Module 3 Flashcards
Artherosclerosis
Focal thickening of walls in medium and large arteries
With reduced compliance and elasticity
Arteriolosclerosis
Diffuse thickening of walls in small arteries and arterioles. Assoc with prolonged hypertension
WHO definition of artherosclerosis
A variable combination of changes of the intima of arteries, consisting of a focal accumulation of lipids, complex carbohydrates, blood and blood products, fibrous tissue and calcium deposits and associated medial changes.
What makes up an artheroma?
A necrotic center with lipids and cellular debris. Surrounding this is a halo of live and dead cells filled with fat. There is a proliferation of smooth muscle cells that surround th encore. Collagen, elastin and ground substance are deposited in the intima forming a white fibrous cap over lesion.
What factors support the hypothesis that artherosclerosis from in response-to-injury ?
- location that artheromas form are at sites of turbulent blood flow ; downstream of branching points, bends in arteries.
Also probable that when blood platelets hit the endothelial wall they can release materials that increases the permeability to lipids and cells - factors that cause endothelial damage increases chances of artherosclerosis is - smoking, hypertension, low density lipoproteins and diabetes.
-chronic injury to arterial endothelium in experimental animals trigger development of artherosclerosis
-damaged endothelial cells are known to secrete chemicals which promote cellular migration and proliferation
The fatty streak
Precursor to artherosclerosis, detectable even at infancy. In is an aggregation of lipid filled macrophages. And smooth muscle cells in the intima at sites where there is turbulent blood flow.
Formation of an artheroma
Hemodynamics forces compromise the endothelial barrier. Blood myocyte are attracted to the site by products of cell injury, these are then converted to phagocytize macrophages. These cells have receptors to low density lipid proteins which the engulf and digest. - gives cel foamy appearance. Marcrophages comprise the bulk of foam cells the rest are smooth muscle cells. - once established macrophages secrete chemotatic and growth factors that cause cells within the artheroma to migrate and proliferate.
Smooth muscle cells of the artheroma
Have LDL receptors like macrophages and accumulate lipid proteins. The lose contractile ability, myofibrils degenerate and they begin to secrete connective tissue components (collagen, elastin, mucopolysaccharides). The cell eventually dies.
Risk factors of artherosclerosis
1) hyperlipidemia - high intake of blood lipids (can also be hereditary)
2)hypertension risk is directly proportion to the duration and severity of hypertension
Hypercholesterolemia - high plasma concentration of cholesterol increases rate of deposition in the lesion.
Smoking Obesity Inactivity Being male Diabetes
Low density lipid proteins (LDL) carry most of the cholersterol in the blood and are a major risk factor.
Consequences of Artherosclerosis
-narrowing of arterial lumen and reduced tissue perfusion. Ischemia causes atrophy- atrophied gradually replaced by scar tissue- deciding pumping ability of heart.
- an increases in peripheral resistance. Narrowing of arteries = increas peripheral resistance ->hypertension -> accelerates artherosclerosis -> increase risk for aneurysm or rupture
-reduced arterial compliance - compliance and elasticity reduced due to scarring and calcification
- arterial spasm - arteries damaged are vulnerable to spasm which causes temporary ischemia - can lead to permanent injury and atypical angina
- Aneurysm - rarely found in coronary arteries. Develop because normal diffusion is impaired by thickened scarred walls- muscle atrophied, wall weakens - focal dilation may occur
-superimposed thrombosis
-dystrophic calcification
Rupture of artheroma
