ARTERIOSCLEROSIS •Hardening of arteries due to thickening and loss of elasticity.
elasticity
•The three types of arteriosclerosis are‐
•1)Atherosclerosis (AS): #1 Killer, CVS dia
•2)Monckeberg’s arteriosclerosis –Medial
calcification, >50 yrs of age
3)Arteriolosclerosis: associated with
威麟x5hypertension.
无分别心Atherosclerosis (AS):
•slow progressive dia of large and medium sized muscular and large elastic arteries
i d l d l l ti t i •characterized by an elevated fibro fatty intimal plaques formed by lipid deposition,smooth muscle proliferation and synthesis of extra cellular matrix.
•It begins in childhood and manifests in
middle and later life
•Risk Factors: Major –Non Modifiable: age,
红尘来去一场梦male gender,family history •Potentially controllable: Hyperlipidemia,
hypertension, cig.smoking & D.Mellitus
(deadly quartet)
•Minor –obesity, ÈHDL, Physical inactivity, stress, post menopau, carbohydrate stress menopau High
diet, alcohol, homocysteine, lipoprotein (a), chlamydial infection etc.
Etio‐Pathogenesis •Hypothes:
•1) Insudation hypothesis (Virchow)
•2) Encrustation hypothesis (Rokitansky) •3) Monoclonal hypothesis (Benditt)返校通知
•4) Reaction to injury hypothesis (Ross).
唐宋诗词名篇欣赏
Reaction to Injury
Chronic endothelial injury Hyperlipid,HTN,smoking, DM,Hemodyn,Homocyst,Toxins etc
Endothelial Dysfunction SMC emigration & Macrophage activation Chronic
inflammatory
dia
学生守则IL, TNF,GF’s,Metaloprot, Adh
mol,
东山诗经
SMC proliferation, Lipid, collagen &
ECM deposition –Well formed plaque
HTN Toxins cig
smoke Hemodynamic
stress
ÇLDL
D d
Damage to endo PTL adh
Diff.Plasma Prot
Mig Mono
Oxidation
PDGF Oxidation LDL
横向研究Uptake Foam cells
Cytokine relea
Collagen
Syn Prolif.SMC
