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Pharm I Fall 2016 NUNM Jensen > Angina > Flashcards

Angina Flashcards

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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
Atenolol: indications?
MI, HTN, angina
26
Atenolol: contraindications?
Heart block or severe bradycardia
27
Atenolol: onset and duration?
< 1hr | 12-24 hrs
28
Atenolol: interactions?
Apple
29
Propranolol: MOA?
Nonselective B1 and B2
30
Propranolol: indications?
MI, HTN, angina, migraine prophylaxis, supraventricular arrhythmias
31
Propranolol: contraindications?
Heart block or severe bradycardia
32
Propranolol: onset and duration?
1-2 hrs | 6-12 (IR) or 24 hrs (ER)
33
Propranolol: interactions
Indian snakeroot and St. John's Wort
34
Carvedilol: MOA?
Nonselective w/ alpha-1 adrenergic blockade activity
35
Carvedilol: indications?
MI, HTN, CHF, angina
36
Carvedilol: contraindications?
Heart block or severe bradycardia
37
Carvedilol: onset and duration?
< 1hr | 24 hrs
38
Carvedilol: interactions?
Grapefruit juice
39
Which beta blockers are more likely to interact with beta agonists used in asthma?
Carvedilol and propranolol
40
What are the four roles of therapy for Calcium channel blockers in angina?
1. Prophylaxis 2. Decrease BP 3. Dilates coronary blood vessels 4. Dilates peripheral blood vessels
41
What is the MOA for Calcium channel blockers?
Blocks calcium influx leading to relaxation of cardiac and smooth muscles
42
What are the side effects of calcium channel blockers?
TACHYCARDIA, EDEMA, ha, fatigue, exercise intolerance, hypotension (varies with selectivity)
43
Calcium channel blockers differ based on their selectivity towards what, which are predominantly found in the periphery?
Dihydropyridine receptors
44
What are the three dihydropyridines?
Nifedipine Felodipine Amlodipine
45
What calcium channel blocker should you avoid for stable angina?
Immediate release nifedipine
46
What are the two non-dihydropyridines?
Diltiazem and verapamil
47
Contraindications for non-dihydropyridines?
Pts w/ ejection fraction < 35% (heart failure) | Cholea, grapefruit, St. John's Wort
48
Interactions to avoid with non-dihydropyridines?
Combination with beta blocker (reduces HR)
49
Amlodipine: indications?
HTN, chronic stable angina, variant angina, disorder of CV system
50
Verapamil: indications?
HTN, CSA, variant angina, angina, SVT, afib/aflutter
51
Verapamil: contraindications?
Hypotension, LVEF < 30%, AV block, sick-sinus syndrome, certain arrhythmias
52
Verapamil: interactions?
Cholea, grapefruit, st. john's wort
53
Diltiazem: indications?
Atrial arrhythmia, HTN, SVT, angina
54
Diltiazem: contraindications?
Hypotension, LVEF < 30%, AV block, sick-sinus, certain arrhythmias
55
Diltiazem: interactions?
Cholea, grapefruit, st. john's wort
56
Why are calcium channel blockers more likely to have drug interactions with other therapeutic moieties?
CYP450 pathways lead to a lot of interactions
57
Aspirin: MOA?
Nonselective, irreversible COX inhibitor
58
Aspirin: contraindications?
< 18 years old due to assoc. w/ Reye's syndrome
59
Aspirin: interactions?
Cocoa, danshen, dong quai, evening primrose, policosanol, willow bark
60
Aspirin: metabolism?
Hydrolyzed to salicylate by esterases
61
Aspirin: side effects?
increased bleeding (GI), disruption of renal perfusion
62
Do other NSAIDs like aspirin have effects on platelets?
Yes, but they are reversible
63
Clopidogrel: MOA?
Irreversibly blocks P2Y12 component of ADP receptors on platelet surface (reduces platelet activation)
64
Clopidogrel: indications?
Post-NSTEMI, ACS, CVA, PCI, and arterial occlusive disease to prevent clots
65
Clopidogrel: onset?
Detected second day of tx
66
Clopidogrel: interactions?
Cocoa, danshen, dong quai, evening primrose, policosanol, willow bark, grapefruit, st. john's wort
67
Ticagrelor: MOA?
Reversibly blocks P2Y12 component of ADP receptors on platelet surface (duration depends on potency)
68
Ticagrelor: side effects?
increased risk of bleeding, increased uric acid levels
69
Ticagrelor: indications?
Prophylaxis post ACS, MI or PCI
70
Ticagrelor: interactions?
Cocoa, danshen, dong quai, evening primrose, policosanol, willow bark, grapefruit, st. john's wort
71
Prasugrel: MOA?
Irreversibly blocks P2Y12 component of ADP receptors on platelet surface
72
Prasugrel: contraindications?
Prior TIA or stroke (also, increased risk for bleeding with body weight < 60kg)
73
Prasugrel: interactions?
Cocoa, danshen, dong quai, evening primrose, policosanol, willow bark, grapefruit, st. johns wort
74
What is different about the P2Y12 pathway that ticagrelor goes through compared to prasugrel and clopidogrel?
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
Warfarin: MOA?
Inhibits Vit. K oxide reductase (the enzyme responsible for regenerating vit. K so it can activate clotting factors)
76
What are the Vitamin K dependent clotting factors?
II, VII, IX, X
77
Warfarin: onset?
Effects on INR seen 2-5 days after dose changes
78
Warfarin: interactions [in addition to the usual blood thinner interactors]
Alfalfa, american ginseng, alcohol, EDTA, glucosamine HCL and sulfate, licorice, N-acetyl glucosamine, Vit. K, wintergreen, plus the usuals.
79
Rivaroxaban: MOA?
Direct, reversible inhibition of factor Xa
80
Apixaban: MOA?
Direct, reversible inhibition of factor Xa
81
Dabigatran: MOA?
Direct thrombin inhibitor
82
Enoxaparin (Low Molecular Weight Heparin): MOA?
Enhances the inhibition rate of clotting proteases by antithrombin III, impairing normal hemostasis and inhibition of factor Xa
83
Enoxaparin (Low Molecular Weight Heparin): indications?
Typically used as initial treatment and then as bridging therapy
84
What is the reversal agent for warfarin and how does it work?
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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