Cardiovascular Pathologies

Question 1

Hypertension:

Answer 1

AAA

Question 2

Atherosclerosis:

Answer 2

1. Fatty streak: (precursor lesion)
   - Earliest significant lesion present in young children
   - The yellow linear elevation of the intimal lining consist of lipid laden macrophages (mainly LDL’s)
   - No clinical significance and may disappear
2. Early atheromatous plaque:
   - Smooth yellow patches in the intima consisting of lipid laden macrophages
   - Non reversible and progress to established plaques
3. Fully developed atheromatous plaque:
   Central lipid core (containing foam cells and cholesterol crystals) covered by a fibrous tissue cap (containing macrophages, T cells and mast cells) within the intimal lining. Dystrophic calcification is extensive which occurs late in plaque development at arterial branching points which have turbulent blood flow (extensive markers on CT scans). Foamy macrophages due to uptake of oxidised lipoproteins. HIGHLY THROMBOGENIC

Complicated atheromas result in:

• Haemorrhage (calcification)
• Thrombosis
• Plaque rupture

Hypercholesterolaemia = Most important risk factor and occur due to mutation (lower functional LDL receptors leads to increase in LDL in the blood)

Question 3

Sable Angina:

Answer 3

• Atheromatous plaques in the coronary arteries obstruct blood flow (ischaemia = occlusion, narrowing)
• There is a mismatch between the supply of oxygen and the demand of oxygen to the myocardium (not enough oxygen is meeting the demands of the myocardium)
• Due to reduction is coronary artery blood blood flow. This can be due to atheroma (very common, most common cause of angina), spasm (tightening, uncommon) or inflammation/arteritis (very rare)
• Development of atheromatous plaque: Fatty streak, then early atheromatous plaque, then fully developed atheromatous plaque
• When myocardial demand does increase, it can be due to increase in HR or BP

Question 4

STEMI/NSTEMI/Unstable Angina (ACS):

Answer 4

First the development of the atheromatous plaque (as seen in stable angina):

• Fatty streak
• Early atheromatous plaque
• Fully developed atheromatous plaque

Then:
- Plaque rupture 
- Inflammation 
- Thrombosis 
leading to STEMI, NSTMEI and unstable angina 

• There is death of the heart muscle (myocardium) due to PROLONGED, chronic severe ischameia (atheroma occluding coronary artery), usually involving the left ventricle = MYOCARDIAL NECROSIS (which releases troponin, see investigations)
• The plaque rupture in STEMI leads to a more complete thrombus occlusion of coronary lumen
• Foam cells are macrophages that have engulfed oxidised LDL’s

Question 5

Mitral Stenosis:

Answer 5

MITRAL VALVE DOES NOT OPEN PROPERLY

• The mitral valve orifice is < 2 cm squared
• This increases the AV gradient and the pressure inside the left atrium,
• Pulmonary venous and capillary pressures increase
• Peripheral vascular resistance increases
• Pulmonary artery pressure increases and pulmonary hypertension develops
• Right heart dilatation with tricuspid regurgitation and pulmonary regurgitation

Question 6

Mitral Regurgitation:

Answer 6

MITRAL VALVE DOES NOT CLOSE PROPERLY

Question 7

Aortic Stenosis:

Answer 7

AORTIC VALVE DOES NOT OPEN PROPERLY

• Increase in left ventricular systolic pressure
• Increase in left ventricular end diastolic pressure, therefore increase in left atrial pressure
• Increase in myocardial oxygen consumption
• Myocardial ischaemia
• Left ventricular failure

Question 8

Aortic Regurgitation:

Answer 8

AORTIC VALVE DOES NOT CLOSE PROPERLY

Question 9

Heart Failure

Answer 9

• Heart is unable to pump sufficient blood to the body, therefore blood is not cleared from the right and left ventricles
• Reduction in cardiac output reduced glomerular filtration rate due to less blood in the systemic circulation
• Activates the Renin-angiotensin- aldosterone system (to increase volume)

Question 10

Atrial Fibrillation

Answer 10

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