CR2.4 Pathology of the vascular and heart

Question 1

Describe modifiable and non-modifiable risk factors for atherosclerosis.

Answer 1

Non-modifiable:

• increasing age
• male gender
• family histoy (i.e. genetics)

Modifiable:

• dyslipidaemia
• smoking
• hyertension
• obesity
• diabetes

Question 2

Discuss the development of atherosclerosis.

Answer 2

Risk factors (e.g. hypertension, smoking, smoking) damage the endothelium within the liver. This causes inflammation (i.e. platlet aggregation, permeability increase, cell adhesion). Cells move inside the intima along with LDL cholestrol. Macrophages within the intima oxidase LDL with release of free-radicals. Oxidized LDL is highly toxic and is phagocytosed by the macrophages and become foam cells. Activated macrophages produce more free-radicals, cytokines (e.g. IL-1) and growth factors. Growth factors attract smooth muscle cells from the media into the intima. Smooth muscle cells also engulf LDL and become foam cells. Smooth muscle cells produce ECM that thickens the intima. The proliferation of smooth muscle cells at the periphery create a fibrous cap.

Question 3

List the steps of natural progression of a plaque.

Answer 3

1. Macrophage infiltrate
2. Intimal thickening
3. Lipid accumulation
4. Smooth muscle migration
5. Fibrosis
6. Calcification
7. Thrombosis

Question 4

Describe the difference between stable and unstable plaques.

Answer 4

Question 5

Describe three aeitology of aneurysm and list congenital and aquired causes.

Answer 5

1. Smooth muscle loss
2. Decreased extracellular matrix (ECM)
3. Abnormal tissue perfusion

Marfan Syndrome is a congenital condition that causes connective tissue defects (i.e. cystic medial degeneration).

Question 6

List common signs of abdominal aortic aneurysm (AAA).

Answer 6

• Tearing chest pain
• Pain radiating to lower back
• Hypertension
• Unequal carotid pulse

Question 7

Define ischaemic heart disease (IHD).

Answer 7

Represents a group of pathophysiological syndromes resulting from myocardial ischemia.

This includes:

• Acute coronary syndrome
  
  • Myocardial infarction
  • Unstable angina
• Stable angina
• Chronic IHD with heart failure
• Sudden cardiac arrest

Question 8

Briefly describe the microscopic change to the myocardium in the case of myocardial infarction.

Answer 8

Muscle fibers with increased eosinophilia and loss of nuclie. Associated neutrofilic infiltrate. Coagulative necrosis begins after 4 hours and represents irreversible injury.

Question 9

Briefly describe exacerbations and mitigating factors of chest pain in pericarditis.

Answer 9

Exacerbated: inspiration, coughing and lying down

Relieved: sitting up and leaning forward

N.B. Always consider patient Hx for possible infection.

Question 10

Describe common types of pericarditis.

Answer 10

• Serous (No adhesion resulting from non-infectious inflammations e.g. Rheumatic fever, SLE)
• Fibrinous and serofibrinus (Serous fluid and fibrin exudate usually found in acute MI, post infarction-Dressler syndrome) –> pericardial friction rub
• Purulent or suppurative (i.e Presence of infective organisms and a large volume can cause cardiac tamponade)
• Haemorrhagic (Is the prescence of blood and serous/fibrinous/suppurative exudate e.g. seen in malignant neoplastic involvement)
• Caseous (e.g. Usually TB)