1. Overview

Atherosclerosis is a chronic, progressive disease characterized by the buildup of fatty deposits within the walls of medium-large arteries, leading to narrowing (stenosis) and reduced blood flow (ischemia). It begins with endothelial dysfunction and lipid accumulation, evolving over decades from early fatty streaks to complex plaques. This condition often remains asymptomatic until critical stenosis or plaque rupture causes clinical events such as heart attack, stroke, or limb ischemia. The process involves multiple stages from initiation to complication, with various risk factors influencing its development.

2. Core Concepts & Key Elements

Definition & Pathology: Hardening of arteries due to patchy fatty deposits (atheromas) in the intima.

Location: Mainly affects medium-large arteries, especially coronary, carotid, and peripheral arteries.

Development Timeline: Starts at ages 10-20, symptoms by 35-40.

Risk Factors:

Hypercholesterolemia: Total cholesterol >200 mg/dl, LDL >160 mg/dl
Hypertension: Systolic ≥140, Diastolic ≥90
Smoking
Diabetes: Fasting glucose 70-110 mg/dl
Others: Age, sex, obesity, inactivity

Atherogenesis Process:

Endothelial dysfunction due to risk factors.
LDL crossing endothelium, oxidized in sub-endothelial space.
Monocyte attraction and transformation into macrophages (foam cells).

Plaque Evolution:

Fatty streak: accumulation of foam cells.
Fibrous plaque: VSMC migrate, produce collagen, forming a fibrous cap.
Advanced plaque: lipid and necrotic core, surrounded by collagen and smooth muscle.
Complicated plaque: rupture or fissure leading to thrombus.

Plaque Types:

Stable (non-vulnerable): hard, collagen-rich.
Unstable (vulnerable): soft, lipid-rich.

Symptoms & Clinical Events:

Often asymptomatic; symptoms occur with >70-75% stenosis.
Chronic ischemia from stable plaques.
Acute events: plaque rupture, thrombus formation.

Affected arteries & Possible Diseases:

Coronaries: angina, myocardial infarction.
Carotids: stroke, TIA.
Lower limbs: claudication, gangrene.

Progression & Morphology:

Fatty streak → fibrous plaque → calcification → complexity → rupture.

3. High-Yield Facts

Definitions:

Atherosclerosis: fatty deposit accumulation → arterial hardening.
LDL cholesterol: >160 mg/dl = risk factor.
Cholesterol: >200 mg/dl = hypercholesterolemia.

Numbers/Values:

Age onset of fatty streaks: 10-20.
Symptoms onset: 35-40.
Critical stenosis: >70-75% lumen narrowing.

Mechanisms:

Endothelial damage → lipid infiltration → inflammatory response.
Foam cell formation: macrophages engorged with oxidized LDL.

Clinical Relevance:

Asymptomatic until critical stenosis or rupture.
Stable vs. unstable plaques determine chronic vs. acute events.

4. Summary Table

Concept	Key Points	Notes
Pathogenesis	Endothelial injury → LDL infiltration → foam cells → plaque formation	Starts at ages 10-20
Risk Factors	Hypercholesterolemia, hypertension, smoking, diabetes	Major modifiable factors
Evolution	Fatty streak → fibrous plaque → complicated plaque	Over decades, age-related
Plaque Stability	Collagen-rich = stable; lipid-rich = unstable	Determines risk of rupture
Key Lesions	Critical stenosis >70-75%; rupture leads to thrombus	Causes clinical events
Affected arteries	Coronary, carotid, peripheral arteries	Manifestations vary
Symptoms	Asymptomatic early; ischemia, infarction, stroke	When stenosis >70-75% or rupture occurs

5. Mini-Schema

Atherosclerosis ├─ Initiation │ └─ Endothelial dysfunction ├─ Lipid accumulation │ └─ LDL infiltration and oxidation ├─ Foam cell formation │ └─ Monocytes → macrophages ├─ Plaque development │ ├─ Fatty streak │ ├─ Fibrous plaque │ └─ Advanced plaque with necrosis ├─ Plaque stability │ ├─ Stable (collagen-rich) │ └─ Unstable (lipid-rich) └─ Clinical outcomes ├─ Chronic ischemia └─ Acute rupture → thrombus

6. Rapid-Review Bullets

Atherosclerosis affects medium-large arteries.

Starts at ages 10-20, symptoms by 35-40.

Major risk factors: hypercholesterolemia, hypertension, smoking, diabetes.

LDL crosses endothelium, oxidizes, triggers inflammation.

Foam cells derive from monocytes ingesting oxidized LDL.

Plaque evolves from fatty streak to fibrous and complicated forms.

Stable plaques have collagen; unstable have lipids.

Critical stenosis is >70-75%, causes ischemic symptoms.

Plaque rupture causes thrombus, leading to acute events.

Commonly affects coronary, carotid, peripheral arteries.

Clinical spectrum: asymptomatic, angina, MI, stroke, gangrene.

1. 📌 Essentials

Atherosclerosis is a chronic disease characterized by fatty deposits in arterial walls causing stenosis.
Primarily affects medium to large arteries like coronary, carotid, and peripheral arteries.
Initiates with endothelial dysfunction due to risk factors such as hypercholesterolemia, hypertension, smoking, and diabetes.
Lipid infiltration, especially oxidized LDL, promotes inflammation and foam cell formation.
Progressive stages include fatty streaks, fibrous plaques, and complicated lesions.
Stable plaques are collagen-rich; unstable plaques are lipid-rich and prone to rupture.
Critical stenosis >70–75% causes ischemic symptoms; rupture can lead to thrombosis.
Clinical manifestations include angina, MI, stroke, limb ischemia, often asymptomatic early.
Plaque development is a slow process spanning decades, beginning in youth.
Morphological evolution: fatty streak → fibrous plaque → calcified and complex plaque.

2. 🧩 Key Structures & Components

Endothelium — lines arteries, regulates vessel permeability and tone.
Lipid core — composed of cholesterol, phospholipids, necrotic debris.
Foam cells — macrophages engorged with oxidized LDL.
Vascular smooth muscle cells (VSMCs) — migrate, proliferate, produce collagen.
Fibrous cap — collagen layer stabilizing plaque.
Necrotic core — lipid and cell debris prone to rupture.
Calcifications — deposits within chronic plaques.
Thrombus — clot formed after plaque rupture.
Risk factors — hypercholesterolemia, hypertension, smoking, diabetes.
Risk modifiers — age, sex, obesity, inactivity.

3. 🔬 Functions, Mechanisms & Relationships

Endothelial dysfunction allows LDL to penetrate intima.
Oxidized LDL induces monocyte adhesion and infiltration.
Monocytes differentiate into macrophages, phagocytose lipids forming foam cells.
Foam cells and lipid accumulation form fatty streaks.
VSMCs migrate from media to intima, secrete collagen → fibrous cap.
Stable plaques have thick collagen caps; unstable plaques have thin caps and large lipid cores.
Plaque rupture exposes thrombogenic material, leading to thrombus formation.
Critical stenosis (>70–75%) causes ischemic symptoms; rupture causes acute events.
Calcification stabilizes plaques but can contribute to brittleness.

Endothelium
   │
   ├─ LDL infiltration
   │
   ▼
Oxidized LDL
   │
   ├─ Monocyte recruitment
   │
   ├─ Monocytes → macrophages → foam cells
   │
   ├─ Fatty streak formation
   │
   ├─ VSMC migration and collagen deposition
   │
   └─ Fibrous plaque
           │
           ├─ Stable (thick collagen)
           │
           └─ Unstable (lipid-rich core)

4. Comparative Table: Stable vs. Unstable Plaques

Feature	Stable Plaque	Unstable Plaque
Composition	Collagen-rich, dense cap	Lipid-rich, thin cap
Risk of rupture	Low	High
Presence of necrotic core	Small or absent	Large
Clinical risk	Chronic ischemia (angina)	Acute MI or stroke due to rupture
Morphology	Thick, fibrous	Thin, susceptible to fissure or rupture

5. 🗂️ Hierarchical Diagram

Atherosclerosis
 ├─ Initiation
 │   └─ Endothelial dysfunction
 ├─ Lipid infiltration
 │   └─ LDL cross-and oxidation
 ├─ Inflammatory response
 │   └─ Monocyte adhesion and infiltration
 ├─ Foam cell formation
 │   └─ Macrophages ingest oxidized LDL
 ├─ Plaque development
 │   ├─ Fatty streak
 │   ├─ Fibrous plaque (VSMC collagen)
 │   └─ Complex/ruptured plaque
 └─ Clinical outcome
     ├─ Chronic ischemia
     └─ Acute rupture leading to thrombus

6. ⚠️ High-Yield Pitfalls & Confusions

Confusing fatty streaks with advanced plaques; fatty streaks are non-obstructive and benign.
Mistaking stable plaques for unstable ones; stability depends on collagen content.
Overlooking the role of oxidized LDL vs. native LDL.
Ignoring the contribution of VSMCs to plaque stability.
Misinterpreting the timing: initiation in youth (ages 10–20), symptoms often not until 35–40.
Assuming all plaques cause symptoms; most early plaques are asymptomatic.
Confusing atherosclerosis with arteriosclerosis (general arterial stiffening).
Overemphasizing calcification as a sign of instability; often stabilizes plaques.

7. ✅ Final Exam Checklist

Define atherosclerosis and identify affected arteries.
List key risk factors: hypercholesterolemia, hypertension, smoking, diabetes.
Describe the sequence: endothelial damage → LDL entry → foam cells → fatty streaks.
Differentiate stable vs. unstable plaques.
Know the critical stenosis percentage (>70–75%) causing symptoms.
Understand the process of plaque rupture and thrombus formation.
Recognize clinical presentations: angina, MI, stroke, gangrene.
Recognize the significance of oxidized LDL in pathogenesis.
Describe the morphological evolution of plaques.
Recall age-related development starting at age 10–20.
Be aware of factors that stabilize or destabilize plaques (collagen vs. lipids).
Know the common arteries affected and related diseases.

Atherosclerosis Pathogenesis and Clinical Implications

Crée tes propres fiches en 30 secondes

1. Overview

2. Core Concepts & Key Elements

3. High-Yield Facts

4. Summary Table

5. Mini-Schema

6. Rapid-Review Bullets

Atherosclerosis Pathogenesis and Clinical Implications

Crée tes propres fiches en 30 secondes

1. 📌 Essentials

2. 🧩 Key Structures & Components

3. 🔬 Functions, Mechanisms & Relationships

4. Comparative Table: Stable vs. Unstable Plaques

5. 🗂️ Hierarchical Diagram

6. ⚠️ High-Yield Pitfalls & Confusions

7. ✅ Final Exam Checklist

End of Revision Sheet

Atherosclerosis Pathogenesis and Clinical Implications

Atherosclerosis Pathogenesis and Clinical Implications

What is the initial pathological change in arteries that initiates atherosclerosis?

Atherosclerosis Pathogenesis and Clinical Implications

Progression globale

Détail par thème

Introduction au système

Les différents types

Structure axiale

Structure appendiculaire

Suivi de progression par thème