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CV II Exam 3 > Anti-anginal agents > Flashcards

Anti-anginal agents Flashcards

1
Q

Chronic coronary artery disease medications

A 
Aspirin
B blockers
Nitrates
CCBs
ACEIs
Ranolazine
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2
Q

Acute coronary syndrome medications

A

Aspirin
B blockers
Nitrates

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3
Q

If patient has unstable angina or NSTMI add medications

A 
Heparin
Gp IIa-IIIb antagonist
ADP receptor antagonist
or
Bivalirudin
ADP receptor antagonist
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4
Q

If patient has STMI with thrombolysis add medications

A

Thrombolytic agent
Heparin
ADP receptor antagonist

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5
Q

If patient has STMI with angioplasty add medications

A 
Heparin
Gp IIa-IIIb antagonist
ADP receptor antagonist
or
Bivalirudin
ADP receptor antagonist
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6
Q

Post MI medications

A

Statin
ACEI
Aldosterone receptor antagonist

Continue aspirin and ADP receptor antagonist

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7
Q

Angina pectoris

A

Primary symptom of ischemic heart disease

Temporary and reversible imbalance between myocardial O2 supply and demand

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8
Q

Usual underlying cause of angina

A

CAD

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9
Q

Increase demand on heart seen with

A

Increase HR, ventricular contraction and wall tension

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10
Q

Decrease O2 supply seen with

A

Decrease coronary blood flow, and O2 carrying capacity of blood (or both)

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11
Q

How does angina feel to patient?

A

Heavy pressing substernal discomfort

Often radiating to left shoulder, flexor aspect of left arm, jaw, or epigastrium

Women, elderly, and diabetes most likely to have atypical symptoms

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12
Q

Typical angina

A

Usually fixed atherosclerotic narrowing of an epicardial coronary artery on which exertion or emotional stress superimposes an increase in myocardial O2 demand

Angina induced by exercise, relieved by rest and/or nitro and lasts no longer than 15 min with 5 - 15 episodes per week

ST segment depression

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13
Q

Atypical angina

A

Angina at rest
Also called Variant, Vasospastic, or Prinzmetal’s
Focal or diffuse coronary vasospasm episodically reduces coronary flow
Transient ST segment elevation during angina

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14
Q

Unstable angina

A

Rupture of an atherosclerotic plaque, with consequent platelet adhesion and aggregation leading to decrease coronary blood flow

Abrupt decreases in blood flow due to thrombus or embolus signals impending MI

If symptoms not relieved by 3 NTG tablets within 15 minutes should call 911 or get to nearest ED immediately

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15
Q

Pathophysiology of angina

A

O2 supply available to the heart is significantly lowered
O2 demands of exertional situations can no longer be met
Autoregulatory mechanisms usually fail to mitigate this imbalance

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16
Q

Agents decreasing O2 demand

A

B blockers and some CCBs (HR and contractility)

Nitrates and CCBs (Preload and afterload)

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17
Q

Agents increasing O2 supply

A

Vasodilators (especially CCBs)

Also statins and antithrombins

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18
Q

Therapeutic approach to angina

A

Increase oxygen supply

Decrease oxygen demand

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19
Q

Increasing oxygen supply difficult with

A

Atherosclerotic plaque

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20
Q

Exertion angina therapeutic approach

A

Decrease work on heart

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21
Q

Unstable angina therapeutic approach

A

Decrease work and increase blood flow

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22
Q

Prinzmetal’s angina therapeutic approach

A

Relax the vasculature

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23
Q

Treatment of typical angina

A

Decrease demand by decreasing HR, contractility and wall tension

Initial therapy:
B blocker and aspirin
B blocker and aspirin and long-acting nitrate

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24
Q

When to use clopidogrel for typical angina

A

When aspirin is contraindicated

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25
Q

When to use ACEIs for typical angina

A

Diabetes or left ventricular dysfunction

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26
Q

When to use CCB DHPs or long-acting nitrates for typical angina

A

When initial therapy with B blocker is contraindicated, not successful, or leads to unacceptable side effects

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27
Q

Treatment of unstable angina

A

Unstable angina can lead to MI
**MONA

Add B blocker unless contraindicated
If B blocker contraindicated use verapamil or diltiazem if no LV dysfunction

Increase blood flow - antiplatelet agent (aspirin)

Add heparin to decrease thrombus

Percutaneous coronary interventions - Angioplasty and stents
Coronary bypass grafts (cabbage)

Thrombolytics (Alteplase, Reteplase, Tenecteplase, Streptokinase)

28
Q

Organic nitrate mechanism

A

Prodrugs that are sources of nitric oxide -> vasodilation

Increase NO -> increase cGMP -> increase removal of PO4 from Myosin -> relaxation

29
Q

Pharmacodynamics of organic nitrates

A

Decrease both preload and afterload
Relax vascular smooth muscle (V>A)
Decrease venous return, preload, **O2 demand, afterload
Directly dilate coronary arteries, especially subendocardial regions compressed during systole
Transient increase in oxygen supply
Prevent coronary vasospasm

30
Q

How should NTG be administered

A

Sublingual
Miss first pass effect
Needs to be converted to NO first

31
Q

Nitroglycerin (NTG)

A

Nitro

Several routes of administration

32
Q

Isosorbide dinitrate

A

Long acting

33
Q

Isosorbide-5-mononitrate

A

Long acting

34
Q

Adverse effects of nitrates

A

Headaches, facial flush, dizziness

Orthostatic hypotension - alcohol worsens

35
Q

Tolerance of NTG

A

Effectiveness diminishes significantly with continued use
Limitation to therapy

Loss of capacity to convert to NO?

36
Q

Drug holidays

A

Can alleviate effects of tolerance

37
Q

Contraindications of nitrates

A

Acute MI - right ventricular infarction

Patients on erectile dysfunction drugs - potentially dangerous fall in BP

38
Q

Increased intracellular contraction in SM

A

Ca++ -> calmodulin ->MLCK -> add PO4 to myosin -> contraction

39
Q

CCB and SM contraction

A

Block increase in calcium
Bind L-type calcium channels

Block contraction = dilation (mostly arterioles)

40
Q

CCBs with prominent cardiac effects

A

Non-DHPs

Verapamil and Diltizem

41
Q

CCBs with prominent arteriolar vasodilation effects

A

DHPs

Nifedipine, Amlodipine, Felodipine, Isradapine, Nicardipine, Nisoldipine, Nimodipine

42
Q

PD of CCB in angina

A

Relax arteriolar SM
Decrease afterload -> decrease O2 demand

Dilation of coronary arteries = increase O2 supply

43
Q

CCB and cardiac cells

A

Calcium binding to troponin allows for contraction
Calcium involved in conduction through slow channels

CCBs have negative ionotropic effect but reflex tachycardia from decreased BP negates effects

44
Q

CCB and SA/AV Nodes

A

Depolarization is through Ca channels
All CCBs block channels but only non-DHPs effect recovery and frequency

Non-DHPs decrease rate of SA firing and decrease AV nodal conduction

45
Q

Supraventricular tachycardias

A

Treat with Non-DHP CCBs

46
Q

CCB and hemodynamic effects

A

Decrease coronary vascular resistance and increase coronary blood flow

47
Q

DHP CCB hemodynamic effects

A

More potent vasodilators
Decrease arterial pressure, reflex increase HR and contractility, CO increase, ventricular function improved, peripheral blood flow improved, venous tone unchanged

48
Q

Non-DHP CCB hemodynamic effects

A

Verapamil - reflex tachycardia due to arterial dilation is blunted by direct negative inotropic effect
Diltiazim - less negative HR

49
Q

PK of CCBs

A

Good oral absorption but high 1st pass effect
Amlodipine, felodipine, isradipine slowly absorbed, with long half life
Verapamil sometimes used IV

50
Q

Adverse effects of CCBs

A

**Constipation (Verapamil)
Peripheral edema, coughing, wheezing, pulmonary edema
Excessive vasodilation - dizziness, hypotension, headache, flushing, nausea
Coronary steal with angina

51
Q

Contraindications of CCBs

A

Use with B blocker - potential AV block

Should not be used in patients with ventricular dysfunction, SA or AV nodal conduction defects and systolic BP < 90 mmHg

52
Q

B blockers in anginal therapy

A

Major - decrease HR
Minor - decrease contractility
(decrease work and O2 demand)

Long term - decrease peripheral resistance

53
Q

Ideal B blockers for anginal therapy

A

Atenolol, Metoprolol

54
Q

Cheap B blockers for anginal therapy

A

Propranolol

55
Q

B blockers in chronic stable angina

A

Monotherapy for mild to moderate angina of effort
Combination therapy with long acting nitrate or DHP CCB
Always after MI

56
Q

What angina cannot be treated with B blocker?

A

Vasospasm - Prinzmetal’s

57
Q

Limitations to using B blocker for chronic stable angina

A

Bradyarrhythmias or AV block
Compensated congestive heart failure
Asthmatics and diabetics use with extreme caution

58
Q

Antiplatelet agent for angina

A

Aspirin
Decrease mortality in patients with unstable angina - reduce MI and death
Inhibit platelet aggregation that would lead to MI

59
Q

Sufficient dose of aspirin

A

85-325 mg per day

60
Q

Aspirin mechanism

A

Blocks production of prostaglandins
Irreversibly inhibits cyclooxygenase
Platelets have no nuclei and cannot produce new cyclooxygenase

61
Q

Clopidogrel

A

Plavix
Blocks ADP receptor binding mediated activation of GPIIa/IIIb complex
Irreversible, long-term inhibition of platelet aggregation
Useful for unstable angina, prophylaxis and treatment of TIA and completed stroke
Treatment for stent placement

62
Q

Drugs used during angioplasty

A

Abciximab - Monoclonal antibody against glycoprotein IIb/IIIa receptor
Tirofiban and eptifibatide inhibit ligand binding to IIb/IIIa receptor

Treatment of unstable angina when angioplasty or atherectomy planned within 24 hrs

63
Q

Acute prophylaxis and treatment of single anginal attacks

A

NTG

Onset: 1-3 min, duration: 20-30 min

64
Q

Maintenance therapy of chronic stable angina

A

B blockers, CCBs, or long duration nitrates

or combination

65
Q

Vasospastic angina

A

CCBs or nitrates

CV II Exam 3 (13 decks)

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