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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 |