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USMLE
CV Pharm 3
Question | Answer |
---|---|
sotalol toxicity | torsades, excessive beta-block |
ibutilide toxicity | torsades |
bretylium toxicity | new arrhythmias, hypotension |
amiodorone toxicity | hypothyrodism/hyperthyrodism, pulmonary fibrosis, hepatic toxicity, corneal deposits, skin deposits (photodermatitis), neurologic defects, constipation, bradycardia, heart block, chf |
what 3 tests to do before using amiodarone? | PFT, LFT, TFT |
name 2 class IV antiarrhytmics | verapamil, diltiazem |
mechanism for class IV antiarrhythmics | blocks Ca channels; affect AV nodal cells, decrease conduction velocity, incrase ERP, increase PR. |
what are class IV antiarrhythmics used for | prevent nodal arryhtmias (SVT) |
what are 4 general side effects for class IV | constipation, flushing, edema, cv (chf, av block, sinus node depression) |
bepridil toxicity | torsades |
adenosine function | hyperpolarizes cells by facilitating K movement out of cells. drug of choice in diagnosing/abolishing AV nodal arryhtmias |
potassium function | depress ectopic pacemaker, esp in dig toxicity |
magnesium function | torsades and dig toxicity use |
what are the adverse effects of nifedipine and verapamil? (5) | dizziness, flushing, nausea (verapamil also has constipation and AV block) |
adverse effects of Diazoxide? | hypoglycemia - reduces insulin release |
what is the first-line treatment of hypertension in pregnancy? | hydralazine with methyldopa |
what is the mechanism of minoxidil? | K channel opener --> hyperpolarizes and relaxes vascular smooth muscle |
what is the toxicity of minoxidil? | hypertrichosis, pericardial effusion |
what is the treatment for malignant hypertension? | nitroprusside, fenoldopam and diazoxide |
what is the mechanism of action of fenoldopam? | Dopoamine D1 receptor agonist --> relaxes renal vascular smooth muscle |
what is the mechanism of diazoxide? | K channel opener --> hyperpolarizes and relaxes vascular smooth muscle |
what are the HMG-CoA reductase inhibitors? | lovastatin, pravastatin, simvastatin, atorvastatin |
What effects do the statins have on LDL, HDL and TGs? | greatly decreases LDL, increases HDL and decreases TGs |
what is the mechanism of action of the Statins? | inhibit cholesterol precursor, mevalonate |
side effects of statins? | reversible increase in LFTs and myositis |
What effect does Niacin have on LDL, HDL and TGs? | decreases LDL, increases HDL, lesser decrease in TGs |
what is the mechanism of action of niacin? | inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation |
what effect do the Bile acid resins have on LDL, HDL, and TGs? | decrease LDL, slight increase in HDL, slight increase in TGs |
what are the bile acid resins? | cholestyramine, colestipol |
what is the mechanism of action of cholestyramine and colestipol? | prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more |
what are side effects of cholestyramine and colestipol? | bad taste, causes GI discomfort, decreased absorption of fat-soluble vitamins |
What effect does ezetimibe have on LDL, HDL and TGs? | decreases LDL; no effect on others |
what is the mechanism of action of ezetimibe? | prevents cholesterol reabsorption at small intestine brush border |
What are the Fibrates? | gemfibrozil, clofibrate, bezafibrate, fenofibrate |
what effect do the fibrates have on LDL, HDL and TGs? | mainly decrease TGs, lesser decrease LDL and increase HDL |
what is the mechanism of action of the fibrates? | upregulate LPL --> increase TG clearance |
what are the side effects of fibrates? | myositis, and increase in LFTs |
what Beta blockers are contraindicated in angina and why? | labetalol, pindolol and acebutolol, due to partial agonist effects |