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CVPR Exam I > 7, 8. Molecular Mechanisms of Arrhythmias and Drugs > Flashcards

7, 8. Molecular Mechanisms of Arrhythmias and Drugs Flashcards

1
Q

Cardiac arrhythmias are acquired subsequent to what 7 things?

A

MI, ischemia, acidosis, alkalosis, electrolyte abnormalities, drug toxicitiy, or excessive catecholamine exposure

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2
Q

Name a cardiac glycoside that can cause arrhythmias.

A

digoxin

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3
Q

Name some antihistamines that can cause arrhythmias.

A

astemizole, terfenadine

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4
Q

Name an antibiotic that can cause arrhythmias.

A

sulfamethoxazole

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5
Q

What are the 1a targets of antiarrhythmic drugs?

A
  1. cardiac Na+ channels (INa)
    2, Ca2+ channels (ICa-L)
  2. K+ channels (IKs and IKr)
  3. β-adrenergic receptors
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6
Q

What drugs can reduce the incidence of sudden cardiac death?

A

β-blockers

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7
Q

What is familial long QT syndrome?

A

a genetic prolongation of the duration of the cardiac AP (phase 2 plateau phase in the QT interval) that can lead to ventricular arrhythmia and death

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8
Q

What is torsades de pointes?

A

a polymorphic ventricular tachycardia that can degenerate into v-fib

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9
Q

What triggers torsades de pointes?

A

an abrupt increase in sympathetic tone

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10
Q

How are long QT patients treated?

A

β-adrenergic receptor blockers (β-blockers)

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11
Q

What is Brugada syndrome?

A

an inherited v-fib with only 40% survival to age 5- caused by mutations in Na+ channels

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12
Q

What is yotiao?

A

a protein that normally targets PKA, the effector of β receptors in cardiac Ca and K channels

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13
Q

What are the 2 general mechanisms of arrhythmia generation?

A
  1. inappropriate impulse initiation at the SA node or ectopically
  2. disturbed impulse conduction in nodes, Purkinje cells, or myocytes
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14
Q

Why do ectopic foci occur?

A

SA nodal pacemaker is abnormally slow or ectopic focus is abnormally fast; infarct

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15
Q

What does EAD stand for?

A

early afterdepolarizations

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16
Q

When do EADs occur?

A

in late phase 2 or early phase 3

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17
Q

What causes EADs?

A

re-activation of Ca2+ channels in response to elevated Ca2+

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18
Q

What does DAD stand for?

A

delayed afterdepolarizations

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19
Q

When do DADs occur?

A

during early phase 4

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20
Q

What causes DADs?

A

initiated by elevated [Ca2+]in and elevated Na+/Ca2+ exchange

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21
Q

What is NCX?

A

the sodium-calcium exchanger

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22
Q

What is the current the NCX generates?

A

I NCX

23
Q

Re-entrant arrhythmias require what two conditions?

A
  1. uni-directional conduction block in a functional circuit

2. conduction time around the circuit is longer than the refractory period

24
Q

In many cases, arrhythmia is triggered by _____ but is maintained by _____.

A

afterdepolarizations; re-entry

25
Q

Why does increased sympathetic tone increase the likelihood of triggered afterdepolarizations?

A

Ca2+ influx is enhanced by β-adrenergic receptor activity

26
Q

What is the mechanism of action of Class I Anti-arrhythmic Drugs?

A

voltage-gated Na+ channel blockers

27
Q

All Na+ channel blockers decrease _____ and

nearly all increase _____.

A

conduction rate; refractory period

28
Q

All _____ decrease conduction rate and nearly all increase refractory period.

A

Na+ channel blockers

29
Q

Class I action results in _____.

A

slowed upstroke

30
Q

_____ action results in slowed upstroke.

A

Class I

31
Q

_____ drugs slow upstroke and also decrease action potential duration.

A

Class Ib

32
Q

Class Ib drugs slow _____ and also decrease _____.

A

upstroke; action potential duration

33
Q

_____ and _____ drugs delay phase 3 onset by blocking K+ channels.

A

Class Ia; class Ic

34
Q

Class Ia and class Ic drugs delay ____ onset by blocking K+ channels.

A

phase 3

35
Q

Class Ia and class Ic drugs delay phase 3 onset by blocking _____.

A

K+ channels

36
Q

Name 3 specific class 1a Na+ channel blockers.

A

quinidine, procainamide, disopyramide

37
Q

All ____ drugs slow the upstroke of the fast response, and they also delay the onset of repolarization.

A

class Ia

38
Q

All class Ia drugs slow the _____, and they also delay the ____.

A

upstroke of the fast response; onset of repolarization

39
Q

Class Ia drugs prolong the refractory period via two processes: _______ and _____.

A
  1. classic, use-dependent mechanism, similar to local anesthetics in action
  2. depolarization (phase 2 duration) is prolonged
40
Q

Quinidine has important effects not related to Na+ channel block, including ____, ____, and ____.

A
  1. blocks K+ channels particularly well, thereby prolonging action potential duration
  2. it is a vagal inhibitor (anti-cholinergic)
  3. it is an α-adrenergic receptor antagonist
41
Q

Name 3 specific Class Ib Na+ channel blockers.

A

lidocaine, mexiletine, phenytoin

42
Q

Lidocaine, mexiletine, and phenytoin are all what kind of drug?

A

Class Ib Na+ channel blockers

43
Q

How are class 1b drugs similar to class 1a drugs?

A

they are use-dependent blockers of voltage-gated Na+ channels

44
Q

In contrast to class Ia drugs, ____ drugs do not prolong phase 2 of the action potential.

A

class Ib

45
Q

In contrast to class Ia drugs, class Ib drugs do not ____.

A

prolong phase 2 of the action potential

46
Q

What is the most important class 1b drug for the treatment of arrhythmias?

A

lidocaine

47
Q

Name 3 specific Class Ic Na+ channel blockers.

A

propafenone, flecainide, encainide

48
Q

Propafenone, flecainide, and encainide are all what kind of drug?

A

Class Ic Na+ channel blockers

49
Q

_____ produce the most pronounced slowing of upstroke rate; the net effect is powerful prolongation of tissue refractory period.

A

Class Ic drugs

50
Q

Class Ic drugs produce the most pronounced slowing of upstroke rate; the net effect is powerful ____.

A

prolongation of tissue refractory period

51
Q

What does it mean that class 1c drugs preferentially target cells?

A

Na+ channels in myocytes with abnormally high firing rates or abnormally depolarized membranes will be blocked to a greater degree than are Na+ channels in normal, healthy myocyte

52
Q

What is the mechanism of action for class 1c drugs that allows their preferential targeting?

A

the channel must be open

53
Q

_____ is the fundamental mechanism of prolongation of cellular refractory period.

A

Prolongation of channel inactivation

54
Q

How do use-dependent channel blockers prolong the refractory period?

A

they stabilize the inactive state after entering the open channel

CVPR Exam I (29 decks)

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