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