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Antiarrhythmic Drugs-Test-2-Questions

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Arrhythmia/Antiarrhythmic Drugs-Test-2-Questions

1. Cardiac Action potential: Phase 3: Repolarization

A K+ channels open --> outward (polarizing) current

B Na+ channels inactivate

C Net result = gain of Na+ and loss of K+ (imbalance is corrected by Na+/K+- ATPase)

D Voltage-sensitive Ca2+ channels close

E Voltage-sensitive Ca2+ channels open

2. Procaninamide is metabolized how?

A CYP 2D6

B CYP 3A4

C Partly acetylated to N-acetylprocainamide (NAPA) which prolongs duration of action potential (class
III)

D Partly acetylated to N-acetylprocainamide (NAPA) which Shortens duration of action potential (class
II)

3. Class I - fast channel blockers (Na+) Which drugs are class 1C?

A Flecainide,

B mexiletine

C procainamide,

D propafenone

E Quinidine,

4. Class 2 Antiarrythmics are B blockers like what?

A esmolol
B metoprolol,

C Pindolol

D propafenone

E Propranolol,

5. Cardiac Action potential: Phase 4: Resting potential

A --> Cell is brought to threshold of next action potential

B Increasing depolarization due to gradual increase in Na+ permeability

C K+ channels open

D Net result = gain of Na+ and loss of K+ (imbalance is corrected by Na+/K+- ATPase)

E Voltage-sensitive Ca2+ channels close

6. antiarrhythmic drugs by class : Class 4

A (b-blockers)

B (Ca2+ channel blockers)

C (K+ channel blockers)

D (Na+ channel blockers)

7. Miscellaneous antiarryhthmics are which drugs?

A adenosine,

B atropine,

C Digoxin,

D magnesium,

E Potassium chloride
8. Quinidine AE causes which of the following conditions?

A Dilated Cardiomyopathy

B PVCs

C SA & AV block or asystole

D torsades de pointes

E ventricular tachycardia (exacerbated by hyperkalemia)

9. Cardiac action potential : Phase 1: Initial repolarization

A --> transient outward current

B K+ channels rapidly open & close

C Na+ channels inactivate

D Na+ channels open

E Upstroke ends as Na+ channels are inactivated

10. Block fast inward Na+ channels • Decreased Na+ entry slows rate of rise of Phase 0 depolarization •
Cause in excitability and conduction velocity • Different properties depending on their affinity for Na+
channel • Possess use / state-dependence

A Anti Arrhythmic Class 1

B Anti Arrhythmic Class 2

C Anti Arrhythmic Class 3

D Anti Arrhythmic Class 4

11. cells discharging at abnormally high frequency are preferentially blocked Definition ?

A Na+ gated dependence

B Refractory dependence

C Use/state dependence
12. Quinidine, procainamide, disopyramide belong to what class of antiarrhythimics

A Class I : 1 A

B Class I : 1 B

C Class I : 1 C

13. • Quinidine sulfate = rapid oral absorption • Forms active metabolites (CYP 3A4) What does it
inhibit? (3)

A CYP 2D6

B CYP 3A4

C CYP 3E5

D CYP 4E3

E P-glycoprotein

14. Cinchonism (blurred vision, tinnitus, headache, psychosis) is caused by which of the following drugs?

A Disopyramide

B Esmmolol

C Losartan

D Procainamide

E Quinidine

15. Contraindications/ extreme caution for Quinidine?

A Chronic Renal Failure/ Bilateral renal stenosis

B Complete heart block/ Incomplete heart block

C History of Torsades de Pointes

D Myocarditis/ Severe myocardial damage


E Prolonged QT interval/ Uncompensated heart failure

16. Class 3 antiarrhytmics work by?

A Blocking the repol of K+ channels prolonging repol, and thus increasing QRS interval

B Blocking the repol of K+ channels prolonging repol, and thus increasing QT interval

C Blocking the repol of Na channels prolonging repol, and thus increasing QT interval

D Blocking the repol of Na+ channels prolonging repol, and thus increasing QRS interval

17. MOA of what drug? • Derivative of local anesthetic procaine • Similar actions to quinidine •
Blockade of Na + channels in activated state • Blockade of K + channels • Antimuscarinic properties

A Disopyramide

B Gonna die

C I'm boned

D Procainamide

E Quinidine

18. Contraindications for Procanimide (3)

A 3rd degree AV block

B Complete heart block/2nd degree AV block

C Systemic lupus erythematosus (SLE)

D Torsades de Pointes

19. Phase 0: Rapid upstroke & depolarization Cardiac action potential

A --> transient outward current

B -> Fast inward current

C K+ channels rapidly open & close


D Na+ channels open

E Upstroke ends as Na+ channels are inactivated

20. Strong negative inotropic effect Strong antimuscarinic properties • Causes peripheral
vasoconstriction • Blocks K+ channels Clinical Applications • Suppression of supraventricular and
ventricular arrhythmias Describes the MOA for which Class 1 Anti-arrhythmic?

A Disopyramide

B Esmolol

C Lostartan

D Procainamide

E Quinidine

21. Severe symptomatic ventricular arrhythmias, premature ventricular contraction or ventricular


tachycardia resistant to other therapy • Severe symptomatic supraventricular arrhythmias & prevention
of paroxysmal atrial fibrillation MOA for which antiarrhythmic

A amioderone

B Flecaninde

C Lidocaine

D Mexiletine

E Propafenone

22. Negative inotropic efffect (aggravates CHF) • CNS effects: dizziness, blurred vision, headache • GI
effects: nausea, vomiting, diarrhea • Life-threatening arrhythmias & ventricular tachycardia Describes
the AE of which Class 1C anti arrhythymic

A Flecainide

B Lidocaine

C Mexiletine

D Propafenone
23. Flecainide, propafenone belong to what class of antiarrhythimics

A (IA)

B (IB)

C (IC)

24. Clinical Applications • Suppression of supraventricular and ventricular arrhythmias Due to


proarrhythmic effects use should be reserved for life-threatening arrhythmias What anti-arrhythmic ?

A Disopyramide

B Procainamide

C Quinidine

25. antiarrhythmic drugs by class : Class 1

A (b-blockers)

B (Ca2+ channel blockers)

C (K+ channel blockers)

D (Na+ channel blockers)

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