Cardiovascular Pharmacology Flashcards Preview

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Flashcards in Cardiovascular Pharmacology Deck (91):
1

treating hypertension in heart failure

use beta blockers unless HF is decompensated

2

treating hypertension in pregnancy

nifedipine
methyldopa
hydralazine
labetalol

"No More Home Life" :)

3

-dipine drugs are:

dihydropyridine CCBs

4

non-dihydropyridine CCBs include:

verapamil, diltiazem

5

all CCBs work via what mechanism?

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

6

clinical use of dihydropyridine CCBs

- HTN
- Prinzmetal angina, regular angina
- Raynaud phenomenon

7

clinical use of nimodipine

SA hemorrhage (prevents cerebral vasospasm)

8

clinical use of non-dihydropyridine CCBs

- HTN
- angina
- atrial fib/flutter

9

SEs non-dihydropyridine CCBs

- cardiac depression via AV block
- hyperprolactinemia
- constipation

10

SEs of dihydropyridine CCBs

- peripheral edema
- flushing
- lightheadedness
- gingival hyperplasia

11

mechanism of hydralazine

arteriole > vein dilation via increase in cGMP

12

clinical use of hydralazine

- along with nitrates in HF
- acute, severe HTN
- pregnancy

13

hydralazine often given with ___ to prevent reflex tachycardia

beta blocker

14

SEs of hydralazine

- edema
- lupus-like syndrome
- reflex tachycardia --> angina

15

treatment of hypertensive emergency

- clevidipine, nicardipine
- nitroprusside
- fenoldopam
- labetalol

16

nitroprusside is known to cause ____ toxicity

CN

17

mechanism of fenoldopam

DA-1 agonist --> vasodilation

18

mechanism of nitrates

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

19

clinical use of nitrates

- angina
- ACS
- pulmonary edema

20

SEs of nitrates

- reflex tachycardia (give with BBs for this reason)
- flushing
- headaches/dizziness (Monday disease in industrial exposure)

21

Never use ____ during a RV infarct.

nitrates

22

mechanism of ranolazine

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

23

use ranolazine for

refractory angina

24

SEs of ranolazine

- dizziness, headache
- constipation
- nausea
- long QT

25

mechanism of milrinone

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

26

clinical use of milrinone

acute decompensated HF

27

SEs of milrinone

hypotension, arrhythmias

28

mechanism of cilostazole

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

29

lipid profile effect of statins

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

30

mechanism of statins

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

31

SEs of statins

- hepatotoxicity
- myopathy (esp with fibrates, niacin)

32

lipid profile effect of cholestyramine, colestipol, colesevelam

decreased LDL, increased tris

33

mechanism of cholestyramine, colestipol, colesevelam

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

34

SEs of cholestyramine, colestipol, colesevelam

- GI upset
- decreased absorption of fat-soluble stuff

35

lipid profile effect of ezetimibe

decreased LDL, decreased tris

36

mechanism of ezetimibe

prevents cholesterol absorption from intestine

37

SEs of ezetimibe

- diarrhea
- hepatotoxicity (rare)

38

lipid profile effect of fibrates

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

39

mechanism of fibrates

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

40

SEs of fibrates

- gallstones
- myopathy (with statins)

41

lipid profile effect of niacin

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

42

mechanism of niacin

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

43

SEs of niacin

- hyperglycemia
- hyperuricemia
- flushing of face via increase in PGs (treat with ASA)

44

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

increased HDL, decreased tris

45

lipid profile effect of PCSK9 inhibitors (alirocumab, evolocumab)

same as a statin

46

mechanism of PCSK9 inhibitors (alirocumab, evolocumab)

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

47

SEs of PCSK9 inhibitors (alirocumab, evolocumab)

- neurocognitive (dementia, delirium)
- myopathy

48

mechanism of digoxin

- 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

clinical use of digoxin

- HF (increases contractility)
- a. fib. (decreases AV nodal conduction)

50

SEs of digoxin

- GI: nausea, vomiting, diarrhea
- color vision changes
- arrhythmias due to AV block
- hyperkalemia

51

quinidine and its SEs

- class 1A antiarrythmic
- cinchonism: HA, tinnitus

52

procainamide and its SEs

- class 1A antiarrythmic
- drug-induced SLE (ANA and anti-histone abs present)

53

disopyramide and its SEs

- class 1A antiarrythmic
- HF

54

mechanism of class 1A antiarrythmic

- 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

clinical use of class 1A antiarrythmic

re-entrant/ectopic SVT/VT

56

SEs of all class 1A antiarrythmic

- thrombocytopenia
- TDP due to QT prolongation

57

lidocaine

class 1B antiarrythmic

58

mexiletine

class 1B antiarrythmic

59

tocanide

class 1B antiarrythmic

60

phenytoin (in the heart)

class 1B antiarrythmic

61

mechanism of class 1B antiarrythmic

- 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

clinical use of class 1B antiarrythmic

post-MI ventricular arrhythmias

63

SEs of class 1B antiarrythmic

CNS stimulation/depression

64

flecainide

class 1C antiarrythmic

65

propafenone

class 1C antiarrythmic

66

mechanism of class 1C antiarrythmic

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

67

clinical use of class 1C antiarrythmic

SVTs like atrial fibrillation

68

SEs of class 1C antiarrythmic

contraindicated in structural/ischemic heart disease due to arrhythmias

69

mechanism of BBs (class II antiarrhythmics)

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

clinical use of BBs (class II antiarrhythmics)

SVT - a fib/flutter

71

SEs of BBs (class II antiarrhythmics)

- impotence
- exacerbates COPD/asthma
- bradycardia, AV block
- CNS depression
- hypoglycemia in OD

72

amiodarone

class III antiarrhythmic

73

ibutilide

class III antiarrhythmic

74

dofetilide

class III antiarrhythmic

75

sotalol

class III antiarrhythmic with atypical BB properties as well!

76

dronedarone

class III antiarrhythmic

77

mechanism of class III antiarrhythmic

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

78

clinical use of class III antiarrhythmic

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

79

class III antiarrhythmic with least risk of TdP

amiodarone

80

SEs of amiodarone

- pulmonary fibrosis
- hepatotoxicity
- hyper/hypothyroidism
- blue/grey skin deposits
- bradycardia/heart block

81

verapamil

class IV antiarrythmic

82

diltiazem

class IV antiarrythmic

83

mechanism of class IV antiarrythmic

- 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

clinical use of class IV antiarrythmic

prevents nodal arrhythmias (a. fib.)

85

SEs of class IV antiarrythmic

- constipation
- flushing
- edema
- SA depression, AV block

86

clinical use of Mg 2+

- TdP
- digoxin toxicity (with anti-dig Fab fragments)

87

mechanism of adenosine

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

88

clinical use of adenosine

SVTs

89

mechanism of ivabradine

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

clinical use of ivabradine

chronic, stable angina in pts who cannot take BBs

91

SEs of ivabradine

visual phenomena, HTN, bradycardia