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USMLE Step I Pharmacology > Cardiovascular Pharmacology > Flashcards

Cardiovascular Pharmacology Flashcards

1
Q

Treatment of Primary (Essential) Hypertension by drug type

A

thiazide diuretics

ACE inhibitors

angiotensin II receptor blockers (ARBs)

dihydropyridine Ca2+ channel blockers

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2
Q

Treatment of HTN in Heart Failure by drug type

A

diuretics

ACE inhibitors/ARBs

beta blockers (for compensated HF)–must use cautiously with decompensated HF and are contraindicated in cardiogenic shock

aldosterone antagonists

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3
Q

Treatment of HTN with diabetes mellitus by drug type

A

ACE inhibitors/ARBs

Ca2+ channel blockers

thiazide diuretics

beta blockers

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4
Q

treatment of HTN in pregnancy by drug type

A

hydralazine

labetalol

methyldopa

nifedipine

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5
Q

why are ACE I inhibitors used for HTN with diabetes mellitus?

A

they are protective against diabetic neuropathy

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6
Q

name the Calcium channel blockers

A

amlodipine

clevidipine

nicardipine

nifedipine

nimodipine

verapamil

diltiazem

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7
Q

Calcium channel blockers–mechanism

A

block voltage dependent L type calcium channels of cardiac and smooth muscle–>reduce muscle contractility

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8
Q

which calcium channel blockers act more on vascular smooth muscle?

A

amlodipine = nifedipine > diltiazem > verapamil

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9
Q

which calcium channel blockers act more on the heart?

A

verapamil > diltizem > amlodipine = nifedipine

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10
Q

Calcium channel blockers Dihydropyridines (except nimodipine)–clinical use

A

HTN

angina (including Prinzmetal)

Raynaud phenomenon

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11
Q

Calcium channel blockers Nimodipine–clinical use

A

subarachnoid hemorrhage–prevents cerebral vasospasm

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12
Q

Calcium channel blockers Clevidipine–clinical use

A

hypertensive urgency or emergency

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13
Q

Calcium channel blockers Non-dihydropyridines–clinical use

A

HTN

angina

atrial fibrillation/flutter

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14
Q

Calcium channel blockers non dihydropyridine–toxicity

A

cardiac depression

AV block

hyperprolactinemia

constipation

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15
Q

Calcium channel blockers dihydropyridine–toxicity

A

peripheral edema

flushing

dizziness

gingival hyperplasia

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16
Q

Hydralazine–mechanism

A

increase cGMP–smooth muscle relaxation

vasodilates arterioles more than veins, so afterload reduces

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17
Q

hydralazine–clinical use

A

severe HTN (particularly acute)

HF (with organic nitrate)

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18
Q

what is the first line of therapy for HTN in pregnant women?

A

hydralazine with methyldopa

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19
Q

what is hydralazine often coadministered with?

why?

A

beta blocker

to prevent reflex tachycardia

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20
Q

hydralazine–toxicity

A

compensatory tachycardia–so contraindicated in angina/CAD

fluid retention

headache

angina

Lupus like syndrome

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21
Q

drugs used for treatment of hypertensive emergency

A

clevidipine

fenoldopam

labetalol

nicardipine

nitroprusside

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22
Q

Nitroprusside–clinical use

A

hypertensive emergency

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23
Q

nitroprusside–mechanism

A

short acting

increases cGMP via direct release of NO

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24
Q

nitroprusside–toxicity

A

releases cyanide, so can lead to cyanide toxicity

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25
Q

fenoldopam–use

A

hypertensive emergency

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26
Q

fenoldopam–mechanism

A

dopamine D1 receptor agonist–coronary, peripheral, renal, and splanchnic vasodilation

decreases BP, inc natriuresis

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27
Q

fenoldopam–toxicity

A

HTN

tachycardia

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28
Q

name the nitrate drugs

A

nitroglycerin

isosorbide dinitrate

isosorbide mononitrate

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29
Q

nitrates–mechanism

A

vasodilate by increasing NO in vascular smooth muscle –> inc in cGMP and smooth muscle relaxation

dilate veins >> arteries, so dec preload

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30
Q

nitrates–use

A

angina

acute coronary syndrome

pulmonary edema

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31
Q

nitrates–toxicity

A

reflex tachycardia (treat with beta blockers)

HTN

flushing headache

“Monday disease” in industrial exposure–development of tolerance for vasodilating action during the work week and loss of tolerance over the weekend –> results in tahcycardia, dizziness, headache upon reexposure

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32
Q

antianginal therapy–use

A

reduce myocardial O2 consumption by decreasing 1 or more of the determinants of myocardial O2 consumption; end diastolic volume, BP, HR, contractility

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33
Q

ranolazine–mechanism

A

inhibits the late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption

does not affect heart rate or contractility

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34
Q

ranolazine–use

A

angina refractory to other medical therapies

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35
Q

ranolazine–toxicity

A

constipation

dizziness

headache

nausea

QT prolongation

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36
Q

name lipid lowering agents

A

HMG CoA reductase inhibitors

bile acid resins

ezetimibe

fibrates

niacin (B3)

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37
Q

what type of Lipid lowering agent decreases LDL the most?

A

HMG CoA reductase inhibitor

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38
Q

what type of lipid lowering agent increases HDL the most?

A

niacin (B3)

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39
Q

what type of lipid lowering agent decreases triglycerides the most?

A

fibrates

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40
Q

what type of lipid lowering agent has NO effect on HDL and triglycerides?

A

ezetimibe

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41
Q

what type of lipid lowering agent has the smallest effect on lowering LDL?

A

fibrates

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42
Q

what type of lipid lowering agent only slightly elevates triglycerides?

A

bile acid resins

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43
Q

HMG CoA reductase inhibitors–mechanism

A

inhibit conversion of HMG CoA to mevalonate (a cholesterol precursor)

dec mortality in CAD patients

44
Q

name 5 HMG CoA reductase inhibitors

A

(-vastatins)

atorvastatin

lovastatin

pravastatin

simvastatin

rosuvastatin

45
Q

HMG CoA reductase inhibitors–toxicity

A

hepatotoxicity (inc LFTs)

myopathy (especially when used with fibrates or niacin)

46
Q

niacin–mechanism

A

inhibits lipolysis (hormone sensitive lipase) in adipose tissue

reduces hepatic VLDL synthesis

47
Q

niacin–toxicity

A

red, flushed fase, which is dec by NSAIDS or long term use

hyperglycemia

hyperuricemia

48
Q

name 3 bile acid resins

A

cholestyramine

colestipol

colesevelam

49
Q

bile acid resins–use

A

prevent intestinal reabsorption of bile acids

liver must use cholesterol to make more

50
Q

bile acid resins–toxicity

A

GI upset

decrease absorption of other drugs and fat soluble vitamins

51
Q

ezetimibe–mechanism

A

prevent cholesterol absorption at small intestine brush borders

52
Q

ezetimibe–toxicity

A

rare inc LFTs; diarrhea

53
Q

name fibrate drugs

A

gemfibrozil

bezafibrate

fenofibrate

54
Q

fibrates–mechanism

A

upregulate LDL –> inc triglyceride clearance

activates PPAR alpha to induce HDL synthesis

55
Q

fibrates–toxicity

A

myopathy–inc risk with statins

cholesterol gallstones

56
Q

name a cardiac glycoside

A

digoxin

57
Q

cardiac glycosides–mechanism

A

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

increase concentration of Ca –> positive intropy

stimulates vagus nerve –> dec HR

58
Q

cardiac glycosides–use

A

HF (inc contractility)

atrial fibrillation (dec conduction at AV node and depression of SA node)

59
Q

cardiac glycosides–toxicity

A

cholinergic–nausea, vomiting, diarrhea, blurry yellow vision (think van Gogh), arrhythmia, AV block

can lead to hyperkalemia, which indicates poor prognosis

60
Q

factors that predispose to toxicity with cardiac glycosides

A

renal failure–dec excretion

hypokalemia–permissive for digoxin binding to K+ binding site on Na/K ATPase

drugs that replace digxin from tissue binding sites

decreased clearance (eg. verapamil, amiodarine, quinidine)

61
Q

cardiac glycosides–antidote

A

slowly normalize K+

cardiac pacer

anti digoxin Fab fragments

Mg2+

62
Q

what are class I antiarrhythmics, and how do they work?

A

sodium channel blockers

slow or block (dec) conduction especially in depolarized cells

dec slope of phase 0 depolarization

are state dependent (selectively depress tissue that is frequently depolarized, ie. tachycardia)

63
Q

what causes toxicity in all class I antiarrhythmics?

A

hyperkalemia

64
Q

what are the class IA antiarrhythmic drugs?

A

Quinifine, Procainamide, Disopyramide

“The Queen Proclaims Diso’s pyramid.”

65
Q

class IA antiarrhythmics–mechanism

A

inc AP duration

inc effective refractory period (ERP) in ventricular action potential

inc QT interval

66
Q

class IA antiarrhythmics–use

A

both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT

67
Q

class IA antiarrhythmics–toxicity

A

cinchonism–headache, tinnitus with quinidine

reversible SLE like syndrome (procainamide)

heart failure (dispyramide)

thrombocytopenia

torsades de pointes due to inc QT interval

68
Q

what are the class IB antiarrhythmic drugs?

A

Lidocaine

MexileTine

“I‘d Buy Liddy’s Mexican Tacos”

69
Q

class IB antiarrhythmics–mechanism

A

dec AP duration

preferentially affect ischemic or depolarized Purkinje and ventricular tissue

Phenytoin can also fall into the IB category

70
Q

class IB antiarrhythmics–use

A

acute ventricular arrhythmias (especially post MI)

digitalis-induced arrhythmias

“IB is Best post MI”

71
Q

class IB antiarrhythmics–toxicity

A

CNS stimulation/depression

cardiovascular depression

72
Q

what is the best antiarrhythmic drug to use for a post MI patient?

A

class IB

73
Q

what are the class IC antiarrhythmic drugs?

A

Flecainide

Propafenone

“Can I have Fries, Please?”

74
Q

class IC antiarrhythmics–mechanism

A

significantly prolongs ERP in AV node and accessory bypass tracts

no effect on ERP in purkinje and ventricular tissue

minimal effect on AP duration

75
Q

class IC antiarrhythmics–toxicity

A

proarrhythmics, especially post-MI (contraindicated)

IC is Contraindicated in structural and ischemic heart disease

76
Q

which class IA antiarrhythmic drug may cause digoxin toxicity?

A

Quinidine–decreases digoxin clearance and displaces digoxin from tissue binding sites

77
Q

class IC antiarrhythmics–use

A

SVTs, including atrial fibrillation

only as a last resort in refractory VT

do not affect AP duration

78
Q

when are class IC antiarrhythmics contraindicated?

A

structural heart diseases and post MI

79
Q

what are class II antiarrhythmics?

name 5

A

beta blockers

metoprolol

propranolol

esmolol

atenolol

timolol

80
Q

class II antiarrhythmics–mechanism

A

decrease SA and AV nodal activity by decreasing cAMP, dec Ca currents

suppress abnormal pacemakers by dec slope of phase 4

81
Q

what node is most sensitive to class II antiarrhythmics? and what is the effect of class II antiarrhythmics on the node?

A

AV node

inc PR interval

82
Q

which class II antiarrhythmic is most short acting?

A

esmolol

83
Q

class II antiarrhythmics–use

A

SVT

ventricular rate control for atrial fibrillation and atrial flutter

84
Q

class II antiarrhythmics–toxicity

A

impotence

exacerbation of COPD and asthma

cardiovascular effects (bradycardia, AV block, HF)

CNS effects (sedation, sleep alterations)

may mask signs of hypoglycemia

beta blockers (except non selective alpha and beta antagonists carvedilol and labetalol) cause unopposed alpha 1 agonism if given alone for pheochromocytoma or cocaine toxicity

85
Q

metoprolol toxicity and how to treat

A

(classII antiarrhythmic)

can cause dyslipidemia

treat with glucagon

86
Q

propranolol toxicity

A

(class II antiarrhythmic)

can exacerbate vasospasm in Prinzmetal angina

87
Q

how to treat beta blocker overdose

A

saline

atropine

glucagon

88
Q

what are class III antiarrhythmics and name 4

A

potassium channel blockers

Amiodarone

Ibutilide

Dofetilide

Sotalol

“AIDS”

89
Q

class III antiarrhythmics–mechanism

A

inc AP duration

inc ERP

inc QT interval

90
Q

class III antiarrhythmics–use

A

atrial fibrillaiton

atrial flutter

ventricular tachycardia (amiodarone, sotalol)

91
Q

what is the indication for class III antiarrhythmics?

A

when all other antiarrhythmics fail

92
Q

sotalol toxicity

A

(class III antiarrhythmic)

torsades de pointes

excessive beta blockade

93
Q

ibutilide–toxicity

A

(class III antiarrhythmic)

torsades de pointes

94
Q

amiodarone–toxicity

A

(class III antiarrhythmic)

pulmonary fibrosis

hepatotoxicity

hypothyroidism/hyperthyroidism (amiodarone is 40% iodine by weight)

acts as hapten–corneal deposits, blue/gray skin deposits causing photodermatitis

neurologic effects

constipation

cardiovascular effects–bradycardia, heart block, HF

95
Q

what should you always check when using amiodarone?

A

pulmonary function tests

liver function tests

thyroid function tests

96
Q

amiodarone has effects of which classes and why?

A

I, II, III, IV

b/c lipophilic–alters lipid membrane

97
Q

what are class IV antiarrhythmics and name 2?

A

calcium channel blockers

verapail

diltiazem

98
Q

class IV antiarrhythmic–mechanism

A

dec conduction velocity

inc ERP

inc PR interval

99
Q

class IV antiarrhythmic–use

A

prevention of nodal arrhythmias (eg. SVT)

rate control in atrial fibrillation

100
Q

class IV antiarrhythmic–toxicity

A

flushing

constipation

edema

cardiovascular effects–HF, AV block, sinus node depression

101
Q

name 2 antiarrhythmics other than those in classes

A

adenosine

Mg2+

102
Q

what is the antiarrhythmic mechanism of adenosine?

A

inc K+ out of cells –> hyperpolarizes the cell and dec intracellular Ca

103
Q

adenosine–use as a antiarrhythmic

A

diagnosing/terminating certain forms of SVT

104
Q

how long does adenosine last?

A

~15 seconds

105
Q

what are 2 things that block the effects of adenosine?

A

theophylline and caffeine–adenosine receptor antagonists

106
Q

adenosine as a antiarrhythmic–toxicity

A

flushing, hypotension, chest pain, sense of impending doom, bronchospasm

107
Q

when would you use Mg as an antiarrhythmic?

A

torsades de pointes

digoxin toxicity

USMLE Step I Pharmacology (17 decks)

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