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Semester 2 - CVS > Week 9 - Drugs > Flashcards

Week 9 - Drugs Flashcards

1
Q

What may result in ectopic pacemaker activity?

A
  • Damaged myocardium becoming depolarised, and firing APs

- Ischaemia activating a latent pacemaker region

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2
Q

What are “after-depolarisations”?

A

Abnormal depolarisations following an action potential

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3
Q

What usually causes delayed after-depolarisations, and what is their consequence?

A

Usually triggered by increased intracellular calcium levels, which results in an early action potential, and hence tachycardia.

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4
Q

What are the three main causes of an arrhythmia?

A
  1. Ectopic pacemaker activity
  2. After-depolarisations
  3. Re-entry loop
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5
Q

What usually causes early after-depolarisations, and what is their consequence?

A

Prolonged action potential

Long QT syndrome

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6
Q

What is a re-entry loop?

A

If there is incomplete conduction damage (unidirectional block), excitation will travel the wrong way through the damaged area, creating a short circuit.

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7
Q

What causes atrial fibrillation?

A

Several re-entry loops in the atria, resulting in uncoordinated contraction.
Could also be due to ectopic excitation, however.

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8
Q

What is the difference between supraventricular tachycardia and ventricular tachycardia?

A 
Supraventricular = tachycardia resulting from problem in atria or AV node.
Ventricular = problem originates in ventricles, Purkinjie fibres or bundle of Hiss.
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9
Q

What types of drug can be used to treat arrhythmias?

A
  1. Voltage-sensitive Na+ channel blockers (class I)
  2. B-blockers (class II)
  3. Potassium channel blockers (class III)
  4. Calcium channel blockers (class IV)
  5. Adenosine
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10
Q

Give an example of a class I anti-arrhythmic drug

A

Lidocaine

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11
Q

What is the mechanism of lidocaine, a class I anti-arrhythmic drug?

A

Use-dependent voltage-sensitive Na+ channel blocker.

Blocks damaged areas of myocardium which are depolarised, and hence likely to fire APs.

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12
Q

In what situations may lidocaine be used?

A

After an MI, to prevent VF.

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13
Q

Give an example of a class II anti-arrhythmic drug, and state what the general function of these drugs is.

A

Propanolol.

B-adrenoreceptor antagonists (B-blockers)

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14
Q

Explain the mechanism by which B-blockers decrease heart rate, in reference to the pacemaker potential.

A

Act on B1-adrenoreceptors in the heart, hence decreasing sympathetic activity.
This means the slope of the pacemaker potential is decreased, and hence it takes longer to reach an AP threshold –> HR down.

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15
Q

How do B-blockers reduce ischaemia?

A

Reduce HR, so reduce O2 demand.

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16
Q

Apart from slowing heart rate, what else do B-blockers do?

A

Slow conduction at AV node, thus preventing supraventricular tachycardia.

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17
Q

What class of anti-arrhythmic drugs are potassium channel blockers?

A

Class III

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18
Q

What is the mechanism of potassium channel blockers?

A

Prolong the action potential, hence lengthening absolute refractory period, which delays the next action potential - i.e. slow heart rate.

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19
Q

Why are potassium channel blockers now usually not the choice drugs for tachycardia?

A

They can be pro-arrhythmic.

20
Q

Give an example of a potassium channel blocker which IS still used.
What is it used for?

A

Amiodarone

Used to treat Wolff-Parkinson-White syndrome, in which extra conduction pathway leads to re-entry loops.

21
Q 
What class of anti-arrhythmic drugs does Verapamil belong to?
What is their general action?
A

Class IV

Calcium channel blockers

22
Q

What is the mechanism of calcium channel blockers?

A

Similar to B-blockers -
- decrease slope of pacemaker potential
- decrease AV nodal conduction
But also have -ve inotropic effect

23
Q

What is the mechanism of adenosine?

A

Acts on a1-adrenoreceptors at the AV node
Enhances K+ conductance, which results in hyperpolarisation.
This briefly stops the heart so it can “reset”.

24
Q

What are the two major types of positive inotropes?

A

Cardiac glycosides

B-adrenoreceptor agonists

25
Q

Do positive inotropes work long-term?

When are they used?

A

No - increase cardiac output, but this stresses heart, so no real effect on long-term survival.
Used in palliative care to improve quality of life.

26
Q

Give an example of a cardiac glycoside

A

Digoxin

27
Q

How do cardiac glycosides act to increase the force of contraction of the heart?

A

Block Na+/K+-ATPase, hence Na+ is no longer extruded.
This means that a Na+ concentration gradient is not established, and therefore Na+ no longer enters the cell via NCX.
In turn, this means that Ca2+ does not leave the cell via NCX, and builds up –> stronger contraction.

28
Q

Apart from a +ve inotropic effect, what other effect do cardiac glycosides have?

A 
Increase vagal (parasympathetic) activity, therefore slowing the heart.
Thus only used in tachycardia.
29
Q

Give an example of a B-adrenoreceptor agonist.

A

Dobutamine

30
Q

When might B-adrenoreceptor agonists be used?

A

Cardiogenic shock

Acute, but reversible, cardiac failure.

31
Q

Name 3 types of drug which are used to reduce the workload of the heart.

A

ACE-inhibitors
B-blockers
Diuretics

32
Q

What is the mechanism of ACE-inhibitors?

A

Block “angiotensin converting enzyme”, preventing production of angiotensin II.
This reduces both preload and afterload of heart, as it prevents angiotensin II acting as a vasoconstrictor and stimulating water retention.

33
Q

What are the two general mechanisms by which angina may be treated?

A

Reduce workload of the heart, hence reducing O2 demand.

Improving blood supply, hence increasing O2 supply.

34
Q

What 3 types of drug may be used to treat angina?

A
  1. B-blockers
  2. Organic nitrates
  3. Calcium channel antagonists
35
Q

Give an example of an organic nitrate

A

Glyceryl trinitrate

36
Q

How do organic nitrates cause vasodilation?

A

React with thiols in the vascular smooth muscle, to release NO2-, which is reduced to NO (nitric oxide).
NO activates guanylate cyclase, which increases cGMP.
In turn, this reduces the concentration of Ca2+ in the cell, hence reducing the smooth muscle contraction.

37
Q

What is the primary site of organic nitrate action?

A

The venous system –> venodilation

This reduces preload

38
Q

Where else, apart from the venous system, may organic nitrates act?
Why is this beneficial?

A

The collateral coronary arteries.

Means vessels providing a route around blockage can accommodate more blood.

39
Q

What conditions make it more likely for blood clots to develop?

A

Atrial fibrillation
After an MI
If you have prosthetic heart valves

40
Q

Which two types of drug may be used to prevent blood clot formation?

A

Anticoagulants

Antiplatelet drugs

41
Q

Compare and contrast heparin and warfarin.

A

Both anticoagulants.
Heparin - only used short-term. Inhibits thrombin.
Warfarin - can be used long-term. Antagonises action of vitamin K.

42
Q

Name a common antiplatelet drug.

A

Aspirin

43
Q

What may cause hypertension?

A

Increase blood volume

Increased TPR

44
Q

What are the 3 main ways that hypertensive drugs act?

A
  • Reduce blood volume
  • Reduce TPR
  • Reduce cardiac output
45
Q

Which 5 types of drug may be used to treat hypertension?

A
  1. Diuretics
  2. ACE-inhibitors
  3. B-blockers
  4. Calcium channel blockers
  5. a1 - adrenoreceptor antagonists

Semester 2 - CVS (8 decks)

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