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Pharmacology I > Anti-Anginal > Flashcards

Anti-Anginal Flashcards

1
Q

what is angina

A

A lack of sufficient oxygen (ischemia) to the heart causes pain, “angina”

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2
Q

why does angina happen

A

Coronary artery obstruction limits blood supply to part of the myocardium

Atherosclerosis and thrombosis blocks blood flow (unstable angina)

Vasospasm blocks blood flow (variant or Prinzmetal’s angina)

Coronary circulation can meet oxygen demands of myocardium at rest, but not when heart work increased by exercise (exertional angina) due to atherosclerosis.

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3
Q

types of angina

A

unstable
variant
exertional

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4
Q

what is an unstable angina

A

Recurrent angina associated with minimal exertion

Prolonged and frequent pain

Thought to be due to fissuring of atherosclerotic plaques and subsequent platelet aggregation

High correlation with myocardial infarction

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5
Q

what is variant angina

A

a direct result of reduction in coronary flow due to vasospasm, not an increase in myocardial oxygen demand

Normal coronary angiograms

Excellent prognosis

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6
Q

what is exertional angina

A

usually due to fixed coronary vascular obstruction (surgical revascularization or angioplasty may be beneficial)

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7
Q

approaches for treating angina

A

Increase coronary blood flow (Nitrates, CCB)

Reduce myocardial oxygen consumption (mvo2) by:

Prevent platelet deposition/aggregation: aspirin

Coronary artery bypass surgery and eluting stents

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8
Q

how do you reduce the myocardial oxygen consumption?

A

NEGATIVE CHRONOTROPIC EFFECT: decrease heart rate

NEGATIVE INOTROPIC EFFECT: decrease myocardial contractility

Decreased ventricular workload (wall stress):
Reduced preload (venodilation) 
Reduced afterload (vasodilation)
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9
Q

Cellular Mechanism for anti-Anginal action of Nitrates (nitrovasodilators)

A

denitration to release nitric oxide (NO) which activates guanylate cyclase and elevates intracellular cyclic GMP producing relaxation of vascular (and other) smooth muscle and produces venodilation and coronary vasodilation (endogenous NO produced by nitric oxide synthase)

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10
Q

Cardiovascular Venodilation Effects of Nitrates

A

results in decreased preload

decreased pressure during diastole in ventricles of heart and reduced wall stress and McO2

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11
Q

Cardiovascular Vasodilation Effects of Nitrates

A

redistribution of blood flow to areas of ischemia

Selective dilatation of epicardial and collateral coronary vessels

prevents or reverses coronary vasospasm

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12
Q

Overall effect on hemodynamics (nitrates)

A

(at usual antianginal doses)

BP: unchanged or slight decrease

HR: unchanged or slight increase

Pulmonary Vascular Resistance: decreased

Cardiac Output: reduced (slight)

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13
Q

adverse effects of nitrates

A

hypotension
headache
drug rash

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14
Q

contraindication of nitrates

A

Do not take Sildenafil with Nitrates

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15
Q

recommended dose of nitrate

A

8-12 hour “nitrate free” interval each day, usually at night but in some individuals during day

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16
Q

MOA of non-dihydropyridine

A

Ca2+ channel blockers

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17
Q

Non-dihydropyridine

A

Verapamil

Diltiazem

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18
Q

Effects of non-dihydropyridine

A

decreased heart rate
decreased myocardial contractility
slowed AV conduction

reduces MvO2 by reducing heart rate, contractility, afterload

prevents or reverses vasospasm (coronary vasodilation)

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19
Q

MOA of dihydropyridine

A

Ca2+ channel blockers

reduced afterload, coronary vasodilation

more potent vasodilators = reflex cardiac stimulation

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20
Q

dihydropyridines

A

nifedipine

felodipine

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21
Q

dihydropypridine effects

A

heart rate, myocardial contractility usually unchanged

AV node conduction unaffected

reduces MvO2 by reducing afterload

22
Q

when to use dihydropyridine-type?

A

In combination with ß-Blocker for coronary vasodilation, reduced afterload. (avoid Verapamil/Diltiazem + β-Blocker… AV block)

Sinus bradycardia, SA/AV block

Valvular Insufficiency (Aortic, Mitral): reduces afterload

23
Q

when to use non-dihydropyridine-type?

A

Asthma/Bronchospastic COPD (cannot use beta-blockers)

Severe Peripheral Vascular Disease with rest painDepression

Labile (variable glucose levels) insulin dependent diabetes

24
Q

MOA of antianginal effect of B-blockers

A

Reduce afterload (CNS)

Do not reduce preload (may paradoxically increase short term).

Do not prevent coronary vasospasm

25
Q

drug of choice of angina

A

B blockers

26
Q

Cardiac effects (β1AR) are responsible for therapeutic effects

A

reduce resting heart rate, myocardial contractility

attenuate increased heart rate, contractility in response to exercise

reduces myocardial oxygen consumption

27
Q

Non-cardiac effects (β2AR) are responsible for many adverse effects of β-blockers

A

Bronchospasm

Hypoglycemia

lethargy, confusion, nightmares

alopecia (hair loss)

28
Q

B Blocker contraindications

A

Sinus bradycardia

SA/AV block

decompensated CHF

Labile or “brittle”

Diabetes, Asthma

COPD

29
Q

what does withdraw from B blocker cause

A

rebound tachycardia, unstable angina or MI

30
Q

what B-blockers used for unstable angina

A

nitrates
aspirin
heparin

31
Q

B-blockers action on exertional angina

A

reduces HR

myocardial contractility

32
Q

action of B blocker on vasopastic angina

A

ineffective

33
Q

impact of B blocker on myocardial infarction

A

Reduce chest pain, ST elevation, cardiac enzyme elevation

Reduced Ventricular ectopy and ventricular fibrillation

Reduced reinfarction and ischemic episodes during hospitalization

Reduced mortality during 2-3 years following MI

34
Q

treatment plan for acute MI/Unstable Angina

A

ß-blocker IV following by PO therapy provided no CHF, hypotension, or sinus bradycardia/heart block

35
Q

MOA of Ranolazine (RANEXA®)

A

Partial fatty acid oxidase inhibitor, increasing glucose oxidation and efficiency of O2 utilization in the heart.

Late sodium current inhibitor with NO effect on HR or BP. It reduces sodium overload and hence ameliorates disturbed ion homeostasis.

36
Q

what is Ranolazine (RANEXA®)?

A

Novel metabolic modulator

37
Q

Ranolazine (RANEXA®) indications

A

chronic stable angina in combination with amlodipine, ß-blockers or nitrates`

38
Q

adverse of Ranolazine (RANEXA®)

A

Dizziness, headache, constipation, nausea

Syncope and asthenia

39
Q

contraindications Ranolazine (RANEXA®)

A

Concurrent use of CYP3A4 inhibitors (grape fruit juice, verapamil, diltiazem and others)

Use of tricyclic antidepressants, fluoxetine, Haldol, nefazodone

Digoxin concentrations increase 40-60% through p-glycoprotein inhibition.

Pregnancy category C.

Cost: expensive adjunct therapy with marginal benefit

40
Q

IC50

A

Ranolazine has the lowest IC50 in inhibiting late sodium current in the heart

41
Q

aspirin

A

provide after unstable angina or MI

reduces reinfarction and CHD death

reduces stroke

warfarin has comparable effect but is costly and has higher morbidity.

42
Q

T/F: All patients with CHD should receive aspirin therapy unless contraindicated

A

TRUE

43
Q

ACE inhibitors

A

Improve survival Post-MI with LV dysfunction (SAVE, AIRE, GISSI-3)

Reduces MI in high risk patients (HOPE study, Ramipril)

44
Q

revascularization

A

Surgical and interventional revascularization is an invaluable adjunct to treatment of medically refractory angina: including: coronary angioplasty, coronary atherectomy, intracoronary laser, coronary artery bypass grafting (CABG)

45
Q

thrombolytic therapy

A

results in myocardial salvage, reduction in mortality within first year following MI

46
Q

LDL reduction with HMG-RI

A

reduces recurrent MI

may acutely stabilize coronary plaque

47
Q

HDL raising/Triglyceride Lowering

A

reduces recurrent MI/CHD death (Helsinki, LRC-CPTT,VA-HIT) (gemfibrozil, niacin)

48
Q

MOA of nitrates

A 
coronary vasodilation 
reduced preload (venous) 
reduced afterload (aterial)
49
Q

MOA of nifedipine

A 
coronary vasodilation 
reduced afterload (aterial)
50
Q

MOA of non-dihydro-P

A

coronary vasodilation
reduced heart rate
decreased contractile force
reduced afterload (aterial)

51
Q

MOA beta-blocker

A

reduced heart rate
reduced contractile force
reduced afterload (aterial)

Pharmacology I (7 decks)

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