Chest Pain & Breathlessness

Question 1

IHD Syndromes

Answer 1

MI
Angina (stable and unstable)
Sudden cardiac death

Question 2

Most common cause of IHD

Answer 2

Atheroma of coronary arteries

Question 3

Causes of IHD

Answer 3

Atheroma of coronary arteries
Coronary artery Vasculitis
Coronary artery vasospasm

Question 4

RF for IHD

Answer 4

Male
Old
FH
Hyperlipidaemia
Hypertension
Diabetes Mellitus
Smoking
Obesity
Stress
Lack of exercise

Question 5

Stage 1 of atherosclerosis

Answer 5

Blood flow forms eddies

Loose platelet aggregation

Question 6

Stage 2 of atherosclerosis

Answer 6

Arterial wall injury at platelet reaction sites
Loosened injured endothelium
Low grade inflammation
Oedema
Ruptured internal elastic membrane

Question 7

Stage 3 of atherosclerosis

Answer 7

Smooth muscle cells proliferate and produce collagen

Question 8

Stage 4 of atherosclerosis

Answer 8

Blood lipids leak into vessel wall
Smooth muscle cells take up fat and store as droplets
Macrophages take up released fat droplets by phagocytosis
Collagen fibres form

Question 9

Stage 5 of atherosclerosis

Answer 9

Collagen increases

Cellularity decreases

Question 10

Stage 6 of atherosclerosis

Answer 10

Acellular plaque with abundant collagen

Question 11

Stage 7 of atherosclerosis

Answer 11

Necrotic centre and calcified

Question 12

Stage 8 of atherosclerosis

Answer 12

Calcified necrotic area becomes gruel like
Cholesterol crystals form
Vasa vasorum vessels grow into intima

Question 13

Complications of atherosclerosis

Answer 13

Ulceration
Fissuring
Haemorrhage
Thrombosis
Aneurysm

Question 14

Stage 9 of atherosclerosis

Answer 14

Risk of massive thrombus formation as exposure of collagen, coagulation and blood flow
Plaque suddenly ruptures

Question 15

Stage 10 of atherosclerosis

Answer 15

Eddies downstream form plaque stenosis

Platelets thrombus formed = may grow and occlude lumen

Question 16

Acute MI Types

Answer 16

Transmural

Subendocardial

Question 17

Transmural Infarction

Answer 17

• involving whole thickness of ventricular wall

- underlying lesion is atheromatous plaque undergone fissuring and occlusive thrombosis

Question 18

Subendocardial infarction

Answer 18

• inner third or half of myocardium

- from generalised underperfusion of myocardium

Question 19

MI in L. coronary artery

Answer 19

Massive anterolateral MI

Question 20

MI in LAD

Answer 20

Anteroseptal MI

Question 21

MI in L circumflex

Answer 21

Lateral MI

Question 22

MI in RCA

Answer 22

Posterior MI

Question 23

0-12hrs MI appearance

Answer 23

No changes

Question 24

12-24hrs MI appearance

Answer 24

• pale blotchy discolouration

- bright eosinophilia of muscle fibres

Question 25

24-72hrs MI appearance

Answer 25

- soft, pale, yellow - loss of nuclei striations - heavy interstitial neutrophil infiltrate

Question 26

3-10d MI appearance

Answer 26

- soft yellow/brown - hyperaemic border - replacement of infarcted area with granulation tissue

Question 27

weeks- months appearance

Answer 27

- white fibrous scar | - collagenous scar tissue

Question 28

ST MI complications

Answer 28

- L ventricular failure - cardiac dysrhythmias - ventricular wall rupture - papillary muscle infarction - mural thrombus - fibrinous pericarditis - DVT -> PE

Question 29

LT MI complications

Answer 29

- intractable L. ventricular failure - ventricular aneurysm - Dressler's syndrome - recurrent MI

Question 30

What do effects of PE depends on?

Answer 30

- size of occluded vessel - number of emboli - adequacy of bronchial blood supply

Question 31

Define large PE

Answer 31

- large embolus coils within 1 pulmonary artery - saddle embolus blocks both pulmonary artery = circulatory collapse

Question 32

Define medium sized PE

Answer 32

- dural blood supply protects lungs from pulmonary artery obstruction

Question 33

How does a pulmonary infarction occur?

Answer 33

multiple emboli combined with poor bronchial blood supply

Question 34

Pathogenesis of atheroma

Answer 34

- encrustation (platelets form thrombi over injured endothelium) - inhibition (inflammation = plasma filtration) - Reaction to injury (increased permeability and SM accumulation - Monoclonal hypothesis (SM cells)