Endothelial Dysfunction — role?
Initiates atherogenesis by increasing permeability.
Atherosclerosis — definition?
Progressive buildup of LDL in arteries.
LDL oxidation — process?
LDL crosses endothelium and oxidizes beneath it.
Affected arteries?
Coronary, carotid, peripheral arteries.
Fatty streak — composition?
Accumulation of foam cells from monocytes.
Plaque stability — stable?
Collagen-rich, fibrous cap.
Monocyte transformation — role?
Monocytes become foam cells in fatty streaks.
Critical stenosis threshold?
Occlusion >70-75%.
Fibrous plaque — features?
VSMC migration, collagen synthesis, extracellular lipid.
Endothelium — role?
Initiates atherogenesis when dysfunctional.
Collagen production — source?
Vascular smooth muscle cells.
Foam cells — origin?
Lipid-laden macrophages from monocytes.
Advanced plaque — contents?
Lipid core, necrotic debris, collagen, smooth muscle.
Unstable plaque — feature?
Thin fibrous cap, large lipid core.
Lipid core — location?
Central necrotic area of advanced plaque.
Plaque rupture — trigger?
Thin fibrous cap overlying lipid core fissures.
Thrombosis — result of?
Plaque rupture exposing thrombogenic material.
Hypercholesterolemia — LDL level?
Greater than 160 mg/dl.
Risk factors — examples?
Hypertension, smoking, diabetes, obesity.
Plaque stability — determinants?
Collagen content and lipid core size.
Stable plaque — features?
Collagen-rich, hard, low rupture tendency.
Unstable plaque — features?
Lipid-rich, soft, high rupture risk.
Critical stenosis — percentage?
Over 70-75% narrowing.
Symptoms — when occur?
When stenosis exceeds critical threshold.
Chronic ischemia — cause?
Partially narrowed arteries, stable plaques.
Acute ischemia — cause?
Vessel occlusion after plaque rupture.
Affected arteries — common sites?
Coronary, carotid, peripheral arteries.
Progression — early age?
Lesions can develop from ages 10-20.
Plaque stability — importance?
Affects rupture risk and clinical events.
Clinical manifestation — asymptomatic?
Until significant stenosis causes symptoms.
Bystander event — in coronary artery?
Myocardial infarction or unstable angina.
Brain ischemia — presenting?
TIA or cerebral infarction.
Limb ischemia — signs?
Intermittent claudication, gangrene.
Lesion development — stages?
Endothelial dysfunction, fatty streak, fibrous, complicated.
Atherogenesis — initiators?
Endothelial injury and LDL oxidation.
Plaque rupture consequence?
Thrombosis and potential vessel occlusion.
Chronic vs acute — classification?
Based on stability and occlusion severity.
Testez vos connaissances avec un QCM de 21 questions sur Understanding Atherosclerosis Development.
1. Which process primarily initiates endothelial dysfunction that leads to LDL oxidation in atherosclerosis?
2. What is the primary component that initiates atherogenesis when dysfunctional?
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