Flashcards: Understanding Atherosclerosis Development — 37 cards

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.