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OSCE Pharmacology > CVS drugs - Anti-arrhythmics, diuretics and anti-fat > Flashcards

CVS drugs - Anti-arrhythmics, diuretics and anti-fat Flashcards

1
Q

What four types of drugs are in the vaughn williams classification?

A

Na+ channel blockers
B-blockers
K+ channel blockers
Ca2+ channel blockers

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2
Q

What are the three mechanisms of action of Na+ channel blockers?

A

Decrease conduction velocity
Increase depolarisation threshold
Decrease automacity

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3
Q

Why would you use fleicanide?

A

Atrial Fib

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4
Q

Give two CIs for Flecainide

A 
Heart failure (make it worse at beating)
History of MI (can worsen arrhythmias)
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5
Q

What is the mechanism of action of felcainide?

A

Block fast, inward Na+ channels

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6
Q

Give three ADRs for flecanide

A

 Dizziness, visual disturbances, arrhythmias

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7
Q

What could effect metabolism of flecainide?

A

GO-DEVICES

Grapefruit juice, omeprazole

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8
Q

When would you use lidocaine?

A

Ventricular arrhytmia following MI

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9
Q

What is the mech of action for lidocaine?

A

Blocks fast, inward Na+ channels

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10
Q

Give three adverse drug reactions for lidocaine

A

Hypotension, bradycardia (Negative inotrope)
Nystagmus (brain)
Seizures (Brain)

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11
Q

What do beta blockers do to ventricular action potential?

A

Shift to right

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12
Q

Give four indications for beta blockers

A

Angina
Post myocardial infarctioin
Hypertension
Arrhytmias

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13
Q

How do beta blockers work as anti-arrhytmics?

A

 Antagonise β-adrenoreceptors. β1-receptors are found in the heart, when they are activated they cause increased Chronotropy and Inotropy.
 Inhibit renin release

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14
Q

Give some of the 6 ADRs of beta blockers?

A 
Bronchospasm
Fatigue and insomnia
Hypotension 
Bradycardia 
Decreased glucose tolerance - Don't feel adrenaline from hypoglycaemia due to B blockers
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15
Q

Give two significant DDIs of beta blockers

A

 Prevents Salbutamol working (β2-adrenoagonist)

 Verapamil – Both have –‘ve inotropic action

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16
Q

How do potassium channel blockers work?

A

Block potassium channels which -
Increases absolute refractory period
Increased AP duration
Suprress re-entry circuits by closing excitable gap

17
Q

What is torsades de pointes

A

Ventricular tachycardia which can result in death

18
Q

Why must you be careful using amiodarone in a patient on warfarin?

A

Amiodarione inhibits cyp450 which requires dose reduction of everything else which undergoes liver metabolism

19
Q

How do calcium channel blockers work?

A

Decrease slop of pacemaker aciton potential at SA node and AV node - Dependent on Ca2+ influx and efflux!
This increaes refractory period, chronotrophy and inotropy

20
Q

When should calcium channel blockers not be used?

A

Heart failure
Bradycardia
AV node block

21
Q

What are four ADRs of calcium channel blockers?

A

Hypotension
Bradycardia
Heart failure
Heart block

22
Q

What does adenosine effect?

A

AV node blocker

23
Q

When is digoxin used?

A

Atrial fib

Heart failure

24
Q

Give the mechanism of action and effects of digoxin

A 
o	Inhibits Na/K-ATPase
o	Direct Cardiac Effects
 Increased Inotrope – Used in heart failure, no mortality benefit
o	CNS Effects
 Decreased Sympathetic outflow
 Increased Parasympathetic outflow
	Sensitises baroreceptor reflex
o	Combined Effects
	 Automaticity of SAN and AVN
	 AVN refractory period
	 Conduction velocity of AVN
25
Q

Why is digoxin dangerous?

A

Narrow therapeutic index

26
Q

What three things happen in digoxin toxicity?

A

bradycardia, AVN block, atrial tachycardia

27
Q

What amplifies toxicity of digoxin?

A

Hypokalaemia

28
Q

What increases digoxin levels in blood?

A

Quinidine, amiodarone, verapamil, spironolactone

29
Q

What increases effect of digoxin in blood already?

A

Beta blockers (both decrease AV node conduction)
Verapamil (both decrease cardiac contractility)
Loop and thiazide diuretic (both cause hypokalaemia)

30
Q

How must digoxin be given?

A

Two separate doses to minimise toxicity risk

OSCE Pharmacology (10 decks)

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