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Pharm I Fall 2016 NUNM Jensen > Angina > Flashcards

Angina Flashcards

1
Q

What is a distinguishing feature of chronic stable angina?

A

Symptom reversibility (pain relieved by rest or sublingual nitroglycerine)

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2
Q

What is the MOA of nitrates?

A

Relaxation of vascular smooth muscle (vasodilation)

Venous dilation is greater than arterial, leading to reduced preload, resulting in reduced O2 consumption

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3
Q

What are the side effects of nitrates?

A

Hypotension, HA, flushing, light headedness

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4
Q

What are the two specific nitrates commonly used?

A

Nitroglycerin and Isosorbide mononitrate

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5
Q

What is/are the indications for Nitroglycerin?

A

Angina (prophylactic and acute)

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6
Q

What interactions should you be conscious of with nitroglycerin?

A

Avoid use of PDE-5 inhibitors like sildenafil

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7
Q

What is the time of onset and duration of nitroglycerin?

A

Onset: 1-3 min (sublingual)
Duration: 25 min

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8
Q

What is/are the indications for Isosorbide mononitrate?

A

Angina pectoris

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9
Q

What interactions should you be conscious of with isosorbide mononitrate?

A

PDE-5 inhibitors like sildenafil

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10
Q

What is the time of onset and duration for isosorbide mononitrate?

A

Onset: 30-45 min.
Duration: >6 hrs

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11
Q

Name four natural products that have hypotensive effects and should be used with caution with blood pressure lowering agents?

A

Coleus, Hawthorn, L-citrulline, and N-acetyl cysteine

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12
Q

Why not combine nitrates with sildenafil?

A

Hypotension

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13
Q

Are nitrates more specific to arterial or venous blood vessels?

A

Venous

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14
Q

What are the four roles of therapy for beta blockers in regard to angina?

A
  1. Prophylaxis
  2. Blunt cardiac stimulation
  3. Prevents reflex tachycardia
  4. Decreases HR, contractility, and BP
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15
Q

What is the MOA for beta blockers?

A

Blocks beta adrenergic receptors and can be selective or non-selective to the heart

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16
Q

What are potential side effects of beta blockers?

A

Bradycardia, heart block, HA, fatigue, dizziness, depression, exercise intolerance, hypotension, erectile dysfunction (varies with selectivity)

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17
Q

What type of agents should you not combine beta blockers with?

A

Those with intrinsic sympathomimetic activity

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18
Q

What are the primary locations for Beta-1, -2, and -3 receptors?

A

Beta-1: heart

  • 2: lungs (but also on the heart)
  • 3: adipose tissue and heart
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19
Q

What can happen with abrupt discontinuation of beta blockers?

A

Reflex tachycardia (taper gradually)

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20
Q

Metoprolol: MOA?

A

Cardioselective beta-1 competitive antagonist

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21
Q

Metoprolol: indications?

A

MI, CHF, angina, HTN

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22
Q

Metoprolol: contraindications?

A

Heart block or severe bradycardia (HR < 60)

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23
Q

Metoprolol: onset and duration?

A

Onset: < 1hr
Duration: 3-6 (IR) or 25hrs (ER)

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24
Q

Atenolol: MOA?

A

Cardioselective beta-1 competitive antagonist

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25
Q

Atenolol: indications?

A

MI, HTN, angina

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26
Q

Atenolol: contraindications?

A

Heart block or severe bradycardia

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27
Q

Atenolol: onset and duration?

A

< 1hr

12-24 hrs

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28
Q

Atenolol: interactions?

A

Apple

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29
Q

Propranolol: MOA?

A

Nonselective B1 and B2

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30
Q

Propranolol: indications?

A

MI, HTN, angina, migraine prophylaxis, supraventricular arrhythmias

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31
Q

Propranolol: contraindications?

A

Heart block or severe bradycardia

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32
Q

Propranolol: onset and duration?

A

1-2 hrs

6-12 (IR) or 24 hrs (ER)

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33
Q

Propranolol: interactions

A

Indian snakeroot and St. John’s Wort

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34
Q

Carvedilol: MOA?

A

Nonselective w/ alpha-1 adrenergic blockade activity

35
Q

Carvedilol: indications?

A

MI, HTN, CHF, angina

36
Q

Carvedilol: contraindications?

A

Heart block or severe bradycardia

37
Q

Carvedilol: onset and duration?

A

< 1hr

24 hrs

38
Q

Carvedilol: interactions?

A

Grapefruit juice

39
Q

Which beta blockers are more likely to interact with beta agonists used in asthma?

A

Carvedilol and propranolol

40
Q

What are the four roles of therapy for Calcium channel blockers in angina?

A
  1. Prophylaxis
  2. Decrease BP
  3. Dilates coronary blood vessels
  4. Dilates peripheral blood vessels
41
Q

What is the MOA for Calcium channel blockers?

A

Blocks calcium influx leading to relaxation of cardiac and smooth muscles

42
Q

What are the side effects of calcium channel blockers?

A

TACHYCARDIA, EDEMA, ha, fatigue, exercise intolerance, hypotension (varies with selectivity)

43
Q

Calcium channel blockers differ based on their selectivity towards what, which are predominantly found in the periphery?

A

Dihydropyridine receptors

44
Q

What are the three dihydropyridines?

A

Nifedipine
Felodipine
Amlodipine

45
Q

What calcium channel blocker should you avoid for stable angina?

A

Immediate release nifedipine

46
Q

What are the two non-dihydropyridines?

A

Diltiazem and verapamil

47
Q

Contraindications for non-dihydropyridines?

A

Pts w/ ejection fraction < 35% (heart failure)

Cholea, grapefruit, St. John’s Wort

48
Q

Interactions to avoid with non-dihydropyridines?

A

Combination with beta blocker (reduces HR)

49
Q

Amlodipine: indications?

A

HTN, chronic stable angina, variant angina, disorder of CV system

50
Q

Verapamil: indications?

A

HTN, CSA, variant angina, angina, SVT, afib/aflutter

51
Q

Verapamil: contraindications?

A

Hypotension, LVEF < 30%, AV block, sick-sinus syndrome, certain arrhythmias

52
Q

Verapamil: interactions?

A

Cholea, grapefruit, st. john’s wort

53
Q

Diltiazem: indications?

A

Atrial arrhythmia, HTN, SVT, angina

54
Q

Diltiazem: contraindications?

A

Hypotension, LVEF < 30%, AV block, sick-sinus, certain arrhythmias

55
Q

Diltiazem: interactions?

A

Cholea, grapefruit, st. john’s wort

56
Q

Why are calcium channel blockers more likely to have drug interactions with other therapeutic moieties?

A

CYP450 pathways lead to a lot of interactions

57
Q

Aspirin: MOA?

A

Nonselective, irreversible COX inhibitor

58
Q

Aspirin: contraindications?

A

< 18 years old due to assoc. w/ Reye’s syndrome

59
Q

Aspirin: interactions?

A

Cocoa, danshen, dong quai, evening primrose, policosanol, willow bark

60
Q

Aspirin: metabolism?

A

Hydrolyzed to salicylate by esterases

61
Q

Aspirin: side effects?

A

increased bleeding (GI), disruption of renal perfusion

62
Q

Do other NSAIDs like aspirin have effects on platelets?

A

Yes, but they are reversible

63
Q

Clopidogrel: MOA?

A

Irreversibly blocks P2Y12 component of ADP receptors on platelet surface (reduces platelet activation)

64
Q

Clopidogrel: indications?

A

Post-NSTEMI, ACS, CVA, PCI, and arterial occlusive disease to prevent clots

65
Q

Clopidogrel: onset?

A

Detected second day of tx

66
Q

Clopidogrel: interactions?

A

Cocoa, danshen, dong quai, evening primrose, policosanol, willow bark, grapefruit, st. john’s wort

67
Q

Ticagrelor: MOA?

A

Reversibly blocks P2Y12 component of ADP receptors on platelet surface (duration depends on potency)

68
Q

Ticagrelor: side effects?

A

increased risk of bleeding, increased uric acid levels

69
Q

Ticagrelor: indications?

A

Prophylaxis post ACS, MI or PCI

70
Q

Ticagrelor: interactions?

A

Cocoa, danshen, dong quai, evening primrose, policosanol, willow bark, grapefruit, st. john’s wort

71
Q

Prasugrel: MOA?

A

Irreversibly blocks P2Y12 component of ADP receptors on platelet surface

72
Q

Prasugrel: contraindications?

A

Prior TIA or stroke (also, increased risk for bleeding with body weight < 60kg)

73
Q

Prasugrel: interactions?

A

Cocoa, danshen, dong quai, evening primrose, policosanol, willow bark, grapefruit, st. johns wort

74
Q

What is different about the P2Y12 pathway that ticagrelor goes through compared to prasugrel and clopidogrel?

A

Ticagrelor goes through no in vivo biotransformation, whereas prasugrel goes through hydrolysis by esterases and CYP dependent oxidation. Clopidogrel also goes through CYP dependent oxidation

75
Q

Warfarin: MOA?

A

Inhibits Vit. K oxide reductase (the enzyme responsible for regenerating vit. K so it can activate clotting factors)

76
Q

What are the Vitamin K dependent clotting factors?

A

II, VII, IX, X

77
Q

Warfarin: onset?

A

Effects on INR seen 2-5 days after dose changes

78
Q

Warfarin: interactions [in addition to the usual blood thinner interactors]

A

Alfalfa, american ginseng, alcohol, EDTA, glucosamine HCL and sulfate, licorice, N-acetyl glucosamine, Vit. K, wintergreen, plus the usuals.

79
Q

Rivaroxaban: MOA?

A

Direct, reversible inhibition of factor Xa

80
Q

Apixaban: MOA?

A

Direct, reversible inhibition of factor Xa

81
Q

Dabigatran: MOA?

A

Direct thrombin inhibitor

82
Q

Enoxaparin (Low Molecular Weight Heparin): MOA?

A

Enhances the inhibition rate of clotting proteases by antithrombin III, impairing normal hemostasis and inhibition of factor Xa

83
Q

Enoxaparin (Low Molecular Weight Heparin): indications?

A

Typically used as initial treatment and then as bridging therapy

84
Q

What is the reversal agent for warfarin and how does it work?

A

Prothrombin complex concentrate (PCC) and fresh frozen plasma (FFP) covers the period before K1 has reached its full effect.

Pharm I Fall 2016 NUNM Jensen (11 decks)

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