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Pharmacology Test #3 > Cardiac Ischemia > Flashcards

Cardiac Ischemia Flashcards

1
Q

Angina pectoris is the result of

A

the build up of metabolites in the heart as a result of inadequate coronary blood flow

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2
Q

The goal of antianginal therapy is

A

to re-establish adequate blood supply to the myocardium (heart muscle)

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3
Q

Myocardial oxygen demand is related to

A

heart rate, contractility, and wall tension

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4
Q

Double Product (Estimate):

A

heart rate X systolic BP

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5
Q

conditions that compromise blood flow through the coronary arteries can cause

A

angina

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6
Q

What can exacerbate angina?

A

factors that increase the work load of the myocardium

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7
Q

Factor affecting blood flow to the myocardium

A

pre-load, after-load, heart rate

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8
Q

Pre-load

A

left ventricular end-diastolic pressure

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9
Q

After-load

A

force distributed in ventricular wall during systole

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10
Q

What is pre-load decreased by?

A

decreased by dilation of the veins

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11
Q

A decrease in pre-load leads to

A

decrease in oxygen consumption and an increase in myocardial perfusion

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12
Q

What is after-load decreased by?

A

decreased by dilation of the arteries

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13
Q

A decrease in after-load leads to

A

decrease in oxygen consumption

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14
Q

What is the blood flow through the coronary arteries during systole?

A

little or no flow through coronaries during systole

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15
Q

Stable or classic angina (angina of effort)

A

Chronic obstruction of coronary arteries - usually atherosclerotic; perfusion is inadequate to meet increased oxygen demand

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16
Q

When does stable angina occur

A

occurs with increased physical exertion - predictable

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17
Q

Variant (Vasospastic, Prinzmetal’s) angina

A

caused by sudden, transient constriction of large coronary arteries; occurs at rest, often at night; not predictable

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18
Q

Unstable (pre-infarct, crescendo) angina

A

new or sudden worsening of angina at rest; caused by thrombosis (clot formation) usually secondary to atherosclerotic rupture; often first warning of MI

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19
Q

Therapy for unstable angina is based on

A

inhibiting platelet function and dissolving clot

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20
Q

goal of treatment for stable and variant angina

A

goal is to dilate coronary arteries and increase perfusion and/or decrease myocardial oxygen demand

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21
Q

Agents used in treating stable and variant angina

A

organic nitrates
calcium channel blockers
beta-adrenergic receptor antagonists (beta blockers)

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22
Q

Mechanism of organic nitrates

A

NO donating compounds; activators of guanylate cyclase

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23
Q

Activity of organic nitrates

A

marked dilation of veins; some dilation of arteries (esp. coronaries); some inhibition of platelet aggregation

24
Q

When/how are organic nitrates given?

A

given sublingually in treatment of acute attacks of angina

given orally or transdermally for prolonged prophylaxis

25
Q

What happens with continuous administration of organic nitrates?

A

tolerance develops; mechanism involves inhibition of ALDH2

26
Q

How do you avoid tolerance with organic nitrates

A

avoided by brief periods (several hours) without the drug

27
Q

Mechanism of calcium channel blockers in angina

A

decrease influx of Ca2+, the trigger for contraction

28
Q

Which calcium channel blocker has high vascular selectivity?

A

DHPs

29
Q

Activity calcium channel blockers in angina?

A

dilation of arteries: decrease in afterload

no dilation of veins: no effect on preload

30
Q

Mechanism of beta blockers in angina

A

block of epinephrine stimulation of myocardium; negative inotropic and chronotropic effect; lower heart rate increases coronary perfusion

31
Q

Activity of beta blockers in angina

A

decreases oxygen demand by depressing myocardium, especially during exertion

32
Q

Automaticity is caused by

A

HCN2/4 channels - depolarizing Na+ current activated at “resting” membrane potential

33
Q

SA and AV node rate is increased by

A

hypokalemia; beta-adrenergic stimulation; fiber stretch; acidosis; depolarized resting potential (injury)

34
Q

beta1-adrenergic antagonists inhibit

A

the HCN conductance mediated by endogenous epinephrine and norepinephrine

35
Q

Ivabradine (Procoralan)

A

selective blocker of the HCN channel; reduces HR; approved for symptomatic treatment of angina in Europe and Asia for patients who can’t take beta-blockers

36
Q

PKA phosphorylation of Cav1.2 does what?

A

increases Ca2+ influx; increases contractility/force of contraction; increased AV nodal action potential conduction rate

37
Q

Combination therapies for angina:

A
  1. organic nitrates and beta-blockers
  2. calcium channel blockers and beta-blockers
  3. calcium channel blockers and organic nitrates
  4. calcium channel blockers, organic nitrates, and beta blockers
38
Q

combination therapy particularly effect in stable angina

A

organic nitrates and beta-blockers

39
Q

combination therapy effective in stable angina refractory to organic nitrate/beta-blocker combination

A

calcium channel blockers and beta-blockers

40
Q

combination therapy contraindicated in angina associated with heart failure

A

calcium channel blockers and organic nitrates

41
Q

combination therapy effective in the treatment of severe vasospastic or stable angina

A

calcium channel blockers and organic nitrates

42
Q

combination therapy that may be effective when double therapy is not

A

calcium channel blockers, organic nitrates, beta-blockers

43
Q

Side effects of Diltiazem

A

low incidence of intolerance

44
Q

Side effects of Verapamil

A

constipating

45
Q

Side effects of beta-blockers

A

exacerbate bronchoconstriction

46
Q

Side effects of DHPs

A

have no antiarrhythmic activty

47
Q

Ranolazine inhibits

A

late sodium current

48
Q

Ranolazine (Ranexa) is used to prevent

A

angin

49
Q

Ranolazine is not effective in

A

terminating angina attacks

50
Q

Ranolazine is metabolized by

A

CYP3A (major) and CYP2D6 (minor)

51
Q

Ranolazine is a substrate for

A

P-glycoprotein transporter

52
Q

Side effects of Ranolazine

A

dizziness; may cause lengthening of the QT interval

53
Q

Factors that lead to plaque instability

A

large lipid pool, thin fibrous cap, inflammation

54
Q

Strategies to stabilize plaques and prevent rupture

A

Reduce LDL
Increase HDL
Inhibit Lp-PLA2
Inhibit MMPs
Inhibition of inflammation (esp. IL-1, IL-6)
Inhibition of cholesterol crystallization

55
Q

Paclitaxel

A

binds microtubules and stabilizes polymerization

56
Q

Sirolimus

A

macrolide that binds FKBP12 and inhibits mTOR to prevent cell cycle progression

57
Q

How do paclitaxel and sirolimus prevent restenosis

A

by inhibiting smooth muscle cell proliferation

Pharmacology Test #3 (13 decks)

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