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Year 2 > Drugs and Cardiac Conduction Disorders > Flashcards

Drugs and Cardiac Conduction Disorders Flashcards

1
Q

Role of Class 1A Na Channel Blockers

A

Lengthens duration of action potential

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2
Q

Role of a Class 1B Na Channel Blockers

A

Shortens or has no effect on the duration of the action potential

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3
Q

Name a Class 1B Na Blocker

A

Lidocaine

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4
Q

Role of Class 1C Blockers

A

No effect on AP

Promote greater Na current depression than other two groups

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5
Q

Name a Class 1C drug

A

Flecainide

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6
Q

What condition is Quinidine used for

A

Atrial arrhythmias, tachycardias and atrial ectopic beats

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7
Q

What condition is Lidocaine used for

A

Ventricular arythmias

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8
Q

What is the modulated receptor hypothesis

A

A - Anti-arrythmic drugs bind to receptor
B - Drugs associated channel differ from drug free channels as they don’t conduct ions and voltage depentace is mor -ve
C - Affinity of receptor is modulated by channel state
D - Each channel state has a different kinetic integration with the drug
E - Affinity of receptor for drug is modulated by mV

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9
Q

In what channel state does Quinidine have highest affinity to receptor

A

Activated

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10
Q

In what channel state does Lidocaine have the highest affinity to receptor

A

Inactivated

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11
Q

How does Quinidine effect HR

A

Unaffected

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12
Q

How does Lidocaine effect the heart

A

Coupled beats inhibited

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13
Q

How does Quinidine (Class 1A) effect electrical conduction of heart

A

No effect

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14
Q

How does Quinidine (Class 1 A drugs) effect K channels

A

Blocks them - prevents REPOLARISATION

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15
Q

How does Quinidine (Class 1A drugs) effect Cholinergic muscarinic receptors

A

Antagonises them

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16
Q

What is Procaineamide used for

A

Ventricular tachycardia, ectopic beats

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17
Q

Why is Lidocaine used for ventricles and Quinidine used for Atria

A

Lidocaine, as a class 1B drug, shortens the duration of the long AP in the ventricles

Quinidine is being used to lengthen the short AP duration of the atria

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18
Q

Why is the fact that Lidocaine (Class 1B) has a very fast dissociation beneficial in certain condition s

A

Used in fibrillation or early extrasystole

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19
Q

Why is Lidocaine (Class 1B drugs) effective in damaged tissues

A

Hypoxia INCREASES extracellular K depolarising channel to inactivated form

Very slow dislocation from channel when tissue is depolarised

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20
Q

Tocainide/Mexiletine vs Lidocaine

A

Orally active

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21
Q

When is Tocainide/Mexiletine (Class 1B) given

A

Reduce incidence of secondary heart attack

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22
Q

Name two Class II anti-arryhtmic drugs

A

Beta adrenceptor antagonists

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23
Q

What ion does Propranolol activity effect

A

Na

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24
Q

What ion does Stall activity effect

A

K

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25
Q

What beta-blocker is given in early stages of MI

A

I/v propranolol in first 4 hours

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26
Q

Why is Propranolol given in first 4 hours of MI

A

25% Reduced risk of ventricular fibrillation/chest pains

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27
Q

How long do we treat a patient with propranolol for in order to give them an extra year of life

A

30

28
Q

How do Class III anti-arhythmic drugs effect the body

A

Delays repolarisation by prolonging refractory period

29
Q

In what heart conditions are Class III anti-arhythmic drugs beneficial

A

Supraventircular and ventricular tachycardias

WPW Syndrome

30
Q

Property of Amiodarone

A

Long elimination half life

Fat Soluble

31
Q

Advantage of amiodarone being fat-soluble

A

Slow accumulation in plasma needs loading dose

32
Q

Where is Amiodarone metabolised

A

Liver by P450

33
Q

Effect of Amiodarone of CYP P450 system

A

Inhibits it

34
Q

Consequence of CYP inhibition by Amiodarone

A

Reduces clearance of many drugs like quinidine

35
Q

How can Amiodarone effect the lungs

A

Fibrosis and interstitial lung disease

36
Q

How can Amiodarone effect thyroid

A

25% becomes hypothyroid

37
Q

How does Amiodarone effect the eye

A

Corneal micro crystalline deposits

38
Q

What is inward rectifier channel

A

Maintains resting mV and closes with depolarisation to prolong plateau

39
Q

What is Transient Outward current channel

A

Opens briefly after depolarisation

40
Q

What is Outward delayed rectifier channels

A

Open at end of plateau initiates depolarisation

41
Q

What channel does Dofetilide target

A

Transient outward current

42
Q

When is Dofetilde given

A

Atrial fibrillation and flutter

43
Q

How does Dofetilide prevent atrial fibrillation

A
  1. Prolongs repolarisation
44
Q

How is Dofetilide taken in

A

Orally active

45
Q

Can Dofetilide be used in heart failure or post infarction

A

Yes

46
Q

Adverse effect of dofetilide

A

Ventricular Tachycardia

47
Q

What kind of drug is Verapamil

A

Calcium blocker

48
Q

In what channel state does Verapamil bind to its receptors

A

Activated/Inactivated state NOT at rest

49
Q

When does verapamil binding increase

A

Increased HR

50
Q

What interrupts binding of verapamil

A

Intracellular pore blocker (like a gatekeeper)

51
Q

How does Verapamil effect SA Node

A

Protected by reflex tachycardia

52
Q

How does Verapamil effect AV Node

A

Conduction and refractory period prolonged

53
Q

How does Verapamil effect SV tachycardia

A

Converts back to sinus rhythm

54
Q

How does Verapamil effect digoxin

A

suppresses it

55
Q

Are Dihydropyridines anti-arhythmic

A

Nope

56
Q

Where are T-channels found

A

Smooth muscle cells

57
Q

Property of T-channels

A

Low conductance pathway

58
Q

How does Mibefradil effectVerapamil binding

A

Displaces it

59
Q

Are there T-channels in the ventricles

A

No

60
Q

How does Clinidipine effect the body

A

Inhibits NE release from sympathetic nerves

61
Q

Name a Class V drug

A

Digoxin

62
Q

How is Digoxin delivered to the body

A

Orally usually (sometimes IV)

63
Q

How is Digoxin excreted

A

Really

64
Q

What drugs increase plasma Digoxin and why

A

Quinidine, Verapamil, amiodarone because it replaces tissue binding sites and reduces digoxin clearance

65
Q

What channel does Digoxin inhibit

A

Na+/K+ ATPase in myocardium

66
Q

How does Digoxin’s inhibition of Na/K ATPase effect intracellular Na levels

A

Increases them which decreases Na/Ca exchanger which ould usually import 3Na into cell and one Ca out of cell

67
Q

How does Digoxin’s effect on Na/K change cardiac action potential

A

Lengthens them, reducing the heart rate as Ca conc. rises due to slower Na/Ca exchanger

Year 2 (155 decks)

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