Atherosclerosis Flashcards
Atherosclerosis
Fibro-inflammatory lipid plaque affecting elastic and muscular arteries
Develops over decades
Affects M 40-60 and post menopausal women
Arteriosclerosis
Caused by Ath/degenerative changes
Arteriolosclerosis
Thickening of arteriolar walls
Hyalinisation and hyperplasia
Stages of atherosclerosis and distribution
Initiation and formation/adaptation/clinical stages
Ath affects Abdominal aorta/coronary/popliteal/internal carotid/descending thoracic aorta/circle of Willis arteries
UL/renal/mesenteric arteries are spared
Macroscopic changes in atherosclerosis
White fibrous cap/Yellow grumous core
3-15mm diameter
Single or multiple and raised
Microscopic changes in atherosclerosis
Fibrous cap- SM/CT/proteoglycans/collagen/elastin
Core- lipid debris/plasma proteins/TL/fibrin/chol and chol esters/PC/SM/foamy Mac
Peripheral neovascularisation and CI
Effects of ath plaque
Asymptomatic
Calcification
Fissure/ulceration/embolisation/thrombosis/Hm leading to stenosis/infarct/atrophy/ischemia/aneurysm (may rupture due to high P)
Ath evolution
Foamy cells (IL-1/6/8 TNF MCP-1)
Fatty streak
Intimal lesions (ICAM/VCAM/selectins)
Fibrous lesions (MMP/PDGF/MPO/oxLDL/IL-18)
Complicated lesions and rupture (CD40-L and PAPP-A)
Ass. Acute phase reactants- Crp/SAA/WBC/PLA-2/fibrinogen
Ath risk factors
HTN >160/110 mm/hg
Smoking/stress/low PA/family history/coloured people
high fat diet/increased age/M>F/homocysteinemia/dyslipidemia
alterations in chol metabolism
Theories of ath
Lipid theory
Thrombotic theory
Monoclonal growth of SM cells
Fatty plaque
Precursor of atheroma and Ass. To high fat diet
Fatty spot 1mm to 10mm streak
Progression- recede/persist/conversion to fibrous plaque
Composition- fat laden mac and SM/fat droplets/TL/proteoglycans/collagen and elastin
Intimal cushion
Ass. To ath changes (gelatinous lesion) White areas of intimal thickening (intimal SM and matrix) Little collagen and lipids Occurs at Ostia (openings at BV exits) Affect BP over time
Intimal lesion
Ass. To HTN/smoking/stress
Caused by mechanical changes/hemodynamic stress/immune complex deposition/chemotherapy
Leads to increased intimal permeability/SM and Mac adhesion and proliferation/atheroma formation
Macrophages in atheroma
Monocytes/MGC/epithelioid mac/granulocytes/histiocytes
Monocyte (in blood)–> Mac (in tissues)
Adhesion/migration/phagocytosis
Mac produce IL-1/TNF (increase adhesion) and ROS/PDGF/TGF (SM chemotaxis)
Mac have scavenger R (modified VLDL-R) thus lipids are internalised/hydrolysed/esterified
SM cells
SM derived from (myo)intima
Stimulation of prol by PDGF/FbGF/EGF/TGF alpha
Inhibition of prol by heparin and TGF beta
SM cells proliferate/become fat laden/increased ECM production> atheroma