9. Atherosclerosis Flashcards
What is the definition of atherosclerosis?
Accumulation of intracellular and extracellular lipid in the intima and media of large and medium sized arteries
What is the fatty streak in atherosclerosis and how does it appear?
Lipid deposits in the intima.
Yellow and slightly raised
What is a plaque in atherosclerosis and how does it appear both to the eye and microscopically?
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.
What is the definition of arteriosclerosis?
Thickening of the walls of arteries and arterioles usually as a result of hypertension or diabetes mellitus.
What happens when a plaque leads to haemorrhage?
New vessel that has developed within the plaque haemorrhages, expanding the plaque, leading to vessel occlusion or breaking open of the plaque.
What happens in thrombus formation on a plaque?
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.
What happens in aneurysm formation from a plaque?
Elastic tissue within the arterial wall is destroyed by the plaque, weakening the wall, leading to local dilatation, and possible vessel rupture.
What can be seen, especially in cerebral arteries, when a patient has hypertension in addition to atherosclerosis?
Rupture of the atherosclerotic artery
Name 3 common sites of atherosclerosis
Aorta (abdominal) Coronary arteries Carotid arteries Cerebral arteries Leg arteries
What are the three basic components of atherosclerotic plaque?
Cells - eg macrophages, leukocytes, smooth muscle cells.
Intra and extracellular lipid.
Extracellular matrix - eg collagen, elastin, proteoglycans.
What result in endothelial dysfunction as proposed initiating factors for plaque formation in atherosclerosis?
Hyperlipidaemia, hypertension, smoking, haemodynamic factors.
What happens in fatty streak formation?
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.
Once a fatty streak has formed, what happens in its maturation into a plaque?
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.
What are cholesterol clefts?
Linear holes in a tissue section left behind when cholesterol crystals are removed from a plaque.
What 3 diseases does arteriosclerosis include?
Atherosclerosis
Atheriolosclerosis
Monkeberg’s disease
Name 5 conditions that atherosclerosis can cause at different locations
Ischaemic heart disease Cerebral ischaemia Mesenteric ischaemia Peripheral vascular disease Abdominal aortic aneurysm
Name 3 complications of ischaemic heart disease
Sudden death MI Angina pectorals Arrhythmias Cardiac failure
What are the two major complication of an aortic aneurysm?
Rupture and thrombus.
Plaque material embolism.
Where do dissecting aneurysms usually occur and what happens to cause them?
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.
What is the injury hypothesis for atherosclerosis formation?
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.
What is the encrustations hypothesis for atherosclerosis formation?
Plaques formed by repeated thrombi overlying thrombi. Lipid core is derived from the thrombi.
What is the monoclonal hypothesis for atherosclerosis formation?
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.
Name 3 non-modifiable risk factors for atherosclerosis
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.
Name 4 modifiable risk factors for atherosclerosis
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.
