Endothelial dysfunction — role?
Initiates atherosclerosis by increasing permeability.
LDL oxidation — location?
Occurs beneath the endothelium.
Foam cells — formation?
Macrophages ingest oxidized LDL.
Fatty streaks — composition?
Clusters of foam cells in the vessel wall.
VSMC migration — function?
Contributes to fibrous cap formation.
Collagen production — cell type?
Vascular smooth muscle cells (VSMC).
Fibrous cap — stability?
Collagen-rich, stabilizes the plaque.
Plaque rupture — consequence?
Thrombosis, arterial occlusion.
Unstable plaque — feature?
Lipid-rich, thin fibrous cap.
Stable plaque — feature?
Collagen-rich, thick fibrous cap.
Critical stenosis — percentage?
Greater than 70-75% narrowing.
Ischemic symptoms — cause?
Severe stenosis or plaque rupture.
Coronary arteries — clinical manifestation?
Angina, myocardial infarction.
Cerebral arteries — clinical event?
Stroke or transient ischemic attack (TIA).
Peripheral arteries — clinical symptom?
Claudication, gangrene.
Plaque stability — determined by?
Composition: collagen vs lipids.
Plaque development timeline?
Starts in youth, symptomatic age >35.
Atherogenesis process?
Endothelial dysfunction, LDL oxidation, foam cell formation, fibrous cap development.
Major risk factors?
High LDL, hypertension, smoking, diabetes.
Plaque complication?
Fissuring or rupture leads to thrombosis.
Atherosclerosis — definition?
Fatty plaque formation in arteries.
LDL cholesterol — role?
Main lipid in plaque deposits.
Plaque rupture — consequence?
Thrombosis and vessel occlusion.
Stable vs unstable plaque — difference?
Collagen-rich vs lipid-rich.
Critical stenosis — percentage?
Greater than 70-75% narrowing.
Foam cells — origin?
Macrophages with oxidized LDL.
Necrotic core — composition?
Dead foam cells and cholesterol crystals.
Answer 16 questions on Understanding Atherosclerosis Formation and Risks.
1. Which process is primarily involved in the initiation of atherosclerosis related to endothelial dysfunction and LDL oxidation?
2. What is the hallmark feature of foam cells in the development of fatty streaks in atherosclerosis?
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