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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

(67 cards)

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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
Name 2 ways of reducing nitrate tolerance
1. Allow 8-12 hours nitrate free period each day | 2. Reversal by SH donors
26
Name an SH donor
N-acetylcysteine
27
Name a drug used for acute relief of chest pain during the management of angina pectoris
Sublingual GTN
28
Name 3 types of drugs used to prevent angina attacks during the management of angina pectoris
1. Beta-blockers 2. Rate-limiting calcium channel modulator 3. Isosorbide mononitrate
29
Describe the direct effect of beta-blockers during treatment of angina
Reduce myocardial oxygen demand by reducing heart rate and contractility
30
Describe the indirect effect of beta-blockers during treatment of angina
Reduce peripheral vascular resistance, blood pressure, afterload and oxygen demand
31
How are beta-blockers used in the treatment of angina?
Used in prophylaxis of stable angina
32
Why are beta-blockers only used in stable angina?
May exacerbate vasospasm in variant angina
33
How are calcium channel modulators used in the treatment of angina?
Used in prophylaxis of stable and variant angina
34
Describe how calcium channel modulators decrease oxygen demand during the treatment of angina
- Lower blood pressure - Reduce afterload - Decrease oxygen demand
35
Describe how calcium channel modulators increase oxygen supply during the treatment of angina
- Dilate epicardial coronary arteries - Improve blood flow to ischaemic sub-endocardium - Increase oxygen supply
36
Why are rate-limiting calcium channel modulators preferable during the treatment of angina?
Have negative inotropic, chronotropic effects, further reducing cardiac work and oxygen demand
37
Why are rate-limiting calcium channel modulators and beta-blockers not used in conjunction?
Both reduce heart work so can lead to significant bradycardia
38
Name 2 ways in which nicorandil functions
1. Potassium channel opener | 2. Organic nitrate
39
Describe how nicorandil decreases oxygen demand during the treatment of angina
- Arterial and venous dilatation - Decrease in cardiac work - Decrease in oxygen demand
40
Describe how nicorandil increases oxygen supply during the treatment of angina
- Dilatation of coronary arteries | - Increased oxygen supply
41
Name 4 side effects of nicorandil
1. Flushing 2. Dizziness 3. Headache 4. Oral ulceration (uncommon)
42
What does ivabradine target?
Inhibits If mixed NaK inward pacemaker current
43
Describe how ivabradine decreases oxygen demand during the treatment of angina
- Decrease in heart rate - Decrease in cardiac work - Decrease in oxygen demand
44
Name 4 side effects of ivabradine
1. Bradycardia 2. Heat block 3. Enhanced brightness 4. Blurred vision
45
Name 3 major drugs in long term management of post myocardial infarction
1. Beta-blockers 2. ACE inhibitors / ARBs 3. Statins / Anti-platelets / Nitrates
46
Name 4 reasons why beta-blockers are useful in the long term management of post myocardial infarction
- Attenuate ischaemia-related remodelling - Reduced incidence of ventricular dysrhythmias - Some decreased recurrence of myocardial infarction - Decrease morbidity and mortality
47
Name a reason why ACE inhibitors / ARBs are useful in the long term management of post myocardial infarction
Attenuate left ventricular dysfunction / remodelling
48
What are 2 main types of cardiac arrhythmias?
1. Supraventricular tachycardia | 2. Atrial fibrilation
49
Describe supraventricular tachycardia
- Abnormally fast heart bate - Decreased pumping efficiency, output and blood pressure - Increased oxygen consumption and risk of myocardial ischaemia
50
Name 2 drugs used to treat supraventricular tachycardia
1. Beta-blockers (metoprolol) | 2. Rate-limiting calcium channel modulators
51
Describe atrial fibrillation
- Chaotic electrical activity in atria resulting in irregular rhythm - Less efficient pumping of heart and increased risk of stroke - Absence of P waves
52
Name 2 treatments of atrial fibrillation
1. Rate control (beta-blockers) and anti-coagulants | 2. Rhythm control (digoxin) and anti-coagulants
53
What is heart failure?
When the heart is unable to supply sufficient blood to tissues to meet the body's metabolic needs
54
Name 2 acute causes of heart failure
1. Severe myocardial infarction | 2. Cariotoxicity
55
Name 4 chronic causes of heart failure
1. Progressive coronary atherosclerosis 2. Hypertension 3. Valve disease 4. Cardiomyopathies
56
Name 3 major symptoms of heart failure
1. Reduced exercise tolerance / fatigue 2. Breathless due to pulmonary oedema (left failure) 3. Ankle swelling / jugular vein distension (right failure)
57
Describe the consequences of heart failure
- 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
Name 4 types of drugs which are used to treat heart failure
1. Diuretics 2. ACE inhibitors / ARBs / Aldosterone antagonists 3. Beta-blockers (chronic) 4. Digoxin (chronic)
59
Describe diuretics in the treatment of heart failure
- Mostly loop diuretics (furosemide) - Symptomatic relief of oedema - Do not increase survival
60
Name 4 adverse effects of loop diuretics
1. Hypokalaemia 2. Hypocalcaemia 3. Metabolic disturbances - Tinnitus
61
Why are drugs which suppress excessive RAAS activity used in the treatment of heart failure?
- Prolong survival - Vasodilatation reduces after-load - Sodium and water loss reduces pre=load - Cardiac work decreases - Reduction of adverse remodelling
62
Why are beta-blockers contraindicated during acute heart failure?
May compromise cardiac output
63
Why are beta-blockers useful in chronic stable heart failure?
- 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
What is the mechanism for the positive inotropic effect of digoxin?
- Inhibits the sodium potassium ATPase pump | - Sodium accumulates intracellularly causing calcium to enter the cell leading to increased contraction
65
How does digoxin control ventricular rate?
- Decreases heart rate - Decreases conductivity of AV node - Enables more effective filling of the ventricle
66
Describe 4 adverse effects of digoxin on the GI system
1. Anorexia 2. Nausea 3. Vomiting 4. Diarrhoea
67
Describe 3 adverse effects of digoxin on CNS
1. Confusion / depression 2. Disturbances of colour vision 3. Vertigo

DEN 2026 - Pharmacology (22 decks)

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