis?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What are the factors responsible for causing Ascariasis? [/INST] \n A. lumbricoides, a roundworm, infects humans when an ingested fertilised egg becomes a larval worm that penetrates the wall of the duodenum and enters the blood stream. From there, it is carried to the liver and heart, and enters pulmonary circulation to break free in the alveoli, where it grows and molts. In three weeks, the larva passes from the respiratory system to be coughed up, swallowed, and thus returned to the small intestine, where it matures to an adult male or female worm. Fertilization can now occur and the female produces as many as 200,000 eggs per day for a year. These fertilized eggs become infectious after two weeks in soil; they can persist in soil for 10 years or more. The eggs have a lipid layer which makes them resistant to the effects of acids and alkalis, as well as other chemicals. This resilience helps to explain why this nematode is such a ubiquitous parasite.</s>
Hypomagnesemia should be differentiated from other causes of abnormal parathyroid hormone levels for example, hypoparathyroidism (genetic and idiopathic), acrodysostosis and pseudohypoparathyroidism.	What is Hypomagnesemia and how can it be distinguished from other illnesses?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is Hypomagnesemia and how can it be distinguished from other illnesses? [/INST] \n Hypomagnesemia should be differentiated from other causes of abnormal parathyroid hormone levels for example, hypoparathyroidism (genetic and idiopathic), acrodysostosis and pseudohypoparathyroidism.</s>
Secondary adrenal insufficiency is also caused by genetic disorders. Combined pituitary hormone deficiency (CPHD) Proopiomelanocortin deficiency (POMC) POMC deficiency is transmitted in autosomal recessive transmission pattern. Genes involved in the pathogenesis of POMC deficiency include POMC gene. Genes involved in the pathogenesis of CPHD include PROP-1 where ACTH deficiency occurs in the end after GH, Prolactin, TSH, and LH / FSH deficiencies. Other genes in CPHD include HESX1, LHX3, LHX4 and SOX3.	What is the pathophysiology behind secondary adrenal insufficiency?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the pathophysiology behind secondary adrenal insufficiency? [/INST] \n Secondary adrenal insufficiency is also caused by genetic disorders. Combined pituitary hormone deficiency (CPHD) Proopiomelanocortin deficiency (POMC) POMC deficiency is transmitted in autosomal recessive transmission pattern. Genes involved in the pathogenesis of POMC deficiency include POMC gene. Genes involved in the pathogenesis of CPHD include PROP-1 where ACTH deficiency occurs in the end after GH, Prolactin, TSH, and LH / FSH deficiencies. Other genes in CPHD include HESX1, LHX3, LHX4 and SOX3.</s>
In the United States, prevalence of diabetic nephropathy (DN) has increased from 7.4% to 9.6% within a 20 years period (1988 to 2008), and this trend will likely continue due to the increasing incidence of diabetes in the American populace. Studies by de Boer et al showed that DN accounts for 44% of new ESRD cases with 6% attributed to type 1 DM, 38% attributed to type 2 DM, and a projected increase of 3 million cases over the course of 20 years. This increased incidence and prevalence of DN is notably greater among African Americans, Asians, and Native Americans than it is among Caucasians.	Can you provide a summary of diabetic nephropathy?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Can you provide a summary of diabetic nephropathy? [/INST] \n In the United States, prevalence of diabetic nephropathy (DN) has increased from 7.4% to 9.6% within a 20 years period (1988 to 2008), and this trend will likely continue due to the increasing incidence of diabetes in the American populace. Studies by de Boer et al showed that DN accounts for 44% of new ESRD cases with 6% attributed to type 1 DM, 38% attributed to type 2 DM, and a projected increase of 3 million cases over the course of 20 years. This increased incidence and prevalence of DN is notably greater among African Americans, Asians, and Native Americans than it is among Caucasians.</s>
Hyperlipidemia Hypertriglyceridemia	What is pseudohyponatremia and what are the underlying factors that contribute to it?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is pseudohyponatremia and what are the underlying factors that contribute to it? [/INST] \n Hyperlipidemia Hypertriglyceridemia</s>
The MD TV: Comments on Hot Topics, State of the Art Presentations in Cardiovascular Medicine, Expert Reviews on Cardiovascular Research Clinical Trial Results: An up to date resource of Cardiovascular Research Risk Assessment Tool for Estimating Your 10-year Risk of Having a Heart Attack - based on information of the Framingham Heart Study, from the United States National Heart, Lung and Blood Institute Heart Attack - overview of resources from MedlinePlus. Heart Attack Warning Signals from the Heart and Stroke Foundation of Canada Regional PCI for STEMI Resource Center - Evidence based online resource center for the development of regional PCI networks for acute STEMI STEMI Systems - Articles, profiles, and reviews of the latest publications involved in STEMI care. Quarterly newsletter. American College of Cardiology (ACC) Door to Balloon (D2B) Initiative. American Heart Association's Heart Attack web site - Information and resources for preventing, recognizing and treating heart attack. v t e ST Elevation Myocardial Infarction Background Overview • Epidemiology and Demographics • Classification Risk factors and Triggers Risk Factors • Triggers Pathophysiology Pathophysiology of Vessel Occlusion • Pathophysiology of Reperfusion • Gross Pathology • Histopathology Diagnosis Diagnosis • Symptoms • Differential Diagnosis of Chest Pain • Physical Examination • Electrocardiogram • Right ventricular myocardial infarction • Atrial Infarction • Cardiac Markers • Coronary Angiography Treatment Pre-Hospital Care Pre-Hospital Care Initial Care Initial Care • Oxygen • Nitrates • Analgesics • Aspirin • Beta Blockers Pharmacologic Reperfusion • Reperfusion Therapy (Overview of Fibrinolysis and Primary PCI) • Fibrinolysis Mechanical Reperfusion • The Importance of Reducing Door-to-Balloon Times • Primary PCI • Adjunctive and Rescue PCI • Rescue PCI • Facilitated PCI • Adjunctive PCI • CABG • Management of Patients Who Were Not Reperfused • Assessing Success of Reperfusion Antithrombin Therapy • Antithrombin therapy • Unfractionated heparin • Low Molecular Weight Heparinoid Therapy • Direct Thrombin Inhibitor Therapy • Factor Xa Inhibition Antiplatelet Agents • Aspirin • Thienopyridine Therapy • Glycoprotein IIbIIIa Inhibition Inhibition of the Renin-Angiotensin-Aldosterone System • Inhibition of the Renin-Angiotensin-Aldosterone System Other Adjunctive Therapies • Magnesium Therapy • Glucose Control • Calcium Channel Blocker Therapy Monitoring Arrhythmia Monitoring Complications Complications Discharge Care Secondary Prevention • Cardiac Rehabilitation • Prognosis Template:WikiDoc Sources	What is the initial treatment for ST-elevation myocardial infarction?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the initial treatment for ST-elevation myocardial infarction? [/INST] \n The MD TV: Comments on Hot Topics, State of the Art Presentations in Cardiovascular Medicine, Expert Reviews on Cardiovascular Research Clinical Trial Results: An up to date resource of Cardiovascular Research Risk Assessment Tool for Estimating Your 10-year Risk of Having a Heart Attack - based on information of the Framingham Heart Study, from the United States National Heart, Lung and Blood Institute Heart Attack - overview of resources from MedlinePlus. Heart Attack Warning Signals from the Heart and Stroke Foundation of Canada Regional PCI for STEMI Resource Center - Evidence based online resource center for the development of regional PCI networks for acute STEMI STEMI Systems - Articles, profiles, and reviews of the latest publications involved in STEMI care. Quarterly newsletter. American College of Cardiology (ACC) Door to Balloon (D2B) Initiative. American Heart Association's Heart Attack web site - Information and resources for preventing, recognizing and treating heart attack. v t e ST Elevation Myocardial Infarction Background Overview • Epidemiology and Demographics • Classification Risk factors and Triggers Risk Factors • Triggers Pathophysiology Pathophysiology of Vessel Occlusion • Pathophysiology of Reperfusion • Gross Pathology • Histopathology Diagnosis Diagnosis • Symptoms • Differential Diagnosis of Chest Pain • Physical Examination • Electrocardiogram • Right ventricular myocardial infarction • Atrial Infarction • Cardiac Markers • Coronary Angiography Treatment Pre-Hospital Care Pre-Hospital Care Initial Care Initial Care • Oxygen • Nitrates • Analgesics • Aspirin • Beta Blockers Pharmacologic Reperfusion • Reperfusion Therapy (Overview of Fibrinolysis and Primary PCI) • Fibrinolysis Mechanical Reperfusion • The Importance of Reducing Door-to-Balloon Times • Primary PCI • Adjunctive and Rescue PCI • Rescue PCI • Facilitated PCI • Adjunctive PCI • CABG • Management of Patients Who Were Not Reperfused • Assessing Success of Reperfusion Antithrombin Therapy • Antithrombin therapy • Unfractionated heparin • Low Molecular Weight Heparinoid Therapy • Direct Thrombin Inhibitor Therapy • Factor Xa Inhibition Antiplatelet Agents • Aspirin • Thienopyridine Therapy • Glycoprotein IIbIIIa Inhibition Inhibition of the Renin-Angiotensin-Aldosterone System • Inhibition of the Renin-Angiotensin-Aldosterone System Other Adjunctive Therapies • Magnesium Therapy • Glucose Control • Calcium Channel Blocker Therapy Monitoring Arrhythmia Monitoring Complications Complications Discharge Care Secondary Prevention • Cardiac Rehabilitation • Prognosis Template:WikiDoc Sources</s>
Problems arise when this pathway creates an electrical circuit that bypasses the AV node. The AV node has rate-slowing electrical regulatory properties, whereas the pathway via the bundle of Kent does not. When an aberrant electrical impulse travels through the Kent bundle, tachyarrhythmia ensues.	What does "Bundle: of Kent" mean?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What does "Bundle: of Kent" mean? [/INST] \n Problems arise when this pathway creates an electrical circuit that bypasses the AV node. The AV node has rate-slowing electrical regulatory properties, whereas the pathway via the bundle of Kent does not. When an aberrant electrical impulse travels through the Kent bundle, tachyarrhythmia ensues.</s>
CDC chikungunya virus	What does primary prevention for Chikungunya involve?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What does primary prevention for Chikungunya involve? [/INST] \n CDC chikungunya virus</s>
Burn injury may be caused by chemicals, friction, electricity, radiation, extreme temperatures (hot and cold) and Inhalation injury in burn s.	What is the definition of burn and what are its possible causes?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the definition of burn and what are its possible causes? [/INST] \n Burn injury may be caused by chemicals, friction, electricity, radiation, extreme temperatures (hot and cold) and Inhalation injury in burn s.</s>
The pathogenesis of HPV infection causing cancer is mainly linked to high risk types of HPV (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 68). Following HPV proteins play a significant role in the development of cancers associated with HPV. E6 and E7 protein products of HPV interact with two important cell cycle regulatory protiens, P53 and Rb proteins of host cell, causing unchecked cellular replication accumulating mutations leading to cancer. Inhibition of P53 P53 protein is a cellular check point at G0/G1 to S phase of cell cycle and is also responsible for cell apoptosis for unrepaired DNA mutations. E6 protein binds P53 which results in degradation of P53, leaving cell without any check for mutations and unregulated cell. growth. Inhibition of Rb protein Rb protein is negative regulator of cell growth. It binds E2F transcription factor which controls DNA replication and cyclin protein induced entering of cell into S phase of cell cycle. E7 protein binds Rb/E2F, releasing E2F from the inhibitory effect of Rb causing increased cyclin induced entry of cell into S phase of cell cycle, resulting in increased replication rate of cells accumulating mutations.	What is the pathophysiology of papillomavirus in humans?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the pathophysiology of papillomavirus in humans? [/INST] \n The pathogenesis of HPV infection causing cancer is mainly linked to high risk types of HPV (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 68). Following HPV proteins play a significant role in the development of cancers associated with HPV. E6 and E7 protein products of HPV interact with two important cell cycle regulatory protiens, P53 and Rb proteins of host cell, causing unchecked cellular replication accumulating mutations leading to cancer. Inhibition of P53 P53 protein is a cellular check point at G0/G1 to S phase of cell cycle and is also responsible for cell apoptosis for unrepaired DNA mutations. E6 protein binds P53 which results in degradation of P53, leaving cell without any check for mutations and unregulated cell. growth. Inhibition of Rb protein Rb protein is negative regulator of cell growth. It binds E2F transcription factor which controls DNA replication and cyclin protein induced entering of cell into S phase of cell cycle. E7 protein binds Rb/E2F, releasing E2F from the inhibitory effect of Rb causing increased cyclin induced entry of cell into S phase of cell cycle, resulting in increased replication rate of cells accumulating mutations.</s>
Cryptosporidiosis is primarily transmitted via fecal oral route and dwells in water resevoirs. Primary prevention of cryptosporidiosis lies in appropriate hygiene after contact with sources or environments that may be contaminated with fecal material such as: after using the toilet, after contact with animals, after contact with children, after gardening or outdoor activities, after engaging in anal sex. Other primary preventive measures include avoidance public swimming areas or water recreation parks for two weeks after resolution of an episode of diarrhea, avoidance of contact with someone who has diagnosed cryptospiroidosis, and caution when traveling in countries where the safety of the food or water supply is unknown or in question. People who are immunocompromised should be particularly cautious to follow these prevention strategies. A cryptosporidiosis infection may have serious and possibly life-threatening sequelae in immune compromised patients.	Can you provide a summary of Cryptosporidiosis?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Can you provide a summary of Cryptosporidiosis? [/INST] \n Cryptosporidiosis is primarily transmitted via fecal oral route and dwells in water resevoirs. Primary prevention of cryptosporidiosis lies in appropriate hygiene after contact with sources or environments that may be contaminated with fecal material such as: after using the toilet, after contact with animals, after contact with children, after gardening or outdoor activities, after engaging in anal sex. Other primary preventive measures include avoidance public swimming areas or water recreation parks for two weeks after resolution of an episode of diarrhea, avoidance of contact with someone who has diagnosed cryptospiroidosis, and caution when traveling in countries where the safety of the food or water supply is unknown or in question. People who are immunocompromised should be particularly cautious to follow these prevention strategies. A cryptosporidiosis infection may have serious and possibly life-threatening sequelae in immune compromised patients.</s>
Prevalence of strongyloidiasis is higher in patients with conditions such as: Systemic rheumatic diseases Chronic renal failure Diabetes mellitus Malnutrition Alcoholism	What is the explanation behind the pathological processes involved in Strongyloidiasis?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the explanation behind the pathological processes involved in Strongyloidiasis? [/INST] \n Prevalence of strongyloidiasis is higher in patients with conditions such as: Systemic rheumatic diseases Chronic renal failure Diabetes mellitus Malnutrition Alcoholism</s>
Infants who survive listeriosis may have long-term neurological damage and delayed development.	What is the natural life cycle of Listeria?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the natural life cycle of Listeria? [/INST] \n Infants who survive listeriosis may have long-term neurological damage and delayed development.</s>
Patients with acute lung abscess may present with fever, cough with purulent sputum, gag reflex may be absent in patients with an underlying neurologic disorder such as stroke. Digital clubbing is present in patients with a chronic abscess. On examination of the chest, there will be features of consolidation. Abscess typically localizes in the upper lobes or apical segments of the lower lobes.	What does the physical examination for a lung abscess entail?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What does the physical examination for a lung abscess entail? [/INST] \n Patients with acute lung abscess may present with fever, cough with purulent sputum, gag reflex may be absent in patients with an underlying neurologic disorder such as stroke. Digital clubbing is present in patients with a chronic abscess. On examination of the chest, there will be features of consolidation. Abscess typically localizes in the upper lobes or apical segments of the lower lobes.</s>
Different species of the following genera of mosquitoes are vectors of W. bancrofti filariasis depending on geographical distribution. Among them are: Culex (C. annulirostris, C. bitaeniorhynchus, C. quinquefasciatus, and C. pipiens); Anopheles (A. arabinensis, A. bancroftii, A. farauti, A. funestus, A. gambiae, A. koliensis, A. melas, A. merus, A. punctulatus and A. wellcomei); Aedes (A. aegypti, A. aquasalis, A. bellator, A. cooki, A. darlingi, A. kochi, A. polynesiensis, A. pseudoscutellaris, A. rotumae, A. scapularis, and A. vigilax); Mansonia (M. pseudotitillans, M. uniformis); Coquillettidia (C. juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound (1). They develop in adults that commonly reside in the lymphatics (2). The female worms measure 80 to 100 mm in length and 0.24 to 0.30 mm in diameter, while the males measure about 40 mm by.1 mm. Adults produce microfilariae measuring 244 to 296 μm by 7.5 to 10 μm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood (3). A mosquito ingests the microfilariae during a blood meal (4). After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles (5). There the microfilariae develop into first-stage larvae (6) and subsequently into third-stage infective larvae (7). The third-stage infective larvae migrate through the hemocoel to the mosquito's prosbocis (8) and can infect another human when the mosquito takes a blood meal (1). The typical vector for Brugia malayi filariasis are mosquito species from the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound (1). They develop into adults that commonly reside in the lymphatics (2). The adult worms resemble those of Wuchereria bancrofti but are smaller. Female worms measure 43 to 55 mm in length by 130 to 170 μm in width, and males measure 13 to 23 mm in length by 70 to 80 μm in width. Adults produce microfilariae, measuring 177 to 230 μm in length and 5 to 7 μm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the blood stream reaching the peripheral blood (3). A mosquito ingests the microfilariae during a blood meal (4). After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles (5). There the microfilariae develop into first-stage larvae (6) and subsequently into third-stage larvae (7). The third-stage larvae migrate through the hemocoel to the mosquito's prosbocis (8) and can infect another human when the mosquito takes a blood meal (1). A wide range of mosquitoes can transmit the parasite, depending on the geographic area. In Africa, the most common vector is Anopheles and in the America, it is Culex quinquefasciatus. Aedes and Mansonia can transmit the infection in the Pacific and in Asia. Shown below is an image of an Anopheles gambiae mosquito taking a blood meal. Shown below is an image of many species in the genera Anopheles that can transmit the infective larvae that cause lymphatic filariasis. Shown below is an image of Culex quinquefasciatus, a vector of lymphatic filariasis. Shown below is an image of Culex that transmits the infective larva of Waucheria bancrofti and brugia malayi. Shown below is an image of an Aedes aegypti female mosquito taking a blood meal. Shown below is an image of Aedes that transmits the infective larvae of Waucheria bancrofti and brugia malayi. Shown below is an image of microfilaria of Wuchereria bancrofti. Shown below is an image of microfilaria of Brugia malayi.	What is the underlying mechanism or medical condition that leads to lymphatic filariasis?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the underlying mechanism or medical condition that leads to lymphatic filariasis? [/INST] \n Different species of the following genera of mosquitoes are vectors of W. bancrofti filariasis depending on geographical distribution. Among them are: Culex (C. annulirostris, C. bitaeniorhynchus, C. quinquefasciatus, and C. pipiens); Anopheles (A. arabinensis, A. bancroftii, A. farauti, A. funestus, A. gambiae, A. koliensis, A. melas, A. merus, A. punctulatus and A. wellcomei); Aedes (A. aegypti, A. aquasalis, A. bellator, A. cooki, A. darlingi, A. kochi, A. polynesiensis, A. pseudoscutellaris, A. rotumae, A. scapularis, and A. vigilax); Mansonia (M. pseudotitillans, M. uniformis); Coquillettidia (C. juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound (1). They develop in adults that commonly reside in the lymphatics (2). The female worms measure 80 to 100 mm in length and 0.24 to 0.30 mm in diameter, while the males measure about 40 mm by.1 mm. Adults produce microfilariae measuring 244 to 296 μm by 7.5 to 10 μm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood (3). A mosquito ingests the microfilariae during a blood meal (4). After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles (5). There the microfilariae develop into first-stage larvae (6) and subsequently into third-stage infective larvae (7). The third-stage infective larvae migrate through the hemocoel to the mosquito's prosbocis (8) and can infect another human when the mosquito takes a blood meal (1). The typical vector for Brugia malayi filariasis are mosquito species from the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound (1). They develop into adults that commonly reside in the lymphatics (2). The adult worms resemble those of Wuchereria bancrofti but are smaller. Female worms measure 43 to 55 mm in length by 130 to 170 μm in width, and males measure 13 to 23 mm in length by 70 to 80 μm in width. Adults produce microfilariae, measuring 177 to 230 μm in length and 5 to 7 μm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the blood stream reaching the peripheral blood (3). A mosquito ingests the microfilariae during a blood meal (4). After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles (5). There the microfilariae develop into first-stage larvae (6) and subsequently into third-stage larvae (7). The third-stage larvae migrate through the hemocoel to the mosquito's prosbocis (8) and can infect another human when the mosquito takes a blood meal (1). A wide range of mosquitoes can transmit the parasite, depending on the geographic area. In Africa, the most common vector is Anopheles and in the America, it is Culex quinquefasciatus. Aedes and Mansonia can transmit the infection in the Pacific and in Asia. Shown below is an image of an Anopheles gambiae mosquito taking a blood meal. Shown below is an image of many species in the genera Anopheles that can transmit the infective larvae that cause lymphatic filariasis. Shown below is an image of Culex quinquefasciatus, a vector of lymphatic filariasis. Shown below is an image of Culex that transmits the infective larva of Waucheria bancrofti and brugia malayi. Shown below is an image of an Aedes aegypti female mosquito taking a blood meal. Shown below is an image of Aedes that transmits the infective larvae of Waucheria bancrofti and brugia malayi. Shown below is an image of microfilaria of Wuchereria bancrofti. Shown below is an image of microfilaria of Brugia malayi.</s>
Osteosarcoma must be differentiated from other diseases such as: any type of bone lesions caused by infection and/or tumors. Features such as the eccentric location of the tumor in the metaphyseal portion of the bone and the skeletal location help to distinguish osteosarcoma from Ewing sarcoma. Bone metastases from other primary tumours, less frequent in the young than in adult patients, should also be considered.	What is Osteosarcoma and how can it be distinguished from other diseases?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is Osteosarcoma and how can it be distinguished from other diseases? [/INST] \n Osteosarcoma must be differentiated from other diseases such as: any type of bone lesions caused by infection and/or tumors. Features such as the eccentric location of the tumor in the metaphyseal portion of the bone and the skeletal location help to distinguish osteosarcoma from Ewing sarcoma. Bone metastases from other primary tumours, less frequent in the young than in adult patients, should also be considered.</s>
For treatment to be successful, the child's family needs to be closely involved. Parents can learn techniques to help manage their child's problem behavior. In cases of abuse, the child may need to be removed from the family and placed in a less chaotic home. Treatment with medications or talk therapy may be used for depression and attention-deficit disorder, which commonly occur with conduct disorder. Many behavioral modification schools, wilderness programs, and boot camps are sold to parents as solutions for conduct disorder. These programs may use a form of attack therapy or confrontation, which can actually be harmful. There is no research to support these techniques. Research suggests that treating children at home, along with their families, is more effective. If you are considering an inpatient program, be sure to check it out thoroughly. Serious injuries and deaths have occurred with some programs. They are not regulated in many states.	What information relates to disruptive behavior?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What information relates to disruptive behavior? [/INST] \n For treatment to be successful, the child's family needs to be closely involved. Parents can learn techniques to help manage their child's problem behavior. In cases of abuse, the child may need to be removed from the family and placed in a less chaotic home. Treatment with medications or talk therapy may be used for depression and attention-deficit disorder, which commonly occur with conduct disorder. Many behavioral modification schools, wilderness programs, and boot camps are sold to parents as solutions for conduct disorder. These programs may use a form of attack therapy or confrontation, which can actually be harmful. There is no research to support these techniques. Research suggests that treating children at home, along with their families, is more effective. If you are considering an inpatient program, be sure to check it out thoroughly. Serious injuries and deaths have occurred with some programs. They are not regulated in many states.</s>
Class I Abnormal-appearing heart on general fetal ultrasound examination. Fetal tachycardia, bradycardia, or persistent irregular rhythm on clinical or screening ultrasound examination. Maternal/family risk factors for cardiovascular disease, such as a parent, sibling, or first-degree relative with congenital heart disease. Maternal diabetes. Maternal systemic lupus erythematosus. Teratogen exposure during a vulnerable period. Other fetal system abnormalities (including chromosomal). Performance of transplacental therapy or presence of a history of significant but intermittent arrhythmia. Re-evaluation examinations are required in these conditions. Class IIa Fetal distress or dysfunction of unclear etiology. Class IIb Previous history of multiple fetal losses. Multiple gestation. Class III Low-risk pregnancies with normal anatomic findings on ultrasound examination. Occasional premature contractions without sustained tachycardia or signs of dysfunction or distress. Presence of a noncardiovascular system abnormality when evaluation of the cardiovascular system will not alter either management decisions or fetal outcome.	What are the guidelines for performing echocardiography?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What are the guidelines for performing echocardiography? [/INST] \n Class I Abnormal-appearing heart on general fetal ultrasound examination. Fetal tachycardia, bradycardia, or persistent irregular rhythm on clinical or screening ultrasound examination. Maternal/family risk factors for cardiovascular disease, such as a parent, sibling, or first-degree relative with congenital heart disease. Maternal diabetes. Maternal systemic lupus erythematosus. Teratogen exposure during a vulnerable period. Other fetal system abnormalities (including chromosomal). Performance of transplacental therapy or presence of a history of significant but intermittent arrhythmia. Re-evaluation examinations are required in these conditions. Class IIa Fetal distress or dysfunction of unclear etiology. Class IIb Previous history of multiple fetal losses. Multiple gestation. Class III Low-risk pregnancies with normal anatomic findings on ultrasound examination. Occasional premature contractions without sustained tachycardia or signs of dysfunction or distress. Presence of a noncardiovascular system abnormality when evaluation of the cardiovascular system will not alter either management decisions or fetal outcome.</s>
Freckles are small colored spots of melanin on the exposed skin or membrane of people with complexions fair enough for them to be visible. Having freckles is genetic and is related to the presence of the melanocortin-1 receptor MC1R gene variant, which is dominant. Freckling can also be triggered by long exposure to sunlight, such as suntanning. When the sun’s rays penetrate the skin, they activate melanocytes which can cause freckles to become darker and more numerous, although the distribution of melanin is not the same. Fair hair such as blonde, or more commonly red hair, are usually common with the genetic factor of freckles, but none so much as fair or pale skin. Freckles are predominantly found on the face, although they may appear on any skin exposed to the sun. Freckles are rare on infants, and more common on children before puberty; they are less common on adults. Children who do not produce enough melanin to protect their skin against harmful rays from the sun develop temporary freckles associated with childhood that usually go away upon puberty, once more melanin is produced. People with the fairest skin often do not produce enough melanin, and so freckles are present after puberty and into adulthood, indicating that individual as a genetic carrier for freckles. Upon exposure to the sun, freckles will reappear if they have been altered with creams or lasers and not protected from the sun, but do however fade with age in some cases. Freckles are not a skin disorder. People with a predisposition to freckles may be especially susceptible to sunburn and skin cancer, and should therefore take extra care to protect themselves in the sun with a daily sunblock of at least 15 SPF. During the Middle Ages and up until the early 15th century in Europe, an excess of freckles ("witchmarks" or "witchspots") became associated with witchcraft and witche, most likely because of genetic pairing with red hair, also considered to be a quality of witches. Ephelides is a genetic trait. It’s used to describe a freckle that is flat, light brown or red, and fades in the winter. Ephelides are more common in those with light complexions and with the regular use of sunblock, can be suppressed. Liver spot (also known as sun spots) are freckles that do not fade in the winter. Rather, they form after years of exposure to the sun. Lentigines are more common in older people.	Can you provide an explanation and overview of freckles, please?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Can you provide an explanation and overview of freckles, please? [/INST] \n Freckles are small colored spots of melanin on the exposed skin or membrane of people with complexions fair enough for them to be visible. Having freckles is genetic and is related to the presence of the melanocortin-1 receptor MC1R gene variant, which is dominant. Freckling can also be triggered by long exposure to sunlight, such as suntanning. When the sun’s rays penetrate the skin, they activate melanocytes which can cause freckles to become darker and more numerous, although the distribution of melanin is not the same. Fair hair such as blonde, or more commonly red hair, are usually common with the genetic factor of freckles, but none so much as fair or pale skin. Freckles are predominantly found on the face, although they may appear on any skin exposed to the sun. Freckles are rare on infants, and more common on children before puberty; they are less common on adults. Children who do not produce enough melanin to protect their skin against harmful rays from the sun develop temporary freckles associated with childhood that usually go away upon puberty, once more melanin is produced. People with the fairest skin often do not produce enough melanin, and so freckles are present after puberty and into adulthood, indicating that individual as a genetic carrier for freckles. Upon exposure to the sun, freckles will reappear if they have been altered with creams or lasers and not protected from the sun, but do however fade with age in some cases. Freckles are not a skin disorder. People with a predisposition to freckles may be especially susceptible to sunburn and skin cancer, and should therefore take extra care to protect themselves in the sun with a daily sunblock of at least 15 SPF. During the Middle Ages and up until the early 15th century in Europe, an excess of freckles ("witchmarks" or "witchspots") became associated with witchcraft and witche, most likely because of genetic pairing with red hair, also considered to be a quality of witches. Ephelides is a genetic trait. It’s used to describe a freckle that is flat, light brown or red, and fades in the winter. Ephelides are more common in those with light complexions and with the regular use of sunblock, can be suppressed. Liver spot (also known as sun spots) are freckles that do not fade in the winter. Rather, they form after years of exposure to the sun. Lentigines are more common in older people.</s>
There are a vast number of causes of palpitations, including namely any condition that causes the heart to be rapidly, forcefully, or irregularly. In general, palpitations may be caused by primary abnormalities in the heart (tachycardia or forceful heart beating), reductions in oxygen carrying capacity (anemia), reductions in the volume of blood circulating (dehydration), sympathetic nervous system stimulation (fever, exertion, panic attacks, drugs), excess hormone production (hyperthyroidism). Pharmacological causes should also be taken into consideration.	Can you provide an overview of palpitation?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Can you provide an overview of palpitation? [/INST] \n There are a vast number of causes of palpitations, including namely any condition that causes the heart to be rapidly, forcefully, or irregularly. In general, palpitations may be caused by primary abnormalities in the heart (tachycardia or forceful heart beating), reductions in oxygen carrying capacity (anemia), reductions in the volume of blood circulating (dehydration), sympathetic nervous system stimulation (fever, exertion, panic attacks, drugs), excess hormone production (hyperthyroidism). Pharmacological causes should also be taken into consideration.</s>
The diagnosis of systemic mastocytosis is based on the presence of one major criterion and one minor criterion or three minor criteria. Major criteria include the presence of multifocal dense infiltrates of mast cells observed in bone marrow sections or other extra cutaneous organs. Four minor criteria include the presence >25% abnormal spindle-shaped mast cells in bone marrow and/or tissues, detection of Kit mutation at codon 816 in bone marrow or extracutaneous organ(s), the expression of CD2 and CD25 surface markers in C-kit positive mast cells from bone marrow or other organs, and elevated serum tryptase levels >20 ng/mL.	What is the preferred diagnostic test for identifying mast cell tumors?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the preferred diagnostic test for identifying mast cell tumors? [/INST] \n The diagnosis of systemic mastocytosis is based on the presence of one major criterion and one minor criterion or three minor criteria. Major criteria include the presence of multifocal dense infiltrates of mast cells observed in bone marrow sections or other extra cutaneous organs. Four minor criteria include the presence >25% abnormal spindle-shaped mast cells in bone marrow and/or tissues, detection of Kit mutation at codon 816 in bone marrow or extracutaneous organ(s), the expression of CD2 and CD25 surface markers in C-kit positive mast cells from bone marrow or other organs, and elevated serum tryptase levels >20 ng/mL.</s>
Endometrial ablation is a medical procedure that is used to remove (ablate) or destroy the endometrial lining of a woman's uterus. This technique is most often employed for women who suffer from excessive or prolonged bleeding during their menstrual cycle but can not or do not wish to undergo a hysterectomy. The procedure is most commonly done on an outpatient basis. Uterine ablation is contraindicated in patients who may want to get pregnant.	Could you please explain what endometrial ablation means?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Could you please explain what endometrial ablation means? [/INST] \n Endometrial ablation is a medical procedure that is used to remove (ablate) or destroy the endometrial lining of a woman's uterus. This technique is most often employed for women who suffer from excessive or prolonged bleeding during their menstrual cycle but can not or do not wish to undergo a hysterectomy. The procedure is most commonly done on an outpatient basis. Uterine ablation is contraindicated in patients who may want to get pregnant.</s>
A reduced concentration of serum alpha1-antitrypsin level is diagnostic of AATD. Laboratory findings consistent with the diagnosis of AATD include moderate-to-severe airflow obstruction with an FEV1 in the range of 30-40% of the predicted value, reduced vital capacity, increased lung volumes secondary to air trapping (residual volume >120% of predicted value) are usually present, diffusing capacity values are reduced substantially (<50% of predicted value) in most symptomatic patients. Serum alpha1-antitrypsin levels are determined by nephelometry. Serum testing is used for diagnostic testing in those patients with family histories compatible with the alpha1-antitrypsin deficiency or with siblings with known alpha1-antitrypsin deficiency. In patients with clinical features that are highly suggestive of alpha1-antitrypsin deficiency but whose serum levels are within the reference range the next best step is to perform a functional assay of alpha1 antiprotease, which measures the ability of the patient's serum to inhibit human leukocyte elastase.	What laboratory results indicate Alpha-1 antitrypsin deficiency?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What laboratory results indicate Alpha-1 antitrypsin deficiency? [/INST] \n A reduced concentration of serum alpha1-antitrypsin level is diagnostic of AATD. Laboratory findings consistent with the diagnosis of AATD include moderate-to-severe airflow obstruction with an FEV1 in the range of 30-40% of the predicted value, reduced vital capacity, increased lung volumes secondary to air trapping (residual volume >120% of predicted value) are usually present, diffusing capacity values are reduced substantially (<50% of predicted value) in most symptomatic patients. Serum alpha1-antitrypsin levels are determined by nephelometry. Serum testing is used for diagnostic testing in those patients with family histories compatible with the alpha1-antitrypsin deficiency or with siblings with known alpha1-antitrypsin deficiency. In patients with clinical features that are highly suggestive of alpha1-antitrypsin deficiency but whose serum levels are within the reference range the next best step is to perform a functional assay of alpha1 antiprotease, which measures the ability of the patient's serum to inhibit human leukocyte elastase.</s>
Surgery is not a mainstay or a preferred method of treatment for pulseless ventricular tachycardia.	What surgical procedure is performed for ventricular tachycardia in a patient who has no pulse?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What surgical procedure is performed for ventricular tachycardia in a patient who has no pulse? [/INST] \n Surgery is not a mainstay or a preferred method of treatment for pulseless ventricular tachycardia.</s>
Avian influenza was first described by Perroncito in 1878 in northern Italy following an outbreak of contagious disease of poultry. In 1918, the avian-descended influenza A H1N1 caused the first major human influenza pandemic. The first avian influenza A H5N1 virus infection in humans was described in 1997 in Hong Kong, where 18 cases were documented (including 6 deaths). The first human-to-human transmission of avian influenza infection was described in 2003 during the outbreaks in Southeast and Central Asia.	What exactly is avian influenza?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What exactly is avian influenza? [/INST] \n Avian influenza was first described by Perroncito in 1878 in northern Italy following an outbreak of contagious disease of poultry. In 1918, the avian-descended influenza A H1N1 caused the first major human influenza pandemic. The first avian influenza A H5N1 virus infection in humans was described in 1997 in Hong Kong, where 18 cases were documented (including 6 deaths). The first human-to-human transmission of avian influenza infection was described in 2003 during the outbreaks in Southeast and Central Asia.</s>
Acute myeloblastic leukemia is a quickly progressing disease in which too many immature white blood cells (not lymphocytes) are found in the blood and bone marrow. Also called AML, acute myeloid leukemia, acute myelogenous leukemia, acute nonlymphocytic leukemia, and ANLL.	Can you provide a synopsis of Acute Myeloblastic Leukemia?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Can you provide a synopsis of Acute Myeloblastic Leukemia? [/INST] \n Acute myeloblastic leukemia is a quickly progressing disease in which too many immature white blood cells (not lymphocytes) are found in the blood and bone marrow. Also called AML, acute myeloid leukemia, acute myelogenous leukemia, acute nonlymphocytic leukemia, and ANLL.</s>
Patients with Glanzmann's thrombasthenia may be asymptomatic, or they could manifest mucosal bleeding, ecchymoses, petechiae and purpura or current bleeding on physical exam.	What does the physical examination for Glanzmann's thrombasthenia entail?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What does the physical examination for Glanzmann's thrombasthenia entail? [/INST] \n Patients with Glanzmann's thrombasthenia may be asymptomatic, or they could manifest mucosal bleeding, ecchymoses, petechiae and purpura or current bleeding on physical exam.</s>