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Pharmacology > Lecture 12: Anti-Arrhythmic Drugs (Part II) > Flashcards

Lecture 12: Anti-Arrhythmic Drugs (Part II) Flashcards

1
Q

What three drugs make up the Class 1A Anti-Arrythmic Class?

A

Quinidine, Procainamide, Disopyramide

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2
Q

How do Class 1A Anti-Arrythmics raise the threshold for AP and slow rate of depolarization in cardiac muscles?
(hint: what channels do they block?)

A

Block Na+ channels (preference for open channels)

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3
Q

How do Class 1A Anti-Arrythmics affect phase 0 upstroke? myocardial conduction velocity?

A

Class 1A Anti-Arrythmics
- Phase 0 upstroke: decrease
- Myocardial conduction velocity: decrease

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4
Q

True or False: Class 1A Anti-Arrythmics block Na and K channels

A

True

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5
Q

How do Class 1A Anti-Arrythmics affect outward K+ current, which is responsible for repolarization of membrane?

A
  • Decrease outward K current
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6
Q

How do Class 1A Anti-Arrythmics affect ERP and AP duration?

A

Class 1A Anti-Arrythmics
- ERP: Increase
- AP duration: Increase

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7
Q

Quinidine, a Class 1A Anti-Arrythmic, increases conduction velocity in the nodes. Why is this?

A

Has a strong ANTI-CHOLINERGIC effect (in addition to Na+ blocking effect)

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8
Q

Contraindications for Quinidine?
Contraindications fro Disopyramide?

A

Quinidine: atrial flutter
Disopyramide: glaucoma, uropathy

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9
Q

DDI for Quinidine?

A

Quinidine and Digoxin (can lead to Digoxin toxicity)

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10
Q

True or False: Both quinidine and disopyramide have anti-cholinergic effects, but the latter is more severe

A

True

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11
Q

Of the three Class 1A Anti-Arrythmic drugs (Quinidine, Procainamide, Disopyramide) - which has the FEWEST anticholinergic effects and does NOT have a DDI with Digoxin?

A

Procainamide

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12
Q

All Class 1A agents are contraindicated in patients with _____ or with drugs that predispose patients to QT prolongation, leading to TdP

A

QT prolongation

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13
Q

True or False: Class 1B Anti-Arrythmics bind to both open and inactivated Na+ Channels

A

True

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14
Q

Binding perference for Class 1A Anti-Arrythmics vs. Class 1B Anti-Arrythmics?

A

Class 1A: Open
Class 1B: Inactive

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15
Q

How do Class 1B Anti-Arrythmics act on Na+ channels?

A

Block open and inactivated Na+ channels

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16
Q

What are the three drugs part of the Class 1B Anti-Arrythmics?

A

1) Lidocaine
2) Mexiletine
3) Phenytoin

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17
Q

Why can Class 1B Anti-Arrythmics lead to seizures or dizzyness?

A

Can cross BBB

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18
Q

True or False: Mexiletine is an analogue of lidocaine and has a negligible influence on QT interval compared to lidocaine, has less vagolytic affects

A

True

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19
Q

True or False: Phenytoin can be used as an anti-epileptic medication

A

True

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20
Q

Which class of anti-arrythmic drugs has the most potent Na+ channel blockers

A

Class 1C

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21
Q

How do Class 1B Anti-Arrythmics affect ERP and AP duration?

A

ERP: Decreased
AP Duration: Decreased

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22
Q

How do Class 1C Anti-Arrythmics affect phase 0 of ventricular cells?

A

Decrease phase 0 of ventricular cells
(as a result, suppresses pre-mature ventricular contraction)

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23
Q

Do Class 1C Anti-Arrythmics bind to open/active Na+ channel or closed/inactive Na+ channel?

A

Open/Active Na+ channel

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24
Q

What are the three Class 1C anti-arrythmics?

A

1) Flecainide
2) Encainide
3) Propafenone

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25
Q

True or False: Class 1B Anti-arrythmics can worsen a pre-existing arrythmia. Therefore: only approved for life-threatening situations, such as: paroxysmal supraventricular arrythmia

A

False - this is the case for class 1C anti-arrythima drugs

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26
Q

How do Class 1C Anti-arrythmics affect AP duration and ERP?

A

Normal - do not change

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27
Q

What two class 1C drugs can lead to developing cardiac arrest/mortality, as per NHLBI study?

A

Encainide
Flexainide

28
Q

True or False: Propafenone can cause mortality

A

True

29
Q

Order the anti-arrythmic drug class from strongest to weakest Na+ channel blocking ability

A

Na+ Blocking Ability
Class 1C > Class 1A > Class 1B

30
Q

In the SA Node, the beta1 receptor triggers an increase in pacemaker activity via _____

A

Funny current/HCN

31
Q

Typically, beta 1 receptors lead to increase SA nodal firing, which increases the phase ___ depolarization rate in pacemaker cells

A

phase 4

32
Q

True or False: In the AV Node - beta 1 receptors increase calcium current, resulting in enhanced conduction velocity and decreased refractory period

A

True

33
Q

Beta blockers belong to which class of anti-arrythmic drugs?

A

Class II anti-arrythmia drug

34
Q

Beta 1 blockers act on both __ and ___ nodes to decrease phase ___ in pacemaker cells.

How does this effect ERP and rate of automaticity?

A

Beta 1 blockers act on: SA/AV Nodes to decrease phase 4 in pacemaker cells

  • Prolongs ERP, decreases rate of automaticity
35
Q

True or False: Non-specific beta blockers (propranolol, sotalol) come with warning of life threatening pro-arrythmia

A

True

36
Q

What type of beta blockers are labetolol and carvediolol?

Atenolol and metoprolol?

A

Beta and alpha 1 receptor blockers

Specific beta 1 blockers

37
Q

AE of non-specific beta blockers?

AE of beta blockers?

A

Bronchospasm (due to blocking B2)

Negative inotropic effect, bradycardia, block

38
Q

What four drugs belong to the class III anti-arrythmic drug class?

A

1) Amiodarone
2) Dronedarone
3) Ibutilide
4) Dofetilide

39
Q

____ channels play a major role in regulating plateau phase, specifically outward delayed rectifying K+ currents (K efflux)

A

K+ channels

40
Q

Which class of Anti-Arrythmia drugs are K+ channel blockers?

A

Class III

41
Q

How do K+ channel blockers (Class III) affect K+ efflux? Plateau phase, repolarization, and ERP?

A

K+ blockers prevent K+ efflux
- Longer plateau phase and re-polarization
- Increased ERP

42
Q

____ shows K+ blocking activity and is considered to be a mixed class II and class III drug

A

Sotalol

43
Q

AE associated with use of Class III drugs?

A
  • Prolongation of plateau duration can give rise to EAD
  • Can result in TdP
44
Q

What is the metabolite of Amiodarone, a K+ channel blocker?

A

Des-ethyl Amiodarone

45
Q

___ is a benzofuran compounds with 37% iodine that has HIGH affinity for thyroid cells and is toxic to thyroid follicular cells, ultimately leads to destruction of thyroid gland and hypothyroidism

A

Amiodarone

46
Q

True or False: Amiodarone is known to inhibit 5-deiodinase activity, thereby decreasing conversion of T4 to T3; also known to be depositied in eyes, skin, and liver

A

True

47
Q

True of False: Dronedarone is known to cause optic neuropathy, corneal deposits, and keratopathy with long-term use

A

False - Amiodarone

48
Q

What anti-arrythmic drugs are associated with ocular toxicity?

A

Amiodarone
Quinidine and Disopyramide (Class 1A)

49
Q

What drug and its metabolite are known to decrease dose of UV radiation known to cause erythema? Cause?

A

Amiodarone
- Induction of ROS and DNA damage by amiodarone and DEA (metabolite) by cutaneous tissue

50
Q

What is a substitute for Amiodarone, with reduced toxic effects? Why is this substitute less toxic?

A

Dronedarone (or Ibutilide or Dofetilide)
- Sulfonamide moiety, results in less iodide toxicity and decreased 1/2 life

51
Q

Calcium channel blockers belong to which type of anti-arrythmia drugs?
A. Class II
B. Class I
C. Class III
D. Class IV

A

D. Class IV

52
Q

Calcium channel blockers primarily cat on which tissues?

A

SA and AV Nodal Tissues (these effects are more prominent than atrial and ventricular muscles)

53
Q

How do Ca2+ blockers affect AP and conduction of impulses in nodal tissues?

A

Slows down AP and impulse conduction

54
Q

True or False: The mechanism used by Ca channel blockers could be helpful in regulating AV Node mediated re-entry phenomenon

A

True

55
Q

What two drugs belong to Class IV Anti-arrythmia drugs?

A

Verapamil and Diltiazem

56
Q

Which class of Anti-Arrythmic drugs can cause AV nodal block?

A

Class IV

57
Q

Class IV Anti-Arrythmia drugs - contraindications?

A

With beta-blockers, can precipitate HF

58
Q

True or False: If Digoxin is co-admin with Verapamil or Diltiazem, could result in enhanced Digoxin toxicity

A

True

59
Q

How does Ivabradine affect Na+ entry?

A

Inhibits Na entry and funny current through HCN in the SA Node

60
Q

What can Ivabradine (Class 0) treat?

A

Arrythmias due to SA nodal origin
(e.g sinus tacchycardiacs)

61
Q

What drug can treat A fib / Paroxysmal Supraventricular Tachy?

A

Digoxin

62
Q

Which drug inhibits M3 receptors in SA and AV Nodes to normalize sinus rhythm and reverse AV Nodal block?

CI?

A

Atropine
- Glaucoma

63
Q

True or False: Afib can lead to stroke

A

True

64
Q

What drugs can be given as anti-coags to prevent stroke?

A

1) Dabigatran; Rivaroxaban; Apixaban - ban/tran

65
Q

Treatment for A-fib induced stroke?

A

1) Heart rate controlling meds - Beta or Ca2+ blockers

2) Heart rhythm controlling meds - Na/K+ channel blockers

Pharmacology (53 decks)

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