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Atherosclerosis A pathological process rather than a single disease…
Atherosclerosis
A pathological process rather than a single disease entity
Injury to endothelial cells that line the artery walls
Injured endothelial cells become inflamed and cannot make normal amounts of antithrombic and vasodilating substances
Impaired clot prevention and vasodilating abilities
Platelets aggregation and seretonin and endothelin are released causing vasoconstriction
Decreased blood flow and ischaemia
SNS activation causes vasoconstriction when noradrenaline is released
ACE enzyme in endothelium converts ANG I to ANG II
Vasoconstriction and increased clotting
Inflamed endothelial cells express adhesion molecules that bind monocytes and other inflammatory and immune cells
Monocytes adhere to the injured endothelium and release numerous inflammatory cytokines and enzymes that further injure the vessel wall
Toxic oxygen radicals are released and cause oxidation of low-density lipoprotein (LDL)
Oxidised LDL engulfed by macrophages enters the intima of the vessel
These lipid-laden macrophages are called foam cells and form a lesion called fatty streak when accumulate in significant amounts
Fatty streaks produce more toxic oxygen radicals and cause immunological and inflammatory changes
Progressive damage to the vessel wall
Macrophages release growth factors that stimulate smooth muscle cell proliferation, producing collagen and migrate over fatty streak forming fibrous plaque
Fibrous plaque may calcify, protrude into the vessel lumen and obstruct blood flow to distal tissues and cause angina
Many plaques are unstable which may rupture (complicated plaques)
The exposure of underlying tissue results in platelet adhesion, initiation of coagulation cascade and rapid thrombus formation
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