Cardiovascular drugs Flashcards

1
Q

thiazides, ACE inhibitors, AngII receptor blockers, dihydropyridine CCB

A

tx for primary/essential HTN

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2
Q

diuretics, ACE inhib, ARBs, beta blockers, aldosterone antagon

A

tx for HTN with HF

beta blockers for compensated HF

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3
Q

ACE inhib/ARBs, CCB, thiazides, beta blockers

A

tx for HTN + DM (protect against diabetic nephropathy)

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4
Q

hydralazine, labetalol, methyldopa, nifedipine

A

tx for HTN in pregnancy (no ACE-I or ARBs!!)

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5
Q

amlodipine, clevidipine, nicardipine, nifedipine, nimodipine

A

dihydropyridine CCB- act on vascular smooth m.

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6
Q

diltiazem, verapamil

A

non dihydropyridine CCB- act on heart smooth m.

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7
Q

CCB used to tx HTN, angina (Prinzmetal’s), Raynaud phenomenon

A

dihydropyridines (act on vasculature) EXCEPT for nimodipine

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8
Q

CCB used to prevent cerebral vasospasm in SAH

A

nimodipine

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9
Q

CCB used for HTN urgency or emergency

A

clevidipine

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10
Q

CCB used to tx HTN, angina, a-fib or atrial flutter

A

non dihydropyridines

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11
Q

increases cGMP to relax smooth m.
vasodilates arterioles > veins (reduces afterload)
used to tx severe HTN (acute), HF, safe for pregnancy
give w/ beta blocker to block reflex tachy

A

hydralazine

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12
Q

these drugs are used as tx regimen for…

clevidipine, fenoldopam, labetalol, nicardipine, nitroprusside

A

HTN emergency

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13
Q

short acting increase in cGMP via direct release of NO
may cause cyanide toxicity
used during HTN emergency

A

Nitroprusside

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14
Q

D1 agonist causing coronary, peripheral, renal, splanchnic vasodilation - lowers BP, increases natriuresis
used during HTN emergency

A

fenoldopam

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15
Q

vasodilate by increasing NO in vasc smooth m - increases cGMP & smooth m. relaxation
dilates veins»arteries, lowers preload
used to tx angina, acute coronary syndrome, pulm edema

A

nitrates: nitroglycerin, isosorbide dinitrate, isosorbide mononitrate

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16
Q

partial beta agonists contraindicated in angina d/t partial increase in HR

A

pindolol & acebutolol

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17
Q

inhib conversion of HMG CoA to mevalonate (cholest precursor), lowers mortality in CAD pt
lowers LDL***, raises HDL, lowers TG’s
best agents for reducing LDL levels

A

HMG CoA reductase inhibitors: lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin

18
Q

prevent intestinal reabsorp of bile acids - liver must then use cholest to make more bile acids
lowers LDL, slightly raises HDL, slightly raises TGs

A

bile acid resins: cholestyramine, colestipol, colesevelam

19
Q

prevents cholest absorption at sm int brush border

lowers LDL

A

ezetimibe

20
Q

upregulate LPL - increased TG clearance
activates PPAR alpha to induce HDL synthesis
lowers LDL, raises HDL, lowers TGs**
the only significant tx to lower TGs

A

fibrates: gemfibrozil, clofibrate, bezafibrate, fenofibrate

21
Q

inhib lipolysis via hormone sensitive lipase in adipose tissue, reduces hepatic VLDL synthesis
lowers LDL, raises HDL***, lowers TGs

A

niacin (B3)

22
Q

direct inhibition of Na/K ATPase - indirect inhib of Na/Ca exchanger - increased intracell Ca - pos inotropy
stimulates vagus n to lower HR
use: to increase contractil for HF, decreases AV & SA conduction for a-fib

A

digoxin (cardiac glycoside)

23
Q

quinidine, procainamide, disopyramide

A

class IA anti arrhythmics- Na channel blockers

24
Q

slow/block conduction - slows phase 0 depol, selective to tissue that is frequently depolarized (tachy)
increases AP duration, increases ERF in vent AP, increases QT interval

A

class IA anti arrhythmics MOA

25
Q

tx for atrial & ventricular arrhythmias esp re-entrant & ectopic SVT & VT

A

class IA anti arrhythmics

26
Q

lidocaine, mexiletine

A

class IB anti arrhythmics- Na channel blockers

27
Q

slow/block conduction via slowing phase 0 depol

decreases AP duration, preferential to ischemic or depol Purkinje & ventricular tissue

A

class IB anti arrhythmics MOA

28
Q

tx for acute ventricular arrhythmias esp post MI, digitalis induced arrhythmias

A

class IB anti arrhythmics

29
Q

flecainide, propafenone

A

class IC anti arrhythmics- Na channel blockers

30
Q

slow/block conduction via slower phase 0 depol, selective to tachycardic tissue
prolongs ERP in AV node & accessory bypass tracts
no effect on ERP in purkinje or vent tissues, minimal effect on AP duration

A

class IC anti arrhythmics MOA

31
Q

tx for SVTs including a-fib

only as last resort in refractory VT

A

class IC anti arrhythmics

32
Q

metoprolol, propanolol, esmolol, atenolol, timolol, carvedilol

A

class II anti arrhythmics- beta blockers

33
Q

decrease SA & AV nodal activity by decreasing cAMP & Ca currents, suppress abnormal pacemakers by decr slope of phase 4 (resting potential)
AV node esp sensitive- increased PR interval

A

class II anti arrhythmic beta blockers MOA

34
Q

tx for SVT, vent rate control for a-fib & a-flutter

A

class II anti arrhythmic beta blockers

35
Q

amiodarone, ibutilide, dofetilide, sotalol

A

class III anti arrhythmics- K channel blockers

36
Q

increase AP duration, increase ERP, increase QT

A

class III anti arrhythmic MOA

37
Q

tx for a-fib, a-flutter, vent tachy

A
class III anti arrhythmic 
amiodarone & sotalol for VT
38
Q

verapamil, diltiazem

A

class IV anti arrhythmics- CCB

39
Q

decrease conduction velocity, increase ERP, increase PR

A

class IV anti arrhythmics MOA

40
Q

used to prevent nodal arrhythmias (SVT), control rate in a-fib

A

class IV anti arrhythmics

41
Q

increases K exit of cells - hyperpolarizes cell & decreases conduction of Ca
drug of choice to diagnose/abolish SVT
very short acting (15sec)
SE: sense of impending doom

A

adenosine

42
Q

effective for torsades de pointe & digoxin toxicity

A

Mg2+