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33 Cards in this Set
- Front
- Back
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which lipid-lowering agent has best effect on HDL?
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niacin (side effects: flushing which is dec'd by aspirin or longterm use)
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which statin is NOT metabolized by P450 system?
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pravastatin
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which lipid lowering agent causes a slight increase in TG?
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bile acid resins (cholestyramine, colestipol)
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which lipid loweirng agents have biggest lowering effect on TGs?
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"fibrates"--gemfibrozil, clofibrate, bezafibrate, fenofibrate
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which lipid lowering agents work by decreasing production of VLDL?
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niacin
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which lipid lowering agents work by stimulating LPL/enhancing rate of catabolism of VLDL?
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fibrates (gemfribrozil, clofibrate, bezafibrate, fenofibrate)
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which class of lipid lowering agents is safest and what is the effect?
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cholesterol absorption blockers (ezetimibe). only decreases LDL. no effect on HDL or TGs
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which antihypertensive can cause a positive Coombs test?
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methyldopa (cental acting alpha agonist, safe for preggers)
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which CCB should NOT be used for arrhythmias?
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nifedipine
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MOA of nitroglycerin
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vasodilate by releasing NO in smooth muscle--> increase in cGMP and smooth muscle relaxation; dilates veins>> arteries
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which heart drug has "Monday dz" as a toxicity
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(tolerance during the work week and loss of tolerance over weekend-> tachycardia, dizzinesss, headache); nitroglycerin
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what diuretics should go with digoxin?
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spironolactone/K+ sparers b/c hypokalemia potentiates dig toxicity
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what increases toxicities of digoxin
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renal failure, hypokalemia, quinidine (dec'd clearance, displaces dig from tissue binding sites)
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antidote to digoxin toxicity
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slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments
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compare the class I antiarr in terms of effect on AP duration
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IA (Na, intermediate acting)--increase duration; IB (Na, fast acting)--decrease duration; IC (Na, slow acting)--no change in AP
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usefulness of IA antiarr?
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(quinidine, amiodarone, procainamide, disopyramide) affect both ATRIAL and VENTRICULAR s, esp reenrant and ectopic tachycardias
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which antiarrhythmics useful in acute ventricular arrhytmias, esp post MI?
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IB (lidocaine, mexiletine, tocainide)
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drug of choice in diagnosing/abolishing AV nodal arrhythmias
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adenosine (maybe cause flushing)
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which antiarr contraindicated post-MI?
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class IC (flecainide, encainide, propafenone)
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when use class IC antiarr?
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usually only as last resort in refractory tachyarrhythmias
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which antiarr only work on AV and SA nodes?
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class II (beta blockers)
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which antiarr can cause dyslipidemia?
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metoprolol (class II)
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amiodarone toxicities
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pulmonary fibrosis, hepatotoxicity, thyroidisms, corneal deposits, photodermatitis, neurologic effects, constipation; check PFTs, LFTs, TFTs!!!
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use of class IV antiarr?
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(nondihydropyridine CCBs; verpamil, diltiazem); primarily affect AV nodal cells--> good for prevention of nodal arrhythmias
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antiarrhythmic effect of K+?
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depresses ectopic pacemakers, esp in digoxin toxicity
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what lipid lowering agent causes flushing ?
what is the flushing mediated by? |
niacin
prostaglandins |
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what are the side effects of niacin?
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red flushed face (can be decreased by aspirin)
hyperglycemia hyperuricemia (exacerbates gout) |
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what lipid lowering agents cause muscle problems?
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Statins (rhabdomyolysis) and Fibrates (myositis)
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Which lipid lowering agents cause gall stones?
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fibrates and bile acids
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what two agents would you use for hypertriglyceridemia?
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niacin and fibrates
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If you use a statin what protiens increase in production?
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LDL receptors
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whats the MOA of niacin?
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inhibits lipolysis in adipose tissue and reduces hepatic VLDL secretion into circulation
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what increases HDL?
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NIACIN THE MOST
and statins and fibrates a little too |
