Exam (elaborations)
FPGEE Review Test Questions and Answers 2024
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Exam of 115 pages for the course FPGEE at FPGEE (FPGEE Review Test)
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FPGEE Review TestIn 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)
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