Karteikarten: Understanding Atherosclerosis and Its Clinical Impact — 36 Karten

Endothelial dysfunction — role?

Initiates atherosclerosis by increasing permeability and adhesion.

Atherosclerosis — definition?

Chronic arterial disease with lipid-rich plaques.

LDL oxidation — consequence?

Promotes monocyte attraction and foam cell formation.

LDL — role?

Main lipid infiltrating arterial walls.

Foam cells — origin?

Macrophages ingest oxidized LDL.

Fatty streaks — composition?

Foam cells and lipid accumulation.

Fatty streaks — first lesion?

Early accumulation of foam cells in arterial wall.

Plaque rupture — consequence?

Thrombosis and vessel occlusion.

Fibrous plaque — composition?

Smooth muscle, collagen, lipid core.

Stable vs unstable plaque — difference?

Stable: thick collagen cap; unstable: thin, lipid-rich.

Plaque stability — high collagen content?

Leads to stable, less rupture-prone plaque.

Endothelium — role?

Initiates atherogenesis when dysfunctional.

Plaque rupture — cause?

Thin fibrous cap over lipid-rich core.

Risk factors — examples?

Hypertension, smoking, hypercholesterolemia, diabetes.

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.