Revision sheet: Understanding Atherosclerosis Formation and Risks

Atherosclerosis Revision Sheet

1. 📌 Essentials (Key Facts)

• Atherosclerosis = formation of fatty plaques (atheromas) in medium-large arteries.
• Deposits are mainly LDL cholesterol beneath the endothelium.
• Lesions start as fatty streaks in ages 10-20; symptomatic disease occurs after 35-40 years.
• Major risk factors: high LDL, hypertension, smoking, diabetes, age, obesity.
• Pathogenesis involves endothelial dysfunction, LDL oxidation, foam cell formation, and fibrous cap development.
• Plaques are classified as stable (collagen-rich) and unstable (lipid-rich).
• Critical stenosis causing symptoms: >70-75% narrowing.
• Plaque rupture exposes necrotic core, causing thrombosis and potential occlusion.
• Clinical syndromes: angina, MI, stroke, claudication, gangrene.
• Atheromatous deposits lead to ischemia in heart, brain, lower limbs.

2. 🧩 Key Structures & Components

• Endothelium — lines arteries, initial site of dysfunction.
• LDL cholesterol — main lipoprotein involved in plaque formation.
• Foam cells — macrophages laden with oxidized LDL, form fatty streaks.
• Vascular smooth muscle cells (VSMC) — migrate and produce collagen in fibrous cap.
• Fibrous cap — collagen-rich layer over necrotic core, stabilizes plaque.
• Lipid/necrotic core — consists of dead foam cells, cholesterol crystals, cellular debris.
• Plaque types — stable vs unstable based on composition.
• Thrombus — clot formed upon cap rupture.

3. 🔬 Functions, Mechanisms & Relationships

• Endothelial dysfunction allows LDL influx and oxidation beneath endothelium.
• Oxidized LDL attracts monocytes, which transform into foam cells.
• Foam cells accumulate into fatty streaks, the earliest lesion.
• VSMCs migrate from media into intima, producing collagen and forming fibrous cap.
• Plaque growth involves lipid accumulation, necrosis, and VSMC proliferation.
• Plaque rupture exposes necrotic core, activates clotting cascade, forming thrombus.
• Stable plaques retain collagen, are less prone to rupture; unstable plaques have large lipid cores.
• Critical stenosis (>70%) impairs blood flow, causing ischemic symptoms.
• Plaque instability leads to acute events: MI, stroke, gangrene.

4. Comparative Table: Stable vs Unstable Plaques

Item	Stable Plaque	Unstable Plaque
Composition	Collagen-rich, VSMC predominance	Lipid-rich, foam cells
Appearance	Hard, dense	Soft, friable
Risk of rupture	Low	High
Clinical risk	Less likely to cause sudden events	Prone to fissure, thrombosis
Example effect	Chronic ischemia	Acute coronary syndrome, stroke

5. 🗂️ Hierarchical Diagram

Atherosclerosis
 ├─ Risk Factors
 │    ├─ High LDL
 │    ├─ Hypertension
 │    ├─ Smoking
 │    └─ Diabetes
 ├─ Pathogenesis
 │    ├─ Endothelial dysfunction
 │    ├─ LDL infiltration & oxidation
 │    ├─ Monocyte recruitment
 │    ├─ Foam cell formation
 │    ├─ Fatty streak development
 │    ├─ VSMC migration & collagen synthesis
 │    └─ Fibrous cap formation
 ├─ Plaque Evolution
 │    ├─ Stable plaques
 │    └─ Unstable plaques
 ├─ Complications
 │    ├─ Cap rupture
 │    └─ Thrombus formation
 └─ Clinical Outcomes
      ├─ Ischemia
      ├─ MI
      ├─ Stroke
      └─ Gangrene

6. ⚠️ High-Yield Pitfalls & Confusions

• Confusing fatty streaks with advanced plaques; fatty streaks are benign.
• Assuming all plaques cause symptoms; many are silent until critical stenosis.
• Overlooking the difference between stable and unstable plaques—stability depends on collagen vs lipid content.
• Misidentifying the role of foam cells—they are key in early lesion formation.
• Ignoring that plaque rupture is the main trigger for acute events.
• Thinking hypertension and hyperglycemia are the root causes; they are risk factors, not causes per se.
• Confusing clinical syndromes: angina vs MI, TIA vs stroke.
• Underestimating the importance of plaque composition in prognosis.

7. ✅ Final Exam Checklist

• Define atherosclerosis and identify its main features.
• List significant risk factors and their cutoff values.
• Describe stages of atherogenesis: initiation, fatty streak, fibrous plaque, complications.
• Explain the differences between stable and unstable plaques.
• Recognize histological features: foam cells, fibrous cap, necrotic core.
• Know the critical stenosis percentage for symptoms (>70-75%).
• Understand how plaque rupture leads to thrombosis.
• Match clinical syndromes to affected arteries: coronary, cerebral, limb.
• Recall key organs involved and their clinical manifestations.
• Explain the role of LDL cholesterol levels (>160 mg/dl) in risk.
• Identify the typical age range for disease onset.
• Recognize the importance of hypertension (≥140/90 mmHg).
• Understand that atherosclerosis causes ischemia, infarction, and organ damage.
• Know that prevention targets control of cholesterol, BP, smoking cessation, and diabetes management.
• Be familiar with pathological progression: endothelial dysfunction → lipid accumulation → foam cells → fibrous cap → rupture → thrombosis.

---