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

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

Flashcards in CVS drugs - Anti-arrhythmics, diuretics and anti-fat Deck (30):
1

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

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

2

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

Decrease conduction velocity
Increase depolarisation threshold
Decrease automacity

3

Why would you use fleicanide?

Atrial Fib

4

Give two CIs for Flecainide

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

5

What is the mechanism of action of felcainide?

Block fast, inward Na+ channels

6

Give three ADRs for flecanide

 Dizziness, visual disturbances, arrhythmias

7

What could effect metabolism of flecainide?

GO-DEVICES
Grapefruit juice, omeprazole

8

When would you use lidocaine?

Ventricular arrhytmia following MI

9

What is the mech of action for lidocaine?

Blocks fast, inward Na+ channels

10

Give three adverse drug reactions for lidocaine

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

11

What do beta blockers do to ventricular action potential?

Shift to right

12

Give four indications for beta blockers

Angina
Post myocardial infarctioin
Hypertension
Arrhytmias

13

How do beta blockers work as anti-arrhytmics?

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

14

Give some of the 6 ADRs of beta blockers?

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

15

Give two significant DDIs of beta blockers

 Prevents Salbutamol working (β2-adrenoagonist)
 Verapamil – Both have –‘ve inotropic action

16

How do potassium channel blockers work?

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

17

What is torsades de pointes

Ventricular tachycardia which can result in death

18

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

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

19

How do calcium channel blockers work?

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

When should calcium channel blockers not be used?

Heart failure
Bradycardia
AV node block

21

What are four ADRs of calcium channel blockers?

Hypotension
Bradycardia
Heart failure
Heart block

22

What does adenosine effect?

AV node blocker

23

When is digoxin used?

Atrial fib
Heart failure

24

Give the mechanism of action and effects of digoxin

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

Why is digoxin dangerous?

Narrow therapeutic index

26

What three things happen in digoxin toxicity?

bradycardia, AVN block, atrial tachycardia

27

What amplifies toxicity of digoxin?

Hypokalaemia

28

What increases digoxin levels in blood?

Quinidine, amiodarone, verapamil, spironolactone

29

What increases effect of digoxin in blood already?

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

30

How must digoxin be given?

Two separate doses to minimise toxicity risk