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U4 Drug table > Angina > Flashcards

Angina Flashcards

1
Q

What is the class for Aspirin (Unit IV)

A

NSAID

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2
Q

What is the mechanism for Aspirin (Unit IV)

A

Irreversible inhibition of platelet COX

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3
Q

What are the therapeutics for Aspirin (Unit IV)

A

Reduction in adverse events (MI, CVA, death); for those w/stable angina, unstable angina, acute MI, prophylaxis

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4
Q

What are the miscellaneous for Aspirin (Unit IV)

A

Low-doses; if you’re allergic, you’ll get asthma

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5
Q

What is the class for Ticlopidine (Ticlid)

A

Thienopyridine derivitive

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6
Q

What is the mechanism for Ticlopidine (Ticlid)

A

Inhibits platelet aggregation by ADP; reduces blood viscosity by decreasing plasma fibrinogen and increasing RBC deformability

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7
Q

What are the therapeutics for Ticlopidine (Ticlid)

A

Aspirin alternative

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8
Q

What are the important side effects for Ticlopidine (Ticlid)

A

Neutropenia and, rarely, TTP

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9
Q

What are the miscellaneous for Ticlopidine (Ticlid)

A

Not really used anymore

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10
Q

What is the class for Clopidogrel (Plavix)

A

Thienopyridine derivitive

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11
Q

What is the mechanism for Clopidogrel (Plavix)

A

Selectively and irreversibly inhibits ADP binding to P2Y12 (blocks ADP-dependent activation of glycoprotein IIb/IIIa complex)

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12
Q

What are the therapeutics for Clopidogrel (Plavix)

A

Great antithrombotic

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13
Q

What are the important side effects for Clopidogrel (Plavix)

A

Bleeding

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14
Q

What are the miscellaneous for Clopidogrel (Plavix)

A

No surgical or dental procedures if patient taking this

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15
Q

What is the class for Prasugrel (Effient)

A

Thienopyridine derivitive

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16
Q

What is the mechanism for Prasugrel (Effient)

A

Irreversibly binds P2Y12 receptor (G protein-coupled chemoreceptor for ADP)

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17
Q

What are the therapeutics for Prasugrel (Effient)

A

Reduce thrombotic events in those w/percutaneous coronary intervention (e.g., stent)

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18
Q

What are the important side effects for Prasugrel (Effient)

A

Massive bleeding risk

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19
Q

What is the class for Dipyradimole (Persantine)

A

Pyrimido-pyrimidine derivitive

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20
Q

What is the mechanism for Dipyradimole (Persantine)

A

Increases platelet intracellular cAMP (inhibits phosphodiesterase 5, activates adenylate cyclase, inhibits uptake of adenosine from vascular endothelium and RBCs)

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21
Q

What are the therapeutics for Dipyradimole (Persantine)

A

Decrease peripheral vascular disease (as an adjunct); stress test of heart

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22
Q

What are the important side effects for Dipyradimole (Persantine)

A

Vasodilation of coronary arteries can enhance exercise-induced ischemia (because it elevates extracellular adenosine levels)

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23
Q

What is the class for ACE inhibitors

A

ACE inhibitor

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24
Q

What is the mechanism for ACE inhibitors

A

Blocks endothelial ACE from converting angiotensin I to angiotensin II (potent vasoconstrictor); as a side effect, also prevents breakdown of bradykinin (potent vasodilator)

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25
Q

What are the therapeutics for ACE inhibitors

A

Often used as an add-on antihypertensive for anyone with chronic kidney disease/proteinuria, CHF, left ventricular hypertrophy, or post-MI (prevents left ventricular remodeling); reduces incidence of future CAD events, may reduce risk of diabetes

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26
Q

What are the important side effects for ACE inhibitors

A

Dry cough, angioedema, decreased renal function, hypotension

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27
Q

What are the miscellaneous for ACE inhibitors

A

Short-acting; contraindicated in pregnancy, renal artery stenosis, hyperkalemia, and prior angioedema (no ARB allowed, either); caution in renal failure

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28
Q

What is the class for Metoprolol, propranolol, bisoprolol

A

?-blocker

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29
Q

What is the mechanism for Metoprolol, propranolol, bisoprolol

A

Decrease contractility, HR (reduced myocardial O2 demand); class II antiarrhythmics (inhibit sympathetic influence on cardiac electrical activity, increase AP duration and effective refractory period in AV node)

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30
Q

What are the therapeutics for Metoprolol, propranolol, bisoprolol

A

Prevent MIs, prevent sudden cardiac death, increase survival post-MI (if patients suddenly stop, really bad!)

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31
Q

What are the important side effects for Metoprolol, propranolol, bisoprolol

A

Fatigue, worsening claudication, impotence (so men don’t take)

32
Q

What are the other side effects for Metoprolol, propranolol, bisoprolol

A

Decreased exercise tolerance, lethargy, insomnia,

33
Q

What are the miscellaneous for Metoprolol, propranolol, bisoprolol

A

Contraindicated in severe bradycardia, high degree AV block, sick sinus syndrome, unstable LV failure; relative contraindication is asthma, severe depression, peripheral vascular disease

34
Q

What is the class for Nitrates

A

Vasodilator

35
Q

What is the mechanism for Nitrates

A

Endothelium independent vasodilator; endothelial effects (inhibits platelet aggregation, inhibits leukocyte-endothelial interactions (anti-inflammatory))

36
Q

What are the therapeutics for Nitrates

A

For acute episodes; long-acting formulations are for those already on other drugs and still can’t control angina

37
Q

What are the important side effects for Nitrates

A

Tolerance w/chronic use (need nitrate free periods of 8-12 hours), headaches, hypotension, activation of Bezold-Jarisch reflex (causes bradycardia)

38
Q

What are the other side effects for Nitrates

A

Increase preload

39
Q

What are the miscellaneous for Nitrates

A

Contraindicated in hypertrophic cardiomyopathy, severe aortic stenosis, significant hypotension, use of phosphodiesterase inhibitors

40
Q

What is the class for Nefedipine (Procardia)

A

Calcium channel blockers (dihydropyridines, 1st generation)

41
Q

What is the mechanism for Nefedipine (Procardia)

A

Interact with L-type voltage gated plasma membrane Ca channel –> decreased calcium entry into vascular smooth muscle cell, preventing contraction; causes dilation of epicardial coronary arteries, arteriolar resistance arteries; less heart-specific activity, but more than 1st generation

42
Q

What are the therapeutics for Nefedipine (Procardia)

A

Hypertension, Raynauds, angina (3rd choice drug)

43
Q

What are the important side effects for Nefedipine (Procardia)

A

Leg edema, heart failure, AV nodal blockade, reflex tachycardia (lipophilic agents gain entry to brain and depress vasomotor center, rapidly dropping BP; this causes more reflex sympathetic activation (leading to adverse CV effects); long-acting agents are less lipophilic, and will cause less sympathetic activation and initial fall in BP)

44
Q

What are the other side effects for Nefedipine (Procardia)

A

Constipation (most common), headache, flushing

45
Q

What are the miscellaneous for Nefedipine (Procardia)

A

Contraindicated in overt decompensated heart failure, bradycardia, sinus node dysfunction, high-degree AV block

46
Q

What is the class for Amlodipine (Norvasc)

A

Calcium channel blockers (dihydropyridines, 2nd generation)

47
Q

What is the mechanism for Amlodipine (Norvasc)

A

Interact with L-type voltage gated plasma membrane Ca channel –> decreased calcium entry into vascular smooth muscle cell, preventing contraction; causes dilation of epicardial coronary arteries, arteriolar resistance arteries; less heart-specific activity

48
Q

What are the therapeutics for Amlodipine (Norvasc)

A

Hypertension, Raynauds, angina (3rd choice drug)

49
Q

What are the important side effects for Amlodipine (Norvasc)

A

Leg edema (less than 1st generation), heart failure, AV nodal blockade, reflex tachycardia (lipophilic agents gain entry to brain and depress vasomotor center, rapidly dropping BP; this causes more reflex sympathetic activation (leading to adverse CV effects); long-acting agents are less lipophilic, and will cause less sympathetic activation and initial fall in BP)

50
Q

What are the other side effects for Amlodipine (Norvasc)

A

Constipation (most common), headache, flushing

51
Q

What are the miscellaneous for Amlodipine (Norvasc)

A

Contraindicated in overt decompensated heart failure, bradycardia, sinus node dysfunction, high-degree AV block

52
Q

What is the class for Felodipine (Plendil)

A

Calcium channel blockers (dihydropyridines, 2nd generation)

53
Q

What is the mechanism for Felodipine (Plendil)

A

Interact with L-type voltage gated plasma membrane Ca channel –> decreased calcium entry into vascular smooth muscle cell, preventing contraction; causes dilation of epicardial coronary arteries, arteriolar resistance arteries; less heart-specific activity

54
Q

What are the therapeutics for Felodipine (Plendil)

A

Hypertension, Raynauds

55
Q

What are the important side effects for Felodipine (Plendil)

A

Leg edema (less than 1st generation), heart failure, AV nodal blockade, reflex tachycardia (lipophilic agents gain entry to brain and depress vasomotor center, rapidly dropping BP; this causes more reflex sympathetic activation (leading to adverse CV effects); long-acting agents are less lipophilic, and will cause less sympathetic activation and initial fall in BP)

56
Q

What are the other side effects for Felodipine (Plendil)

A

Constipation (most common), headache, flushing

57
Q

What are the miscellaneous for Felodipine (Plendil)

A

Contraindicated in overt decompensated heart failure, bradycardia, sinus node dysfunction, high-degree AV block

58
Q

What is the class for Isradipine (Dynacirc)

A

Calcium channel blockers (dihydropyridines, 2nd generation)

59
Q

What is the mechanism for Isradipine (Dynacirc)

A

Interact with L-type voltage gated plasma membrane Ca channel –> decreased calcium entry into vascular smooth muscle cell, preventing contraction; causes dilation of epicardial coronary arteries, arteriolar resistance arteries; less heart-specific activity

60
Q

What are the therapeutics for Isradipine (Dynacirc)

A

Hypertension, Raynauds

61
Q

What are the important side effects for Isradipine (Dynacirc)

A

Leg edema (less than 1st generation), heart failure, AV nodal blockade, reflex tachycardia (lipophilic agents gain entry to brain and depress vasomotor center, rapidly dropping BP; this causes more reflex sympathetic activation (leading to adverse CV effects); long-acting agents are less lipophilic, and will cause less sympathetic activation and initial fall in BP)

62
Q

What are the other side effects for Isradipine (Dynacirc)

A

Constipation (most common), headache, flushing

63
Q

What are the miscellaneous for Isradipine (Dynacirc)

A

Contraindicated in overt decompensated heart failure, bradycardia, sinus node dysfunction, high-degree AV block

64
Q

What is the class for Verapamil (Calan)

A

Calcium channel blockers (nondihydropyridines, phenylalkamine type)

65
Q

What is the mechanism for Verapamil (Calan)

A

Interact with L-type voltage gated plasma membrane Ca channel –> decreased calcium entry into vascular smooth muscle cell, preventing contraction; causes decreased contractility, firing rate of aberrant pacemaker sites, and conduction velocity; prolongs repolarization in SA node and AV node (–> decreases HR); less vasodilation

66
Q

What are the therapeutics for Verapamil (Calan)

A

Hypertension, anti-anginal (chronotropic effects –> decreased myocardial oxygen demand), SVT (class IV anti-arrhythymic)

67
Q

What are the important side effects for Verapamil (Calan)

A

Leg edema, bradycardia, AV nodal blockade, hypotension, worsening heart failure

68
Q

What are the other side effects for Verapamil (Calan)

A

Constipation (most common), headache, flushing

69
Q

What are the miscellaneous for Verapamil (Calan)

A

Contraindicated in overt decompensated heart failure, bradycardia, sinus node dysfunction, high-degree AV block

70
Q

What is the class for Diltiazem (Cardizem)

A

Calcium channel blockers (nondihydropyridines, benzothiazepine type)

71
Q

What is the mechanism for Diltiazem (Cardizem)

A

Interact with L-type voltage gated plasma membrane Ca channel –> decreased calcium entry into vascular smooth muscle cell, preventing contraction; causes decreased contractility, firing rate of aberrant pacemaker sites, and conduction velocity; prolongs repolarization in SA node and AV node (–> decreases HR); less vasodilation

72
Q

What are the therapeutics for Diltiazem (Cardizem)

A

Hypertension, anti-anginal (chronotropic effects –> decreased myocardial oxygen demand), SVT (class IV anti-arrhythymic)

73
Q

What are the important side effects for Diltiazem (Cardizem)

A

Leg edema, bradycardia, AV nodal blockade, hypotension, worsening heart failure

74
Q

What are the other side effects for Diltiazem (Cardizem)

A

Constipation (most common), headache, flushing

75
Q

What are the miscellaneous for Diltiazem (Cardizem)

A

Contraindicated in overt decompensated heart failure, bradycardia, sinus node dysfunction, high-degree AV block

U4 Drug table (7 decks)

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