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Spring 2024 Therapeutics 3 > Exam 2 Antiarrhythmic Drug Pharmacology YangYang > Flashcards

Exam 2 Antiarrhythmic Drug Pharmacology YangYang Flashcards

1
Q

What is the flow of movement of electrical conduction in the heart?

A

Pacemaker cells found in SA node fire first

Excitation spreads through atrial myocardium (down and right)

AV node fires (bottom of left atrium)

Excitation spreads down AV bundle (to bottom of heart)

Purkinje fibers distribute excitation through ventricular myocardium (across bottom of heart)

**moves from top to bottom

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2
Q

Pacemaker cells have automaticity, what does this mean?

A

Work without external stimulation

-regulate themselves
-work even when asleep
-have ability to generate action potentials

*Note: SNS and PSNS can control this

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3
Q

What affect does the SNS have on HR?

A

Increases it
(fight or flight)

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4
Q

What affect does the PSNS have on HR?

A

Decreases it
(rest and digest)

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5
Q

What 3 conduction systems contribute to the P wave?

A

SA node
Atrium
AV node

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6
Q

What 4 conduction systems contribute to the QRT interval?

A

Purkinje Fiber
Endocardium
Mid-myocardium
Epicardium

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7
Q

What is the name of the only sodium channel in the heart?

A

Nav1.5

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8
Q

What are the two calcium channels in the heart?

A

N-type Cav2.2

T-type Cav3.x

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9
Q

What are the 2 potassium channels in the heart?

A

Kir

Kv

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10
Q

What are the 2 HCN channels in the heart?

A

HCN1

HCN4

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11
Q

What are the 2 hERG channels in the heart?
*know

A

KCNH2

KV11.1

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12
Q

What ion channel in the heart is most important to avoid when developing new drugs?

A

hERG channels
(KCNH2 and KV11.1)

*reason why many good drugs are abandoned
*if it is blocked as a peripheral effect it causes a heart side effect

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13
Q

What is the goal of CiPA (Comprehensive In Vitro Proarrhythmia Assay)?

A

Work to take drugs that were abandoned due to their affects on hERG channels and develop them into new drugs

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14
Q

What is the typical membrane potential outside the cell?

A

0 mV

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15
Q

What is the typical membrane potential inside the cell?

A

-70 mV

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16
Q

What is the concentration of potassium (K) inside and outside the cell?

A

Inside: 148 mM

Outside: 5mM

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17
Q

What is the concentration of sodium (Na) inside and outside the cell?

A

Inside: 10 mM

Outside: 142 mM

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18
Q

What is the concentration of calcium (Ca) inside and outside the cell?

A

Inside: < 1 um

Outside: 5 mM

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19
Q

What is the concentration of chloride (Cl) inside and outside the cell?

A

Inside: 4 mM

Outside 103 mM

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20
Q

What ions want to move out of the cell based on concentrations only (K, Na, Ca, Cl)?

A

Potassium (K)

*only ion with high intracellular concentration and low extracellular concentration

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21
Q

What ions want to move into a cell based on concentrations only (K, Na, Ca, Cl)?

A

Sodium (Na)
Calcium (Ca)
Chloride (Cl)

*these all have higher extracellular concentrations and low intracellular concentrations

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22
Q

What ions want to move into a cell based on charge only? (K, Na, Ca, Cl)

A

Potassium (K)
Sodium (Na)
Calcium (Ca)

**these are all positively charged molecules and are attracted to the negative charge in the cell

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23
Q

What ion wants to move out of a cell based on charge only? (K, Na, Ca, Cl)

A

Cl

*this is a negatively charged ion, wants to escape the negatively charged intracellular environment

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24
Q

How many K are pumped into the cell by the Na/K ATPase and how many Na are pumped out?

A

2 K pumped in

3 Na pumped out

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25
Q

In a cardiac action potential, what is the movement of ions during Phase 0 (depolarization)?

A

Calcium increases
Sodium increases

-membrane potential rapidly increases

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26
Q

In a cardiac action potential, what happens at Stage 1?

A

Sodium channels close

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27
Q

In a cardiac action potential, what happens at phase 2?

A

Calcium keeps increasing but potassium decreases

-they balance each other out and a membrane potential plateau forms

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28
Q

In a cardiac action potential, what happens to ions in phase 3 (rapid repolarization)?

A

Potassium continues to decrease while calcium channels close

-causes membrane potential to rapidly decrease

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29
Q

In a cardiac action potential, what happens to ions in phase 4 (resting potential)?

A

Leaky potassium channels
Ca channels still closed

-membrane potential is below baseline during this time

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30
Q

Note:

A

see quizlet for remaining note cards

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31
Q

What are the 2 types of ion channels that mediate cardiac action potentials?

A

Pacemaker Cell

Ventricular Myocyte

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32
Q

Where do pacemaker cells action potentials occur?

A

SA and AV node

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33
Q

What is the automaticity of pacemaker cells vs ventricular myocytes?

A

Pacemaker: High automaticity
(maintain regular beating)

Myocyte: Low automaticity
(require signal from AV node to fire)

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34
Q

What ion are pacemaker cell spikes dependent on?

A

Ca-dependent spikes

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35
Q

What ion are ventricular myocyte cell spikes dependent on?

A

Na-dependent spikes

36
Q

What is the resting membrane potential of pacemaker cells?

37
Q

What is the resting membrane potential of ventricular myocytes?

38
Q

What is the function of the iCa action potential?

A

Carries action potential upstroke

(works on phase 0 when calcium is increasing)

39
Q

What is the function of the iK action potential?

A

Repolarizes the K current

(works on phase 3 where potassium levels drop, causing repolarization and decreased membrane potential)

40
Q

What is the function of the if action potential?

A

“Funny current”

controls the diastolic pacemaker current in phase 4
-when membrane potential goes low, the channels open

41
Q

What is the function of the iK(ACh) action potential?

A

K current activated by the vagus nerve
(phase 4)

42
Q

When is norepinephrine release the highest?

A

During fight-or-flight response

43
Q

What is the movement of Norepinephrine (NE) through the signaling cascade?

A

-Bound to beta AR receptors
-Binds GPCR
-Goes through signaling cascade
-PKA activates the sodium and calcium channels
-Na influx (through HCN channel*) leads to more action potential firing, HR increases

44
Q

What does the HCN channel do?

A

Lets more Na into the cell which leads to more action potential firing and increased HR

45
Q

What is the function of acetylcholine?

A

Slows down heart rate

46
Q

What is the movement of acetylcholine in ion signaling?

A

-Bound to MR1
-Binds to different GPCR than NE
-Blocks adenocyclines and cAMP
-Blocks the activation of sodium channels (HCN channel)
-Blocks activation of calcium channels
-**Opens potassium channel (GIRK) *hyperpolarization

**Overall: this slows down heart
*Less Na and Ca influx, more K influx
*Never 100% blockade

47
Q

What do GIRK channels do?

A

Allow for influx of K

48
Q

What phase do neurons not have in their action potential?

A

Do not have a plateau phase

(only myocyte action potentials do)

49
Q

What is the ball-and-chain model used for in Phase 0 of myocyte action potentials?

A

Sodium influx is very strong and changing from one confirmation of a voltage-gated Na channel to another takes time

-ball is used to block the pathway and stop sodium from flowing inside in the time it takes for the voltage-gated channel to close

*inactivates sodium channel

50
Q

What is the structural basis of a re-entry arrhythmia?

A

Signals go around the non-excitable region
-go left, right, and around the bottom
-the signal at the bottom meets up from either side and cancels each other out

*if the cancelling out does not happen this creates a problem

*if cells are dead on one side of the non-excitable region, this causes one side of the signal to not conduct
-the other side of the signal goes around the bottom, around the side, and back up
(re-entry)

*affects heart beat
-creates trigger signal for cell to fire again

51
Q

What is the re-entrant circuit?

A

Circuit by which the signal keeps going around the non-excitable region in re-entry arrhythmia

52
Q

How does re-entry arrhythmia affect heart rate?

A

Creates heart rate almost double normal

*causes Sustained V Tach and Occasional PVCs

53
Q

What are the 3 requirements for re-entry arrhythmia?

A
  1. Multiple parallel pathways
  2. Unidirectional block
  3. Conduction time greater than effective refractory period (ERP)
54
Q

What drug class is a Class 1 antiarrhythmic?

A

Na Channel Blockers

55
Q

What drug class is a Class 2 antiarrhythmic?

A

Beta Blockers

56
Q

What drug class is a Class 3 antiarrhythmic?

A

K Channel Blockers
(prolong refractory period)

57
Q

What drug class is a Class 4 antiarrhythmic?

A

Ca Channel Blockers

58
Q

What affect do Beta Blockers (Class 2) have on the shape of an action potential?

A

DO NOT REDUCE PEAK HEIGHT

-move the action potential graph to the right

DO NOT CHANGE SHAPE OF GRAPH ONLY CHANGE TIMING

59
Q

What affect do CCBs (Class 4) have on the shape of an action potential?

A

REDUCE PEAK HEIGHT
(blocking calcium reduces peak)

-Timing shifts slightly to the right

60
Q

What are the antiarrhythmic actions of beta blockers (Class 2)?

A

-Slow pacemaker and Ca currents in SA, AV node

-Increase refractoriness of SA, AV node

-Increase P-R interval

61
Q

What are the antiarrhythmic actions of calcium channel blockers (Class 4)?

A

-Frequency-dependent block

-Increase refractoriness of AV node and P-R interval

-Protect ventricular rate from atrial tachycardia

62
Q

What are the 3 beta blockers used as antiarrhythmics?

A

Esmolol***

Acebutolol

Propranolol

63
Q

What are beta blockers used for regarding arrhythmias?

A

Arrhythmias involving catecholamines

(epinephrine)

64
Q

What are the calcium channels that can be used as antiarrhythmics?

A

Verapamil

Diltiazem

65
Q

What are calcium channels used for regarding arrhythmias?

A

Block re-entrant arrhythmias INVOLVING THE AV NODE

Protect ventricular rate (in atrial flutter and afib)

66
Q

What do Class 1A antiarrhythmics block?

A

Mixed block: Na and K channels

67
Q

What affect do Class 1A antiarrhythmics have on an action potential?

A

Widen QRS

Prolong QT

*image is missing stage 1 point, moved to right

68
Q

What do Class 1B antiarrhythmics block?

A

Na channel block

69
Q

What affect do Class 1B antiarrhythmics have on an action potential?

A

No clinically significant effect on an ECG

*move graph slightly to LEFT

70
Q

What do Class 1C antiarrhythmics block?

A

STRONG Na channel block

71
Q

What affect do Class 1C antiarrhythmics have on an action potential?

A

Widen QRS

*moves only the phase 0 line out to the right
*rest of graph is the same

72
Q

What is the most common Class 1A antiarrhythmic drug?
(NA channel blocker)

73
Q

What are the 2 most common Class 1B antiarrhythmic drugs?
(NA channel blocker)

A

Lidocaine
Mexiletine

74
Q

What is the most common Class 1C antiarrhythmic drug?
(NA channel blocker)

A

Flecainide

75
Q

What is the MOA of Class 3 Antiarrhythmics (K channel blockers)?

A

Prolong action potential duration and QT interval

Increases effective refractory period
*used for re-entrant arrhythmias

76
Q

What is a downside to Class 3 antiarrhythmics (K channel blockers)?

A

Dangerous, not often used

*hERG channel blockers!
*Can cause Torsades de Pointes

77
Q

What is the most common Class 3 antiarrhythmic drug (K channel blocker)?

A

Amiodarone

78
Q

When is amiodarone used?

A

Top choice for:

Rate control in A-fib

Suppression of post-MI ventricular arrhythmias

79
Q

What genetic mutations can cause Long QT Syndrome (LQTS)?

A

KCNQ1 (K channel)
KCNH2 (K channel)
SCN5A (sodium channel)

80
Q

Where do Class 1 (Na Channel Blocker) drugs affect the action potential?

81
Q

Where do Class 4 (CCB) drugs affect the action potential?

82
Q

Where do Class 3 (K Channel Blockers) drugs affect the action potential?

83
Q

Where do Class 2 (Beta Blocker) drugs affect the action potential?

84
Q

How can Digoxin treat arrhythmias?

A

Inhibits AV node

Increases inotropy, used for HF

85
Q

How can Adenosine treat arrhythmias?

A

Depresses pacemaker cells
-Suppresses atrial tachycardia
-Given IV

**Brief but potent slowing of the heart

Spring 2024 Therapeutics 3 (24 decks)

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