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Semester 5 - Farmocology > Session 10 - Drugs Rate and Rhythm > Flashcards

Session 10 - Drugs Rate and Rhythm Flashcards

1
Q

What is the cardiac resting membrane potential?

A

-90mV

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2
Q

What sets the resting membrane potential for cardiac cells?

A

The relative permeability of the cardiac myocyte to K+

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3
Q

What is the equilibrium potential of K+?

A

-80mV

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4
Q

Outline a contraction of a ventricular myocyte?

A

o In diastole, the resting membrane potential of cardiac cells is close to the equilibrium potential of K+ (4).
o Initial depolarisation due to spread of electrical activity from pacemaker cells. Once threshold has been reached, fast voltage gated sodium channels are opened, causing depolarisation towards Na+’s equilibrium potential (0).
o Following the rapid depolarisation, a brief repolarisation caused by the outward flow of K+ returns the membrane potential to ~0. (1)
o Na+ channels deactivate, but the depolarisation causes the opening of voltage gated Ca2+ channels, which take longer to activate, keeping the membrane depolarised (2).
o Influx of Ca2+ causes the release of further Ca2+ from cellular stores, causing contraction (See M&R Session 5).
o After ~250ms, Ca2+ channels close.
o Efflux of K+ returns membrane potential to resting (3).

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5
Q

Give the classification of anti-arythmic drugs

A

Class 1 - Na+ blockes
Class 2 - B blocekrs
Class 3 - K+ channel blockers
Class 4 - Ca2+ channel blockers

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6
Q

Give three types of Na+ channel blockers

A

1a) Quinidine
1b) Lidocaine
1c) Felcainide

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7
Q

Give a type of beta blocker

A

Atenolol
Bisoprolol
Metoprolol

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8
Q

Give a widely used K+ channel blocker

A

Amiodarone

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9
Q

Give a Ca2+ channel blocker

A

Verapamil

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10
Q

What are the effects of Flecainide and Lidocaine?

A

Decrease conduction velocity
Increase depolarisation threshold
Decrease automacity

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11
Q

What is the route of administration of flecainide?

A

Oral and intravenous

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12
Q

What are the indications for flecinaide?

A

Supraventricular tachyarrythmias (atrial arrhythmia)

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13
Q

Give two contraindications for Flecainide?

A

Heart failure, History of MI

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14
Q

What is the mechanism of action for Flecainide?

A

Blocks fast, inward Na+ ion channel (Phase 0)

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15
Q

Give three adverse reactions of flecainide

A

 Dizziness, visual disturbances, arrhythmias

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16
Q

What are the drug-drug interactions for Flecainide?

A

 Metabolised by CYP2D6 and eliminated renally. Inducers/inhibitors

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17
Q

How is lidocaine adminstered?

A

Intravenously

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18
Q

What are the indications for lidocaine?

A

Ventricular arrhythmias following MIO

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19
Q

What are the contraindications for Lidocaine (2)

A

AV block

Heart failure

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20
Q

Give three adverse drug reactions for lidocaine

A

Hypotension, bradycardia
Nystagmus
Seizures

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21
Q

What do beta blockers act on?

A

B1 receptors in the heart

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22
Q

What is the action of B blockers

A

Block sympathetic action
Decrease slop of pacemaker potential in SAN
Decrease chronotrophy
Inhibits adenyl cyclase, decrease inotrophy

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23
Q

What do B blockers do to ventricular action potential?

A

Shifts it to the right

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24
Q

What are the indications for B blockers? (4)

A

 Angina
 Post myocardial infarction
 Hypertension
 Arrhythmias

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25
Q

What are the two main contraindications for beta blockers?

A

Asthma

General decreased heart function

26
Q

What is the mechanism of action for beta blockers?

A

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

27
Q

Give some adverse drug reactions for beta blockers

A

 Bronchospasm, fatigue and insomnia, dizziness, cold extremities, hypotension, bradycardia and decreased glucose tolerance in diabetic patients – Don’t feel adrenaline from hypoglycaemia due to B blockers, dangerous

28
Q

Give two drug-drug interactions of Beta blockers

A

 Prevents Salbutamol working (β2-adrenoagonist)

 Verapamil – Both have –‘ve inotropic action

29
Q

What do K+ channel blockers do?

A

Prolong the absolute refractory period by increase AP duration
Also suppress re-entry circuits by closing excitable gap

30
Q

Why are they not generally used?

A

Torsades de pointes

31
Q

Give an example of a potassium channel blocker

A

Amiodarone

32
Q

What is the route of administration of potassium channel blockers?

A

Oral or intravenous

33
Q

What are the indications for potassium channel blockers

A

Ventricular and supraventricular arrythmia

34
Q

What are some drug-drug interactions of amiodarone?

A

Inhibits CYP3A4, CYP2C9 and P-glycoprotein

 Dose reductions of Warfarin, Digoxin, Flecainide needed

35
Q

What do Ca2+ blockers do?

A

Increased refractory period

Decreased Chronotrophy and Inotropy

36
Q

Give two examples of Calcium channel blockers

A

Verapamil

Diltiazem

37
Q

Give a route of admin for calcium

A

Oral

38
Q

Give three indications for Ca2+ blockers

A

Supraventriuclar arrhythmias

Prophylaxis and treatment of angina nad hypertension

39
Q

Give three contraindications for Calcium channel blockers

A

Heart failure
Bradycardia
AV node block

40
Q

Give four adverse reactions to calcium channel blockers?

A

Hypotension
Bradycardia
Heart failure
Heart block

41
Q

What is used to treat torsades de pointes?

A

Digoxin

Adenosine

42
Q

What does adenosine do?

A

Blocks AV node

43
Q

What are the two main effects of adenosine?

A

Decrease automacity

Increased AVN refractory period

44
Q

What are two main indications for digoxin?

A

Supraventricular arrhythmias, Heart Failure

45
Q

Give two contraindications for digoxin

A

Heart block

Hypokalaemia

46
Q

Outline the mech of action of digoxin

A 
o	Inhibits Na/K-ATPase
o	Direct Cardiac Effects
	 Inotrope – Used in heart failure, no mortality benefit
o	CNS Effects
	 Sympathetic outflow
	 Parasympathetic outflow
	Sensitises baroreceptor reflex
o	Combined Effects
	 Automaticity of SAN and AVN
	 AVN refractory period
	 Conduction velocity of AVN
47
Q

What are three adverse drug reactions to digoxin?

A

o Narrow therapeutic index
o Toxicity enhanced with hypokalaemia
o Cardiac toxicity – bradycardia, AVN block, atrial tachycardia

48
Q

Give some drugs which increase digoxin levels

A

Popafenone, Quinidine, Amiodarone, Verapamil, Spironolactone, Cylosporine

49
Q

Give some drugs which decrease digoxin levels

A

Erythromycin, Tetracycline (gut bacteria metabolise digoxin)

50
Q

Why do you split loading dose of digoxin in two?

A

To minimise toxicity risk

51
Q

How much of digoxin is protein bound

A

20-30%

52
Q

What is digoxin clearance proportional to?

A

GFR

53
Q

Give three examples of ACE inhibitors

A

 Ramipril
 Lisinopril
 Captopril

54
Q

Give three indications for ACE inhibitors

A

 Hypertension
 Heart failure
 Renal dysfunction

55
Q

Give three contraindications for ACE inhibitors

A

Pregnancy
Renovascular
Aortic stenosis

56
Q

Outline mech of action of ACE inhibitors

A

 ACE inhibitors cause inhibition of Angiotensin Converting Enzyme, consequently reducing Angiotensin II and Aldosterone levels. This causes vasodilation and consequent reduction in peripheral resistance and reduced sodium retention.
 Reduce breakdown of the vasodilator Bradykinin

57
Q

Give five adverse reactions of ACE inhibitors

A

 Characteristic dry cough
 Angio-oedema (rare, but more common in black population)
 Renal Failure
 Hyperkalaemia
 Hypotension, dizziness and headache, diarrhoea and muscle cramps

58
Q

Give two angiotensin blockers

A

Losartan

Valsartan

59
Q

What is an indication for angiotensin blocker?

A

Hypertension

60
Q

Give four contraindications

A

 Pregnancy, breastfeeding

 Caution in renal artery stenosis and aortic stenosis

61
Q

What is the mech of action of angiotensin blocker?

A

 Bind to and antagonise the receptor for Angiotensin II – Angiotensin 1 Receptor (AT1 R).
 Inhibits vasoconstriction and aldosterone stimulation by angiotensin II.

62
Q

Give two adverse drug reactions to angiotensin receptor blockers

A

 Renal failure

 Hyperkalaemia

Semester 5 - Farmocology (27 decks)

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