output
stringlengths
2
68.9k
input
stringlengths
15
295
instruction
stringclasses
1 value
prompt
stringlengths
158
69.1k
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>
Typically patients of subependymoma are asymptomatic and small lesions are discovered incidentally. Symptoms of subependymoma include: Symptoms due to elevated intracranial pressure Headache Nausea Vomiting Neurological symptoms Seizures Sudden loss of awareness Transient loss of memory Patients with subependymoma usually appear normal. Physical examination may be remarkable for: Abnormal pupillary reflex Visual field defects Gait changes Bilateral Babinski sign Depressed Glasgow coma score (GCS) Decreased muscle strength Decreased deep tendon reflexes Sensation defects Hearing problems and abnormal Rinne and Weber tests There are no specific laboratory findings associated with subependymoma. There are no ECG findings associated with subependymoma. There are no x-ray findings associated with subependymoma. There are no echocardiography / ultrasound findings associated with sybependymoma. Head CT scan is helpful in the diagnosis of subependymoma. On CT scan, subependymoma is characterized by: Iso- and hypodense intraventricular mass Positive mass effect No enhancement If large, it may have cystic or even calcific components No vasogenic edema Brain MRI is helpful in the diagnosis of subependymoma. On MRI, subependymoma is characterized by: MRI component Findings T1 weighted image Iso - hypointense compared to white matter Homogeneous but may be heterogeneous in larger lesions T2 weighted image Hyperintense compared to adjacent white and grey matter Heterogeneity may be seen in larger lesions, with susceptibility related signal drop-out due to calcifications No adjacent parenchymal edema (as no brain invasion is present) T1 weighted image with contrast Little or no enhancement There are no other imaging findings associated with subependymoma. There are no other diagnostic studies associated with subependymoma. There is no medical therapy available for the treatment of subependymoma. Surgery is the mainstay of therapy for subependymoma. Incidental intraventricular subependymoma can be managed conservatively through MRI surveillance. Surgical resection is indicated for: Symptomatic tumors Tumors without a clear imaging diagnosis There are no established measures for the secondary prevention of subependymoma. There are no established measures for the primary prevention of subependymoma.
What is Subependymoma and how is it diagnosed?
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 Subependymoma and how is it diagnosed? [/INST] \n Typically patients of subependymoma are asymptomatic and small lesions are discovered incidentally. Symptoms of subependymoma include: Symptoms due to elevated intracranial pressure Headache Nausea Vomiting Neurological symptoms Seizures Sudden loss of awareness Transient loss of memory Patients with subependymoma usually appear normal. Physical examination may be remarkable for: Abnormal pupillary reflex Visual field defects Gait changes Bilateral Babinski sign Depressed Glasgow coma score (GCS) Decreased muscle strength Decreased deep tendon reflexes Sensation defects Hearing problems and abnormal Rinne and Weber tests There are no specific laboratory findings associated with subependymoma. There are no ECG findings associated with subependymoma. There are no x-ray findings associated with subependymoma. There are no echocardiography / ultrasound findings associated with sybependymoma. Head CT scan is helpful in the diagnosis of subependymoma. On CT scan, subependymoma is characterized by: Iso- and hypodense intraventricular mass Positive mass effect No enhancement If large, it may have cystic or even calcific components No vasogenic edema Brain MRI is helpful in the diagnosis of subependymoma. On MRI, subependymoma is characterized by: MRI component Findings T1 weighted image Iso - hypointense compared to white matter Homogeneous but may be heterogeneous in larger lesions T2 weighted image Hyperintense compared to adjacent white and grey matter Heterogeneity may be seen in larger lesions, with susceptibility related signal drop-out due to calcifications No adjacent parenchymal edema (as no brain invasion is present) T1 weighted image with contrast Little or no enhancement There are no other imaging findings associated with subependymoma. There are no other diagnostic studies associated with subependymoma. There is no medical therapy available for the treatment of subependymoma. Surgery is the mainstay of therapy for subependymoma. Incidental intraventricular subependymoma can be managed conservatively through MRI surveillance. Surgical resection is indicated for: Symptomatic tumors Tumors without a clear imaging diagnosis There are no established measures for the secondary prevention of subependymoma. There are no established measures for the primary prevention of subependymoma.</s>
Meigs syndrome (also known as "Meigs-Cass syndrome") is defined as the triad of ascites, pleural effusion, and benign ovarian tumor. Meigs syndrome was first discovered by Otto von Spiegelberg, a German gynecologist, in 1866. There is no classification system established for Meigs syndrome. Other variants of Meigs syndrome include pseudo-meigs syndrome, and atypical Meigs' syndrome. Meigs syndrome may be caused by either ovarian fibroma, Brenner tumor, ovarian thecoma, or granulosa cell tumor. The pathogenesis of Meigs syndrome is characterized by a transudative process. The prevalence of benign ovarian tumors is approximately 2-10%, and only 1-2% develop Meigs syndrome. Meigs syndrome is more commonly observed among postmenopausal women. The median age at diagnosis is approximately 50 years. The majority of patients with Meigs syndrome are asymptomatic. Early clinical features include bloating, fatigue, and shortness of breath. Computed tomography is the imaging modality of choice for Meigs syndrome. On conventional radiography, Meigs syndrome is characterized by blunting of the costophrenic angle or fluid within the horizontal or oblique fissures (250-600 ml of fluid is required before the pleural effusion becomes evident). Surgery is the mainstay of therapy for Meigs syndrome. Exploratory laparotomy with surgical staging is the most common approach to the treatment of Meigs syndrome. Once diagnosed and successfully treated, patients with Meigs syndrome are followed-up every 6 months. Follow-up testing includes; serum cancer antigen 125, ultrasound, and basic metabolic profile.
What is the meaning of Meigs' 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 meaning of Meigs' syndrome? [/INST] \n Meigs syndrome (also known as "Meigs-Cass syndrome") is defined as the triad of ascites, pleural effusion, and benign ovarian tumor. Meigs syndrome was first discovered by Otto von Spiegelberg, a German gynecologist, in 1866. There is no classification system established for Meigs syndrome. Other variants of Meigs syndrome include pseudo-meigs syndrome, and atypical Meigs' syndrome. Meigs syndrome may be caused by either ovarian fibroma, Brenner tumor, ovarian thecoma, or granulosa cell tumor. The pathogenesis of Meigs syndrome is characterized by a transudative process. The prevalence of benign ovarian tumors is approximately 2-10%, and only 1-2% develop Meigs syndrome. Meigs syndrome is more commonly observed among postmenopausal women. The median age at diagnosis is approximately 50 years. The majority of patients with Meigs syndrome are asymptomatic. Early clinical features include bloating, fatigue, and shortness of breath. Computed tomography is the imaging modality of choice for Meigs syndrome. On conventional radiography, Meigs syndrome is characterized by blunting of the costophrenic angle or fluid within the horizontal or oblique fissures (250-600 ml of fluid is required before the pleural effusion becomes evident). Surgery is the mainstay of therapy for Meigs syndrome. Exploratory laparotomy with surgical staging is the most common approach to the treatment of Meigs syndrome. Once diagnosed and successfully treated, patients with Meigs syndrome are followed-up every 6 months. Follow-up testing includes; serum cancer antigen 125, ultrasound, and basic metabolic profile.</s>
There are no other diagnostic study findings associated with neurofibroma.
What other diagnostic tests are used for neurofibroma?
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 are used for neurofibroma? [/INST] \n There are no other diagnostic study findings associated with neurofibroma.</s>
Uveitis specifically refers to inflammation of the middle layer of the eye, termed the " uvea ". In common usage, it may refer to an inflammatory process involving the interior of the eye. The uvea consists of the iris, ciliary body, and choroid; it provides most of the blood supply to the retina. Uveitis may occur unilaterally or bilaterally, affect the anterior, intermediate, or posterior segment of the eye, may be infectious or non infectious, and granulomatous or non-granulomatous. The exact pathogenesis of uveitis is not fully understood. It is thought that uveitis is mediated by a genetic predisposition and an acquired cross immunity to infectious agents, or cross immunity to self-antigens due to underlying autoimmune diseases. Common causes of uveitis include seronegative spondyloarthropathy, sarcoidosis, juvenile idiopathic arthritis, systemic lupus erythematosus, Behçet syndrome, multiple sclerosis, AIDS, syphilis, and tuberculosis. Uveitis must be differentiated from other diseases such as conjunctivitis, endophthalmitis, or scleritis. A history of cigarette smoking is associated with all etiologies and subtypes of uveitis. Uveitis is estimated to be responsible for approximately 10% of the blindness in the United States. If left untreated uveitis can progress to permanent vision loss or result in complications such as cataracts, glaucoma, and retinal detachment. A history of an underlying associated condition along with symptoms of eye pain, redness, photophobia, floaters, and blurry vision is strongly suggestive of uveitis. There are no specific laboratory or physical examination findings associated with uveitis. Imaging modalities may assist in diagnosing an underlying condition, though have no diagnostic utility for uveitis itself. Slit lamp test is the diagnostic modality of choice. Other ophthalmologic studies may assist in further characterizing the disease. Mainstay medical therapy is by high dose corticosteroids. Targeted antimicrobials may be required to treat an underlying infection. Surgical intervention is reserved for managing complications of uveitis such as cataract surgery or glaucoma surgery. The only indicated guideline for screening is in patients suspected of or diagnosed with juvenile idiopathic arthritis. Prompt treatment of a potential underlying infection may help prevent development of uveitis.
What is an overview of Uveitis?
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 an overview of Uveitis? [/INST] \n Uveitis specifically refers to inflammation of the middle layer of the eye, termed the " uvea ". In common usage, it may refer to an inflammatory process involving the interior of the eye. The uvea consists of the iris, ciliary body, and choroid; it provides most of the blood supply to the retina. Uveitis may occur unilaterally or bilaterally, affect the anterior, intermediate, or posterior segment of the eye, may be infectious or non infectious, and granulomatous or non-granulomatous. The exact pathogenesis of uveitis is not fully understood. It is thought that uveitis is mediated by a genetic predisposition and an acquired cross immunity to infectious agents, or cross immunity to self-antigens due to underlying autoimmune diseases. Common causes of uveitis include seronegative spondyloarthropathy, sarcoidosis, juvenile idiopathic arthritis, systemic lupus erythematosus, Behçet syndrome, multiple sclerosis, AIDS, syphilis, and tuberculosis. Uveitis must be differentiated from other diseases such as conjunctivitis, endophthalmitis, or scleritis. A history of cigarette smoking is associated with all etiologies and subtypes of uveitis. Uveitis is estimated to be responsible for approximately 10% of the blindness in the United States. If left untreated uveitis can progress to permanent vision loss or result in complications such as cataracts, glaucoma, and retinal detachment. A history of an underlying associated condition along with symptoms of eye pain, redness, photophobia, floaters, and blurry vision is strongly suggestive of uveitis. There are no specific laboratory or physical examination findings associated with uveitis. Imaging modalities may assist in diagnosing an underlying condition, though have no diagnostic utility for uveitis itself. Slit lamp test is the diagnostic modality of choice. Other ophthalmologic studies may assist in further characterizing the disease. Mainstay medical therapy is by high dose corticosteroids. Targeted antimicrobials may be required to treat an underlying infection. Surgical intervention is reserved for managing complications of uveitis such as cataract surgery or glaucoma surgery. The only indicated guideline for screening is in patients suspected of or diagnosed with juvenile idiopathic arthritis. Prompt treatment of a potential underlying infection may help prevent development of uveitis.</s>
Currently there is no cure for Goodpasture syndrome. The mainstay of therapy for Goodpasture syndrome consist of corticosteroids, cyclophosphamide and plasmapheresis.
What is the medical treatment for Goodpasture 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 medical treatment for Goodpasture syndrome? [/INST] \n Currently there is no cure for Goodpasture syndrome. The mainstay of therapy for Goodpasture syndrome consist of corticosteroids, cyclophosphamide and plasmapheresis.</s>
Treatment of esthesioneuroblastoma depends on the following features: Stage of the tumor Regional or distant metastatic disease. Surgery is best reserved for patients with small tumors located in the sinonasal cavity without involvement of the orbit or skull base. For more advanced tumors, the successful treatment includes surgery and radiation therapy with most of the institutions favoring delivery of postoperative, rather than preoperative, radiotherapy. Large and bulky tumors (T3 and T4) are treated with preoperative chemotherapy and radiotherapy followed by surgery. The optimal treatment of esthesioneuroblastoma includes complete surgical resection of the tumor followed by radiation therapy. However, some institutions have reported success with alternative treatment modalities, including surgery without radiation. Dulguerov’s 2001 meta-analysis showed lower recurrence rates for the combination of surgery and radiotherapy. The literature gives little support to single-modality treatments; only few studies have advocated either radiation or surgery alone. Some institutions advocate surgery alone for Kadish stage A tumors, whereas the majority suggest adjuvant radiotherapy for these lesions. The traditional surgical approach for esthesioneuroblastoma, is craniofacial resection (CFR). Craniofacial resection is a combined transcranial and transfacial approach, which includes a lateral rhinotomy or midfacial degloving and frontal craniotomy. The objective of this approach is to achieve an en bloc resection of tumor and involved structures. It also involves removal of the olfactory bulbs, cribriform plate, roof of the ethmoid sinuses, upper septum, medial maxillae, and as much of the anterior cranial fossa dura as necessary. The advent of craniofacial resection is credited with increase in overall survival for esthesioneuroblastoma patients. The postoperative morbidity (approximately 35%) and mortality (2-5%) with craniofacial resection is relatively high, although the complication rate associated with craniofacial resection has decreased over the last few decades. Although traditional craniofacial resection remains the gold standard, less invasive endoscopic techniques have become increasingly utilized. Minimally invasive endoscopic resection (MIER) is a complete endoscopic approach, most suited for tumors that have not invaded the brain tissue. Endoscopic-assisted cranionasal resection (EA-CNR) combines transnasal endoscopic approach with craniotomy and addresses large tumors that have invaded brain tissue. There are distinct advantages of EA-CNR and MIER over traditional CFR. Endoscopic techniques allow great access to anatomic areas where external approaches are notoriously known to fail, such as frontal recess and the sphenoid sinus region. The endoscope plays an important role in tumor surveillance, in the postoperative period. Finally, the endoscopic approach eliminates the need for disfiguring facial incisions. Endoscopic techniques have shown to have comparable success rates but fewer complications compared with traditional craniofacial resection.
What role does surgery play in the treatment of esthesioneuroblastoma?
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 role does surgery play in the treatment of esthesioneuroblastoma? [/INST] \n Treatment of esthesioneuroblastoma depends on the following features: Stage of the tumor Regional or distant metastatic disease. Surgery is best reserved for patients with small tumors located in the sinonasal cavity without involvement of the orbit or skull base. For more advanced tumors, the successful treatment includes surgery and radiation therapy with most of the institutions favoring delivery of postoperative, rather than preoperative, radiotherapy. Large and bulky tumors (T3 and T4) are treated with preoperative chemotherapy and radiotherapy followed by surgery. The optimal treatment of esthesioneuroblastoma includes complete surgical resection of the tumor followed by radiation therapy. However, some institutions have reported success with alternative treatment modalities, including surgery without radiation. Dulguerov’s 2001 meta-analysis showed lower recurrence rates for the combination of surgery and radiotherapy. The literature gives little support to single-modality treatments; only few studies have advocated either radiation or surgery alone. Some institutions advocate surgery alone for Kadish stage A tumors, whereas the majority suggest adjuvant radiotherapy for these lesions. The traditional surgical approach for esthesioneuroblastoma, is craniofacial resection (CFR). Craniofacial resection is a combined transcranial and transfacial approach, which includes a lateral rhinotomy or midfacial degloving and frontal craniotomy. The objective of this approach is to achieve an en bloc resection of tumor and involved structures. It also involves removal of the olfactory bulbs, cribriform plate, roof of the ethmoid sinuses, upper septum, medial maxillae, and as much of the anterior cranial fossa dura as necessary. The advent of craniofacial resection is credited with increase in overall survival for esthesioneuroblastoma patients. The postoperative morbidity (approximately 35%) and mortality (2-5%) with craniofacial resection is relatively high, although the complication rate associated with craniofacial resection has decreased over the last few decades. Although traditional craniofacial resection remains the gold standard, less invasive endoscopic techniques have become increasingly utilized. Minimally invasive endoscopic resection (MIER) is a complete endoscopic approach, most suited for tumors that have not invaded the brain tissue. Endoscopic-assisted cranionasal resection (EA-CNR) combines transnasal endoscopic approach with craniotomy and addresses large tumors that have invaded brain tissue. There are distinct advantages of EA-CNR and MIER over traditional CFR. Endoscopic techniques allow great access to anatomic areas where external approaches are notoriously known to fail, such as frontal recess and the sphenoid sinus region. The endoscope plays an important role in tumor surveillance, in the postoperative period. Finally, the endoscopic approach eliminates the need for disfiguring facial incisions. Endoscopic techniques have shown to have comparable success rates but fewer complications compared with traditional craniofacial resection.</s>
Treatment with infusions of plasma or purified apotransferrin may stabilise or correct the anemia and growth defects.
What is transferrinemia and what are the treatments for 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 transferrinemia and what are the treatments for it? [/INST] \n Treatment with infusions of plasma or purified apotransferrin may stabilise or correct the anemia and growth defects.</s>
Two roots make up the ansa cervicalis. The superior root (descendens hypoglossi) of the ansa cervicalis is formed by a branch of spinal nerve C1. These nerve fibers travel in the hypoglossal nerve before leaving to form the superior root. The superior root goes around the occipital artery and then descends in the carotid sheath. It sends off branches to the superior belly of the omohyoid muscle, and the upper parts of the sternothyroid and sternohyoid muscles and is then joined by the inferior root. The inferior root (descendens cervicalis) is formed by fibers from spinal nerves C2 and C3. The inferior root gives off branches to the inferior belly of the omohyoid muscle, and the lower parts of the sternothyroid and sternohyoid muscles.
What is the Ansa cervicalis?
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 Ansa cervicalis? [/INST] \n Two roots make up the ansa cervicalis. The superior root (descendens hypoglossi) of the ansa cervicalis is formed by a branch of spinal nerve C1. These nerve fibers travel in the hypoglossal nerve before leaving to form the superior root. The superior root goes around the occipital artery and then descends in the carotid sheath. It sends off branches to the superior belly of the omohyoid muscle, and the upper parts of the sternothyroid and sternohyoid muscles and is then joined by the inferior root. The inferior root (descendens cervicalis) is formed by fibers from spinal nerves C2 and C3. The inferior root gives off branches to the inferior belly of the omohyoid muscle, and the lower parts of the sternothyroid and sternohyoid muscles.</s>
It is a more sensitive test than a CT scan. It is better in identifying lesions of stroke, white matter, and the posterior fossa. It can't be used as a first line of investigation. It is more expensive than a CT scan.
What is causing confusion with MRI?
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 causing confusion with MRI? [/INST] \n It is a more sensitive test than a CT scan. It is better in identifying lesions of stroke, white matter, and the posterior fossa. It can't be used as a first line of investigation. It is more expensive than a CT scan.</s>
Infection with Naegleria is very rare. However, when it does occur, infection is most common during the dry, summer months, when the air temperature is hot, the water is warm, and water levels are low. The number of infections increase during years characterized by heat waves.
What is a Naegleria infection?
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 a Naegleria infection? [/INST] \n Infection with Naegleria is very rare. However, when it does occur, infection is most common during the dry, summer months, when the air temperature is hot, the water is warm, and water levels are low. The number of infections increase during years characterized by heat waves.</s>
AVNRT starts and stops abruptly. Patients may develop syncope. The prognosis is good.
Could you explain the definition of nodal reentrant tachycardia?
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 explain the definition of nodal reentrant tachycardia? [/INST] \n AVNRT starts and stops abruptly. Patients may develop syncope. The prognosis is good.</s>
Common risk factors in the development of chorioamnionitis include: Preterm premature rupture of membranes (PPROM) Prolonged rupture of membranes Prolonged labor Prolonged second stage Intrapartum Hypertension Prematurity Postterm Pregnancy Nulliparity Cesarean section due either to fetal heart rate decelerations or dystocia Internal fetal monitoring Multiple digital vaginal examinations Epidural anesthesia Meconium stained amniotic fluid Immunocompromised state Behavioral conditions Smoking Alcohol Drug Abuse Infections Maternal genital tract colonization with group B Streptococcus Sexually transmitted diseases (STDs) Maternal genital colonization with ureoplasma
What are the factors that increase the risk of chorioamnionitis?
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 that increase the risk of chorioamnionitis? [/INST] \n Common risk factors in the development of chorioamnionitis include: Preterm premature rupture of membranes (PPROM) Prolonged rupture of membranes Prolonged labor Prolonged second stage Intrapartum Hypertension Prematurity Postterm Pregnancy Nulliparity Cesarean section due either to fetal heart rate decelerations or dystocia Internal fetal monitoring Multiple digital vaginal examinations Epidural anesthesia Meconium stained amniotic fluid Immunocompromised state Behavioral conditions Smoking Alcohol Drug Abuse Infections Maternal genital tract colonization with group B Streptococcus Sexually transmitted diseases (STDs) Maternal genital colonization with ureoplasma</s>
Ultrasound is not required for the diagnosis of tonsillitis.
Can ultrasound (USG) be used to diagnose tonsillitis?
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 ultrasound (USG) be used to diagnose tonsillitis? [/INST] \n Ultrasound is not required for the diagnosis of tonsillitis.</s>
Prompt treatment of disorders that can cause valve disease reduces your risk of tricuspid regurgitation. Treat strep infections promptly to prevent rheumatic fever. Any invasive procedure, including dental work and cleaning, can introduce bacteria into your bloodstream. The bacteria can infect a damaged mitral valve, causing endocarditis. Always tell your health care provider and dentist if you have a history of heart valve disease or congenital heart disease before treatment. Taking antibiotics before dental or other invasive procedures may decrease your risk of endocarditis.
What information is currently available on tricuspid regurgitation?
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 is currently available on tricuspid regurgitation? [/INST] \n Prompt treatment of disorders that can cause valve disease reduces your risk of tricuspid regurgitation. Treat strep infections promptly to prevent rheumatic fever. Any invasive procedure, including dental work and cleaning, can introduce bacteria into your bloodstream. The bacteria can infect a damaged mitral valve, causing endocarditis. Always tell your health care provider and dentist if you have a history of heart valve disease or congenital heart disease before treatment. Taking antibiotics before dental or other invasive procedures may decrease your risk of endocarditis.</s>
There is insufficient evidence to recommend routine screening for scleroderma, however screening is recommended for pulmonary arterial hypertension and malignancy in scleroderma patients: According to the ACCF/AHA expert consensus document, screening for pulmonary arterial hypertension (PAH) by transthoracic echocardiogram (TTE) and pulmonary function tests (PFTs) is recommended every year among patients with scleroderma. Enhanced screening for malignancy is recommended in scleroderma patients at high risk. Regular blood pressure monitoring at home is encouraged in patients with scleroderma to screen for renal involvement and prevention of scleroderma renal crisis.
What does screening for scleroderma 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 screening for scleroderma entail? [/INST] \n There is insufficient evidence to recommend routine screening for scleroderma, however screening is recommended for pulmonary arterial hypertension and malignancy in scleroderma patients: According to the ACCF/AHA expert consensus document, screening for pulmonary arterial hypertension (PAH) by transthoracic echocardiogram (TTE) and pulmonary function tests (PFTs) is recommended every year among patients with scleroderma. Enhanced screening for malignancy is recommended in scleroderma patients at high risk. Regular blood pressure monitoring at home is encouraged in patients with scleroderma to screen for renal involvement and prevention of scleroderma renal crisis.</s>
Primary prevention strategies intend to avoid the development of disease. Different strategies like dietary modification, increasing physical activity and weight reduction are found useful in the primary prevention (development) of metabolic syndrome.
What is the main preventive measure for metabolic 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 main preventive measure for metabolic syndrome? [/INST] \n Primary prevention strategies intend to avoid the development of disease. Different strategies like dietary modification, increasing physical activity and weight reduction are found useful in the primary prevention (development) of metabolic syndrome.</s>
Supportive laboratory findings: Presence of normal or increased synthesis of testosterone by the testes Presence of normal conversion of testosterone to dihydrotestosterone (DHT) Presence of normal or increased luteinizing hormone (LH) production by the pituitary gland In CAIS (complete androgen insensitivity syndrome), but not in PAIS (partial androgen insensitivity syndrome): possible reduction in postnatal (0-3 months) surge in serum luteinizing hormone (LH) and serum testosterone concentrations. In the “predominantly male” phenotype: In response to a standard dose of the anabolic androgen, stanozolol there would be less than normal decline of sex hormone-binding globulin During the first year of life or after the beginning of puberty, there would be higher than normal levels of anti-müllerian hormone (AMH) If a phenotypic female has 46XY karyotype and if the androgen receptor (AR) variant in the family is determined, then the next step would be molecular genetic testing which incluides: Single-gene testing Multi-gene panel Genomic testing which would be including the exome sequencing and the genome sequencing may be considered if single-gene testing (and/or use of a multi-gene panel that includes androgen receptor (AR)) fails to confirm a diagnosis in patients with features of AIS. While performing prenatal amniocentesis, the male karyotype is not determined by the ultrasound or obvious female appearance at birth. If an androgen receptor (AR) variant has not been identified in the family, then androgen binding assays may be considered. By the extensive use of prenatal testing modalities such as pre-implantation genetic screening, noninvasive prenatal screening, and ultrasonography there would be more disagreement in coming to a final conclusion which would require expert navigation to identify true pathology. Molecular Genetic Testing Used in Androgen Insensitivity Syndrome Gene Test Method Proportion of 46,XY Probands w/a Pathogenic Variant 2 Detectable by This Method AR Sequence analysis ~95%-97% Gene-targeted deletion/duplication analysis ~3%-5%
What are the laboratory test results for individuals with androgen insensitivity 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 are the laboratory test results for individuals with androgen insensitivity syndrome? [/INST] \n Supportive laboratory findings: Presence of normal or increased synthesis of testosterone by the testes Presence of normal conversion of testosterone to dihydrotestosterone (DHT) Presence of normal or increased luteinizing hormone (LH) production by the pituitary gland In CAIS (complete androgen insensitivity syndrome), but not in PAIS (partial androgen insensitivity syndrome): possible reduction in postnatal (0-3 months) surge in serum luteinizing hormone (LH) and serum testosterone concentrations. In the “predominantly male” phenotype: In response to a standard dose of the anabolic androgen, stanozolol there would be less than normal decline of sex hormone-binding globulin During the first year of life or after the beginning of puberty, there would be higher than normal levels of anti-müllerian hormone (AMH) If a phenotypic female has 46XY karyotype and if the androgen receptor (AR) variant in the family is determined, then the next step would be molecular genetic testing which incluides: Single-gene testing Multi-gene panel Genomic testing which would be including the exome sequencing and the genome sequencing may be considered if single-gene testing (and/or use of a multi-gene panel that includes androgen receptor (AR)) fails to confirm a diagnosis in patients with features of AIS. While performing prenatal amniocentesis, the male karyotype is not determined by the ultrasound or obvious female appearance at birth. If an androgen receptor (AR) variant has not been identified in the family, then androgen binding assays may be considered. By the extensive use of prenatal testing modalities such as pre-implantation genetic screening, noninvasive prenatal screening, and ultrasonography there would be more disagreement in coming to a final conclusion which would require expert navigation to identify true pathology. Molecular Genetic Testing Used in Androgen Insensitivity Syndrome Gene Test Method Proportion of 46,XY Probands w/a Pathogenic Variant 2 Detectable by This Method AR Sequence analysis ~95%-97% Gene-targeted deletion/duplication analysis ~3%-5%</s>
Hemangioma is primarily diagnosed based on the clinical presentation. Investigations such as Ultrasound, CT scan or MRI are needed when hemagioma in organs is suspected. The gold standard for diagnosing lumbosacral hemangioma is MRI.
What is the preferred diagnostic study for Hemangioma?
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 study for Hemangioma? [/INST] \n Hemangioma is primarily diagnosed based on the clinical presentation. Investigations such as Ultrasound, CT scan or MRI are needed when hemagioma in organs is suspected. The gold standard for diagnosing lumbosacral hemangioma is MRI.</s>
There is no clinically proven method to prevent appendicitis.
What is appendicitis, and what details can be given about 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 appendicitis, and what details can be given about it? [/INST] \n There is no clinically proven method to prevent appendicitis.</s>
Atrial fibrillation Atrial Flutter Supraventricular tachycardia Ventricular tachycardia
What does catheter ablation 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 catheter ablation mean? [/INST] \n Atrial fibrillation Atrial Flutter Supraventricular tachycardia Ventricular tachycardia</s>
Antigen NMDA receptor NR1 Lgil CASPR2 AMPA receptor GABA B receptor Glycine receptor MgluR5 Age(median)/gender female: male 0·6–85 (21) 4:1 30–80 (60) 1:2 46–77 (60) 1:4 38–87 (60) 9:1 24–75 (62) 1:1 5–69 (43) 6:5 46, 15 1:1 Clinical syndrome 1.Prodromal Syndrome 2. Psychiatric Syndrome, seizures, amnesia 3.Movement disorders catatonia, autonomic instability, Limbic encephalitis, tonic or facio-brachial dystonic seizures, myoclonus Morvan Syndrome, encephalitis, neuromyotonia Limbic encephalitis, psychiatric syndrome Limbic encephalitis Encephalomyelitis with rigidity and myoclonus, hyperekplexia, stiff-person syndrome, (retinopathy) Limbic encephalitis, myoclonus MRI T2/FLAIR hyperintensities, medial temporal 25% 80% 40% 90% 70% 10% 50% CSF pleocytosis or Oligoclonal Bands 95% 40% 25% 90% 90% some oligoclonal bands 2/2 only cases reported and present in them ocb: oligoclonal bands; EEG: electroencephalograph; NMDA: N-methyl-D-aspartate; AMPA: α-amino-3-hydroxy-5-methyl-4-isoxazol-propionic acid; GABA: γ-amino-butyric acid receptor; CASPR2: contactin-associated protein-like 2; Lgi1: leucine-rich, glioma-inactivated 1; mGluR5: metabotrophic glutamate receptor 5. Other etiologies causing Anti NMDA encephalitis like features Differential diagnosis Bacterial and viral infections of the brain Herpes simplex virus type 1, Human herpes virus type 6, Enterovirus, Mycoplasma Autoimmune-associated encephalitis PANDAS, Sydenham chorea, Hashimoto encephalopathy, Rasmussen encephalitis, Encephalitis lethargica Autoimmune synaptic receptor encephalitides Neuronal antibodies to GABA, AMPA, and LGI1receptors CNS vasculitis Primary CNS angiitis, Secondary (due to chronic infection, inflammatory processes) Demyelinating disorders Acute disseminated encephalomyelitis, Neuromyelitis optica Medication Overdose Ketamine, Phencyclidine
What is the method for distinguishing between Anti-NMDA receptor encephalitis and 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 the method for distinguishing between Anti-NMDA receptor encephalitis and other illnesses? [/INST] \n Antigen NMDA receptor NR1 Lgil CASPR2 AMPA receptor GABA B receptor Glycine receptor MgluR5 Age(median)/gender female: male 0·6–85 (21) 4:1 30–80 (60) 1:2 46–77 (60) 1:4 38–87 (60) 9:1 24–75 (62) 1:1 5–69 (43) 6:5 46, 15 1:1 Clinical syndrome 1.Prodromal Syndrome 2. Psychiatric Syndrome, seizures, amnesia 3.Movement disorders catatonia, autonomic instability, Limbic encephalitis, tonic or facio-brachial dystonic seizures, myoclonus Morvan Syndrome, encephalitis, neuromyotonia Limbic encephalitis, psychiatric syndrome Limbic encephalitis Encephalomyelitis with rigidity and myoclonus, hyperekplexia, stiff-person syndrome, (retinopathy) Limbic encephalitis, myoclonus MRI T2/FLAIR hyperintensities, medial temporal 25% 80% 40% 90% 70% 10% 50% CSF pleocytosis or Oligoclonal Bands 95% 40% 25% 90% 90% some oligoclonal bands 2/2 only cases reported and present in them ocb: oligoclonal bands; EEG: electroencephalograph; NMDA: N-methyl-D-aspartate; AMPA: α-amino-3-hydroxy-5-methyl-4-isoxazol-propionic acid; GABA: γ-amino-butyric acid receptor; CASPR2: contactin-associated protein-like 2; Lgi1: leucine-rich, glioma-inactivated 1; mGluR5: metabotrophic glutamate receptor 5. Other etiologies causing Anti NMDA encephalitis like features Differential diagnosis Bacterial and viral infections of the brain Herpes simplex virus type 1, Human herpes virus type 6, Enterovirus, Mycoplasma Autoimmune-associated encephalitis PANDAS, Sydenham chorea, Hashimoto encephalopathy, Rasmussen encephalitis, Encephalitis lethargica Autoimmune synaptic receptor encephalitides Neuronal antibodies to GABA, AMPA, and LGI1receptors CNS vasculitis Primary CNS angiitis, Secondary (due to chronic infection, inflammatory processes) Demyelinating disorders Acute disseminated encephalomyelitis, Neuromyelitis optica Medication Overdose Ketamine, Phencyclidine</s>
Intrahepatic Cholestasis of Pregnancy (ICP), also termed Obstetric Cholestasis in the United Kingdom, gives rise to troublesome itching during pregnancy but may lead to possibly serious complications for the mother and very serious outcomes for the fetus. Itching has long been considered to be a common symptom of pregnancy. The vast majority of times, itching, or pruritus is a minor annoyance caused by changes to the skin, especially that of the abdomen. However, there are instances when itching is a symptom of ICP. ICP occurs most commonly in the third trimester, but can begin at any time during the pregnancy.
What does the term "intrahepatic cholestasis of pregnancy" 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 the term "intrahepatic cholestasis of pregnancy" mean? [/INST] \n Intrahepatic Cholestasis of Pregnancy (ICP), also termed Obstetric Cholestasis in the United Kingdom, gives rise to troublesome itching during pregnancy but may lead to possibly serious complications for the mother and very serious outcomes for the fetus. Itching has long been considered to be a common symptom of pregnancy. The vast majority of times, itching, or pruritus is a minor annoyance caused by changes to the skin, especially that of the abdomen. However, there are instances when itching is a symptom of ICP. ICP occurs most commonly in the third trimester, but can begin at any time during the pregnancy.</s>
This test may be done in a hospital or clinic radiology department. The patient lies on the X-ray table and a preliminary X-ray is taken. The patient is then asked to lie on the side while a well lubricated enema tube is inserted into the rectum. As the enema enters the body, the patient might have the sensation that their stomach is being filled. The barium, a radiopaque (shows up on X-ray) contrast medium, is then allowed to flow into the colon. A small balloon at the tip of the enema tube may be inflated to help keep the barium inside. The flow of the barium is monitored by the health care provider on an X-ray fluoroscope screen (like a TV monitor). Air may be puffed into the colon to distend it and provide better images (often called a "double-contrast" exam). If air is used, the enema tube will be reinserted (if it had been removed; whether it is depends on who does the exam) and a small amount of air will be introduced into the colon, and more X-ray pictures are taken. The patient is usually asked to move to different positions and the table is slightly tipped to get different views. If there is a suspected bowel perforation, a water-soluble contrast is used instead of barium. The study is otherwise very similar, although the images are not quite as good. (The concern with existing perforation is that contrast will leak from the bowel to the peritoneal cavity, and water-soluble material is safer than barium, which must be removed.)
What does lower gastrointestinal series 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 lower gastrointestinal series mean? [/INST] \n This test may be done in a hospital or clinic radiology department. The patient lies on the X-ray table and a preliminary X-ray is taken. The patient is then asked to lie on the side while a well lubricated enema tube is inserted into the rectum. As the enema enters the body, the patient might have the sensation that their stomach is being filled. The barium, a radiopaque (shows up on X-ray) contrast medium, is then allowed to flow into the colon. A small balloon at the tip of the enema tube may be inflated to help keep the barium inside. The flow of the barium is monitored by the health care provider on an X-ray fluoroscope screen (like a TV monitor). Air may be puffed into the colon to distend it and provide better images (often called a "double-contrast" exam). If air is used, the enema tube will be reinserted (if it had been removed; whether it is depends on who does the exam) and a small amount of air will be introduced into the colon, and more X-ray pictures are taken. The patient is usually asked to move to different positions and the table is slightly tipped to get different views. If there is a suspected bowel perforation, a water-soluble contrast is used instead of barium. The study is otherwise very similar, although the images are not quite as good. (The concern with existing perforation is that contrast will leak from the bowel to the peritoneal cavity, and water-soluble material is safer than barium, which must be removed.)</s>
Volume overload of the right side of heart can lead to right heart failure that may present with symptoms of swelling of the extremities, difficulty breathing and signs such as hepatomegaly and an elevated jugular venous pulse. On cardiovascular examinations there is a fixed splitting of second heart sound. Also, a systolic ejection murmur that is attributed to the increased flow of blood through the pulmonic valve can be heard.
What is involved in the physical examination for atrial septal defect?
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 involved in the physical examination for atrial septal defect? [/INST] \n Volume overload of the right side of heart can lead to right heart failure that may present with symptoms of swelling of the extremities, difficulty breathing and signs such as hepatomegaly and an elevated jugular venous pulse. On cardiovascular examinations there is a fixed splitting of second heart sound. Also, a systolic ejection murmur that is attributed to the increased flow of blood through the pulmonic valve can be heard.</s>
Always suspect acute pericarditis in the presence of characteristic pleuritic chest pain and pericardial friction rub. Also suspect pericarditis in a patient with persistent fever and pericardial effusion or new unexplained cardiomegaly. Always first suspect acute cardiac tamponade in any patient presenting with Beck's triad: hypotension, muffled heart sounds and distended neck veins (or elevated jugular venous pressure). Initiate systemic corticosteroid therapy to treat pericarditis due to autoreactive or connective tissue diseases and uremia. Use intrapericardial application to avoid systemic side effects. Use moderate initial dosing of steroids followed by a slow taper and introduce ibuprofen or colchicine early during tapering of steroids. Order an analysis of pericardial effusion in required cases for different etiologies according to the clinical presentation. Assess for the presence of coagulopathy or the intake of antithrombotic medications before choosing the modality of drainage of the pericardial fluid. Choose pericardiocentesis rather than surgical drainage as a therapeutic option unless the patient has an indication for surgical drainage. When surgical drainage is indicated but the patient has severe hypotension prohibiting the induction of anesthesia, perform pericardiocentesis in the operating room before surgery. Monitor closely patients who underwent pericardiocentesis for postdrainage decompensation. Heparin is recommended under strict observation for patients who need anticoagulant therapy.
What is the survival guide for residents to manage pericarditis?
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 survival guide for residents to manage pericarditis? [/INST] \n Always suspect acute pericarditis in the presence of characteristic pleuritic chest pain and pericardial friction rub. Also suspect pericarditis in a patient with persistent fever and pericardial effusion or new unexplained cardiomegaly. Always first suspect acute cardiac tamponade in any patient presenting with Beck's triad: hypotension, muffled heart sounds and distended neck veins (or elevated jugular venous pressure). Initiate systemic corticosteroid therapy to treat pericarditis due to autoreactive or connective tissue diseases and uremia. Use intrapericardial application to avoid systemic side effects. Use moderate initial dosing of steroids followed by a slow taper and introduce ibuprofen or colchicine early during tapering of steroids. Order an analysis of pericardial effusion in required cases for different etiologies according to the clinical presentation. Assess for the presence of coagulopathy or the intake of antithrombotic medications before choosing the modality of drainage of the pericardial fluid. Choose pericardiocentesis rather than surgical drainage as a therapeutic option unless the patient has an indication for surgical drainage. When surgical drainage is indicated but the patient has severe hypotension prohibiting the induction of anesthesia, perform pericardiocentesis in the operating room before surgery. Monitor closely patients who underwent pericardiocentesis for postdrainage decompensation. Heparin is recommended under strict observation for patients who need anticoagulant therapy.</s>
Hepatitis B Immunoglobulin (HBIG) is a form of passive immunization when given shortly before or soon after exposure to hepatitis B virus. It is also administered in combination with HBV vaccines to the newborns of HBsAg positive mothers.
What are the secondary prevention methods for Hepatitis B?
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 secondary prevention methods for Hepatitis B? [/INST] \n Hepatitis B Immunoglobulin (HBIG) is a form of passive immunization when given shortly before or soon after exposure to hepatitis B virus. It is also administered in combination with HBV vaccines to the newborns of HBsAg positive mothers.</s>
Lab evaluation gives a picture of partial or panhypopituitarism. Laboratory findings consistent with the diagnosis of Sheehan's syndrome are including hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia, hypophosphatemia, anemia, pancytopenia, eosinophilia, hypoalbuminemia, low fasting plasma glucose, and decreased levels of anterior pituitary hormones (free thyroxine, estradiol, cortisol levels). The most sensitive tests are inadequate prolactin and gonadotropin responses to stimulation.
What are the laboratory results for Sheehan's 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 are the laboratory results for Sheehan's syndrome? [/INST] \n Lab evaluation gives a picture of partial or panhypopituitarism. Laboratory findings consistent with the diagnosis of Sheehan's syndrome are including hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia, hypophosphatemia, anemia, pancytopenia, eosinophilia, hypoalbuminemia, low fasting plasma glucose, and decreased levels of anterior pituitary hormones (free thyroxine, estradiol, cortisol levels). The most sensitive tests are inadequate prolactin and gonadotropin responses to stimulation.</s>
The majority of patients with lymphocytosis remain asymptomatic unless there is significant lymphadenopathy or infection. Early clinical features can include, but do not necessarily need to include, fever, fatigue, night sweats, weight loss, and lymphadenopathy. If left untreated, 1.1% of patients with monoclonal B lymphocytosis may progress to develop CLL per year. Common complications of CLL include fatigue due to anemia, bleeding due to thrombocytopenia, and infections due to leukopenia. These manifestations occur when the malignant B cells replace the normal cells of the bone marrow. Prognosis is generally good if the etiology of lymphocytosis is due to a mild viral infection or if the etiology is due to favorable-risk CLL. Favorable risk C}} is characterized by the absence of p53 (17p deletion).
What is the cause of lymphocytosis, and what are its natural progression, potential complications, and likelihood of recovery?
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 cause of lymphocytosis, and what are its natural progression, potential complications, and likelihood of recovery? [/INST] \n The majority of patients with lymphocytosis remain asymptomatic unless there is significant lymphadenopathy or infection. Early clinical features can include, but do not necessarily need to include, fever, fatigue, night sweats, weight loss, and lymphadenopathy. If left untreated, 1.1% of patients with monoclonal B lymphocytosis may progress to develop CLL per year. Common complications of CLL include fatigue due to anemia, bleeding due to thrombocytopenia, and infections due to leukopenia. These manifestations occur when the malignant B cells replace the normal cells of the bone marrow. Prognosis is generally good if the etiology of lymphocytosis is due to a mild viral infection or if the etiology is due to favorable-risk CLL. Favorable risk C}} is characterized by the absence of p53 (17p deletion).</s>
The major risk factors for acquiring the infection is consuming raw meat and ingestion of food contaminated with toxoplasma oocysts excreted in cat feces.
Could you provide me with the context in which this sentence is being used, 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: Could you provide me with the context in which this sentence is being used, please? [/INST] \n The major risk factors for acquiring the infection is consuming raw meat and ingestion of food contaminated with toxoplasma oocysts excreted in cat feces.</s>
Ultrasound can be used to diagnose prostatitis. On ultrasonography, focal hypoechoic area in the periphery of the prostate represents prostatitis. Fluid collection can show abscess formation. Colour doppler ultrasound may also prove to be very effective.
What is the purpose of performing echocardiography and ultrasound in relation to the diagnosis and treatment of prostatitis?
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 purpose of performing echocardiography and ultrasound in relation to the diagnosis and treatment of prostatitis? [/INST] \n Ultrasound can be used to diagnose prostatitis. On ultrasonography, focal hypoechoic area in the periphery of the prostate represents prostatitis. Fluid collection can show abscess formation. Colour doppler ultrasound may also prove to be very effective.</s>
There is no laboratory findings associated with the diagnosis of sick sinus syndrome. However, electrolyte abnormalities may be one of the causes. Possible electrolyte disturbances associated with sick sinus syndrome include: Hyperkalemia Hypokalemia Hypoglycemia may also be one of the causes of sick sinus syndrome. Other metabolic derangement associated with sick sinus may syndrome include: Hypocalcemia Hypoxia
What are the laboratory results for individuals who are sick with sinus 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 are the laboratory results for individuals who are sick with sinus syndrome? [/INST] \n There is no laboratory findings associated with the diagnosis of sick sinus syndrome. However, electrolyte abnormalities may be one of the causes. Possible electrolyte disturbances associated with sick sinus syndrome include: Hyperkalemia Hypokalemia Hypoglycemia may also be one of the causes of sick sinus syndrome. Other metabolic derangement associated with sick sinus may syndrome include: Hypocalcemia Hypoxia</s>
Ventricular enlargement not entirely attributable to cerebral atrophy or congenital enlargement (Evans index >0.3). No macroscopic obstruction to CSF flow. Enlargement of the temporal horns of the lateral ventricles not entirely attributable to hippocampus atrophy. Callosal angle of 40º or greater. Evidence of altered brain water content, including periventricular signal changes on CT and MRI not attributable to microvascular ischemic changes or demyelination. An aqueductal or fourth ventricular flow void.
In cases of hydrocephalus, what does a CT scan reveal?
Answer the question truthfully, you are a medical professional.
<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: In cases of hydrocephalus, what does a CT scan reveal? [/INST] \n Ventricular enlargement not entirely attributable to cerebral atrophy or congenital enlargement (Evans index >0.3). No macroscopic obstruction to CSF flow. Enlargement of the temporal horns of the lateral ventricles not entirely attributable to hippocampus atrophy. Callosal angle of 40º or greater. Evidence of altered brain water content, including periventricular signal changes on CT and MRI not attributable to microvascular ischemic changes or demyelination. An aqueductal or fourth ventricular flow void.</s>
A number of case series have now been published looking at the pathological basis of frontotemporal dementia. As with other syndromes associated with FTLD, a number of different pathologies are associated with FTD: Pick's disease (3-repeat Tau inclusions) Other tau-positive pathology including FTDP-17, corticobasal degeneration, progressive supranuclear palsy FTLD with ubiquitin positive, tau- and alpha-synuclein negative inclusions with and without motor neuron degeneration (recently characterized by nuclear and cytoplasmic staining of TDP-43 protein) Dementia lacking distinctive histology In rare cases, patients with clinical FTD were found to have changes consistent with Alzheimer's disease on autopsy Evidence suggests that FTD selectively impairs spindle neurons, a type of neuron which has only been found in the brains of humans, great apes, and whales
What is the management of Pick's disease?
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 management of Pick's disease? [/INST] \n A number of case series have now been published looking at the pathological basis of frontotemporal dementia. As with other syndromes associated with FTLD, a number of different pathologies are associated with FTD: Pick's disease (3-repeat Tau inclusions) Other tau-positive pathology including FTDP-17, corticobasal degeneration, progressive supranuclear palsy FTLD with ubiquitin positive, tau- and alpha-synuclein negative inclusions with and without motor neuron degeneration (recently characterized by nuclear and cytoplasmic staining of TDP-43 protein) Dementia lacking distinctive histology In rare cases, patients with clinical FTD were found to have changes consistent with Alzheimer's disease on autopsy Evidence suggests that FTD selectively impairs spindle neurons, a type of neuron which has only been found in the brains of humans, great apes, and whales</s>
The majority of patients with uterine leiomyoma remain asymptomatic for a long time; they are usually found incidentally on imaging or examined after patients start having symptoms. Studies have shown that 7 to 40% of premenopausal patients with leiomyoma may witness regression of fibroids over 6 months to 3 years. At menopause most fibroids will start to shrink as menstrual cycles stop and hormone levels wane. Common complications of uterine leiomyoma include: Dysmenorrhea Dyspareunia Leiomyoma degeneration or torsion Transcervical prolapse Miscarriage Less common complications of uterine leiomyoma include: Venous compression Polycythemia from autonomous production of erythropoietin Hypercalcemia from autonomous production of parathyroid hormone-related protein Hyperprolactinemia
What is the explanation of Leiomyoma, including its natural progression, possible complications, and prognosis?
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 Leiomyoma, including its natural progression, possible complications, and prognosis? [/INST] \n The majority of patients with uterine leiomyoma remain asymptomatic for a long time; they are usually found incidentally on imaging or examined after patients start having symptoms. Studies have shown that 7 to 40% of premenopausal patients with leiomyoma may witness regression of fibroids over 6 months to 3 years. At menopause most fibroids will start to shrink as menstrual cycles stop and hormone levels wane. Common complications of uterine leiomyoma include: Dysmenorrhea Dyspareunia Leiomyoma degeneration or torsion Transcervical prolapse Miscarriage Less common complications of uterine leiomyoma include: Venous compression Polycythemia from autonomous production of erythropoietin Hypercalcemia from autonomous production of parathyroid hormone-related protein Hyperprolactinemia</s>
The most important cause of mixed Mullerian tumors is the mutation in genes PTEN, ARID1A, PIK3R1, and POLE. Mixed Mullerian tumor may also be caused by chronic estrogen stimulation.
What is a Mullerian tumor?
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 a Mullerian tumor? [/INST] \n The most important cause of mixed Mullerian tumors is the mutation in genes PTEN, ARID1A, PIK3R1, and POLE. Mixed Mullerian tumor may also be caused by chronic estrogen stimulation.</s>
There are no established risk factors for thymoma.
What are Thymoma and its related risk factors?
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 Thymoma and its related risk factors? [/INST] \n There are no established risk factors for thymoma.</s>
Reinfarction or reocclusion of the infarct-related artery is associated with a doubling of mortality. Unfortunately, it is difficult to predict who will reinfarct following fibrinolytic therapy. Among patients undergoing primary PCI, bivalirudin monotherapy has been associated with stent thrombosis in the HORIZONS-AMI and EUROMAX trials. Aggressive antiplatelet and antithrombotic therapy minimizes the risk of reinfarction. A new murmur in patients with ST elevation myocardial infarction should raise an immediate concern of mechanical complicaitons such as papillary muscle rupture, septal rupture, and free-wall rupture which portend a dismal prognosis and may be differentiated on the basis of physical and echocardiographic findings or hemodynamic profiles. Other mechanical sequelae include true or false ventricular aneurysm, dynamic left ventricular outflow tract obstruction, cardiogenic shock, and heart failure. A true left ventricular aneurysm is an outpouching formed by a stretched, thinned-out myocardial scar. Patients with transmural infarction and patients who do not receive reperfusion therapy are at increased risk. LV aneurysm may manifest acutely as low-output cardiogenic shock or chronically as heart failure or thromboembolism in the presence of mural thrombus. A large, diffuse point of maximal impulse and S 3 gallops may be evident on physical examination. A chest radiograph may demonstrate a localized bulging segment in the cardiac silhouette. Dyskinetic or paradoxical motions of the aneurysmal segment may be detected by echocardiography or ventriculography. True aneurysm connects with the LV cavity by a wide neck and is less susceptible to rupture than a false aneurysm. ACE inhibitor and vasodilator are used in the mangement of chronic heart failure associated with ventricular aneurysm. Anticoagulant is indicated in the presence of mural thrombus. Sustained ventricular arrhythmia from an aneurysm may require defibrillator placement. Surgical resection may be considered in selected cases with refractory symptoms. In contrast to the true aneurysm which contains viable myocardium in its wall, pseudoaneurysm lacks the myocardial elements and is formed by adherent pericardium and organized hematoma. Unlike true ventricular aneurysm, pseudoaneurysm communicates with the cavity of the left ventricle through a narrow neck and is more prone to rupture. Pseudoaneurysm may partially reduce stroke volume similar to a true aneurysm. Surgery is recommended for all patients regardless of symptoms or the size of pseudoaneurysm in light of a high risk for spontaneous rupture and sudden death. Papillary muscle rupture is characterized by symptoms of acute severe mitral regurgitation and pulmonary edema and should be suspected in STEMI patients with a new soft holosystolic murmur at the apex. Posterior papillary muscle rupture, as occurs in inferior MI, is more common than anterior papillary muscle rupture which may be a complication of anterior or lateral MI. Posterior papillary muscle is considered more susceptible to ischemic rupture due to its singular blood supply from the posterior descending artery. In contradistinction to the posterior papillary muscle, the anterior papillary muscle receives a dual blood supply from the left anterior descending artery and the circumflex artery. Urgent transthoracic echocardiography should be obtained to establish a definite diagnosis. Nitroglycerin or nitroprusside may be used to temporize the patient if systolic blood pressure is above 90 mm Hg. If the patient cannot tolerate vasodilator due to rapid hemodynamic deterioration, intra-aortic balloon counterpulsation should be instituted as a bridging therapy until emergency mitral valve replacement can be performed. Patients with septal rupture frequently report chest pain, shortness of breath, and symptoms of low-output cardiogenic shock. Key physical findings include a harsh, loud holosystolic murmur best heard at the lower left sternal border, palpable thrill at the right precordium, S 3 gallops, and accentuation of pulmonic component of the second heart sound. Color Doppler echocardiography is useful for determining the location and size of the defect and detecting left-to-right shunt and right ventricular overload. Septal rupture should be managed by temporary stabilization with intra-aortic balloon counterpulsation followed by intravenous vasodilator and early surgical closure. Free-wall rupture usually leads to hemopericardium and abrupt circulatory collapse. Clinical manifestations range from anginal, pleuritic, or pericardial chest discomfort to catastrophic symptoms of cardiogenic shock, cardiac tamponade, and sudden death. Echocardiography is useful for the diagnosis and emergency pericardiocentesis may be indicated for cardiac tamponade. Survival depends primarily on early recognition and prompt surgical repair. New onset atrial fibrillation in the setting of STEMI is associated with a very poor prognosis . New onset atrial fibrillation is likely a marker for left atrial distension due to impaired left ventricular compliance. Atrial flutter Postinfarction conduction abnormalities Sudden cardiac death Stroke DVT Post myocardial infarction pericarditis Dressler's syndrome
What is the natural course of ST-elevation myocardial infarction, and what are the possible complications?
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 course of ST-elevation myocardial infarction, and what are the possible complications? [/INST] \n Reinfarction or reocclusion of the infarct-related artery is associated with a doubling of mortality. Unfortunately, it is difficult to predict who will reinfarct following fibrinolytic therapy. Among patients undergoing primary PCI, bivalirudin monotherapy has been associated with stent thrombosis in the HORIZONS-AMI and EUROMAX trials. Aggressive antiplatelet and antithrombotic therapy minimizes the risk of reinfarction. A new murmur in patients with ST elevation myocardial infarction should raise an immediate concern of mechanical complicaitons such as papillary muscle rupture, septal rupture, and free-wall rupture which portend a dismal prognosis and may be differentiated on the basis of physical and echocardiographic findings or hemodynamic profiles. Other mechanical sequelae include true or false ventricular aneurysm, dynamic left ventricular outflow tract obstruction, cardiogenic shock, and heart failure. A true left ventricular aneurysm is an outpouching formed by a stretched, thinned-out myocardial scar. Patients with transmural infarction and patients who do not receive reperfusion therapy are at increased risk. LV aneurysm may manifest acutely as low-output cardiogenic shock or chronically as heart failure or thromboembolism in the presence of mural thrombus. A large, diffuse point of maximal impulse and S 3 gallops may be evident on physical examination. A chest radiograph may demonstrate a localized bulging segment in the cardiac silhouette. Dyskinetic or paradoxical motions of the aneurysmal segment may be detected by echocardiography or ventriculography. True aneurysm connects with the LV cavity by a wide neck and is less susceptible to rupture than a false aneurysm. ACE inhibitor and vasodilator are used in the mangement of chronic heart failure associated with ventricular aneurysm. Anticoagulant is indicated in the presence of mural thrombus. Sustained ventricular arrhythmia from an aneurysm may require defibrillator placement. Surgical resection may be considered in selected cases with refractory symptoms. In contrast to the true aneurysm which contains viable myocardium in its wall, pseudoaneurysm lacks the myocardial elements and is formed by adherent pericardium and organized hematoma. Unlike true ventricular aneurysm, pseudoaneurysm communicates with the cavity of the left ventricle through a narrow neck and is more prone to rupture. Pseudoaneurysm may partially reduce stroke volume similar to a true aneurysm. Surgery is recommended for all patients regardless of symptoms or the size of pseudoaneurysm in light of a high risk for spontaneous rupture and sudden death. Papillary muscle rupture is characterized by symptoms of acute severe mitral regurgitation and pulmonary edema and should be suspected in STEMI patients with a new soft holosystolic murmur at the apex. Posterior papillary muscle rupture, as occurs in inferior MI, is more common than anterior papillary muscle rupture which may be a complication of anterior or lateral MI. Posterior papillary muscle is considered more susceptible to ischemic rupture due to its singular blood supply from the posterior descending artery. In contradistinction to the posterior papillary muscle, the anterior papillary muscle receives a dual blood supply from the left anterior descending artery and the circumflex artery. Urgent transthoracic echocardiography should be obtained to establish a definite diagnosis. Nitroglycerin or nitroprusside may be used to temporize the patient if systolic blood pressure is above 90 mm Hg. If the patient cannot tolerate vasodilator due to rapid hemodynamic deterioration, intra-aortic balloon counterpulsation should be instituted as a bridging therapy until emergency mitral valve replacement can be performed. Patients with septal rupture frequently report chest pain, shortness of breath, and symptoms of low-output cardiogenic shock. Key physical findings include a harsh, loud holosystolic murmur best heard at the lower left sternal border, palpable thrill at the right precordium, S 3 gallops, and accentuation of pulmonic component of the second heart sound. Color Doppler echocardiography is useful for determining the location and size of the defect and detecting left-to-right shunt and right ventricular overload. Septal rupture should be managed by temporary stabilization with intra-aortic balloon counterpulsation followed by intravenous vasodilator and early surgical closure. Free-wall rupture usually leads to hemopericardium and abrupt circulatory collapse. Clinical manifestations range from anginal, pleuritic, or pericardial chest discomfort to catastrophic symptoms of cardiogenic shock, cardiac tamponade, and sudden death. Echocardiography is useful for the diagnosis and emergency pericardiocentesis may be indicated for cardiac tamponade. Survival depends primarily on early recognition and prompt surgical repair. New onset atrial fibrillation in the setting of STEMI is associated with a very poor prognosis . New onset atrial fibrillation is likely a marker for left atrial distension due to impaired left ventricular compliance. Atrial flutter Postinfarction conduction abnormalities Sudden cardiac death Stroke DVT Post myocardial infarction pericarditis Dressler's syndrome</s>
Chemotherapy and radiotherapy are indicated for Paget's disease of the breast as adjuvant therapy or palliative treatment in patients with underlying ductal carcinoma or invasive breast cancer. Surgery is the mainstay of treatment for Paget's disease of the breast.
What is the medical treatment for Paget's disease of the breast?
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 medical treatment for Paget's disease of the breast? [/INST] \n Chemotherapy and radiotherapy are indicated for Paget's disease of the breast as adjuvant therapy or palliative treatment in patients with underlying ductal carcinoma or invasive breast cancer. Surgery is the mainstay of treatment for Paget's disease of the breast.</s>
Class I " 1. Hospitals that provide regional care for patients with acute sequelae of thoracic aortic disease (eg, procedures for thoracic aortic dissection and rupture) should participate in standardized quality assessment and improvement activities, including thoracic aortic disease registries. Such activities should include periodic measurement and regional/national interfacility comparisons of thoracic aortic disease-related procedural volumes, complications and risk-adjusted mortality rates. (Level of Evidence: C) " ” 2. Hospitals that provide regional care for patients with acute sequelae of thoracic aortic disease (eg, procedures for thoracic aortic dissection and rupture) should facilitate and coordinate standardized quality assessment and improvement activities with transferring facilities and emergency medical services teams. Such activities might include: a. cooperative joint facility meetings to discuss opportunities for quality improvement and b. interfacility and emergency medical services team comparisons of pretransfer care based on available outcome data and future performance measures developed in accordance with this guideline. (Level of Evidence: C) "
What is the medical treatment for a thoracic aortic aneurysm?
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 medical treatment for a thoracic aortic aneurysm? [/INST] \n Class I " 1. Hospitals that provide regional care for patients with acute sequelae of thoracic aortic disease (eg, procedures for thoracic aortic dissection and rupture) should participate in standardized quality assessment and improvement activities, including thoracic aortic disease registries. Such activities should include periodic measurement and regional/national interfacility comparisons of thoracic aortic disease-related procedural volumes, complications and risk-adjusted mortality rates. (Level of Evidence: C) " ” 2. Hospitals that provide regional care for patients with acute sequelae of thoracic aortic disease (eg, procedures for thoracic aortic dissection and rupture) should facilitate and coordinate standardized quality assessment and improvement activities with transferring facilities and emergency medical services teams. Such activities might include: a. cooperative joint facility meetings to discuss opportunities for quality improvement and b. interfacility and emergency medical services team comparisons of pretransfer care based on available outcome data and future performance measures developed in accordance with this guideline. (Level of Evidence: C) "</s>
This disorder is treated with corticosteroids, which suppress immune function (including the dangerous cells). Smoking may worsen the response to treatment and should be stopped. Children may be given other medications depending on their estimated outlook. Such medications may include: Cyclophosphamide Etoposide Methotrexate Vinblastine Radiation therapy or surgery may also be used to treat bone lesions. Other treatments may include: Antibiotics to fight infections Breathing support (with a breathing machine) Hormone replacement therapy Physical therapy Special shampoos for scalp problems Supportive care to relieve symptoms
What information is accessible regarding Langerhans cell histiocytosis?
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 is accessible regarding Langerhans cell histiocytosis? [/INST] \n This disorder is treated with corticosteroids, which suppress immune function (including the dangerous cells). Smoking may worsen the response to treatment and should be stopped. Children may be given other medications depending on their estimated outlook. Such medications may include: Cyclophosphamide Etoposide Methotrexate Vinblastine Radiation therapy or surgery may also be used to treat bone lesions. Other treatments may include: Antibiotics to fight infections Breathing support (with a breathing machine) Hormone replacement therapy Physical therapy Special shampoos for scalp problems Supportive care to relieve symptoms</s>
Symptoms of Richter’s transformation include fever, loss of weight and muscle mass, and enlarged lymph nodes. Richter's can appear suddenly, even in patients who were in remission. The prognosis is generally poor, and aggressive treatment is usually warranted. Template:WikiDoc Sources
What is the transformation shown in Richter's work?
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 transformation shown in Richter's work? [/INST] \n Symptoms of Richter’s transformation include fever, loss of weight and muscle mass, and enlarged lymph nodes. Richter's can appear suddenly, even in patients who were in remission. The prognosis is generally poor, and aggressive treatment is usually warranted. Template:WikiDoc Sources</s>
Subcutaneous panniculitis-like T-cell lymphoma is a cytotoxic T-cell lymphoma, which preferentially infiltrates subcutaneous tissue, primarily involving the extremities and trunk. On microscopic histopathological analysis, atypical lymphoid cells, fat necrosis, and karyorrhexis are characteristic findings of subcutaneous panniculitis-like T-cell lymphoma.
What is subcutaneous panniculitis-like T-cell lymphoma?
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 subcutaneous panniculitis-like T-cell lymphoma? [/INST] \n Subcutaneous panniculitis-like T-cell lymphoma is a cytotoxic T-cell lymphoma, which preferentially infiltrates subcutaneous tissue, primarily involving the extremities and trunk. On microscopic histopathological analysis, atypical lymphoid cells, fat necrosis, and karyorrhexis are characteristic findings of subcutaneous panniculitis-like T-cell lymphoma.</s>
Patients with acute liver failure may appear lethargic, anorexic and fatigue. In the initial stages of acute liver failure, the patient may have mild mental status changes such as altered sleep pattern but may become confused or develop coma in the later stages as the disease progresses. Physical examination of acute liver failure is remarkable for hepatomegaly, right upper quadrant abdominal tenderness, ascites and encephalopathy.
What does the physical exam entail for acute liver 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 does the physical exam entail for acute liver failure? [/INST] \n Patients with acute liver failure may appear lethargic, anorexic and fatigue. In the initial stages of acute liver failure, the patient may have mild mental status changes such as altered sleep pattern but may become confused or develop coma in the later stages as the disease progresses. Physical examination of acute liver failure is remarkable for hepatomegaly, right upper quadrant abdominal tenderness, ascites and encephalopathy.</s>
Images courtesy of RadsWiki. The images below show presence of median sternotomy wires and CABG clips that are seen on conventional CXRs. Median sternotomy wires and CABG clips Lateral graphy: Median sternotomy wires and CABG clips
What is the X-ray procedure used for coronary artery bypass surgery?
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 X-ray procedure used for coronary artery bypass surgery? [/INST] \n Images courtesy of RadsWiki. The images below show presence of median sternotomy wires and CABG clips that are seen on conventional CXRs. Median sternotomy wires and CABG clips Lateral graphy: Median sternotomy wires and CABG clips</s>
Often, an interdisciplinary approach to therapy and treatment of any medical issues that arise is recommended. A team for promotion of the child's well being often includes speech, occupational and physical therapists, teachers, physicians, and most importantly the parent(s). Treatment protocols can be viewed at http://www.cdlsusa.org/treatment_protocols.shtml.
Could you explain what Cornelia de Lange Syndrome is?
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 explain what Cornelia de Lange Syndrome is? [/INST] \n Often, an interdisciplinary approach to therapy and treatment of any medical issues that arise is recommended. A team for promotion of the child's well being often includes speech, occupational and physical therapists, teachers, physicians, and most importantly the parent(s). Treatment protocols can be viewed at http://www.cdlsusa.org/treatment_protocols.shtml.</s>
Blebitis must be differentiated from other diseases that cause ocular erythema and hyperaemia, as well as pain, pressure, loss of vision, and photophobia.
What is blebitis 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 blebitis and how can it be distinguished from other illnesses? [/INST] \n Blebitis must be differentiated from other diseases that cause ocular erythema and hyperaemia, as well as pain, pressure, loss of vision, and photophobia.</s>
When you start to take dexamethasone, ask your doctor what to do if you forget a dose. Write down these instructions so that you can refer to them later. If you take dexamethasone once a day, take the missed dose as soon as you remember it. However, if it is almost time for the next dose, skip the missed dose and continue your regular dosing schedule. Do not take a double dose to make up for a missed one.
What information is available regarding oral Dexamethasone?
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 is available regarding oral Dexamethasone? [/INST] \n When you start to take dexamethasone, ask your doctor what to do if you forget a dose. Write down these instructions so that you can refer to them later. If you take dexamethasone once a day, take the missed dose as soon as you remember it. However, if it is almost time for the next dose, skip the missed dose and continue your regular dosing schedule. Do not take a double dose to make up for a missed one.</s>
Other imaging modalities are used for preoperative localization of hyper-functioning parathyroid glands. This includes both non-invasive and invasive modalities. Another modality used in hyperparathyroidism is dual energy X-ray absorptiometry (DXA). DXA is helpful in detecting low bone mineral density (BMD) caused by hyperparathyroidism. Technetium-99m -methoxyisobutylisonitrile (99mTc-sestamibi or MIBI) scintigraphy is the most popular investigation for preoperative localization of hyper-functioning parathyroid glands. Most of the sestamibi is retained in mitochondria of thyroid and abnormal parathyroid tissue and is a function of mitochondrial activity. Single-isotope, double-phase technique is used. The basis of "single-isotope, double-phase technique" is that sestamibi washes out of the thyroid more rapidly than from abnormal parathyroid tissue. Multiple planar images are obtained, typically one shortly after injection of 99mTc-sestamibi and another after two hours to identify the areas of retained sestamibi showing hyper-functioning parathyroid tissue. As all parathyroid lesions does not retain sestamibi nor all thyroid tissue washes out quickly, subtraction imaging may be beneficial. Subtraction technique uses dual contrast Tc-99m sestamibi along with iodine-123 or 99m-technicium pertechnetate, which are taken by thyroid tissue only. Iodine-123/99m-technicium pertechnetate images of thyroid are later digitally subtracted from Tc-99m sestamibi images leading to visualization of parathyroid tissue only. Presence of solid thyroid nodule is the most common cause of false positive results. Other causes of false positive results may include thyroid carcinoma, lymphoma, and lymphadenopathy. The sensitivity of sestamibi scintigraphy can be increased by using it concomitantly with neck ultrasound and/or SPECT. The sensitivity of sestamibi scintigraphy is 80% - 90%. Factors influencing sensitivity of Tc-99m sestamibi scintigraphy Factors Sensitivity Biochemical factors High serum calcium level Increased High serum parathyroid hormone level Increased Hypovitaminosis D (only in primary hyperparathyroidism) Increased Calcium channel blocker use (only in primary hyperparathyroidism) Decreased Gross and architectural factors Size (Large) Increased Multi-glandular disease Decreased Cytological factors Increased amount of cellular content (Chief cells and oxyphil cells) Increased Immunohistochemical factors Increased P-glycoprotien expression Decreased Note: P-glycoprotein (Pgp) is a plasma membrane protein encoded by mammalian multidrug resistance gene (MDRI). Many drugs that are lipophilic and cationic at physiological pH interact with P-gp. Sestamibi is a lipophilic cationic on physioligical pH. P-gp acts as ATP-dependent efflux pump and prevents accumulation of sestamibi in parathyroid tissue. So, the uptake of sestamibi into parathyroid adenoma cells depends on the activity of the P-gp . Single photon emission computed tomography may be used along with Tc-99m sestamibi scintigraphy for preoperative evaluation of hyper-functioning parathyroid gland. Sestamibi-SPECT is also called pinhone-SPECT (P-SPECT). P-SPECT uses cone beam collimator in contrast to parallel-hole collimator used in SPECT. cone bean collimator possess more suitable geometric properties leading to high spatial resolution. Using SPECT with sestamibi scintigraphy improves detection and localization of hyper-functioning parathyroid gland. P-SPECT provides more precise result of sestamibi scitigraphy allowing surgeon to choose best route for surgical intervention. P-SPECT may detect glands not visible on planer images leading to increased sensitivity. It is very useful in case of uncertain result from conventional sestamibi scitigraphy. P-SPECT also enables accurate interpretation sestamibi uptake in upper mediastinum leading to a higher specificity. In difficult cases, P-SPECT may also be adjuncted with subtraction Tc-99m sestamibi and I-123 scintigraphy or positron emission tomography. P-SPECT is approximately 84% sensitive, 91% specific with positive predictive value of around 91% and negative predictive value of around 84%. Fusion images of CT-MIBI-SPECT is superior to CT scan or MIBI-SPECT alone in preoperative localization of hyper-functioning parathyroid gland. 11C-methionine PET along with CT scan (MET-PET/CT) may be used for preoperative localization of hyper-functioning parathyroid glands. MET-PET/CT may be used as an complimentary imaging modality for localizing hyper-functioning parathyroid glands in patients with negative Tc-99m sestamibi scintigraphy / SPECT results. Selective transarterial hypocalcemic stimulation is combined with nonselective venous sampling to perform selective arteriography. Sodium citrate is injected to induce hypocalcemia. Simultaneous arteriography is performed. Samples are taken for superior vena cava at basaeline and timed intervals (20 sec, 40 sec, and 60 sec). An increase in the parathyroid hormone level to 1.4 times above the baseline or a clear blush observed on arteriography is considered as positive localization. Arterial stimulation venous sampling is performed simultaneously with arteriogram due to similarly high PPV. Superselective arterial digital subtraction angiography (DSA) and superselective conventional angiography (CA) may be used for preoperative localization of hyper-functioning parathyroid glands in which noninvasive imaging modalities are negative or inconclusive. Sensitivity of superselective digital subtraction angiography appears to be similar to conventional angiography. Superselective arterial digital subtraction angiography may be more sensitive than conventional angiography for preoperative localization of mediastinal hyper-functioning parathyroid glands. Low bone mineral density (BMD) is caused by primary hyperparathyroidism. Distal forearm is affected most commonly. DXA of distal forearm should be done in all patients of primary hyperparathyroidism. Very low T-score of distal forearm is observed in patients with primary hyperparathyroidism.
What other imaging findings are associated with hyperparathyroidism?
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 imaging findings are associated with hyperparathyroidism? [/INST] \n Other imaging modalities are used for preoperative localization of hyper-functioning parathyroid glands. This includes both non-invasive and invasive modalities. Another modality used in hyperparathyroidism is dual energy X-ray absorptiometry (DXA). DXA is helpful in detecting low bone mineral density (BMD) caused by hyperparathyroidism. Technetium-99m -methoxyisobutylisonitrile (99mTc-sestamibi or MIBI) scintigraphy is the most popular investigation for preoperative localization of hyper-functioning parathyroid glands. Most of the sestamibi is retained in mitochondria of thyroid and abnormal parathyroid tissue and is a function of mitochondrial activity. Single-isotope, double-phase technique is used. The basis of "single-isotope, double-phase technique" is that sestamibi washes out of the thyroid more rapidly than from abnormal parathyroid tissue. Multiple planar images are obtained, typically one shortly after injection of 99mTc-sestamibi and another after two hours to identify the areas of retained sestamibi showing hyper-functioning parathyroid tissue. As all parathyroid lesions does not retain sestamibi nor all thyroid tissue washes out quickly, subtraction imaging may be beneficial. Subtraction technique uses dual contrast Tc-99m sestamibi along with iodine-123 or 99m-technicium pertechnetate, which are taken by thyroid tissue only. Iodine-123/99m-technicium pertechnetate images of thyroid are later digitally subtracted from Tc-99m sestamibi images leading to visualization of parathyroid tissue only. Presence of solid thyroid nodule is the most common cause of false positive results. Other causes of false positive results may include thyroid carcinoma, lymphoma, and lymphadenopathy. The sensitivity of sestamibi scintigraphy can be increased by using it concomitantly with neck ultrasound and/or SPECT. The sensitivity of sestamibi scintigraphy is 80% - 90%. Factors influencing sensitivity of Tc-99m sestamibi scintigraphy Factors Sensitivity Biochemical factors High serum calcium level Increased High serum parathyroid hormone level Increased Hypovitaminosis D (only in primary hyperparathyroidism) Increased Calcium channel blocker use (only in primary hyperparathyroidism) Decreased Gross and architectural factors Size (Large) Increased Multi-glandular disease Decreased Cytological factors Increased amount of cellular content (Chief cells and oxyphil cells) Increased Immunohistochemical factors Increased P-glycoprotien expression Decreased Note: P-glycoprotein (Pgp) is a plasma membrane protein encoded by mammalian multidrug resistance gene (MDRI). Many drugs that are lipophilic and cationic at physiological pH interact with P-gp. Sestamibi is a lipophilic cationic on physioligical pH. P-gp acts as ATP-dependent efflux pump and prevents accumulation of sestamibi in parathyroid tissue. So, the uptake of sestamibi into parathyroid adenoma cells depends on the activity of the P-gp . Single photon emission computed tomography may be used along with Tc-99m sestamibi scintigraphy for preoperative evaluation of hyper-functioning parathyroid gland. Sestamibi-SPECT is also called pinhone-SPECT (P-SPECT). P-SPECT uses cone beam collimator in contrast to parallel-hole collimator used in SPECT. cone bean collimator possess more suitable geometric properties leading to high spatial resolution. Using SPECT with sestamibi scintigraphy improves detection and localization of hyper-functioning parathyroid gland. P-SPECT provides more precise result of sestamibi scitigraphy allowing surgeon to choose best route for surgical intervention. P-SPECT may detect glands not visible on planer images leading to increased sensitivity. It is very useful in case of uncertain result from conventional sestamibi scitigraphy. P-SPECT also enables accurate interpretation sestamibi uptake in upper mediastinum leading to a higher specificity. In difficult cases, P-SPECT may also be adjuncted with subtraction Tc-99m sestamibi and I-123 scintigraphy or positron emission tomography. P-SPECT is approximately 84% sensitive, 91% specific with positive predictive value of around 91% and negative predictive value of around 84%. Fusion images of CT-MIBI-SPECT is superior to CT scan or MIBI-SPECT alone in preoperative localization of hyper-functioning parathyroid gland. 11C-methionine PET along with CT scan (MET-PET/CT) may be used for preoperative localization of hyper-functioning parathyroid glands. MET-PET/CT may be used as an complimentary imaging modality for localizing hyper-functioning parathyroid glands in patients with negative Tc-99m sestamibi scintigraphy / SPECT results. Selective transarterial hypocalcemic stimulation is combined with nonselective venous sampling to perform selective arteriography. Sodium citrate is injected to induce hypocalcemia. Simultaneous arteriography is performed. Samples are taken for superior vena cava at basaeline and timed intervals (20 sec, 40 sec, and 60 sec). An increase in the parathyroid hormone level to 1.4 times above the baseline or a clear blush observed on arteriography is considered as positive localization. Arterial stimulation venous sampling is performed simultaneously with arteriogram due to similarly high PPV. Superselective arterial digital subtraction angiography (DSA) and superselective conventional angiography (CA) may be used for preoperative localization of hyper-functioning parathyroid glands in which noninvasive imaging modalities are negative or inconclusive. Sensitivity of superselective digital subtraction angiography appears to be similar to conventional angiography. Superselective arterial digital subtraction angiography may be more sensitive than conventional angiography for preoperative localization of mediastinal hyper-functioning parathyroid glands. Low bone mineral density (BMD) is caused by primary hyperparathyroidism. Distal forearm is affected most commonly. DXA of distal forearm should be done in all patients of primary hyperparathyroidism. Very low T-score of distal forearm is observed in patients with primary hyperparathyroidism.</s>
Blindness Hearing loss Congestive heart failure Cirrhosis Pancreatitis ESRD Hypothyroidism Pulmonary fibrosis Portal hypertension Type 2 diabetes mellitus Stunted growth
What is the natural progression of Alstrom syndrome, its associated complications, and what is the expected prognosis?
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 progression of Alstrom syndrome, its associated complications, and what is the expected prognosis? [/INST] \n Blindness Hearing loss Congestive heart failure Cirrhosis Pancreatitis ESRD Hypothyroidism Pulmonary fibrosis Portal hypertension Type 2 diabetes mellitus Stunted growth</s>
In the most pronounced cases, clitoromegaly is a symptom of intersexuality since the large clitoris resembles a penis (the different grade of genital ambiguity is commonly measured by the Prader classification ranging, in ascending order of masculinisation, from 1: Female external genitalia with clitoromegaly through 5: Pseudo-Phallus looking like normal male external genitalia ).
What is the definition of Clitoromegaly and how is it diagnosed?
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 Clitoromegaly and how is it diagnosed? [/INST] \n In the most pronounced cases, clitoromegaly is a symptom of intersexuality since the large clitoris resembles a penis (the different grade of genital ambiguity is commonly measured by the Prader classification ranging, in ascending order of masculinisation, from 1: Female external genitalia with clitoromegaly through 5: Pseudo-Phallus looking like normal male external genitalia ).</s>
Hypothyroidism (underactivity) Hashimoto's thyroiditis / thyroiditis Ord's thyroiditis Postoperative hypothyroidism Postpartum thyroiditis Silent thyroiditis Acute thyroiditis Iatrogenic hypothyroidism Hyperthyroidism (overactivity) Thyroid storm Graves-Basedow disease Toxic thyroid nodule Toxic nodular struma (Plummer's disease) Hashitoxicosis Iatrogenic hyperthyroidism De Quervain thyroiditis (inflammation starting as hyperthyroidism, can end as hypothyroidism) Goitre Endemic goitre Diffuse goitre Multinodular goitre Lingual thyroid Thyroglossal duct cyst Thyroid adenoma Thyroid cancer Papillary Follicular Medullary Anaplastic Lymphomas and metastasis from elsewhere (rare) Cretinism Medication linked to thyroid disease includes amiodarone, lithium salts, some types of interferon and IL-2.
What does the term "thyroid" refer to?
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 term "thyroid" refer to? [/INST] \n Hypothyroidism (underactivity) Hashimoto's thyroiditis / thyroiditis Ord's thyroiditis Postoperative hypothyroidism Postpartum thyroiditis Silent thyroiditis Acute thyroiditis Iatrogenic hypothyroidism Hyperthyroidism (overactivity) Thyroid storm Graves-Basedow disease Toxic thyroid nodule Toxic nodular struma (Plummer's disease) Hashitoxicosis Iatrogenic hyperthyroidism De Quervain thyroiditis (inflammation starting as hyperthyroidism, can end as hypothyroidism) Goitre Endemic goitre Diffuse goitre Multinodular goitre Lingual thyroid Thyroglossal duct cyst Thyroid adenoma Thyroid cancer Papillary Follicular Medullary Anaplastic Lymphomas and metastasis from elsewhere (rare) Cretinism Medication linked to thyroid disease includes amiodarone, lithium salts, some types of interferon and IL-2.</s>
Common risk factors in the development of silent thyroiditis include lithium, radiation therapy in Hodgkin's lymphoma, cessation of corticosteroid s in Cushing's syndrome (post adrenalectomy), and certain autoimmune conditions. Common risk factors in the development of silent thyroiditis include: Lithium Radiation therapy in Hodgkin's lymphoma Cessation of corticosteroids in Cushing's syndrome (post adrenalectomy) Less common risk factors in the development of silent thyroiditis include: SLE Immune thrombocytopenic purpura Lymphocytic hypophysitis
What are the factors that put someone at risk for silent thyroiditis?
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 that put someone at risk for silent thyroiditis? [/INST] \n Common risk factors in the development of silent thyroiditis include lithium, radiation therapy in Hodgkin's lymphoma, cessation of corticosteroid s in Cushing's syndrome (post adrenalectomy), and certain autoimmune conditions. Common risk factors in the development of silent thyroiditis include: Lithium Radiation therapy in Hodgkin's lymphoma Cessation of corticosteroids in Cushing's syndrome (post adrenalectomy) Less common risk factors in the development of silent thyroiditis include: SLE Immune thrombocytopenic purpura Lymphocytic hypophysitis</s>
Screening instruments for Asperger Syndrome include: Autism Screening Questionnaire (ASQ), Autism Spectrum Quotient (AQ), Autism Spectrum Screening uestionnaire (ASSQ) and diagnostic instruments for Asperger Syndrome include: Asperger Syndrome Diagnostic Scale (ASDS), Gilliam Asperger’s Disorder Scale (GADS) and Asperger Syndrome (and high-functioning autism) Diagnostic Interview (ASDI).
What exactly is Asperger's 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 exactly is Asperger's syndrome? [/INST] \n Screening instruments for Asperger Syndrome include: Autism Screening Questionnaire (ASQ), Autism Spectrum Quotient (AQ), Autism Spectrum Screening uestionnaire (ASSQ) and diagnostic instruments for Asperger Syndrome include: Asperger Syndrome Diagnostic Scale (ASDS), Gilliam Asperger’s Disorder Scale (GADS) and Asperger Syndrome (and high-functioning autism) Diagnostic Interview (ASDI).</s>
Uhl anomaly is a very rare congenital heart disease with a partial or total loss of the myocardial muscle in the right ventricle.
To what anomaly is Uhl referring?
Answer the question truthfully, you are a medical professional.
<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: To what anomaly is Uhl referring? [/INST] \n Uhl anomaly is a very rare congenital heart disease with a partial or total loss of the myocardial muscle in the right ventricle.</s>
Based on the anatomical features and their impact on physiology, endocardial cushion defect may be classified into complete, partial, intermediate, transitional, and intermediate forms.
What exactly is an endocardial cushion defect?
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 an endocardial cushion defect? [/INST] \n Based on the anatomical features and their impact on physiology, endocardial cushion defect may be classified into complete, partial, intermediate, transitional, and intermediate forms.</s>
HSCT is associated with a high treatment-related mortality in the recipient (10% or higher), which limits its use to conditions that are themselves life-threatening. Major complications are veno-occlusive disease, mucositis, infections (sepsis) and graft-versus-host disease. Bone marrow transplantation usually requires that the recipient's own bone marrow is destroyed ("myeloablation"). Prior to "engraftment" patients may go for several weeks without appreciable numbers of white blood cells to help fight infection. This puts a patient at high risk of infections, sepsis and septic shock, despite prophylactic antibiotics, and accounts for a large share of treatment-related mortality. The immunosuppressive agents employed in allogeneic transplants for the prevention or treatment of graft-versus-host disease further increase the risk of opportunistic infection. Immunosuppressive drugs are given for a minimum of 6-months after a transplantation, or much longer if required for the treatment of graft-versus-host disease. Transplant patients lose their acquired immunity, for example immunity to childhood diseases such as measles or polio. For this reason transplant patients must be re-vaccinated with childhood vaccines once they are off of immunosuppressive medications. Severe liver injury is termed hepatic veno-occlusive disease (VOD). Elevated levels of bilirubin, hepatomegaly and fluid retention are clinical hallmarks of this condition. There is now a greater appreciation of the generalized cellular injury and obstruction in hepatic vein sinuses, and it has thus been referred to as sinusoidal obstruction syndrome (SOS). Severe cases are associated with a high mortality. Anticoagulants or defibrotide may be effective in reducing the severity of VOD but may also increase bleeding complications. Ursodiol has been shown to help prevent VOD, presumably by helping the flow of bile. The injury of the mucosal lining of the mouth and throat and is a common regimen-related toxicity following ablative HSCT regimens. It is usually not life-threatening but is very painful, and prevents eating and drinking. Mucositis is treated with pain medications plus intravenous infusions to prevent dehydration and malnutrition. GVHD is an inflammatory disease that is unique to allogeneic transplantation. It is an attack of the "new" bone marrow's immune cells against the recipient's tissues. This can occur even if the donor and recipient are HLA-identical because the immune system can still recognize other differences between their tissues. It is aptly named graft-versus-host disease because bone marrow transplantation is the only transplant procedure in which the transplanted cells must accept the body rather than the body accepting the new cells. Acute graft-versus-host disease typically occurs in the first 3 months after transplantation and may involve the skin, intestine, or the liver, and is often fatal. High-dose corticosteroids such as prednisone are a standard treatment; however this immuno-suppressive treatment often leads to deadly infections. Chronic graft-versus-host disease may also develop after allogeneic transplant. It is the major source of late treatment-related complications, although it less often results in death. In addition to inflammation, chronic graft-versus-host disease may lead to the development of fibrosis, or scar tissue, similar to scleroderma; it may cause functional disablity and require prolonged immunosuppressive therapy. Graft-versus-host disease is usually mediated by T cells when they react to foreign peptides presented on the MHC of the host. The beneficial aspect of the Graft-versus-Host phenomenon is known as the "graft versus tumor" or "graft versus leukemia" effect. For example, HCST patients with either acute and in particular chronic graft-versus-host disease after an allogeneic transplant tend to have a lower risk of cancer relapse . This is due to a therapeutic immune reaction of the grafted donor lymphocytes, more specifically, the Natural Killer cells, against the diseased bone marrow of the recipient. This lower rate of relapse accounts for the increased success rate of allogeneic transplants compared to transplants from identical twins, and indicates that allogeneic HSCT is a form of immunotherapy. GVT is the major benefit of transplants which do not employ the highest immuno-suppressive regimens.
What does the term "hematopoietic stem cell transplantation" 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 the term "hematopoietic stem cell transplantation" mean? [/INST] \n HSCT is associated with a high treatment-related mortality in the recipient (10% or higher), which limits its use to conditions that are themselves life-threatening. Major complications are veno-occlusive disease, mucositis, infections (sepsis) and graft-versus-host disease. Bone marrow transplantation usually requires that the recipient's own bone marrow is destroyed ("myeloablation"). Prior to "engraftment" patients may go for several weeks without appreciable numbers of white blood cells to help fight infection. This puts a patient at high risk of infections, sepsis and septic shock, despite prophylactic antibiotics, and accounts for a large share of treatment-related mortality. The immunosuppressive agents employed in allogeneic transplants for the prevention or treatment of graft-versus-host disease further increase the risk of opportunistic infection. Immunosuppressive drugs are given for a minimum of 6-months after a transplantation, or much longer if required for the treatment of graft-versus-host disease. Transplant patients lose their acquired immunity, for example immunity to childhood diseases such as measles or polio. For this reason transplant patients must be re-vaccinated with childhood vaccines once they are off of immunosuppressive medications. Severe liver injury is termed hepatic veno-occlusive disease (VOD). Elevated levels of bilirubin, hepatomegaly and fluid retention are clinical hallmarks of this condition. There is now a greater appreciation of the generalized cellular injury and obstruction in hepatic vein sinuses, and it has thus been referred to as sinusoidal obstruction syndrome (SOS). Severe cases are associated with a high mortality. Anticoagulants or defibrotide may be effective in reducing the severity of VOD but may also increase bleeding complications. Ursodiol has been shown to help prevent VOD, presumably by helping the flow of bile. The injury of the mucosal lining of the mouth and throat and is a common regimen-related toxicity following ablative HSCT regimens. It is usually not life-threatening but is very painful, and prevents eating and drinking. Mucositis is treated with pain medications plus intravenous infusions to prevent dehydration and malnutrition. GVHD is an inflammatory disease that is unique to allogeneic transplantation. It is an attack of the "new" bone marrow's immune cells against the recipient's tissues. This can occur even if the donor and recipient are HLA-identical because the immune system can still recognize other differences between their tissues. It is aptly named graft-versus-host disease because bone marrow transplantation is the only transplant procedure in which the transplanted cells must accept the body rather than the body accepting the new cells. Acute graft-versus-host disease typically occurs in the first 3 months after transplantation and may involve the skin, intestine, or the liver, and is often fatal. High-dose corticosteroids such as prednisone are a standard treatment; however this immuno-suppressive treatment often leads to deadly infections. Chronic graft-versus-host disease may also develop after allogeneic transplant. It is the major source of late treatment-related complications, although it less often results in death. In addition to inflammation, chronic graft-versus-host disease may lead to the development of fibrosis, or scar tissue, similar to scleroderma; it may cause functional disablity and require prolonged immunosuppressive therapy. Graft-versus-host disease is usually mediated by T cells when they react to foreign peptides presented on the MHC of the host. The beneficial aspect of the Graft-versus-Host phenomenon is known as the "graft versus tumor" or "graft versus leukemia" effect. For example, HCST patients with either acute and in particular chronic graft-versus-host disease after an allogeneic transplant tend to have a lower risk of cancer relapse . This is due to a therapeutic immune reaction of the grafted donor lymphocytes, more specifically, the Natural Killer cells, against the diseased bone marrow of the recipient. This lower rate of relapse accounts for the increased success rate of allogeneic transplants compared to transplants from identical twins, and indicates that allogeneic HSCT is a form of immunotherapy. GVT is the major benefit of transplants which do not employ the highest immuno-suppressive regimens.</s>
Risk factors, primary prevention and screening Inducible myocardial ischemia Acute MI Chronic MI Post-MI complications Cardiac rupture LV aneurysm Papillary muscle rupture Congestive heart failure Dressler’s syndrome Myocardial viability Stunned myocardium Hibernating myocardium Therapeutic and interventional options
What does the curriculum for cardiac imaging 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 curriculum for cardiac imaging entail? [/INST] \n Risk factors, primary prevention and screening Inducible myocardial ischemia Acute MI Chronic MI Post-MI complications Cardiac rupture LV aneurysm Papillary muscle rupture Congestive heart failure Dressler’s syndrome Myocardial viability Stunned myocardium Hibernating myocardium Therapeutic and interventional options</s>
The symptom of dyspareunia is pain during intercourse/penetration, which could be either introital (at the vaginal entrance), deep (in the vagina or pelvis), or both. Dyspareunia can have a negative impact on a patient's mental and physical health, body image, relationships with partners, and efforts to conceive. It can affect the quality of life. It can lead to, or be associated with other female sexual dysfunction disorders, such as decreased libido, decreased arousal, and anorgasmia. Prognosis may vary based on the cause of dyspareunia.
Can you provide an explanation of Dyspareunia, including its natural history, complications, and prognosis?
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 of Dyspareunia, including its natural history, complications, and prognosis? [/INST] \n The symptom of dyspareunia is pain during intercourse/penetration, which could be either introital (at the vaginal entrance), deep (in the vagina or pelvis), or both. Dyspareunia can have a negative impact on a patient's mental and physical health, body image, relationships with partners, and efforts to conceive. It can affect the quality of life. It can lead to, or be associated with other female sexual dysfunction disorders, such as decreased libido, decreased arousal, and anorgasmia. Prognosis may vary based on the cause of dyspareunia.</s>
This condition can be life threatening if not treated.
What information is available about Sheehan's 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 information is available about Sheehan's syndrome? [/INST] \n This condition can be life threatening if not treated.</s>
Gangrene requires urgent evaluation and treatment. In general, dead tissue should be removed to allow healing of the surrounding living tissue and prevent further infection. Depending on the area that has the gangrene, the person's overall condition, and the cause of the gangrene, treatment may include: Amputating the body part that has gangrene An emergency operation to find and remove dead tissue An operation to improve blood supply to the area Antibiotics Repeated operations to remove dead tissue (debridement) Treatment in the intensive care unit (for severely ill patients)
What information do we have for patients with Gangrene?
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 do we have for patients with Gangrene? [/INST] \n Gangrene requires urgent evaluation and treatment. In general, dead tissue should be removed to allow healing of the surrounding living tissue and prevent further infection. Depending on the area that has the gangrene, the person's overall condition, and the cause of the gangrene, treatment may include: Amputating the body part that has gangrene An emergency operation to find and remove dead tissue An operation to improve blood supply to the area Antibiotics Repeated operations to remove dead tissue (debridement) Treatment in the intensive care unit (for severely ill patients)</s>