Flashcard: Understanding Atherosclerosis Development — 34 carte

Endothelial dysfunction — role?

Initiates atherogenesis by increasing permeability and adhesion.

Atherosclerosis — definition?

Lipid deposits in medium-large arteries

LDL oxidation — process?

LDL becomes oxidized in sub-endothelial space.

Risk factors — examples?

Hypercholesterolemia, hypertension, smoking, diabetes, age

Monocyte recruitment — mechanism?

Attracted by endothelial adhesion molecules.

Initiate with?

Endothelial dysfunction

Foam cells — origin?

Derived from macrophages ingesting oxidized LDL.

LDL — role?

Infiltrates and oxidizes in the arterial wall

Fatty streak — hallmark?

Early atherosclerotic lesion consisting of foam cells.

Foam cells — origin?

Monocytes that migrate and transform

VSMC migration — effect?

Contributes to fibrous plaque formation by collagen production.

Plaque components — include?

Lipid core, fibrous cap, cellular elements

Fibrous plaque — structure?

Core of lipids and foam cells, covered by collagen cap.

Plaque stability depends on?

Collagen content and lipid richness

Lipid core — contents?

Lipids, foam cells, necrotic debris.

Fibrous cap — function?

Protects core; stability depends on collagen content.

Cap rupture — consequence?

Thrombus formation and potential vessel occlusion.

Thrombus — outcome?

Partial or complete vessel blockage.

Critical stenosis — percentage?

Typically >70-75%, leading to symptoms.

Symptoms — common manifestation?

Ischemic symptoms like angina, stroke, or claudication.

LDL threshold — >200 mg/dl?

High risk of atherosclerosis.

Blood pressure — hypertension?

Systolic ≥140 mmHg, diastolic ≥90 mmHg.

Plaque stability — collagen content?

Stable: high collagen; unstable: lipid-rich.

Stages — development sequence?

Initiation, fatty streak, fibrous plaque, complicated plaque.

Affected arteries?

Coronary, carotid, lower limb arteries.

Early lesion — in ages?

10-20 years old.

Symptomatic threshold?

>70-75% stenosis.

Acute event — cause?

Plaque rupture with thrombus formation.

Chronic ischemia — sign?

Stable angina, limb claudication.

Unstable plaque — feature?

Lipid-rich, thin fibrous cap, high rupture risk.

Foam cell role?

Main cell type in early lesion.

Extracellular debris — composition?

Necrotic lipids and cell remnants.

VSMC migration — effect on stability?

Enhances stability via collagen production.

Clinical arteries affected?

Coronary, carotid, limb arteries.