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Step 1 cardiology > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Primary HTN tx

A

thiazide diuretics, ACE inhibitors, ARB, dihydropyridine Ca channel blockers

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2
Q

HTN w/ HF tx

A

diuretics, ACEI, ARBs, BB (compensated HF), aldosterone antagonists

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3
Q

what must be used cautiously in decompensated HF and are contraindicated in cardiogenic shock?

A

BB

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4
Q

HTN w/ DM

A

ACEI, ARBS, Ca channel blockers, thiazide diuretics, BB

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5
Q

what are protective against diabetic nephropathy?

A

ACEI, ARBs

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6
Q

HTN w/ pregnancy

A

hydralazine, labetalol, methyldopa, nifedipine

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7
Q

dihydropyridine Ca channel blockers

A

act on vasc SM

amlodipine, clevidipine, nicardipine, nifedipine, nimodipine

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8
Q

non-dihydropyridine Ca channel blockers

A

act on heart

diltiazem, verapamil

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9
Q

Ca channel blocker MOA

A

block voltage-dependent L-type ca channels on cardiac and SM –> dec. muscle contractility

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10
Q

Ca channel blockers potency order on Vasc SM

A

amlodipine=nifedipine > diltiazem > verapamil

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11
Q

Ca channel blockers potency order on Heart

A

verapamil > diltiazem > amlodipine = nifedipine

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12
Q

dihydropyridines use

A

HTN, angina (incl. Prinzmetal), Raynaud’s

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13
Q

nimodipine use

A

subarachnoid heme (prevents cerebral vasospasm)

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14
Q

clevidipine use

A

HTN, angina, atrial fib/flutter

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15
Q

non-dihydropyridine ca channel blocker ADR

A

cardiac depression, AV block, hyperprolactinemia, constipation

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16
Q

dihydropyridine ca channel blocker ADR

A

peripheral edema, flushing, dizziness, gingival hyperplasia

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17
Q

Hydralazine MOA

A

inc cGMP –> smooth muscle relaxation.

vasodilates arterioles > veins

afterload reduction

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18
Q

Hydralazine use

A

acute severe HTN; HF (w/ organic nitrate)

Safe in pregnancy

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19
Q

Hydralazine codrug

A

BB to prevent reflex tachycardia

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20
Q

Hydralazine ADR

A

compensatory tachycardia, fluid retention, HA, angina, lupus-like syndrome

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21
Q

Hydralazine contraindications

A

pts with angina/CAD

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22
Q

HTN emergency

A

clevidipine, fenoldopam, labetalol, nicardipine, nitroprusside

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23
Q

Nitroprusside MOA

A

short acting; inc cGMP via direct rls of NO

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24
Q

Nitroprusside toxicity

A

cyanide!

25
Q

Fenoldopam MOA

A

D1 agonist, coronary, peripheral, renal, and splanchnic vasodilation

dec. BP, inc. natriuresis

PO anti-HTN

26
Q

Fenoldopam ADR

A

hypotension, tachycardia

27
Q

Nitrates list

A

nitroglycerin, isosorbide dinitrate, isosorbide mononitrate

28
Q

Nitrates MOA

A

vasodilate by inc NO in vasc SM –> inc in cGMP and SM relaxation.

Dilates veins&raquo_space; arteries.

Dec preload

29
Q

Nitrates use

A

angina, acute coronary syndrome, pulmonary edema

30
Q

Nitrates ADR

A

reflex tachycardia (tx with BB), hypotension, flushing, HA ,

“Monday dx” in industrial exposure

31
Q

Monday Disease

A

development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend –> tachycardia, dizziness, HA upon reexposure

32
Q

antianginal therapy

A

goal is reduction of myocardial O2 consumption by dec 1 or more of the determinants of MVO2:

end diastolic volume, BP, HR, contractility

33
Q

Nitrates MVO2 effects

A

Decreased: end diastolic volume, BP, ejection time,

No change: contractility

Increased: HR (reflex response)

34
Q

BB MVO2 effects

A

Decreased: BP, contractility, HR

No change: end diastolic volume

increased: ejection time

35
Q

Nitrates+ BB MVO2 effects

A

greatly decreased: MVO2

decreased: BP

no change: end diastolic volume, contractility, HR, ejection time

36
Q

what partial B-agonists are contraindicated in angina/

A

pindolol and acebutolol

37
Q

Ranolazine MOA

A

inhibits late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption. doesn’t affect HR or contractility

38
Q

ranolazine use

A

angina refractory to other medical therapies

39
Q

ranolazine ADR

A

constipation, dizziness, HA, nausea, QT prolongation

40
Q

HMG-CoA reductase inhibitor MOA

A

inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor

41
Q

HMG-CoA reductase inhibitor use

A

severe dec. in LDL, dec. in triglycerides
increase in HDL

dec mortality in CAD

42
Q

HMG-CoA reductase inhibitor ADR

A

hepatotoxicity, myopathy (esp. when used w/ fibrates or niacin)

43
Q

Bile acid resins MOA

A

cholestyramine, colestipol, colesevelam

prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more

44
Q

Bile acid resins effect

A

moderate decrease in LDL, slight inc in HDL/triglycerides

45
Q

Bile acid resins ADR

A

GI upset, dec absorption of other drugs and fat-soluble vitamins

46
Q

Ezetimibe MOA

A

prevent cholesterol absorption at SI brush border

47
Q

Ezetimibe effect

A

moderate dec in LDL; no change in HDL/trigylcerides

48
Q

Ezetimibe ADR

A

rare inc in LFTs, diarrhea

49
Q

Fibrates MOA

A

Gemfibrozil, Bezafibrate, fenofibrate

upregulate LPL–> inc TG clearance

activates PPAR-a to induce HDL synthesis

50
Q

Fibrates effect

A

severe dec in triglycerides; dec LDL; inc in HDL

51
Q

Fibrates ADR

A

myopathy (inc risk w/ statins); cholesterol gallstones

52
Q

Niacin (vit B3) MOA

A 
inhibits lipolysis (hormone-sensitive) in adipose tissue;
reduces hepatic VLDL synthesis
53
Q

Niacin ADR

A

red flushed face (tx w/ prophylactic NSAIDS)
Hyperglycemia
Hyperuricemia

54
Q

Niacin effect

A

moderate dec in LDL
moderate inc in HDL
dec in triglycerides

55
Q

Digoxin (cardiac glycoside) MOA

A

direct inhibition of Na/K ATPase –> indirect inhibition of Na/Ca exchanger.

inc Ca –> positive inotropy.

Stimulates vagus nerve –> dec HR

56
Q

Digoxin use

A 
HF (inc contractility)
atrial fibrillation (dec conduction at AV node and depression of SA node)
57
Q

Digoxin ADR

A

Cholinergic, blurry yellow vision, AV block

58
Q

Factors predisposing to Digoxin toxicity

A

renal failure, hypokalemia, drugs that displace digoxin from tissue binding sites, dec clearance

(verapamil, amiodarone, quinidine)

59
Q

Digoxin antidotes

A

slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2

Step 1 cardiology (2 decks)

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