Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Pharmacology > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

What is a general class side effect to be aware of?

A
  • several different effects on AP generation and propagation –> may affect autonomic NS**
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why does TdP result? When is it most commonly seen?

A

TdP results from QT prolongation (d/t blockade of K current)

MC with hypokalemia, hypomagnesemia, bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the physio behind each Vaughan-Williams class?

A

I: modulate or block Na+ channels

II: inhibit sympathetic activity

III: block K+ channels

IV: block Ca2+ channels

Other: digoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What drugs are in Class I?

A

Modulate or block Na+ channels

Ia: quinidine, procainamide, disopyramide

Ib: lidocaine, mexiletine

Ic: flecainide, propafenone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What drugs are in Class II?

A

Inhibit sympathetic activity

B-blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What drugs are in Class III?

A

Block K+ channels

  • sotalol
  • dofetilide
  • ibutilide
  • amiodarone
  • dronedarone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What drugs are in Class IV?

A

Block Ca2+ channels

  • verapamil
  • diltiazem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are “class” interactions?

A
  • careful w/other QT prolongers
  • most metabolized by 3A4 or 2D6
  • drugs causing hypokalemia or hypomagnesemia (loop diuretics) INC risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are “class” ADRs?

A

Dysrhythmia

  • QT prolongation / proarrhythmic potential
  • careful with brady and heart blocks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Quinidine syncope?

A

Recurrent lightheadedness and fainting secondary to self-terminating TdP

[drug] usually normal or even subtherapeutic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is cinchonism and which drug is it related to with high concentrations?

A

Quinidine

Dry as a bone (urinary retention) 
Red as a beet (vascular flushing) 
Blind as a bat (blurred vision) 
Mad as a hatter (delirium, psychosis) 
Hotter than hell (anhidrosis, hot skin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are two ADRs of procainamide?

A
  1. Reversible lupus-like syndrome**

2. potentially severe bone marrow suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What ADRs are related to disopyramide?

A

Anticholinergic, esp urinary retention

- careful w/glaucoma and BPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What ADRs are related to Mexiletine?

A

CNS tox

  • dizzy, lightheaded, unsteady gait
  • tremor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What ADRs are related to Lidocaine?

A

CNS tox

  • tremor MC
  • seizure possible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What ADRs are related to Flecainide?

A

** mostly proarrhythmic –> make sure K is normal **

BBW: do not use in pt w/h/o AMI

** need echo to ensure structurally normal heart **

17
Q

What ADRs are related to Propafenone?

A
  • dysguesia (altered taste)
  • lupus-like reaction

** BBW - need echo to ensure structurally normal heart **

18
Q

Sotalol interactions?

A

Avoid concurrent B-blockers and CCBs

Has some b-blocking activity (same precautions)

19
Q

What is ibutilide main ADR?

A

proarrhythmic activity

20
Q

What is Dofetilide main ADR?

A

** dysrhythmia is problematic - death possible **

start med in hospital

21
Q

What are two specifics related to Amiodarone chemistry?

A
  • Iodine containing compound (like thyroxine)

- highly lipid soluble and very long half life (55 days)

22
Q

What are Amio clinical indications?

A

FDA: life threatening recurrent VF or hemodynamically-unstable VT (ACLS)

Common unlabeled: A-fib

  • AF pharm cardioversion
  • AF prophylaxis following open heart surgery
  • Recurrent AF
23
Q

Describe the Pk Interactions of Amio?

A

3A4 substrate
** inhibits multiple isoenzymes moderately**

Pgp substrate & inhibitor
- may INC [digoxin] for up to 3 mo

24
Q

Describe the Pd interactions of Amio?

A
  • additive QTc drugs
  • additive AV block/bradycardia
  • drugs that induce INC K or Mg
25
Q

** Review all interaction alerts closely for Amio **

What are the five examples given?

A
  1. DEC warfarin dose
  2. DEC PO digoxin
  3. Avoid with HCV drugs
  4. Avoid macrolides, FQ, fluconazole
  5. Careful w/statin (use rosuva)
26
Q

What are the ADRs of Amio?

A
  1. Pulm
    - IPF –> ARDs (interstitial infiltrates on imaging)
  2. Thyroid (hypo)
  3. Ocular
    - corneal microdeposits
    - optic neuropathy/neuritis
  4. Derm
    - photosensitivity
    - bluish skin discoloration
  5. CNS
    - gait, ataxia, dizzy, memory, peripheral neuropathy
  6. Cardiac
    - brady, AV nodal block
27
Q

How does Dronedarone compare and contrast to Amiodarone?

A

Some MOA but

  • non-iodinated analog
  • shorter half life and less tissue accumulation

Clinical:
- AF, a flutter [less effective at maintaining NSR compared to amio]

28
Q

Who is Dronedarone C.I. in?

A
  1. HF class IV or II-III w/recent decompensation
  2. Pt who cannot stay in NSR
  3. 2/3 deg AV block
  4. SSS
  5. Brady pt
29
Q

What are 4 drug interactions to be aware of with Dronedarone?

A
  1. strong 3A4 substrate; moderate 3A4/2D6 inhibitor (remember Metoprolol, statins)
  2. Pgp inhibitor (remember digoxin)
  3. QTc prolonger
  4. Elevated INR with Warfarin**
30
Q

What ADRs are related to Dronedarone?

A

Initial

  • NVD
  • photosensitivity (not blue though)

Emerging
- acute liver, renal failure, exacerbation of HF

31
Q

Digoxin has 2 MOA depending on clinical use. What is it for HF? SV arrhythmias?

A

HF

  • reversible inhibition of Na/K ATPase results in INC intracellular Ca
  • increased contractility

SV arrhythmias

  • INC vagal tone
  • DEC conduction through SA, AV nodes
32
Q

What are the two clinical uses of digoxin?

A
  1. Advanced systolic HF
    - does not alter mortality**
  2. 2nd line for AF in HF pts
33
Q

What are three general things to monitor while on digoxin?

A
  • ECGs (baseline, periodic)
  • SCr - renal excretion (baseline, periodic)
  • Cations
34
Q

How can bile acid sequestrants affect digoxin?

A

Bile acid sequestrants may bind and impair absorption of digoxin**

35
Q

How might acute dig tox manifest?

A

Cardiac (greatest concern)**

  • PVCs**
  • various degrees of AV nodal blockade**
  • other electrical problems

GI: anorexia, NV, abd pain
Neuro: confusion, weakness

36
Q

How might chronic dig tox manifest?

A
  • more difficult to dx, sxs develop over days to months

** cardiac effects (rhythm disturbances) - greatest concern **

Neuro: lethargy, delirium, weak

** visual changes - color vision, development of scotomas, blindness **

37
Q

How do you diagnose Dig Tox?

A

Clinical manifestations + ECG

Not isolated INC serum [digoxin]

38
Q

How do you treat Dig Tox?

A
  1. ABCs
  2. Continuous tele & Pox
  3. Place IV
  4. Check BS
  5. Digoxin Immune Fab
    - used for clinically significant arrhythmia or hypotension

Clinical Pharmacology (54 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions