B4-050 Treatment of Angina Flashcards

1
Q

angina occurs when the oxygen need

A

exceeds the supply

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2
Q

immediate relief of angina

A

organic nitrates

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3
Q

angina prophylaxis

A

calcium channel blockers
beta blockers

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4
Q

angina is typically relieved with

A

rest and/or nitroglycerin

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5
Q

typical location of angina

A

retrosternal
radiating to left/both arms

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6
Q

classic or variant angina?

atheromatous obstruction of large coronaries, especially with exercise

A

classic

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7
Q

classic or variant angina?

may require CABG or angioplasty if uncontrolled

A

classic

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8
Q

classic or variant angina?

spasm or constrication in atherosclerotic coronary vessels

A

variant

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9
Q

classic or variant angina?

relieved by nitrates and ca channel blockers

A

variant

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10
Q

oxygen demand is determined by

A
  1. contractility
  2. heart rate
  3. wall stress
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11
Q

main energy source in heart

A

fatty acid oxidation

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12
Q

drugs that can shift myocardial metabolism toward glycolysis and reduce oxygen demand without affecting hemodynamics

A
  • trimetazidine
  • pFOX inhibitors
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13
Q

oxygen supply depends on

A
  • O2 delivery
  • O2 extraction
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14
Q

agents decreasing O2 demand

A
  • beta blockers
  • verapamil/dilitiazem
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15
Q

agents that increase o2 supply

A
  • dehydropyridines
  • statins
  • anti-thrombotics
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16
Q

drugs that can relax vascular smooth muscle work by

A
  • decreasing intracellular Ca (CCB)
  • preventing depolarization (nicorandil)
  • increasing cGMP (NO)
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17
Q

3 drug groups used to treat angina

A
  • organic nitrates
  • CCBs
  • beta blockers
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18
Q

organic nitrates, CCBs, beta blockers

decrease myocardial oxygen demand by decreasing:

A
  • HR
  • ventricular volume
  • blood pressure
  • contractility
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19
Q
  • reduces intracellular Ca+ concentration, reducing cardiac contractility and work
  • recently approved
A

ranolazine

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20
Q

partially inhibits fatty acid oxidation

A

trimetazidine

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21
Q
  • inhibits xanthine oxidase
  • prolongs exercise time in patients with angina
A

allopurinol

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22
Q

direct bradycardic agent inhibiting the hyperpolarization activated Na+ channel in the SA node

A

ivabradine

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23
Q
  • rho-kinase inhibitor
  • reduces coronary vasospasm in experimental animals
A

fasudil

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24
Q

short acting nitrates

3

A
  • amyl nitrate, inhaled
  • nitroglycerin, sublingual
  • isosorbide dinitrate
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25
Q

how are different vessel types affected by NO?

A
  • large veins are markedly dilated
  • arterioles and precapillary spinchters are dilated less
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26
Q

can potentiate action of NO in angina, causing severe hypotension and MI

A

sildenafil

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27
Q

can be used to treat cyanide poisoning

A

NO

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28
Q

effect and result: beneficial nitrate effects

decreased BP and vasodilation

A

reduced myocardial O2 demand

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29
Q

effect and result: beneficial nitrate effects

reduced ventricular diastolic pressure

A

improved subendocardial perfusion

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30
Q

effect and result: beneficial nitrate effects

dilation of epicardial arteries

A

redistribution of coronary flow to ischemic area

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31
Q

effect and result: beneficial nitrate effects

increased collateral flow

A

improved perfusion to ischemic areas

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32
Q

effect and result: harmful nitrate effects

reflex increases in HR and contractility

A

increased myocardial O2 demand

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33
Q

effect and result: harmful nitrate effects

reflex tachycardia

A

reduced perfusion due to shorter diastole

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34
Q

oral nitrates are rapidly metabolized by

A

hepatic reductase

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35
Q

What two nitrates should be given sublingual for rapid absorption and to avoid hepatic destruction?

A
  • nitroglycerin
  • isosorbide dinitrate
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36
Q

what nitrate, if given IV, dilates both arteries and veins equally?

A

sodium nitroprusside

37
Q

fastest acting nitrate preparations

A

amyl nitrate, inhaled
sodium nitroprusside, IV
nitroglycerin, sublingual

38
Q

acute nitrate toxicity can cause

A
  • orthostatic hypertension
  • tachycardia
  • throbbing headaches
39
Q

frequent exposure to nitrates can cause

A

tolerance

Monday disease

40
Q

CCBs are orally active drugs that block

A

L type Ca channels

41
Q

Ca channels are opened by

A

stimulation of B receptors

42
Q

CCBs affects […] more than […]

blood vessels

A

arteries; veins

43
Q
  • dihydropyridine
  • binding site 1A
  • vascular selectivity
A

nifedipine

44
Q
  • benzothiapine
  • binding site 1B
  • selective for both vascular and myocardium
A

diltiazem

45
Q
  • phenylalkylamine
  • binding site 1C
  • selective for myocardial tissue
A

verapamil

46
Q

CCB that is the strongest vasodilator, causes reflex tachycardia

A

nifedipine

47
Q

CCB with strongest cardiac affects, causes myocardial depression, decreases HR

A

verapamil

48
Q

short acting CCBs should be avoided in patients with

A

hypertension

49
Q

beneficial effects of dihydropyridines

A
  • coronary vasodilation (increased O2 supply)
  • systemic arteriole vasodilation (decreased afterload)
50
Q

harmful effects of dyhydropyridines

A

severe hypotension -> reflex tachy -> increased cardiac workload -> increased risk of MI

51
Q

beneficial effects of verapamil and diltiazem

A
  • reduced SA automaticity and AV conduction
  • decreased myocardial contractility and bradycardia –> decreased cardiac work load
52
Q

harmful effects of verapamil and diltiazem

A

cardiac depression, resulting in cardiac arrest, AV block, or CHF

53
Q

may enhance digoxin toxicity

A

verapamil/diltiazem

54
Q

should not be used in patients with ventricular dysfunction or SA/AV node disturbances

A

verapamil/diltiazem

55
Q
  • inhibit insulin secretion
  • interfere with platelet aggregation
  • relatively minor side affects
A

CCBs

56
Q

extremely useful for the mangement of angina associated with effort

A

beta blockers

57
Q

do not dilate coronary arteries

A

beta blockers

58
Q

beneficial effects of beta blockers

A
  • decreased sympathetic activity (decreased cardiac work)
  • direct vasodilation
  • bradycardia (increased perfusion time)
59
Q

may induce or worsen CHF in patients with acute MI or decompensated HF

A

beta blockers

60
Q

potentially harmful in variant angina

A

beta blockers

61
Q

may increase plasma triglycerides and decrease HDL causing atherosclerosis

A

beta blockers

62
Q

most common cause of angina pectoris

A

atherosclerotic disease of the coronaries

63
Q

first line therapy: angina

A
  • modify risk factors
  • antiplatelets
64
Q

what drugs are more effective for variant angina?

A

nitrates and CCBs

65
Q

most effective drug combinations for angina

A
  • b-blockers and CCBs or,
  • 2 CCBs
66
Q

potentially harmful effects of CCBs or beta blockers can be prevented by

A

nitrates

and vice versa

67
Q

relfex tachycardia can be minimized by combining nitrates with

A

CCBs or beta blockers

68
Q

result in pronounced dilation of large vessels, reduce preload

A

nitrates

69
Q

reduce afterload and/or cardiac function

A

CCBs

70
Q

reduce vasocontriction and cardiac function

A

beta blockers

71
Q

increase risk for new onset diabetes

A

beta blockers

72
Q

acute nitrate toxicity

A
  • headaches
  • orthostatic hypertension
  • tachycardia
73
Q

potentiate the action of nitrates and lead to MI

A

PDE-5 inhibitor

sildenafil

74
Q

cause decreased oxygen demand

A

verapamil/dilitiazem

suppress AV and SA nodes

75
Q

decrease preload via venodilation

A

nitrates

76
Q
  • decrease afterload by arteriodilation
  • decrease TPR
A

dihydropyridine and nitrates

77
Q

increase oxygen supply by redistributing blood flow

A

nitrates

78
Q

increase oxygen supply by coronary vasodilation

A

dihydropyridines

79
Q

reduce sympathetic activity on the heart

A

beta 1 blockers

80
Q

decrease peripheral resistance by reducing angiotensin 2

A

ACE/ARBs

81
Q

slow down heart rate by depressing SA and AV node

A

verapamil

82
Q

short acting nitrate used for acute anginal attacks

A

sublingual nitroglycerin

83
Q

short acting nitrate for chronic treatment of angina

A

oral isosorbide mononitrate

84
Q

used to treat hypertension and heart failure but can precipitate angina due to reflex cardiac stimulation

A

hydralazine

85
Q

result in tolerance or marked reduction of effect upon repeated exposure

A

nitroglycerin

86
Q

to reduce nitroglycerin tolerance,

A

use lowest effective dose with nitrate free intervals of 10-12 hrs daily

87
Q

preferentially acts as a vasodilator leading to reflex tachy

A

nefedipine

88
Q

work as vasodilators without causing relfex tachycardia

A

a1 blockers

zosins

89
Q

suppress SA/AV nodes leading to bradycardia

A

verapamil/diltiazem