Atheroma & infarction

Question 1

Atheroma

Answer 1

Degeneration of the walls of the arteries caused by accumulated fatty deposits and scar tissue. Leading to restriction of circulation and risk thrombosis

Question 2

Infarction

Answer 2

Obstruction of the blood supply to an organ or region of tissue, typically by thrombus or embolus, causing local death of the tissue

Question 3

What is atherosclerosis

Answer 3

Complex inflammatory process

Mediated by low density lipoprotein angiotensin II

Question 4

Common sites for atherosclerosis

Answer 4

Larger arteries
Carotid arteries and circle of Willis
Coronary arteries
Iliac arteries
Aorta

Question 5

Steps for initiation

Answer 5

1) Inflammatory triggers active arterial endothelial cells. Oxidation of LDL particles, chiefly stimulated by presence of necrotic cell debris and free radicals in the endothelium
2) LDL and inflammation, endothelial cells start to become activated and express cytokines and adhesion molecules
3) Circulating monocytes bind to the activated endothelium. They start expressing adhesion molecules and begin to move through the tissue and reside in the intimal layer
4) Monocytes differentiate into tissue macrophages which release their own inflammatory mediators. It is an appropriate immunological response to inflammation but in the wrong place here

Question 6

The order for processes to make plaque

Answer 6

Initiation
Plaque formation
Maturation of the plaque

Question 7

Steps for plaque formation

Answer 7

1) Macrophages then begin to accumulate LDL from the circulation and become foam cells
2) Activated foam cells release other growth factors which cause smooth muscle cells to leave the medial layer and cross the internal elastic lamina entering the intima
3) The activated smooth muscle cells also release growth factors and may also begin synthesising collagen and elastin in the intima layer

Question 8

Steps for maturation of the plaque

Answer 8

1) Smooth muscle cells accumulate LDL becoming a second type of foam cells, but they continue to make extracellular matrix of elastin and collagen which forms a fibrous plaque
2) Cells underneath this plaque become oxygen starved and they begin to undergo apoptosis and release their fat which forms a globule of fat that is now accumulating in the intima, known as the lipid core
3) The dying cells release matrix metalloproteases and other enzymes which can breakdown the fibrous matrix towards the edge of the plaque leaving a large lipid core covered by a fibrous plaque that may be vulnerable to enzymatic digestion

Question 9

Calcification

Answer 9

• Later, in life calcium deposits form around the atheroma and these are visible on a CT scan
• The role of calcium deposits remains uncertain, there have been arguments that calcification may stabilise the plaque
• Calcium may be a bad thing, but paradoxically a lot of calcium deposits rather than a few could be a slight advantage

Question 10

Plaque rupture

Answer 10

• If the central core becomes too large plaque rupture can occur and the sub-endothelium is exposed. The endothelium is normally an anticoagulant surface
• Collagen forms a very good bases for clotting along with other proteins and factors in the intima. This gives us a pro-coagulant surface in an artery
• A thrombus now forms which may occlude the artery

Question 11

Consequences of atheroma

Answer 11

Occlusive thrombosis
Thromboembolism
Aneurysm due to wall weakness

Question 12

Occlusive thrombosis

Answer 12

• E.g. myocardial infarction
• Commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle.

Question 13

Thromboembolism

Answer 13

• E.g. ischaemic stroke
• In this case obstruction due to an embolus from elsewhere in the body (usually carotid artery) blocking blood supply to part of the brain. Other types of ischaemic strokes occur.

Question 14

Aneurysm due to wall weakness

Answer 14

• E.g. aortic aneurysm
• Cause weakness in the wall of the aorta and increase the risk of aortic rupture. When rupture occurs, massive internal bleeding results and, unless treated immediately, shock and death can occur.

Question 15

Arterial occlusion

Answer 15

• Particularly cardiac and carotid arteries
• Anything downstream from arterial occlusion becomes starved of oxygen e.g. ischaemia
• The reduced blood flow can lead to symptoms such as angina on exercise
• A thrombus becoming detached can block the cardiac arteries (MI) or cerebral arteries (stroke) and cause death or serious damage very quickly

Question 16

Venous occlusion

Answer 16

• We tend to think of as happening in the legs, but here an occlusion doesn’t cut off the oxygen supple. It will cause pain and swelling as hydraulic pressure – causes oedema
• However, a thrombus may detach and return to the right side of the heart and could enter the pulmonary circulation causing a pulmonary embolism

Question 17

Stable cardiac angina

Answer 17

Due to permanent flow limitation

Not necessarily infarction

Question 18

Unstable cardiac angina

Answer 18

Due to transient thrombosis

Not necessarily infarction

Question 19

Myocardial infarction

Answer 19

Due to complete occlusion

Question 20

ECG changes in Myocardial infarction

Answer 20

ST elevated myocardial infarction - STEMI

Damaged heart tissue doesn’t depolarise properly so is elevated above baseline

Question 21

Complications of MI

Answer 21

• Acute cardiac failure
• Conduction problems – arrhythmia
• Papillary damage – valve dysfunction
• Mural thrombosis – stroke
• Wall rupture
• Chronic heart failure – myocardial scarring

Question 22

Stroke due to thromboembolism

Answer 22

• Thrombus at carotid plaque rupture travels into smaller cerebral vessels
• 85% from carotid atheroma rupture
• 15% from stasis in left atrium due to arrhythmia

Question 23

Non-thromboembolic stroke

Answer 23

Due to hypo-perfusion, loss of blood pressure (e.g. heart failure, haemorrhage, shock) or aneurism rupture and bleeding in the brain