PHARM - Drugs for the Treatment of Ischaemic Heart Disease - Week 5 Flashcards

1
Q

What are ischaemic heart diseases typically a result of?

A

Plaque buildup in the coronary arteries, narrowing them and preventing adequate blood flow to the heart, resulting in ischaemia.

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2
Q

What is the principal artery supplying blood to the heart?

A

Coronary arteries.

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3
Q

In what two ways can blood flow to the heart be increased, and why do they increase flow?

A

Dilating coronary arteries - self explanatory
Decreasing heart rate - arteries are less compressed

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4
Q

What does the O2 demand of the heart depend on?

A

The cardiac workload

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5
Q

Give the formula for cardiac output.

A

Stroke volume x heart rate

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6
Q

Define preload.

A

Degree of stretch pre-contraction

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7
Q

Define afterload.

A

Resistance the heart pumps against

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8
Q

Define angina.

A

Chest pain

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9
Q

Does ischaemic heart disease cause angina?

A

Yes

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10
Q

Name three possible causes of angina.

A

Imbalance between O2 supply and needs
Insufficient O2 to meet cardiac demand
Reduced perfusion rather than inadequate blood O2

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11
Q

Define stable angina, the pain it causes, two means by which it can be induced, and what it is associated with.

A

Chest pain that occurs with exertion or stress. It is associated with coronary artery disease.

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12
Q

Define variant angina, when it occurs, and its mediator.

A

Coronary vasospasm at rest, mediator unknown.

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13
Q

Define unstable angina, when it occurs (2), and what secondary complication it has the potential to cause.

A

Angina at rest and with effort.
Potential for thrombi formation.

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14
Q

Do arterioles typically get plaque buildup?

A

No

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15
Q

Consider stable angina treatment. What three things should treatment accomplish and what 2 effects should drugs have?

A

Treat to:
-prevent attacks
-relieve symptoms
-prevent progression to heart attack
Use drugs to:
-increase O2 supply
-reduce O2 demand

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16
Q

In what two ways can O2 supply be increased?

A

Dilating coronary arteries
Reducing heart rate

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17
Q

Is it relatively easy or difficult to dilate atheromatous arteries?

A

Difficult

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18
Q

Can coronary arteries always be dilated?

A

Not neccessarily, they may already be maximally dilated.

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19
Q

Explain why reducing heart rate increases O2 supply t othe heart.

A

Heart spends longer in relaxation phase
Coronary arteries have longer to fill

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20
Q

In what three ways can O2 demand be decreased?

A

Decrease cardiac output
Reduce preload
Reduce afterload

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21
Q

In what two ways can cardiac output be decreased?

A

Reduce heart rate
Reduce stroke volume

22
Q

In what two ways can preload be decreased? Give an example of a drug class for this.

A

Dilate veins
Reduce venous return
Nitrates

23
Q

In what two ways can afterload be decreased? Give an example of a drug class for this.

A

Dilate arterioles
Decrease resistance
Ca2+ channel blockers

24
Q

How do nitrates work to treat angina?

A

They are biotransformed to NO, which dilates all vessels.

25
Q

Describe the effect of NO on the following vessels (other than it dilates them) and whether it is major or minor:
Veins
Large arteries
Coronary arteries

A

Veins
-decreases preload (major)
Large arteries
-decreases afterload (minor)
Coronary arteries
-no effect

26
Q

Consider nitrates for treating angina. Name two additional effects it has on other smooth muscle, and whether they are clinically significant.

A

Other smooth muscle - brief relaxation of the gut and airways.
Not clinically significant.

27
Q

Name an effect nitrates can have on blood pressure, and why this occurs.

A

Postural hypotension due to venous pooling

28
Q

Name 5 side effects of using nitrates for angina.

A

Headache
Flushing
-due to cerebral, head, and neck arterial dilation
Reflex tachycardia

29
Q

What are nitrates typically used in combination with and to minimise what side effect?

A

B-blockers or cardiac-selective calcium channel blockers to minimise tachycardia.

30
Q

Describe four ways in which tolerance to nitrates can occur with continuous use. Name which of the four is the classic mechanism.

A

-The classic mechanism involves depletion of tissue thoils needed for NO production
-Increased release/sensitivity to constrictors like AII
-Increased endothelial free radical production scavenging NO, reducing bioavailability
-Reduced/abnormal activity of muscle mitochondria, reducing NO production, increasing free radicals

31
Q

How can the classic mechanism of nitrate tolerance be treated? What is required for nitrate tolerance in general?

A

Treatment with N-acetyl cysteine restores GTN (glycerine) effect.
A drug-free period is required to minimise tolerance - removing the patch overnight.

32
Q

Name 2 main ways B-blockers can be used to treat angina.

A

They reduce heart contractility and decrease heart rate.

33
Q

What is the first-line therapy for angina prophylaxis

A

Selective or non-selective B-blockers

34
Q

Name 6 adverse effects and contraindications for B-blockers.

A

Cold extremities
Fatigue
Cardiac depression
Bradycardia
Broncoconstriction
Decreased symptoms of hypoglycaemia

35
Q

What kind of calcium channel blockers can be used for angina treatment?

A

L-type

36
Q

What four effects do calcium channel blockers have on the heart with angina treatment?

A

Decreased heart rate, stroke volume, cardiac output, and decreased O2 demand.

37
Q

What two vascular effects do calcium channel blockers have with angina treatment?

A

Arterial dilation, reducing afterload and demand

38
Q

What two drugs must calcium channel blockers never be taken with?

A

A B-blocker or digoxin

39
Q

What is the effect of ivabradine, and how does it work?

A

Pure heart rate reduction
Specific and selective inhibition of inward sodium/potassium current in the sinus node

40
Q

When is ivabradine given for angina treatment?

A

Only if heart rate is >70 beats per minute

41
Q

Name 3 adverse effects of ivabradine.

A

Brightness in visual field due to retinal effects (same target, different site)
Bradycardia
Conduction abnormalities

42
Q

Name two factors that require precaution when giving ivabradine.

A

Heart rate <70 bpm
Levels are increased by some antibiotics and antifungals

43
Q

Consider angina therapy. Are the drugs used for treatment disease-modifying? Do they lower the risk of infarction or cardiac arrest?

A

They are not disease-modifying, so there is an unchanged risk to heart disease.

44
Q

Are single drugs given for angina treatment is it a combination therapy?

A

Combination therapy

45
Q

Summarise angina therapy by lising the following drugs by whether or not they effect the following factors:
Drugs
-ivabradine
-B-blockers
-Ca2+ channel blockers
-nitrates
Factors
-heart rate
-stroke volume
-afterload
-preload

A

Ivabradine
-lower heart rate
B-blocker
-lower heart rate
-lower stroke volume
Ca2+ channel blocker
-lower heart rate
-lower stroke volume
-lower afterload
Nitrates
-lower preload

46
Q

What effect do the following factors (if decreased) have on O2 supply and demand (2):
Heart rate
Stroke volume
Afterload
Preload

A

They all decrease O2 demand
Decreasing heart rate increases O2 supply

47
Q

How can a coronary spasm be treated?

A

Short-acting nitrate

48
Q

Aside from nitrates, list another drug that can be used to treat variant angina.

A

Ca2+ channel blocker

49
Q

Can B-blockers be used for treating variant angina?

A

No, they are contraindicated

50
Q

How can unstable angina be treated? What additional drug is required and why?

A

Same as for classic angina, with the addition of aspirin to prevent thrombosis.

51
Q

Name 6 ways the risk factor for angina can be reduced.

A

Stop smoking
Increase physical activity
Lose weight
Treat hypertension, dyslipidaemia, and diabetes

52
Q

Name two revascularisation techniques for angina.

A

Percutaneous coronary intervention
Coronary artery bypass graft