Cardio Pharm Flashcards
Direct acting arteriole dilator (increases cGMP). Decreases TPR (afterload).
Hydralazine mechanism of action?
Sever hypertension, CHF. First line HTN tx in pregnancy (with methyldopa).
Hydralazine uses?
Drug-induced SLE in slow acetylators, reflex tachycardia, headache, angina.
Hydralazine side effects?
Inhibits L-type voltage gated calcium channels. Vasodilator (arteiroles). Low heart affinity.
Nifedipine, amlodipine mechanism of action?
Prinzmetal’s angina, Raynaud’s phenomenon, Berry aneurysms, hypertension.
Nifedipine, amlodipine uses?
Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation. Reflex tachycardia, gingival hyperplasia.
Nifedipine, amlodipine side effects?
Inhibits L-type voltage gated calcium channels. Decreases contractility, AV conduction velocity. Low artery affinity. Class IV antiarrhythmics (increase ERP, PR interval).
Verapamil mechanism of action?
Hypertension, angina, arrhythmias (SVT).
Verapamil uses?
Cardiac depression, AV block, peripheral edema, flushing, dizziness, heavy constipation. Gingival hyperplasia.«_space;Increases toxicity of digoxin by displacing from tissue-binding sites.»
Verapamil side effects?
Inhibits L-type voltage gated calcium channels. Decreases contractility, AV conduction velocity. Low artery affinity. Class IV antiarrhythmics (increase ERP, PR interval).
Diltiazem mechanism of action?
Hypertension, angina, arrhythmias (SVT).
Diltiazem uses?
Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation.
Diltiazem side effects?
Vasodilation and venodilation (increases cGMP via direct release of nitrous oxide).
Nitroprusside mechanism of action?
Malignant hypertension.
Nitroprusside uses?
Limit treatment to 24-36 hours. Cyanide toxicity (altered mental status, lactic acidosis). Treat toxicity with nitrites, hydroxocobalamin, and sodium thiosulfate (sulfur).
Nitroprusside side effects?
D1 receptor agonist; relaxes renal vascular smooth muscle. Artery vasodilator.
Fenoldopam mechanism of action?
Malignant hypertension. Increases renal perfusion.
Fenoldopam uses?
Direct acting arteriole vasoldiator. ATP dependent K+ channel opener; hyperpolarizes and relaxes vascular smooth muscle.
Diazoxide mechanism of action?
Malignant hypertension. Insulinomas.
Diazoxide uses?
Hyperglycemia (reduces insulin release).
Diazoxide side effects?
Direct acting arteriole vasoldiator. ATP dependent K+ channel opener; hyperpolarizes and relaxes vascular smooth muscle.
Minoxidil mechanism of action?
Sever hypertension (IV), baldness (topical).
Minoxidil uses?
{{Hypertrichosis, pericardial effusion}}, reflex tachycardia, angina, salt retention. {{Hyperglycemia (reduces insulin release).}}
Minoxidil side effects?
Venodilation (increases cGMP, inducing dephosphorylation of myosin light chain). Has largest effect on large veins. Production of NO requires cystine on glutathione (GSH).
Nitroglycerin, isorbide dinitrate mechanism of action?
Effort angina, pulmonary edema.
Nitroglycerin, isorbide dinitrate uses?
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).
Nitroglycerin, isorbide dinitrate side effects?
Inhibits HMG-CoA reductase (decrease mevalonate/cholesterol production). Improves survival by inhibiting inflammation.
Lovastatin (-statin) mechanism of action?
Decreases VLDL (TGs), LDL (cholesterol). Increases HDL. Primarily used to lower CHOLESTEROL.
Lovastatin (-statin) uses?
Hepatotoxicity, myositis, rhabdomyolysis (especially with gemfibrozil).
Lovastatin (-statin) side effects?
Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation.
Niacin mechanism of action?
Increases HDL, lowers LDL (cholesterol). Greatly lowers VLDL (triglycerides). Primarily used to lower TRIGLYCERIDES.
Niacin uses?
{{Flushing (tx with aspirin)}}. Hyperglycemia (acanthosis nigricans). {{Hyperuricemia }}(exacerbates gout).
Niacin side effects?
Prevents intestinal reabsorption of bile acids; liver must consume cholesterol to make replenish lost bile.
Cholestyramine mechanism of action?
Decreases LDL (cholesterol); mild increase of VLDL and HDL.
Cholestyramine uses?
Patients hate it; tastes horrible and causes GI discomfort. Affects absorption of ADEK vitamins and other medications (digoxin, warfarin). Gallstones. Contraindicate with hypertriglyceridemia.
Cholestyramine side effects?
Prevents intestinal reabsorption of bile acids; liver must consume cholesterol to make replenish lost bile.
Cholestipol mechanism of action?
Decreases LDL (cholesterol); mild increase of VLDL and HDL.
Cholestipol uses?
Patients hate it; tastes horrible and causes GI discomfort. Affects absorption of ADEK vitamins and other medications (digoxin, warfarin). Gallstones. Contraindicate with hypertriglyceridemia.
Cholestipol side effects?
Prevents intestinal reabsorption of bile acids; liver must consume cholesterol to make replenish lost bile.
Colesevelam mechanism of action?
Decreases LDL (cholesterol); mild increase of VLDL and HDL.
Colesevelam uses?
Patients hate it; tastes horrible and causes GI discomfort. Affects absorption of ADEK vitamins and other medications (digoxin, warfarin). Gallstones. Contraindicate with hypertriglyceridemia.
Colesevelam side effects?
Prevent cholesterol reabsorption at small intestine brush border.
Ezetimibe mechanism of action?
Lowers LDL (cholesterol).
Ezetimibe uses?
Hepatotoxicity (elevated AST, ALT).
Ezetimibe side effects?
Induces LPL (via PPAR-alpha) leading to increased TG clearance).
Gemfibrozil mechanism of action?
Hypertryglyceridemia (increases VLDL uptake).
Gemfibrozil uses?
Myositis, hepatotoxicity, gallstones (inhibits 7-alpha hydroxylase), rhabdomyolysis.
Gemfibrozil side effects?
Induces LPL (via PPAR-alpha) leading to increased TG clearance).
Clofibrate, bezafibrate, fenofibrate (-fibrate) mechanism of action?
Hypertryglyceridemia (increases VLDL uptake).
Clofibrate, bezafibrate, fenofibrate (-fibrate) uses?
Hepatotoxicity, gallstones (inhibits 7-alpha hydroxylase). No rhabdomyolysis.
Clofibrate, bezafibrate, fenofibrate (-fibrate) side effects?
Inhibits Na/K-ATPase leading to increase intracellular sodium (hypersensitive neurons) and calcium (increased contractility). Predominately stimulates vagal tone (decrease AV conductivity, decrease HR).
Digoxin mechanism of action?
CHF, atrial fibrillation, SVT.
Digoxin uses?
{{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.
Digoxin side effects?
Recombinant B-type natriuertic peptide. {{Vasodilates}} (increases cGMP).
Nesiritide mechanism of action?
Acute decompensated heart failure.
Nesiritide uses?
Hypotension.
Nesiritide side effects?
Class Ia antiarrhythmic. Inhibits OPEN voltage gated sodium channels. Inhibits voltaged gated potassium channels (increases QT interval, AP duration, and ERP).
Quinidine mechanism of action?
Atrial and ventricular arrhythmias, especially SVT and ventricular tachycardia.
Quinidine uses?
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.
Quinidine side effects?
Class Ia antiarrhythmic. Inhibits OPEN voltage gated sodium channels. Inhibits voltaged gated potassium channels (increases QT interval, AP duration, and ERP).
Procainamide mechanism of action?
Atrial and ventricular arrhythmias, especially SVT and ventricular tachycardia.
Procainamide uses?
{{Thrombocyptopenia, torsades de pointes }}(increased QT), drug induced SLE (hematotoxic). Increased toxicity with hyperkalemia.
Procainamide side effects?
Class Ia antiarrhythmic. Inhibits OPEN voltage gated sodium channels. Inhibits voltaged gated potassium channels (increases QT interval, AP duration, and ERP).
Disopyramide mechanism of action?
Atrial and ventricular arrhythmias, especially SVT and ventricular tachycardia.
Disopyramide uses?
{{Thrombocyptopenia, torsades de pointes}} (increased QT). Increased toxicity with hyperkalemia.
Disopyramide side effects?
Class Ib antiarrhythmic. Inhibits {{INACTIVE}} voltage gated sodium channels {{(targets ISCHEMIC tissue)}}. Activates voltage gated potassium channels (shortens AP, ERP).
Phenytoin mechanism of action?
Acute ventricular arrhytmias (post-MI) and digitalis-induced arrhythmias.
Phenytoin uses?
Class Ib antiarrhythmic. Inhibits INACTIVE voltage gated sodium channels (targets ISCHEMIC tissue). Shortens AP, ERP.
Lidocaine mechanism of action?
Acute ventricular arrhytmias (post-MI) and digitalis-induced arrhythmias.
Lidocaine uses?
CNS stimulation/depression, cardiovascular depression. Increased toxicitiy with hyperkalemia.
Lidocaine side effects?
Class Ib antiarrhythmic. Inhibits INACTIVE voltage gated sodium channels (targets ISCHEMIC tissue). Shortens AP, ERP.
Mexiletine mechanism of action?
Acute ventricular arrhytmias (post-MI) and digitalis-induced arrhythmias.
Mexiletine uses?
CNS stimulation/depression, cardiovascular depression. Increased toxicitiy with hyperkalemia.
Mexiletine side effects?
Class Ib antiarrhythmic. Inhibits INACTIVE voltage gated sodium channels (targets ISCHEMIC tissue). Shortens AP, ERP.
Tocainide mechanism of action?
Acute ventricular arrhytmias (post-MI) and digitalis-induced arrhythmias.
Tocainide uses?