pathology of atherosclerosis Flashcards
list some risk factors for atherosclerosis and explain why they are risk factors according to endothelial damage theory
- smoking - free radicals, nicotine, carbon monoxide
- vaping - nicotine
- old age
- hypertension - force
- poorly controlled diabetes - superoxide anions and glycosylation products
- hyperlipidaemia - direct damage
describe how atheroscelerosis occurs according to endothelial damage theory
- damage will occur
- thrombus will form
- will heal over - covering that part of the vessel where damage occured
- this will happen over and over and eventually begin to block the vessel
define atherosclerosis
- accumulation of fibrolipid plaques in systemic arteries
- limits the blood flow to areas causing ischemia and infarction
outline the time course of the progression of atherosclerosis
- birth - no atherosclerosis
- late teenage/early 20s - fatty streaks in aorta, may not
progress to established atherosclerosis - 30s/40s/50s - development of established atherosclerotic
plaques - 40s-80s - complications of atherosclerotic plaques e.g.
thrombosis, intraplaque haemorrhage
explain the pathogenesis (development) of atherosclerosis
old discredited lipid insudation theory
current endothelial damage theory
- endothelial cells are delicate
- easily damaged by cigarette smoke, shearing forces at
arterial divisions, hyperlipdaemia, glycosylation products
- cumulative damage leads to endothelial ulceration,
microthrombi, eventual development of established atherosclerotic plaques
outline the main complictions of atherosclerosis
- embolism
- infarction
- ischemia
- gangrene
what is the difference between arteriosclerosis and atherosclerosis?
arteriosclerosis - the hardening of arteries
atherosclerosis - lipid plaques cause arteries to become narrowed and hardened
just read this - don’t need to know in detail - how plaques form
- endothelial cells become damaged, leaving gaps in the wall - damaged endothelial cells also lose their preventative functions of clotting and inflammation
- LDLs (cholesterol) get into the wall of the vessel from the lumen
- WBC then enter and oxidise the lipids, turning them into foam cells and causing an inflammatory responce
- this produces calcium salt
- the calcium salt and the LDLs then build up and start to form a plaque, especially as this is a positive feedback loop
- calcification of plaque
- a thrombus then forms on top of the plaque
What is the role of endothelial cells in atherosclerosis?
Endothelial cells line the inner layer of blood vessels, maintaining vessel integrity and preventing clot formation. Injury or dysfunction of these cells is the initial event in atherosclerosis
How do monocytes and macrophages contribute to atherosclerosis?
Monocytes are recruited from the bloodstream to the artery wall, where they differentiate into macrophages and ingest oxidized LDL, transforming into foam cells within the plaque.
What are foam cells, and why are they significant in atherosclerosis?
Foam cells are lipid-laden macrophages that accumulate within plaques and release inflammatory molecules, promoting further plaque growth. They are a hallmark of early atherosclerosis.
What role do smooth muscle cells (SMCs) play in atherosclerosis?
SMCs migrate into the intima, proliferate, and produce extracellular matrix (ECM) proteins, which help stabilize the plaque by forming a fibrous cap.
What is the function of platelets in atherosclerosis?
Platelets are involved in clot formation when a plaque ruptures. They adhere to the exposed lipid core, initiating a clot that can obstruct blood flow.
