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198 Cards in this Set
- Front
- Back
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Hydralazine mechanism of action?
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Direct acting arteriole dilator (increases cGMP). Decreases TPR (afterload).
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Hydralazine uses?
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Sever hypertension, CHF. First line HTN tx in pregnancy (with methyldopa).
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Hydralazine side effects?
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Drug-induced SLE in slow acetylators, reflex tachycardia, headache, angina.
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Nifedipine, amlodipine mechanism of action?
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Inhibits L-type voltage gated calcium channels. Vasodilator (arteiroles). Low heart affinity.
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Nifedipine, amlodipine uses?
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Prinzmetal's angina, Raynaud's phenomenon, Berry aneurysms, hypertension.
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Nifedipine, amlodipine side effects?
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Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation. Reflex tachycardia, gingival hyperplasia.
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Verapamil mechanism of action?
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Inhibits L-type voltage gated calcium channels. Decreases contractility, AV conduction velocity. Low artery affinity. Class IV antiarrhythmics (increase ERP, PR interval).
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Verapamil uses?
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Hypertension, angina, arrhythmias (SVT).
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Verapamil side effects?
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Cardiac depression, AV block, peripheral edema, flushing, dizziness, heavy constipation. Gingival hyperplasia. Increases toxicity of digoxin by displacing from tissue-binding sites.
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Diltiazem mechanism of action?
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Inhibits L-type voltage gated calcium channels. Decreases contractility, AV conduction velocity. Low artery affinity. Class IV antiarrhythmics (increase ERP, PR interval).
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Diltiazem uses?
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Hypertension, angina, arrhythmias (SVT).
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Diltiazem side effects?
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Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation.
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Nitroprusside mechanism of action?
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Vasodilation and venodilation (increases cGMP via direct release of nitrous oxide).
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Nitroprusside uses?
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Malignant hypertension.
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Nitroprusside side effects?
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Limit treatment to 24-36 hours. Cyanide toxicity (altered mental status, lactic acidosis). Treat toxicity with nitrites, hydroxocobalamin, and sodium thiosulfate (sulfur).
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Fenoldopam mechanism of action?
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D1 receptor agonist; relaxes renal vascular smooth muscle. Artery vasodilator.
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Fenoldopam uses?
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Malignant hypertension. Increases renal perfusion.
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Fenoldopam side effects?
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0
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Diazoxide mechanism of action?
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Direct acting arteriole vasoldiator. ATP dependent K+ channel opener; hyperpolarizes and relaxes vascular smooth muscle.
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Diazoxide uses?
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Malignant hypertension. Insulinomas.
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Diazoxide side effects?
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Hyperglycemia (reduces insulin release).
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Minoxidil mechanism of action?
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Direct acting arteriole vasoldiator. ATP dependent K+ channel opener; hyperpolarizes and relaxes vascular smooth muscle.
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Minoxidil uses?
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Sever hypertension (IV), baldness (topical).
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Minoxidil side effects?
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Hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retention. Hyperglycemia (reduces insulin release).
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Nitroglycerin, isorbide dinitrate mechanism of action?
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Venodilation (increases cGMP, inducing dephosphorylation of myosin light chain). Has largest effect on large veins. Production of NO requires cystine on glutathione (GSH).
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Nitroglycerin, isorbide dinitrate uses?
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Effort angina, pulmonary edema.
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Nitroglycerin, isorbide dinitrate side effects?
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Reflex tachycardia, orthostatic hypotension, HEADACHE*. Rapid tolerance (tachyphylaxis due to depletion of GSH). Cardiotoxicity when used with sildenafil (massive drop in TPR causes reflex tachycardia and possible MI).
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Lovastatin (-statin) mechanism of action?
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Inhibits HMG-CoA reductase (decrease mevalonate). Improves survival by inhibiting inflammation.
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Lovastatin (-statin) uses?
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Decreases VLDL (TGs), LDL (cholesterol). Increases HDL. Primarily used to lower CHOLESTEROL.
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Lovastatin (-statin) side effects?
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Hepatotoxicity, myositis, rhabdomyolysis (especially with gemfibrozil).
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Niacin mechanism of action?
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Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation.
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Niacin uses?
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Increases HDL, lowers LDL (cholesterol). Greatly lowers VLDL (triglycerides). Primarily used to lower TRIGLYCERIDES.
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Niacin side effects?
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Flushing (tx with aspirin). Hyperglycemia (acanthosis nigricans). Hyperuricemia (exacerbates gout).
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Cholestyramine mechanism of action?
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Prevents intestinal reabsorption of bile acids; liver must consume cholesterol to make replenish lost bile.
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Cholestyramine uses?
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Decreases LDL (cholesterol); mild increase of VLDL and HDL.
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Cholestyramine side effects?
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Patients hate it; tastes horrible and causes GI discomfort. Affects absorption of ADEK vitamins and other medications (digoxin, warfarin). Gallstones. Contraindicate with hypertriglyceridemia.
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Cholestipol mechanism of action?
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Prevents intestinal reabsorption of bile acids; liver must consume cholesterol to make replenish lost bile.
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Cholestipol uses?
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Decreases LDL (cholesterol); mild increase of VLDL and HDL.
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Cholestipol side effects?
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Patients hate it; tastes horrible and causes GI discomfort. Affects absorption of ADEK vitamins and other medications (digoxin, warfarin). Gallstones. Contraindicate with hypertriglyceridemia.
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Colesevelam mechanism of action?
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Prevents intestinal reabsorption of bile acids; liver must consume cholesterol to make replenish lost bile.
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Colesevelam uses?
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Decreases LDL (cholesterol); mild increase of VLDL and HDL.
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Colesevelam side effects?
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Patients hate it; tastes horrible and causes GI discomfort. Affects absorption of ADEK vitamins and other medications (digoxin, warfarin). Gallstones. Contraindicate with hypertriglyceridemia.
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Ezetimibe mechanism of action?
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Prevent cholesterol reabsorption at small intestine brush border.
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Ezetimibe uses?
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Lowers LDL (cholesterol).
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Ezetimibe side effects?
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Hepatotoxicity (elevated AST, ALT).
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Gemfibrozil mechanism of action?
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Induces LPL (via PPAR-alpha) leading to increased TG clearance).
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Gemfibrozil uses?
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Hypertryglyceridemia (increases VLDL uptake).
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Gemfibrozil side effects?
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Myositis, hepatotoxicity, gallstones (inhibits 7-alpha hydroxylase), rhabdomyolysis.
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Clofibrate, bezafibrate, fenofibrate (-fibrate) mechanism of action?
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Induces LPL (via PPAR-alpha) leading to increased TG clearance).
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Clofibrate, bezafibrate, fenofibrate (-fibrate) uses?
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Hypertryglyceridemia (increases VLDL uptake).
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Clofibrate, bezafibrate, fenofibrate (-fibrate) side effects?
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Hepatotoxicity, gallstones (inhibits 7-alpha hydroxylase). No rhabdomyolysis.
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Digoxin mechanism of action?
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Inhibits Na/K-ATPase leading to increase intracellular sodium (hypersensitive neurons) and calcium (increased contractility). Predominately stimulates vagal tone (decrease AV conductivity, decrease HR).
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Digoxin uses?
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CHF, atrial fibrillation, SVT.
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Digoxin side effects?
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Cholinergic effects (nausea, vomiting, diarrhea, blurry yellow vision). Increases PR interval, decrease QT interval, scooping, T-wave inversion, ventricular arrhythmia. Causes hyperkalemia. Increased toxicity with hypokalemia, renal failure, and quinidine/verapamil. In overdose first treat the hyperkalemia, then use digoxin-Fab, then magnesium.
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Nesiritide mechanism of action?
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Recombinant B-type natriuertic peptide. Vasodilates (increases cGMP).
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Nesiritide uses?
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Acute decompensated heart failure.
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Nesiritide side effects?
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Hypotension.
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Quinidine mechanism of action?
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Class Ia antiarrhythmic. Inhibits OPEN voltage gated sodium channels. Inhibits voltaged gated potassium channels (increases QT interval, AP duration, and ERP).
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Quinidine uses?
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Atrial and ventricular arrhythmias, especially SVT and ventricular tachycardia.
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Quinidine side effects?
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Increases QT interval (torsades). Cinchonism - headache, tinnitus, visual disturbances, constipation or diarrhea). Increased heart rate and hypotension (muscarinic, alpha antagonist). Increased toxicity with hyperkalemia. Increases toxicity of digoxin by displacing from tissue-binding sites.
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Procainamide mechanism of action?
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Class Ia antiarrhythmic. Inhibits OPEN voltage gated sodium channels. Inhibits voltaged gated potassium channels (increases QT interval, AP duration, and ERP).
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Procainamide uses?
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Atrial and ventricular arrhythmias, especially SVT and ventricular tachycardia.
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Procainamide side effects?
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Thrombocyptopenia, torsades de pointes (increased QT), drug induced SLE (hematotoxic). Increased toxicity with hyperkalemia.
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Disopyramide mechanism of action?
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Class Ia antiarrhythmic. Inhibits OPEN voltage gated sodium channels. Inhibits voltaged gated potassium channels (increases QT interval, AP duration, and ERP).
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Disopyramide uses?
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Atrial and ventricular arrhythmias, especially SVT and ventricular tachycardia.
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Disopyramide side effects?
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Thrombocyptopenia, torsades de pointes (increased QT). Increased toxicity with hyperkalemia.
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Phenytoin mechanism of action?
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Class Ib antiarrhythmic. Inhibits INACTIVE voltage gated sodium channels (targets ISCHEMIC tissue). Activates voltage gated potassium channels (shortens AP, ERP).
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Phenytoin uses?
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Acute ventricular arrhytmias (post-MI) and digitalis-induced arrhythmias.
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Phenytoin side effects?
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0
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Lidocaine mechanism of action?
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Class Ib antiarrhythmic. Inhibits INACTIVE voltage gated sodium channels (targets ISCHEMIC tissue). Shortens AP, ERP.
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Lidocaine uses?
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Acute ventricular arrhytmias (post-MI) and digitalis-induced arrhythmias.
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Lidocaine side effects?
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CNS stimulation/depression, cardiovascular depression. Increased toxicitiy with hyperkalemia.
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Mexiletine mechanism of action?
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Class Ib antiarrhythmic. Inhibits INACTIVE voltage gated sodium channels (targets ISCHEMIC tissue). Shortens AP, ERP.
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Mexiletine uses?
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Acute ventricular arrhytmias (post-MI) and digitalis-induced arrhythmias.
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Mexiletine side effects?
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CNS stimulation/depression, cardiovascular depression. Increased toxicitiy with hyperkalemia.
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Tocainide mechanism of action?
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Class Ib antiarrhythmic. Inhibits INACTIVE voltage gated sodium channels (targets ISCHEMIC tissue). Shortens AP, ERP.
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Tocainide uses?
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Acute ventricular arrhytmias (post-MI) and digitalis-induced arrhythmias.
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Tocainide side effects?
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CNS stimulation/depression, cardiovascular depression. Increased toxicitiy with hyperkalemia.
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Flecanide mechanism of action?
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Class Ic antiarrhythmic Inhibits both open and closed voltage gated sodium channels. No effect on AP, ERP.
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Flecanide uses?
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Ventricular tachycardia, SVT.
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Flecanide side effects?
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Proarrhythmic; contraindicated post MI. Significantly prolongs refractory period in AV node. Increased toxicitiy with hyperkalemia.
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Propafenone mechanism of action?
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Class Ic antiarrhythmic Inhibits both open and closed voltage gated sodium channels. No effect on AP, ERP.
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Propafenone uses?
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Ventricular tachycardia, SVT.
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Propafenone side effects?
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Proarrhythmic; contraindicated post MI. Significantly prolongs refractory period in AV node. Increased toxicitiy with hyperkalemia.
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Propranolol mechanism of action?
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Non-selective beta adrenergic antagonist. Increases PR interval, decreases slope of phase 4 in AV/SA node. Decreases renin release.
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Propranolol uses?
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Ventricular tachycardia, SVT, slowing ventricular rate during atrial fibrillation and atrial flutter. Antihypertensive post MI/angina.
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Propranolol side effects?
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Treat overdose with glucagon. Impotence, exacerbation of asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (depression, sleep alterations). May mask signs of hypoglycemia.
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Esmolol mechanism of action?
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Beta-1 selective adrenergic antagonist. Very short acting. Increases PR interval, decreases slope of phase 4 in AV/SA node.
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Esmolol uses?
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Ventricular tachycardia, ACUTE SVT, slowing ventricular rate during atrial fibrillation and atrial flutter. Antihypertensive post MI/angina.
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Esmolol side effects?
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Treat overdose with glucagon. Impotence, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (depression, sleep alterations). May mask signs of hypoglycemia.
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Metoprolol, atenolol, timolol, acebutolol mechanism of action?
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Beta-1 selective adrenergic antagonist. Increases PR interval, decreases slope of phase 4 in SA/AV node. Decreases renin release.
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Metoprolol, atenolol, timolol, acebutolol uses?
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Ventricular tachycardia, SVT, slowing ventricular rate during atrial fibrillation and atrial flutter. Antihypertensive post MI/angina.
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Metoprolol, atenolol, timolol, acebutolol side effects?
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Treat overdose with glucagon. Impotence, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (depression, sleep alterations). May mask signs of hypoglycemia. Dyslipidemia (increase LDLs and TGs).
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Ibutilide mechanism of action?
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Blocks voltage-gated potassium channels. Increases AP, ERP. Increases QT interval.
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Ibutilide side effects?
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Torsades de pointes.
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Sotalol mechanism of action?
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Beta-1 adrenergic antagonist. Blocks voltage-gated potassium channels. Increases AP, ERP. Increases QT interval.
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Sotalol side effects?
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Torsades de pointes.
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Bretylium mechanism of action?
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Blocks voltage-gated potassium channels. Increases AP, ERP. Increases QT interval.
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Bretylium uses?
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0
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Bretylium side effects?
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Not associated with torsades de pointes.
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Amiodarone mechanism of action?
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Blocks voltage-gated potassium channels. Increases AP, ERP. Increases QT interval.
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Amiodarone uses?
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Any arrhythmias. Extremely long half life (80 days).
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Amiodarone side effects?
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Doesn't increase risk of torsades de pointes. Pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism, corneal deposits, blue/gray skin deposits resulting in photodermatitis, neurological effects, constipation, bradycardia/heart block/CHF.
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Dofetilide mechanism of action?
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Blocks voltage-gated potassium channels. Increases AP, ERP. Increases QT interval.
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Dofetilide uses?
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0
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Dofetilide side effects?
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Torsades de pointes.
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Adenosine mechanism of action?
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Increaes potassium efflux, hyperpolarizing the cell. Causes G(i)-coupled decrease in cAMP. Decreases SA/AV nodal activity.
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Adenosine uses?
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Drug of choice for paroxysmal SVT.
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Adenosine side effects?
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Flushing, hypotension, chest pain, bronchospasm/dyspnea. Effects blocked by theophylline/caffeine.
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Magnesium mechanism of action?
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Decreases neuron excitability.
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Magnesium uses?
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Digoxin toxicity, torsades de pointes.
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Magnesium side effects?
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0
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Captopril (-pril) mechanism of action?
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Inhibits ACE, reducing levels of A-II and preventing inactivation of bradykinin (vasodilation). Increased renin release.
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Captopril (-pril) uses?
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Hypertension with CHF or diabetic renal disease. Prevents unfavorable heart remodeling as a result of chronic hypertension (increases survival).
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Captopril (-pril) side effects?
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Cough, angioedema, proteinuria, taste changes, hypotension, rash, increased renin, hyperkalemia. Contraindicate with pregnancy (fetal renal damage) and bilateral renal stenosis (causes decrease in GFR by preventing constriction of efferent arterioles leading to increased creatinine).
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Losartan (-sartan) mechanism of action?
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Angiotensin II receptor type 1 antagonist.
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Losartan (-sartan) uses?
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Hypertension with CHF or diabetic renal disease. Prevents unfavorable heart remodeling as a result of chronic hypertension (increases survival).
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Losartan (-sartan) side effects?
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NO COUGH OR ANGIOEDEMA. Proteinuria, taste changes, hypotension, rash, increased renin, hyperkalemia***. Contraindicate with pregnancy (fetal renal damage) and bilateral renal stenosis (causes decrease in GFR by preventing constriction of efferent arterioles leading to increased creatinine).
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Furosemide, torsemide mechanism of action?
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Inhibits NaKCC of the TAL. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilation of afferent arteriole); inhibited by NSAIDs.
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Furosemide, torsemide uses?
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Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia.
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Furosemide, torsemide side effects?
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Ototoxicity, hypokalemic metabolic alkalosis, dehydration, sulfa allergy, interstitial nephritis, hyperuricemia (gout), hypocalcemia/hypomagnesemia.
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Ethacrynic acid mechanism of action?
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Inhibits NaKCC of the TAL. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilation of afferent arteriole); inhibited by NSAIDs.
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Ethacrynic acid uses?
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Diuresis in patients allergic to sulfa drugs.
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Ethacrynic acid side effects?
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NO SULFA ALLERGY, can be used with gout. Otoxoticity (more toxic than furosemide), hypokalemic metabolic alkalosis, dehydration, nephritis, hypocalcemia/hypomagnesemia.
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Hydrochlorothiazide, indapamide, metolazone mechanism of action?
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Inhibits NaCl reabsorption in the early distal tubule. Opens ATP-dependent K+ channel (beta islet cells, arterioles).
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Hydrochlorothiazide, indapamide, metolazone uses?
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Hypertension, CHF, idiopathic hypercalcinuria (nephrolithiasis), nephrogenic diabetes insipidus. DON'T USE IN PATIENTS WITH DIABETES MELLITUS TYPE 2.
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Hydrochlorothiazide, indapamide, metolazone side effects?
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Hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia (inhibits insulin release), hyperlipidemia (LDL, cholesterol), hyperuricemia, and hypercalcemia. Sulfa allergy.
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Spironlactone mechanism of action?
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Aldosterone antagonist on principle cells of the cortical collecting tubule. Potassium sparing diuretic.
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Spironlactone uses?
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Hyperaldosteronism (Conn's syndrome), reverses hypokalemia, CHF. Slows cardiac remodeling. Anti-androgen (for acne, hirsutism).
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Spironlactone side effects?
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Hyperkalemic metabolic acidosis. Gynectomastia (anti-androgen effects).
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Eplerenone mechanism of action?
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Selective aldosterone antagonist on principle cells of the cortical collecting tubule. Potassium sparing diuretic.
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Eplerenone uses?
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Hyperaldosteronism (Conn's syndrome), reverses hypokalemia, CHF. Slows cardiac remodeling.
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Eplerenone side effects?
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Hyperkalemic metabolic acidosis. No anti-androgen effects.
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Triamterene mechanism of action?
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Block sodium channels in the cortical collecting tubule. Potassium sparing diuretic.
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Triamterene uses?
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Reverses hypokalemia, CHF, lithium-induced nephrogenic diabetes insipidus.
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Triamterene side effects?
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Hyperkalemic metabolic acidosis.
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Amiloride mechanism of action?
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Block sodium channels in the cortical collecting tubule. Potassium sparing diuretic.
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Amiloride uses?
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Reverses hypokalemia, CHF, lithium-induced nephrogenic diabetes insipidus.
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Amiloride side effects?
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Hyperkalemic metabolic acidosis.
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Aliskiren mechanism of action?
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Direct renin inhibitor.
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Aliskiren uses?
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Hypertension with CHF or diabetic renal disease. Prevents unfavorable heart remodeling as a result of chronic hypertension (increases survival).
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Aliskiren side effects?
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Hyperkalemia. No cough or edema. Contraindicate with renal artery stenosis.
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anti-digoxin Fab fragments mechanism of action?
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0
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anti-digoxin Fab fragments uses?
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Digoxin toxicity
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anti-digoxin Fab fragments side effects?
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0
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Clopidogrel, parsugrel, ticagrelor mechanism of action?
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Inhibits platelet aggregation by irreversibly blocking ADP receptors. Inhibits fibrinogen by binding and preventing glycoprotein Iib/IIIa expression.
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Clopidogrel, parsugrel, ticagrelor uses?
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Acute coronary syndrome; coronary stenting. Decreased incidence or recurrence of thrombotic stroke.
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Clopidogrel, parsugrel, ticagrelor side effects?
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0
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Ticlopidine mechanism of action?
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Inhibits platelet aggregation by irreversibly blocking ADP receptors. Inhibits fibrinogen by binding and preventing glycoprotein Iib/IIIa expression.
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Ticlopidine uses?
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Acute coronary syndrome; coronary stenting. Decreased incidence or recurrence of thrombotic stroke.
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Ticlopidine side effects?
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Neutropenia, acute thrombocytopenic purpura.
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Cilostazol mechanism of action?
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Phosphodiesterase III inhibitor; increases cAMP in platelets thus inhibiting platelet aggregation. Vasodilator.
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Cilostazol uses?
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Peripheral artery disease. Intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (combined with aspirin), angina prophylaxis.
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Cilostazol side effects?
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Nausea, headache, facial flushing, hypotension, abdominal pain.
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Dipyridamole mechanism of action?
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Phosphodiesterase III inhibitor; increases cAMP in platelets thus inhibiting platelet aggregation. Vasodilator. Thromboxane synthase inhibitor.
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Dipyridamole uses?
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Peripheral artery disease. Intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (combined with aspirin), angina prophylaxis.
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Dipyridamole side effects?
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Nausea, headache, facial flushing, hypotension, abdominal pain.
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Abciximab mechanism of action?
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Monoclonal antibody that binds to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation.
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Abciximab uses?
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Acute coronary syndrome, percutaneous transulminal coronary angioplasty.
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Abciximab side effects?
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Bleeding, thrombocytopenia.
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Eptifibatide mechanism of action?
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Glycoprotein receptor IIb/IIIa antagonist on activated platelets, preventing aggregation.
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Eptifibatide uses?
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Acute coronary syndrome, percutaneous transulminal coronary angioplasty.
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Eptifibatide side effects?
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Bleeding, thrombocytopenia.
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Tirofiban mechanism of action?
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Glycoprotein receptor IIb/IIIa antagonist on activated platelets, preventing aggregation.
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Tirofiban uses?
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Acute coronary syndrome, percutaneous transulminal coronary angioplasty.
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Tirofiban side effects?
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Bleeding, thrombocytopenia.
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Streptokinase, urokinase mechanism of action?
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Converts both clot bound and free blood plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increase PT, PTT, but no effect on platelet count.
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Streptokinase, urokinase uses?
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Early MI, DVT. NEVER USE IN STROKE.
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Streptokinase, urokinase side effects?
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Hypersensitivity (immunogenic). Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension. Treat toxicity with aminocaproic acid.
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Alteplase mechanism of action?
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Tissue plasminogen activator (tPA). Clot specific. Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increase PT, PTT, but no effect on platelet count.
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Alteplase uses?
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Early MI, early ischemic stroke.
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Alteplase side effects?
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No hypersensitivity. Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension. Treat toxicity with aminocaproic acid.
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APSAC (anistreplase) mechanism of action?
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Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increase PT, PTT, but no effect on platelet count.
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APSAC (anistreplase) uses?
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Early MI, early ischemic stroke.
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APSAC (anistreplase) side effects?
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Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension. Treat toxicity with aminocaproic acid.
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Protamine sulfate mechanism of action?
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Positively charged molecule that binds negatively charged heparin.
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Protamine sulfate uses?
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Rapid antidote to heparin toxicity.
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Protamine sulfate side effects?
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0
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Enoxaparin, fondaparinux mechanism of action?
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Low-molecular-weight heparin. Acts more on factor Xa. Better bioavailability, longer half life.
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Enoxaparin, fondaparinux uses?
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0
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Enoxaparin, fondaparinux side effects?
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Not easily reversible. Doesn't need lab monitoring (doesn't affect PTT). Less likely to cause HIT.
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Heparin mechanism of action?
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Cofactor for the activaiton of antithrombin III, decreases thrombin (IIa), decreases factor Xa. Also IXa and XIIa. Short half life. Works in blood. Rapid onset. Works in vitro.
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Heparin uses?
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Immediate anticoagulation for pulmonary embolism, stroke, acute coronary syndrome, MI, DVT. May be used during pregnancy (unlike warfarin). Water soluble (must give IV, short half life).
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Heparin side effects?
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Must monitor PTT. Bleeding, heparin-induced thrombocytopenia, osteoporosis, drug-drug interactions. Treat overdose with protamine sulfate.
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Warfarin (coumadin) mechanism of action?
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Interferes with vitamin K synthesis (gamma-carboxylation), thus decreases factors II, VII, IX, X, protein C and S. Works on the liver. Slow onset. Only works in vivo.
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Warfarin (coumadin) uses?
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Chronnic anticoagulation therpay (DVT, post STEMI). Don't use in pregnant women. Lipid soluble (give orally, long half life).
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Warfarin (coumadin) side effects?
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Must monitor PT/INR. Bleeding, teratogenic (bone disruption), skin/tissue necrosis (with protein C and S deficiency), drug-drug interactions. Treat overdose with fresh frozen plasma (for immediate recovery) or vitamin K (gradual). Increased toxiicity with sulfonamides, sulfonylureas, NSAIDs. Decreased absorption with cholestyramine.
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Lepirudin, bivalirudin mechanism of action?
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Direct thrombin inhibitor; hirudin derivative.
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Lepirudin, bivalirudin uses?
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Used as an alternative to heparin for anticoagulating in patients with heparin-induced thrombocytopenia. Used in unstable angina prior to percutaneous fibrinolysis.
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Lepirudin, bivalirudin side effects?
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Doesn't cause HIT.
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EACA mechanism of action?
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Epsilon-aminocaproic acid
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EACA uses?
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Treats thrombolytic (alteplase) toxicity.
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Argatroban, dabigatran mechanism of action?
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Direct thrombin inhibitor; (blocks factor IIa). Prevents fibrin formation.
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Argatroban, dabigatran side effects?
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Doesn't cause HIT.
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Tranexamic acid uses?
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Treats thrombolytic (alteplase) toxicity.
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Rivaroxaban mechanism of action?
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Oral factor Xa inhibitor.
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Milrinone, inamrinone mechanism of action?
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Phosphodiesterase inhibitor (increases cAMP), thus increasing inotropy and decreasing TPR.
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Milrinone, inamrinone uses?
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Congestive heart failure. Override beta-blockers.
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