Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacology I > Anti-Anginal > Flashcards

Anti-Anginal Flashcards

(51 cards)

Start Studying
1
Q

what is angina

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

types of angina

A

unstable
variant
exertional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is exertional angina

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

adverse effects of nitrates

A

hypotension
headache
drug rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

contraindication of nitrates

A

Do not take Sildenafil with Nitrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

recommended dose of nitrate

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MOA of non-dihydropyridine

A

Ca2+ channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Non-dihydropyridine

A

Verapamil

Diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

MOA of dihydropyridine

A

Ca2+ channel blockers

reduced afterload, coronary vasodilation

more potent vasodilators = reflex cardiac stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

dihydropyridines

A

nifedipine

felodipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

dihydropypridine effects

Study These Flashcards
A

heart rate, myocardial contractility usually unchanged

AV node conduction unaffected

reduces MvO2 by reducing afterload

22
Q

when to use dihydropyridine-type?

Study These Flashcards
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?

Study These Flashcards
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

Study These Flashcards
A

Reduce afterload (CNS)

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

Do not prevent coronary vasospasm

25
drug of choice of angina
B blockers
26
Cardiac effects (β1AR) are responsible for therapeutic effects
reduce resting heart rate, myocardial contractility attenuate increased heart rate, contractility in response to exercise reduces myocardial oxygen consumption
27
Non-cardiac effects (β2AR) are responsible for many adverse effects of β-blockers
Bronchospasm Hypoglycemia lethargy, confusion, nightmares alopecia (hair loss)
28
B Blocker contraindications
Sinus bradycardia SA/AV block decompensated CHF Labile or "brittle" Diabetes, Asthma COPD
29
what does withdraw from B blocker cause
rebound tachycardia, unstable angina or MI
30
what B-blockers used for unstable angina
nitrates aspirin heparin
31
B-blockers action on exertional angina
reduces HR | myocardial contractility
32
action of B blocker on vasopastic angina
ineffective
33
impact of B blocker on myocardial infarction
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
treatment plan for acute MI/Unstable Angina
ß-blocker IV following by PO therapy provided no CHF, hypotension, or sinus bradycardia/heart block
35
MOA of Ranolazine (RANEXA®)
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
what is Ranolazine (RANEXA®)?
Novel metabolic modulator
37
Ranolazine (RANEXA®) indications
chronic stable angina in combination with amlodipine, ß-blockers or nitrates`
38
adverse of Ranolazine (RANEXA®)
Dizziness, headache, constipation, nausea Syncope and asthenia
39
contraindications Ranolazine (RANEXA®)
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
IC50
Ranolazine has the lowest IC50 in inhibiting late sodium current in the heart
41
aspirin
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
T/F: All patients with CHD should receive aspirin therapy unless contraindicated
TRUE
43
ACE inhibitors
Improve survival Post-MI with LV dysfunction (SAVE, AIRE, GISSI-3) Reduces MI in high risk patients (HOPE study, Ramipril)
44
revascularization
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
thrombolytic therapy
results in myocardial salvage, reduction in mortality within first year following MI
46
LDL reduction with HMG-RI
reduces recurrent MI | may acutely stabilize coronary plaque
47
HDL raising/Triglyceride Lowering
reduces recurrent MI/CHD death (Helsinki, LRC-CPTT,VA-HIT) (gemfibrozil, niacin)
48
MOA of nitrates
``` coronary vasodilation reduced preload (venous) reduced afterload (aterial) ```
49
MOA of nifedipine
``` coronary vasodilation reduced afterload (aterial) ```
50
MOA of non-dihydro-P
coronary vasodilation reduced heart rate decreased contractile force reduced afterload (aterial)
51
MOA beta-blocker
reduced heart rate reduced contractile force reduced afterload (aterial)

Pharmacology I (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions