1. Overview

Atherosclerosis involves the development of fatty deposits (atheromas) in medium-large arteries.

Located beneath the intima (endothelium), causing arterial narrowing (stenosis) and reduced blood flow (ischemia).

It is a slowly progressing, chronic disease beginning early in life and potentially causing clinical symptoms around ages 35-40.

Key ideas include atherogenesis process, risk factors, plaque evolution, symptom presentation, and complications.

2. Core Concepts & Key Elements

Definition: Fatty deposits (LDL cholesterol) in arterial walls forming atheromatous plaques.

Affected arteries: Medium-large arteries, primarily coronary, carotid, peripheral arteries.

Atherogenesis stages:

Initiation: Endothelial dysfunction, LDL crossing and oxidizing beneath endothelium.
Early lesion: Monocyte attraction, transformation into foam cells, formation of fatty streak.
Plaque formation: Foam cell accumulation, VSMC migration, collagen synthesis, extracellular lipid buildup, resulting in a fibrous cap.
Advanced plaque: Lipid core, necrotic debris, surrounded by collagen and smooth muscle cells.
Complication: Plaque rupture/fissure leading to thrombus formation and vessel occlusion.

Risk factors: Hypercholesterolemia (LDL >160 mg/dl), hypertension (SBP >=140; DBP >=90), smoking, diabetes (fasting glucose 70-110 mg/dl), age, sex, obesity, inactivity.

Plaque stability:

Stable (non-vulnerable): Collagen-rich, hard, low rupture risk.
Unstable (vulnerable): Lipid-rich, soft, high rupture risk.

Clinical presentation:

Asymptomatic until significant stenosis (>70-75%).
Symptoms:
- Chronic: Partial ischemia (stable plaques).
- Acute: Complete occlusion due to plaque rupture (vulnerable plaques).

Disease outcomes:

Chronic: Progressive ischemia.
Acute: Thrombosis, infarction, and ischemia.

3. High-Yield Facts

LDL cholesterol: >160 mg/dl; total cholesterol: >200 mg/dl.

Hypertension: SBP ≥140, DBP ≥90.

Normal fasting glycemia: 70-110 mg/dl.

Plaque types:

Stable: collagen-rich, low rupture risk.
Unstable: lipid-rich, high rupture risk.

Critical stenosis threshold: >70-75%.

Clinical syndromes:

Heart: Stable angina, ACS (unstable angina, MI).
Brain: TIA, cerebral infarction.
Lower limbs: Intermittent claudication, gangrene.

4. Summary Table

Concept	Key Points	Notes
Atherogenesis	Initiation, fatty streak, fibrous plaque, complicated plaque	Progressive wall thickening and narrowing
Risk factors	Hypercholesterolemia, hypertension, smoking, diabetes	Age, sex, obesity, inactivity
Plaque stability	Stable: collagen-rich; Unstable: lipid-rich	Determines risk of rupture and clinical events
Symptoms	Asymptomatic until significant stenosis	Chronic ischemia or acute thrombosis
Ischemic outcomes	Partial (chronic), complete (acute) occlusion	Depends on plaque stability and rupture

5. Mini-Schema

Atherosclerosis ├─ Development Stages │ ├─ Endothelial dysfunction │ ├─ Fatty streak formation │ ├─ Fibrous plaque │ └─ Complicated plaque (rupture, thrombus) ├─ Risk Factors │ ├─ Hypercholesterolemia │ └─ Hypertension, smoking, diabetes └─ Clinical Manifestations ├─ Chronic ischemia └─ Acute ischemic events (MI, stroke, gangrene)

6. Rapid-Review Bullets

Atherosclerosis is characterized by LDL-rich atheromas in arterial walls.

Initiated by endothelial dysfunction and LDL oxidation.

Monocytes adhere, become foam cells, forming fatty streaks.

VSMCs produce collagen, forming a fibrous cap over lipid core.

Plaque stability depends on collagen content and lipid core composition.

Critical stenosis occurs at >70-75% narrowing.

Plaque rupture leads to thrombus formation and vascular occlusion.

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

Common clinical syndromes: stable angina, MI, stroke, intermittent claudication.

Atheromas can be stable (low rupture risk) or unstable (high rupture risk).

Symptoms may be chronic (partial ischemia) or acute (full occlusion).

Blood flow is compromised as atherosclerosis progresses.

Lipid-laden core and fibrous cap are hallmarks of advanced plaques.

Thrombosis following plaque rupture causes acute infarctions.

Early lesions detectable from ages 10-20.

Atherosclerosis is often asymptomatic until advanced stages.

Atherosclerosis Revision Sheet

1. 📌 Essentials

Definition: Progressive buildup of LDL cholesterol-rich fatty deposits in arterial walls forming atheromatous plaques.
Affected arteries: Primarily coronary, carotid, peripheral arteries.
** process:** Endothelial dysfunction → fatty streak → fibrous plaque → complicated lesion.
Major risk factors: Hypercholesterolemia (>160 mg/dl LDL), hypertension, smoking, diabetes.
Plaque stability: Collagen-rich → stable; Lipid-rich → vulnerable/unstable.
Critical stenosis: Occlusion >70-75% causes ischemia symptoms.
Complications: Plaque rupture → thrombosis → vessel occlusion → infarction.
Clinical manifestations: Asymptomatic initially; symptoms arise from chronic ischemia or acute thrombosis.
Progression timeline: Begins early in life, becomes symptomatic around ages 35-40.
Major outcomes: Chronic ischemia, acute MI, stroke, gangrene.

2. 🧩 Key Structures & Components

Endothelium: Innermost arterial lining, initiates atherogenesis when dysfunctional.
LDL (Low-Density Lipoprotein): Carries cholesterol into the arterial wall.
Foam cells: Lipid-laden macrophages from monocytes.
Vascular Smooth Muscle Cells (VSMCs): Migrate, proliferate, produce collagen.
Fibrous cap: Collagen-rich layer covering the lipid core.
Lipid core: Necrotic, cholesterol-rich necrotic debris.
Plaque components:
- Stable plaque: Thick fibrous cap, lipid.
- Unstable plaque: Thin fibrous cap, large lipid necrotic core.

3. 🔬 Functions, Mechanisms & Relationships

Endothelial dysfunction allows LDL infiltration and oxidation.
Oxidized LDL attracts monocytes that enter intima → convert to foam cells.
Foam cells form fatty streaks, an early lesion in atherogenesis.
VSMCs migrate from media to intima, proliferate, produce collagen → stabilize plaque.
Lipid accumulation enlarges necrotic core, thinning fibrous cap in vulnerable plaques.
Plaque rupture exposes thrombogenic material → thrombus formation.
Thrombus can cause partial or complete vessel occlusion, resulting in ischemia or infarction.
Progressive narrowing of arteries impairs blood flow → clinical symptoms.

4. 📊 Comparative Table

Feature	Stable Plaque	Unstable (Vulnerable) Plaque
Fibrous cap	Thick, collagen-rich	Thin, collagen-poor
Lipid content	Low	High
Macrophage infiltration	Moderate	Extensive
Rupture risk	Low	High
Clinical risk	Less likely to cause sudden events	Major cause of acute events

5. 🗂️ Hierarchical Diagram

Atherosclerosis
 ├─ Endothelial Dysfunction
 │    ├─ LDL Infiltration & Oxidation
 │    └─ Monocyte Adhesion
 ├─ Fatty Streak
 │    ├─ Foam Cell Formation
 │    └─ Initial Lesion
 ├─ Fibrous Plaque
 │    ├─ VSMC Migration & Collagen Deposition
 │    └─ Lipid Core Development
 ├─ Complicated Plaque
 │    ├─ Rupture / Fissure
 │    └─ Thrombus Formation

6. ⚠️ High-Yield Pitfalls & Confusions

Mistaking stable plaques (fibrous, collagen-rich) for unstable ones.
Confusing foam cells with degenerating smooth muscle cells.
Underestimating early lesions like fatty streaks as benign or unimportant.
Thinking that significant stenosis always correlates with symptoms.
Overlooking the role of plaque rupture over size in clinical events.
Confusing atherosclerosis with arteriosclerosis (general arterial stiffening).
Misidentifying risk factors; e.g., assuming only cholesterol causes plaque.
Ignoring the importance of VSMC stability in plaque rupture.

7. ✅ Final Exam Checklist

Define atherosclerosis and its key features.
List common arteries affected by atheromatosis.
Describe stages of atherogenesis.
Explain the difference between stable and unstable plaques.
Recall major risk factors: hypercholesterolemia, hypertension, smoking, diabetes.
Identify critical stenosis threshold (>70-75%).
Recognize clinical syndromes: stable angina, MI, stroke, peripheral ischemia.
Understand the pathophysiology of plaque rupture and thrombosis.
Know the composition of atheromatous plaques.
Differentiate early fatty streaks from advanced plaques.
Describe how VSMCs contribute to plaque stability.
Recognize that plaques can be asymptomatic for decades.
Recall that lipid core and thin fibrous cap predispose to rupture.
Interpret histological features of stable vs vulnerable plaques.
Understand the timeline from early lesion to clinical symptoms.
Be aware of complications: thrombosis, infarction, gangrene---

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

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. 📊 Comparative Table

5. 🗂️ Hierarchical Diagram

6. ⚠️ High-Yield Pitfalls & Confusions

7. ✅ Final Exam Checklist

Understanding Atherosclerosis Development

Understanding Atherosclerosis Development

Which process primarily initiates endothelial dysfunction that leads to LDL oxidation 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