Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

Imminent myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why does the mismatch of oxygen supply and demand occur?

A

Heart has to work harder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are 2 markers of acute coronary syndrome?

A
  1. Troponin levels

2. ECGs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is an ECG affected by a STEMI?

A

The ST segment of the ECG becomes elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is an ECG affected by a non-STEMI?

A

The ST segment of the ECG becomes depressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Name 3 examples of organic nitrate drugs

A
  1. Glyceryl Trinitrate (GTN)
  2. Isosorbide dinitrate (ISDN)
  3. Isosorbide mononitrate (ISMN)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the ADME of GTN

A
  • Poor oral bioavailability
  • Given as transdermal patch / sublingual spray
  • Rapidly enters through sublingual means
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the ADMA of ISDN / ISMN

A
  • ISMN has better oral bioavailability

- Oral administration causes delayed onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe 3 functions of nitrates

A
  1. Dilate systemic veins
  2. Dilate coronary arteries
  3. Redistribute blood in heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Name 6 adverse effects of organic nitrates

A
  1. Postural hypotension
  2. Flushing
  3. Headache
  4. Xerostomia
  5. Tachycardia
  6. Nausea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is nitrate tolerance?

A

Loss of effectiveness with continued therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why does nitrate tolerance occur?

A
  • Depletion of tissue sulfhydryl groups

- Organic nitrate cannot be converted into NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Name an SH donor

A

N-acetylcysteine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions