USA Pharm 578 Exam 4
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Chapter 18 HYPERTHYROIDISM antihyper/diuretics (45 &51) exam #2... 320 exa
52 terms Teacher 51 terms 217 terms 96 terms
kaitlyncook13 Preview P maite_avila Preview barkbark126 Preview tsio
major contraindication for use of quinidine hx of long QT syndrome or drug-induced torsades
paroxysmal AF definition AF that terminates spontaneously or with intervention within 7 d of onset
persistent AF definition continuous AF that is sustained > 7 d
long-standing persistent AF continuous AF sustained > 7 d
permanent AF when pt and clinician make decision to stop further attempts to restore and/or
maintain sinus rhythm
nonvalvular AF AF in absence of rheumatic mitral stenosis, a mechanic or biosynthetic heart valve,
or mitral valve repair
ADRs of cinchonism tinnitus, headache, dizziness, confusion
Explain the total body clearance of procainamide procainamide (PA) is cleared about 50% renally (as the unchanged drug) and 50%
by hepatic metabolism
how the major metabolite NAPA is formed -the principal metabolite is N-acetylprocainamide (NAPA) formed by acetylation
(conjugation) in the liver
-fast acetylators have higher levels of NAPA
pharmacologic actions of NAPA active metabolite NAPA contributes to the overall antiarrhythmic activity by
exerting Class III effects; may be responsible for production of torsades when it
accumulates in renal failure patients
State the drug which is the most frequent cause of drug- Procainamide - most frequent cause of drug-induced lupus (10-30% incidence on
induced lupus long-term use)
, Describe the activity of lidocaine against AF or atrial ineffective vs. AF and Aflutter
flutter
Describe the activity of lidocaine against nonsustained VT a. acute management of ventricular arrhythmias occurring during cardiac
manipulation or in relation to acute
MI
b. conversion of nonsustained VT to NSR
lidocaine antiarrhythmic class Ib--Na+ channel blocker
State the major ADR of flecainide and the limitations this -ADR--inc incidence of SCD or non-fatal cardiac arrest; proarrhythmic effects in
places on its clinical use pts w/ AF/Aflutter
-DUE TO PROARRHYTHMIC EFFECTS, USE OF FLECAINIDE IS UNACCEPTABLE
IN
PATIENTS WHOSE ARRHYTHMIAS ARE NOT LIFE-THREATENING
State the indications for propafenone a. documented life-threatening ventricular arrhythmias
b. in patients without structural heart disease, propafenone prolongs the time to
recurrence of PAF
(paroxysmal atrial fibrillation/flutter) and PSVT associated with disabling
symptoms
Explain the mechanisms which account for the action of 1. controls ventricular rate response in AF by slowing AV conduction:
Class II antiarrhythmics a. increases the refractory period of the AV node
b. decreases conduction velocity through the AV node
2. depresses phase 4 depolarization (automaticity) of the SA node
why are class II antiarrhythmics advantageous in these drugs have the best potential to control ventricular rate in pts whose AF is
thyrotoxicosis? due to enhanced sympathetic activity as in thyrotoxicosis
State the indications for esmolol and describe its duration a. rapid control of ventricular rate in AF or AFlutter in circumstances where short-
of action term ventricular rate control is needed
b. noncompensatory sinus tachycardia where rapid heart rate requires
intervention
Describe the effects of amiodarone on the APD, ERP, i. prolongs the APD (through blockade of potassium channels, Class III effects)
automaticity, conduction velocity, and AV nodal and ERP of all
conduction time. cardiac excitable tissue; increases QRS width and prolongs the QT interval and the
JT interval
(QT - QRS)
ii. decreases the slope of diastolic depolarization and the sinus discharge rate by
20-30%; very
strong inhibitor of both normal and abnormal automaticity
iii. decreases conduction velocity in all cardiac tissues and increases AV nodal
conduction time
ADR of amiodarone -pulmonary fibrosis
-hypothyroidism
-bradycardia or heart block in preexisting SA or AV nodal dz
-proarrhythmic effects can exacerbate Vtach and may cause torsades
-skin (photodermatitis, pigmentation)
Save
Students also studied
Chapter 18 HYPERTHYROIDISM antihyper/diuretics (45 &51) exam #2... 320 exa
52 terms Teacher 51 terms 217 terms 96 terms
kaitlyncook13 Preview P maite_avila Preview barkbark126 Preview tsio
major contraindication for use of quinidine hx of long QT syndrome or drug-induced torsades
paroxysmal AF definition AF that terminates spontaneously or with intervention within 7 d of onset
persistent AF definition continuous AF that is sustained > 7 d
long-standing persistent AF continuous AF sustained > 7 d
permanent AF when pt and clinician make decision to stop further attempts to restore and/or
maintain sinus rhythm
nonvalvular AF AF in absence of rheumatic mitral stenosis, a mechanic or biosynthetic heart valve,
or mitral valve repair
ADRs of cinchonism tinnitus, headache, dizziness, confusion
Explain the total body clearance of procainamide procainamide (PA) is cleared about 50% renally (as the unchanged drug) and 50%
by hepatic metabolism
how the major metabolite NAPA is formed -the principal metabolite is N-acetylprocainamide (NAPA) formed by acetylation
(conjugation) in the liver
-fast acetylators have higher levels of NAPA
pharmacologic actions of NAPA active metabolite NAPA contributes to the overall antiarrhythmic activity by
exerting Class III effects; may be responsible for production of torsades when it
accumulates in renal failure patients
State the drug which is the most frequent cause of drug- Procainamide - most frequent cause of drug-induced lupus (10-30% incidence on
induced lupus long-term use)
, Describe the activity of lidocaine against AF or atrial ineffective vs. AF and Aflutter
flutter
Describe the activity of lidocaine against nonsustained VT a. acute management of ventricular arrhythmias occurring during cardiac
manipulation or in relation to acute
MI
b. conversion of nonsustained VT to NSR
lidocaine antiarrhythmic class Ib--Na+ channel blocker
State the major ADR of flecainide and the limitations this -ADR--inc incidence of SCD or non-fatal cardiac arrest; proarrhythmic effects in
places on its clinical use pts w/ AF/Aflutter
-DUE TO PROARRHYTHMIC EFFECTS, USE OF FLECAINIDE IS UNACCEPTABLE
IN
PATIENTS WHOSE ARRHYTHMIAS ARE NOT LIFE-THREATENING
State the indications for propafenone a. documented life-threatening ventricular arrhythmias
b. in patients without structural heart disease, propafenone prolongs the time to
recurrence of PAF
(paroxysmal atrial fibrillation/flutter) and PSVT associated with disabling
symptoms
Explain the mechanisms which account for the action of 1. controls ventricular rate response in AF by slowing AV conduction:
Class II antiarrhythmics a. increases the refractory period of the AV node
b. decreases conduction velocity through the AV node
2. depresses phase 4 depolarization (automaticity) of the SA node
why are class II antiarrhythmics advantageous in these drugs have the best potential to control ventricular rate in pts whose AF is
thyrotoxicosis? due to enhanced sympathetic activity as in thyrotoxicosis
State the indications for esmolol and describe its duration a. rapid control of ventricular rate in AF or AFlutter in circumstances where short-
of action term ventricular rate control is needed
b. noncompensatory sinus tachycardia where rapid heart rate requires
intervention
Describe the effects of amiodarone on the APD, ERP, i. prolongs the APD (through blockade of potassium channels, Class III effects)
automaticity, conduction velocity, and AV nodal and ERP of all
conduction time. cardiac excitable tissue; increases QRS width and prolongs the QT interval and the
JT interval
(QT - QRS)
ii. decreases the slope of diastolic depolarization and the sinus discharge rate by
20-30%; very
strong inhibitor of both normal and abnormal automaticity
iii. decreases conduction velocity in all cardiac tissues and increases AV nodal
conduction time
ADR of amiodarone -pulmonary fibrosis
-hypothyroidism
-bradycardia or heart block in preexisting SA or AV nodal dz
-proarrhythmic effects can exacerbate Vtach and may cause torsades
-skin (photodermatitis, pigmentation)
