Endothelial dysfunction — role?
Initiates atherosclerosis by increasing permeability and adhesion.
LDL oxidation — consequence?
Promotes monocyte attraction and foam cell formation.
Foam cells — origin?
Macrophages ingest oxidized LDL.
Fatty streaks — first lesion?
Early accumulation of foam cells in arterial wall.
Fibrous plaque — composition?
Smooth muscle, collagen, lipid core.
Plaque stability — high collagen content?
Leads to stable, less rupture-prone plaque.
Plaque rupture — cause?
Thin fibrous cap over lipid-rich core.
Thrombosis — result of rupture?
Clot formation occludes artery.
Vessel stenosis — symptom threshold?
>70-75% narrowing for symptoms.
Affected arteries — common sites?
Coronary, carotid, iliac, femoral.
Cholesterol levels — high risk?
Total >200 mg/dl, LDL >160 mg/dl.
Risk factors — key influences?
Hypercholesterolemia, hypertension, smoking, diabetes.
Stages of lesion — order?
Initiation, fatty streak, fibrous, complicated.
Pathogenesis schema — initial event?
Endothelial dysfunction from risk factors.
Symptoms — chronic vs acute?
Chronic: ischemia; Acute: thrombosis from rupture.
Plaque composition — stabilizing?
High collagen and smooth muscle content.
Thrombus formation — danger?
Obstructs blood flow, causing ischemia.
Prevention — key strategies?
Manage cholesterol, blood pressure, stop smoking.
Initiation — triggered by?
Endothelial injury and LDL entry.
Fatty streaks — features?
Foam cells, monocytes, T lymphocytes.
Fibrous plaque — features?
Smooth muscle, collagen, lipid core.
Unstable plaque — risk?
Lipid-rich, thin cap, prone to rupture.
Plaque rupture — consequence?
Thrombosis and potential acute occlusion.
Major affected arteries?
Coronary, carotid, iliac, femoral.
Blood pressure threshold?
Systolic ≥140 mmHg, diastolic ≥90 mmHg.
Impact of risk factors?
Accelerate endothelial damage and plaque progression.
Lesion progression — main features?
From fatty streak to fibrous and complex plaque.
Advanced lesion — characteristic?
May cause luminal narrowing and rupture.
Plaque stabilization — method?
Increase collagen, reduce lipids.
Atherosclerosis — definition?
Chronic arterial disease with lipid-rich plaques.
LDL — role?
Main lipid infiltrating arterial walls.
Fatty streaks — composition?
Foam cells and lipid accumulation.
Plaque rupture — consequence?
Thrombosis and vessel occlusion.
Stable vs unstable plaque — difference?
Stable: thick collagen cap; unstable: thin, lipid-rich.
Endothelium — role?
Initiates atherogenesis when dysfunctional.
Risk factors — examples?
Hypertension, smoking, hypercholesterolemia, diabetes.
Answer 21 questions on Understanding Atherosclerosis and Its Clinical Impact.
1. Which of the following is a key risk factor that contributes to endothelial dysfunction in the development of atherosclerosis?
2. How does LDL oxidation contribute to monocyte attraction in the development of atherosclerosis?
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