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Cardiovascular > 04.22 - IHD Pharm (Ostrom) > Flashcards

04.22 - IHD Pharm (Ostrom) Flashcards

1
Q

What determines myocardial demand?

A

HR, Contractility, Wall tension (afterload)

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2
Q

2 Main CV effects of Nitrates

A

(1) Venodilation reduces Preload; (2) Coronary Vasodilation

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3
Q

2 major non-dihydropyridine CCB’s, and which is better

A

Verapamil > Diltiazem

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4
Q

2 mechanisms of Ranolazine

A

Late sodium current inhibitor; Partial FA oxidase inhibitor –> Increase glucose oxidation and efficiency of O2 utilization in heart

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5
Q

2 Non-Dihydro CCB’s

A

Verapamil, Diltiazem

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6
Q

3 Widespread Uses of CCB’s

A

Angina, HTN, Supraventricular Arrhythmias

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7
Q

5 Dihydro CCB’s

A

Nifedipine, Nicardipine, Isradipine, Felodipine, Amlodipine

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8
Q

Absolute Contraindication for Nitrates

A

PDE inhibitors

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9
Q

Action of Ca2+ in cardiac muscle cell

A

Binding to Troponin C reduces inhibition of actin-myosin cross-bridges

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10
Q

Action of Ca2+ in smooth muscle cell

A

Binding to Calmodulin activates MLCK, which phosphorylates myosin and triggers contraction

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11
Q

Adverse Effects of Nitrates

A

Hypotension, Headache, Drug Rash

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12
Q

Adverse reactions with Ranolazine

A

Dizziness, headache, constipation, nausea (4-6%)

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13
Q

AE’s caused by all CCB’s

A

Hypotension, Peripheral Edema

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14
Q

AE’s of DHP CCB’s

A

Excessive Vasodilation, GI, Per Edema, Coronary Steal

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15
Q

AE’s of Verapamil, Diltiazem

A

Bradycardia, Asystole, AV Block; Constipation; CHF

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16
Q

All patients with CHD should receive

A

Aspirin

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17
Q

Another source of concern for CCB’s

A

may increase cancer risk (not shown in ALLHAT)

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18
Q

Are CCB’s good at treating HTN

A

One study says yes, other no

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19
Q

Best choice for oral anti-HTN in patient with Prinzmetal’s would be

A

DHP CCB

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20
Q

Cardiac cells rely on L-type Ca channels for

A

Contraction (contractile cells) and Upstroke of AP in Nodal Cells

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21
Q

CCB’s act on what type of Ca channels

A

L-Type

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22
Q

CCB’s are highly effect for relief of symptoms in

A

Exertional and Vasospastic Angina

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23
Q

CCB’s in patients with CAD

A

fail to consistently reduce reinfarction or CAD mortality; Imparied LV function

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24
Q

Chemical class of Diltiazem

A

Benzothiazepines

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25
Q

Chemical class of Verapamil

A

Phenylalkylamines

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26
Q

Con to Ranolazine

A

Cost; Will not relieve acute angina attacks

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27
Q

Conclusion: When should CCB’s be used

A

Unable to tolerate BB’s; Or add-on for angina uncontrolled by BB + nitrate

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28
Q

Contraindications for All CCB’s

A

Hypotension, Advance HF

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29
Q

Contraindications for Non-DHP CCB’s only

A

Sinus Bradycardia, AV conduction defects (also Hypotension, Advance HF)

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30
Q

DHP =

A

Vasodilation = Baroreceptor Reflex

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31
Q

Direct effects of Non-Di CCB’s predominate to

A

Reduce Heart Work: HR, Contractility, Slowed AV conduction

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32
Q

Do BB’s prevent vasospasm?

A

No

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33
Q

Drug of choice in Angina overall

A

Beta blockers

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34
Q

Effect of Nitrates on BP and HR

A

BP unchanged or slight decrease, HR unchanged or slight increase

35
Q

Effect of Nitrates on Coronary Arteries

A

Vasodilate, Prevents or reverses coronary vasospasm

36
Q

Effect of Nitrates on Pulmonary Vascular Resistance and CO

A

PVR decreased, CO reduced slightly

37
Q

Effects of Nitrate Venodilation

A

Decreased Preload –> Reduces wall stress and MvO2, Subendocardial blood flow increased

38
Q

For Exertional Angina, use BB why?

A

Reduces HR, contractility

39
Q

For Unstable Angina, use BB’s with

A

Nitrates, ASA, and Heparin

40
Q

For Vasospastic Angina, use BB why?

A

DON’T

41
Q

How do CCB’s effect CV function w/out significant side effects

A

Specific for L-type Ca Channels

42
Q

How do CYP inducers affect Verapamil, Diltiazem

A

Reduce their levels

43
Q

How do Di CCB’s reduce MvO2

A

Vasodilation = Reduced afterload

44
Q

How do Non-Di CCB’s reduce MvO2

A

Reduce heart work (demand)

45
Q

How does increased Diastole affect coronary perfusion?

A

Increases

46
Q

Indications of Ranolazine

A

Chronic, stable agina in combo with Amlodapine, BB, or Nitrates

47
Q

Major Contraindications of Ranolazine

A

Digoxin (conc. increases); CYP; Long QT

48
Q

Mechanisms of Tolerance to Nitrates

A

Volume Expansion, Neurohumoral Activation, Depletion of Tissue Cysteine Stores

49
Q

MOA of Milrinone

A

PDE4 inhibitor

50
Q

Most common side effects of DHP’s are due to

A

Vasodilation

51
Q

Most common ventricular dysfunction

A

Heart Failure

52
Q

Notable pharmacokinetics for CCB’s

A

Extensive First-Pass metab; CYP3A4; Short plasma half-life; Bolus effect

53
Q

Pharmacodynamic interactions with Verapamil, Diltiazem

A

BB’s increase risk of Nodal Block

54
Q

Primary drug class of choice for most types of angina

A

Nitrates

55
Q

Problem with Di CCB’s

A

Reflex cardiac stimulation: HR, Contractility

56
Q

Properties of L-Type Ca Channels

A

V-dep, Large Conductance, Slow inactivation

57
Q

Rationale for combining BB with CCBs (Di)

A

Prevent coronary vasospasm, reduce systemic vascular resistance

58
Q

Rationale for combining BB with Nitrates:

A

Reduces LVEDP, LV Volume, Dilates coronary arteries

59
Q

Situations favoring Di CCB

A

With BB for Coronary Vasodilation, reduced afterload; Sinus brady, Nodal block; Valvular insufficiency

60
Q

Special effect of non-Di CCB’s on coronary arteries

A

Coronary Vasodilation: Prevents or reverses Vasospasm

61
Q

Special feature of lipophilic BB’s

A

Can reduce afterload thru CNS effects

62
Q

Vascular specificity of CCBs

A

Induce relaxation of arterial SM but not Venous (reduce afterload, not preload)

63
Q

What does voltage-dep binding of Nifedipine select for smooth muscle ca channels?

A

SM voltage less variable

64
Q

What is target of nitrates?

A

*–> NO –> GC –> Increase cGMP

65
Q

What type of Ca channels mediate NT release in neurons

A

N- and P-type

66
Q

When should Renolazine be used:

A

Increase exercise tolerance and time to onset of angina; Adjunct when refractory to other tx’s

67
Q

When would Non-Di CCB’s be indicated

A

Pt can’t use BB: Asthma/COPD, Insuline-dep DM, PVD

68
Q

Which anti-anginal(s) doesn’t vasodilate coronaries?

A

BB

69
Q

Which anti-anginal(s) doesn’t reduce HR

A

Nitrates, Dihydro CCBs

70
Q

Which anti-anginal(s) reduce afterload?

A

All

71
Q

Which anti-anginal(s) reduce preload?

A

Nitrates

72
Q

Which CCB causes constipation

A

Verapamil

73
Q

Which CCB class binds in use-dependent way

A

Non-DHP

74
Q

Which CCB class binds in voltage-dependent way

A

DHP

75
Q

Which CCB class is a selective vasodilator

A

Dihydro –> Can cause reflex

76
Q

Which CCB class needs to be used with Beta blocker

A

Dihydropyridine to prevent reflex cardiac stimulation

77
Q

Which CCB worsens CHF

A

Verapamil

78
Q

Which CCB’s are CYP3A4 substrates

A

Verapamil, Diltiazem

79
Q

Which CCB’s slow the recovery of the L-type channel?

A

Verapamin, Diltiazem (non-dihydro)

80
Q

Which class of CCB’s affect AV node conduction

A

Non-Di CCB’s slow

81
Q

Which is preferred, Di or Non-Di CCB’s?

A

Dihydropyridine, unless patient can’t tolerate BB

82
Q

Which of the following decrease CHD events: BBs, Nitrates, CCBs

A

BBs do, Nitrates don’t, CCBs are variable

83
Q

Why do Nitrates cause Headache

A

Vasodilation of Meningeal arteries

84
Q

Worst choice of oral anti-HTN in patient with Prinzmetal’s

A

Beta Blocker

Cardiovascular (18 decks)

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