9. Atherosclerosis Flashcards

1
Q

What is the definition of atherosclerosis?

A

Accumulation of intracellular and extracellular lipid in the intima and media of large and medium sized arteries

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2
Q

What is the fatty streak in atherosclerosis and how does it appear?

A

Lipid deposits in the intima.

Yellow and slightly raised

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3
Q

What is a plaque in atherosclerosis and how does it appear both to the eye and microscopically?

A

Fatty streak grows to form plaque. Raised and white to yellow in colour, impinge on lumen of artery.
Fibrosis, cholesterol clefts, disruption of internal elastic lamina and extension into the media.

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4
Q

What is the definition of arteriosclerosis?

A

Thickening of the walls of arteries and arterioles usually as a result of hypertension or diabetes mellitus.

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5
Q

What happens when a plaque leads to haemorrhage?

A

New vessel that has developed within the plaque haemorrhages, expanding the plaque, leading to vessel occlusion or breaking open of the plaque.

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6
Q

What happens in thrombus formation on a plaque?

A

Usually on an ulcerated plaque, where the fibrous cap is eroded from underneath and the core of the plaque is exposed to the blood which i high thrombogenic. The thrombus may occlude the vessel.

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7
Q

What happens in aneurysm formation from a plaque?

A

Elastic tissue within the arterial wall is destroyed by the plaque, weakening the wall, leading to local dilatation, and possible vessel rupture.

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8
Q

What can be seen, especially in cerebral arteries, when a patient has hypertension in addition to atherosclerosis?

A

Rupture of the atherosclerotic artery

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9
Q

Name 3 common sites of atherosclerosis

A
Aorta (abdominal)
Coronary arteries
Carotid arteries
Cerebral arteries
Leg arteries
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10
Q

What are the three basic components of atherosclerotic plaque?

A

Cells - eg macrophages, leukocytes, smooth muscle cells.
Intra and extracellular lipid.
Extracellular matrix - eg collagen, elastin, proteoglycans.

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11
Q

What result in endothelial dysfunction as proposed initiating factors for plaque formation in atherosclerosis?

A

Hyperlipidaemia, hypertension, smoking, haemodynamic factors.

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12
Q

What happens in fatty streak formation?

A

Lipid droplets (LDLs) and monocytes cross endothelium, accumulate in intima. Become oxidised and macrophages ingest lipid, forming foam cells. Cause endothelium to bulge, smooth muscle cells migrate to lesion from media, proliferate.

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13
Q

Once a fatty streak has formed, what happens in its maturation into a plaque?

A

Grows as number of foam cells and smooth muscle cells increases, some smooth muscle cells take up lipid, appear foamy, and some lie over plaque but underneath endothelium, forming roof, reinforced by collagen, elastic, matrix proteins, forming fibrous cap. Endothelium stretched, gaps appear between endothelial cells, platelets adhere to gaps. Cells in centre plaque die, necrosis, dead cells release cholesterol, crystals appear, small blood vessels grow in plaque from adventitia and plaque may undergo calcification.

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14
Q

What are cholesterol clefts?

A

Linear holes in a tissue section left behind when cholesterol crystals are removed from a plaque.

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15
Q

What 3 diseases does arteriosclerosis include?

A

Atherosclerosis
Atheriolosclerosis
Monkeberg’s disease

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16
Q

Name 5 conditions that atherosclerosis can cause at different locations

A
Ischaemic heart disease
Cerebral ischaemia
Mesenteric ischaemia
Peripheral vascular disease
Abdominal aortic aneurysm
17
Q

Name 3 complications of ischaemic heart disease

A
Sudden death
MI
Angina pectorals
Arrhythmias
Cardiac failure
18
Q

What are the two major complication of an aortic aneurysm?

A

Rupture and thrombus.

Plaque material embolism.

19
Q

Where do dissecting aneurysms usually occur and what happens to cause them?

A

Aorta and its major branches.
Inner layer of arterial wall tears open, blood enters, separated media into 2 layers. Fills with blood and lumen of artery becomes occluded.

20
Q

What is the injury hypothesis for atherosclerosis formation?

A

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, cells of the arterial wall.

21
Q

What is the encrustations hypothesis for atherosclerosis formation?

A

Plaques formed by repeated thrombi overlying thrombi. Lipid core is derived from the thrombi.

22
Q

What is the monoclonal hypothesis for atherosclerosis formation?

A

Some plaques are monoclonal or oligoclonal. Plaques are benign neoplastic growths, induced by cholesterol or a virus. However some areas of normal arteries are colonal.

23
Q

Name 3 non-modifiable risk factors for atherosclerosis

A

Age - progressive throughout adult life.
Gender - higher rates in men, incidents in women increase after menopause.
Genetic - clustering of risk factors (eg hypertension, diabetes), hypercholesterolaemia (some of the genotype associated with high LDL levels, so predisposition to atherosclerosis.

24
Q

Name 4 modifiable risk factors for atherosclerosis

A

Hyperlipidaemia - increase in LDL, increasing incidence of atherosclerosis.
Hypertension - increased pressure damages blood vessel walls, predisposes plaque formation.
Cigarette smoking - inflammation in and damage to blood vessel wall, predisposition to thrombosis, oxidation of lipids.
Geography - developed countries have higher risk.
Obesity - leads to hypertension, diabetes, hypertiglyceridaemia, reduced HDL.
Infection - Chlamydia pneumoniae, CMV both reported to increase risk of atherosclerosis.

25
Q

How is HDL protective against atherosclerosis?

A

HDL removed cholesterol from atheromatous plaques and delivers it to the liver for excretion in bile.

26
Q

What 2 things are levels of HDL increased with, and what 2 things are they decreased with?

A

Increased - exercise and moderate alcohol.

Decreased - obesity and smoking.

27
Q

Name 4 prevention strategies for preventing atherosclerosis

A

Dietary measures including low fat and high fibre to reduce circulating lipid, and lipid-lowering drugs to reduce LDL and cholesterol, and increase HDL.
Stopping smoking.
Controlling hypertension.
Controlling weight and regular exercise.
Sensible alcohol intake.
Treating diabetes.
Antioxidants eg vitamin E, may be protective.

28
Q

Name 2 intervention strategies for atherosclerosis

A

Lipid-lowering drugs eg statins and aspirin prophylaxis.

Thrombolysis, angioplasty, sends, coronary artery bypass grafts (CABG).