Cardiovascular system and diseases II Flashcards
what is atherosclerosis
hardening of arteries, causing thickening and loss of elasticity
- INTIMAL LESIONS can be atheromatous or fibrofatty, they protrude and obstruct the vascular lumens
where do atherosclerotic plaques generally develop
in elastic arteries (aorta, carotid) and large and medium sized muscular arteries (coronary)
atherosclerosis is associated with what
high LDL cholesterol
low HDL cholesterol
what are the non-modifiable risk factors associated with atherosclerosis (4 of them)
- age
- gender (m>f)
- positive family history
- genetic abnormality (ACE gene)
what are the modifiable risk factors associated with atherosclerosis (6 of them)
- hyperlipidaemia
- hypertension
- smoking
- Diabetes
- obesity
- physical inactivity
what is the pathological feature of atherosclerosis
what does it consist of
atherosclerotic PLAQUES
- consists of: raised lesion with a soft, yellow, grumous core of LIPID (mainly chol and chol esters) covered by a white FIBROUS CAP
describe the structure of atherosclerotic plaques
- superficial FIBROUS CAP: SMOOTH MUSCLE cells, dense collagen
- SHOULDER: cellular area cont MACROPHAGES, T CELLS, SMOOTH MUSCLE cells
- NECROTIC CORE: cont LIPID, DEAD CELL DEBRIS, FOAM CELLS, FIBRIN, variably organised THROMBUS and other plasma proteins
- CHOLESTEROL: often present as crystalline aggregates or CLEFTS
- NEOVASCULARISATION: at the periphery of lesion
what are the 3 principle components of a plaque
1) CELLS: smooth musc, macrophages, other leukocytes
2) EXTRACELLULAR MATRICES: collagen, elastin, proteoglycans
3) INTRACELLULAR and EXTRACELLULAR lipid
what is the morphology of the lesions
EARLIEST aortic atherosclerosis:
- fatty streaks
- lipid-filled foamy macrophages
- begin as multiple minutw flat yellow spots
ADVANCED complicated atherosclerosis in abdominal aorta:
- many lesions have ruptured
- become thrombosed
what are the key pathological events in atheroscleorsis
1) ENDOTHELIAL INJURY: inc vascular permeability, leukocyte adhesion and thrombosis
2) ACCUMULATION OF LIPOPROTEINS: mainly LDLin vessel wall
3) MONOCYTE ADHESION to the endothelium, followed by MIGRATION into the INTIMA and TRANSFORMATION into macrophages and foam cells
4)
what are the key pathological events in atheroscleorsis
1) ENDOTHELIAL INJURY: inc vascular permeability, leukocyte adhesion and thrombosis
2) ACCUMULATION OF LIPOPROTEINS: mainly LDLin vessel wall
3) MONOCYTE ADHESION to the endothelium, followed by MIGRATION into the INTIMA and TRANSFORMATION into macrophages and foam cells
4) PLATELET ADHESION
5) FACTOR RELEASE from activated platelets, macrophages and vascular cell walls –> SMC recruitment and further accumulation of macrophages
6) SMC proliferation and ECM production
7) Lipid accumulation both extracellulary and intracellularly (macrophages and SMCs)
what are the consequences of atherosclerotic plaques
1) RUPTURE, ULCERATION, EROSION of the intimal surface–> high thrombogenic substances –> THROMBOSIS
2) HAEMORRHAGE INTO A PLAQUE: rupture of the fibrous cap –> intra-plaque haemorrhage –> plaque rupture
3) ATHEROEMBOLISM: plaque rupture–> atherosclerotic debris into blood stream –> microemboli
4) ANEURYSM FORMATION: atherosclerosis-induced pressure, ischaemic atrophy, loss of eleatic tissue–> weakness –> aneurysmal dilation and potential rupture
what are the 3 clinical phase outocomes of an atheroscleotic plaque
1) rupture (can cause anyeurism and rupture)
2) occlusion (by thrombus)
3) stenosis (narrowing of vessel)
what are the outcomes of atheroscleotic diseases dependant on
- size of involved vessels
- relative stability of the plaque itself
- degree of degeneration (underlying arterial wall)
what are the MAJOR consequences of atherosclerotic diseases
- myocardial infarction (MI) (heart attack)
- cerebral infarction (stroke)
- aortic aneurysms
- peripheral vascular disease (gangrene of the legs)
