Cardio Pharm Flashcards

1
Q

which lipid-lowering agent has best effect on HDL?

A

niacin (side effects: flushing which is dec’d by aspirin or longterm use)

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2
Q

which statin is NOT metabolized by P450 system?

A

pravastatin

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3
Q

which lipid lowering agent causes a slight increase in TG?

A

bile acid resins (cholestyramine, colestipol)

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4
Q

which lipid loweirng agents have biggest lowering effect on TGs?

A

fibrates”–gemfibrozil, clofibrate, bezafibrate, fenofibrate”

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5
Q

which lipid lowering agents work by decreasing production of VLDL?

A

niacin

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6
Q

which lipid lowering agents work by stimulating LPL/enhancing rate of catabolism of VLDL?

A

fibrates (gemfribrozil, clofibrate, bezafibrate, fenofibrate)

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7
Q

which class of lipid lowering agents is safest and what is the effect?

A

cholesterol absorption blockers (ezetimibe). only decreases LDL. no effect on HDL or TGs

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8
Q

which antihypertensive can cause a positive Coombs test?

A

methyldopa (cental acting alpha agonist, safe for preggers)

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9
Q

which CCB should NOT be used for arrhythmias?

A

nifedipine

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10
Q

MOA of nitroglycerin

A

vasodilate by releasing NO in smooth muscle–> increase in cGMP and smooth muscle relaxation; dilates veins» arteries

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11
Q

which heart drug has Monday dz” as a toxicity”

A

(tolerance during the work week and loss of tolerance over weekend-> tachycardia, dizzinesss, headache); nitroglycerin

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12
Q

what diuretics should go with digoxin?

A

spironolactone/K+ sparers b/c hypokalemia potentiates dig toxicity

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13
Q

what increases toxicities of digoxin

A

renal failure, hypokalemia, quinidine (dec’d clearance, displaces dig from tissue binding sites)

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14
Q

antidote to digoxin toxicity

A

slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments

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15
Q

compare the class I antiarr in terms of effect on AP duration

A

IA (Na, intermediate acting)–increase duration; IB (Na, fast acting)–decrease duration; IC (Na, slow acting)–no change in AP

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16
Q

usefulness of IA antiarr?

A

(quinidine, amiodarone, procainamide, disopyramide) affect both ATRIAL and VENTRICULAR s, esp reenrant and ectopic tachycardias

17
Q

which antiarrhythmics useful in acute ventricular arrhytmias, esp post MI?

A

IB (lidocaine, mexiletine, tocainide)

18
Q

drug of choice in diagnosing/abolishing AV nodal arrhythmias

A

adenosine (maybe cause flushing)

19
Q

which antiarr contraindicated post-MI?

A

class IC (flecainide, encainide, propafenone)

20
Q

when use class IC antiarr?

A

usually only as last resort in refractory tachyarrhythmias

21
Q

which antiarr only work on AV and SA nodes?

A

class II (beta blockers)

22
Q

which antiarr can cause dyslipidemia?

A

metoprolol (class II)

23
Q

amiodarone toxicities

A

pulmonary fibrosis, hepatotoxicity, thyroidisms, corneal deposits, photodermatitis, neurologic effects, constipation; check PFTs, LFTs, TFTs!!!

24
Q

use of class IV antiarr?

A

(nondihydropyridine CCBs; verpamil, diltiazem); primarily affect AV nodal cells–> good for prevention of nodal arrhythmias

25
Q

antiarrhythmic effect of K+?

A

depresses ectopic pacemakers, esp in digoxin toxicity

26
Q

what lipid lowering agent causes flushing ?

what is the flushing mediated by?

A

niacin

prostaglandins

27
Q

what are the side effects of niacin?

A

red flushed face (can be decreased by aspirin)

hyperglycemia

hyperuricemia (exacerbates gout)

28
Q

what lipid lowering agents cause muscle problems?

A

Statins (rhabdomyolysis) and Fibrates (myositis)

29
Q

Which lipid lowering agents cause gall stones?

A

fibrates and bile acids

30
Q

what two agents would you use for hypertriglyceridemia?

A

niacin and fibrates

31
Q

If you use a statin what protiens increase in production?

A

LDL receptors

32
Q

whats the MOA of niacin?

A

inhibits lipolysis in adipose tissue and reduces hepatic VLDL secretion into circulation

33
Q

what increases HDL?

A

NIACIN THE MOST

and statins and fibrates a little too