FPGEE Review Exam Questions with Correct Answers
In FAST response fibers - Electrolyte involved in phase 0 - AnswerNa+ influx
/.In FAST response fibers - Electrolyte involved in phase 2 - AnswerCa+ influx, K+
outflux plateau
/.In FAST response fibers - Electrolyte involved in phase 3 - AnswerK+ outflux (Ca+
drops off) rapid repolarization
/.In SLOW response fibers - Electrolyte involved in phase 0 - AnswerCa+(few Na+
channels in Nodal fibers)
/.In SLOW response fibers - Electrolyte involved in phase 3 - AnswerK+ outflux
repolarization
/.In SLOW response fibers - Electrolyte involved in phase 4 - Answer"Mainly Na+ (This
is the pacemaker current) aarapim. "
/.Ectopic rhythm can result from - Answerischemia, electrolyte abnormalities, or
heightened sympathetic tone
/.If an early afterdepolarization is sustained - Answertorades de pointes (QRS
complexes of varying amplitudes)
/.ECG of a patient with an accessory pathway (bundle of Kent) - Answer"Wide QRS
complexes, early ventricular upstroke (also predisposed to re-entry loops) (Wolff
Parkinson White (WPW) syndrome) wolff-parkinson-white-accessory-bundle-bundle-of-
Kent "
/.MOA of quinidine - AnswerBlocks (open-activated) Na+ channels: In SA Nodal tissue -
Shift to a more positive threshold and decrease the pacemaker slope (phase 4), In
Ventricular tissue - Decreases the phase 0 slope (depolarization) and block K+
channels prolongs repolarization (longer refractory period protected from reentry
currents): Anticholanergic (vagolytic effect faster conduction through AV node)
/.Indications of quinidine - Answer"atrial flutter or fibrillation maintain normal sinus
rhythm,Paroxysmal supraventricular tachycardia, Premature atrial or ventricular
contractions, paroxysmal AV junctional rhythm 9"
/.When taking this drug patients must be monitored for lupus (with ANA) -
AnswerProcainamide
,/.Take with quinidine to prevent rapid ventricular response in patient with atrial flutter -
Answerβ-blocker or Ca2+ channel blocker
/.Which 1A antiarrhythmic for a patient on digoxin - AnswerProcainamide (doesn't alter
digoxin levels)
/.MOA of Lidocaine and Phenytoin - Answer( 1B) block of voltage-gated Na+ in
ventricular myocytes (decrease phase 0 upstroke)
/.MOA of Encainide, Flecainide, Moricizine, Propafenone - Answer( 1C) block of
voltage-gated Na+ channelsin ventricular myocytes
/.MOA of Propranolol, Atenolol, Metoprolol... - Answer( ) block β1-adrenergic receptors
SLOW SA and AV nodal activity,(decreases phase 4 slope)
/.MOA of Ibutilide, Dofetilide, Sotalol, Amiodarone - Answer( I) Block K+ channels longer
action potential plateau and prolonged repolarization
/.MOA of Verapamil, Diltiazem - Answer( IV) Ca2+ channel blocker slows action
potential upstroke in SA and AV nodes
/.This 1A drug is associated with the development of Lupus, hematotoxicity, but less
likely to cause torsades - Answerprocainamide
/.Antiarrhythmics of choice for post ischemic insults - Answer1B
/.Drug used for Supraventricular tachycardias, and post-MI prophylaxis -
Answerantiarrhythmics (β-blockers)
/.What does Quinidine do to AV node - Answerincreases conduction velocity (via
anticholinergic effects)
/.This 1A drug is meolized to a meolite with a pure I effect (prolonging refractory,
lengthening QT interval) - AnswerProcainamide
/.DOC or ventricular arrhythmias in ER situations (like in MI) - AnswerLidocaine
/.LidocaineMexiletine should be (increased or decreased) in patients with drug inducible
P0 - Answerincreased
/.Moderate Na+ channel block decrease phase 0, and prolonged repolarization ( 1A, 1B
or 1C) - Answer1A
/.Mild Na+ channel block slight pahse 0 slope decrease, shortened repolarization( 1A,
1B or 1C) - Answer1B
,/.Marked Na+ channel block severe decreased in phase 0 slope, No change in
repolarization ( 1A, 1B or 1C) - Answer1C
/.This drug can worsen the arrhythmia in patients with pre-existing ventricular
tachyarrythmias and those with a history of MI - AnswerFlecainide (a 1C)
/.Drug used when other measure fail to help life threatening paroxysmal
supraventricular or vventricular arrhythmias - AnswerFlecainide (a 1C)
/.MOA of β1-blockers - Answerblock sympathetic input to AV (and SA nodes) decrease
the rate of phase 4 depolarization (pacemaker current), prolong repolarization
/.Non-selective β1 and β2 blockers that DO NOT prolong repolarization - AnswerFirst
generation β-blockers (Propranolol, Nadolol, Timolol) and carvedilol and labetalol
/.Β-blocker also used for glaucoma - AnswerTimolol
/.This β-blocker can cause liver damage - Answerlabetalol
/.These β-blockers cause vasodilationvia α1-blockage - AnswerCarvedilol and labetalol
/.Selective β1-blocker with a very short half-life - AnswerEsmolol
/.Used in ER treatment to block β in thyroid storm - Answeresmolol
/.A selective β1-blocker and selective β2-agonist - Answerceliprolol
/.MOA of K+ channel blockers - AnswerI antiarrhythmics lengthen the plateau (phase 2)
and prolong repolarization
/.Lengthening the plateau phase does what (in I) - Answerincreases the refractory
period (prevents re-entry), On the bad side: increases likely-hood of afterdepolarizations
and torsades de pointes
/.Drug for conversion of atrial flutter - Answerquinidine, ibutilide, dofetilide
/.of amiodarone - AnswerMainly I, but has effects in all es
/.Unique MOA of amiodarone - Answeralters lipid membrane where ion channela and
receptors are located
/.The most dreaded complication of Amiodarone - AnswerPneumonitis leading to
pulmonary fibrosis
/.Amiodirone can exert an negative inotropic effect how - Answerinhibiting β-receptors
, /.Why do Ca2+ channel blockers act preferentially on nodal tissue - AnswerBecause the
pacemaker current depend on Ca2+
/.Major effect of Ca2+ blockers - Answerslow the action potential upstroke in AV nodal
tissue
/.This Ca2+-blocker has a greater effect in vascular smooth muscle - Answernifedipine
(a dihydropyridine)
/.IV drug used to treat hypertension and prinzmental angina - AnswerVerapamil
/.Taking a Ca2+-blocker with a β-blocker can result in - Answerheart failure, irreversible
electromechanical dissociation
/.Indication for Ranolazine - Answerchronic sle angina (MOA seems to involve late Na+
current)
/.MOA of adenosine - Answeropens G protein-coupled K+ channel inhibits AV nodal
conduction (also atrial, and SA condution): also suppresses Ca2+-dependant action
potentials
/.Indications for adenosine - Answerfirst-line agent for converting narrow paroxysmal
supraventricular tachycardia to normal SA rhythm
/.Time it takes for amount of drug to fall to half of its value, constant in first order kinetics
(majority of drugs) - AnswerHalf-lafe (T)
/.Inhibitors of CYP0 - AnswerCimetidine, ketoconazole, erythromycin, isoniazid, and
grapefruit
/.Ability of a drug to produce a biologic effect - AnswerEfficacy
/.Mechanism of action (MOA) utilizes intracellular receptors - Answer"Thyroid and
steroid hormones 03_Binding_of_Lipid-Soluble_Hormones. "
/.MOA utilizes transmembrane receptors - Answer"Insulin loadBinary_3 "
/.Antidote used for organophosphateanticholinesterase poisoning - AnswerAtropine,
pralidoxime (2-P)
/.Antidote used for warfarin toxicity - AnswerVitamin K and fresh frozen plasma (FFP)
/.Antidote used for opioid toxicity - AnswerNaloxone (IV), naltrexone (PO)
/.Antidote used for benzodiazepine toxicity - AnswerFlumazenil