CVS

Question 1

Pathogenesis of ischaemic heart disease

Answer 1

1. Occlusion (75% occlusion, but degree of occlusion does not parallel severity of disease)
2. Increased myocardial demand (eg. exercise, infection, pregnancy)
3. Oxygen availability (eg. anaemia, CO poisoning, pulmonary disease)

Question 2

Pathogenesis of atherosclerosis

Answer 2

1. Chronic endothelial injury —> hyperlipidaemia (more lipoproteins below endothelial layer = increased permeability of endothelial cells), hypertension, hemodynamic factors
2. Endothelial dysfunction (in hyperlipidaemia) —> monocytes produce free radicals, oxidised LDLs for macrophages to engulf —> too much lipoproteins, accumulate in macrophages —> foam cells
3. Smooth muscle recruitment to intima —> macrophage activation, secrete cytokines to attract T-lymphocytes, recruit smooth muscle cells
4. Macrophage and smooth muscle cells engulf lipid
5. Smooth muscle proliferation, collagen, other ECM deposition, extracellular lipid —> create fibrous cap, prevents contents from leaking into bloodstream

Question 3

Define atherosclerosis. What is an atheroma?

Answer 3

Atherosclerosis: Degenerative and inflammatory disease affecting large and medium sized arteries —> thickening and loss of elasticity

Atheroma:
- Plaque —> raised lesion with soft, yellow core of lipid —> covered by white fibrous cap
- Soft, yellow core of lipid —> soft, necrotic centre, contains macrophage, foam cells —> exposure to bloodstream triggers coagulation cascade (pro thrombotic)
- Protrudes into the lumen —> causes fibrosis —> grows bigger and causes ischaemic changes

Question 4

Risk factors for atherosclerosis (modifiable and non-modifiable)

Answer 4

Non-modifiable: Age, Gender, Family history, Genetics

Modifiable: Hyperlipidaemia, hypertension, diabetes, cigarette smoking, formation of “C-reactive” protein (inflammation)

Question 5

Consequences of atherosclerosis

Answer 5

1. Vessel thickening (clogged with atherosclerotic plaque) —> narrowed lumen —> poor tissue perfusion —> distal tissue ischaemia —> distal tissue necrosis
2. Loss of elasticity —> predisposes to aneurysm formation, rupture, haemorrhage
3. Endothelial changes —> predisposes to thrombus formation —> luminal obstruction —> distal tissue necrosis

Question 6

Clinical diagnosis of myocardial infarction

Answer 6

Symptoms: severe, crushing chest pain (may radiate to arm/jaw)
ECG changes —> ST elevation
Elevated cardiac enzymes (troponin I and II)

Question 7

Complications of MI

Answer 7

1. Ventricles:
   - LV failure —> congestive heart failure
   - Rupture myocardium —> cardiac tamponade (blood flows into pericardial sac, places pressure on heart, difficulty pumping)
   - fibrosis and aneurysm —> scar forms
   - thrombus (abnormal dilation in wall of LV)
2. Conduction system:
   - electrical pulses unable to be conducted due to fibrous tissue, heart unable to pump in synchronous manner
3. Pericarditis:
   - pericardial sac can get stuck to areas of fibrosis/inflammation —> infection spreads to pericardium
4. Valves —> ruptured papillary muscle