Atherosclerosis

Atherosclerosis

Atherosclerosis

Defn
a progresiv inflmatory disorder of arterial wall i.e charctrised by focal lipid-rich deposits of atheroma dat remain clinicaly silent until they becom large enough 2 impair arterial perfusion / until ulceration / disruption of lesion results in thrombotic oclusion / embolisation of afectd vessel.

Risk factors

i)major constitutionl risk factors
-age mostly byond 4th d
-sex more in men
-genetic factors
-familial & racial factrs

ii)major acquird risk factrs
-hyperlipidaemia
-HTN
-smoking
-DM

iii)minor risk factrs
-obesity
-exognous harmons lik oral contraceptivs
-endogenous estrogen defi
-physicl inactivity
-stresful lif style
-environmental influencs
-heavy alcohol

pathophysiology

i)early atherosclerosis
fatty streaks @ alterd arterial shear stress -> abnormal endothlial function -> dvlpmnt of inflmn -> inflmatry cels mainly monocyts binds 2 receptors of endothelial cels -> migrate into intima -> take up oxidizd LDL 4m plasma -> lipid laden foam cels or macrophages -> extracelular lipid pool in intima -> foam cels die -> releas of contents -> cytokines, grwth factrs releasd -> smooth muscle cels migration into intima & change 4m contractile 2 a repair phenotype in atempt 2 stabiliz atherosclrotic lesion -> formn of atherosclerotic plaque

ii)Advancd athrsclros
-in establishd atherosclerotic plaque macrophages mediate inflmn & smooth muscl cels promot repair
-if inflmn predominates plaque becmes active/unstabl & may b complicted by ulceration & superaded thrombosis
-cytokines by activtd macrophges & may caus intiml smoth muscl cels ovrlying plaque 2 becom senescent
-thining of fibrous cap
-any breach in intgrity of plaque wil expose contents 2 circulatry bld
-platlet agregation & thrombosis dat extnds in2 athromtous plaque & arterial lumen

Clinicl efects

dpends on siz, typ of artries
1)slow luminl narowing causing ischaemia & atrophy
2)suden luminl oclusn causing infarction necr
3)propagation of plaque by formn of thrombi, emboli
4)formn of aneurysml dilatation & eventual ruptur


#Primary prevention
2 complementary strategies

1)Population strategy
-risk factors in whole population thru diet & lifstyle
-advice on smoking / avg cholestrol / exercise / diet / obesity

2)Targeted strategy
-treat high risk
-consider absolut risk of atheromatous cvs diseas
-antihypertensivs, lipid lowring therapy
-apropriate Rx

#Secondry prevention

in whom evidnc of atheromtous vascular diseas e.g periphral vasc diseas / MI offered a variety of Rx
-energetic corection of risk factors lik smoking, HTN, hypercholstrolmia