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DEN 2026 - Pharmacology > Angina, Myocardial Infarction and Heart Failure (Cardiovascular Disease II) > Flashcards

Angina, Myocardial Infarction and Heart Failure (Cardiovascular Disease II) Flashcards

1
Q

Describe angina pectoris

A
  • Chest pain radiating to arm, neck and jack due to ischaemic heart disease caused by coronary atherosclerosis
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2
Q

What can bring on a bout of angina?

A
  • Transient mismatch of oxygen supply and demand

- Activation of the sympathetic nervous system during physical exercise or emotional anxiety

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3
Q

How do symptoms of stable angina and unstable angina differ?

A
  • Stable angina should resolve at rest

- Persistent pain at rest indicates unstable angina

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4
Q

What can persistent cardiac pain at rest indicate, other than unstable angina?

A

Imminent myocardial infarction

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5
Q

Why does the mismatch of oxygen supply and demand occur?

A

Heart has to work harder

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6
Q

What 3 cardiac diseases come under the umbrella term ‘Acute Coronary Syndrome’?

A
  1. ST elevation myocardial infarction (30%)
  2. Non ST elevation myocardial infarction (25%)
  3. Unstable angina (45%)
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7
Q

What are 2 markers of acute coronary syndrome?

A
  1. Troponin levels

2. ECGs

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8
Q

How does myocardial infarction affect troponin levels?

A
  • Lumen of coronary arteries become occluded
  • Troponin leaks out of damaged heart muscle due to lack of oxygen supply
  • As damage levels increase, troponin secretion levels increase
  • STEMI produces more troponin than non-STEMI due to increased damage
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9
Q

How is an ECG affected by a STEMI?

A

The ST segment of the ECG becomes elevated

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10
Q

How is an ECG affected by a non-STEMI?

A

The ST segment of the ECG becomes depressed

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11
Q

What are 3 rationales for the use of drugs in angina pectoris?

A
  1. Increase coronary blood flow (increase oxygen supply to heart muscle)
  2. Reduce cardiac work (decrease oxygen demand by heart muscle)
  3. Reduce clotting in diseased arteries
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12
Q

Name 6 drugs used to treat angina pectoris

A
  1. Organic nitrates
  2. Nicorandil / Ivabradine
  3. Beta blockers
  4. Calcium channel modulators
  5. Anti-platelet agents
  6. Anticoagulants
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13
Q

Name 3 examples of organic nitrate drugs

A
  1. Glyceryl Trinitrate (GTN)
  2. Isosorbide dinitrate (ISDN)
  3. Isosorbide mononitrate (ISMN)
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14
Q

Describe the ADME of GTN

A
  • Poor oral bioavailability
  • Given as transdermal patch / sublingual spray
  • Rapidly enters through sublingual means
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15
Q

Describe the ADMA of ISDN / ISMN

A
  • ISMN has better oral bioavailability

- Oral administration causes delayed onset

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16
Q

Describe the mechanism of action of nitrates

A
  • Organic nitrates metabolised to NO by enzymes in smooth muscles
  • Sulfhydryl dependent mechanism
  • NO stimulates soluble guanylate cyclase to stimulate cGMP production
  • cGMP is relaxant 2nd messenger for smooth muscle
  • Muscle relaxes causing vasodilatation
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17
Q

Describe 3 functions of nitrates

A
  1. Dilate systemic veins
  2. Dilate coronary arteries
  3. Redistribute blood in heart
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18
Q

Why do nitrates cause more dilatation in veins than in arteries?

A

Reflex sympathetic activation (noradrenaline release) overcomes short lived decrease in after-load in response to arteriolar dilatation

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19
Q

How does the dilatation of systemic veins work to combat acute coronary syndrome?

A
  • Venous return decreases
  • Pre-load decreases
  • Cardiac work decreases
  • Oxygen demand decreases
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20
Q

How does the dilatation of coronary arteries work to combat acute coronary syndrome?

A
  • Improve blood flow and oxygen delivery to ischaemic areas
  • Dilatation of obstructed epicardial arteries or collateral vessels
  • Oppose vascular spasm in variant angina
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21
Q

How do organic nitrates redistribute blood in the heart?

A

Redistribute blood from epicardial to endocardial regions which are more vulnerable to ischaemia

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22
Q

Name 6 adverse effects of organic nitrates

A
  1. Postural hypotension
  2. Flushing
  3. Headache
  4. Xerostomia
  5. Tachycardia
  6. Nausea
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23
Q

What is nitrate tolerance?

A

Loss of effectiveness with continued therapy

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24
Q

Why does nitrate tolerance occur?

A
  • Depletion of tissue sulfhydryl groups

- Organic nitrate cannot be converted into NO

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25
Q

Name 2 ways of reducing nitrate tolerance

A
  1. Allow 8-12 hours nitrate free period each day

2. Reversal by SH donors

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26
Q

Name an SH donor

A

N-acetylcysteine

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27
Q

Name a drug used for acute relief of chest pain during the management of angina pectoris

A

Sublingual GTN

28
Q

Name 3 types of drugs used to prevent angina attacks during the management of angina pectoris

A
  1. Beta-blockers
  2. Rate-limiting calcium channel modulator
  3. Isosorbide mononitrate
29
Q

Describe the direct effect of beta-blockers during treatment of angina

A

Reduce myocardial oxygen demand by reducing heart rate and contractility

30
Q

Describe the indirect effect of beta-blockers during treatment of angina

A

Reduce peripheral vascular resistance, blood pressure, afterload and oxygen demand

31
Q

How are beta-blockers used in the treatment of angina?

A

Used in prophylaxis of stable angina

32
Q

Why are beta-blockers only used in stable angina?

A

May exacerbate vasospasm in variant angina

33
Q

How are calcium channel modulators used in the treatment of angina?

A

Used in prophylaxis of stable and variant angina

34
Q

Describe how calcium channel modulators decrease oxygen demand during the treatment of angina

A
  • Lower blood pressure
  • Reduce afterload
  • Decrease oxygen demand
35
Q

Describe how calcium channel modulators increase oxygen supply during the treatment of angina

A
  • Dilate epicardial coronary arteries
  • Improve blood flow to ischaemic sub-endocardium
  • Increase oxygen supply
36
Q

Why are rate-limiting calcium channel modulators preferable during the treatment of angina?

A

Have negative inotropic, chronotropic effects, further reducing cardiac work and oxygen demand

37
Q

Why are rate-limiting calcium channel modulators and beta-blockers not used in conjunction?

A

Both reduce heart work so can lead to significant bradycardia

38
Q

Name 2 ways in which nicorandil functions

A
  1. Potassium channel opener

2. Organic nitrate

39
Q

Describe how nicorandil decreases oxygen demand during the treatment of angina

A
  • Arterial and venous dilatation
  • Decrease in cardiac work
  • Decrease in oxygen demand
40
Q

Describe how nicorandil increases oxygen supply during the treatment of angina

A
  • Dilatation of coronary arteries

- Increased oxygen supply

41
Q

Name 4 side effects of nicorandil

A
  1. Flushing
  2. Dizziness
  3. Headache
  4. Oral ulceration (uncommon)
42
Q

What does ivabradine target?

A

Inhibits If mixed NaK inward pacemaker current

43
Q

Describe how ivabradine decreases oxygen demand during the treatment of angina

A
  • Decrease in heart rate
  • Decrease in cardiac work
  • Decrease in oxygen demand
44
Q

Name 4 side effects of ivabradine

A
  1. Bradycardia
  2. Heat block
  3. Enhanced brightness
  4. Blurred vision
45
Q

Name 3 major drugs in long term management of post myocardial infarction

A
  1. Beta-blockers
  2. ACE inhibitors / ARBs
  3. Statins / Anti-platelets / Nitrates
46
Q

Name 4 reasons why beta-blockers are useful in the long term management of post myocardial infarction

A
  • Attenuate ischaemia-related remodelling
  • Reduced incidence of ventricular dysrhythmias
  • Some decreased recurrence of myocardial infarction
  • Decrease morbidity and mortality
47
Q

Name a reason why ACE inhibitors / ARBs are useful in the long term management of post myocardial infarction

A

Attenuate left ventricular dysfunction / remodelling

48
Q

What are 2 main types of cardiac arrhythmias?

A
  1. Supraventricular tachycardia

2. Atrial fibrilation

49
Q

Describe supraventricular tachycardia

A
  • Abnormally fast heart bate
  • Decreased pumping efficiency, output and blood pressure
  • Increased oxygen consumption and risk of myocardial ischaemia
50
Q

Name 2 drugs used to treat supraventricular tachycardia

A
  1. Beta-blockers (metoprolol)

2. Rate-limiting calcium channel modulators

51
Q

Describe atrial fibrillation

A
  • Chaotic electrical activity in atria resulting in irregular rhythm
  • Less efficient pumping of heart and increased risk of stroke
  • Absence of P waves
52
Q

Name 2 treatments of atrial fibrillation

A
  1. Rate control (beta-blockers) and anti-coagulants

2. Rhythm control (digoxin) and anti-coagulants

53
Q

What is heart failure?

A

When the heart is unable to supply sufficient blood to tissues to meet the body’s metabolic needs

54
Q

Name 2 acute causes of heart failure

A
  1. Severe myocardial infarction

2. Cariotoxicity

55
Q

Name 4 chronic causes of heart failure

A
  1. Progressive coronary atherosclerosis
  2. Hypertension
  3. Valve disease
  4. Cardiomyopathies
56
Q

Name 3 major symptoms of heart failure

A
  1. Reduced exercise tolerance / fatigue
  2. Breathless due to pulmonary oedema (left failure)
  3. Ankle swelling / jugular vein distension (right failure)
57
Q

Describe the consequences of heart failure

A
  • Reduced cardiac output and blood pressure trigger compensatory activation of SNS and RAAS to maintain tissue perfusion and promote cardiac remodelling
  • Progressively inadequate
  • Frequent hospitalisation
  • Significant morbidity and mortality
58
Q

Name 4 types of drugs which are used to treat heart failure

A
  1. Diuretics
  2. ACE inhibitors / ARBs / Aldosterone antagonists
  3. Beta-blockers (chronic)
  4. Digoxin (chronic)
59
Q

Describe diuretics in the treatment of heart failure

A
  • Mostly loop diuretics (furosemide)
  • Symptomatic relief of oedema
  • Do not increase survival
60
Q

Name 4 adverse effects of loop diuretics

A
  1. Hypokalaemia
  2. Hypocalcaemia
  3. Metabolic disturbances
    - Tinnitus
61
Q

Why are drugs which suppress excessive RAAS activity used in the treatment of heart failure?

A
  • Prolong survival
  • Vasodilatation reduces after-load
  • Sodium and water loss reduces pre=load
  • Cardiac work decreases
  • Reduction of adverse remodelling
62
Q

Why are beta-blockers contraindicated during acute heart failure?

A

May compromise cardiac output

63
Q

Why are beta-blockers useful in chronic stable heart failure?

A
  • Reduce activation of RAAS (reduce pre-load and after-load)
  • Reduce heart rate / heart work / myocardial oxygen demand
  • Increase filling / diastole length / coronary blood flow
  • Anti arrhythmic effects
64
Q

What is the mechanism for the positive inotropic effect of digoxin?

A
  • Inhibits the sodium potassium ATPase pump

- Sodium accumulates intracellularly causing calcium to enter the cell leading to increased contraction

65
Q

How does digoxin control ventricular rate?

A
  • Decreases heart rate
  • Decreases conductivity of AV node
  • Enables more effective filling of the ventricle
66
Q

Describe 4 adverse effects of digoxin on the GI system

A
  1. Anorexia
  2. Nausea
  3. Vomiting
  4. Diarrhoea
67
Q

Describe 3 adverse effects of digoxin on CNS

A
  1. Confusion / depression
  2. Disturbances of colour vision
  3. Vertigo

DEN 2026 - Pharmacology (22 decks)

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