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Pharmacology > Anti-Anginal Drugs > Flashcards

Anti-Anginal Drugs Flashcards

1
Q

what results in myocardial ischemia?

A

imbalance between oxygen supply and demand

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2
Q

what are 2 things that can cause decrease of oxygen/blood supply?

A
  1. plaques obstruct perfusion
  2. coronary artery spasm
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3
Q

what can coronary artery spasm cause?

A

prinzmetal / vasospastic / rest angina

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4
Q

what can cause an increase in oxygen/blood demand?

A

exertion/stress

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5
Q

what is stable/typical angina also called?

A

coronary artery disease

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6
Q

how is typical angina usually managed?

A

lifestyle changes and medications

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7
Q

what is unstable angina also called?

A

acute coronary syndrome (ACS)

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8
Q

what is unstable angina caused by?

A

ruptured plaque with platelet aggregation and thrombi formation

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9
Q

what does angina with increased pain severity, frequency, duration, and occurrence at a lower exercise level indicate?

A

patient is progressing from stable to unstable angina

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10
Q

what is used to prevent ischemic heart disease?

A

statins

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11
Q

what two variables determine oxygen supply?

A
  1. arterial oxygen content
  2. coronary blood flow
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12
Q

what four variables determine oxygen demand?

A
  1. increased HR
  2. increased contractility
  3. increased preload
  4. increased afterload
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13
Q

amount of blood in the ventricle during diastole

A

preload

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14
Q

resistance the heart has to pump against to push blood into systemic circulation

A

afterload

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15
Q

what will an increase in one or all of HR, contractility, preload, and/or afterload cause?

A

increased demand

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16
Q

what is the cardinal symptom of angina?

A

squeezing pain in center of chest that lasts more than a few minutes

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17
Q

what are the classic symptoms of angina? (7)

A
  1. pain to arms, neck, jaw, shoulder or back
  2. SOB
  3. diaphoresis
  4. dizziness, fainting
  5. anxiety
  6. nausea
  7. fatigue
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18
Q

what is the primary function of nitric oxide?

A

dilates blood vessels

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19
Q

what does nitrate combine with to be reduced to nitric oxide?

A

sulfhydryl (SH)

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20
Q

where is sulfhydryl found?

A

endogenously

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21
Q

what is myocardial oxygen consumption (MVO2)?

A

the amount of oxygen used by the heart

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22
Q

when active nitric oxide dilates coronary arteries and veins at low doses, what does is cause?

A

decreased preload

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23
Q

when active nitric oxide dilates large arteries and arterioles at high doses, what does it causes?

A

decreased TPR, afterload, and MVO2

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24
Q

how does cGMP affect contractility?

A

it does not let calcium into the muscle = decreases contractility

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25
Q

what does the activation of nitrate to nitric oxide lead to?

A

activation of guanylyl cyclase to create cGMP

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26
Q

how can nitroglycerine be administered? (2)

A
  1. sublingual
  2. buccal
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27
Q

what is the onset of sublingual or buccal nitroglycerine?

A

2-4 mins

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28
Q

what is the duration of action of sublingual or buccal nitroglycerine?

A

1 hour

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29
Q

if a patient with chest pain is given NTG SL x1 and pain is not relieved within 5 minutes, what does this suggest?

A

unstable angina

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30
Q

how should NTG be administered for acute MI?

A

IV infusion

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31
Q

what is the duration of action for prophylactic NTG administered via ointment?

A

4-8 hours

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32
Q

what is the duration of action for prophylactic NTG administered via patch?

A

24 hours

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33
Q

how should isosorbides be administered?

A

PO

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34
Q

which isosorbide is the active form?

A

isosorbide mononitrate

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35
Q

how does tolerance to nitrate develop?

A

chronic exposure

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36
Q

in the tolerance to nitrate, how is there a decreased capacity of vascular smooth muscle to convert nitrates to nitric oxide?

A

used up sulphydryl groups in the body

37
Q

how can tolerance to nitrate be overcome?

A

short periods (8-12hrs/day) of nitrate absence from the body

38
Q

what causes the adverse effect of SL NTG of postural hypotension?

A

rapid drop in BP and sudden movement

39
Q

what causes reflex tachycardia as an adverse effect of NTG?

A

compensation of drop in BP - heart pumps quicker

40
Q

what causes the flushing and headaches as an adverse effect of NTG?

A

vasodilation of all vessels in the body

41
Q

what administration route of NTG is most likely to cause a rash?

A

transdermal NTG

42
Q

why is it important to give NTG sublingual?

A

avoid extensive first-pass effect by hepatic nitrate reductase

43
Q

which type of nitrite is less effected by first pass effect and is therefore given PO?

A

isosorbide dinitrate

44
Q

what does PDE V do?

A

inactivates cGMP

45
Q

what does PDE V inhibitor do?

A

inhibits the inactivation of cGMP, which leads to increased cGMP

46
Q

what does cGMP do?

A

stimulates smooth muscle relaxation = decreased BP

47
Q

why shouldn’t sildenafil (PDE V inhibitor) be given to a patient taking an organic nitrate?

A

can cause prolonged hypotension

48
Q

what do beta 1 and beta 2 blockers do?

A

block sympathetic nervous system

49
Q

where are beta 1 receptors present on? (2)

A

juxtaglomerular cells in kidney
heart

50
Q

what would a beta 1 blocker do? (3)

A
  1. block renin release
  2. decrease angiotensin II
  3. decrease afterload
51
Q

what are beta 1 blockers typically used for? (2)

A
  1. hypertension
  2. heart failure
52
Q

where are beta 2 receptors typically located?

A

smooth muscle cells on heart, lungs, and liver

53
Q

what does activation of beta 1 receptor cause? (5)

A
  1. increased HR
  2. increased contractility
  3. increased CO
  4. increased renin
    5 increased angiotensin II
54
Q

what does blocking of the beta 1 receptor cause? (4)

A
  1. decreased HR
  2. decreased CO
  3. decreased afterload
  4. decreased angiotensin II
55
Q

what does blocking of beta 1 receptors mask?

A

hypoglycemia

56
Q

what does activation of beta 2 receptors cause? (5)

A
  1. bronchodilation
  2. vasodilation
  3. skeletal m tremor
  4. hepatic glycogenolysis
  5. gluconeogenesis (increased BG)
57
Q

what does blocking of beta 2 receptors cause? (2)

A
  1. bronchoconstriction
  2. hypoglycemia
58
Q

if a patient comes in to the clinic to reverse the blockade of beta 2 receptors, what are they at risk for?

A

acute hypertension with too much vasopressors

59
Q

what does it mean when some beta blockers have membrane stabilizing activity?

A

they can inhibit action potential in cardiac cells

60
Q

what can beta blockers with intrinsic sympathomimetic activity (ISA) do?

A

partially activate receptor

61
Q

what is not a good choice for patients with angina?

A

beta blockers with intrinsic sympathomimetic activity (ISA)

62
Q

which organ metabolizes and eliminates lipid soluble medications?

A

liver

63
Q

which two beta blockers are generation 1 (nonselective)?

A

propranolol
sotalol

64
Q

what receptors do generation 1 (propranolol) beta blockers work on?

A

beta 1 and beta 2 receptors

65
Q

which receptors do generation 2 beta blockers work on?

A

beta 1 (selective)

66
Q

which 3 beta blockers are generation 2? (beta 1 selective)

A

atenolol
metoprolol
acebutolol

67
Q

what are bad effects of generation 1 and 2 beta blockers? (2)

A

increase triglycerides
decrease HDL

68
Q

what receptors do generation 3 beta blockers work on?

A

alpha 1 receptors

69
Q

what 3 alpha blockers are generation 3?

A

carvedilol
labetalol
nebivolol

70
Q

which medication is used in hypertensive emergency?

A

labetalol

71
Q

what is the main function of generation 3 alpha 1 blockers? (2)

A

peripheral vasodilation
better decrease in BP

72
Q

what are beta blockers not effective for? (2)

A
  1. coronary artery spasm
  2. exertion-induced angina
73
Q

why are beta blockers combines with nitrates?

A

antagonize SNS activity

74
Q

what should be avoided in beta blockers?

A

those with intrinsic sympathomimetic activity

75
Q

what can abrupt withdrawal of long-term beta blockers lead to? (2)

A

unstable angina
MI

76
Q

what do calcium channel blockers bind to?

A

L-type Ca channels

77
Q

what do CCBs cause?

A

peripheral and coronary vasodilation

78
Q

what do CCBs decrease? (2)

A

afterload
MVO2

79
Q

what are 2 non-dihydropyridines CCBs?

A

verapamil
ditiazem

80
Q

what do NDHP CCBs decrease?

A

HR
CO
(myocardial contractility)
conduction in SA and AV nodes

81
Q

what do NDHP CCBs work on?

A

the heart

82
Q

what are NDHP CCBs used for? (2)

A

angina and arrhythmias

83
Q

what type of antianginal is contraindicated in patients with heart failure?

A

NDHP CCBs

84
Q

what are 5 dihydropyridines CCBs?

A

Nifedipine
Isradipine
Nicardipine
Felodipine
Amlodipine

85
Q

what do DHP CCBs cause?

A

peripheral vasodilation

86
Q

what is a side effect of DHP CCBs?

A

reflex tachycardia

87
Q

what are DHP CCBs used for?

A

hypertension

88
Q
A

Pharmacology (13 decks)

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