Datasets:

Suriring

/

question-answer-Medicual-Suri-Instruct

like 0

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What information about prostatitis is available?", "role": "user" }, { "content": "During a physical exam, your health care provider may find:\r\nEnlarged or tender lymph nodes in your groin Fluid released from your urethra Swollen or tender scrotum\r\nTo examine your prostate, the health care provider will perform a digital rectal exam. During this exam, the provider will insert a lubricated, gloved finger into your rectum.\r\nThe prostate may feel:\r\nLarge and soft (with a chronic prostate infection) Warm, soft, swollen, or tender (with an acute prostate infection)\r\nYour doctor may do a prostatic massage to see whether you have an infection:\r\nThe health care provider will rub a gloved finger over the prostate gland a few times to release fluid from the urethra. The fluid will be examined for white blood cells and bacteria - signs of an infection.\r\nUrine samples may be collected for urinalysis and urine culture.\r\nProstatitis may affect the results of the prostate-specific antigen (PSA), a blood test used to screen for prostate cancer.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does SSRI sexual dysfunction mean?", "role": "user" }, { "content": "The first case of PSSD, long-term premature ejaculation beginning after discontinuation of citalopram, was published in 2003. Three cases of severe hyposexuality caused by PSSD were published in May 2006, and a fifth case was published soon after. A sixth case was published in late 2007 , and three more cases were published in early 2008 . There have also been several published cases of Persistent Genital Arousal Disorder (PGAD) that lasts long after withdrawal from SSRIs. These symptoms are quite different from, and should not be confused with, hypersexuality.\r\nTo establish, monitor, and regulate causation of PSSD in individual patients, one approach in use by consulation-liaison psychiatrists is to assay measurable parameters of patient health (hormone levels, sexual functioning) with a survey or laboratory tests before and after administering a psychiatric drug, based on individual patient concern regarding each of the listed side effects. If PSSD develops, a correlation can be established between assay results and PSSD, guiding further treatment for the individual patient and others. A lack of education on drug side effects and the presence of clinical depression in a patient who is a candidate for antidepressant therapy can combine to reduce the patient's ability to advocate for tests.\r\nPost-administration reporting of side effects provides useful data for development of new drugs and patient decisions. In America, adverse effects are reported with FDA forms, 3500 for optional use (patients can self-report using this form), and 3500A, for mandatory reporting.\r\nThe ICD-9 codes used for classifying, diagnosing, and reporting sexual dysfunction are available at Chrisendres.com and other sources.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does GUCH mean and can you give me an overview of it?", "role": "user" }, { "content": "GUCH is an acronym for Grown Ups with congenital heart defects. Adults with congenital heart defects is a group of patients which is fast growing in numbers, due to advances in cardiac surgery and intensive care in the 1970s and 80s. In some countries, specialized programs have been established established to provide care for these patients later in life.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "\"What is the importance or meaning behind Kidney and World Kidney Day?\"", "role": "user" }, { "content": "World Kidney Day is observed on the second Thursday of March every year. It was held for the first time in 2006, to increase awareness of kidney disease and educate persons at risk regarding the importance of prevention and early detection. It is a joint initiative by the International Society of Nephrology (ISF) and International Federation of Kidney Foundations (IFKF). The next World Kidney Day will be held on 13 March 2008. In 2007, it was held on 8th March.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can PCI be performed on lesions that are angulated or tortuous?", "role": "user" }, { "content": "Severe vessel tortuosity and the presence of eccentric angulated lesions have long been identified as significant predictors of percutaneous coronary intervention (PCI) failure, as well as worse clinical outcomes . Challenges in the treatment of angulated lesions and lesions in tortuous segments includes difficulty in delivering the interventional equipment and the increased risk of vessel dissection and vessel perforation.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide an overview of Type 1 Endocrine Neoplasia?", "role": "user" }, { "content": "Pharmacologic medical therapies for multiple endocrine neoplasia type 1 include cabergoline, somatostatin analogues, and H2-receptor blockers.\r\nSurgery is the mainstay of treatment for multiple endocrine neoplasia type 1.\r\nThere is no established method for prevention of Multiple endocrine neoplasia 1.\r\nAccording to the National Cancer Institute, surveillance for multiple endocrine neoplasia type 1 by imaging studies such as brain MRI, abdominal CT and abdominal MRI is recommended every 3-5 year among patients with pituitary tumors and pancreatic neuroendocrine tumors respectively. Biochemical tests such as serum prolactin, insulin-like growth factor 1, fasting total serum calcium, ionized calcium, parathyroid hormone, fasting serum gastrin, chromogranin A, pancreatic polypeptide, glucagon and vasointestinal polypeptide are recommended every year among patients with pituitary tumors, pancreatic neuroendocrine tumors and primary hyperparathyroidism.\r\nFuture or investigational therapies of multiple endocrine neoplasia type 1 include TRK-inhibitors (tropomyosin receptor kinase inhibitors), mTOR inhibitors, thienopyrimidine analogs and molecular phenotyping.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you explain what intracranial aneurysms are?", "role": "user" }, { "content": "These aneurysms result from tumor invasion of the vessel wall followed by tumor embolism . They usually occur as a result of a myxoma in the left atrium. The middle cerebral artery is most commonly involved.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you provide me with the context in which this sentence will be used, so I can better tailor my response?", "role": "user" }, { "content": "The diagnosis of MAT is usually not clinical rather the following electrocardiographic diagnostic criteria is used:\r\nECG of MAT has following characteristics:\r\nAtrial rate of greater than 100 beats per minute (although some also suggest a threshold of 90 beats per minute for MAT diagnosis) Irregularly irregular rhythm There are P waves of varying morphology from at least three different foci. There is an absence of one dominant atrial pacemaker. Variable or irregular PP intervals, RR intervals, and PR intervals (however, variation in PR intervals is not yet included in the diagnostic criteria because of the variation of PR interval depends on the length of the preceding RP interval). Can be mistaken for atrial fibrillation if the p waves are of low amplitude.\r\nAs multifocal atrial tachycardia is mostly associated with the underlying medical conditions such as cardiac and pulmonary disease, so its diagnosis does not typically warrant any additional workup, other than the workup required for the suspected underlying conditions. If the arrhythmia persists despite of treating the underlying medical conditions, following tests should be done to check for any signs of infection, anemia, or electrolyte abnormalities such as hypokalemia and hypomagnesemia: Complete blood count Serum chemistry panel\r\nPediatric practitioners usually face the following four challenges regarding MAT in children:\r\nChallenges faced by pediatric practitioners while treating children with multifocal atrial tachycardia Challenges Details How to detect MAT early Early detection of MAT is very important in order to prevent the worse outcome in the case of infantile -onset MAT. Usually, tachycardia is first detected during the newborn period and the incidental detection of MAT not based on the clinical suspicion is rather high. Clinical suspicion of the infantile -onset of MAT is very important for its early detection. MAT lasting longer over several days without any proper management can lead to myocardial dysfunction which can further cause congestive heart failure due to tachycardia-induced cardiomyopathy. Hence, it is necessary to detect MAT early and immediately treat it with appropriate management to prevent CHF. How to control MAT Complete control of the MAT is not easily achievable even with high- dose combinations of multiple antiarrhythmic medications. A more realistic treatment goal is to initially reduce the percentage of MAT by achieving ventricular rate control. Various drugs such as beta-blockers, digoxin, and amiodarone have been used for the purpose, but there is not enough data to support the superiority of any one of these approaches. How deep to investigate etiologies of MAT As there are many varieties of etiologies of MAT in children, these etiologies should be described in detail in order to treat the underlying problems and get a better clinical outcome. Idiopathic infantile -onset group shows a favorable outcome compared to the other groups such as syndromic disease. RASopathy has been reported to be associated with a high incidence of atrial arrhythmias hence, MAT in children should be checked for the association of RASopathy and vice versa. How to predict another arrhythmia and outcome Atrial premature beats, atrial fibrillation (AF), or atrial flutter are known to accompany MAT in both adults and pediatric patients. MAT may be an early manifestation of catecholaminergic polymorphic ventricular tachycardia (CPVT) with additional findings of atrioventricular nodal reentrant tachycardia. Phenotypical progression of MAT into CPVT and an association between the RyR2 mutation and AF and ectopic atrial tachycardia have been reported. MAT in young children may be the initial manifestation of a potentially life -threatening arrhythmia of CPVT. Hence, aggressive evaluations and close follow-ups might be required for the non- infantile form of MAT with a structurally normal heart.\r\nMostly patients with multifocal atrial tachycardia are asymptomatic. MAT is often incidentally found during the routine electrocardiogram. Once the diagnosis of MAT is made, a thorough history should be obtained with main focus on commonly associated conditions such as cardiac and pulmonary diseases particularly congestive heart failure and chronic obstructive pulmonary disease respectively. The clinical manifestations of MAT differ from those of other tachyarrhythmias in that symptoms predominantly relate to the underlying precipitating illness rather than the arrhythmia itself. Patients usually present with: Irregular heart rate greater than 100 beats per minute (mostly identified only during the physical examination by the health care provider) Palpitations (rare) Presyncope (rare) Syncope (rare) Picture of a typical MAT patient is as follows: Elderly patient Decompensated pulmonary disease Decompensated heart failure Postoperative Usually hemodynamically stable (no severe hemodynamic compromise associated with MAT) High mortality ECG features in MAT patients include: P waves with ≥3 forms Atrial rate usually 100 to 200 bpm Irregular atrial rate Variable PR interval Isoelectric baseline between P waves May progress to atrial fibrillation\r\nPhysical examination findings of patients with multifocal atrial tachycardia include: Elevated heart rate usually greater than 100 bpm Irregularly irregular rhythm Hemodynamically stable (mostly) As MAT is associated with underlying medical conditions, hence, it is suggested to carry out a general assessment for the signs of cardiopulmonary disease, especially because MAT can trigger the decompensation of underlying cardiac and pulmonary disease.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is Erysipeloid and how is it categorized?", "role": "user" }, { "content": "Erysipeloid may be classified into the following categories according to the severity of the condition: \r\nUsually a mild, localized infection Patients present with localized swelling and redness of the skin Commonly referred to as \"erysipeloid of Rosenbach\"\r\nPatients may present with fever\r\nManifests as bacteremia with associated complications (e.g., endocarditis, arthritis)", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the natural progression, potential complications, and outlook of Lyme disease?", "role": "user" }, { "content": "Patients develops red, expanding rash called erythema migrans (EM). Flu-like symptoms such as fatigue, arthralgia, myalgias, headache, fever and/or chills, stiff neck, anorexia, and regional lymphadenopathy may be present.\r\nSome people may get these flu-like symptoms in addition to an EM rash, but in some, these flu-like symptoms may be the only evidence of infection.\r\nSome people get a small bump or redness at the site of a tick bite that goes away in 1-2 days, like a mosquito bite. This is not a sign that one has Lyme disease. However, ticks can spread other organisms that may cause a different type of rash. For example, Southern tick-associated rash illness (STARI) causes a rash with a very similar appearance. \r\nEM occurs in approximately 70-80% of infected persons and begins at the site of a tick bite after a delay of 3-30 days (average is about 7 days). Early EM may be homogenously erythematous without any central clearing.\r\nEM gradually expands over a period of several days, and can reach up to 12 inches (30 cm) across. Parts of the rash may clear as it enlarges, resulting in a bullseye appearance.\r\nThe rash usually feels warm to touch but is rarely itchy or painful.\r\nEM lesions may appear on any area of the body but is present the majority of the time on the axilla, inguinal region, or popliteal fossa. EM resolves in approximately 28 days in untreated patients. \r\nUntreated infection may spread from the site of the bite to other parts of the body, producing a range of symptoms including: Multiple EM lesions in other areas of the body. Multiple lesions are secondary to dissemination and are not to be confused with multiple tick bites Facial or Bell's palsy Severe headaches and neck stiffness due to meningitis Pain and swelling in the large joints (such as knees) Shooting pains that may interfere with sleep Heart palpitations and dizziness due to changes in heartbeat\r\nMany of these symptoms will resolve over a period of weeks to months, even without treatment. However, lack of treatment can result in additional complications.\r\nLyme arthritis is the hallmark of stage 3 Lyme disease. Lyme arthritis is the most frequently presented symptom in late disseminated Lyme disease. Lyme arthritis is not necessarily preceded by erythema migrans. Approximately 60% of patients with untreated infection may begin to have intermittent attacks of arthritis with severe joint pain and swelling. Intermittent attacks of Lyme arthritis range from 3 days to 11.5 months with a mean of 3 months. During early years of illness, attacks of Lyme arthritis are more frequent and longer in duration. Both frequency and duration of attacks subsequently decrease. There may be months or years of complete remission between each attack of Lyme arthritis. The majority of the time, Lyme arthritis involves large joints. The most commonly affected joint is knee joint, but any joint can be affected including the shoulder, ankle, elbow, temporomandibular joint, and wrist. Lyme arthritis manifests differently than other causes of arthritis and must be distinguished from other causes of arthralgias. Up to 5% of untreated patients may develop chronic neurological complaints months to years after infection. These include shooting pains, numbness or tingling in the hands and/or feet, and short-term memory disturbances.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the historical background of autoimmune lymphoproliferative syndrome?", "role": "user" }, { "content": "Autoimmune Lymphoproliferative Syndrome was first discovered by Canale and Smith, in 1967.Five patients were reported with lymphadenopathy, cytopenia and splenomegaly. The syndrome was initially named as Canale-Smith Syndrome. In 1990, ALPS was first characterized In 1992, a mutation of lpr (lymphoproliferation phenotype) and gld (generalized lymphoproliferative disease phenotype), a human equivalent of murine disease is reported. In 1995, association between inborn mutation of Fas gene and the development of Autoimmune lymphoproliferative syndrome was discovered. In 2003, new mutation in Fas Ligand (FasL) gene mutation and caspase 8 or 10 gene mutations.\r\nIn 1995, FAS gene mutation in ALPS was discovered. In 2009, an international workshop held at NIH in Uthe United States, announced revised diagnostic criteria and classification of ALPS. In 2017, mTOR inhibitor found to be an effective treatment for treatment refractory cytopenias related to ALPS.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does the physical examination of a dermoid cyst entail?", "role": "user" }, { "content": "Periorbital dermoid cyst in left eyebrow. The cyst was present at birth but was not noticeable at the time.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What information is currently available regarding Transient Tic Disorder?", "role": "user" }, { "content": "Transient tic disorder is a temporary condition in which a person makes one or many brief, repeated, difficult to control movements or noises (tics).", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you please clarify what you mean by \"proper English\"? The sentence \"What is peripheral neuropathy?\" is already in proper English. It is a grammatically correct and complete sentence.", "role": "user" }, { "content": "The pathophysiologic processes that can adversely affect peripheral nerves is very extensive. Processes which can damage the peripheral nerves at multiple levels via many molecular pathways include: Immunologic, metabolic, genetic, infectious, toxic and traumatic processes. Any pathologic process affecting the cell body will result in downstream degeneration of the cell's axon. Primary motor neuron diseases, such as ALS or SMA, demonstrate axonal pathology peripherally when central neurons degenerate. Similarly, metabolic conditions, such as diabetes, the metabolic syndrome, nutritional deficiencies, or chronic renal failure, affect DRG cell bodies by mechanisms involving insulin resistance, oxidative stress, and apoptosis. Pathologic damage may also be considered to take place directly at the axon, independent of the cell body. Schwann cells and the myelin sheath are often selectively targeted in immune-mediated processes such as GBS, CIDP, paraproteinemias, and their variants. It is theorized that a phenomenon of molecular mimicry occurs in these diseases, wherein glycoprotein epitopes found in myelin bear structural similarity to those found in other infectious agents. Immune recognition of these pathogens then spreads to include normal epitopes on the myelin sheath. Pathologic studies reveal both humoral and cellular immune activation and lymphocytic infiltration with patchy demyelination and remyelination. A number of GBS variants which are more prevalent in Asia and Central/South America also damage axons along with myelin, and are commonly associated with Campylobacter jejuni infection. Hereditary neuropathies can also affect both axons and/or their myelin sheaths. The most common type, hereditary motor sensory neuropathy (HMSN or Charcot-Marie-Tooth disease), is classified into many clinical subtypes. Many other genetic syndromes also produce varying disruption of Schwann cell, axon and/or neuronal function. Both the Schwann cells and axons of the peripheral nerve depend upon delicate vasa nervorum for perfusion and metabolic support. Many metabolic and inflammatory processes, while directly affecting peripheral nerves and neuronal cell bodies, can also result in damage to nerve vasculature and indirectly produce ischemic damage, particularly to axons. Primary vasculitides as well as other rheumatologic disorders (systemic lupus erythematosus, Sjögren's syndrome, nonsystemic vasculitis of the peripheral nerves, etc.)", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide an explanation of Hypoxemia and its classification?", "role": "user" }, { "content": "There is no established system for the classification of disease name.\r\nOR\r\nDisease name may be classified according to classification method into number subtypes/groups: group1, group2, group3, and group4.\r\nOR\r\nDisease name may be classified into large number > 6 subtypes based on classification method 1, classification method 2, and classification method 3. Disease name may be classified into several subtypes based on classification method 1, classification method 2, and classification method 3.\r\nOR\r\nBased on the duration of symptoms, disease name may be classified as either acute or chronic.\r\nOR\r\nIf the staging system involves specific and characteristic findings and features: According to the staging system + reference, there are number stages of malignancy name based on the finding1, finding2, and finding3. Each stage is assigned a letter/number1 and a letter/number2 that designate the feature1 and feature2.\r\nOR\r\nThe staging of malignancy name is based on the staging system.\r\nOR\r\nThere is no established system for the staging of malignancy name.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What exactly is Rickettsia rickettsii?", "role": "user" }, { "content": "In vivo studies reveal that Rickettsia rickettsii invade endothelial lining of small to medium vessels in the human host, causing vascular permeability. When tested in vitro, it is shown that the bacterium infects every kind of cell of the mammalian host.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you provide me the exact sentence to rephrase?", "role": "user" }, { "content": "Adrenal insufficiency may be classified according to location of pathology into three subtypes primary adrenal insufficiency, secondary adrenal insufficiency, and tertiary adrenal insufficiency.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does Coxsackie mean?", "role": "user" }, { "content": "Coxsackie (virus) is a cytolytic virus of the picornaviridae family, an enterovirus (a group containing the polioviruses, coxsackieviruses, and echoviruses). There are 61 non-polio enteroviruses that can cause disease in humans, of which 23 are coxsackie A viruses (6 are coxsackie B viruses). Enterovirus are the second most common viral infectious agents in humans (after the rhinoviruses).", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you explain what sinus tachycardia means?", "role": "user" }, { "content": "Inappropriate sinus tachycardia is an uncommon form of supraventricular tachycardia (SVT).", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What exactly is cholangiocarcinoma, and what are the factors that contribute to its development?", "role": "user" }, { "content": "Common causes of cholangiocarcinoma include cirrhosis, viral hepatitis, gallstones and primary sclerosing cholangitis.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is metabolic syndrome, and which information is currently available regarding it?", "role": "user" }, { "content": "The goal of treatment is to reduce your risk of heart disease and diabetes. Your doctor will recommend lifestyle changes or medicines to help reduce your blood pressure, LDL cholesterol, and blood sugar.\r\nRecommendations include:\r\nLose weight. The goal is to lose between 7% and 10% of your current weight. You will probably need to eat 500 - 1,000 fewer calories per day. Get 30 minutes of moderate intensity exercise, such as walking, 5 - 7 days per week. Lower your cholesterol using weight loss, exercise, and cholesterol lowering medicines, if needed. Lower your blood pressure using weight loss, exercise, and medicine, if needed.\r\nSome people may need to take daily low-dose aspirin. People who smoke should quit.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the laboratory findings associated with cancer of the small intestine?", "role": "user" }, { "content": "Laboratory findings in patients with small intestine cancer include: \r\nComplete blood count and differential count - anemia Fecal occult blood test (FOBT) - demonstrates occult bleeding from the intestines Serum carcino-embryogenic antigen (CEA) and CA 19-9 - elevated concentrations are associated with large tumor masses, and have a poor prognosis Low serum iron levels Low serum vitamin B12 and folate levels Hypercalcemia - with metastasis to the bone\r\nAbnormal liver function tests Abnormal pulmonary function tests", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the main methods of prevention for dysplastic nevus?", "role": "user" }, { "content": "The following preventive measures reduce the risk of melanoma: \r\nAvoid sunlight and ultraviolet radiation exposure\r\nUse sunblocks (at least 15 SPF) when exposed to sunlight. Reapply sunblock every 2-3 hours and after sweating/swimming Seek shaded areas Wear wide-brimmed hats Avoid sunbeds", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the possible conditions that could be causing a thoracic aortic aneurysm?", "role": "user" }, { "content": "Abdominal aortic aneurysms Acute myocardial infarction Congestive heart failure Aortic regurgitation Blunt chest trauma Hypertensive emergency Hemothorax Pneumothorax Pericarditis Pulmonary embolism Cardiac tamponade Superior vena cava syndrome\r\nThoracic aortic aneurysm should be differentiated from other diseases presenting with chest pain, shortness of breath and tachypnea. The differentials include the following: \r\n\r\nDiseases Diagnostic tests Physical Examination Symptoms Past medical history Other Findings CT scan and MRI EKG Chest X-ray Tachypnea Tachycardia Fever Chest Pain Hemoptysis Dyspnea on Exertion Wheezing Chest Tenderness Nasalopharyngeal Ulceration Carotid Bruit Pulmonary embolism On CT angiography: Intra-luminal filling defect On MRI: Narrowing of involved vessel No contrast seen distal to obstruction Polo-mint sign (partial filling defect surrounded by contrast) S1Q3T3 pattern representing acute right heart strain Fleischner sign (enlarged pulmonary artery), Hampton hump, Westermark's sign ✔ ✔ ✔ (Low grade) ✔ ✔ (In case of massive PE) ✔ - - - - Hypercoagulating conditions (Factor V Leiden, thrombophilia, deep vein thrombosis, immobilization, malignancy, pregnancy) May be associated with metabolic alkalosis and syncope Congestive heart failure On CT scan: Mediastinal lymphadenopathy Hazy mediastinal fat On MRI: Abnormality of cardiac chambers (hypertrophy, dilation) Delayed enhancement MRI may help characterize the myocardial tissue (fibrosis) Late enhancement of contrast in conditions such as myocarditis, sarcoidosis, amyloidosis, Anderson-Fabry's disease, Chagas disease) Goldberg's criteria may aid in diagnosis of left ventricular dysfunction: (High specificity) S V1 or S V2 + R V5 or R V6 ≥3.5 mV Total QRS amplitude in each of the limb leads ≤0.8 mV R / S ratio <1 in lead V4 Cardiomegaly ✔ ✔ ✔ - - ✔ - - - - Previous myocardial infarction Hypertension (systemic and pulmonary) Cardiac arrythmias Viral infections (myocarditis) Congenital heart defects Right heart failure associated with: Hepatomegaly Positive hepato-jugular reflex Increased jugular venous pressure Peripheral edema Left heart failure associated with: Pulmonary edema Eventual right heart failure Percarditis On contrast enhanced CT scan: Enhancement of the pericardium (due to inflammation) Pericardial effusion Pericardial calcification On gadolinium -enhanced fat-saturated T1-weighted MRI: Pericardial enhancement (due to inflammation) Pericardial effusion ST elevation PR depression Large collection of fluid inside the pericardial sac (pericardial effusion) Calcification of pericardial sac ✔ ✔ ✔ (Low grade) ✔ (Relieved by sitting up and leaning forward) - ✔ - - - - Infections: Viral (Coxsackie virus, Herpes virus, Mumps virus, HIV) Bacteria (Mycobacterium tuberculosis -common in developing countries) Fungal (Histoplasmosis) Idiopathic in a large number of cases Autoimmune Uremia Malignancy Previous myocardial infarction May be clinically classified into: Acute (< 6 weeks) Sub-acute (6 weeks - 6 months) Chronic (> 6 months) Pneumonia On CT scan: (not generally indicated) Consolidation (alveolar /lobar pneumonia) Peribronchial nodules (bronchopneumonia) Ground-glass opacity (GGO) Abscess Pleural effusion On MRI: Not indicated Prolonged PR interval Transient T wave inversions Consolidation (alveolar /lobar pneumonia) Peribronchial nodules (bronchopneumonia) Ground-glass opacity (GGO) ✔ ✔ ✔ ✔ - ✔ ✔ - - - Ill-contact Travelling Smoking Diabetic Recent hospitalization Chronic obstructive pulmonary disease Requires sputum stain and culture for diagnosis Empiric management usually started before culture results Vasculitis On CT scan: (Takayasu arteritis) Vessel wall thickening Luminal narrowing of pulmonary artery Masses or nodules (ANCA -associated granulomatous vasculitis) On MRI: Homogeneous, circumferential vessel wall swelling Right or left bundle-branch block (Churg-Strauss syndrome) Atrial fibrillation (Churg-Strauss syndrome) Non-specific ST segment and T wave changes Nodules Cavitation ✔ ✔ ✔ ✔ ✔ ✔ - ✔ ✔ ✔ Takayasu arteritis usually found in persons aged 4-60 years with a mean of 30 Giant-cell arteritis usually occurrs in persons aged > 60 years Churg-Strauss syndrome may present with asthma, sinusitis, transient pulmonary infiltrates and neuropathy alongwith cardiac involvement Granulomatous vasculitides may present with nephritis and upper airway (nasopharyngeal) destruction Chronic obstructive pulmonary disease (COPD) On CT scan: Chronic bronchitis may show bronchial wall thickening, scarring with bronchovascular irregularity, fibrosis Emphysema may show alveolar septal destruction and airspace enlargement (Centrilobular- upper lobe, panlobular- lower lobe) Giant bubbles On MRI: Increased diameter of pulmonary arteries Peripheral pulmonary vasculature attentuation Loss of retrosternal airspace due to right ventricular enlargement Hyperpolarized Helium MRI may show progressively poor ventilation and destruction of lung Multifocal atrial tachycardia (atleast 3 distinct P wave morphologies) Enlarged lung shadows (emphysema) Flattening of diaphragm (emphysema) ✔ ✔ - - - ✔ ✔ - - - Smoking Alpha-1 antitrypsin deficiency Increased sputum production (chronic bronchitis) Cough Alpha 1 antitrypsin deficiency may be associated with hepatomegaly\r\nTemplate:WH Template:WS", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does gamma-glutamyl transpeptidase mean?", "role": "user" }, { "content": "Gamma-glutamyl transferase (GGT or GGTP, or Gamma-GT) (EC 2.3.2.2) is primarily a liver enzyme.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the different possible diagnoses for breast cancer?", "role": "user" }, { "content": "ABBREVIATIONS LAP=Lymphadenopathy, HRT=Hormonal replacement therapy, FNA=Fine needle aspiration, DCIS=Ductal carcinoma in-situ\r\n\r\nDiseases Benign or Malignant Clinical manifestation Paraclinical findings Gold standard diagnosis Demography History Symptoms Signs Histopathology Imaging Mass Mastalgia Nipple discharge Breast exam Skin changes LAP Fibroadenoma Benign Very slight increased risk of breast cancer in complex fibroadenoma Most common benign tumor, women aged 20-30 years Increases in size during pregnancy or with estrogen therapy, and regress after menopause + ± – Solitary Well-defined Mobile mass – – Proliferative breast lesion without atypia Ultrasound: Well-defined Solid mass Mammography Ultrasound Biopsy Breast cyst Benign No increased risk of malignancy for simple cyst <1% for complicated cyst <1% to 23% for complex cyst Common masses found in premenopausal, perimenopausal, and postmenopausal women Mostly seen among HRT users May resolve after aspiration Further evaluation for unresolved masses + ± – Solitary Cluster of small masses or an ill-defined mass Smooth, firm, and frequently tender – – Nonproliferative breast lesions Ultrasound: Simple cyst: Well circumscribed, posterior acoustic enhancement without internal echoes Complicated cyst: Homogenous low-level internal echoes due to without solid components Complex cyst: Thick walls greater than 0.5 mm with solid component Ultrasound Fine needle aspiration (FNA) Fibrocystic change Benign No increased risk of malignancy Slightly increased risk of malignancy in presence of positive familial history of breast cancer Unknown prevalence among adolescents >50% in women of reproductive age Present before menses and improve during menstruation + + ± Painful breast tissue Tender, nodular swelling – – Nonproliferative breast lesions Ultrasound: Small cysts in mammary zone Fibroglandular tissue around the mass Ultrasound Mammography (it is not recommended for adolescents) Galactocele Benign No increased risk of malignancy Milk retention cysts with fluid collection among pregnant women and during breast-feeding After ending lactation, the cysts resolve + ± ± Soft masses Cystic masses – – Inflammation of lactate ducts due to extension, results in wall fibrosis Mammography: Intermediate mass in absence of classic fat-fluid level Ultrasound: Complex mass Ultrasound Mammography Cysts of montgomery Benign No increased risk of malignancy Most common in age of 10-20 years old More than 80% resolve spontaneously Drainage is essential in rare cases + ± ± Asymptomatic subareolar mass Drainage of clear to brownish fluid ± – Acute inflammation due to obstruction of the Montgomery's gland Ultrasound: Single cystic lesion in retroareolar area Ultrasound Hamartoma Benign Coexisting malignancy may be present Common in women older than 35 years old Asymptomatic ones found incidentally or painless breast lump Usually excised ± – – Soft breast lump Breast enlargement without palpable mass ± – Benign proliferation of fibrous, glandular, and fatty tissue Thin capsule of connective tissue Mammography: Well-described Discrete, solid, and encapsulated lesion Ultrasound Mammography Breast abscess Benign No increased risk of malignancy Complication of lactational mastitis in 14% of cases Common among African-American women, heavy smokers, and obese patients Resolve after drainage/ antibiotic therapy + + – Localized inflammation of breast Tenderness + – Mixed inflammatory feature by neutrophils. Granulation tissue and chronic inflammation feature caused by Gram-positive cocci Ultrasound: Fluid collection Ultrasound Mastitis Benign No increased risk of malignancy Common among lactating women (first three months of breast-feeding) Periductal mastitis among smokers and associated with squamous metaplasia Resolve after drainage/ antibiotic therapy ± + ± Breast tenderness Swollen breast tissue + – Breast parenchyma inflammation: Acute mastitis: Staphylococcus infection Granulomatous mastitis: Tuberculosis or sarcoidosis infection Ultrasound: Ill-defined area with hyperechogenicity with inflamed fat lobules Skin thickening Ultrasound Diseases Benign or Malignant Demography History Mass Mastalgia Nipple discharge Breast exam Skin changes LAP Histopathology Imaging Gold standard diagnosis Breast carcinoma Malignant Most common diagnosed cancer among women Leading cause of cancer death in women 40-49 years old Positive family history + – ± Hard Immobile Solitary Irregular margin ± ± Molecular alteration in epithelial cells Ductal Lobular Ductal/lobular Mucinous Tubular Medullary Papillary Mammography: Spiculated soft tissue, mass microcalcification Ultrasound: Spiculated, hypoechoic lesion, shadowing, internal calcification Ultrasound Mammography Ductal carcinoma in situ (DCIS) Malignant Approximately 25% of all breast cancers Increase risk with ageing Positive family history Nulliparity Obesity ± – ± May have normal physical exam – – Noninvasive breast cancer Heterogenous group of neoplastic lesions Mammography: Suspicious microcalcification Mammography Microinvasive breast cancer Malignant Rare Commonly referred to DCIS with microinvasion Average age 50-60 years old Nulliparity Positive family history + – ± Solitary Firm palpable mass – ± Associated with high grade DCIS Mammography: A mass with or without calcification Stromal reaction Mammography Breast sarcoma Malignant Rare type, < 1% of all breast malignancies Average age of between 45-50 years Positive history of breast cancer Rapid increase in size + – – Well-defined Firm mass ± – Heterogeneous nonepithelial malignancies from connective tissue of breast Mammography: Noncalcified oval mass Indistinct margins Mammography Phyllodes tumor Benign or Malignant Most common in premenopausal women (40-50 years) Represent 1% of breast tumors Grow aggressively Classify in benign, borderline, and malignant groups ± – – Smooth and multinodular Well-defined Firm mass Mobile – – Nonepithelial breast neoplasm with average size of 5 cm Ultrasound: Solid mass Hypoechoic Well-circumscribed Mammography: Smooth mass Polylobulated mass Ultrasound Mammography Lymphoma Malignant Extremely rare (0.04%-0.5%) Average age 55-60 years Unilateral mass in older women In childbearing women, bilateral and similar to inflammatory breast cancer, possibly having Burkitt lymphoma + – – Well-defined, firm mass Multiple – ± Diffuse growth pattern with large cells like immunoblast associated with neutrophils Mammography: Nonspecific circumscribed masses Without calcification Mammography Core biopsy Duct ectasia Benign Common among perimenopausal women Usually resolve spontaneously ± ± ± Usually asymptomatic – – Distention of subareolar ducts Ultrasound: Dilated milk ducts Fluid-filled ducts Ultrasound Intraductal papilloma Benign Common in women between 35-55 years old Possibly benign Harbor areas of atypia or DCIS Surgical excision is recommended + ± ± Solitary or multiple lesion Large lump near nipple – – Growth of papillary cell into a lumen Ultrasound: Well-defined Solid nodule Core needle biopsy Lipoma Benign Common between age of 40-60 years old Benign tumors May experience recurrence + – – Solitary Mobile Soft mass – – Mature adipocytes without lipoblasts or atypia Ultrasound: Well-Circumscribed Hypoechoic lesion Core needle biopsy Excisional biopsy Sclerosing adenosis Small risk of malignancy Recurrent pain during mensturation May present as a mass or incidental finding on mammogram No treatment is needed ± + – Multiple lesion Firm Tender nodules ± – Proliferative disease Mammography: Well-defined or irregular mass Microcalcification Mammography Pseudoangiomatous stromal hyperplasia Benign Common in reproductive age women Benign stromal proliferation Stimulation of vascular lesion + – – Solitary firm mass Thickening – – Slit-like spaces between glandular units Maybe confused with mammary angiosarcoma Mammography and ultrasound: Well-defined Solid mass Noncalcified Ultrasound Mammography Mondor's disease Benign Uncommon benign disease Occur on outer side of breast or under nipple Benign and self-limiting disease Resolve after 4-6 weeks + + – Thick and tender cord on breast skin + – N/A Ultrasound: Tubular anechoic structure Multiple narrowing areas Clinical examination Ultrasound Diseases Benign or Malignant Demography History Mass Mastalgia Nipple discharge Breast exam Skin changes LAP Histopathology Imaging Gold standard diagnosis Diabetic mastopathy Benign Lymphocytic mastitis or mastopathy Common among premenopausal women Longstanding diabetes mellitus type 1 Suspicious breast mass After diagnosis, excision is not required + – – Ill-defined mass Immobile – – Dense keloid-like fibrosis Periductal, lobular, and perivascular lymphocytic infiltration Ultrasound: Irregular mass Hypoechoic Dense lesion Ultrasound Core needle biopsy Gynecomastia Benign Benign breast tissue swelling among men and boys around puberty Benign proliferation of the male breast glandular tissue Usually underlying nipple mass At least 0.5 cm + ± ± Unilateral or bilateral firm mass Breast swelling Rubbery mass – – Glandular breast changes Ultrasound: Nodular pattern Dendritic pattern Diffuse glandular pattern Ultrasound Sarcoidosis Benign Rare in patients with systemic involvement Benign palpable mass May mimic malignancy feature + – – Firm mass Hard mass – – Epithelioid granulomas with multinucleated giant cell with rare necrosis Mammography: Irregular Ill-defined Spiculated solid mass Biopsy Fat necrosis Benign Common among women May mimic malignancy features Benign breast lumps develop after trauma / surgery Suspicious lumps required biopsy No excision in established diagnosis + ± – Hard or smooth mass Solitary mass Mobile – – Collections of liquefied fat Ultrasound: Collections of liquefied fat Oil cysts Ultrasound", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is Panniculitis and what conditions are associated with it?", "role": "user" }, { "content": "Lipoatrophy (the loss of subcutaneous tissue) can occur in any of these conditions.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide an overview of the infection caused by cytomegalovirus?", "role": "user" }, { "content": "Primary infection in majority of patients have a mononucleosis like presentation. Patients with immunosuppression have symptoms related to the affected organ system. Retinitis presents with blurred vision and floaters. Colitis presents with abdominal pain and bloody diarrhea. Pneumonitis is usually asymptomatic. Neurologic infection presents with altered mental status and focal neurological deficits.\r\nThe appearance of the patient depends on the stage of the disease. The patient may look very healthy or be ill-looking and cachectic. On fundus examination fluffy yellow-white retinal lesions, with or without intraretinal hemorrhages can be demonstrated in patients with CMV retinitis. Abdominal distension and tenderness can be present on examination in patients with CMV colitis. In patients with CMV encephalitis altered mental status and focal neurological deficits are present.\r\nThere are no specific laboratory findings associated with CMV infection. Elevated ESR and a low lymphocyte count may be present in patients with complications. Diagnosis is usually done by demonstration of the inclusion bodies from the tissue biopsies or by a positive PCR for CMV DNA.\r\nThere are no EKG changes associated with cytomegalovirus infection.\r\nChest X-Ray in cytomegalovirus pneumonitis demonstrates diffuse pulmonary interstitial infiltrates.\r\nCT scan of the abdomen in patients with CMV colitis demonstrates colonic thickening. On brain CT, the presence of periventricular enhancement is suggestive of ventriculoencephalitis which is a common (but non-specific) finding in CMV encephalitis.\r\nPeriventricular enhancement is present in patients with ventriculoencephalitis on brain MRI.\r\nThere are no echocardiography findings associated with CMV infection.\r\nCMV infection is diagnosed by demonstration of intranuclear inclusion bodies and a positive PCR, therefore there are no other specific imaging findings for CMV infection.\r\nOther diagnostic studies helpful for the diagnosis of CMV infection include upper GI endoscopy, colonoscopy, serology and PCR.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the potential treatments or therapies being currently researched for Hemophilia in the future?", "role": "user" }, { "content": "Future and investigational therapies of hemophilia include co-transplantation of endothelial colony-forming cells (ECFCs) and placenta -derived mesenchymal stromal cells (PMSCs) at the neonatal age and prevention of the anti- factor VIII memory B-cell response.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you suggest some additional diagnostic tests for Acne Vulgaris?", "role": "user" }, { "content": "There are no other diagnostic studies associated with acne vulgaris.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the recommended imaging technique, either echocardiography or ultrasound, for diagnosing follicular thyroid cancer?", "role": "user" }, { "content": "Key ultrasound findings in thyroid cancer are:\r\nLarge size, microcalcifications, and hypoechogenicity Lymphadenopathy Microcalcifications- most specific finding associated with malignancy (~95%) Coarse calcifications Peripheral rim calcification Isoechoic solid nodule A nodule taller than it is wide Irregular margins\r\nThe lymph node findings are:\r\nEnlarged regional lymph nodes are suspicious for thyroid malignancy Microcalcifications in regional lymph nodes are highly suspicious Lymph nodes with cystic change are highly suspicious Loss of normal fatty hilum, irregular node appearance Increased colour Doppler flow is suspicious Low threshold criteria for lymph node biopsy Biopsy if suspicious features Consider biopsy if >8 mm", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide a summary of Waldenström's macroglobulinemia?", "role": "user" }, { "content": "Primary prevention of Waldenstrom's macroglobulinemia depends on avoiding the type of modifiable risk factor causing the disease such as hepatitis C, HIV, rickettsiosis, hay fever, human T-lymphotrophic virus type 1 infection, epstein-Barr virus infection, environmental factors, history of helicobacter pylori infection, history of immunosuppressant drug therapy after an organ transplant, diet rich in meat and fat and history of past treatment for hodgkin lymphoma.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the laboratory results of pre-eclampsia?", "role": "user" }, { "content": "Laboratory findings consistent with the diagnosis of preeclampsia include: elevated liver enzyme tests, thrombocytopenia, elevated serum creatinine, and elevated serum uric acid. An elevated concentration of liver enzymes, low platelets, and hemolysis are diagnostic of HELLP syndrome.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does antepartum hemorrhage mean?", "role": "user" }, { "content": "Bloody show (benign) - most common cause of APH Placental abruption - most common pathological cause Placenta previa - second most common pathological cause Vasa previa - often difficult to diagnose, frequently leads to fetal demise Uterine rupture Bleeding from the lower genital tract Cervical bleeding - cervicitis, cervical neoplasm, cervical polyp Bleeding from the vagina itself - trauma, neoplasm Bleeding that may be confused with vaginal bleeding GI bleed - hemorrhoids, inflammatory bowel disease Urinary tract bleed - urinary tract infection", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the potential future or experimental treatments for mantle cell lymphoma?", "role": "user" }, { "content": "Recent advances in the understanding of the pathogenesis of mantle cell lymphoma have led to the development of targeted therapies which have shown potential promise as effective therapeutic approaches in the future.. In addition to the ongoing assessment of new monoclonal antibody-based therapies, the continued development of targeted molecular signaling inhibitors based on the underlying biology of MCL is an approach that will potentially yield fruitful results in this disease. Some of the current therapies under clinical investigation are as follows: BCL-2 inhibitor venetoclax (ABT-199) and the phosphatydilinosytol 3-kinase δ (PI3K δ) inhibitor idelalisib were tested in a phase I study and have shown promising results. Chimeric antigen receptor T-cell (CAR-T) therapy is being used in a phase II study of CAR-T therapy in relapsed MCL. Due to the male to female predominance of approximately 4:1 in MCL, investigators are investigating androgen receptor (AR) blockers like enzalutamide as means of decreasing MCL cell proliferation. A few next-generation proteasome inhibitors (carfilzomib, oprozomib, ixazomib) are undergoing clinical testing in MCL and have shown an acceptable safety profile in bortezomib -resistant MCL patients.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What information is available on folliculitis?", "role": "user" }, { "content": "Folliculitis may return Infection may spread to other body areas", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What do hand and foot rashes refer to?", "role": "user" }, { "content": "The content on this page was first contributed by\r\nList of contributors:", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you provide me with the current phrasing of the sentence so that I can rephrase it for you correctly?", "role": "user" }, { "content": "Medical history questions may include:\r\nDid this problem develop suddenly or slowly? Is it getting worse (progressive)? How bad is it? How many pillows does the patient need to help make breathing comfortable? Is there any ankle, feet, or leg swelling ? Does the patient have difficulty breathing at other times? How tall is the patient? How much does the patient weigh? What other symptoms does the patient have?", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What information is available regarding Empty Sella Syndrome?", "role": "user" }, { "content": "Primary empty sella syndrome is most often discovered during radiological imaging of the brain. Pituitary function is usually normal.\r\nThe health care provider may test pituitary gland function to make sure that the gland is working normally.\r\nSometimes tests for high pressure in the brain will be done, such as:\r\nExamination of the retina by an ophthalmologist Lumbar puncture (spinal tap)\r\nThe hormone prolactin is a little high in a small percentage of patients, which may interfere with the normal function of the testicles or ovaries.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the potential diagnoses to consider for parathyroid cancer?", "role": "user" }, { "content": "Parathyroid cancer must be differentiated from other conditions presenting as a neck swelling.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the criteria for performing percutaneous coronary intervention in cases of stable angina with a chronic diagnosis?", "role": "user" }, { "content": "Class III \" 1. PCI is not recommended in patients with asymptomatic ischemia or CCS class I or II angina who do not meet the criteria as listed under the class II recommendations or who have 1 or more of the following: a. Only a small area of viable myocardium at risk. (Level of Evidence: C) b. No objective evidence of ischemia. (Level of Evidence: C) c. Lesions that have a low likelihood of successful dilatation. (Level of Evidence: C) d. Mild symptoms that are unlikely to be due to myocardial ischemia. (Level of Evidence: C) e. Factors associated with increased risk of morbidity or mortality. (Level of Evidence: C) f. Left main disease and eligibility for CABG. (Level of Evidence: C) g. Insignificant disease (less than 50% coronary stenosis). (Level of Evidence: C) \"\r\nClass IIa \" 1. PCI is reasonable in patients with asymptomatic ischemia or CCS class I or II angina and with 1 or more significant lesions in 1 or 2 coronary arteries suitable for PCI with a high likelihood of success and a low risk of morbidity and mortality. The vessels to be dilated must subtend a moderate to large area of viable myocardium or be associated with a moderate to severe degree of ischemia on noninvasive testing. (Level of Evidence: B) \" \" 2. PCI is reasonable for patients with asymptomatic ischemia or CCS class I or II angina, and recurrent stenosis after PCI with a large area of viable myocardium or high-risk criteria on noninvasive testing. (Level of Evidence: C) \" \" 3. Use of PCI is reasonable in patients with asymptomatic ischemia or CCS class I or II angina with significant left main CAD (greater than 50% diameter stenosis) who are candidates for revascularization but are not eligible for CABG. (Level of Evidence: B) \"\r\nClass IIb \" 1. The effectiveness of PCI for patients with asymptomatic ischemia or CCS class I or II angina who have 2- or 3-vessel disease with significant proximal LAD CAD who are otherwise eligible for CABGwith 1 arterial conduit and who have treated diabetes or abnormal LV function is not well established. (Level of Evidence: B) \" \" 2. PCI might be considered for patients with asymptomatic ischemia or CCS class I or II angina with non-proximal LAD CAD that subtends a moderate area of viable myocardium and demonstrates ischemia on noninvasive testing. (Level of Evidence: C) \"\r\nClass III \" 1. PCI is not recommended for patients with CCS class III angina with single-vessel or multivessel CAD, no evidence of myocardial injury or ischemia on objective testing, and no trial of medical therapy, or who have 1 of the following: a. Only a small area of myocardium at risk. (Level of Evidence: C) b. All lesions or the culprit lesion to be dilated with morphology that conveys a low likelihood of success. (Level of Evidence: C) c. A high risk of procedure-related morbidity or mortality. (Level of Evidence: C) d. Insignificant disease (less than 50% coronary stenosis). (Level of Evidence: C) e. Significant left main CAD and candidacy for CABG. (Level of Evidence: C) \"\r\nClass IIa \" 1. It is reasonable that PCI be performed in patients with CCS class III angina and single-vessel or multi-vessel CAD who are undergoing medical therapy and who have 1 or more significant lesions in 1 or more coronary arteries suitable for PCI with a high likelihood of success and low risk of morbidity or mortality. (Level of Evidence: B) \" \" 2. It is reasonable that PCI be performed in patients with CCS class III angina with single-vessel or multi-vessel CAD who are undergoing medical therapy with focal saphenous vein graft lesions or multiple stenoses who are poor candidates for reoperative surgery. (Level of Evidence: C) \" \" 3. Use of PCI is reasonable in patients with CCS class III angina with significant left main CAD (greater than 50% diameter stenosis) who are candidates for revascularization but are not eligible for CABG. (Level of Evidence: B) \"\r\nClass IIb \" 1. PCI may be considered in patients with CCS class III angina with single-vessel or multivessel CAD who are undergoing medical therapy and who have 1 or more lesions to be dilated with a reduced likelihood of success. (Level of Evidence: B) \" \" 2. PCI may be considered in patients with CCS class III angina and no evidence of ischemia on noninvasive testing or who are undergoing medical therapy and have 2- or 3-vessel CAD with significant proximal LAD CAD and treated diabetes or abnormal LV function. (Level of Evidence: B) \"", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the role of ultrasound in the management of acute viral nasopharyngitis?", "role": "user" }, { "content": "There are no ultrasound findings associated with acute viral nasopharyngitis.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the explanation of the relationship between Endoscopy and History?", "role": "user" }, { "content": "The first endoscope, of a kind, was developed in 1806 by Philip Bozzini with his introduction of a \"Lichtleiter\" (light conductor) \"for the examinations of the canals and cavities of the human body\". However, the Vienna Medical Society disapproved of such curiosity. An endoscope was first introduced into a human in 1822 by William Beaumont, an army surgeon at Mackinac Island, Michigan. The use of electric light was a major step in the improvement of endoscopy. The first such lights were external. Later, smaller bulbs became available making internal light possible, for instance in a hysteroscope by Charles David in 1908. Hans Christian Jacobaeus has been given credit for early endoscopic explorations of the abdomen and the thorax with laparoscopy (1912) and thoracoscopy (1910). Laparoscopy was used in the diagnosis of liver and gallbladder disease by Heinz Kalk in the 1930s. Hope reported in 1937 on the use of laparoscopy to diagnose ectopic pregnancy. In 1944, Raoul Palmer placed his patients in the Trendelenburg position after gaseous distention of the abdomen and thus was able to reliably perform gynecologic laparoscopy.\r\nThe first gastrocamera was released in 1950 by Olympus Optical Co., Ltd. The device took pictures on monochromatic film using a small light bulb that was triggered manually. The device was of limited use, however, because it did not implement real-time optical capability. Olympus continued its development of endoscopes by incorporating fiber optics in the early 1960s, leading to the first useful endoscopes. In 1964, it released a gastrocamera guided by a fiberscope. A few articles claim that Dr.Basil Hirschowitz of Univ.Of Michigan,Ann Arbor discussed the endoscope in early 50's. \r\nAs endoscopic technology improved, so did the methods of gastrointestinal endoscopy. Owing primarily to the efforts of Dr. Hiromi Shinya in the late 1960s, GI endoscopy developed into what is more recognizable as today's colonoscopy. While many doctors experimented with techniques to take advantage of the new iterations of endoscopes, Dr. Shinya focused on techniques that would allow for successful operation of the endoscope by an individual, rejecting the common practice at the time of utilizing two people. Consequently, many of the fundamental methods and procedures of modern colonoscopy were developed by Dr. Shinya.\r\nDr. Shinya's other great contribution was to therapeutic endoscopy, in his invention of the electrosurgical polypectomy snare with the aid of Olympus employee Hiroshi Ichikawa. Shinya sketched his first plans for the device on January 8, 1969. He envisioned a loop of wire attached to the end of a colonoscope that would allow for easy removal of polyps during investigation by passing a current through the wire. By September of 1969, the first polypectomy using this device was performed. Polypectomy has since become the most common therapeutic procedure performed with an endoscope. Template:Wikiref\r\nBy 1980, laparoscopy training was required by gynecologists to perform tubal ligation procedures and diagnostic evaluations of the pelvis. The first laparoscopic cholecystectomy was performed in 1984 and the first video-laparoscopic cholecystectomy in 1987. During the 1990s, laparoscopic surgery was extended to the appendix, spleen, colon, stomach, kidney, and liver. Wireless capsule endoscopy or Capsule Endoscopy is now approved in all the countries including Japan where government reimbusement will be available from Oct.2007.Capsule Endoscopy increases detection of Small Bowel tumors where traditional Endoscopy is not very efficient.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the factors that increase the risk of hyperosmolar hyperglycemic state?", "role": "user" }, { "content": "The following factors are associated with an increased risk of hyperosmolar hyperglycemic state (HHS): \r\nOld age Obesity High mean glycosylated hemoglobin A1c (HbA1c) Infection Physiological stressors: Acromegaly Thrombosis Cerebrovascular accident Cushing's disease Hemochromatosis Pregnancy\r\nHeatstroke Hypothermia Dialysis Burns Neuroleptic malignant syndrome Rhabdomyolysis Depression Lack of health insurance Low body mass index (BMI) Delayed or improper management of diabetes\r\nThe following factors are associated with a reduced risk of hyperosmolar hyperglycemic state (HHS): \r\nOptimum management of diabetes Optimum fluid intake Adequate renal functions Adequate cardiac functions Higher education level of patient Higher education level of care giver", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the laboratory results for pertussis?", "role": "user" }, { "content": "There are differences in the diagnostic needs of the clinical versus the public health setting. In the clinical setting, the goal is to optimize sensitivity while providing rapid results. This ensures rapid diagnosis and appropriate treatment to prevent further transmission. In the public health setting, a high degree of specificity is needed to avoid unnecessary and ineffective public health interventions. Several types of laboratory tests are commonly used for the diagnosis of Bordetella pertussis. Culture is considered the gold standard because it is the only 100% specific method for identification. Other tests that can be performed include polymerase chain reaction (PCR) and serology.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What laboratory findings are associated with Otitis media?", "role": "user" }, { "content": "Laboratory tests are not usually used for diagnosing otitis media. The following test results may, however, indicate otitis media as general markers of inflammation:\r\nWhite Blood Cell Count A complete blood count test performed on otitis media patients may reveal abnormal lymphocyte and other white blood cell counts, lesser or greater than normal. Markers for Inflammation Otitis media patients may display markers for inflammation, determined by the following tests: Erythrocyte sedimentation rate C-reactive protein", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What information is currently available about Von Willebrand disease?", "role": "user" }, { "content": "http://www.nlm.nih.gov/medlineplus/ency/article/000544.htm\r\nTemplate:WH Template:WS", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the reasons for the occurrence of eosinophilia?", "role": "user" }, { "content": "Adrenal insufficiency Asthma Atheroembolic disease Atopic dermatitis Fungal infections Hypereosinophilic syndromes Immunodeficiency states Leukemia Lymphoma Mastocytosis Medication-related eosinophilia Parasitic infections Rhinitis syndromes Vasculitis\r\nAcanthocheilonemiasis Acute eosinophilic leukemia Acute lymphoblastic leukemia Acute myeloid leukemia Addison's disease Adrenocortical insufficiency Aggressive systemic mastocytosis Aldesleukin Alfotax Allergic bronchopulmonary aspergillosis Allergic inflammation Allergic rhinitis Allopurinol Alveolar hydatid disease Amebiasis Amikacin sulfate Amikafur Amikayect Amikin Amitriptyline Ampicillin Amoxicillin Ancylostoma caninum Ancylostoma duodenale Angiolymphoid hyperplasia with eosinophilia Angiostrongyliasis costaricensis Anisakiasis Anthelmintic Artemether and lumefantrin Ascariasis Aspergillosis Aspirin Asthma Atheroembolic disease Atopic and related diseases Atopic dermatitis Auranofin Autoimmune lymphoproliferative syndrome type 1 Autoimmune lymphoproliferative syndrome type 2 Aztreonam B cell non-Hodgkin lymphoma Baylisascaris infection Benaxima Besnier-Boeck-Schaumann disease Beta blockers Biclin Biosint Boceprevir Brain tumors Bronchial asthma Brucellosis Buerger's disease Capastat sulfate Capillaria Capreomycin sulfate Capreomycin Carbamazepine Carcinoma especially with radiation therapy Caspofungin Cat-scratch fever Cefaclor Cefadroxil Cefaxim Cefizox Cefoclin Cefotaxime sodium Cefoxitin sodium Cefprozil Ceftazidime Ceftazim Ceftin Ceftizoxime Cefuroxime Cephalosporin Ceptaz Chlamydial pneumonia of infancy Chlorphenesin carbamate Chlorpropamide Cholesterol embolism Chromosome 21 partial deletion Chronic eosinophilic leukemia Chronic active hepatitis Chronic eosinophilic leukemia Chronic eosinophilic pneumonia Chronic myeloid leukaemia Churg-Strauss syndrome Cirrhosis Claforan Clofibrate Clomipramine Clonorchis sinensis Coccidioidomycosis Connective tissue disease Cysticercosis Cytomegalovirus Dantrolene Dapsone Daptomycin Dermatitis herpetiformis Dermatomyositis Desipramine Dicrocoelium dendriticum fluke Dientamoeba fragilis Diethylcarbamazine Diffuse proliferative glomerular nephritis Dothiepin Doxycycline Dracunculiasis Dressler's syndrome Duhring's disease Echinococcosis Echinococcus granulosus Echinococcus Eczema Endomyocardial fibrosis Enfuvirtide Eosinophilia-myalgia syndrome Eosinophilic cellulitis Eosinophilic cystitis Eosinophilic fasciitis Eosinophilic folliculitis Eosinophilic gastroenteritis Eosinophilic granuloma Eosinophilic leukemia Eosinophilic myocarditis Eosinophilic panniculitis Eosinophilic pneumonia Eosinophilic pulmonary syndrome Eosinophilic pustular folliculitis Episodic angioedema with eosinophilia Erythema multiforme Ethosuximide Etravirine Exfoliative dermatitis Extrinsic allergic alveolitis Familial eosinophilia Familial reticuloendotheliosis with eosinophilia Farmer's lung Fasciola hepatica Fascioliasis Fasciolopsis buski Filariases Flukes Food allergy Fortaz Fortum Fotexina Froxal Fungal infections Gamikal GM-CSF Gnathostoma hispidum Gnathostoma spinigerum Gnathostomiasis Gold salts Graft versus host immunologic reactions Granulocyte-macrophage colony stimulating factor Helminth infections Hemodialysis Heterophyiasis Histiositosis with cutaneous involvement Hodgkin lymphoma Hookworm infection Human T-lymphotropic virus (HTLV)-I Human T-lymphotropic virus (HTLV)-II Hydralazine Hyper-IgE syndrome Hypereosinophilic syndrome Hypersensitivity Hypoadrenalism Idiopathic eosinophilic chronic pneumopathy Idiopathic eosinophilic synovitis IgA deficiency Imipramine Immunoblastic lymphadenopathy Infectious lymphocytosis Infectious mononucleosis Inflammatory Bowel Disease Interleukin-2 Interstitial nephritis Isoniazid Isospora belli Kefurox Ketorolac Kimura disease Kostmann disease Kostmann syndrome L-tryptophan contaminant Lepromatous leprosy Leukemia Loa loa Loeffler endocarditis Loeffler's syndrome Lymphomas Lyphocin maolate Magrassi-Leonardi syndrome Malaria Malignancy Mansonella ozzardi Mansonelliasis Maolate Mastocytosis Medication-related eosinophilia Mefoxin Metagonimiasis Micafungin Milk protein allergy Minocycline Modafinil Mycobacterium tuberculosis Myeloproliferative disorders Nalidixic acid Nasal polyposis Nitrofurantoin Nonallergic rhinitis with eosinophilia syndrome (NARES) Nonsteroidal antiinflammatory agents Nortriptyline NSAID nephropathy Occupational lung diseases Ocular larva migrans Olanzapine Omenn syndrome Onchocerciasis Opisthorchiasis Oxaprozin Oxytetracycline Papaverine Paragonimiasis Paraneoplastic syndrome Parasitic infection Pemphigus vulgaris Penicillin Pentostatin Pergolide Peritoneal dialysis Phenytoin Pneumocystis jirovecii Polyarteritis nodosa Polymyositis Praziquantel Precursor B-cell acute lymphoblastic leukemia with t(5;14) Precursor T-cell lymphoblastic lymphoma with t(8;13) Primary sclerosing cholangitis Procarbazine Progressive systemic sclerosis Proleukin Psoriasis Pulmonary eosinophilia Pyrimethamine Radiotherapy Ranitidine Renal cell carcinoma Rheumatoid arthritis Rice millers syndrome River Blindness Sarcoidosis Sarcoptes scabiei Scabies Scarlet fever Schistosoma haematobium Schistosoma mansoni Selective serotonin reuptake inhibitor Shulman’s syndrome Simple pulmonary eosinophilia Sipuleucel-T Sjögren's syndrome Spirometra erinace-ieuropaei Spirometra mansoni Spirometra mansonoides Spirometra theileri Stevens-Johnson syndrome Strongyloidiasis Sulphonamides Systemic lupus erythematosus Systemic mastocytosis Tagal Taloken Tapeworms Taporin TAR syndrome Tazicef Tazidime Tetracyclines Thrombocytopenia with absent radii Thrombotic thrombocytopenic purpura Thymoma Tissue invasion by parasites Tobacco smoking Toxic oil syndrome Toxocara canis Toxocariasis Transplant rejection Trichinella spiralis Tropical pulmonary eosinophilia Tryptophan Urticaria Vancoled Vancomycin Hydrochloride Vancomycin Vasculitis Viken Visceral larva migrans Waytrax Wegener granulomatosis White blood cells Wiskott-Aldrich syndrome Wuchereria bancrofti Yectamid Zimelidine Zinacef", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide information on the natural history, complications, and prognosis associated with malignant peripheral nerve sheath tumors?", "role": "user" }, { "content": "In general Malignant peripheral nerve sheath tumor is known to have high metastatic potential and poor prognosis. long-term outcomes vary widely across multiple series, with 5-year survival ranging between 15% and 50%. Large tumor size at presentation (typically >5 cm) has been the most consistently determined adverse prognostic factor. Other reported factors include tumor grade, truncal location, surgical margin status, local recurrence, and heterologous rhabdomyoblastic differentiation. The true prognostic impact of NF1 syndrome in MPNST remains somewhat in flux. Several large series report significantly worse outcomes for MPNST arising in the setting of NF1 compared with sporadic disease, with inferior responses to cytotoxic chemotherapy and 5-year survivals that are up to 50% worse.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "During a physical examination, how is an umbilical hernia detected?", "role": "user" }, { "content": "Physical exam findings for umbilical hernia are as follows: \r\nPhysical examination of patients with umbilical hernia is usually remarkable for a protruding umbilical mass examined in the standing and supine positions to determine the size of a hernia +/- valsalva maneuver.\r\nPatients with umbilical hernia usually appear normal.\r\nVital signs in umbilical hernia are normal.\r\nSkin examination of patients with umbilical hernia is usually normal.\r\nHEENT examination of patients with umbilical hernia is usually normal.\r\nNeck examination of patients with umbilical hernia is usually normal.\r\nPulmonary examination of patients with umbilical hernia is usually normal.\r\nCardiovascular examination of patients with umbilical hernia is usually normal.\r\nAbdominal examination of patients with umbilical hernia is usually normal with the exception of a protruding umbilical mass. If strangulated then it presents with: Pain Hard umbilical mass Tenderness\r\nBack examination of patients with umbilical hernia is usually normal.\r\nGenitourinary examination of patients with umbilical hernia is usually normal.\r\nNeuromuscular examination of patients with umbilical hernia is usually normal.\r\nExtremities examination of patients with umbilical hernia is usually normal.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide a synopsis or summary of Osteosarcoma?", "role": "user" }, { "content": "Bone cancer is a malignant (cancerous) tumor of the bone that destroys normal bone tissue. Osteosarcoma is the most common type of malignant bone cancer, accounting for 35% of primary bone malignancies. It is a malignant tumor that is characterized by the direct formation of bone or osteoid tissue by the tumor cells. Malignant tumors that begin in bone tissue are called primary bone cancer. Osteosarcoma may be classified according to the World Health Organization ’s histologic classification of bone tumors into three groups. The osteosarcomas may be localized at the end of the long bones (commonly in the metaphysis). Most often it affects the upper end of the tibia, humerus, or lower end of the femur. On gross pathology, areas of bone formation, hemorrhage, fibrosis, and cystic degeneration on cut surface are characteristic findings of osteosarcoma. On microscopic histopathological analysis, presence of osteoid within the tumor, pleomorphic cells, anaplastic cells, and atypical mitoses are characteristic findings of osteosarcoma. There are no established causes for osteosarcoma. The common risk factors in the development of osteosarcoma are radiation to bones, alkylating antineoplastic agents, Paget disease, multiple hereditary osteochondromas, fibrous dysplasia, Bloom syndrome, Rothmund-Thomson syndrome, and Li-Fraumeni syndrome. Common complications of osteosarcoma include pathologic fracture and metastasis. The most common symptoms of osteosarcoma include bone pain that may be worse at night, swelling, and redness at the site of the tumor. On x-ray, osteosarcoma is characterized by medullary and cortical bone destruction, periosteal reaction, tumor matrix calcification, and soft tissue mass. On MRI, osteosarcoma is characterized by intermediate intensity of soft tissue and low signal intensity of ossified components on T1. High signal intensity of soft tissue and low signal intensity of ossified components on T2. The predominant therapy for osteosarcoma is neoadjuvant chemotherapy (chemotherapy given before surgery) followed by surgical resection. The most common drugs used to treat osteosarcoma are cisplatin, doxorubicin and high-dose methotrexate.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the criteria used for diagnosing molluscum contagiosum?", "role": "user" }, { "content": "Histologic examination can confirm the clinical diagnosis. Hematoxylin and eosin (H&E) staining of a molluscum contagiosum lesion will reveal cells and keratinocytes containing eosinophilic cytoplasmic inclusion bodies that are also known as molluscum bodies or Henderson-Paterson bodies.\r\nDermoscopic examination can also be useful for supporting a clinical diagnosis and confirmation of molluscum contagiosum. In dermoscopic exam, a central umbilication with polylobular, white to yellow amorphous structures will be visualized which is typical for the disease. This exam allows physicians to evaluate primary morphology of skin lesions. \r\nIn dermoscopic exam a peripheral crown of radiating or punctiform vessels may also be seen. Dermoscopy exams of molluscum contagiosum lesions provide a higher specificity for the disease than other diagnostic methods. The presence of vessels, orifices, and specific vascular patterns helps in determining the diagnosis and in differentiating molluscum contagiosum from other diseases. \r\nElectron microscopy of biopsies is not usually indicated due to the cost and feasibility, but if done, will demonstrate typical brick-shaped poxvirus particles. Electron microscopy can also identify infected cells that may be missed with light microscopy due to normal appearance.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you provide me with the current sentence or phrase that needs to be rephrased?", "role": "user" }, { "content": "Hereditary elliptocytosis (HE) includes inherited a spectrum of red blood cell (RBC) disorders, that present heterogeneity in clinical symptoms, biochemistry and genetics. All of the Hereditary elliptocytosis subtypes have the elliptical morphologic shape RBCs in common, which leads to reduced RBC survival. \r\nQuality and quantity defects of the cytoskeletal proteins are responsible in Hereditary elliptocytosis. These cytoskeletal proteins are necessary for maintenance of RBCs structure, specially their biconcave morphology.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the possible diagnoses for folate deficiency?", "role": "user" }, { "content": "To review the differential diagnosis of anemia, click here.\r\nDisease Genetics Clinical manifestation Lab findings History Symptoms Signs Hemolysis Intrinsic/Extrinsic Hb concentration MCV RDW Reticulocytosis Haptoglobin levels Hepcidin Iron studies Specific finding on blood smear Serum iron Serum Tfr level Transferrin or TIBC Ferritin Transferrin saturation Folate deficiency Impaired DNA synthesis Alcohol consumption History of using drugs like methotrexate, trimethoprim, and phenytoin Low socioeconomic groups with poor nutrition Older people Pregnant and lactating women No neurological symptoms vs B12 deficiency Odynophagia Angular stomatitis Glossitis Signs of heart failure Anencephaly and spina bifida − − Anisochromic Macrocytic ↑ ↓ Nl Nl ↑ ↑ ↓ ↑ ↑ RBC macrocytosis Hypersegmented neutrophils Pancytopenia in severe cases Vitamin B12 deficiency Impaired DNA synthesis Pernicious anemia Crohn's disease Gastrectomy Veganism Diphyllobothrium latum infection Psychosis Insomnia Depression Cognitive slowing Restless leg syndrome Neurological deficit Myelopathy Memory loss with reduced attention span Nystagmus Positive romberg sign Positive Lhermitte's sign − − Anisochromic Macrocytic ↑ ↓ Nl Nl ↑ ↑ ↓ ↑ ↑ Senile neutrophil Anisocytosis Ovalocytes Orotic aciduria Autosomal recessive Deficiency of enzyme UMPS Episodic vomiting Rhabdomyolysis Coma Gastrointestinal manifestation Neurological manifestation − − Anisochromic Macrocytic ↑ ↓ Nl Nl ↑ ↑ ↓ ↑ ↑ NA Fanconi anemia Autosomal recessive X-linked recessive History of anemia at age 16 Hypopigmentation Cafe-au-lait patches Radial ray anomaly Significant for bilateral short thumbs − − Anisochromic Macrocytic ↑ ↓ Nl Nl ↑ ↑ ↓ ↑ ↑ Nl appearing WBC, RBC and Platelets But the number is greatly reduced Disease Genetics History Symptoms Signs Hemolysis Intrinsic/Extrinsic Hb concentration MCV RDW Reticulocytosis Haptoglobin levels Hepcidin Serum iron Serum Tfr level IBC Ferritin Transferrin saturation Specific finding on blood smear Diamond-Blackfan anemia Mutations in: RPL5 RPL11 RPL35A RPS7 RPS10 RPS17 RPS19 RPS24 RPS26 Associated with myelodysplastic syndrome Increased risk of AML Pale skin Sleepiness Heart murmurs Triphalangeal thumbs Short stature Microcephaly Hypertelorism Ptosis Micrognathia − − Anisochromic Macrocytic Nl ↓ Nl Nl ↑ ↑ ↓ ↑ ↑ NA Liver disease − Hepatitis Binge drinking Gall bladder disease Jaundice Abdominal pain Itchy skin Ascites Right upper quadrant pain Hepatomegaly Swelling in the legs Ankle swelling − − Anisochromic Macrocytic ↑ ↑ Nl Nl ↑ ↑ ↓ ↑ ↑ Round macrocytes Target macrocytes Alcoholism − History of increased alcohol intake Folic acid deficiency Memory impairment Nausea Sweating Truncal obesity Asterixis Encephalopathy Spider angiomas Hematemesis Gynecomastia − − Anisochromic Macrocytic ↑ ↑ Nl Nl ↑ ↑ ↓ ↑ ↑ Oval macrocytes Hypersegmented neutrophils Disease Genetics History Symptoms Signs Hemolysis Intrinsic/Extrinsic Hb concentration MCV RDW Reticulocytosis Haptoglobin levels Hepcidin Serum iron Serum Tfr level IBC Ferritin Transferrin saturation Specific finding on blood smear", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the history and what are the symptoms associated with Hematemesis?", "role": "user" }, { "content": "Patients may experience the following symptoms:\r\nVomiting blood Nausea Abdominal pain Fatigue and weakness Sweat Dark colored, tar like stools Hypotension Shock\r\nOther health problems may also cause these symptoms.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What exactly is Marjolin's ulcer?", "role": "user" }, { "content": "Histologically, the tumour is a well- differentiated squamous cell carcinoma. This carcinoma is aggressive in nature, spreads locally and is associated with a poor prognosis .", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What information is available regarding congenital cases of protein C or S deficiency?", "role": "user" }, { "content": "Childhood stroke More than one pregnancy loss (recurrent miscarriage) Recurrent clots in the veins Pulmonary embolism\r\nIn rare cases, using warfarin to thin the blood and prevent clots can cause brief increased clotting and severe skin wounds. Patients are at risk if they are not treated with the blood-thinning drug heparin before taking warfarin.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you explain what intrahepatic cholestasis is and how it affects a person's health?", "role": "user" }, { "content": "BRIC is a rare disorder. Although the prevalence is unknown, this condition is less common than the related disorder PFIC, which affects approximately 1 in 50,000 to 100,000 people worldwide.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the explanation of the pathophysiology of thymoma?", "role": "user" }, { "content": "Thymus is the site of maturation of T cells. This makes thymus the primary center responsible for adaptive immunity.\r\nThe exact pathogenesis of the primary tumor development is not completely understood.\r\nPrimary tumors of thymus are relatively rare. Thymoma is the most common type of primary tumor of thymus. Thymoma is histologically comprised of abnormally conditioned T cells. The mingling of these abnormal T cells into the circulation is believed to be involved in the causality of the associated autoimmune disorders.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is meant by adrenocortical carcinoma?", "role": "user" }, { "content": "Adrenocortical carcinoma must be differentiated from other adrenal tumors such as adrenocortical adenoma, adrenal metastasis, adrenal medullary tumors, and Cushing's syndrome.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is Hereditary Multiple Exostoses?", "role": "user" }, { "content": "HME is estimated to occur in 1 in 50,000 people. It is characterized by the growth of cartilage-capped benign bone tumours around areas of active bone growth, particularly the metaphysis of the long bones. HME can lead to the shortening and bowing of bones, as such affected individuals often have a short stature. Depending on their location the exostoses can cause the following problems: pain or numbness from nerve compression, vascular compromise, inequality of limb length, irritation of tendon and muscle, as well as a limited range of motion at the joints upon which they encroach. Generally, when a person with HME reaches maturity, and their bones stop growing, the exostoses also stop growing. A person with HME is also more likely to develop a rare form of bone cancer called chondrosarcoma as an adult.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the importance of performing a physical examination in cases of stromal ovarian tumors?", "role": "user" }, { "content": "Patients with sexcord/ stromal ovarian tumors usually appear normal except few abdominal or pelvic and genitourinary findings on examination. Abdominal findings include Abdominal distension, increased abdominal girth, abdominal tenderness in the right /left lower abdominal quadrant, a palpable abdominal mass in the right/left lower abdominal quadrant, guarding, ascites, hemoperitoneum.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does post-traumatic endophthalmitis mean?", "role": "user" }, { "content": "In 1903, post-traumatic fungal endophthalmitis was first reported by Romer. In 1933, exogenous fungal endophthalmitis was first described by Rychener.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the explanation of the pathophysiology underlying autoimmune hepatitis?", "role": "user" }, { "content": "Autoimmune hepatitis is a chronic disease characterized by inflammation of the liver which results from the combination of genetic predisposition and environmental triggers\r\nNormal physiology of liver: \r\nLiver is known to be an organ with special innate immune features. Liver has distinct cellular composition with predominance of Kupffer cells (KCs), natural killer (NK) cells and natural killer T (NKT). Liver is constantly exposed to microbial products,(toxic) environmental substances and food antigens from the portal stream draining the intestine, the liver plays an important role in the induction and maintenance of immune tolerance. Liver is a target of adverse immune reactions in chronic inflammatory liver diseases like autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC).", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "\"What does multiple endocrine neoplasia type 2 refer to?\"", "role": "user" }, { "content": "Multiple endocrine neoplasia type 2 has a variable natural history. Life threatening complications of multiple endocrine neoplasia type 2 include malignant hypertension, megacolon, and metastasis. Prognosis of multiple endocrine neoplasia type 2 is mainly related to the stage-dependent prognosis of medullary thyroid cancer.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is Chloroxolone and what does an overview of it include?", "role": "user" }, { "content": "Clorexolone is a low-ceiling sulfonamide diuretic.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is a Naegleria infection?", "role": "user" }, { "content": "Only one species (type) of Naegleria infects people: Naegleria fowleri.'", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What treatment is recommended for gonadoblastoma?", "role": "user" }, { "content": "Gonadectomy is the primary surgery for gonadblastoma. \r\nBilateral gonadectomy is indicated when the contralateral gonad is abnormal or undescended.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What information is available regarding demeclocycline?", "role": "user" }, { "content": "Amoxicillin and clavulanic acid may cause side effects. Tell your doctor if any of these symptoms are severe or do not go away:\r\nDiarrhea\r\nItching of the rectum or vagina\r\nSore mouth\r\nChanges in skin color\r\nIf you experience any of the following symptoms, call your doctor immediately:\r\nSevere headache\r\nBlurred vision\r\nSkin rash\r\nRedness of the skin (sunburn)\r\nHives\r\nDifficulty breathing or swallowing\r\nYellowing of the skin or eyes\r\nItching\r\nDark-colored urine\r\nLight-colored bowel movements\r\nLoss of appetite\r\nUpset stomach\r\nVomiting\r\nStomach pain\r\nExtreme tiredness or weakness\r\nConfusion\r\nDecreased urination\r\nIf you experience a serious side effect, you or your doctor may send a report to the Food and Drug Administration's (FDA) MedWatch Adverse Event Reporting program online at http://www.fda.gov/MedWatch/report.htm or by phone 1-800-332-1088.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you provide me with the exact sentence that needs to be rephrased? It appears to be already proper English.", "role": "user" }, { "content": "Premenstrual syndrome Dysmenorrhea Bipolar disorder Major depressive disorder Persistent depressive disorder (dysthymia) Use of hormonal therapy \r\nPMDD is similar to premenstrual syndrome (PMS), but differs from it in severity and in that it requires treatment, because it interferes with the sufferer's ability to function in her environment. The cardinal symptom--surfacing between ovulation and menstruation, and disappearing within a few days after the onset of the bleeding--is irritability. Anxiety, anger, and depression may also occur. The main symptoms, which can be disabling, include", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the laboratory test results for bacterial meningitis?", "role": "user" }, { "content": "Labortary tests which may help identify the bacterial meningitis include non specific tests and specific diagnostic tests.\r\nNon specific tests include blood tests such as complete blood count, liver function tests, renal function tests, biochemistry, and coagulation profile. \r\nLaboratory findings Test Findings Complete blood count Decreased hemoglobin Decreased hematocrit Elevated CRP White blood cell count Elevated or decreased leukocyte count(severe infection) with a left shift To detect meningococcal septicemia, routine assessment of the neutrophil counts must be considered, as follows: Absolute Neutrophil Count (ANC): ≤1000/mm or ≥10,000/mm Immature Neutrophil Count (INC): ≥500/mm Immature-to-Total Neutrophil Ratio (ITR): ≥0.20 Biochemistry Hypoglycemia Elevated creatinine Elevated ALT, AST Possible hyponatremia Acidosis: High lactate; Low bicarbonate (shock) Coagulation Thrombocytopenia -poor prognosis Increased D-Dimers, Increased PT/APTT- DIC Blood culture Positive in 50 to 90 percent of patients Two sets of blood cultures needed before antimicrobials\r\nSpecific diagnostic tests include lumbar puncture with CSF examination and CSF culture. CSF examination findings in bacterial meningitis are as follows:\r\nCSF gram stain findings include the following: \r\nCSF Gram Stain Finding Causative Organism Culture medium Growth on culture medium Gram positive diplococcus Streptococcus Pneumonia Blood agar plate Small, grey, moist (sometimes mucoidal), watery colonies with green zone of allpha hemolysis Gram negative diplococcus Neisseria Meningitides Blood agar plate and chocolate agar plate Round, smooth, moist, glistening, and convex Gram positive coccobacillus Listeria Monocytogenes Brain heart infusion Isolated small 1mm colonies creamy white in colour and dome shaped Small pleomorphic gram - negative coccobacilli Haemophilus Influenzae Chocolate agar plate enriched with NAD and hematin (X) Large, colorless-to-grey, opaque colonies", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you provide a context or details for me to accurately rephrase the given sentence?", "role": "user" }, { "content": "The aorta is an elastic artery, and as such is quite distensible. When the left ventricle contracts to force blood into the aorta, the aorta expands. This stretching gives the potential energy that will help maintain blood pressure during diastole, as during this time the aorta contracts passively.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the primary prevention method for Beriberi?", "role": "user" }, { "content": "The most important preventive measure against Beriberi is increasing thiamine intake in diet. Other measures include reducing alcohol consumption and proper prenatal care of women in susceptible geographical areas.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the meaning of double-outlet right ventricle with echo?", "role": "user" }, { "content": "Yale Congenital Heart Disease- DORV\r\nTemplate:WikiDoc Sources", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you give me details about hydrocele and the relevant information associated with it?", "role": "user" }, { "content": "Hydroceles are usually not dangerous, and they are usually only treated when they cause discomfort or embarrassment, or if they are large enough to threaten the testicle's blood supply.\r\nOne option is to remove the fluid in the scrotum with a needle, a process called aspiration. However, surgery is generally preferred. Aspiration may be the best alternative for people who have certain surgical risks.\r\nSclerosing (thickening or hardening) medications may be injected after aspiration to close off the opening. This helps prevent the future build up of fluid.\r\nHydroceles associated with an inguinal hernia should be repaired surgically as quickly as possible. Hydroceles that do not go away on their own over a period of months should be evaluated for possible surgery. A surgical procedure, called a hydrocelectomy, is often performed to correct a hydrocele.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the medical treatment for Stage III Seminoma?", "role": "user" }, { "content": "Surgery is a primary treatment for stage III seminoma. Chemotherapy is usually given after surgery.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the natural history, complications, and prognosis associated with osteoma?", "role": "user" }, { "content": "Osteoma prognosis is related to proximity to anatomic structures and surgical resection. Features associated with worse prognosis after surgery depend on tumor location, depth, and size. About 20% of osteomas have symptomatic recurrences.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is cancer of the small intestine and what information is currently available on it?", "role": "user" }, { "content": "Symptoms of abdominal and whole body have no specificity. Other health problems may also cause similar symptoms. Go to see your doctor to verify your diseases as early as possible. Diseases with similar symptoms are listed in the following:\r\nCrohn's disease Intestinal tuberculosis Ulcerative colitis Large intestine cancer Irritable bowel syndrome (IBS) Depression", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is a Lisch nodule?", "role": "user" }, { "content": "A hamartoma is defined as a benign tumor or nodular growth that is composed of proliferating mature histologically normal cells that normally reside at the affected tissue. NF1 is due to mutations in the NF1 gene, located at chromosome 17q11.2. Lisch nodules are generally not present in central NF(neurofibromatosis)/NF(neurofibromatosis)-2. Neurofibromin, the protein product encoded by the gene, is expressed in many tissues, including brain, kidney, spleen, and thymus. Mutations in the NF1 gene result in loss of production or reduced function of protein; this causes a wide spectrum of clinical findings, including NF1 -associated tumors. Histopathologically, Lisch nodules are composed of melanocytes and spindle cells, usually concentrated on the superficial layers of the iris stroma. The spindle cells are larger than the normal iris melanocytes. Immunohistochemical studies show positive reaction against the following Vimentin Smooth muscle actin Neuron specific enolase.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What laboratory findings are associated with Adiposogenital dystrophy?", "role": "user" }, { "content": "Laboratory findings are crucial in the diagnosis of adiposogenital dystrophy. Pituitary hormones are low and there may be downstream hormonal deficiencies as well.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does lactose intolerance mean?", "role": "user" }, { "content": "The most common cause of lactose intolerance is acquired primary lactase deficiency. Less common causes of lactose intolerance include Small intestinal bacterial overgrowth, Infections such as giardiasis, Drug induced enteritis, Celiac sprue, Tropical sprue, and Whipple's disease.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the reasons behind cyanosis?", "role": "user" }, { "content": "Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.\r\nCarbon monoxide poisoning Cyanide poisoning Malathion Parathion Ethylene glycol Epiglottitis Foreign body aspiration Pulmonary embolism Tension pneumothorax Hemothorax Pulmonary hemorrhage Pulmonary hypertension Myocardial infarction Congestive heart failure Disseminated intravascular coagulation Tetralogy of fallot Cardiac tamponade Eisenmenger syndrome Anaphylaxis Birth asphyxia Amniotic fluid embolism \r\nThere following are some of the common causes of central cyanosis:\r\nConditions associated with decreased concentration of inspired oxygen (FiO2): Smoke inhalation most commonly from house fires Carbon monoxide poisoning Hydrogen cyanide poisoning Intentional or unintentional exposure to asphyxiating gases (eg, Propane, methane, butane, hydrogen sulphide) Impairment of chest wall or lung expansion: External compression Pneumothorax Hemothorax Flail chest Hypoventilation: Upper airway obstruction: Foreign body aspiration Pertussis / Croup Epiglottitis Bacterial tracheitis Traumatic disruption (thermal injury, fractures) Acute chest syndrome Congenital airway abnormalities: Choanal atresia Laryngotracheomalacia Macroglossia Micrognathia or retrognathia (eg, Pierre-Robin syndrome) Neurologic abnormalities: CNS depression Birth asphyxia Severe head trauma Apnea of prematurity Obstructive sleep apnea Infections (eg, meningitis, encephalitis) Intraventricular hemorrhage Seizures Cyanotic breath holding spells Coma Neuromuscular disorders: Myasthenia gravis Injury to the phrenic nerve Type 1 spinal muscular dystrophy (Wernig-Hoffman disease) Intrinsic lung diseases: Asthma COPD Pneumonia Bronchiolitis Respiratory distress syndrome (Hyaline membrane disease) Empyema Pleural effusion Cystic fibrosis Atelectasis Bronchopulmonary dysplasia Alveolar capillary dysplasia Vascular causes: Cardiac tamponade Cyanotic congenital heart diseases (Right to left shunts): Decreased pulmonary flow: Tetralogy of fallot Tricuspid valve anomalies: Tricuspid atresia Tricuspid stenosis Ebstein's anomaly Pulmonary stenosis (critical valvular) Pulmonary atresia with intact ventricular septum Increased pulmonary flow: TGA (Transposition of great arteries, most common dextro type) Truncus arteriosus TAPVC (Total anamalous pulmonary venous connection) Heart failure: Conditions that present with cyanosis and severe heart failure include: Left sided obstructive lesion (HLHS) Coarctation of aorta Critical valvular aortic stenosis Eisenmenger syndrome Congestive heart failure Atrial septal defect Pulmonary hypertension Pulmonary edema Pulmonary hemorrhage Pulmonary embolism Pulmonary arteriovenous malformations Multiple small intrapulmonary shunts Shock Sepsis Amniotic fluid embolism Hematologic abnormalities: Methemoglobinemia (congenital or acquired) Sulfhemoglobinemia (acquired) Hemoglobin mutations with low oxygen affinity: Hb Kansas Hb Beth Israel Hb Saint Mande Hb Bruxells Polycythemia vera Disseminated intravascular coagulation Metabolic disorders: Severe hypoglycemia Inborn errors of metabolism Miscellaneous: Drugs and chemicals: Beta blockers Nitrite or nitrate-containing compounds (eg, nitroglycerin) Dapsone Sulfonamides Benzocaine Chloroquine Heroin Venomous snakebites Brief resolved unexplained events (BRUE) High altitude Congenital diaphragmatic hernia Cirrhosis of liver Drowning Chocking Hanging Hypothermia\r\nThere following are some of the common causes of peripheral cyanosis: \r\nVarious conditions that cause central cyanosis can also present with peripheral cyanosis. Common conditions where peripheral cyanosis is more specific: Cold exposure Acrocyanosis Erythrocyanosis Raynaud's phenomenon Raynaud's disease Arterial obstruction: Peripheral vascular disease Buergers disease Venous obstruction: Thromboembolism Deep vein thrombosis Superior vena cava syndrome Decreased cardiac output: Left-sided heart failure Shock Hypovolemia Redistribution of blood flow from extremities\r\nMetals: Silver nitrate Silver iodide Silver Lead Drugs: Phenothiazines Amiodarone Chloroquine hydrochloride Pigmentary lesions (eg, Mongolian spot s, large birthmarks) Extensive tattoos Consumption of blue or purple-dyed food\r\n1p36 deletion syndrome 2,4,6-Trinitrotoluene 4-Nitrophenol Aberrant subclavian artery Acetaminophen and hydrocodone Acrocephalopolysyndactyly Acrocyanosis Acrodynia Acrofacial dysostosis Acute histoplasmosis Acute interstitial pneumonitis Adams-Oliver syndrome Adrenal hemorrhage Air embolism Air leak syndromes Airway obstruction Al Gazali-Aziz-Salem syndrome Alveolar capillary dysplasia Amiodarone Amyl nitrite Anchovy poisoning Angioneurotic edema Aniline Anisidine Anthracosis Antifreeze Aotic arch defects Aortic coarctation Aortic stenosis Apnea of prematurity Apple seed poisoning Apricot seed poisoning Arsine gas Arterial occlusion Asbestosis Aspiration Asthma Atelectasis Atrial myxoma Atrial septal defect Bacterial tracheitis Benign familial neonatal convulsions Benzocaine Benzodiazepines Berylliosis Besnier-Boeck-Schaumann disease Beta blockers Bicisate dihydrochloride Bindewald-Ulmer-Muller syndrome Bird cherry seed poisoning Birth asphyxia Bitter almond poisoning Blalock-Taussig shunt Bland-White-Garland syndrome Blood transfusion Blue baby syndrome Boerhaave syndrome Bordetella pertussis Bronchiectasis Bronchiolitis Bronchopulmonary dysplasia Bronchospasm Buergers disease Brown snake poisoning Bufotenin Carbamates Cardiac tamponade Cardiomyopathy Cassirer disease Cast syndrome Cerebral hypoxia Chloramphenicol Chlorate salts Chlorobenzene Chloroquine Choanal atresia Choking Cholesterol emboli syndrome Cholesterol pneumonia Chromhidrosis Chromosome 22q11 deletion Chronic bronchitis Chronic mercury exposure Chronic obstructive pulmonary disease Chylothorax Cirrhosis of liver Clonazepam Clorazepate Clupeotoxin Coal worker's pneumoconiosis Codeine Cold exposure Community-acquired pneumonia Congenital central hypoventilation syndrome Congenital cystic adenomatoid malformation Congenital diaphragmatic hernia Congenital heart disease Congenital hyperinsulinism Congenital pulmonary lymphangiectasia Congestive heart failure Cor biloculare Cor triatriatum Coronary artery anomaly Critical valvular aortic stenosis Crocq disease Croup Cyanide poisoning Cyanotic congenital heart disease Cystic fibrosis Cystic hygroma Dapsone Deep vein thrombosis Dehydration Demeton-S-methyl Desmopressin Diaphragmatic paralysis Diazepam Diazinon Dichlorvos Dicrotophos DiGeorge syndrome Dilaudid Dinitrocresol Dioxathion Diphosphoglycerate mutase deficiency Disseminated intravascular coagulation Disulfoton Double inlet left ventricle Double outlet right ventricle Drowning Drug overdose Duodenal atresia Ebstein anomaly Eisenmenger syndrome Emphysema Empyema Encephalitis Endosulfan Epichlorohydrin Epiglottitis Erythrocyanosis Esophageal atresia Ethion Ethylene Ethylene glycol Ethylene oxide Exercise-induced asthma Extrinsic allergic alveolitis Familial interstitial fibrosis Familial pulmonary capillary hemangiomatosis Fensulfothion Fenthion Fibrosing alveolitis Flail chest Foreign body aspiration Goodpasture syndrome Gray baby syndrome Hamman-Rich syndrome Hanging Head trauma Heart attack Hemoglobinopathy Hemothorax Heroin Herring poisoning High altitude HMG-CoA lyase deficiency Hyaline membrane disease Hydrocodone Hydrogen sulfide Hydroquinone Hypermagnesemia Hypersensitivity pneumonitis Hypoadrenalism Hypocalcemia Hypoglycemia Hypomagnesemia Hypoplastic left heart syndrome Hypothermia Hypoventilation Hypovolemia Hypoxemia Hypoxia (medical) Hypoxic ischemic encephalopathy Ibuprofen Idiopathic diffuse interstitial pulmonary fibrosis Idiopathic pulmonary fibrosis Idiopathic pulmonary hemosiderosis Idiopathic pulmonary hypertension Idiopathic subglottic tracheal stenosis Immobility Infant respiratory distress syndrome Infantile apnea Insect sting allergy Intermittent claudication Interrupted aortic arch Interstitial lung disease Intracranial hemorrhage Intraventricular hemorrhage Iron poisoning Isaac's syndrome Ischemic heart disease Isolated ventriculoarterial discordance Ivemark syndrome Jervell and Lange-Nielsen syndrome Kugel-Stoloff syndrome Lantana poisoning Laryngeal cleft Laryngeal edema Laryngomalacia Laryngotracheomalacia Lead Legionellosis Legionnaire's disease Lethal chondrodysplasia Moerman type Lobar emphysema Lorazepam Lortab Ludwig's angina Lung abscess Lupus Macroglossia Malathion Malignancy-related superior vena cava syndrome Marfan syndrome Maternal sedation Matthew-Wood syndrome Meadows syndrome Meconium aspiration syndrome Melioidosis Mendelson's syndrome Meningitis Meperidine Methadone Methemoglobinemia Methidathion Methiocarb Methomyl Metoclopramide Microcephalic osteodysplastic primordial dwarfism type 1 Micrognathia Midazolam Mitral atresia in infants Monomelic amyotrophy Morphine Mountain sickness Myocardial infarction Narcotics Neonatal myasthenia gravis Neuromyotonia Nitrates Nitrazepam Nitrites Nitroglycerin Obstructive sleep apnea Organophosphate poisoning Osler-Vaquez disease Oxazepam Pancoast tumor Paraquat Parathion Partial atrioventricular canal Patent ductus arteriosus Patent foramen ovale Penetrating chest wounds Pergolide Perinatal asphyxia Peripartum cardiomyopathy Peripheral arterial disease Persistent pulmonary hypertension of the newborn Persistent truncus arteriosus Pertussis Pneumothorax Phenazopyridine Phenol Phenothiazines Phlegmasia alba dolens Phlegmasia cerulea dolens Phosdrin Phrenic nerve injury Pickwickian syndrome Pierre Robin syndrome Pleural effusion Pneumoconiosis Pneumonia Pneumothorax Polycythemia vera Primaquine Profenofos Propane Pseudoaldosteronism Pseudocyanosis Pulmonary alveolar proteinosis Pulmonary arteriovenous fistula Pulmonary arteriovenous malformation Pulmonary artery sling Pulmonary atresia Pulmonary edema Pulmonary embolism Pulmonary fibrosis Pulmonary hemorrhage Pulmonary hypertension Pulmonary hypoplasia Pulmonary stenosis Pulmonary veno-occlusive disease Pulmonary venous return anomaly Raynaud's disease Raynaud's phenomenon Respiratory depression Respiratory distress syndrome Respiratory failure Respiratory muscle paralysis Retrognathia Ribavirin Rifampin Right ventricle hypoplasia Right ventricular outflow tract obstruction Sakati syndrome Sakati-Nyhan-Tisdale syndrome Sarcoidosis Sea snake venom Sedatives Seizure Sepsis Shaken baby syndrome Shaver's disease Shock Shprintzen syndrome Silicosiderosis Silicosis Silver Silver iodide Silver nitrate Sleep apnea Smoke inhalation Snakebites Sneddon syndrome Spontaneous pneumothorax Stachybotrys chartarum exposure Streptococcal Group B invasive disease Strychnine Subpulmonary stenosis Sudden infant death syndrome Suffocation Sulfhemoglobinemia Sulfonamides Sulfur dioxide Superior vena cava syndrome Surfactant metabolism dysfunction Syndromic microphthalmia type 9 TAPVC Taussig-Bing syndrome Tension pneumothorax Terbufos Tetraethyl Pyrophosphate Tetralogy of Fallot Tetrodotoxin Thermal injury Thioglycolic acid Thoracic dystrophy Tonic-clonic seizures Total anomalous pulmonary venous connection Tracheal agenesis without tracheoesophageal fistula Tracheal stenosis Tracheoesophageal fistula Transient tachypnea of the newborn Transposition of the great vessels Trichloroethylene Tricuspid atresia Tricuspid stenosis Truncus arteriosus Type 1 pseudohypoaldosteronism Unilateral pulmonary agenesis Unilateral pulmonary hypoplasia Vaquez disease Vascular malposition Vascular rings Vein of Galen aneurysm Velocardiofacial syndrome Ventricular septal defect VLCAD deficiency Vocal cord paralysis Waterhouse-Friderichsen syndrome Weinstein Kliman Scully syndrome Werdnig-Hoffman disease Western equine encephalitis Whooping cough\r\n1p36 deletion syndrome 2,4,6-Trinitrotoluene 4-Nitrophenol Aberrant subclavian artery Acetaminophen and hydrocodone Acrodynia Acrofacial dysostosis Acute histoplasmosis Acute interstitial pneumonitis Adams-Oliver syndrome Adrenal hemorrhage Air embolism Air leak syndromes Airway obstruction Al Gazali-Aziz-Salem syndrome Alveolar capillary dysplasia Amiodarone Amyl nitrite Anchovy poisoning Angioneurotic edema Aniline Anisidine Anthracosis Antifreeze Aotic arch defects Aortic coarctation Aortic stenosis Apnea of prematurity Apple seed poisoning Apricot seed poisoning Arsine gas Arterial occlusion Asbestosis Aspiration Atelectasis Atrial myxoma Atrial septal defect Bacterial tracheitis Benign familial neonatal convulsions Benzocaine Benzodiazepines Berylliosis Besnier-Boeck-Schaumann disease Bindewald-Ulmer-Muller syndrome Bird cherry seed poisoning Birth asphyxia Bitter almond poisoning Blalock-Taussig shunt Bland-White-Garland syndrome Blood transfusion Blue baby syndrome Boerhaave syndrome Bordetella pertussis Bronchiectasis Bronchiolitis Bronchopulmonary dysplasia Bronchospasm Brown snake poisoning Bufotenin Carbamates Cardiac tamponade Cardiomyopathy Cassirer disease Cast syndrome Cerebral hypoxia Chloramphenicol Chlorate salts Chlorobenzene Chloroquine Choanal atresia Choking Cholesterol emboli syndrome Cholesterol pneumonia Chromhidrosis Chromosome 22q11 deletion Chronic bronchitis Chronic mercury exposure Chronic obstructive pulmonary disease Chylothorax Cirrhosis of liver Clonazepam Clorazepate Clupeotoxin Coal worker's pneumoconiosis Codeine Community-acquired pneumonia Congenital central hypoventilation syndrome Congenital cystic adenomatoid malformation Congenital diaphragmatic hernia Congenital heart disease Congenital hyperinsulinism Congenital pulmonary lymphangiectasia Congestive heart failure Cor biloculare Cor triatriatum Coronary artery anomaly Critical valvular aortic stenosis Crocq disease Croup Cyanide poisoning Cyanotic congenital heart disease Cystic fibrosis Cystic hygroma Dapsone Deep vein thrombosis Dehydration Demeton-S-methyl Desmopressin Diaphragmatic paralysis Diazepam Diazinon Dichlorvos Dicrotophos DiGeorge syndrome Dilaudid Dinitrocresol Dioxathion Diphosphoglycerate mutase deficiency Disseminated intravascular coagulation Disulfoton Double inlet left ventricle Double outlet right ventricle Drowning Drug overdose Duodenal atresia Ebstein anomaly Eisenmenger syndrome Emphysema Empyema Encephalitis Endosulfan Epichlorohydrin Epiglottitis Esophageal atresia Ethion Ethylene Ethylene glycol Ethylene oxide Exercise-induced asthma Extrinsic allergic alveolitis Familial interstitial fibrosis Familial pulmonary capillary hemangiomatosis Fensulfothion Fenthion Fibrosing alveolitis Flail chest Foreign body aspiration Goodpasture syndrome Gray baby syndrome Hamman-Rich syndrome Hanging Head trauma Heart attack Hemoglobinopathy Hemothorax Heroin Herring poisoning High altitude HMG-CoA lyase deficiency Hyaline membrane disease Hydrocodone Hydrogen sulfide Hydroquinone Hypermagnesemia Hypersensitivity pneumonitis Hypoadrenalism Hypocalcemia Hypoglycemia Hypomagnesemia Hypoplastic left heart syndrome Hypoventilation Hypovolemia Hypoxemia Hypoxia (medical) Hypoxic ischemic encephalopathy Ibuprofen Idiopathic diffuse interstitial pulmonary fibrosis Idiopathic pulmonary fibrosis Idiopathic pulmonary hemosiderosis Idiopathic pulmonary hypertension Idiopathic subglottic tracheal stenosis Immobility Infant respiratory distress syndrome Infantile apnea Insect sting allergy Intermittent claudication Interrupted aortic arch Interstitial lung disease Intracranial hemorrhage Intraventricular hemorrhage Iron poisoning Isaac's syndrome Ischemic heart disease Isolated ventriculoarterial discordance Ivemark syndrome Jervell and Lange-Nielsen syndrome Kugel-Stoloff syndrome Lantana poisoning Laryngeal cleft Laryngeal edema Laryngomalacia Laryngotracheomalacia Lead Legionellosis Legionnaire's disease Lethal chondrodysplasia Moerman type Lobar emphysema Lorazepam Lortab Ludwig's angina Lung abscess Lupus Macroglossia Malathion Malignancy-related superior vena cava syndrome Marfan syndrome Maternal sedation Matthew-Wood syndrome Meadows syndrome Meconium aspiration syndrome Melioidosis Mendelson's syndrome Meningitis Meperidine Methadone Methemoglobinemia Methidathion Methiocarb Methomyl Metoclopramide Microcephalic osteodysplastic primordial dwarfism type 1 Micrognathia Midazolam Mitral atresia in infants Monomelic amyotrophy Morphine Mountain sickness Myocardial infarction Narcotics Neuromyotonia Nitrates Nitrazepam Nitrites Nitroglycerin Obstructive sleep apnea Organophosphate poisoning Osler-Vaquez disease Oxazepam Pancoast tumor Paraquat Parathion Partial atrioventricular canal Patent ductus arteriosus Patent foramen ovale Penetrating chest wounds Pergolide Perinatal asphyxia Peripartum cardiomyopathy Peripheral arterial disease Persistent pulmonary hypertension of the newborn Persistent truncus arteriosus Pertussis Pneumothorax Phenazopyridine Phenol Phenothiazines Phlegmasia alba dolens Phlegmasia cerulea dolens Phosdrin Phrenic nerve injury Pickwickian syndrome Pierre Robin syndrome Pleural effusion Pneumoconiosis Pneumonia Pneumothorax Polycythemia vera Primaquine Profenofos Propane Pseudoaldosteronism Pseudocyanosis Pulmonary alveolar proteinosis Pulmonary arteriovenous fistula Pulmonary arteriovenous malformation Pulmonary artery sling Pulmonary atresia Pulmonary edema Pulmonary embolism Pulmonary fibrosis Pulmonary hemorrhage Pulmonary hypertension Pulmonary hypoplasia Pulmonary stenosis Pulmonary veno-occlusive disease Pulmonary venous return anomaly Respiratory depression Respiratory distress syndrome Respiratory failure Respiratory muscle paralysis Retrognathia Ribavirin Rifampin Right ventricle hypoplasia Right ventricular outflow tract obstruction Sakati syndrome Sakati-Nyhan-Tisdale syndrome Sarcoidosis Sea snake venom Sedatives Seizure Shaken baby syndrome Shaver's disease Shock Shprintzen syndrome Silicosiderosis Silicosis Silver Silver iodide Silver nitrate Sleep apnea Smoke inhalation Snakebites Sneddon syndrome Spontaneous pneumothorax Stachybotrys chartarum exposure Streptococcal Group B invasive disease Strychnine Subpulmonary stenosis Sudden infant death syndrome Suffocation Sulfhemoglobinemia Sulfonamides Sulfur dioxide Superior vena cava syndrome Surfactant metabolism dysfunction Syndromic microphthalmia type 9 TAPVC Taussig-Bing syndrome Tension pneumothorax Terbufos Tetraethyl Pyrophosphate Tetralogy of Fallot Tetrodotoxin Thermal injury Thioglycolic acid Thoracic dystrophy Tonic-clonic seizures Total anomalous pulmonary venous connection Tracheal agenesis without tracheoesophageal fistula Tracheal stenosis Tracheoesophageal fistula Transient tachypnea of the newborn Transposition of the great vessels Trichloroethylene Tricuspid atresia Tricuspid stenosis Truncus arteriosus Type 1 pseudohypoaldosteronism Unilateral pulmonary agenesis Unilateral pulmonary hypoplasia Vaquez disease Vascular malposition Vascular rings Vein of Galen aneurysm Velocardiofacial syndrome Ventricular septal defect VLCAD deficiency Vocal cord paralysis Waterhouse-Friderichsen syndrome Weinstein Kliman Scully syndrome Werdnig-Hoffman disease Western equine encephalitis Whooping cough\r\n\r\nAcrocyanosis Buerger's disease Cold exposure Deep vein thrombosis Erythrocyanosis Hypovolemia Left sided heart faiure Peripheral vascular disease Raynaud's disease Raynaud's phenomenon Shock Superior vena cava syndrome Thromboembolism", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you explain what the gastrocolic reflex refers to?", "role": "user" }, { "content": "The gastrocolic reflex or gastrocolic response is one of a number of physiological reflexes controlling the motility, or peristalsis, of the gastrointestinal tract. It involves an increase in motility of the colon in response to stretch in the stomach and byproducts of digestion in the small intestine. The small intestine also shows a similar motility response.\r\nThe reflex was demonstrated by myoelectric recordings in the colons of animals and humans, which showed an increase in electrical activity within as little as 15 minutes after eating. The recordings also demonstrated that the gastrocolic reflex is uneven in its distribution throughout the colon. The sigmoid colon is more greatly affected than the right side of the colon in terms of a phasic response; however, the tonic response across the colon is uncertain. A number of neuropeptides have been proposed as mediators of the gastrocolic reflex. These include serotonin, neurotensin, cholecystokinin (CCK), and gastrin.\r\nClinically, the gastrocolic reflex has been implicated in pathogenesis of irritable bowel syndrome. Also, the serotonin (5HT 3) antagonist ondansetron decreases the tonic response to stretch.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What exactly is ovarian sarcoma?", "role": "user" }, { "content": "There are no established measures for the secondary prevention of ovarian sarcoma.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide a summary of pneumomediastinum?", "role": "user" }, { "content": "Pneumomediastinum is considered a benign entity with good prognosis. The main symptom of pneumomediastinum is chest pain. The onset of the pain is sudden and acute or follows exacerbations of underlying pathology such as asthma. Spontaneous pneumomediastinum usually resolves by itself, but prolonged cases have also been reported (>2 months). There also have been incidences of recurrence.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you please explain what Superior vena cava syndrome is?", "role": "user" }, { "content": "If left untreated, patients with superior vena cava syndrome may progress to develop a complete blood flow obstruction and a decreased cardiac output with hypotension, leading to heart failure and death. Common complications of superior vena cava syndrome include airway obstruction, increased ICP, laryngeal edema, and cerebral edema. The prognosis will vary depending on the cause of the syndrome, and the amount of blockage that has already occurred. Prognosis is generally poor and the survival rate of patients with superior vena cava syndrome is approximately 10-20% at 6 months.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the anatomy and underlying mechanisms of mitral stenosis?", "role": "user" }, { "content": "When the mitral valve area goes below 2 cm 2, the valve causes an impediment to the flow of blood into the left ventricle, creating a pressure gradient across the mitral valve. This gradient may be increased by increases in the heart rate or cardiac output. As the gradient across the mitral valve increases, the amount of time necessary to fill the left ventricle with blood increases. Eventually, the left ventricle requires the atrial kick to fill with blood. As the heart rate increases, the amount of time that the ventricle is in diastole and can fill up with blood (called the diastolic filling period) decreases. When the heart rate goes above a certain point, the diastolic filling period is insufficient to fill the ventricle with blood and pressure builds up in the left atrium, leading to pulmonary congestion.\r\nWhen the mitral valve area goes less than 1 cm 2, there will be an increase in the left atrial pressures (required to push blood through the stenotic valve). Since the normal left ventricular diastolic pressures is about 5 mmHg, a pressure gradient across the mitral valve of 20 mmHg due to severe mitral stenosis will cause a left atrial pressure of about 25 mmHg. This left atrial pressure is transmitted to the pulmonary vasculature and causes pulmonary hypertension. Pulmonary capillary pressures in this level cause an imbalance between the hydrostatic pressure and the oncotic pressure, leading to extravasation of fluid from the vascular tree and pooling of fluid in the lungs (congestive heart failure causing pulmonary edema).\r\nIncreases in the heart rate will allow less time for the left ventricle to fill, also causing an increase in left atrial pressure and pulmonary congestion.\r\nThe constant pressure overload of the left atrium will cause the left atrium to increase in size. As the left atrium increases in size, it becomes more prone to develop atrial fibrillation. When atrial fibrillation develops, the atrial kick is lost (since it is due to the normal atrial contraction).\r\nIn individuals with severe mitral stenosis, the left ventricular filling is dependent on the atrial kick. The loss of the atrial kick due to atrial fibrillation can cause a precipitous decrease in cardiac output and sudden congestive heart failure.\r\nThe mitral annulus changes in shape and size during the cardiac cycle. It is smaller at the end of atrial systole due to the contraction of the left atrium around it, like a sphincter. This reduction in annulus size at the end of atrial systole may be important for the proper coapting of the leaflets of the mitral valve when the left ventricle contracts and pumps blood .\r\nThe closing of the mitral valve and the tricuspid valve constitutes the first heart sound (S1). It is not actually the valve closure which produces a sound but rather the sudden cessation of blood flow caused by the closure of the mitral and tricuspid valves. The mitral valve opening is normally not heard except in mitral stenosis as the opening Snap. Flow of blood into the heart during rapid filling is not normally heard except in certain pathological states where it constitutes the third heart sound (S3).\r\nThickening and immobility of the mitral valve leaflets causes an obstruction in blood flow from the left atrium to left ventricle (Mitral stenosis). As a result, the pressure in the left atrium increases, also the pressure in the pulmonary vasculature and right side of the heart increases. Mitral stenosis may cause left ventricular dysfunction if it is associated with mitral regurgitation .\r\nAlmost all cases of mitral stenosis are due to disease in the heart secondary to rheumatic fever and the consequent rheumatic heart disease (a condition that may develop after strep throat or scarlet fever). Around 90% of cases of rheumatic heart disease are associated with mitral stenosis . The valve problems develop 5 - 10 years after the rheumatic fever, a tiny nodules forms along the valve leaflets , the leaflets eventually thicken with deposition of fibrin. The cusps may become fibrosed, calcified and thickened over a span of a decade . Chronic turbulent flow through a deformed valve appears to cause these changes and as a result the valve losses it's normal morphology . The degree of leaflet thickening and calcification and the severity of chordal involvement are variable. Rheumatic fever is becoming rare in the United States, so mitral stenosis is also less common .\r\nSeverity of Mitral stenosis\r\nThe severity of mitral stenosis depends on the pressure gradient between the left atrium and ventricle which depends on the cross sectional area of the mitral valve. The normal mitral valve orifice has a cross sectional area of about 4.0 cm2.\r\nMitral stenosis is mild if the cross sectional area is about 2 cm2 and the pressure gradient is small. Mitral stenosis is moderate if the cross sectional area is about 1.0 to 1.5 cm2. Mitral stenosis is severe if the cross sectional area is ≤1.0 cm2 and the pressure gradient between the left atrium and left ventricle is significant.\r\nUsually, the rate of decrement in the valve area is about 0.1 cm2/year once mitral stenosis is present .\r\nIn pregnancy, the pressure gradient between the left atrium and ventricle is usually increased due to the increase in the heart rate and cardiac output during pregnancy. This can lead to the diagnosis of previously asymptomatic case of mitral stenosis, or worsening of the symptoms of previously diagnosed case.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the explanation for the relationship between ARVD1, epidemiology, and demographics?", "role": "user" }, { "content": "The incidence of ARVD is about 1/10,000 in the general population in the United States, although some studies have suggested that it may be as common as 1/1,000. It accounts for up to 17% of all sudden cardiac deaths in the young. In Italy, the incidence is 40/10,000, making it the most common cause of sudden cardiac death in the young population. It is more common in Northern Italy.\r\nThe male to female ratio is 3:1.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you please tell me the definition of pulmonic regurgitation?", "role": "user" }, { "content": "Pulmonary valve is located at the junction of the right ventricular outflow tract and pulmonary artery. Three equal-sized, semilunar cusps or leaflets make up the pulmonary valve. Pulmonary valve opens during right ventricular systole and closes during right ventricular diastole. Pulmonary regurgitation (PR) may be caused by an acquired alteration in the valvular morphology, idiopathic dilatation of the pulmonary artery (IDPA), pulmonic valve ring dilatation, congenital absence or malformation of the valve, and increasing regurgitation causing right ventricular volume overload. The pathophysiologic mechanism of pulmonic regurgitation includes right ventricular overload resulting in the right ventricular remodeling and progressive decline in function. The rate of decline in right ventricular systolic function is affected by associated conditions such as peripheral pulmonary artery stenosis and pulmonary hypertension which further increase the severity of pulmonary regurgitation. Among patients with severe PR, the gene expression pattern of GRK2 and β2- adrenoceptor (molecular markers of cardiac dysfunction) has been reported to be altered. Isolated PR is uncommon and is usually demonstrated with other valvular abnormalities or in certain conditions. Conditions associated include TOF, rheumatic heart disease and syphilis. On gross pathology vegetative lesions on the pulmonic valve leaflets may be observed among patients with acquired alteration in the valvular leaflet morphology.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is the natural history of Endophthalmitis, as well as its complications and prognosis?", "role": "user" }, { "content": "Endophthalmitis is a medical emergency. If left untreated, it may lead to panophthalmitis, corneal infiltration, corneal perforation, and permanent vision loss.\r\nCommon complications of endophthalmitis include:\r\nPanophthalmitis Decrease or loss of vision Chronic pain Cataract development Retinal detachment Vitreous hemorrhage Hypotony and phthisis bulbi\r\nEarly diagnosis and treatment with antimicrobial therapy are fundamental to optimize visual outcome.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What information about avian influenza is available?", "role": "user" }, { "content": "If you think you have been exposed to avian influenza, call your health care provider before your visit. This will give the staff a chance to take proper precautions that will protect them and other patients during your office visit. Tests to identify the avian flu exist but are not widely available. A test for diagnosing strains of bird flu in people suspected of having the virus gives preliminary results within 4 hours. Older tests took 2 to 3 days. Your doctor might also perform the following tests:\r\nAuscultation (to detect abnormal breath sounds) Chest x-ray Nasopharyngeal culture White blood cell differential\r\nOther tests may be done to look at the functions of your heart, kidneys, and liver.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide an overview of ventricular remodeling?", "role": "user" }, { "content": "Many factors influence the time course and extent of remodeling, including the severity of the insult, secondary events (recurrent ischemia or infarction), neurohormonal activation, genetic factors and gene expression, and treatment. Medications may attenuate remodeling. Angiotensin-converting enzyme (ACE) inhibitors have been consistently shown to decrease remodeling in animal models or transmural infarction and chronic pressure overload. Clinical trials have shown that ACE inhibitor therapy after myocardial infarction leads to improved myocardial performance, improved ejection fraction, and decreased mortality compared to patients treated with placebo. Early correction of congenital heart defects, if appropriate, may prevent remodeling, as will treatment of chronic hypertension or valvular heart disease. Often, reverse remodeling, or improvement in left ventricular function, will also be seen.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What does the term \"hyperkalemic periodic paralysis\" mean?", "role": "user" }, { "content": "Although much rarer, hyperkalemic periodic paralysis has also been observed in humans. In humans the disorder causes episodes of extreme muscle weakness, usually beginning in the second decade and depending on the type and severity of the HYPP will increase or stabilize until the fourth or fifth decade where attacks usually decline and can altogether stop. Factors that can trigger attacks include rest after exercise, potassium-rich foods, stress, fatigue, certain pollutants (eg: Cigarette smoke) and periods of fasting. Muscle strength improves between attacks, although many affected people may have increasing bouts of muscle weakness as time goes on (abortive attacks). Sometimes with HYPP those affected may experience degrees of muscle stiffness and spasms (myotonia) in the affected muscles. This can be caused by the same things that trigger the paralysis, dependant on the type of mytonia. (See also paramyotonia).\r\nSome people with hyperkalemic periodic paralysis have increased levels of potassium in their blood (hyperkalemia) during attacks. In other cases, attacks are associated with normal blood potassium levels (normokalemia). Ingesting potassium can trigger attacks in affected individuals, even if blood potassium levels do not go up.\r\nThe most common underlying cause is one of several possible point mutations in the gene SCN4A. The SCN4A gene provides instructions for making a protein that plays an essential role in muscles used for movement (skeletal muscles). For the body to move normally, these muscles must tense (contract) and relax in a coordinated way. Muscle contractions are triggered by the flow of certain positively charged atoms (ions), including sodium, into muscle cells. The SCN4A protein forms channels that control the flow of sodium ions into these cells. Mutations in the SCN4A gene alter the usual structure and function of sodium channels. The altered channels cannot properly regulate the flow of sodium ions into muscle cells, which reduces the ability of skeletal muscles to contract. Because muscle contraction is needed for movement, a disruption in normal ion transport leads to episodes of muscle weakness or paralysis.\r\nThis condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Could you provide me the existing text, so I can rephrase it?", "role": "user" }, { "content": "Vachel and Stevens were the first to describe a case of cystic dilatation of the intrahepatic bile ducts in 1906, but Jacques Caroli in 1958 gave a more thorough description of a syndrome of congenital malformation of the intrahepatic ducts with segmental cystic dilatation, increased biliary lithiasis, cholangitis and liver abscesses, associated with renal cystic disease or tubular ectasia. The disease is uncommon, with about 180 cases reported in the literature.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Which diagnostic imaging technique should be recommended to identify autoimmune hepatitis, echocardiography or ultrasound?", "role": "user" }, { "content": "There are few ultrasound findings helps in diagnosing autoimmune hepatitis. However, an ultrasound is more helpful in the diagnosis of complications of autoimmune hepatitis which include: \r\nFibrosis Heterogeneous hepatic echotexture Hepatomegaly Splenomegaly Irregular nodular liver", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "Can you provide an overview of prostatitis?", "role": "user" }, { "content": "There is no gold standard for the diagnosis and evaluation of patients presenting with prostatitis. The evaluation of a patient with acute and chronic bacterial prostatitis consists of history and physical examination and urine culture for lower urinary tract localization cultures, respectively. The evaluation of chronic pelvic pain syndrome includes tests which can be broadly divided into mandatory, recommended and optional.\r\nA detailed and thorough history from the patient is necessary. Specific areas of focus when obtaining a history from the patient include previous history of sexually transmitted diseases, any new sexual partners, known urogenital disorders, and recent catheterization or other genitourinary instrumentation. Common symptoms of acute and chronic bacterial prostatitis include urinary frequency, urinary urgency, burning during urination, nocturia, urinary retention and pain in the genital area, groin, lower abdomen, or lower back. Symptoms of acute prostatitis may also include fever, nausea, and vomiting. \r\nPatients with chronic prostatitis are usually well-appearing. Patients with acute prostatitis may appear ill and have systemic symptoms such as fever, chills, and nausea. In acute prostatitis, palpation of the prostate reveals a tender and enlarged prostate. In chronic prostatitis, palpation of the prostate reveals a tender and soft (boggy) prostate gland. A prostate massage should never be done in a patient with suspected acute prostatitis, since it may induce sepsis.\r\nThe laboratory tests used in the diagnosis of prostatitis are CBC, urinalysis, serum PSA (prostate-specific antigen) levels, urine culture, postvoid residual volume levels, 2-glass pre and post-prostatic massage test, Stamey-Meares four-glass test, and a semen analysis. Laboratory findings consistent with the diagnosis of acute prostatitis include increased leukocytes on complete blood picture, bacteria seen on urine culture, elevated C-reactive protein, and transiently elevated PSA (prostate specific antigen) levels. Laboratory findings consistent with the diagnosis of chronic bacterial prostatitis include negative pre-massage urine culture results, more than 10 to 20 leukocytes per high-power field in both the pre and the post massage urine specimen, bacteriuria in the postmassage urine specimen, and lower leukocyte and bacterial counts in voided bladder urine specimens as compared to bacterial count in post-prostatic massage voided urine or expressed prostatic secretions. The absence of bacterial growth on cultures is diagnostic of chronic nonbacterial prostatitis. \r\nCT scan in a patient with prostatitis shows edema of the prostate gland with diffuse enlargement, mostly in the peripheral zone. An abscess may be seen as a rim enhancing hypodensity which can either have single or multiple loci. Ultrasound can be used to diagnose prostatitis. On ultrasonography, focal hypoechoic area in the periphery of the prostate represents prostatitis. Fluid collection can show abscess formation. Colour doppler ultrasound may also prove to be very effective. MRI can also be used to diagnose prostatitis. Though it is not used commonly, its utilisation when suspecting alternate diagnosis like prostatic carcinoma etc is very important. MRI in case of a patient wit prostatitis depicts diffuse enlargement of the gland.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What laboratory findings are typically connected with Pneumoconiosis?", "role": "user" }, { "content": "There are no diagnostic laboratory findings associated with pneumoconiosis. Findings are generally nonspecific and therefore not of clinical significance. Rheumatoid factor and ESR may be present, but do not indicate disease activity or severity.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What are the preventative measures for Giardiasis?", "role": "user" }, { "content": "There is no vaccine against giardiasis. Prophylaxis against giardiasis, per se, is not recommended. Although some patients may benefit from antibiotic prophylaxis against traveler's diarrhea, antiparasitic regimens against giardiasis are not used prophylactically. To prevent and control infection with the Giardia parasite, it is important to: The following practices may help reduce the risk of Giardia transmission:\r\nPractice good handwashing and hygiene Avoid water (drinking or recreational) that may be contaminated Avoid eating food that may be contaminated Safe sexual practices, especially regarding anal sex, may decrease the risk of contracting or spreading giardiasis", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What do coronary arteries refer to?", "role": "user" }, { "content": "The coronary arteries supply oxygenated blood to the heart muscle itself. Although blood fills the chambers of the heart, the muscle tissue of the heart, or myocardium, is so thick that it requires coronary blood vessels to deliver blood deep into it. There are two primary arteries supplying the heart, the left coronary artery and the right coronary artery. These two epicardial coronary arteries course along the surface of the heart and this is why they are called \"epicardial\" (on top of the heart) arteries. Smaller arteries dive deep into the heart muscle and are called subendocardial coronary arteries. The cardiac veins are the vessels that remove the deoxygenated blood from the heart muscle and return it to the right atrium.", "role": "assistant" } ]

[ { "content": "Answer the question truthfully, you are a medical professional.", "role": "system" }, { "content": "What is Omegaven and what is an overview of it?", "role": "user" }, { "content": "WikiDoc Resources for Omegaven Articles Most recent articles on Omegaven Most cited articles on Omegaven Review articles on Omegaven Articles on Omegaven in N Eng J Med, Lancet, BMJ Media Powerpoint slides on Omegaven Images of Omegaven Photos of Omegaven Podcasts & MP3s on Omegaven Videos on Omegaven Evidence Based Medicine Cochrane Collaboration on Omegaven Bandolier on Omegaven TRIP on Omegaven Clinical Trials Ongoing Trials on Omegaven at Clinical Trials.gov Trial results on Omegaven Clinical Trials on Omegaven at Google Guidelines / Policies / Govt US National Guidelines Clearinghouse on Omegaven NICE Guidance on Omegaven NHS PRODIGY Guidance FDA on Omegaven CDC on Omegaven Books Books on Omegaven News Omegaven in the news Be alerted to news on Omegaven News trends on Omegaven Commentary Blogs on Omegaven Definitions Definitions of Omegaven Patient Resources / Community Patient resources on Omegaven Discussion groups on Omegaven Patient Handouts on Omegaven Directions to Hospitals Treating Omegaven Risk calculators and risk factors for Omegaven Healthcare Provider Resources Symptoms of Omegaven Causes & Risk Factors for Omegaven Diagnostic studies for Omegaven Treatment of Omegaven Continuing Medical Education (CME) CME Programs on Omegaven International Omegaven en Espanol Omegaven en Francais Business Omegaven in the Marketplace Patents on Omegaven Experimental / Informatics List of terms related to Omegaven\r\nOmegaven is a fatty acid emulsion produced by Fresenius Kabi. It is used for total parenteral nutrition (feeding directly into a venous catheter), e.g. in short bowel syndrome. It is rich in omega-3 fatty acids.\r\nIt has gained popularity in children in preference to the more commonly used Intralipid after case reports that it reduced the risk of liver damage. \r\nA recent study indicated that the use of Omegaven may be an appropriate intervention strategy for newborns with a very low birth weight, gastrochisis, and jejunal atresia. \r\nIt is currently undergoing a clinical trial at National Taiwan University Hospital. \r\nAlthough the use of Omegaven in children in the United States is experimental, the use of it in adults in Europe is less controversial. In European studies, Omegaven has been associated with a reduction in psoriasis, when contrasted to administration of omega-6 fatty acid Lipoven. Omegaven has also been associated with reduced mortality and antibiotic use during hospital stays.", "role": "assistant" } ]