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Pharmacology Test #3 > Cardiac Ischemia > Flashcards

Cardiac Ischemia Flashcards

(57 cards)

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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

Study These Flashcards
A

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

24
Q

When/how are organic nitrates given?

Study These Flashcards
A

given sublingually in treatment of acute attacks of angina

given orally or transdermally for prolonged prophylaxis

25
What happens with continuous administration of organic nitrates?
tolerance develops; mechanism involves inhibition of ALDH2
26
How do you avoid tolerance with organic nitrates
avoided by brief periods (several hours) without the drug
27
Mechanism of calcium channel blockers in angina
decrease influx of Ca2+, the trigger for contraction
28
Which calcium channel blocker has high vascular selectivity?
DHPs
29
Activity calcium channel blockers in angina?
dilation of arteries: decrease in afterload | no dilation of veins: no effect on preload
30
Mechanism of beta blockers in angina
block of epinephrine stimulation of myocardium; negative inotropic and chronotropic effect; lower heart rate increases coronary perfusion
31
Activity of beta blockers in angina
decreases oxygen demand by depressing myocardium, especially during exertion
32
Automaticity is caused by
HCN2/4 channels - depolarizing Na+ current activated at "resting" membrane potential
33
SA and AV node rate is increased by
hypokalemia; beta-adrenergic stimulation; fiber stretch; acidosis; depolarized resting potential (injury)
34
beta1-adrenergic antagonists inhibit
the HCN conductance mediated by endogenous epinephrine and norepinephrine
35
Ivabradine (Procoralan)
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
PKA phosphorylation of Cav1.2 does what?
increases Ca2+ influx; increases contractility/force of contraction; increased AV nodal action potential conduction rate
37
Combination therapies for angina:
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
combination therapy particularly effect in stable angina
organic nitrates and beta-blockers
39
combination therapy effective in stable angina refractory to organic nitrate/beta-blocker combination
calcium channel blockers and beta-blockers
40
combination therapy contraindicated in angina associated with heart failure
calcium channel blockers and organic nitrates
41
combination therapy effective in the treatment of severe vasospastic or stable angina
calcium channel blockers and organic nitrates
42
combination therapy that may be effective when double therapy is not
calcium channel blockers, organic nitrates, beta-blockers
43
Side effects of Diltiazem
low incidence of intolerance
44
Side effects of Verapamil
constipating
45
Side effects of beta-blockers
exacerbate bronchoconstriction
46
Side effects of DHPs
have no antiarrhythmic activty
47
Ranolazine inhibits
late sodium current
48
Ranolazine (Ranexa) is used to prevent
angin
49
Ranolazine is not effective in
terminating angina attacks
50
Ranolazine is metabolized by
CYP3A (major) and CYP2D6 (minor)
51
Ranolazine is a substrate for
P-glycoprotein transporter
52
Side effects of Ranolazine
dizziness; may cause lengthening of the QT interval
53
Factors that lead to plaque instability
large lipid pool, thin fibrous cap, inflammation
54
Strategies to stabilize plaques and prevent rupture
Reduce LDL Increase HDL Inhibit Lp-PLA2 Inhibit MMPs Inhibition of inflammation (esp. IL-1, IL-6) Inhibition of cholesterol crystallization
55
Paclitaxel
binds microtubules and stabilizes polymerization
56
Sirolimus
macrolide that binds FKBP12 and inhibits mTOR to prevent cell cycle progression
57
How do paclitaxel and sirolimus prevent restenosis
by inhibiting smooth muscle cell proliferation

Pharmacology Test #3 (13 decks)

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