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The Cardiovascular System > Drugs Used in the Treatment of Ichaemic Heart Disease > Flashcards

Drugs Used in the Treatment of Ichaemic Heart Disease Flashcards

1
Q

What two things can ischaemic heart disease lead to

A

Angina and myocardial infarction

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2
Q

In what circumstances does angina arise from ischaemic heart disease

A

When there is a stable plaque that causes narrowing of the coronary arteries.

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3
Q

In what circumstances does myocardial infarction arise from ischaemic heart disease

A

When there is an unstable plaque and thrombus formation.

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4
Q

What does vascular endothelium regulate

A

Smooth muscle tone, permeability and leukocyte adhesion, platelet aggregation and tendency for thrombus formation.

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5
Q

What are four causes of endothelial dysfunction

A
  • elevated and modified LDL, e.g. in hypercholesterolaemia
  • Oxygen free radicals caused by smoking, hypertension and activated inflammatory cells
  • infectious micro-organisms
  • physical damage by turbulent flow.
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6
Q

What are foam cells

A

Macrophages that take up low density lipoprotiein oxidised by the interaction with oxygen free radicals. They are a component of fatty streaks.

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7
Q

What are the three methods of management of coronary artery disease

A
  • Reduce risk factors for development
  • Pharmacological measures
  • Surgical intervention.
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8
Q

What risk factors for the development of coronary artery disease can be reduced

A

Diet, smoking, blood pressure, diabetes

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9
Q

Why are women more protected from endothelial dysfunction until menopause

A

Due to the presence of oestrogen.

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10
Q

What pharmalogical measures can be used to prevent the development of coronary artery disease

A

The use of lipid lowering drugs such as statins and fibrates

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11
Q

What are two examples of lipid lowering drugs

A

Statins and fibrates

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12
Q

What pharmacological measures can be used to treat the angina symptoms of coronary artery disease

A

Use of nitrates which are cleaved to produce nitric oxide - a potent vasodilator.

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13
Q

What pharmacological measures can be used to prevent thrombosis and myocardial infarction in coronary artery disease

A

Anti-platelet and anti-coagulant drugs.

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14
Q

What surgical measures can be used in the management of coronary artery disease

A
  • Balloon angioplasty for plaque removal
  • Stenting
  • Coronary artery bypass grafting.
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15
Q

What are the risk factors for coronary artery disease

A
  • Genetic
  • Smoking
  • Diet
  • Hyperlipidaemia
  • Hypertension
  • Diabetes
  • Age
  • Male sex.
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16
Q

What is an example of a fibrate

A

Benzafibrate

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17
Q

What do fibrates do

A

They are lipid lowering drugs. They decrease circulating VLDL and triglyceride and increase HDL.

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18
Q

What do statins do

A

They are lipid lowering drugs which lower LDL levels. They are HMG-CoA reductase inhibitors. This is the rate determining step of cholesterol formation.

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19
Q

What is an example of a statin

A

Simvastatin

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20
Q

What is the mechanism of action of statins as HMG-CoA reductase inhibitors

A

LDL is formed by cholesterol which is synthesised in the liver. HMG-CoA reductase is important in the rate limiting step of this process. Statins block the formation of LDL by inhibiting the HMG-CoA reductase enzyme.

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21
Q

What is mevalonate

A

A precursor for cholesterol

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22
Q

As well as inhibiting the formation of LDL, what else do statins do

A

They increase the expression of LDL receptors to increase the uptake of LDL.

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23
Q

What is angina

A

Intermittent chest pain caused by mismatch between demand of oxygen by the heart and supply of oxygen to the heart.

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24
Q

How is angina managed

A

By reducing the demand on the heart or increasing the oxygen supply to the heart to reduce the imbalance between supply and demand.

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25
Q

What is used to treat angina during an acute attack

A
  • Rest

- Nitrates

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26
Q

What is an example of a nitrate used for treatment of an acute angina attack

A

Glyceryl trinitrate

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27
Q

What types of drugs are used for prophylaxis of angina to reduce the likelihood of an attack

A
  • Beta adrenoceptor antagonists
  • Calcium antagonists
  • KATP channel opener
  • Longer lasting nitrate
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28
Q

What is an example of a beta adrenocepttor antagonist used for prophylaxis of angina

A

Atenolol

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29
Q

What is an example of a calcium antagonist used for prophylaxis of angina

A

Nifedipine

30
Q

What are two examples of a KATP channel openers used for prophylaxis of angina

A

Nicorandil and ivabradine

31
Q

What is an example of a longer lasting nitrate used in prophylaxis of angina

A

Isosorbide dinitrate

32
Q

What is the mechanism of action of nitrates

A

Nitric oxide is released which acts to bring about the conversion of GTP to cGMP at guanylate cyclase. This reduces the availability of calcium ions and causes relaxation of smooth muscle.

33
Q

What route is used to take nitrates

A

The parenteral route for rapid absorption.

34
Q

Why are nitrates effective

A

They dilate veins, decrease venous return, decreasing the volume of blood returned to the heart and decreasing the strain on the heart. They also decrease peripheral resistance, reducing demand.

35
Q

What is nicorandil

A

A potassium channel opener (KATP opener)

36
Q

What is the mechanism of action of nicorandil

A

It increases the action of ATP sensitive channels in smooth muscle cells which prevents contraction and relaxes the muscle. This reduces the load on the heart.

37
Q

Where do beta adrenoceptor blockers act

A

Beta adrenoceptor blockers block beta-1 receptors in the heart and also in the kidney.

38
Q

What is the mechanism of action of beta-adrenoceptor blockers

A

On cardiac beta 1 adrenoceptors, beta blockers reduce heart rate and therefor oxygen demand. On renal beta 1 adrenoceptors, beta blockers reduce blood volume by reducing renin release and the activation of RAAS. Resistance in the arterioles and therefore preload is reduced so oxygen demand is reduced.

39
Q

What is ivabradine

A

It is an ATP sensitive potassium channel opener

40
Q

What is the mechanism of action of ivabradine

A

It opens ATP sensitive calcium channels, allowing an inflex of potassium ions and reducing the rate of spontaneous depolarisation during action potential generation in SA node cells. This reduced heart rate and O2 demand.

41
Q

What are nifedipine and dilthiazem

A

Calcium antagonists

42
Q

What is the action of calcium antagonists

A

Calcium antagonists prevent the opening of voltage dependent calcium ion channels. This prevents the re-entry of calcium into the cardiac muscle so this reduces the availability of calcium ions for contractility. This reduces the force of contraction and oxygen demand.

43
Q

What are anti-thrombotic drugs used for

A

To reduce the risk of thrombus formation if an atherosclerotic plaque ruptures.

44
Q

What two drugs are usually used in anti-thrombotic therapy

A

Anti-coagulants and anti-platelets.

45
Q

What happens if there is damage to the endothelium

A

There is collagen in the sub-endothelial layer which is exposed and triggers the aggregation of platelets to the area of damage.

46
Q

What stabilises the thrombus

A

Fibrin strands.

47
Q

What happens to platelets when they are activated

A

They change shape and degranulate to release ADP and ATP.

48
Q

What are two types of anti-platelet drugs

A

Cyclooxygenase inhibitors, P2Y12 inhibitors and thrombin receptor antagonists.

49
Q

What is an example of a cyclooxygenase

A

Aspirin

50
Q

What does aspirin do

A

It irreversibly inhibits COX, and prevents the formation of TxA2 and platelet activation.

51
Q

What are the roles of cyclooxygenase in thrombosis

A
  • To convert arachidonic acid into prostaglandin precursors

- To produce prostacyclin which is responsible for producing mucus in the stomach

52
Q

Why should aspirin not be used in people with decreased mucus in their stomach

A

Because aspirin is a cyclooxygenase inhibitor and cyclooxygenase is responsible for the production of prostacyclins which produce mucus in the stomach.

53
Q

What are two examples of P2Y12 inhibiors

A

Clopidogrel and ticagrelor

54
Q

What do P2Y12 inhibitors do

A

Blocks the effect of ADP and prevents platelet activation.

55
Q

What is the role of P2Y12 in the normal production of a thrombus

A

P2Y12 receptors are present on the surface of platelets and ATP acts on these to increase the activity of calcium and activate the platelets.

56
Q

What happens if P2Y12 receptors are inhibited

A

The platelets are not activated so there is less platelet activity and thrombus formation decreases.

57
Q

What is an example of a thrombin receptor antagonist

A

Voripaxar

58
Q

What do thrombin receptor antagonists do

A

Prevent the activation of PAR-1 receptors on platelets.

59
Q

What is the risk associated with anti-thrombotic drugs

A

Bleeding.

60
Q

What is ATIII

A

Antithrombin III

61
Q

What is the role of ATIII

A

The body’s own anti-thrombotic mechanism. It prevents the formation of fibrin which binds to receptors on platelets and stabilises thrombi.

62
Q

What is the role of heparin

A

To bind to antithrombin III and promote its anti-thrombotic action

63
Q

What is the role of anti-coagulant drugs

A

To prevent the formation of fibrin which stabilises the platelet plug

64
Q

What are three examples of anti-coagulant drugs

A

Heparin, warfarin and rivaroxaban

65
Q

Which anti-coagulant drug can be given intravenously

A

Heparin

66
Q

Which anti-coagulant drugs can be given orally

A

Warfarin and rivaroxaban.

67
Q

What is the mechanism of action of rivaroxaban

A

It is a factor 10a inhibitor which inhibits the formation of thrombi as it stops the conversion of prothrombin to thrombin and therefore fibrinogen to fibrin.

68
Q

What is the mechanism of action of warfarin

A

Warfarin is a vitamin K inhibitor. Some of the products of oxidised vitamin K are used in the clotting cascade - factors 2,7,9 and 10 so warfarin inhibits the formation of these factors and stops the progression of the clotting cascade.

69
Q

What are the negative aspects of the use of warfarin

A
  • It has a narrow therapeutic index
  • There is a high risk of bleeding
  • Blood levels must be checked regularly
70
Q

What are the consequences of MI

A
  • Ischaemia
  • Cell death
  • Heart failure.

The Cardiovascular System (15 decks)

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