Flashcards in atheroma, thrombosis and embolism Deck (64)
what is the significance of this?
major cause of mortality and morbidity
what conditions do these include?
myocardial and cerebral infarction and pulmonary embolism
what is an atheroma?
it is a intimal (innermost) lesions that protrudes into a vessel wall. it consists of a raised lesion with a soft core of lipid and a fibrous cap.
what forms the soft core of lipids?
cholesterol and cholesterol esters
what is the function of the IEL?
the internal elastic lamina separates the media from the intima
what is in the fibrous cap?
foam cells, macrophages, elastin, collagen, lymphocytes, soft muscle cells
what is in the necrotic core?
cell debris, foam cells, cholesterol crystals and calcium
what are foam cells?
they are macrophages or smooth muscle cells that have migrated from the media and engulfed lipids
how is the necrotic core formed?
cells die, and lipid escapes from them
what do macrophages and SMCs do?
they produce collagen and elastin - these are the ECM proteins that form the fibrous cap of atheroma / top of lesion
how can atheroma form?
chronic inflammation within the intima
how can thrombosis form?
processes damaging the media
what are commonly affected vessels?
sites of bifurcation - turbulent slow - occurs at ostia
circle of willis
why does atherosclerosis occur?
it is a response to injury to the overlying endothelium - triggers a cascade of events leading to atherosclerosis
how does oestrogen link with MI?
prior to menopause men are more likely to have MI, post menopause women are due to levels of oestrogen
how can abnormalities in the transport of cholesterol impact these conditions?
LDL transports cholesterol to site of atherosclerosis and HDL away - abnormalities can change this and therefore mean more cholesterol is taken to the site
what are modifiable risk factors for atheroma and thrombosis?
cigarette smoking, CRP, diabetes, hyperlipidaemia and hypertension
what are non-modifiable risk factors?
gender, age, family history and genetic abnormalities
what is atherosclerosis?
chronic inflammatory response to injury to the endothelium
how does progression of lesion occur?
interaction between normal cellular constituents of the arterial wall, T lymphocytes, monocyte derived macrophages and modified lipoproteins
what is the response to endothelial injury?
increased permeability, leukocytes adhere to endothelium and emigrate through into intima. Cyto and chemokines cause the smooth muscle cells to emigrate from media to intima and activate macrophages - try to engulf the lipids. SMCs help engulf and produce ECM proteins for a fibrous plaque - cells start to die resulting in necrotic core and neovascularisation - small vessels form at edges of lesion
what is the fatty streak?
it is the earliest lesion in atherosclerosis, composed of lipid filled foamy macrophages, begining as multiple minute flat yellow spots and then coalescing into streaks - not significantly raised and do not cause disturbance to flow
what is an atherosclerotic plaque?
consists of lipid accumulation and intimal thickening
appear white yellow and superimposed thrombus on plaque is red
plaque will impinge on the vessel lumen
what are ostia and what are the complications here?
ostia are holes where branching arteries come off the aorta. Streaks form around the ostia, which sometimes contain calcium, and as lesion progresses, it becomes more severe. If lesion ruptures can cause blood clots here.
what can result in thrombosis?
increase in pressure or overlying turbulence, athero-embolisms, aneurysms and haemorrhages
what is an embolus?
when part of the plaque dislodges
how do thrombi form?
when there is rupture, ulceration or erosion of the intimal surface then the blood is exposed to the highly thrombogenic core which induces thrombosis - lumen occlusion - ischaemia
what is a thrombus?
it is a solid mass of blood constituents formed in the vascular system in vivo
what is the most common cause of arterial thrombosis?
to be superimposed on an atheroma - the lesion causes turbulent blood flow and exposes to thrombogenic substances - rupture of plaque