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