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Cardiovascular Pharmacology Flashcards

1
Q

treating hypertension in heart failure

A

use beta blockers unless HF is decompensated

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2
Q

treating hypertension in pregnancy

A

nifedipine
methyldopa
hydralazine
labetalol

“No More Home Life” :)

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3
Q

-dipine drugs are:

A

dihydropyridine CCBs

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4
Q

non-dihydropyridine CCBs include:

A

verapamil, diltiazem

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5
Q

all CCBs work via what mechanism?

A

blockage of L-type Ca 2+ channels in cardiac (particularly AV node) or smooth muscle (preferentially pre-capillary arterioles)

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6
Q

clinical use of dihydropyridine CCBs

A
  • HTN
  • Prinzmetal angina, regular angina
  • Raynaud phenomenon
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7
Q

clinical use of nimodipine

A

SA hemorrhage (prevents cerebral vasospasm)

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8
Q

clinical use of non-dihydropyridine CCBs

A
  • HTN
  • angina
  • atrial fib/flutter
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9
Q

SEs non-dihydropyridine CCBs

A
  • cardiac depression via AV block
  • hyperprolactinemia
  • constipation
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10
Q

SEs of dihydropyridine CCBs

A
  • peripheral edema
  • flushing
  • lightheadedness
  • gingival hyperplasia
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11
Q

mechanism of hydralazine

A

arteriole > vein dilation via increase in cGMP

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12
Q

clinical use of hydralazine

A
  • along with nitrates in HF
  • acute, severe HTN
  • pregnancy
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13
Q

hydralazine often given with ___ to prevent reflex tachycardia

A

beta blocker

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14
Q

SEs of hydralazine

A
  • edema
  • lupus-like syndrome
  • reflex tachycardia –> angina
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15
Q

treatment of hypertensive emergency

A
  • clevidipine, nicardipine
  • nitroprusside
  • fenoldopam
  • labetalol
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16
Q

nitroprusside is known to cause ____ toxicity

A

CN

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17
Q

mechanism of fenoldopam

A

DA-1 agonist –> vasodilation

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18
Q

mechanism of nitrates

A

increase in NO from arginine –> increased cGMP to vascular (especially veins) smooth muscle –> vasodilation –> decrease in both preload AND afterload

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19
Q

clinical use of nitrates

A
  • angina
  • ACS
  • pulmonary edema
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20
Q

SEs of nitrates

A
  • reflex tachycardia (give with BBs for this reason)
  • flushing
  • headaches/dizziness (Monday disease in industrial exposure)
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21
Q

Never use ____ during a RV infarct.

A

nitrates

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22
Q

mechanism of ranolazine

A

inhibition of late phase of Na current which leads to decreased preload

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23
Q

use ranolazine for

A

refractory angina

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24
Q

SEs of ranolazine

A
  • dizziness, headache
  • constipation
  • nausea
  • long QT
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25
Q

mechanism of milrinone

A

PDE-3 inhibitor so increases cAMP in cardiomyocytes (increase in chronotropy and inotropy) and vascular smooth muscle (vasodilation)

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26
Q

clinical use of milrinone

A

acute decompensated HF

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27
Q

SEs of milrinone

A

hypotension, arrhythmias

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28
Q

mechanism of cilostazole

A

PDE inhibitor causing arterial vasodilation and inhibition of platelet aggregation/degranulation

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29
Q

lipid profile effect of statins

A

decreased** LDL, increased HDL, decreased tris

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30
Q

mechanism of statins

A

HMG-CoA reductase inhibitors that inhibit the rate-limiting step of cholesterol production

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31
Q

SEs of statins

A
  • hepatotoxicity

- myopathy (esp with fibrates, niacin)

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32
Q

lipid profile effect of cholestyramine, colestipol, colesevelam

A

decreased LDL, increased tris

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33
Q

mechanism of cholestyramine, colestipol, colesevelam

A

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

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34
Q

SEs of cholestyramine, colestipol, colesevelam

A
  • GI upset

- decreased absorption of fat-soluble stuff

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35
Q

lipid profile effect of ezetimibe

A

decreased LDL, decreased tris

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36
Q

mechanism of ezetimibe

A

prevents cholesterol absorption from intestine

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37
Q

SEs of ezetimibe

A
  • diarrhea

- hepatotoxicity (rare)

38
Q

lipid profile effect of fibrates

A

decreased LDL, increased HDL, decreased** tris

39
Q

mechanism of fibrates

A

upregulation of lipoprotein lipase via PPARa activation –> increased tris into adipose tissue via clearance of chylomicrons/VLDL which also frees up HDL

40
Q

SEs of fibrates

A
  • gallstones

- myopathy (with statins)

41
Q

lipid profile effect of niacin

A

decreased LDL, increased ***** HDL, decreases tris

42
Q

mechanism of niacin

A

inhibits hormone sensitive lipase in adipose tissue (decreased FFAs to the blood stream) and production of VLDL in the liver

43
Q

SEs of niacin

A
  • hyperglycemia
  • hyperuricemia
  • flushing of face via increase in PGs (treat with ASA)
44
Q

lipid profile effect of omega-3 FAs (fish oil)

A

increased HDL, decreased tris

45
Q

lipid profile effect of PCSK9 inhibitors (alirocumab, evolocumab)

A

same as a statin

46
Q

mechanism of PCSK9 inhibitors (alirocumab, evolocumab)

A

inhibition of degredation of LDL receptors in liver (more LDL receptors in liver!)

47
Q

SEs of PCSK9 inhibitors (alirocumab, evolocumab)

A
  • neurocognitive (dementia, delirium)

- myopathy

48
Q

mechanism of digoxin

A
  • direct inh of Na/K ATPase pump –> more Na in cell –> indirect inh of Na/Ca exchanger –> more Ca in cell and increase in inotropy
  • parasympathetic stimulation
49
Q

clinical use of digoxin

A
  • HF (increases contractility)

- a. fib. (decreases AV nodal conduction)

50
Q

SEs of digoxin

A
  • GI: nausea, vomiting, diarrhea
  • color vision changes
  • arrhythmias due to AV block
  • hyperkalemia
51
Q

quinidine and its SEs

A
  • class 1A antiarrythmic

- cinchonism: HA, tinnitus

52
Q

procainamide and its SEs

A
  • class 1A antiarrythmic

- drug-induced SLE (ANA and anti-histone abs present)

53
Q

disopyramide and its SEs

A
  • class 1A antiarrythmic

- HF

54
Q

mechanism of class 1A antiarrythmic

A
  • intermediate inh. of phase 0 depolarization in cardiomyocytes –> increase in refractory period
  • increase in AP duration due to QT prolongation from some K channel blocking effects on phase 3
55
Q

clinical use of class 1A antiarrythmic

A

re-entrant/ectopic SVT/VT

56
Q

SEs of all class 1A antiarrythmic

A
  • thrombocytopenia

- TDP due to QT prolongation

57
Q

lidocaine

A

class 1B antiarrythmic

58
Q

mexiletine

A

class 1B antiarrythmic

59
Q

tocanide

A

class 1B antiarrythmic

60
Q

phenytoin (in the heart)

A

class 1B antiarrythmic

61
Q

mechanism of class 1B antiarrythmic

A
  • weak inh. of phase 0 depolarization in cardiomyocytes –> no real effect on conduction velocity or refractory period, just preferentially treats depolarized tissue
  • shortens AP
62
Q

clinical use of class 1B antiarrythmic

A

post-MI ventricular arrhythmias

63
Q

SEs of class 1B antiarrythmic

A

CNS stimulation/depression

64
Q

flecainide

A

class 1C antiarrythmic

65
Q

propafenone

A

class 1C antiarrythmic

66
Q

mechanism of class 1C antiarrythmic

A
  • strong inhibition of phase 0 depolariation in cardiomyocytes - prolongs refractory period in AV node and accessory bypass tracts
  • no effect on AP duration
67
Q

clinical use of class 1C antiarrythmic

A

SVTs like atrial fibrillation

68
Q

SEs of class 1C antiarrythmic

A

contraindicated in structural/ischemic heart disease due to arrhythmias

69
Q

mechanism of BBs (class II antiarrhythmics)

A

decreased cAMP –> decreased Ca 2+ –> suppresses SA/AV nodal conduction by decreasing slope of phase 4 (takes longer for these cells to repolarize) –> decreases rate and contractility

  • decreased SA discharge
  • decreased AV conduction
  • increased refractory period
70
Q

clinical use of BBs (class II antiarrhythmics)

A

SVT - a fib/flutter

71
Q

SEs of BBs (class II antiarrhythmics)

A
  • impotence
  • exacerbates COPD/asthma
  • bradycardia, AV block
  • CNS depression
  • hypoglycemia in OD
72
Q

amiodarone

A

class III antiarrhythmic

73
Q

ibutilide

A

class III antiarrhythmic

74
Q

dofetilide

A

class III antiarrhythmic

75
Q

sotalol

A

class III antiarrhythmic with atypical BB properties as well!

76
Q

dronedarone

A

class III antiarrhythmic

77
Q

mechanism of class III antiarrhythmic

A

prolongs repolarization of cardiomyocytes in phase 3 –> increased AP duration and QT interval, increased refractory period

78
Q

clinical use of class III antiarrhythmic

A

a. fib/flutter, ventricular tachycardia especially post-MI (first-line > IB like lidocaine)

79
Q

class III antiarrhythmic with least risk of TdP

A

amiodarone

80
Q

SEs of amiodarone

A
  • pulmonary fibrosis
  • hepatotoxicity
  • hyper/hypothyroidism
  • blue/grey skin deposits
  • bradycardia/heart block
81
Q

verapamil

A

class IV antiarrythmic

82
Q

diltiazem

A

class IV antiarrythmic

83
Q

mechanism of class IV antiarrythmic

A
  • block L-type Ca channels, so inhibits phase 0 of AP in nodal cells and prolongs repolarization
  • slows SA discharge rate and AV conduction rate
84
Q

clinical use of class IV antiarrythmic

A

prevents nodal arrhythmias (a. fib.)

85
Q

SEs of class IV antiarrythmic

A
  • constipation
  • flushing
  • edema
  • SA depression, AV block
86
Q

clinical use of Mg 2+

A
  • TdP

- digoxin toxicity (with anti-dig Fab fragments)

87
Q

mechanism of adenosine

A

AT1 receptors activate K+ channels in nodal and hyperpolarize them –> decreased AV node conduction

88
Q

clinical use of adenosine

89
Q

mechanism of ivabradine

A

selective inh of “funny” Na channels in nodal cells which prolongs phase 4 and leads to decreased SA node firing –> decreases HR without affective contractility –> lowers MVO2

90
Q

clinical use of ivabradine

A

chronic, stable angina in pts who cannot take BBs

91
Q

SEs of ivabradine

A

visual phenomena, HTN, bradycardia

Pharmacology (22 decks)

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