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Flashcards in cardio drugs Deck (82)
1

primary essential HTN treatment

diuretics, ACE inh, ARBs, Ca2+ channel blockers

2

HTN with CHF treatment

diuretics, ACE inh, ARBs, beta-blockers (compensated CHF, not decompensated or cardiogenic shock), aldosterone antagonists

3

HTN with DM treatment

ACE inhibitors/ARBs, Ca2+ channel blockers, diuretics, beta-blockers, alpha-blockers

4

MOA of calcium channel blockers

block the V-dep L-type Ca++ channels of cardiac and smooth muscle --> reduce muscle contractility

5

which ca++ channel blockers work on the vascular smooth muscle?

amlodipine = nifedipine > diltiazem > verapamil

6

which ca++ channel blockers work on the heart?

verapamil > diltiazem > amlodipine = nifedipine

7

clinical use of ca++ channel blockers

dihydropyridine (except nimodipine): HTN, angina, raynauds
non-dihydropyridine: HTN, angina, atrial fibrillation/flutter
nimodipine: subarachnoid hemorrhage

8

toxicity of ca++ channel blockers

cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, constipation

9

amlodipine

dihydropine ca++ channel blocker

10

nimodipine

dihydropine ca++ channel blocker

11

nifedipine

dihydropine ca++ channel blocker

12

diltiazem

non-dihydropine ca++ channel blocker

13

verapamil

non-dihydropine ca++ channel blocker

14

hydralazine MOA

inc cGMP --> smooth muscle relaxation, vasodilates arterioles > veins; afterload reductino

15

clinical use of hydralazine

severe HTN, CHF, first line for HTN in pregnancy, methyldopa, with beta blockers to prevent reflex tach

16

toxicity of hydralazine

compensatory tach, fluid retention, nausea, headache, angina, lupus like syndrome

17

hypertensive emergency drugs

nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam

18

nitroprusside

SA
increase cGMP via NO
may cause CN tox beause it releases CN

19

fenoldopam

D1R agaonist - oronary, peripheral, renal and splanchnic vasodilation, decrease BP and natriuresis

20

MOA of nitroglycerin and isosorbide dinitrate

vasodilate via increase NO in vascular smooth muscles --> increased cGMP and smooth muscle relaxation
dilates veins more than arteries
decreased preload

21

clinical use of nitroglycerin and isosorbide dinitrate

angina, ACS, PE

22

nitroglycerine and isosorbide dinitrate toxicity

reflex tach, hypoTN, flushing, headache

23

MOA of HMG - CoA reductase inhibitors

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

24

Side effects of statins

hepatotoxicity
rhabdomyolysis

25

MOA of niacin

inhibits lipolysis in adipose tissue, reduces hepatic VLDL synthesis

26

Side effects of niacin

red flushed face which is decreased with aspirin or long term use
hyperglycemia (acanthosis nigricans)
hyperuricemia (exacerbates gout)

27

what are the bile acid resins?

cholestyramine, colestipol, colesevelam

28

MOA of bile acid resins

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

29

side effects of bile acid resins

tastes bad, GI discomfort, decreased absorption of fat soluble vitamins, cholesterol gallstones

30

MOA of fibrates

upregulates LPL leading to TG clearance
activates PPAR-a to induce HDL synthesis

31

side effects of fibrates

myositis (increased risk of concurrent statins)
hepatotoxicity
cholesterol gallstones

32

cardiac glycoside drug

digoxin

33

moa of cardiac glycoside

direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca++ exchanger/antiport --> increased intracellular calcium --> positive inotropy --> vagus nerve stimulation --> decreased HR

34

clinical use of cardiac glycosides

CHF, atrial fib

35

toxicity of cardiac glycosides

cholinergic: nausea, vomiting, diarrhea, blurry yellow vision, hyperkalemia

36

what does ECG show with cardiac glycoside use?

increased PR
decreased QT
ST scooping
T wave inversion
arrhythmia
AV block

37

what factors predispose to toxicity

renal failure, hypokalemia, verapamil, amiodarone, quinidine

38

antidote to cardiac glycoside use

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

39

quinidine

class 1a

40

procainamide

class 1a

41

disopyramide

class 1a

42

lidocaine

class 1b

43

mexiletine

class 1b

44

flecainide

class 1c

45

propafenone

class 1c

46

metoprolol

class 2

47

propranolol

class 2

48

esmolol

class 2

49

atenolol

class 2

50

timolol

class 2

51

carvedilol

class 2

52

amiodarone

class 3

53

ibutilide

class 3

54

dofetilide

class 3

55

sotalol

class 3

56

verapamil

class 4

57

diltiazem

class 4

58

class 1 antiarrhythmics moa

Na+ channel blockers, slow or block conduction
decrease slope of phase 0 depolarization and increased threshold for firing in abnormal pacemaker cells
state dependent
hyperkalemia causes increased toxicity

59

moa of class 1a

increased AP duration, increased effective refractory period, increased QT

60

clinical use of class 1a

both atrial and ventricular arrhythmias, especially reentrant and ectopic SVT and VT

61

toxicity of class 1a

cinchonism, reversible SLE like syndrome (procainamide), heart failure (disopyramide), thrombocytopenia, torsades de points due to increased QT

62

MOA of class 1b

Myositis (increased risk of concurrent statins)
hepatotoxicity
cholesterol gallstones

63

clinical use of class 1b

acute ventricular arrhythmias, digitalis induced arrhythmias. Best post-MI

64

toxicity

CNS stimulation/depression, cardiovascular depression

65

MOA of class 1c

prolongs refractory period in AV node
minimal effect on AP duration

66

clinical use of class 1c

SVTs, including atrial fib last resort in refractory VT

67

toxicity of class 1c

proarrhythmic, especially post-MI contraindicated in structural and ischemic heart disease

68

MOA of class 2

decrease SA and AV nodal activity by decreasing cAMP and ca++ currents
suppresses abnormal pacemaker by decreasing slope of phase 4

69

clinical use of class 2

SVT, slowing ventricular rate during atrial fibrillation and atrial flutter

70

toxicity of class 2

impotence
COPD, asthma exacerbation
cardiovascular effects, CNS effects
metoprolol: dyslipidemia
propanolol: exacerbates vasospasm in Prinzmetal angina
contraindiated in cocaine users

71

how do you treat class 2 overdose?

glucagon

72

class 3 moa

K+ channel blocker
AP duration increase with increased ERP
increase QT

73

clinical use of class 3

atrial fibrillation, atrial flutter, ventricular tach (amiodarone, sotalol)

74

toxicity of sotalol

torsades de points, excessive beta blockade

75

toxicity of ibutilide

torsades de points

76

toxicity of amiodarone

pulmonary fibrosis, hepatotoxicity, hypothyroidism, hyperthyroidism, corneal deposits, skin deposits, photodermatitis, neurological effects, constipation, cardiovascular effects

77

moa of class 4

ca++ channel blocker, decreased conduction velocity, increased ERP, PR interval increase

78

clinical use of class 4

prevention of nodal arrhythmias, rate control in atrial fibrillation

79

toxicity of class 4

constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

80

what are the other antiarrhythmics

adenosine, Mg++

81

adenosine

increased K+ out of cells --> hyperpolarizing the cell and decreasing calcium current
used for diagnosing and abolishing supraventricular tachycardia
very short acting (15 seconds)
adverse effects: flushing, hypotension, chest pain
effects blocked by theophylline and caffeine

82

mg2+

effective in torsades de points and digoxin