1. Overview

Atherosclerosis involves patchy deposits of LDL cholesterol (atheromas or plaques) in medium-large arteries’ intima layer.

Leads to arterial lumen narrowing (stenosis) and blood flow reduction (ischemia).

Develops slowly from early intimal thickening in ages 10-20, manifesting symptoms around 35-40.

Key stages include initiation, early lesion (fatty streak), fibrous plaque, and complicated plaque.

Affected arteries include coronary, carotid, and lower limb arteries.

Major risk factors: hypercholesterolemia, hypertension, smoking, diabetes, age, sex, obesity, inactivity.

2. Core Concepts & Key Elements

Atherogenesis initiation:

Endothelial dysfunction due to risk factors.
LDL crossing endothelium and oxidizing in sub-endothelial space.

Early lesion:

Monocyte attraction → transformed into macrophages forming foam cells.
Manifest as fatty streaks.

Progression to fibrous plaque:

Foam cells increase.
Vascular smooth muscle cells (VSMC) migrate inward, produce collagen and extracellular matrix.
Plaque core: extracellular lipids, foam cells, debris.
Surrounded by collagen-rich fibrous cap and endothelial coverage.

Complicated plaque:

Cap rupture or fissure.
Thrombus formation leading to partial or complete vessel occlusion.

Plaque characteristics:

Stable plaques: collagen-rich, hard, low rupture risk.
Unstable (vulnerable) plaques: lipid-rich, soft, high rupture risk.

Symptoms:

Typically asymptomatic until >70-75% stenosis.
Chronic: partial ischemia.
Acute: plaque rupture → thrombus → complete ischemia.

Affected arteries and clinical manifestations:

Heart: stable angina, ACS (unstable angina, MI).
Brain: T.I.A., stroke.
Lower limbs: intermittent claudication, gangrene.

3. High-Yield Facts

LDL cholesterol thresholds:

Total cholesterol >200 mg/dl.
LDL >160 mg/dl.

Blood pressure:

Hypertension: systolic ≥140 mmHg, diastolic ≥90 mmHg.

Normal fasting glucose:

70-110 mg/dl.

Atheroma core components:

Lipids, foam cells, necrotic debris.

Plaque stability:

Stable: collagen-rich.
Unstable: lipid-rich.

Severity thresholds:

70-75% stenosis critical for symptoms.

Clinical consequences:

Partial ischemia: chronic.
Total ischemia: acute, risk of infarction or stroke.

4. Summary Table

Concept	Key Points	Notes
Initiation	Endothelial dysfunction, LDL oxidation	Risk factor-driven
Early lesion	Fatty streak, foam cells	Monocytes → macrophages
Fibrous plaque	VSMC migrate, collagen, lipid core	Stable vs. vulnerable
Complicated plaque	Cap rupture, thrombosis	May cause ischemia
Symptoms	Asymptomatic, become symptomatic >70% stenosis	Chronic vs. acute
Clinical manifestations	Heart (angina, MI), brain (stroke), limbs (claudication)	Depends on artery affected

5. Mini-Schema (ASCII)

Atherosclerosis ├─ Initiation │ ├─ Endothelial dysfunction │ └─ LDL oxidation in sub-endothelial space ├─ Early lesion │ ├─ Monocyte attraction │ └─ Foam cell formation (fatty streak) └─ Progression ├─ Foam cell increase ├─ VSMC migration & collagen production └─ Formation of fibrous plaque ├─ Lipid core ├─ Fibrous cap └─ Endothelial covering └─ Complicated plaque ├─ Cap rupture or fissure └─ Thrombus formation → vessel occlusion

6. Rapid-Review Bullets

LDL deposits in artery wall initiate atherosclerosis.

Endothelial dysfunction is the first step.

Fatty streaks appear from monocyte-derived foam cells.

VSMCs migrate and produce extracellular matrix, forming a fibrous cap.

Plaque core contains lipids, foam cells, debris.

Stable plaques have collagen-rich walls; vulnerable plaques are lipid-rich.

Rupture leads to thrombus, causing acute ischemic events.

Symptoms are usually asymptomatic until critical stenosis (>70-75%).

Clinical signs: stable angina, MI, stroke, limb ischemia.

Risk factors include high LDL, hypertension, smoking, diabetes, age.

Critical thresholds: LDL >160 mg/dl, BP ≥140/90, fasting glucose >110 mg/dl.

Plaque rupture risk influences clinical outcome and management.

Atherosclerosis Revision Sheet

1. 📌 Essentials

A disease characterized by lipid deposits (atheromas) in medium-large arteries' intima.
Main risk factors: hypercholesterolemia, hypertension, smoking, diabetes, age.
Initiates with endothelial dysfunction precipitated by risk factors.
LDL cholesterol infiltration and oxidation trigger early lesion development.
Foam cells derive from monocytes that migrate and transform in the vessel wall.
Plaques consist of a lipid core, fibrous cap, and cellular components.
Plaque stability depends on collagen content and lipid richness.
Cap rupture leads to thrombus formation, causing ischemia or infarction.
Symptoms are often asymptomatic until >70% arterial narrowing.
Affected arteries: coronary, carotid, lower limb arteries.

2. 🧩 Key Structures & Components

Endothelial cells — regulate vascular permeability; initial site of dysfunction.
LDL cholesterol — deposits in arterial wall, oxidizes contributing to atherogenesis.
Monocytes/Macrophages — attracted to early lesion, become foam cells.
Foam cells — lipid-laden macrophages; main component of fatty streaks.
Vascular smooth muscle cells (VSMC) — migrate inward, produce collagen and extracellular matrix (ECM).
Fibrous cap — collagen-rich layer covering the plaque, maintaining stability.
Lipid core — necrotic debris, extracellular lipids, foam cells.
Thrombus — formed after cap rupture, causes occlusion.

3. 🔬 Functions, Mechanisms & Relationships

Risk factors (hypercholesterolemia, hypertension) cause endothelial dysfunction.
Endothelial damage increases permeability, allowing LDL infiltration.
LDL oxidation triggers immune response: monocytes migrate and turn into foam cells.
Accumulating foam cells secrete cytokines, recruiting more immune cells.
VSMCs migrate from media to intima, produce collagen, forming a protective fibrous cap.
Stable plaques are collagen-rich; unstable are lipid-rich prone to rupture.
Rupture exposes thrombogenic material, activating clotting cascade.
Thrombus formation can cause partial or complete arterial occlusion.
Progressive plaque growth leads to luminal narrowing, impairing blood flow.

4. 🗂️ Hierarchical Diagram (ASCII)

Atherosclerosis
 ├─ Initiation
 │    ├─ Endothelial dysfunction
 │    └─ LDL oxidation
 ├─ Early lesion
 │    ├─ Monocyte recruitment
 │    └─ Foam cell formation (fatty streak)
 ├─ Plaque development
 │    ├─ Foam cell accumulation
 │    ├─ VSMC migration and collagen production
 │    └─ Formation of fibrous plaque
 │        ├─ Lipid core
 │        └─ Fibrous cap
 └─ Plaque complication
      ├─ Cap rupture / fissure
      └─ Thrombus formation → occlusion

5. ⚠️ High-Yield Pitfalls & Confusions

Confusing fatty streaks (early) with advanced fibrous plaques.
Overlooking the distinction between stable and unstable plaques.
Misinterpreting thin-cap fibroatheromas (vulnerable plaques) as stable.
Mistaking cap rupture for simple plaque erosion.
Assuming all plaques cause symptoms; many remain asymptomatic.
Believing LDL oxidation occurs only in plasma, ignoring sub-endothelial space.
Confusing causes of ischemia: plaque rupture vs. superimposed thrombosis.
Underestimating the role of VSMCs in plaque stability.

6. ✅ Final Exam Checklist

Know the stages of atherogenesis: initiation, fatty streak, fibrous plaque, complicated plaque.
Identify the key cellular players: endothelial cells, monocytes, foam cells, VSMCs.
Understand plaque composition: lipid core, fibrous cap, cellular elements.
Differentiate between stable and vulnerable plaques.
Recognize the pathological role of LDL cholesterol and oxidized LDL.
Be familiar with common arteries affected: coronary, carotid, limb arteries.
Comprehend the clinical manifestations based on artery and plaque stability.
Know risk factor thresholds: LDL >160 mg/dl, BP ≥140/90 mmHg, fasting glucose >110 mg/dl.
Understand the consequences of plaque rupture: thrombosis, ischemia, infarction.
Recall symptoms: asymptomatic until significant stenosis; then angina, MI, stroke, claudication.
Associate risk factors with development and progression of atherosclerosis.
Be aware of the importance of plaque stability in clinical outcomes.
Link pathophysiological processes to clinical symptoms and management.

End of Revision Sheet

Understanding Atherosclerosis Development

Crée tes propres fiches en 30 secondes

1. Overview

2. Core Concepts & Key Elements

3. High-Yield Facts

4. Summary Table

5. Mini-Schema (ASCII)

6. Rapid-Review Bullets

Understanding Atherosclerosis Development

Crée tes propres fiches en 30 secondes

Atherosclerosis Revision Sheet

1. 📌 Essentials

2. 🧩 Key Structures & Components

3. 🔬 Functions, Mechanisms & Relationships

4. 🗂️ Hierarchical Diagram (ASCII)

5. ⚠️ High-Yield Pitfalls & Confusions

6. ✅ Final Exam Checklist

Understanding Atherosclerosis Development

Understanding Atherosclerosis Development

Which of the following is a primary risk factor that contributes to endothelial dysfunction in atherosclerosis?

Understanding Atherosclerosis Development

Progression globale

Détail par thème

Introduction au système

Les différents types

Structure axiale

Structure appendiculaire

Suivi de progression par thème