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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
What beta-blocker is given in early stages of MI
I/v propranolol in first 4 hours
26
Why is Propranolol given in first 4 hours of MI
25% Reduced risk of ventricular fibrillation/chest pains
27
How long do we treat a patient with propranolol for in order to give them an extra year of life
30
28
How do Class III anti-arhythmic drugs effect the body
Delays repolarisation by prolonging refractory period
29
In what heart conditions are Class III anti-arhythmic drugs beneficial
Supraventircular and ventricular tachycardias WPW Syndrome
30
Property of Amiodarone
Long elimination half life Fat Soluble
31
Advantage of amiodarone being fat-soluble
Slow accumulation in plasma needs loading dose
32
Where is Amiodarone metabolised
Liver by P450
33
Effect of Amiodarone of CYP P450 system
Inhibits it
34
Consequence of CYP inhibition by Amiodarone
Reduces clearance of many drugs like quinidine
35
How can Amiodarone effect the lungs
Fibrosis and interstitial lung disease
36
How can Amiodarone effect thyroid
25% becomes hypothyroid
37
How does Amiodarone effect the eye
Corneal micro crystalline deposits
38
What is inward rectifier channel
Maintains resting mV and closes with depolarisation to prolong plateau
39
What is Transient Outward current channel
Opens briefly after depolarisation
40
What is Outward delayed rectifier channels
Open at end of plateau initiates depolarisation
41
What channel does Dofetilide target
Transient outward current
42
When is Dofetilde given
Atrial fibrillation and flutter
43
How does Dofetilide prevent atrial fibrillation
1. Prolongs repolarisation
44
How is Dofetilide taken in
Orally active
45
Can Dofetilide be used in heart failure or post infarction
Yes
46
Adverse effect of dofetilide
Ventricular Tachycardia
47
What kind of drug is Verapamil
Calcium blocker
48
In what channel state does Verapamil bind to its receptors
Activated/Inactivated state NOT at rest
49
When does verapamil binding increase
Increased HR
50
What interrupts binding of verapamil
Intracellular pore blocker (like a gatekeeper)
51
How does Verapamil effect SA Node
Protected by reflex tachycardia
52
How does Verapamil effect AV Node
Conduction and refractory period prolonged
53
How does Verapamil effect SV tachycardia
Converts back to sinus rhythm
54
How does Verapamil effect digoxin
suppresses it
55
Are Dihydropyridines anti-arhythmic
Nope
56
Where are T-channels found
Smooth muscle cells
57
Property of T-channels
Low conductance pathway
58
How does Mibefradil effectVerapamil binding
Displaces it
59
Are there T-channels in the ventricles
No
60
How does Clinidipine effect the body
Inhibits NE release from sympathetic nerves
61
Name a Class V drug
Digoxin
62
How is Digoxin delivered to the body
Orally usually (sometimes IV)
63
How is Digoxin excreted
Really
64
What drugs increase plasma Digoxin and why
Quinidine, Verapamil, amiodarone because it replaces tissue binding sites and reduces digoxin clearance
65
What channel does Digoxin inhibit
Na+/K+ ATPase in myocardium
66
How does Digoxin's inhibition of Na/K ATPase effect intracellular Na levels
Increases them which decreases Na/Ca exchanger which ould usually import 3Na into cell and one Ca out of cell
67
How does Digoxin's effect on Na/K change cardiac action potential
Lengthens them, reducing the heart rate as Ca conc. rises due to slower Na/Ca exchanger

Year 2 (155 decks)

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