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[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does the term \"aortic sinus\" mean?", "role": "user" }, { "content": "The aortic sinus is a section of the ascending aorta that is normally dilated (enlarged or widened) just above the aortic valve.\r\nThere are generally three aortic sinuses, the left, the right and the posterior.\r\nThe left aortic sinus gives rise to the left coronary artery. The right aortic sinus gives rise to the right coronary artery. Usually, no vessels arise from the posterior aortic sinus, which is therefore known as the non-coronary sinus.\r\nShown below is a drawing depicting the aortic sinus anatomy. Note that the aortic sinus has three cusps: the left coronary cusp, the right coronary cusp and the non coronary cusp.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide an overview of spontaneous bacterial peritonitis?", "role": "user" }, { "content": "Spontaneous bacterial peritonitis is a blood-borne infection caused by Enteric organisms in 70% of cases (Mono-microbial origin in 90% of cases). Aerobic gram-negative bacteria like Escherichia coli account for half of the cases. Gram-positive cocci Streptococcus species in 20% cases with enterococcus accounting for 5% of the cases. Staphylococcus aureus and Streptococcus salivarius are less frequent causes. Poly-microbial infection is Iatrogenic (more likely associated with abdominal paracentesis) or intra-abdominal source of infection. The cause of SBP has not been established definitively but is believed to involve hematogenous spread of organisms in a patient with a diseased liver and altered portal circulation resulting in defect in the usual filtration function. In adults, spontaneous bacterial peritonitis occurs most commonly in conjunction with cirrhosis of the liver and portal hypertension (frequently as a result of alcoholism and hepatitis).", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the various phases of chronic myelogenous leukemia?", "role": "user" }, { "content": "Chronic myelogenous leukemia may be classified according to the clinical characteristics and laboratory findings into five phases: chronic phase, accelerated phase, blast crisis, relapsed or recurrent CML and refractory disease. The earliest phase is the chronic phase and generally has the best response to treatment. The accelerated phase is a transitional phase and blastic phase is an aggressive phase that becomes life-threatening. Relapsed CML means that the number of blast cells in the blood and bone marrow increase after remission. Finally, primary refractory disease means the leukemia did not respond to initial treatment.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the natural history, potential complications, and likely outcome of cystic fibrosis?", "role": "user" }, { "content": "Life expectancy of patients with cystic fibrosis has been increased over past decades because of better symptomatic treatment strategies. In patients with cystic fibrosis, obstructive lung disease and other lung complications are currently the primary causes of morbidity and are responsible for 80% of mortality. At present, the survival probability of children is 40-50 years. Women with cystic fibrosis have a shortened life expectancy compared to men. Women also become colonized with certain common CF pathogens earlier and have a lower life expectancy in the setting of respiratory infections.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "According to Fournier, what are the causes of gangrene?", "role": "user" }, { "content": "Fournier gangrene is caused by mixed aerobic and anaerobic organisms which normally exist below the pelvic diaphragm in the perineum and genitalia. Fournier gangrene may be caused by the following organisms: \r\nAerobic organisms\r\nMost common aerobic organisms are: \r\nGroup A streptococcus Escherichia coli Klebsiella pneumoniae Staphylococcus aureus\r\nAnaerobic organisms\r\nMost common anaerobic organisms are:\r\nBacteroides fragilis\r\nStreptococcus Enterococcus Corynebacterium Clostridium Pseudomonas proteus species Candida species Lactobacillus gasseri \r\nLess than quarter of cases of Fournier gangrene are idiopathic.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide a summary or description of Asperger's syndrome?", "role": "user" }, { "content": "It is believed that 20% of Asperger Syndrome patients'grow out’ of their disorder and and do not meet the diagnostic criteria as adults, whereas many other patients improve. Diagnosis of AS is often delayed and sometimes done in adulthood. Social impairment is lifelong. Early diagnosis and intervention in patients with AS may improve adaptation and adjustment of the child. Asperger Syndrome (AS) is associated with several conditions such as attention deficit hyperactivity disorder (ADHD) (most common in pediatric patients) , depression (most common in adolescent and adult patients) and anxiety disorders.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the medical therapy for reperfusion injury?", "role": "user" }, { "content": "Various proposed medical managements studied are:\r\nTherapeutic hypothermia It has been shown in rats that neurons sometimes die completely 24 hours after the blood flow returns . This delayed reaction is the result of the multiple inflammatory immune responses that occur during reperfusion. Such inflammatory reactions cause increase in ntracranial pressure, a pressure that leads to cell damage and cell death in some cases. Hypothermia has been shown to help reduce intracranial pressure and thus decrease the adverse effects of inflammatory immune responses during reperfusion. Besides that, reperfusion also increases free radical development. Hypothermia has also been shown to decrease the patient's development of deadly free radicals during reperfusion.\r\nHydrogen sulfide treatment There are several preliminary studies in mice that seem to show that treatment with hydrogen sulfide (H2S) could have a protective effect against reperfusion injury. \r\nCyclosporine In addition to its well-known immunosuppressive capabilities, the one-time administration of cyclosporine at the time of percutaneous coronary intervention (PCI) has been found to deliver a 40 percent reduction in infarct size in a small group proof of concept study of human patients with reperfusion injury published in The New England Journal of Medicine in 2008. Cyclosporine works by inhibiting the action of Cyclophilin D which usually helps in opening Mitochondrial membrane transport protein (MPT Pore). So once cyclophilin D action is inhibited, there is no more MPT pore opening and in turn, saves the mitochondria from getting damaged. The opening of MTP Pore results in major cell destruction by causing the influx of water into mitochondria, impairing its function and ultimately leading to the collapse. The strategy to protect mitochondria is the most important thing associated with the treatment part.\r\nTRO40303 TRO40303 is a new cardio protective compound that was shown to inhibit the MP T pore and reduce infarct size after ischemia - reperfusion .\r\nIschemic Conditioning Flow chart- Ischemic Conditioning Mechanism- Role of ischemic conditioning in preventing and minimizing the damage associated with Reperfusion injury. Stem cell therapy Recent investigations suggest a possible beneficial effect of mesenchymal stem cells on heart and kidney reperfusion injury \r\nSuperoxide dismutase Superoxide dismutase is an important antioxidant enzyme that transforms superoxide anions into water and hydrogen peroxide. Recent work has demonstrated important therapeutic effects on pre-clinical models of reperfusion damage following an ischemic stroke \r\nMetformin Some studies proved the role of metformin in preventing Ischemia-Reperfusion injury by inhibiting the opening of MPT Pore and Mitochondrial complex inhibition. Although the studies are done in rats only still the correlation can be derived clinically for humans as well. \r\nCannabinoids A synthetic analog of cannabis helps to prevent hepatic ischemia and injury by reducing the inflammation and oxidative stress occurring through CB2 receptors . This in turn lowers the tissue damage and provides protective effects. The various synthetic analogs of phytocannabinoid that play major role are: THCV- Tetrahydrocannabivarin 8- Tetrahydrocannabivarin 11-OH-8-THCV", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What other imaging findings are associated with Hepatocellular Carcinoma?", "role": "user" }, { "content": "Hepatic angiography maybe helpful in the diagnosis of hepatocellular carcinoma, findings suggestive of hepatocellular carcinoma include: Hepatic angiography, which demonstrates: Early opacification of portal vein and/or hepatic vein branches Thread and streak signs Filling defects in the portal / hepatic venous system Portal vein tumor thrombus Obliterations of common hepatic artery", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the underlying cause of interstitial nephritis?", "role": "user" }, { "content": "70 to 75 percent (with antibiotics responsible for 30 to 49 percent of these cases) \r\nAny drug has the potentiality to cause AIN, among case reports of many drugs causing AIN, but only a few have been reported with biopsy-proven AIN. The most common proven drugs cause of AIN includes: \r\nNonsteroidal anti-inflammatory agents (NSAIDs)\r\nPenicillins and cephalosporins Antimicrobial sulfonamides, including trimethoprim-sulfamethoxazole Rifampin Diuretics, including loop diuretics such as furosemide and bumetanide, and Thiazide-type diuretics Ciprofloxacin and, perhaps to a lesser degree other quinolones Cimetidine Allopurinol Proton pump inhibitors such as omeprazole and lansoprazole Indinavir 5-aminosalicylates (eg, mesalamine)\r\nMultiple organisms may cause TIN including bacterial viral fungal parasitic infections. \r\nLegionella, Leptospira, Streptococcus, Mycobacterium tuberculosis, Corynebacterium diphtheriae Yersinia, Enterococcus Escherichia coli\r\nCytomegalovirus (CMV) Epstein-Barr virus (EBV), Aolyomavirus, Adenovirus, Candida\r\nLeishmania Toxoplasma\r\nSarcoidosis\r\nSLE,\r\nSjögren's syndrome\r\nLess common causes of TIN include:\r\nHeavy metals (eg, lead, cadmium, mercury) Obstructive uropathy, nephrolithiasis, reflux disease Neoplasia (eg, myeloma, leukemia, amyloidosis) Metabolic diseases (eg, hypercalcemia, cystinosis, potassium depletion, hyperoxaluria)\r\nAcetaminophen Acyclovir Adenovirus Aldomet Allopurinol Alpha-interferon Alport syndrome Amlodipine Ampicillin Anitrim Anti-tubular basement membrane antibodies Apo-sulfatrim Aristolochia Aspirin Azathioprine Bactelan Bardet-biedl syndrome Batrizol Brucella Bumetanide Candida Captopril Carbamazepine Cefaclor Cefotaxime sodium Cefoxitin sodium Cephalosporin Chlamydia Chlorthalidone Cimetidine Ciprofloxacin Clofibrate Cocaine Coccidioidomycosis Corynebacterium diphtheriae Cox-2 inhibitors Creatine Cytomegalovirus Dabrafenib mesylate Diazepam Diclofenac Diflunisal Diltiazem Diphenylhydantoin Diphtheria Diuretics Doxycycline Ectaprim Enterobacticel Enterococcus Epstein-barr virus Erythromycin Escherichia coli Esteprim Ethambutol Famotidine Fenoprofen Flurbiprofen Francisella Furosemide Granulomatosis with polyangiitis Griseofulvin Hantaan virus Histoplasmosis Hiv infection Hydralazine Hydrochlorothiazide Hypercalcemia Hyperkalaemic distal renal tubular acidosis Hyperuricemia Hypokalemia Ibuprofen Igg4-related disease Indinavir Indomethacin Inflammatory bowel disease Isobac Isoniazid Kawasaki's disease Kelfiprim Ketoprofen Lansoprazole Legionellosis Leishmaniasis Leptospirosis Macrolides Mesalamine Mesalazine Methicillin Metoxiprim Minocycline hydrochloride Mycobacterium tuberculosis Mycoplasma infection Myeloma Naproxen Novo-trimel Nu-cotrimox Olsalazine Omeprazole Oxacillin Oxaprozin Oxytetracycline Pegylated interferon alfa-2b Penicillin Phenindione Phenobarbital Phenteramine Phenylpropanolamine Phenytoin Piperacillin/tazobactam Piroxicam Polymyxin Polyomavirus Pranlukast Propylthioruacil Pro-trin Quinine Rabeprazole Ranitidine Reflux nephropathy Renal failure Rickettsia infection Rifampin Roubac Rubeola infection Sarcoidosis Sensenbrenner syndrome Sicca syndrome Sickle cell disease Sjogren syndrome Streptococcal infection Streptomycin Sulfatrim ds Sulfinpyrazone Sulfonamide Sulfoxaprim Sulindac Syphilis Syraprim Systemic lupus erythematosus Tenofovir disoproxil fumarate Tetracycline Thiazide diuretics Tolmetin Toxoplasmosis Treponema Triamterene Trimesuxol Trimethoprim-sulfamethoxazole Trimetoger Trimetox Trimzol Trisulfa Trisulfam Tubulointerstitial nephritis Uroplus ds Uroplus ss Uveitis Vancomycin Wegener's granulomatosis Yersinia", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the X-ray for Lutembacher's syndrome?", "role": "user" }, { "content": "Chest X-ray findings on an anteroposterior view may include:", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide a summary of Lassa fever?", "role": "user" }, { "content": "Lassa fever is endemic in West Africa and is rare in developed countries. The annual incidence of Lassa virus is 100,000-300,000 individuals with a case fatality rate typically reaching 1-5% but may be as high as 65% during outbreaks. There is no predilection to specific age groups, gender, or race. However, young age and pregnancy are associated with increased risk of Lassa fever-associated", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the cause of large cell carcinoma in the lung?", "role": "user" }, { "content": "Less common causes of large cell carcinoma of the lung, include: \r\nInorganic arsenic exposure Chromium, nickel exposure Vinyl chloride exposure Radon exposure Halogen ether exposure", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the causes and symptoms of jaundice in newborns?", "role": "user" }, { "content": "Family and maternal history is important for diagnosing neonatal jaundice and the management approach. For the family history, the following should be evaluated: History of previous sibling developed neonatal jaundice Family history of jaundice Family history of anemia or hereditary hemolytic disorders Family members with liver disease\r\nFor the maternal history, the following should be evaluated: The history of pregnancy and delivery Any maternal complications or illness during the pregnancy Breastfeeding history Usage of any drugs", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the potential complications associated with bleeding and transfusion in patients who have unstable angina and non-ST elevation myocardial infarction?", "role": "user" }, { "content": "5-10% of NSTEMI patients receive blood transfusions. \r\nThe appropriate use of blood transfusion administration is highly subjective due to lack of definitive data on transfusion triggers in patients with CAD. However, there is an association between transfusion and short-term mortality among NSTEMI patients.\r\nYang and colleagues analyzed data from 74,271 NSTEMI / unstable angina patients and found a significant association between blood transfusion and in-hospital mortality. Wu and colleagues analyzed 78,974 elderly patients with acute MI and associated the reception of blood transfusion with a significant increased risk of 30-day death when baseline hematocrit was > 33%. Rao and colleagues examined 24,111 NSTEMI patients and found that blood transfusion was associated with a significantly higher risk of 30-day mortality if the nadir hematocrit was > 24%. \r\nGiven this equipoise, it seems reasonable to conclude that routine use of transfusion to maintain arbitrary hemoglobin levels in asymptomatic patients should be avoided.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What factors increase the risk of developing tumor lysis syndrome?", "role": "user" }, { "content": "The followings are risk factors for developing tumor lysis syndrome after initiating chemotherapy: \r\nCommon risk factors in the development of tumor lysis syndrome include: acute lymphoblastic leukemia Non-Hodgkin lymphoma Burkitts lymphoma Older age Dehydration Non-steroidal anti-inflammatory drugs Angiotensin converting enzyme inhibitors angiotensin receptor blockers\r\nLess common risk factors in the development of TLS include: Multiple myeloma Melanoma Breast cancer Ovarian cancer Hepatocellular carcinoma Lung cancer Sarcomas", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the syndrome of cholesterol emboli?", "role": "user" }, { "content": "Cholesterol embolism (often cholesterol crystal embolism or atheroembolism, sometimes blue toe or purple toe syndrome or trash foot) occurs when cholesterol is released, usually from an atherosclerotic plaque, and travels along with the bloodsteam (embolism) to other places in the body, where it obstructs blood vessels. Most commonly this causes skin symptoms (usually livedo reticularis), gangrene of the extremities and sometimes renal failure; problems with other organs may arise, depending on the site at which the cholesterol crystals enter the bloodstream. When the kidneys are involved, the disease is referred to as atheroembolic renal disease (AERD). The diagnosis usually involves biopsy (removing a tissue sample) from an affected organ. Cholesterol embolism is treated by removing the cause and with supportive therapy; statin drugs have been found to improve the prognosis. CES is underdiagnosed and may mimic other diseases.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the natural occurrences or progression, potential complications, and prognosis associated with jaundice?", "role": "user" }, { "content": "The prognosis for individuals with jaundice varies with the underlying cause of the condition. There are certain conditions that has the most favorable prognosis leading to full recovery. However, more serious causes of jaundice like acute suppurative cholangitis or fulminant hepatic failure can sometimes be fatal despite medical or surgical intervention. The mortality can be as high as 80%. The development and severity of complications as well as patient's underlying health and comorbidities have a huge impact on the prognosis of patients.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does Loeffler's Endocarditis refer to?", "role": "user" }, { "content": "The diagnosis of Loeffler endocarditis should be considered in individuals exhibiting signs and symptoms of poor heart contractility and/or valve disease in the presence of significant increases in blood eosinophil counts. Ancillary tests may help in the diagnosis. However, the only definitive test for Loeffler endocarditis is cardiac muscle biopsy showing the presence of eosinophilic infiltrates.\r\nThe definite diagnosis of Loeffler endocarditis is based on cardiac muscle biopsy, showing the presence of eosinophilic infiltrates and sometimes fibrosis. Since the disorder may be patchy, multiple tissue samples taken during the procedure improve the chances of uncovering the pathology but in any case negative results do not exclude the diagnosis.\r\nThe most common symptoms of Loeffler endocarditis include weight loss, fever, cough, a rash (possibly pruritic) and symptoms of congestive heart failure.\r\nCommon physical examination findings of Loeffler endocarditis include peripheral oedema, elevated jugular venous pressure, tachycardia, murmur of mitral regurgitation, S3 gallop and possibly S4 sound. (physical findings of heart failure)\r\nPalpable apex beat and mitral regurgitation help to differentiate restrictive cardiomyopathy may be very similar to those of constrictive pericarditis.\r\nHypereosinophilia (i.e. blood eosinophil counts at or above 1,500 per microliter) or, less commonly, eosinophilia (counts above 500 but below 1,500 per microliter) are found in the vast majority of cases and are valuable clues pointing to this rather than other types of cardiomyopathies. However, elevated blood eosinophil counts may not occur during the early phase of the disorder. Other, less specific laboratory findings implicate a cardiac disorder but not necessarily eosinophilic myocarditis. These include elevations in blood markers for systemic inflammation (e.g. C reactive protein, erythrocyte sedimentation rate) and cardiac injury (e.g. c reatine kinase, troponin s); Laboratory findings consistent with the diagnosis of Loeffler endocarditis include marked eosinophilia - at least 0.44 x 109/l.\r\nAn ECG may be helpful in the diagnosis of Loeffler endocarditis. Findings on an ECG suggestive of/diagnostic of Loeffler endocarditis include ST segment -T wave abnormalities, and sometimes evidences of atrial enlargement.\r\nAn x-ray may be helpful in the diagnosis of Loeffler endocarditis. Findings on an x-ray suggestive of Loeffler endocarditis include cardiomegaly and presentation of heart failure and pulmonary edema. Nevertheless, these findings are neither specific nor sensitive for the diagnosis of Loeffler endocarditis.\r\nEchocardiography may be helpful in the diagnosis of Loeffler endocarditis. Findings on an echocardiography suggestive of/diagnostic of Loeffler endocarditis include restrictive filling but pretty good left ventricular systolic function. Echocardiography typically gives non-specific and only occasional findings of endocardium thickening, left ventricul ar hypertrophy, left ventricle dilation, and involvement of the mitral and/or tricuspid valve s. Three‐dimensional transthoracic and transesophageal echocardiography might provide additional information to conventional two‐dimensional transthoracic echocardiography alone in patients with Loeffler endocarditis. \r\nImproved detection is imparted by the use of a multi-modality investigation, including the use of transesophageal echocardiography and contrast agents.\r\nA standard transthoracic echocardiogram will typically reveal the following features, which are characteristic of the restrictive cardiomyopathies:\r\nNormal left ventricular systolic function Normal LV cavity dimensions Diastolic dysfunction Majority of cases advanced dysfunction, typically grade III, formerly known as the \"restrictive filling\" profile Early, incidentally detected cases may have lesser degrees of dysfunction Pulsed wave doppler (mitral inflow) and tissue doppler (mitral annuli) demonstrate: An E/A ratio > 2 A deceleration time (DT) < 160 ms A septal e' < 8 cm/s An LVEDP (septal E/e') > 15\r\nFeatures which are specific to the hypereosinophilic syndrome include:\r\nLeft ventricular apical obliteration by laminar thrombosis Diffuse and echogenic thrombus Occurs in the absence of regional wall motion abnormalities The key distinction from the far more common apical thrombosis due to e.g. ischemic heart disease and subsequent apical dyskinesis Thickening and increased echogenicity of subendocardial structures Preferential involvement of the left ventricular posterobasal (inferolateral) wall and posterior leaflet of mitral valve Consequent restricted excursion of mitral valve's posterior leaflet Eccentric mitral regurgitation\r\nAlthough multimodality imaging is recommended in diagnosis and management of Loeffler endocarditis, but CT scan is barely used a an imaging modality. \r\nMRI and echocardiography were used extensively in diagnosis and management of these cases.\r\nCardiac MRI may be helpful in the diagnosis of Loeffler endocarditis. Gadolinium -based cardiac magnetic resonance imaging is the most useful non-invasive procedure for diagnosing eosinophilic myocarditis. Findings on MRI suggestive of/diagnostic of Loeffler endocarditis include at least two of the following abnormalities: An increased signal in T2-weighted images; An increased global myocardial early enhancement ratio between a myocardial and skeletal muscle in enhanced T1 images and One or more focal enhancements distributed in a non-vascular pattern in late enhanced T1-weighted image s. Additionally, and unlike in other forms of myocarditis, eosinophilic myocarditis may also show enhanced gadolinium uptake in the sub-endocardium. Multiparametric cardiac magnetic resonance imaging (CMR) \r\nMultiparametric CMR can not only diagnose Loeffler endocarditis but also reveal the patchy disease state. which could be helpful in prognosis assessment. Furthermore, Multiparametric CMR can also be used for treatment monitoring. and follow up. Compared to echocardiography, cardiac MRI allows multiple scanning planes with excellent spatial resolution and the possibility of tissue characterization.\r\nThere are no other imaging findings associated with Loeffler endocarditis.\r\nThere are no other diagnostic studies associated with Loeffler endocarditis.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the significance of CT scans in detecting Angiomyolipoma?", "role": "user" }, { "content": "Abdominal CT scan may be diagnostic for angiomyolipoma. On CT scan, angiomyolipoma is characterized by: \r\nSmooth tumor margin with low intratumoral fat component Homogenous enhancement on both corticomedullary and excretory phase scans Negative attenuation on unenhanced CT scan Rarely calcification may be present\r\nCT images demonstrate a large kidney angiomyolipoma\r\nCT: Angiomyolipoma. CT: Angiomyolipoma. CT: Angiomyolipoma. CT: Angiomyolipoma. CT: Angiomyolipoma.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does an EKG with 80 leads measure or detect?", "role": "user" }, { "content": "One 80 lead system, the PRIME ECG ® system, is currently approved for use in the US under a 510k.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the factors that lead to the development of cellulitis?", "role": "user" }, { "content": "Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.\r\nGroup A streptococcus Staphylococcus \r\nLess common causes of cellulitis include:\r\nGram-negative aerobic bacilli \r\nAcute bacterial dermohypodermatitis Adenitis Aeromonas hydrophila Animal bite Belimumab Beta-hemolytic streptococci Breast implant infections Candida albicans Capnocytophaga canimorsus Chediak-Higashi syndrome Chronic liver disease Chronic venous insufficiency Cirrhosis Citrobacter Clostridium Clostridium perfringens Coronary artery bypass graft surgery Corticosteroids Cryptococcus neoformans Deep neck space infections Dermatitis Diabetes mellitus Eikenella corrodens Enterobacter Eosinophilic cellulitis Erysipelas Erysipelothrix rhusiopathiae Fusarium Group A streptococcus Haemophilus influenzae Helicobacter cinaedi Herpes simplex Hidradenitis suppurativa HIV Insect bites and stings Ludwig's angina Luliconazole Lymphatic obstruction Lymphedema Mastectomy Mastitis Meningococcus MRSA Mucormycosis Nephrotic syndrome Nocardiosis Non-necrotising cellulitis Orbital cellulitis Oritavancin Panitumumab Paronychia Pasteurella Pasteurella multocida Pelvic lymph node dissection Pergolide Periorbital cellulitis Peripheral vascular disease Peritonsillar abscess Pneumococcus Pseudomonas aeruginosa Quinsy Radiation therapy Radical neck surgery Romidepsin Saphenous vein stripping Serratia Staphylococcus aureus Stasis dermatitis Streptobacillus moniliformis Streptococcus Streptococcus agalactiae Streptococcus iniae Streptococcus pneumoniae Submandibular cellulitis Substance abuse Systemic inflammatory response syndrome Systemic lupus erythematosus Tattoo Tiagabine Trauma Varicella Venectomy Vibrio vulnificus Wells syndrome WHIM syndrome\r\nThe causative pathogen of cellulitis varies with the anatomical location and the patient’s medical and exposure history.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the meaning of the term \"glabrous\" when referring to the skin?", "role": "user" }, { "content": "Tinea corporis is a mycosis that targets glaborous skin.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the explanation of Sulfonylurea in chemistry?", "role": "user" }, { "content": "All sulfonylureas have a central phenyl ring with two branching chains", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide an overview of aortic stenosis?", "role": "user" }, { "content": "The main symptoms of aortic stenosis include angina, syncope and congestive heart failure. Left untreated, the average survival is 5 years after the onset of angina, 3 years after the onset of syncope, and 1 year after the onset of congestive heart failure. Other symptoms include dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea.\r\nAortic stenosis is most often diagnosed when it is asymptomatic and can sometimes be detected during routine examination of the heart and circulatory system. The major signs include pulsus parvus et tardus (a slow-rising, small volume carotid pulse), a lag time between apical and carotid impulses, and a distinct systolic ejection murmur.\r\nThe electrocardiogram in the patient with moderate to severe aortic stenosis may reveal left ventricular hypertrophy and heart block.\r\nExercise testing should not be performed in symptomatic patients with AS but can be used to elicit exercise-induced symptoms and abnormal blood pressure responses in asymptomatic patients. \r\nChest X-ray may be used as a diagnostic tool in the evaluation of aortic stenosis. Findings associated with aortic stenosis include left ventricular hypertrophy and calcification of the aortic valve.\r\nComputed tomography can be helpful as a diagnostic tool in conditions where the echocardiographic findings are inconclusive.\r\nMagnetic resonance imaging is rarely used in the diagnosis of aortic stenosis, except in rare cases where the echocardiographic findings are inconclusive. There is a signal void where the high velocity jet exits the aortic valve.\r\nEchocardiography is the best non-invasive test to evaluate the aortic valve anatomy and function. It is indicated in the case of presence of symptoms suggestive of valvular problems or in the case of detection of a systolic murmur with a grade greater than 3/6. Doppler echocardiography allows the measurement of the maximum jet velocity and can be used to estimate the effective orifice area of the aortic valve as well as the gradient across the aortic valve using the modified Bernoulli equation (gradient = 4 x velocity 2). The flow must be constant, so as the velocity increases, the valve area decreases proportionally. Attention to technical details is important as they may lead to underestimation of the severity of the aortic stenosis. Echocardiography can also be used to assess the severity of left ventricular hypertrophy.\r\nLeft and right heart catheterization as well as angiography may be useful in the assessment of the patient prior to aortic valve replacement surgery. In addition, asymptomatic patients with aortic stenosis should undergo cardiac catherization when echocardiographic findings are inconsistent with the clinical findings .\r\nThe aortic valve area is the size of the orifice for blood to flow from the left ventricle to the aorta. The aortic valve area is reduced in aortic stenosis, and the aortic valve area is the metric that is used to gauge the need for aortic valve replacement surgery. The pressure gradient across a narrowed aortic valve cannot be used to gauge the need for valve replacement as the gradient may be low in patients with impaired left ventricular function.\r\nThe calculation of the aortic valve area is an indirect method used to determine the area of the aortic valve. The calculated aortic valve orifice area is currently one of the measures for evaluating the severity of aortic stenosis. An aortic valve having an area less than 0.8 cm² is considered to be severe aortic stenosis. \r\nThere are many ways to calculate the aortic valve area. The most commonly used methods involve measurements taken during echocardiography. For interpretation of these values, the aortic valve area is generally divided by the body surface area.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the historical context surrounding acute promyelocytic leukemia?", "role": "user" }, { "content": "In 1882, A.C. Doyle reported on the efficacy of arsenic in acute promyelocytic leukemia. In 1957, Leif Hillestad described acute promyelocytic leukemia as a distinct clinical condition for the first time. He noted the syndrome of low fibrinogen levels, fibrin degradation, and life-threatening hemorrhage. It was noted that this condition carried a high mortality rate due to severe hemorrhage. In 1970, scientists in Harbin showed that arsenic trioxide and mercury chloride could treat acute and chronic leukemia. In 1973, Bernard and colleagues showed in clinical studies that therapeutic efficacy of daunorubicin, an chemotherapy agent of the anthracycline class. This medication was shown to induce remission in the majority of patients, with an increase in remission rate from 13% to 58%. The median duration of remission with daunorubicin was more than 2 years. Compared to 6-mercaptopurine, daunorubicin was shown to reduce mortality from bleeding after 5 days. In the early 1990s, it was noted that arsenic trioxide could induce remission in a high proportion of patients. In 1980, Breitman and colleagues showed that all- trans retinoic acid could lead to the differentiation of the HL-60 cell line of myeloid leukemia. This was the first demonstration that differentiation therapy could treat leukemia. This concept was based on the fact that most cancers are primitive and stem-like, which leads to aggressive and chemo -resistant cellular behavior. Blockade of stemness and induction of differentiation could lead to anti-cancer effect. In 1988, Huang and colleagues showed that all- trans retinoic acid could successfully treat acute promyelocytic leukemia in 24 patients. The complete remission rate was more tan 90%. In 1995, D. Head and colleagues showed that higher remission rates and higher survival rates could be achieved with higher doses of daunorubicin, with a survival rate of 61% after 9 years and a 0% relapse after 36 months. In 1997, scientists in Harbin and Shanghai showed that single-agent arsenic trioxide could induce response rates of 90% in patients who relapsed after receiving all- trans retinoic acid and chemotherapy. In 2000, the United States Food and Drug Administration approved arsenic trioxide for treatment of acute promyelocytic leukemia. In 2001, Soignet and colleagues showed that a single, 5-week course of arsenic trioxide carried a complete remission rate of 50%. It was shown that 2 cycles of arsenic trioxide could induce remission in 86% of patients. In 2013, LoCoco and colleagues showed that, in a randomized phase 3 multi-center clinical trial, a non- chemotherapy -based regimen was superior to a chemotherapy-based regimen for low-risk acute promyelocytic leukemia. Specifically, the combination of all-''trans'' retinoic acid and arsenic trioxide resulted in improved overall survival compared to the combination of all- trans retinoic acid plus chemotherapy. This landmark clinical trial, which was conducted by the Italian and German-Austrian Leukemia Study Groups, altered the treatment paradigm for low-risk acute promyelocytic leukemia.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide a summary of LQT1?", "role": "user" }, { "content": "LQT1 is the most common subtype of long QT syndrome making up to 55% of all cases of long QT syndrome. It often presents as a cardiac event that occurs after exercise, and especially during underwater exercise such as swimming or diving. Homozygous recessive mutations in the gene for LQT1 appear to cause the Jervell and Lange-Nielsen syndrome which is characterized clinically by LQTS and sensorineural deafness. Romano-Ward syndrome is an autosomal dominant form of LQTS that is not associated with deafness. Events before the age of 10 years old only occur in the LQT1 subtype of LQTS. Patients with LQT1 paradoxically show a prolongation in the QT segment on EKG after an infusion of epinephrine, which is also used to unmask latent carriers. LQT1 patients are most likely to have the greatest positive response to therapy with beta blockers when compared with the other LQTS subtypes. The mutation occurs on the short arm of chromosome 11.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does the term \"cotton fever\" mean?", "role": "user" }, { "content": "Cotton fever is a syndrome that is often associated with intravenous drug use, specifically the use of cotton to filter drugs like heroin. The cause of the condition is believed to be endotoxin shed by the bacteria Enterobacter agglomerans which colonizes cotton plants. A condition very similar to cotton fever was described in the 18th century among cotton-mill workers. The term cotton fever was coined in 1975 after the syndrome was recognized in intravenous drug users.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the natural history, prognosis and potential complications of glycogen-related type I storage disease?", "role": "user" }, { "content": "If left untreated, patients with GSD I develops complications and dies in infancy or childhood of overwhelming hypoglycemia and acidosis. Surviving individuals have stunted physical growth and delayed puberty due to chronically low insulin levels. Mental retardation as a result of severe and recurrent hypoglycemia is considered preventable with appropriate treatment.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What role does MRI play in detecting cellulitis?", "role": "user" }, { "content": "Soft tissue involvement is seen in cases of untreated or in rapidly spreading progressing cellulitis. MRI can be of great value in such cases. A T2-weighted image may demonstrate hyperintensity and soft tissue thickening whilst T1 may show hypointensity and postcontrast enhancement. CT scans can be helpful in demonstrating involvement of subcutaneous fat and abcess formation.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the importance of performing a physical examination to diagnose sarcomatoid carcinoma of the lung?", "role": "user" }, { "content": "The following physical examination findings may be present among patients with non-small cell lung cancer: \r\nPhysical examination findings of sarcomatoid carcinoma of the lung can be completely normal during the early stage of malignancy. Patient may present with following findings in later stage of malignancy:\r\nWell-appearing Older age in relation to chronological age Lethargic Confused\r\nLow-grade fever Decreased oxygen saturation at room air Tachypnea Tachycardia\r\nLymphadenopathy\r\nPallor Acanthosis nigricans\r\nSlurred speech Confusion\r\nAuscultation\r\nPresent pleural friction rub Present egophony Crackling or bubbling noises Present whispered pectoriloquy Decreased/absent breath sounds\r\nPercussion\r\nHyporesonance Dull percussion Tactile fremitus Reduced chest expansion\r\nHepatomegaly\r\nBack examination of patients with sarcomatoid carcinoma of the lung is usually normal.\r\nGenitourinary examination of patients with sarcomatoid carcinoma of the lung is usually normal.\r\nPalpable soft-tissue mass\r\nClubbing of fingers Swelling of hands and feet Weakness", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What other diagnostic studies are available for pneumoconiosis?", "role": "user" }, { "content": "Pulmonary function tests, bronchoscopy, and lung biopsies may be helpful in the diagnosis of pneumoconiosis.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the definition of anoxic brain injury and how can it be identified through the use of MRI?", "role": "user" }, { "content": "DWI DWI DWI DWI FLAIR FLAIR T1 with GAD", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Is it possible to diagnose hypogonadism using an MRI?", "role": "user" }, { "content": "MRI may be used in cases of hypogonadism to examine pituitary gland for any pituitary or hypothalamic tumors causing the disease. However, the chance of finding pituitary and hypothalamic tumors in hypogonadism patients is very low. Brain MRI is helpful if the patient present with the following features: Visual disorders Neurological manifestations Lab results showing hypopituitarism Possible MRI findings in hypogonadism include: Empty sella turcica: the sella is filled with cerebrospinal fluid (CSF) and the infundibulum can be seen to traverse the space, thereby excluding a cystic mass. Pituitary micro or macro adenomas.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the association between COVID-19 and acute kidney injury?", "role": "user" }, { "content": "COVID-19 -associated AKI must be differentiated from other diseases that cause AKI, such as congestive heart failure, hemorrhage, dehydration, liver failure, urinary tract obstruction, Interstitial nephritis, glomerulonephritis and nephrotoxic medications.\r\nTo review the differential diagnosis of AKI, click here.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What information is available regarding Von Willebrand disease?", "role": "user" }, { "content": "Tests that may be done to diagnose this disease include:\r\nBleeding time (is prolonged) Platelet aggregation test Platelet count (may be low or normal) Ristocetin cofactor test (the primary assay test used to diagnose von Willebrand disease) Von Willebrand factor level (level is reduced)\r\nThis disease may also alter the results of the following tests:\r\nFactor VIII level Von Willebrand factor multimers (parts of the von Willebrand factor protein molecule)\r\nVon Willebrand disease may be hard to diagnose. Low von Willebrand factor levels and bleeding do not always mean you have von Willebrand disease.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the effect of bundle branch block?", "role": "user" }, { "content": "Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.\r\nCitalopram toxicity Cocaine abuse Heart failure Hyperkalemia Myocardial infarction Pulmonary embolism\r\nCocaine abuse COPD Cor pulmonale Coronary heart disease Heart failure Hyperkalemia Hypertension Myocarditis Pulmonary embolism\r\nAtrial septal defect Cardiac catheterization Cardiac transplantation Cardiomyopathy Chagas disease Citalopram toxicity Cocaine abuse COPD Cor pulmonale Coronary artery disease Ebstein anomaly Fabry disease Familial Heart failure HIV Hyperkalemia Hypertension Infective endocarditis Left ventricular noncompaction Kearns-Sayre Syndrome Lev's disease Lyme disease Muscular dystrophy Myocardial infarction Myocarditis Myotonic dystrophy Naloxone Oxycodone Polymyositis Post cardiac surgery Propafenone Pulmonary artery catheterization Pulmonary embolism Pulmonary hypertension Pulmonic stenosis Ritonavir Sarcoidosis Septal ablation Systemic lupus erythematosus Thrombolytic therapy Transjugular intrahepatic portosystemic shunt Trauma Valvular heart disease", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What other imaging findings are typically seen in association with hemothorax?", "role": "user" }, { "content": "There are no other imaging findings associated with hemothorax.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the connection between dermatitis and external links?", "role": "user" }, { "content": "NIH/Medline\r\nv t e Diseases of the skin and subcutaneous tissue (integumentary system) (L, 680-709) Infections Template:Navbox subgroup Bullous disorders acantholysis (Pemphigus, Transient acantholytic dermatosis) · Pemphigoid (Bullous, Cicatricial, Gestational) · Dermatitis herpetiformis Inflammatory Template:Navbox subgroup Radiation -related disorders Sunburn · actinic rays (Actinic keratosis, Actinic cheilitis) · Polymorphous light eruption (Acne aestivalis) · Radiodermatitis · Erythema ab igne Pigmentation disorder hypopigmentation (Albinism, Vitiligo) · hyperpigmentation (Melasma, Freckle, Café au lait spot, Lentigo / Liver spot, Acanthosis nigricans, Acral acanthotic anomaly) Other skin keratosis / hyperkeratosis (Seborrheic keratosis, Callus) · other epidermal thickening (Ichthyosis acquisita, Palmoplantar keratoderma) skin ulcer (Pyoderma gangrenosum, Bedsore) Cutaneous Markers of Internal Malignancy (Florid cutaneous papillomatosis, acanthosis nigricans, sign of Leser-Trelat) atrophic (Lichen sclerosus, Acrodermatitis chronica atrophicans) necrobiosis (Granuloma annulare, Necrobiosis lipoidica) · other granuloma (Granuloma faciale, Pyogenic granuloma) cutaneous vasculitis (Livedoid vasculitis, Erythema elevatum diutinum) Connective tissues collagen disease: Keloid localized connective tissue disorders: Lupus erythematosus (Discoid lupus erythematosus, Subacute cutaneous lupus erythematosus) · Scleroderma / Morphea · Linear scleroderma · Calcinosis cutis · Sclerodactyly · Ainhum see also congenital, neoplasia\r\nTemplate:Inflammation\r\n\r\nTemplate:WikiDoc Sources", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What biochemistry topics can be listed?", "role": "user" }, { "content": "N-formylmethionine - N-formylmethionine leucyl-phenylalanine - N-methyl-D-aspartate receptor - N-methylaspartate - N-terminus - NADH - NADPH - NaKATPase - Native state - nef gene product - neoplasm protein - Nernst equation - nerve - nerve growth factor - nerve growth factor receptor - nerve tissue protein - nerve tissue protein S 100 - nervous system - neurobiology - neurofilament protein - neurokinin A - neurokinin K - neurokinin-1 receptor - neurokinin-2 receptor - neuron - neuronal cell adhesion molecule - neuropeptide - neuropeptide receptor - neuropeptide Y - neuropeptide Y receptor - Neuroscience - neurotensin - neurotensin receptor - neurotransmitter - neurotransmitter receptor - neutral theory of molecular evolution - neutron - neutron activation analysis - NF-kappa B - nicotinic receptor - nitrogen - Nitroglycerine - Nobel Prize in Chemistry - non-competitive inhibition - nuclear lamina - nuclear localization signal - Nuclear magnetic resonance - NMR - nuclear protein - Nucleic acid - nucleic acid regulatory sequence - nucleic acid repetitive sequence - nucleic acid sequence homology - nucleon - Nucleophile - nucleoside - nucleosome - nucleotide - nutrition -", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the meaning of nevus depigmentosus?", "role": "user" }, { "content": "Nevus depigmentosus must be differentiated from vitiligo.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the classification of HIV and AIDS?", "role": "user" }, { "content": "Clinical stage Features Clinical stage 1 Asymptomatic Generalized lymphadenopathy Clinical stage 2 Weight loss of less than 10% body weight Minor mucocutaneous manifestations Herpes Zooster within the last five years Recurrent respiratory tract infections (such as sinusitis, bronchitis, otitis media, pharyngitis) Recurrent oral ulcerations Papular pruritic eruptions Angular cheilitis Seborrhoeic dermatitis Fungal finger nail infections Clinical stage 3 Conditions where a presumptive diagnosis can be made on the basis of clinical signs or simple investigations Unexplained chronic diarrhoea for longer than one month Unexplained persistent fever (intermittent or constant for longer than one month) Severe weight loss (>10% of presumed or measured body weight) Oral candidiasis Oral hairy leukoplakia Pulmonary tuberculosis (TB) diagnosed in last two years Severe presumed bacterial infections (e.g. pneumonia, empyema, meningitis, bacteraemia, pyomyositis, bone or joint infection) Acute necrotizing ulcerative stomatitis, gingivitis or periodontitis Conditions where confirmatory diagnostic testing is necessary Unexplained anaemia (< 80 g/l), and or neutropenia (<500/µl) and or thrombocytopenia (<50 000/ µl) for more than one month Clinical stage 4 Conditions where a presumptive diagnosis can be made on the basis of clinical signs or simple investigations HIV wasting syndrome Pneumocystis pneumonia Recurrent severe or radiological bacterial pneumonia Chronic herpes simplex infection (orolabial, genital or anorectal of more than one month’s duration) Oesophageal candidiasis Extrapulmonary Tuberculosis Kaposi sarcoma Central nervous system toxoplasmosis HIV encephalopathy Conditions where confirmatory diagnostic testing is necessary Extrapulmonary cryptococcosis including meningitis Disseminated non-tuberculous mycobacteria infection Progressive multifocal leukoencephalopathy Candida of trachea, bronchi or lungs Cryptosporidiosis Isosporiasis Visceral herpes simplex infection Cytomegalovirus (CMV) infection (retinitis or of an organ other than liver, spleen or lymph nodes) Any disseminated mycosis (e.g. histoplasmosis, coccidiomycosis, penicilliosis) Recurrent non-typhoidal salmonella septicaemia Lymphoma (cerebral or B cell non-Hodgkin) Invasive cervical carcinoma Visceral leishmaniasis\r\nClinical stage Features Clinical stage 1 Asymptomatic Generalized lymphadenopathy Clinical stage 2 Hepatosplenomegaly Papular pruritic eruptions Seborrhoeic dermatitis Extensive human papilloma virus infection Extensive molluscum contagiosum Fungal nail infections Recurrent oral ulcerations Linear gingival erythema (LGE) Angular cheilitis Parotid enlargement Herpes zoster Recurrent or chronic RTIs (otitis media, otorrhoea, sinusitis) Chronic diarrhoea lasting for more than 30 days in the absence of known etiology Severe persistent or recurrent candidiasis outside the neonatal period Weight loss or failure to thrive in the absence of known etiology Persistent fever lasting for more than 30 days in the absence of known etiology. Recurrent severe bacterial infections other than septicemia or meningitis like osteomyelitis, bacterial pneumonia or abscesses Clinical stage 3 Conditions where a presumptive diagnosis can be made on the basis of clinical signs or simple investigations Moderate unexplained malnutrition not adequately responding to standard therapy Unexplained persistent diarrhoea (14 days or more) Unexplained persistent fever (intermittent or constant, for longer than one month) Oral candidiasis (outside neonatal period) Oral hairy leukoplakia Acute necrotizing ulcerative gingivitis / periodontitis Pulmonary TB Severe recurrent presumed bacterial pneumonia Conditions where confirmatory diagnostic testing is necessary Chronic HIV-associated lung disease including brochiectasis Lymphoid interstitial pneumonitis (LIP) Unexplained anaemia (<80g/l), and or neutropenia (<1000/µl) and or thrombocytopenia (<50 000/µl) for more than one month Clinical stage 4 Conditions where a presumptive diagnosis can be made on the basis of clinical signs or simple investigations Unexplained severe wasting or severe malnutrition not adequately responding to standard therapy Pneumocystis pneumonia Recurrent severe presumed bacterial infections (e.g. empyema, pyomyositis, bone or joint infection, meningitis, but excluding pneumonia) Chronic herpes simplex infection; (orolabial or cutaneous of more than one month’s duration) Extrapulmonary Tuberculosis Kaposi’s sarcoma Oesophageal candidiasis Central nervous system toxoplasmosis (outside the neonatal period) HIV encephalopathy Conditions where confirmatory diagnostic testing is necessary CMV infection (CMV retinitis or infection of organs other than liver, spleen or lymph nodes; onset at age one month or more) Extrapulmonary cryptococcosis including meningitis Any disseminated endemic mycosis (e.g. extrapulmonary histoplasmosis, coccidiomycosis, penicilliosis) Cryptosporidiosis Isosporiasis Disseminated non-tuberculous mycobacteria infection Candida of trachea, bronchi or lungs Visceral herpes simplex infection Acquired HIV associated rectal fistula Cerebral or B cell non-Hodgkin lymphoma Progressive multifocal leukoencephalopathy (PML) HIV-associated cardiomyopathy or HIV-associated nephropathy", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What information can you provide about Chlorothiazide?", "role": "user" }, { "content": "Diuril® Diuril® Sodium Intravenous\r\nTemplate:WS", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the additional diagnostic tests or investigations for Biliary cystadenoma and cystadenocarcinoma?", "role": "user" }, { "content": "There are no additional tests are recommended for the diagnosis of biliary cystadenoma.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is a pineal yolk sac tumor?", "role": "user" }, { "content": "There is so many classification system for pure pineal tumors. The most current system is for World Health Organization (WHO). Louis and associates edited classification of Central Nervous System tumors and published in 2007. \r\nAdapted from WHO:\r\nTUMOR FREQUENCY ORIGIN GERMCELL TOMURS 60% Rest of germ cells Germinoma MATURE TERATOMAMATURE TERATOMATERATOMA with Malignant Transformstion Yolk sac tomur (endodermal sinus tumor) Embryonal carcinoma Choriocarcinoma PINEAL PARANCHIMAL TUMORS 30% pineal glandular tissue pineocytoma (WHO grade ɪ) pineal paranchymal tomur of intermediate diffrentiation(WHO grade ɪɪ or ɪɪɪ) pineoblastoma (WHO grade ɪv) papillary tumor of pineal region\r\nTOMURS OF SUPPORTIVE AND ADJUCENT STRUCTURES 10% ASTROCYTOMAGlioma (glioblastoma or oligodendroglioma) Medulloepithelioma Glial cells Ependymomachoroid plexus papilloma Ependymal lining MENINGIOMA Arachnoid cells HemangiomaHemangiopericytoma or blastomaChemodectomaCraniopharyngioma vascular cells NON-NEOPLASTIC TUMOR LIKE CONDITIONS < 1% Arachnoid cysts Arachnoid cells Degenerative cysts (pineal cysts) Glial cells Cysticercosis parasites Arteriovenous malformations vascularization Cavernomas Aneurysms of the vein Galen METASTASES <.,1% Absence of blood - brain barrier Lung (most common),breast,stomach,kidney, melanoma", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the history and what are the symptoms of endometrial hyperplasia?", "role": "user" }, { "content": "A positive history of irregular menstrual cycles (PCOD) may be present. A detailed drug history may be helpful in the assessment of possible risk factors for endometrial hyperplasia. A history of inappropriate hormone replacement therapy in post menopausal women and history of tamoxifen use in breast cancer patients may be present.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the definition of Endophthalmitis and what is its Pathophysiology?", "role": "user" }, { "content": "Endophthalmitis is an ocular inflammation resulting from the introduction of an infectious agent, either bacterial or fungal, into the posterior segment of the eye. Infectious agents are introduced to the anterior and posterior segments of the eye exogenously or endogenously. \r\nExogenous endophthalmitis occurs following a penetrating ocular injury or ocular surgery. Besides cataract (approximately 90% of all cases), nearly all other type of ocular surgery such as glaucoma, retinal, radial keratotomy, and intravitreal injections may be able to disturb the integrity of the eye globe and contaminate the aqueous humor and/or vitreous humor. \r\nEndogenous endophthalmitis is caused by the hematologic dissemination of an infection to the eyes. The most common extraocular foci of infection include liver abscess, pneumonia, and endocarditis. Endogenous endophthalmitis is commonly associated with immunosuppression or procedures that increase the risk for blood-borne infections such as diabetes, HIV, malignancy, intravenous drug use, transplantation, immunosuppressive therapy, and catheterization. \r\nOn gross pathology, eyelid swelling, eyelid erythema, injected conjunctiva and sclera, hypopyon, chemosis, and mucopurulunt discharge are characteristic findings of bacterial endophthalmitis.\r\nOn microscopic histopathological analysis, infiltration of polymorphonuclear leukocytes or chronic inflammatory cells (depending on the duration of the inflammation) and destruction of ocular structures are characteristic findings of endophthalmitis.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does the physical examination for dengue fever entail?", "role": "user" }, { "content": "Tachycardia, postural hypotension, a narrow pulse pressure (<20 mm Hg) and / or frank hypotension could indicate intravascular volume depletion due to either dehydration or capillary leak. The presence of any of the above is a warning sign of severe disease, and the patient should be hospitalized for observation.\r\nIf the patient is not urinating at least every 6 hours, this may reflect intravascular volume depletion due to capillary leak, and the patient should be observed for the development of severe disease.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the connection between the pancreas and history?", "role": "user" }, { "content": "The pancreas was first identified by Herophilus (335-280 BC), a Greek anatomist and surgeon. Only a few hundred years later, Ruphos, another Greek anatomist, gave the pancreas its name. The term \"pancreas\" is derived from the Greek pan, \"all\", and kreas, \"flesh\", probably referring to the organ's homogeneous appearance.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you provide me with further context about Nilvadipine? How do you want me to rephrase the question?", "role": "user" }, { "content": "Nilvadipine is a calcium channel blocker (CCB) used for the treatment of hypertension and chronic major cerebral artery occlusion.\r\nPathohistochemical studies have revealed that the volume of the infarction in the middle cerebral artery occlusion model could be decreased by nilvadipine.\r\nNilvadipine was tested in clinical trial as a possible treatment for Alzheimer's Disease in Ireland by the Roskamp Institute, Florida, USA and Trinity College, Ireland. \r\nFollowing this study, an international research consortium led by Trinity College Dublin (Ireland) in May 2011 announced the selection for funding of a large-scale European clinical trial of Nilvadipine, an Alzheimer’s disease drug developed at the Roskamp Institute in Sarasota. More than 500 Alzheimer’s patients will participate in the multicenter Phase III clinical trial designed to study the effectiveness of Nilvadipine.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the criteria used for diagnosing idiopathic interstitial pneumonia?", "role": "user" }, { "content": "The diagnosis of IIPs is dynamic as it depends on multidisciplinary approach among different specialists. The histological patterns identified by the pathologists give better distinguishing patterns than imaging patterns identified by radiologists. Clinical-radiological-pathological diagnosis (CRP diagnosis) is rely on histopathological findings as a very informative tool to reach the definitive diagnosis. Also the practice of delaying the biopsy till the patient starts to deteriorate clinically and radiologically is not helpful as it delays the diagnosis and reduce the likelihood of the disease to be accurately identified. \r\nHowever the surgical biopsy is important for classification and confident CRP diagnosis, it is not always necessary to reach diagnosis, especially in the cases where there is a typical clinical-radiological picture of UIP/IPF. The diagnostic criteria for idiopathic pulmonary fibrosis without a surgical biopsy adopted by AT/ERS. \r\nAMERICAN THORACIC SOCIETY / EUROPEAN RESPIRATORY SOCIETY CRITERIA for diagnosing of IDIOPATHIC PULMONARY FIBROSIS in absence of surgical lung biopsy Major criteria:(must have all) Exclusion of other known causes of ILD, such as certain drug toxicities, environmental exposures, and connective tissue diseases Transbronchial lung biopsy/ BAL showing no features to support an alternative diagnosis Restrictive pulmonary function studies (reduced VC, often with an increased FEV1/FVC ratio) and impaired gas exchange (increased PA-aO2, decreased PaO2 with rest or exercise or decreased DLCO) HRCT scans with bibasilar reticular abnormalities with minimal ground-glass opacities Minor criteria: Age > 50 yr Insidious onset of unexplained dyspnea on exertion Duration illness > 3 mo Bibasilar, inspiratory crackles\r\nAdopted from the joint statement of American Thoracic Society.\r\nIn the immunocompetent adult, the presence of all of the major diagnostic criteria + at least three of the four minor criteria increases the likelihood of a correct clinical diagnosis of IPF.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you provide me with the context of this sentence so I can provide the best possible rephrasing?", "role": "user" }, { "content": "The chest x-ray of eosinophilic pneumonia may show reticular or ground glass opacities. The distribution of opacities is localized to the lung periphery in acute pneumonia and diffuse in chronic one.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you explain what thrombotic thrombocytopenic purpura is?", "role": "user" }, { "content": "The exact pathogenesis of thrombotic thrombocytopenic purpura (TTP) is not fully understood. It is thought that TTP is caused by the deficiency of a plasma metalloprotease, ADAMTS13.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the definitions of bleeding complications in patients with unstable angina, non-ST elevation myocardial infarction, and complications related to transfusions?", "role": "user" }, { "content": "Major Bleeding:\r\nFatal, intracranial, retroperitoneal, intraocular leading to vision loss Decrease in Hgb 3 g/dL adjusted for transfusion Transfusion of 2 units\r\nMinor Bleeding: Any other clinically significant bleeding not meeting major criteria leading to study drug interruption, surgery, or transfusion of 1 unit of blood.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does the term Tetralogy of Fallot mean?", "role": "user" }, { "content": "Tetralogy of Fallot occurs in approximately 30 to 60 per 100,000 births. Tetralogy of Fallot represents 5-7% of congenital heart defects. The majority of cases are thought to be sporadic and are not familial. Tetralogy of Fallot occurs slightly more often in males than in females.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the connection between D-dimer and clinical trials?", "role": "user" }, { "content": "Landmark Trials\r\nTemplate:WH Template:WS", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the pathophysiology behind hypoaldosteronism?", "role": "user" }, { "content": "The juxtaglomerular apparatus of the macula densa primarily senses the concentration of plasma sodium and renal perfusion pressure. In response to low plasma sodium concentration or decreased renal perfusion pressure, the juxtaglomerular apparatus secretes renin. On secretion, renin cleaves angiotensinogen (produced by liver) to angiotensin I. Angiotensin-converting enzyme produced in the lungs further cleaves angiotensin I to angiotensin II. The main site of activity for angiotensin II is zona glomerulosa of adrenal cortex, where angiotensin II stimulates aldosterone synthase which converts deoxycorticosterone to aldosterone.\r\nThe renin-angiotensin-aldosterone axis is a tightly controlled feedback mechanism which regulates sodium and blood pressure in our body. Low plasma sodium, decreased perfusion pressure and hyperkalemia stimulates aldosterone secretion. Hypokalemia suppresses aldosterone secretion.\r\nAldosterone is synthesized at a rate of approximately 100 to 150 ug/day.\r\n\r\n\r\nHypoaldosteronism is defined as decreased levels of the hormone aldosterone or a resistance of the target tissue to the actions of aldosterone. Hypoaldosteronism can be due to: Aldosterone deficiency: The deficiency in aldosterone can be due to congenital isolated hypoaldosteronism, primary adrenal insufficiency, diabetic nephropathy, critical illness, and drugs such as ACE inhibitors, NSAID and calcineurin inhibitors. Aldosterone resistance: In aldosterone resistance, the level of aldosterone is normal but there is decreased response of the target tissue to the actions of aldosterone. Aldosterone resistance is seen with mineralocorticoid receptor defects (seen in pseudohypoaldosteronism) and with drugs such as potassium-sparing diuretics and trimethoprim.\r\nHypoaldosteronism results in reduced reabsorption of sodium in the principal cells of cortical collecting tubules (CCT). This leads to decreased excretion of potassium and mild non-anion gap metabolic acidosis.\r\nHyporeninemic hypoaldosteronism is most commonly seen in patients with mild to moderate renal insufficiency and diabetic nephropathy: In patients of renal insufficiency, atrophy of the juxtaglomerular apparatus (JGA) leads to decreased sensing of plasma sodium concentration and renal perfusion pressure. With progression of the renal disease and atrophy of the juxtaglomerular apparatus (JGA) there may be inadequate renin production and release. A decrease in renin production and release leads to decreased angiotensin production, which eventually causes hypoaldosteronism. Renal insufficiency may also cause decreased response of the principal cells in the cortical collecting tubule to aldosterone.\r\nHyperreninemic hypoaldosteronism also known as secondary isolated hypoaldosteronism is seen in patients with severe illness such as sepsis, malignancy, heart failure, adrenal dysfunction and liver cirrhosis. During these stress inducing conditions, increased levels of ACTH and cortisol are seen. Under normal conditions, continuous ACTH secretion for greater than 96 hours leads to suppression of aldosterone synthase activity. Chronically ill patients with prolonged ACTH secretion (>96 hours) have impaired aldosterone synthase activity and decreased levels of aldosterone. In response, the kidneys via its neurohormonal regulation leads to increased levels of renin and hence the term hyperreninemic hypoaldosteronism. In addition, cytokine release from chronic illness or increased levels of atrial natriuretic peptide (in patients with heart failure) also have an inhibitory effect on the zona glomerulosa of adrenal cortex. Hyperreninemic hypoaldosteronism is also seen in patients with adrenal dysfunction such as Addison's disease. Primary adrenal insufficiency or Addison's disease can be due to adrenal dysgenesis, impaired steroidogenesis, and adrenal destruction. In patients of primary adrenal insufficiency, the adrenal glands does not produce sufficient cortisol and aldosterone. The decrease in level of aldosterone leads to decreased absorption of sodium in the kidneys and increased retention of potassium. This in turn activates the juxtaglomerular apparatus (JGA) of the kidneys, which secretes renin in an attempt to normalise plasma sodium concentration and perfusion pressure. However, due to adrenal dysfunction the zona glomerulosa of adrenal cortex is unable to produce aldosterone and presents with hyperreninemic hypoaldosteronism.\r\nIn isolated hypoaldosteronism, there is selective deficiency of aldosterone with normal cortisol production. Isolated hypoaldosteronism may result from dysfunction of zona glomerulosa or aldosterone synthase deficiency. Aldosterone synthase is an enzyme involved in the synthesis of aldosterone. Patients with aldosterone synthase enzyme deficiency (type I and type II) results in defective conversion of deoxycorticosterone to aldosterone and subsequently abnormal levels of aldosterone. Certain drugs such as heparin and nitric oxide have a direct suppressive effect on the zona glomerulosa of adrenal cortex which may lead to decrease production of aldosterone.\r\nPostadrenalectomy hypoaldosteronism is seen in patients with Conn syndrome who undergo surgery for tumor removal: \r\nConn syndrome is most often unilateral and leads to excessive production of aldosterone from the affected adrenal gland. Excessive production of aldosterone causes hypertension and suppression of renin angiotensin aldosterone system (RAAS). Patients with Conn syndrome who are treated with spironolactone and later undergo surgery for tumor removal may develop hypoaldosteronism. Patients with Conn syndrome have increased levels of aldosterone and decreased plasma renin activity (from suppressed RAAS) which leads to chronic suppression of contralateral zona glomerulosa. On surgical removal of aldosterone producing tumor, there is sudden decline in circulating aldosterone which leads to hypoaldosteronism.\r\nMineralocorticoid resistance is characterized by a decrease in response to the hormone aldosterone. In mineralocorticoid resistance the level of aldosterone may be normal or supranormal. It is due to this reason mineralocorticoid resistance is also known as pseudohypoaldosteronism. Mineralocorticoid resistance can be further categorized into: \r\nPseudohypoaldosteronism Type I: The decrease in response to aldosterone is due to heterozygous or homozygous inactivating mutations in the mineralocorticoid receptor. These patients are also resistant to mineralocorticoid therapy. Pseudohypoaldosteronism Type II: This is an extremely rare disorder. It is speculated that these patients have mutations in the genes encoding proteins of the serine threonine kinase family (WKNK1 or WNK4 kinases). Pseudohypoaldosteronism Type II is characterized by low or low-normal plasma renin activity and aldosterone concentrations, leading to hyperkalemia and metabolic acidosis with normal renal function. Pseudohypoaldosteronism type II is also known as Gordon’s syndrome. Pseudohypoaldosteronism Type III: This condition presents with transient mineralocorticoid resistance. Pseudohypoaldosteronism type III is seen in patients with underlying renal conditions with decreased glomerular filtration rate. The exact cause is unknown but is thought to be related to increased levels of TGF -β.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the purpose of using an MRI in relation to Molluscum contagiosum?", "role": "user" }, { "content": "There are no MRI findings associated with molluscum contagiosum.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you please explain what hypertrophic cardiomyopathy is?", "role": "user" }, { "content": "Hypertrophic cardiomyopathy is a condition that is most often passed down through families (inherited). It is thought to result from gene mutations that control heart muscle growth. Genes involved in the pathogenesis of hypertrophic cardiomyopathy include MYH7, TNNT2, TPM1. Nevertheless, a number of chronic medical conditions might be contributed to hypertrophic cardiomyopathy development, among them are thyroid disease, diabetes, and obesity, and hypertension.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is Hypopituitarism and how do you distinguish it from other diseases?", "role": "user" }, { "content": "Hypopituitarism should be differentiated from other diseases causing panhypopituitarism, hypothyroidism, hypogonadism, ACTH deficiency, GH deficiency, ADH deficiency and high prolactin level.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Which laboratory tests are utilized for the diagnosis of Peutz-Jeghers syndrome?", "role": "user" }, { "content": "The following laboratory tests may be helpful in the diagnosis of Peutz-Jeghers syndrome: \r\nStool:\r\nStool guaiac test\r\nBlood:\r\nComplete blood count (CBC) to detect anemia Serum iron, total iron-binding capacity, and serum ferritin to detect iron deficiency anemia", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does a testicular cancer biopsy involve?", "role": "user" }, { "content": "Biopsy is rarely done in the diagnosis of testicular cancer. However, Inguinal biopsy may be done in the contralateral testis if the ultrasound showed the intratesticular mass, cryptorchid testis, marked atrophy, and suspicious mass. Other indications for testicular biopsy are obstructive azoospermia, testicular sperm extraction and diagnosis of carcinoma in situ of the testis.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "\"What is the cause of enteropathy resulting from radiation?\"", "role": "user" }, { "content": "Radiation enteropathy or radiation enteritis is the syndrome that develops after the intestine is exposed to radiation.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the procedure for a physical examination to detect subarachnoid hemorrhage?", "role": "user" }, { "content": "In a patient with thunderclap headache, none of the signs mentioned are helpful in confirming or ruling out hemorrhage, although a seizure makes bleeding from an aneurysm more likely. Physical examination should include vital sign, level of consciousness (Glasgow Coma Scale (GCS)) eye examination, and neurologic examination.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "How is Anti-NMDA receptor encephalitis involved in CT?", "role": "user" }, { "content": "Head computed tomography (CT) is ineffective due to its low sensitivity.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the historical background or context of T-cell prolymphocytic leukemia?", "role": "user" }, { "content": "40 years ago, in 1973, Catovsky first described four cases of T-cell prolymphocytic leukemia. In 1994, Harris a pathologist from Boston and his colleagues made an effort to classify T-cell prolymphocytic leukemia.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are cardiac diseases during pregnancy and peripartum cardiomyopathy?", "role": "user" }, { "content": "PPCM is more common among women with:\r\nPrior PPCM Multiple pregnancies African decent, Haitian descent History of toxemia Long-term tocolytic use Age >30 Twin Pregnancy", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "In cases of cardiac tamponade, what does a chest x-ray indicate?", "role": "user" }, { "content": "Cardiac tamponade can be diagnosed radiographically if the fluid has accumulated slowly over time and if the patient is stable enough to have had a chest x-ray obtained. The chest x-ray will show an enlarged globular heart (cardiomegaly).", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you provide an overview of Asperger's syndrome, please?", "role": "user" }, { "content": "Medical treatments used in Asperger Syndrome include: stimulants, a-2 adrenergic agonists, atypical antipsychotics, antidepressants and anticonvulsants. Many studies believe that medications alone can not improve Asperger Syndrome's (AS) symptoms and other complementary interventions (social and behavioral) are required. \r\nBehavioral therapies in Asperger Syndrome (AS) are used to help the patients with their social communication and to develop social skills. \r\nBased on a prevalence of 1.1 % for autism spectrum disorder (ASD) in the US, the economic burden for ASD has been estimated to be $268.2991 billion (1.467% of GDP) and $460.8002 billion (1.649% of GDP) in 2015 and 2025 respectively. \r\nThere have been some experimental therapy and suggestions such as oxytocin and treatment with stem cells in patients with Asperger Syndrome (AS).", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What medical therapy is recommended for ostium primum atrial septal defect?", "role": "user" }, { "content": "There are no widely used guidelines for medical therapy usage in patients with atrial septal defects. Medical therapy in patients of atrial septal defect is administered in certain conditions like arrhythmias . Also, medical therapy can be used to manage conditions associated with atrial septal defects.\r\nIn asymptomatic patients with small shunts and normal right ventricle size generally no medical therapy is required. Routine follow-up assessment of symptoms like arrhythmia and paradoxical embolic events should be done. Also, a repeat echocardiogram should be obtained every 2 to 3 years.\r\nTreatment of atrial arrhythmia and restoration of sinus rhythm is recommended. In cases with atrial fibrillation, antiarrhythmic and anticoagulation therapy is recommended.\r\nAspirin has been found to decrease the incidence of recurrent stroke and transient ischemic attacks in patients with atrial septal defect and patent foramen ovale . The American Heart Association guidelines support the utilization of sustained warfarin therapy in high-risk atrial septal defect patients. \r\nResearchers have investigated the justification for aspirin therapy in patients with atrial septal defects and patent foramen ovale, who have had stroke or a transient ischemic attack. Aspirin therapy was observed to have an effective role in reducing the incidence of recurrent stroke after four years. Another pharmacologic intervention study indicated that both aspirin and warfarin therapy were effective. The AHA guidelines support the utilization of sustained warfarin therapy in high-risk atrial septal defect patients. \r\nSome recent research has suggested that a proportion of cases of migraine may be caused by patent foramen ovale. While the exact mechanism remains unclear, closure of a PFO can reduce symptoms in certain cases. This remains controversial. 20% of the general population have a PFO, which for the most part, is asymptomatic. 20% of the female population have migraines. And, the placebo effect in migraine typically averages around 40%. The high frequency of these facts makes statistically significant relationships between PFO and migraine difficult (i.e., the relationship may just be chance or coincidence).\r\nAlthough there is no direct evidence to link migraines and atrial septal defects, some research has noted that treatment of patent foramen ovale can reduce the severity of migraine symptoms. \r\nEffective pharmacologic therapies for migraine prevention include:\r\nAnti-hypertensives: Beta blockers (propranolol, timolol, metoprolol, nadolol, and atenolol), calcium channel blockers (verapamil, nifedipine, and nimodipine), and angiotensin converting enzyme inhibitors/angiotensin II receptor blockers (lisinopril, candesartan) Anti-depressants: Amitriptyline, venlafaxine, nortriptyline, doxepin, protriptyline Anti-convulsants: Valproate, gabapentin, topiramate Other prophylaxis: Botuliunum toxin, butterbur, coenzyme Q10, feverfew, magnesium, methysergide, opioids, pizotifen, riboflavin", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "\"What is Intravascular Imaging, and how is it employed during PCI?\"", "role": "user" }, { "content": "Multiple meta-analyses have shown that intravascular ultrasound -guided PCI is more successful in reducing major adverse cardiovascular events (MACE) compared to angiographic-guided PCI. Furthermore, based on a trial named ULTIMATE (Intravascular Ultrasound Guided Drug Eluting Stents Implantation in “All-Comers” Coronary Lesions), intravascular ultrasound -guided PCI is more successful in reducing target- vessel failure compared to angiographic-guided PCI. The following are the list of pre- PCI evaluations that can be done with intravascular ultrasound: Full-thickness evaluation of the vessel wall Plaque burden Calcification extent Length of lesion External elastic lamina diameter for stent sizing The following are the list of post- PCI evaluations that can be done with intravascular ultrasound: Assessment of stent area Stent malposition Stent underexpansion Tissue protrusion Edge disease and dissection", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you please define what cradle cap is?", "role": "user" }, { "content": "Assurances that this condition will clear as the baby matures are very common. However, studies have shown that the condition not infrequently persists into the toddler years, and less commonly into later childhood. It tends to recur in adolescence and persists into adulthood. In an Australian study, about 15% percent of previously diagnosed children still had eczema 10 years later. Sometimes, cradle cap turns into atopic dermatitis. Rarely, it turns out to be misdiagnosed psoriasis.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the historical perspective on the liver in terms of mass?", "role": "user" }, { "content": "Hippocrates was the first to describe pyogenic liver abscess, based on the type of fluid recovered from abscess. In 1843, Dr. Robert Liston, a British surgeon, was the first to describe hemangioma. In 1911, Yamagiwa suggested a new classification system based on the cell of origin and divided hepatobiliary cancers into hepatocellular cancer and cholangiocellular cancer, with the proposed terminology of hepatoma and cholangioma. In 1958, I Bartok discovered hepatoblastoma for the first time. In 1958, Hugh A Edmondson, was the first to discover and describe in detail liver adenoma following 50,000 autopsies. in 1973, association between oral contraceptives and the development of liver tumors was first described.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does a physical examination for Loeffler's syndrome entail?", "role": "user" }, { "content": "Physical examination of patients with Löffler syndrome might be normal, but is usually remarkable for wheezing, rash, and mild fever. \r\nPatients with Löffler syndrome might appear normal or ill.\r\nlow-grade fever Tachycardia with regular pulse or (ir)regularly irregular pulse Tachypnea\r\nSkin examination of patients with Löffler syndrome s usually normal. Nevertheless, patients might develop a rash. Cutaneous features of hypereosinophilic syndrome\r\nHEENT examination of patients with Löffler syndrome is usually normal.\r\nNeck examination of patients with Löffler syndrome is usually normal.\r\nLung auscultation might have crackles on physical examination (common), with or without wheezing.\r\nPulmonary examination of patients with might be normal.\r\nFine/coarse crackles upon auscultation of the lung Rhonchi Wheezing may be present\r\nCardiovascular examination of patients with Löffler syndrome is usually normal.\r\nAbdominal examination of patients with Löffler syndrome is usually normal. Patients subsequently might complain of abdominal pain or other complications of parasitic infections.\r\nBack examination of patients with Löffler syndrome is usually normal.\r\nGenitourinary examination of patients with Löffler syndrome is usually normal.\r\nNeuromuscular examination of patients with Löffler syndrome is usually normal.\r\nExtremities examination of patients with Löffler syndrome is usually normal.\r\nCyanosis is barely reported", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the medical treatment for cutaneous follicle center lymphoma?", "role": "user" }, { "content": "The predominant therapy for primary cutaneous follicle centre lymphoma is radiotherapy. Adjunctive chemotherapy may be required.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What do marine toxins refer to?", "role": "user" }, { "content": "Are there long-term consequences to these diseases?\r\nCiguatera poisoning has resulted in some neurologic problems persisting for weeks, and in rare cases, even years. Symptoms have sometimes returned after eating contaminated fish a second time. Amnesic shellfish poisoning has resulted in long-term problems with short-term memory. Long-term consequences have not been associated with paralytic shellfish poisoning, neurotoxic shellfish poisoning, and scombrotoxic fish poisoning.\r\nhttp://www.cdc.gov/ncidod/dbmd/diseaseinfo/marinetoxins_g.htm#whatsort", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "How are fertility and demographics related?", "role": "user" }, { "content": "The fertility rate is a demographic measure of the number of children per woman. Although it has been until recently considered to be a fairly reliable indicator of population growth, it is no longer so in much of Asia. Due to selective abortion and other factors, the ratio of women relative to men in populations is declining. Therefore, the fertility rate as it has traditionally been defined is no longer an authoritative measure of population growth in China, India, and Myanmar.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What treatment options are available for saphenous vein graft failure, which includes coronary artery bypass surgery and percutaneous coronary intervention (PCI)?", "role": "user" }, { "content": "As with all medical procedures, complications for SVG intervention can occur. Risk factors for complications include: older graft age (>3-5 years), the presence of thrombus, and diffuse disease.\r\nAlthough PCI with stenting is effective for focal lesions, there is uncertainty regarding the best treatment for diffusely degenerated SVGs. In these cases, it is often a better choice to abandon the graft and intervene on the native vessel instead.\r\nAs mentioned above, prevention of no reflow should be attempted with embolic protection devices, pretreatment using nitroprusside and the avoidance of high-pressure inflations and unnecessary pre/post-dilation and oversizing. However, in the event that no reflow develops, it should be aggressively managed with intracoronary vasodilators (i.e. diltiazem, nicardipine, adenosine, and nitroprusside).\r\nImages courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology\r\nSaphenous vein coronary bypass graft: Gross, natural color, external view of heart with thrombosed veins Saphenous vein coronary bypass graft: Thrombosis, Acute: Gross, fixed tissue but well shown cross sections of bypass graft and anastomotic site with thrombosis. 61 yo male, with and acute infarct treated with streptokinase and two days later had bypass. Died 5 days post op. Two veins are thrombosed Myocardial Infarct Acute Reflow Type: Gross, fixed tissue but good color. A very enlarged heart with moderate LV dilation and high anterior wall hemorrhagic infarct. Initially treated with streptokinase and two days later had saphenous vein grafts. Both grafts are thrombosed. He died after 5 days", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What medical treatment is recommended for community-acquired pneumonia?", "role": "user" }, { "content": "“ This recommendation has been removed due to the market withdrawal of drotrecogin alfa. Hypotensive, fluid-resuscitated patients with severe CAP should be screened for occult adrenal insufficiency. (Moderate recommendation; level II evidence) Patients with hypoxemia or respiratory distress should receive a cautious trial of noninvasive ventilation (NIV) unless they require immediate intubation because of severe hypoxemia (arterial oxygen pressure/fraction of inspired oxygen PaO2/FiO2 ratio <150) and bilateral alveolar infiltrates. (Moderate recommendation; level I evidence) Low-tidal-volume ventilation (6 cm3/kg of ideal body weight) should be used for patients undergoing ventilation who have diffuse bilateral pneumonia or acute respiratory distress syndrome. (Strong recommendation; level I evidence) ”\r\nFor Level of evidence and classes click here.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does Sarcoma botryoides mean?", "role": "user" }, { "content": "The majority of patients with sarcoma botryoides remain asymptomatic. If left untreated, patients with sarcoma botryoides may progress to develop direct extension to pelvic soft tissue structures. If a patient presents with the classical presentation of a grape-like vaginal tissue, every doctor should be alarmed and commence rapid diagnosis followed by therapy. Common complications of sarcoma botryoides, include:\r\nBleeding Infertility Death\r\nFavorable prognostic parameters: Disease without deep myometrial invasion Single polyp Embryonal histologic subtype Poor prognostic factors include: Metastatic disease at presentation Poor response to chemotherapy", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is involved in the physical examination for tricuspid atresia?", "role": "user" }, { "content": "Patients with pulmonary stenosis and closed PAD usually appear cyanotic after birth. Conversely, patients with VSD and high pulmonary blood flow without stenotic pulmonary arteries present with signs of overt heart failure without cyanosis.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the laboratory discoveries or results for chronic lymphocytic leukemia?", "role": "user" }, { "content": "Laboratory findings consistent with the diagnosis of chronic lymphocytic leukemia include abnormal complete blood count, immunohistochemistry, and electrophoresis. Monoclonality of kappa and lambda producing B cells is a key diagnostic feature among patients with chronic lymphocytic leukemia.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the risk factors associated with peritonsillar abscess?", "role": "user" }, { "content": "Common risk factors in the development of peritonsillar abscess include: \r\nSmoking Previous peritonsillar abscess episodes History of recurrent pharyngotonsillitis (Inflammation of the pharynx and tonsils) Poor oral hygiene", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the laboratory findings related to seizures?", "role": "user" }, { "content": "The laboratory tests for patients with seizure may include checking for: hypoglycemia, hyponatremia, uremia, and drug intoxication, and levels of ammonia, creatine kinase (CK), lactate, and prolactin. Elevated prolactin level may be helpful in differentiating generalized tonic-clonic or complex partial seizure from psychogenic nonepileptic seizures, only if the patient’s prolactin level is measured 10 to 20 minutes after a suspected seizure event. Analysis of the serum prolactin level is not effective in distinguishing a seizure from syncope. No conclusion could be established regarding serum prolactin changes following status epilepticus, repetitive seizures, and neonatal seizures.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you provide information about Fentanyl Oral Transmucosal?", "role": "user" }, { "content": "In case of overdose, call your local poison control center at 1-800-222-1222. If the victim has collapsed or is not breathing, call local emergency services at 911.\r\nIf an overdose is suspected, the medication unit should be removed from the person's mouth immediately and disposed of properly. If the person is asleep, call their name and shake their arm or shoulder to keep them awake. Contact the numbers listed above for emergency care. Once the emergency situation is taken care of, call the doctor to find out if future doses of fentanyl oral transmucosal should be at a lower dose.\r\nSymptoms of overdose may include:\r\ndrowsiness itching, especially around the nose and eyes dizziness upset stomach vomiting slowed breathing or stopped breathing", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you give me an overview of pharyngitis, please?", "role": "user" }, { "content": "With more than 10 million outpatient visits per year, pharyngitis is one of the most common disorders in adults and children. Viruses are the single most common cause of pharyngitis and account for 25 percent to 45 percent of all cases. Group A streptococcus presents in up to 37% of all children presenting with a sore throat to an outpatient clinic or ED and 24% of those presenting at younger than 5 years. Group A streptococcus is by far the most common bacterial cause of acute pharyngitis, accounting for approximately 15 to 30 percent of cases in children and 5 to 10 percent of cases in adults. Peak seasons for sore throat include late winter and early spring.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the risk categorization and outlook for patients with unstable angina who have experienced a non-ST segment elevation myocardial infarction?", "role": "user" }, { "content": "There are several scoring systems which have been devised as methods of identifying high-risk patients presenting with acute coronary syndrome (ACS). These include, among others, the Braunwald classification system, the Rizik classification system, the TIMI risk score, the GRACE risk score and the PURSUIT risk score. In direct comparisons, the GRACE risk score is superior to TIMI risk score in assessing both prognosis and the severity of coronary artery disease in NSTEMI patients. Regarding predicting the severity of CAD, a cross-sectional study published in 2018 used coronary angiogram to assess the severity of coronary artery disease using the vessel score & Gensini scores and correlated these scores with the GRACE and TIMI scores. The area under the ROC curve for the GRACE score (0.943; 95% CI = 0.893 - 0,993) was significantly superior to the area under the ROC curve for the TIMI score (0.892; 95% CI = 0.853 - 0.937) . Regarding 30 day mortality, a 2016 study correlated 30 day mortality in NSTEMI patients with the NT-proBNP biomarker, TIMI score, and GRACE scores. A total of 1324 patients were included in the study, which found both NT-proBNP (0.85) and the GRACE score (0.87) independently predicted mortality at 30 days, while the TIMI score (0.60) did not .\r\nThe TIMI Risk Score for UA /non-ST-elevation myocardial infarction (NSTEMI) is based on the TIMI 11B and ESSENCE trials and has been shown to be predictive of all-cause mortality, myocardial infarction, and severe recurrent myocardial ischemia prompting urgent revascularization for the first 14 days after presentation. It has also been validated as a tool for 30-day risk stratification of patients presenting to the emergency room with chest pain. It is very likely the most commonly used tool for risk-stratification as it is the easiest to understand and use of those listed.\r\nThe TIMI risk score is determined by the sum of the presence of 7 variables at admission; 1 point is given for each of the following variables: \r\nAge 65 years or older At least 3 risk factors for coronary artery disease Prior coronary artery stenosis of 50% or more ST segment deviation on EKG presentation At least 2 anginal events in prior 24 h Use of aspirin in prior 7 days Elevated serum levels of cardiac biomarkers\r\nIn TIMI risk scoring, prior coronary stenosis of 50% or more remained relatively insensitive to missing information and remained a significant predictor of events. \r\nIncidence of adverse events (all-cause mortality, myocardial infarction, and severe recurrent myocardial ischemia prompting urgent revascularization for the first 14 days after presentation):\r\nTIMI Risk Score 0/1: 4.7% TIMI Risk Score 2: 8.3% TIMI Risk Score 3: 13.2% TIMI Risk Score 4: 19.9% TIMI Risk Score 5: 26.2% TIMI Risk Score 6/7: 40.9%\r\nThe Braunwald Classification of unstable angina pectoris (UAP) stratifies patients according to both the type of anginal pain and the underlying cause of the pain. Increasing class is associated with increasing risk of both recurrent ischemia and death at 6 months.\r\nClass I: Exertional angina (new onset, severe, or accelerated; angina of less than 2 months duration; more frequent angina; angina precipitated by less exertion; no rest angina in the last 2 months) Class II: Rest angina, subacute (rest angina within the last month but none within 48 hours of presentation) Class III: Rest angina, acute (rest angina within 48 hours of presentation)\r\nClass A: Secondary unstable angina (caused by a noncardiac condition such as anemia, infection, thyrotoxicosis or hypoxemia) Class B: Primary unstable angina Class C: Post-infarction unstable angina (within 2 weeks of documented myocardial infarction)\r\nThe Rizik classification scheme of UAP has been shown to be predictive of in-hospital adverse cardiac events and as such could be used to make decisions regarding hospitalization and intensity of treatment. \r\nClass IA: Acceleration of previously existent chronic stable angina without new EKG changes Class IB: Acceleration of previously existent chronic stable angina with new EKG changes Class II: Exertional angina of new onset without respect to EKG morphology Class III: New onset resting angina (either with or without history of prior stable angina) Class IV: Patients with protracted chest pain of > 20 minutes with EKG changes\r\nThe PURSUIT Risk score has been shown to be predictive of the 30-day incidence of death and the composite of death or myocardial (re)infarction in patients presenting with UA / NSTEMI (patients with ACS but without ST-elevation myocardial infarction). Points are given for each of the 7 below risk factors. The points are then summed to provide a risk score which can then be converted to a probability of either death or a composite of death or MI (from 0% to 50% depending on total points). \r\nAge (increased probability for age above 60 and above) Gender (increased probability for men, no increased probability for women) Worst Canadian Cardiovascular Society Classification for angina pectoris in the previous 6 weeks (from angina only during very strenuous activity (Class I) to angina at rest (Class IV), increased probability for Class III or IV) Heart rate (increased probability for heart rate 100 and above) Systolic blood pressure (increased probability for systolic blood pressure 100 and below) Signs of heart failure (i.e., rales) ST-segment depression on presenting EKG\r\nThe GRACE model has been shown to be predictive of in-hospital mortality for patients presenting with ACS. The 8 risk factors listed below were shown to be the most strongly predictive. A probability of in-hospital death can be assigned by adding up the points allocated for each risk factor (range from <0.2% for less than 61 points to > 51% for more than 249 points). This model was validated as a tool to predict 6-month mortality in patients who survived hospital admission for ACS as well. \r\nIncreasing age (0-100 points) Increasing Killip class (0-59 points) Decreasing systolic blood pressure (0-58 points) ST-segment deviation (28 points) Cardiac arrest during presentation (39 points) Increasing serum creatinine level (1-28 points) Elevated initial cardiac enzymes (14 points) Increasing heart rate (0-46 points)", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the factors that increase the risk of acute cholecystitis?", "role": "user" }, { "content": "Common risk factors in the development of acute calculous cholecystitis include advancing age, female gender, obesity, and family history. Long periods of fasting, total parental nutrition (TPN), weight loss are the common risk factors for the development of acute acalculous cholecystitis.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide an overview of sepsis?", "role": "user" }, { "content": "According to IDSA, \"Surviving Sepsis Campaign\" guidelines, the management protocol for sepsis include screening for high-risk patients; taking bacterial cultures soon after the patient arrived at the hospital; starting patients on broad-spectrum intravenous antibiotic therapy before the results of the cultures are obtained; identifying the source of infection and taking steps to control it (e.g., abscess drainage); administering intravenous fluids to correct a loss or decrease in blood volume; and maintaining glycemic (blood sugar) control. \r\nSurgical intervention is not recommended for the management of sepsis\r\nPrevent infections that can lead to sepsis by cleaning scrapes and wounds and getting regular vaccination against infections that cause sepsis can help in the prevention of sepsis.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are some additional diagnostic tests for indigestion?", "role": "user" }, { "content": "People over the age 55 years and those with alarm features are usually investigated by esophagogastroduodenoscopy (EGD). In this painless investigation the esophagus, stomach and duodenum are examined through an endoscope passed down through the mouth. This will rule out peptic ulcer disease, medication related ulceration, malignancy and other rarer causes.\r\nPeople under the age of 55 years with no alarm features do not need EGD but are considered for investigation for peptic ulcer disease caused by Helicobacter pylori infection. Investigation for H.pylori infection is usually performed when there is a moderate to high prevalence of this infection in the local community or the person with dyspepsia has other risk factors for H. pylori infection, related for example to ethnicity or immigration from a high-prevalence area. If infection is confirmed it can usually be eradicated by medication.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the histological presentation of Noncompaction cardiomyopathy?", "role": "user" }, { "content": "Interstitial fibrosis was observed in 5/5 patients with isolated noncompaction cardiomyopathy who underwent right ventricular biopsy Endomyocardial thickening and subendocardial fibroelastosis was observed in 3/5 patients who underwent right ventricular biopsy Myocyte necrosis has been observed in areas of trabeculation .", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the explanation of Adenoids and Pathology?", "role": "user" }, { "content": "Enlarged adenoids, or adenoid hypertrophy, can become nearly the size of a ping pong ball and completely block airflow through the nasal passages.\r\nEven if enlarged adenoids are not substantial enough to physically block the back of the nose, they can obstruct airflow enough so that breathing through the nose requires an uncomfortable amount of work, and inhalation occurs instead through an open mouth.\r\nAdenoids can also obstruct the nasal airway enough to affect the voice without actually stopping nasal airflow altogether.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the cause of ST elevation myocardial infarction?", "role": "user" }, { "content": "Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.\r\nAortic dissection Carbon monoxide poisoning Disseminated intravascular coagulation Infectious endocarditis\r\nPlaque rupture\r\nAcute coronary syndrome Air pollution Amphetamines Amyloidosis Anabolic steroids Anaphylactic shock Anger Anxiety Aortic dissection Aortic stenosis Arrhythmias Atherosclerosis Bereavement Bradyarrhythmias Broken heart syndrome Carbon monoxide poisoning Cocaine Combined oral contraceptive pill Commotio cordis Coronary artery aneurysm Coronary artery dissection Coronary artery vasospasm Coronary heart disease Coronary stent thrombosis Coronary thrombosis Desmopressin Desogestrel and Ethinyl Estradiol Diabetes mellitus Diflunisal Disulfiram Dissecting aortic aneurysm Dyslipidemia Earthquakes Electrocution Electrolyte imbalance Ephedrine Epinephrine overdose Erythropoietin Ethynodiol diacetate and ethinyl estradiol Etonogestrel Fabry's disease Familial hypercholesterolemia Fine particulate matter Heavy meal Homocystinuria Hurler disease Hypercoagulable states Hypertension Hypotension Idarubicin hydrochloride Idiopathic hypertrophic subaortic stenosis Indinavir Infectious endocarditis Interferon gamma Kawasaki disease Malignant hypertension Marijuana Missile attacks Medroxyprogesterone Meloxicam Mucopolysaccharidoses Myocardial contusion Naratriptan Niacin Nitroglycerin Norgestrel and Ethinyl estradiol Nuvaring Oxaprozin Pergolide Pheochromocytoma Physical exertion Piroxicam Plaque rupture Polyarteritis nodosa Polycythemia vera Prinzmetal angina Pseudoxanthoma elasticum Psychological stress Ramucirumab Respiratory failure Sexual activity Sports injury Stress cardiomyopathy Sudden withdrawal of beta blockers Sudden withdrawal of nitrates Sumatriptan Tachyarrhythmias Takayasu arteritis Takotsubo cardiomyopathy Testosterone Thiamine deficiency Thrombocytosis Thyrotoxicosis Tiagabine Transluminal percutaneous coronary angioplasty Trauma Upper respiratory tract infection Wartime bombing", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is Congenital Disorder of Glycosylation?", "role": "user" }, { "content": "A congenital disorder of glycosylation (previously called carbohydrate-deficient glycoprotein syndrome) is one of several rare inborn errors of metabolism in which glycosylation of a variety of tissue proteins and/or lipids is deficient or defective. Congenital disorders of glycosylation are sometimes known as CDG syndromes. They often cause serious, sometimes fatal, malfunction of several different organ systems (especially the nervous system, muscles, and intestines) in affected infants. The most common subtype is CDG-Ia (also referred to as PMM2-CDG) where the genetic defect leads to the loss of phosphomannomutase 2, the enzyme responsible for the conversion of mannose-6-phosphate into mannose-1-phosphate.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is an atrial myxoma?", "role": "user" }, { "content": "A myxoma (Myxo- = Latin for mucus) is the most common primary tumor of the heart. Cardiac myxoma was first described in 1845. In 1951, Prichard described a kind of microscopic endocardial structure of the atrial septum, which was suggested to be associated with cardiac myxoma. Clarence Crafoord, a Swedish cardiovascular surgeon successfully removed a cardiac myxoma for the first time in 1954. Before 1951, cardiac myxoma diagnosis was made only at post-mortem examination. In 1959, the first M-mode echocardiogram of a left atrial myxoma was reported. Cardiac myxomas are classified by the WHO histological classification of tumors of the heart \" Benign tumors and tumor-like lesions\" and categorized into a type of pluripotent mesenchymal tumor. Cardiac myxoma arises from remnants of subendocardial vasoformative reserve cells, which are primitive mesenchymal cells that are normally involved in the supportive structure of the endocardium. Myxomas are usually located in the fossa ovalis and endocardium of the atrial septum. Some symptoms of myxoma may be associated with the release of interleukin 6 (IL-6). On gross pathology, a gelatinous, irregular surface that fills the left atrium is the characteristic finding of myxoma. A common histopathological finding is the Gamna-Gandy Bodies that consist of fibrosis and deposition of iron pigments. The main cause of cardiac myxoma remains unknown. However, in some cases like inherited myxomatosis, there is a strong relation with genetic mutations of PRKAR1A gene. Cardiac myxoma should be differentiated from other benign and malignant primary heart tumors including papillary fibroelastoma, lipoma, rhabdomyoma, and cardiac metastasis. Cardiac myxomas are the most common primary cardiac tumor in adults, with a reported prevalence of 0.03% in general population. The incidence of cardiac myxoma is about 1/ 100,000 per year. The majority of patients with cardiac myxoma are diagnosed between 30 to 60 years; children are rarely affected. Females are more commonly affected with cardiac myxoma than men. The female-to-male ratio is approximately 1.8 to 1. Cardiac myxomas represent 78% of heart tumors. Common risk factors in the development of myxoma are female gender and genetic predisposition. In some cases, right atrial myxoma has been associated with tricuspid stenosis and atrial fibrillation. If left untreated, cardiac myxoma progression occurs slowly. The overlap of various phenomena such as thrombosis, hemorrhage, or fragmentation may influence tumor growth, detachment, and consequently embolism. Constitutional symptoms, such as: weight loss, fatigue, weakness are often the initial clinical onset of cardiac myxoma, and may resemble those from endocarditis. Metastases are uncommon in cardiac myxoma. Since the majority of the cardiac myxomas are left-sided, it may progress to develop mitral valve obstruction or systemic embolic events, such as stroke. Whereas, right atrial myxomas may obstruct the tricuspid valve and can present as right sided heart failure. Approximately 20% of patients with cardiac myxoma are asymptomatic. Overall, clinical features of cardiac myxoma are associated with the size of the tumor, location, size, and mobility. There is no single diagnostic study of choice for myxoma. Myxoma may be diagnosed based on clinical presentation and detecting the cardiac mass. Symptoms associated with cardiac myxomas are typically due to the effect of the mass of the tumor obstructing the normal blood flow within the heart chambers. Left atrial myxoma symptoms may mimic mitral stenosis, while right atrial myxomas rarely produce symptoms until they have grown to be at least 13 cm wide. General symptoms may also mimic those of infective endocarditis. Cardiac myxoma symptoms may occur at any time, but most often they tend to occur with changes in body position. Common symptoms include: chest pain, palpitation, dizziness, syncope and dyspnea on exertion. There are no specific physical findings for cardiac myxoma. The auscultatory presence of a \"tumor plop\" (which is caused by the obstruction of the mitral valve orifice by the tumor) on physical examination is highly suggestive of cardiac myxoma. Common physical examination findings of cardiac myxoma include systolic or diastolic murmurs (depending on size, mobility, and location of the tumor). Laboratory findings consistent with cardiac myxoma are generally non-specific, results often demonstrate anemia, leukocytosis and elevated erythrocyte sedimentation rate. On chest x-ray, cardiac myxoma is characterized by normal results and in some cases a calcification overlying the heart. On CT scan, cardiac myxoma is characterized by low attenuation and areas of dystrophic calcification in cardiac chambers. CT scan may be helpful in the diagnosis of cardiac myxoma because it provides better soft-tissue contrast than echocardiography, and it can also differentiate calcification and fat, and may allow tissue diagnosis of some masses such as lipomas. On Magnetic Resonance Imaging (MRI) or Cardiac Magnetic Resonance (CMR), cardiac myxoma is characterized by a soft tissue mass within the cardiac chambers isointense to skeletal muscle. This imaging modality plays an important role in the evaluation of cardiac masses and is of great value when echocardiographic findings are suboptimal or when the lesion has an atypical location or appearance. The echocardiogram is the initial modality and most useful diagnostic imaging study in cardiac myxoma. On cardiac ultrasound, cardiac myxoma is characterized by the presence of a heterogeneous pedunculated mass that is commonly located in the left atrium. Echocardiography allows for evaluation assessment of tumor mobility, as it often protrudes through valve flaps. As a testing modality, two-dimensional echocardiography is often coupled with other modalities (such as, Doppler echocardiography) to detect vascular abnormalities that frequently occur in cardiac myxomas. Another diagnostic study for cardiac myxoma is cardiac angiography, which often demonstrates contrast media-enhanced tumor vasculature. There is no known medical therapy for cardiac myxomas. Surgery is the mainstay of treatment for cardiac myxoma. The feasibility of surgery depends on the patient hemodynamic stability at diagnosis. Cardiac myxoma surgery has operative mortality around 0 to 3%, depending on risk factors or mechanical damage to a heart valve, as well as adhesion of the tumor to valve leaflets. The short and long-term prognosis is generally regarded as excellent.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you explain what a template for a patient information page is?", "role": "user" }, { "content": "In this section you should outline the treatment options, including medications, lifestyle changes, and surgical interventions.\r\nAdvise the patient to always follow the treatment plan that their doctor has provided them.\r\nFor an example of a treatment section of a patient information page, click here.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the recommended medical treatment for vertebrobasilar insufficiency?", "role": "user" }, { "content": "In the recent decades, interventional therapy became more and more important with the medical therapy as the foundation of the whole treatment.Open surgery is rarely used because its high risk of complication comparing with the catheter-based therapy.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the underlying medical condition and mechanism that causes angiomyolipoma?", "role": "user" }, { "content": "Genes involved in the pathogenesis of angiomyolipoma include: \r\n\r\nTSC1 gene\r\nTSC2 gene", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the infection history and symptoms of whipworm?", "role": "user" }, { "content": "Patients with whipworm infection may present with the following history:\r\nRecent travel to or currently living in an area of known infestation Living in close proximity to water sources Poor personal hygiene Low socioeconomic status", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the name of the surgery used to treat Androgen Insensitivity Syndrome?", "role": "user" }, { "content": "There are no specific contraindications advised as such from a surgical approach point of view. General factors such as a age for consideration of surgery and other co-morbid conditions have to be taken in to consideration before planning for a surgery.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does carotid stenting mean?", "role": "user" }, { "content": "Informed consent obtained and local anaesthetic administered Preparation of both groins with antiseptic and draped Puncture into femoral artery and access through short sheath Guidewire passed through aorta and into arch Arch aortogram obtained if not previously performed to confirm suitability to continue Carotid and cerebral angiogram performed Long access sheath placed after cannulation of common carotid artery (CCA) Guidewire passed through area of carotid narrowing Placement of embolic protection device above the area of narrowing Angioplasty of carotid narrowing, but more commonly proceed straight to deployment of stent into area of narrowing Angioplasty post stent deployment Removal of protection device, guidewires and sheath Aftercare of groin puncture site", "role": "assistant" } ]