Endothelial dysfunction — role?
Initiates atherosclerosis by increasing permeability.
Atherosclerosis — definition?
Fatty plaque formation in arteries.
LDL oxidation — location?
Occurs beneath the endothelium.
LDL cholesterol — role?
Main lipid in plaque deposits.
Foam cells — formation?
Macrophages ingest oxidized LDL.
Plaque rupture — consequence?
Thrombosis and vessel occlusion.
Fatty streaks — composition?
Clusters of foam cells in the vessel wall.
Stable vs unstable plaque — difference?
Collagen-rich vs lipid-rich.
VSMC migration — function?
Contributes to fibrous cap formation.
Critical stenosis — percentage?
Greater than 70-75% narrowing.
Collagen production — cell type?
Vascular smooth muscle cells (VSMC).
Foam cells — origin?
Macrophages with oxidized LDL.
Fibrous cap — stability?
Collagen-rich, stabilizes the plaque.
Necrotic core — composition?
Dead foam cells and cholesterol crystals.
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.
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1. Which process is primarily involved in the initiation of atherosclerosis related to endothelial dysfunction and LDL oxidation?
2. At what age do fatty streaks typically begin to form in arteries, according to the revision sheet?
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