Thrombotic thrombocytopenic purpura is caused by impaired ADAMTS13 protease, which leads to uncleaved von Willebrand factor multimers causing microvascular thrombosis, thrombocytopenia, and hemolytic anemia with schistocyte formation. Disseminated intravascular coagulation results in prolonged prothrombin time and partial thromboplastin time, thrombosis, and bleeding. Epstein-Barr virus infects mature B lymphocytes and causes heterophile antibody production and immunoglobulin M antibodies against horse and sheep red blood cells.
Thrombotic thrombocytopenic purpura is caused by impaired ADAMTS13 protease, which leads to uncleaved von Willebrand factor multimers causing microvascular thrombosis, thrombocytopenia, and hemolytic anemia with schistocyte formation. Disseminated intravascular coagulation results in prolonged prothrombin time and partial thromboplastin time, thrombosis, and bleeding. Epstein-Barr virus infects mature B lymphocytes and causes heterophile antibody production and immunoglobulin M antibodies against horse and sheep red blood cells.
Thrombotic thrombocytopenic purpura is caused by impaired ADAMTS13 protease, which leads to uncleaved von Willebrand factor multimers causing microvascular thrombosis, thrombocytopenia, and hemolytic anemia with schistocyte formation. Disseminated intravascular coagulation results in prolonged prothrombin time and partial thromboplastin time, thrombosis, and bleeding. Epstein-Barr virus infects mature B lymphocytes and causes heterophile antibody production and immunoglobulin M antibodies against horse and sheep red blood cells.
Thrombotic thrombocytopenic purpura is caused by impaired ADAMTS13 protease, which leads to uncleaved von Willebrand factor multimers causing microvascular thrombosis, thrombocytopenia, and hemolytic anemia with schistocyte formation. Disseminated intravascular coagulation results in prolonged prothrombin time and partial thromboplastin time, thrombosis, and bleeding. Epstein-Barr virus infects mature B lymphocytes and causes heterophile antibody production and immunoglobulin M antibodies against horse and sheep red blood cells.
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Thrombotic Thrombocytopenic Purpura
o Impaired ADAMTS13, vWF cleaving protease.
o Uncleaved vWF multimers result in microvascular thrombosis. o Thrombocytopenia and hemolytic anemia with schistocyte formation occur. DIC o Prolonged PT, PTT o Thrombosis, bleeding. EBV o Mature B lymphocytes o Heterophile + o IGM antibodes, horse/sheep RBC Umbilical Hernia o Incomplete closure of the umbilical ring, allow bowel through abdomen. o Covered by skin o Reducibe buglge at the umbilicus with increase abdominal pressure o Associated with Downs o Resolve by itself Tonic clonic and absence seizure o Valproate is used here o Phenobarbital is used for tonic clonic only Gouty Arthiritis o We give them Xanthine oxidase inhibitors, which decrease uric acid production. o Prophylactic therapy is intiated. Cystic Fibrosis o Amino acid 508 base pair deletion causes impaired posttranslational processing(improper folding and glycosylation) of CFTR. o Abnormal protein is targetd for protasomal degradation, preventing it from reaching to cell surface. Mycobacterium TB o Streptomycin(amino glycoside) resistance o Works by inhibiting 30s subunit o Alter structure of bacterial ribosomal proteins IGA Nephropathy is MCC of GN. o Painless hematuria after URI. o Mesangial IgA deposit. Constrictive Pericarditis o Thickened pericardium
o Limiting ventricular expansion during diastolic filling
o Increase JVD, Kussmaul sign, pulsus paradoxus, pericardial knock. During exercise, increase CO2 production o Increased PCO2 of mixed enous blood o Hemeostatic mechanisms maintain arterial blood gas level Transmural inflammation o Edema and fibrosis o Interstinal lumen narrowing. o Causes ulcers, lead to fistula. Phosphoribosyl Pyrophosphate synthetase is responsible for production of activated ribose for de novo synthesis. o Mutation here will cause increased purine production o Result in hyperuricemia and gout. BPH o A1 antagonist work within days to weeks, work on dynamic component of bladder outlet obstruction o 5 Alpha Reductase Inhibitors(dutasteride, finasteride) inhibit conversion of testosterone to dihydro and address fixed component of bladder outlet obstruction. Reduce prostate volume. After a pancreatectomy, all enzymes are normally secreted. o D-xylose does not get affected by the enzymes because it is a monosaccharide. Calcium stones have hypercalciruia, but have normocalcemia due to intact regulation of serum calcium levels by vitamin D and PTH. VIPoma result in watery diarrhea, hypokalemia, achlorhydia syndrome. o Somatostatin inhibits release of VIP. Eye adduction is done by CN3, which enters through the Superior orbital fissure. o CN6, 4, superior ophthalmic vein also enter here. Stable angina, patient is given nitrates o Nitrates venodilate, decrease preload(decrease LV end diastolic volume and pressure), reduce afterload. Results in decreased Myocardial O2 demand, relieves angina symptoms. In Asthmatic patients, only leukotrienes and acetylcholine produce bronchospasm thats reeleived by pharmacologic agents. o Using montelukast or zafirlukast can control asthma by increasing airway caliber and reducing mucosal inflammation.
o Inhaled ipratropium is the MM3 antimuscuranic.
Carbon tetrachloride causes free radical injury. o Happens through lipid peroxidation. o Can culminate in hepatocyte necrosis. Gallbladder hypomotility o Gallbladder absorbs water from bile, hypomotility causes bile concentration, which promotes bile precipitation and accumulation of viscous biliary sludge that obstructs bile duct. o Sludge formation is aprecursor to stone formation.