Session 6 - Atherosclerosis

Question 1

Where does atherosclerosis commonly develop?

Answer 1

It develops in the arteries only. It develops in patches of the intima often where blood flow is disturbed such as around the opening of a branch.

Question 2

What is arteriosclerosis?

Answer 2

Hardening of the arteries. The walls of the arteries are thickened and lose their elasticity. It is an umbrella term for three diseases:

• atherosclerosis - medium and large sized arterial disease that begins in the intima
• arteriolosclerosis - hardening of the arterioles.
• Monkeberg’s disease - calcification of the media of large arteries

Question 3

Name the three main components of an atherosclerotic plaque?

Answer 3

1. Cells - macrophages, leucocytes, smooth muscle cells
2. Intra and extracellular lipid
3. Extracellular matrix - collagen, elastin, proteoglycans.

Question 4

Name some factors that cause chronic endothelial insult?

Answer 4

• smoking
• hypertension
• hyperlipidaemia
• haemodynamic factors resulting in endothelial dysfunction

Question 5

Name the basic processes that occur in atherosclerosis formation?

Answer 5

1. Chronic endothelial insult occurs
2. Lipid droplets (mainly from LDL’s) will cross the endothelium and accumulate in the intima
3. These lipids become oxidsed and they are engulfed by macrophages forming foam cells.
4. Smooth muscle cells will migrate to the lesion and smooth muscle cells will also take up lipid and appear foamy.
5. Some smooth muscle cells will lie over the plaque forming a roof.
6. The roof is enforced by collagen, elastin, and other proteins resulting in the formation of a fibrous cap.
7. Gaps appear in the endothelial cells and platelets aggregate.
8. Cells in the centre of the plaque die and necrosis develops.

Question 6

What is the fatty streak?

Answer 6

The earliest lesion in atherosclerosis. They are flat and cause no disturbance to blood flow. They consist of foam cells, smooth muscle cells and extracellular lipid.

Fatty streaks will grow and become plaques.

Question 7

What is an atherosclerotic plaque?

Answer 7

A plaque that is white to yellow in colour and impinge on the lumen of the artery. Fibrosis, necrosis, cholesterol clefts and disruption of the internal elastic lamina will be seen. Extension into the media and ingrowth of small vessels from the adventitia will occur.

Question 8

What is plaque ulceration?

Answer 8

This is where the fibrous cap is eroded from underneath and the core of the plaque is exposed to the blood. The core is highly thrombogenic.

Question 9

Why do spasms sometimes occur at the site of an atherosclerotic plaque?

Answer 9

This is caused by thrombi that will release vasoconstrictors and will cause the spasm of the smooth muscle in the vasculature.

Question 10

Name some of the complications of atherosclerosis?

Answer 10

1. Embolisation
2. Thrombus formation on the plaque
3. Ulceration
4. Spasm at the area of the thrombus
5. Calcification
6. Haemorrhage
7. Aneurysm formation
8. Rupture of the atherosclerotic artery

Question 11

What is an aneurysm?

Answer 11

This is a local dilatation of an artery due to weakning of the arterial wall. In large arteries they are almost always secondary to atherosclerosis.

Question 12

What are two complications of an aneurysm?

Answer 12

1. Rupture of the aneurysm
2. Plaque material within them may embolise

Question 13

What is a dissecting aneurysm? Is it an acute or chronic clinical event?

Answer 13

It is an acute aneurysm which forms within a couple of minutes and survival is rare. It usually occurs in the aorta and is where the inner layer of the arterial walls tear open and resultedly blood enters the tunica media and separates it into two layers. As the tear fills up with blood the lumen of the artery can be occluded.

Sometimes blood can push back into the lumen by the means of a second tear.

Question 14

What is a saccular aneurysm?

Answer 14

This occurs commonly in the abdominal aorta - usually occurs as a result of an adventitious thrombus as it protects the aneurysm from bursting.

Question 15

Name the three hypotheses that have been suggested for atherogenesis.

Answer 15

• The response to injury hypothesis
• The encrustation hypothesis
• The monoclonal hypothesis

Question 16

What is the response to injury hypothesis?

Answer 16

this postulates that atherosclerosis is a chronic inflammatory response of the arterial wall initiated by injury to the endothelium. Lesion progression is sustained by interaction between modified lipoproteins, macrophages, T lymphocytes and the cells of the arterial wall

Question 17

What is the encrustation hypothesis?

Answer 17

The encrustation hypothesis - plaques are formed by repeated thrombi overlying thrombi. The lipid core is derived from the thrombi.

Question 18

What is the monoclonal hypothesis?

Answer 18

This hypothesis arose following findings that some plaques are monoclonal or oligoclonal. This made people think that plaques could be a benign neoplastic growth perhaps induced by cholesterol or a virus.

Question 19

Name some non-modifiable risk factors of atherosclerosis

Answer 19

• Age
• Gender - more common in men than women but the incidence in women increases after menopause as oestrogen is protective.
• Genetic predisposition

Question 20

Name some modifiable risk factors of atherosclerosis?

Answer 20

• Hyperlipidaemia
• Hypertension
• Smoking
• Geography
• Obesity
• Infection

Question 21

What prevention strategies can you adopt to decrease the likelihood of developing atherosclerosis?

Answer 21

• Eating healthily - keep LDL cholesterol low and increase HDL cholesterol intake.
• Stop smoking
• Control hypertension
• Control weight
• Regular exercise
• Sensible alcohol intake
• Treat diabetes mellitus
• Lipid lowering drugs - eg. statins
• surgery

Question 22

What is a corneal arcus?

Answer 22

This is where you see a pale ring around the edge of the cornea due to fat being deposited around the edges. In younger patients it is a clinical sign of hyperlipidaemia whereas in the elderly it may not be concerning.