Unit 13: Atherosclerosis – Exam Revision Sheet

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1. 📌 Essentials

• Atherosclerosis is a chronic arterial disease characterized by lipid-rich plaques in medium/large arteries.
• The primary lipid involved is LDL cholesterol, which infiltrates and oxidizes in the wall.
• It initiates with endothelial dysfunction from risk factors like hypertension, smoking, and hypercholesterolemia.
• Fatty streaks are early, asymptomatic lesions consisting of foam cells and lipid accumulation.
• Fibrous plaques feature smooth muscle proliferation, collagen, and a lipid core, with potential for stability or rupture.
• Plaque rupture exposes thrombogenic material, leading to thrombus formation and possible vessel occlusion.
• Clinical signs appear when arterial lumen decreases by >70-75%, causing ischemia.
• Major affected arteries include coronary, carotid, iliac, and femoral arteries.
• Risk factors include hyperlipidemia, hypertension, smoking, diabetes, obesity, and inactivity.
• Advanced plaques can cause chronic ischemia or acute events like myocardial infarction or stroke.

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2. 🧩 Key Structures & Components

• Endothelium: Innermost arterial lining; dysfunction initiates atherogenesis.
• Lipid core (necrotic core): Accumulation of cholesterol, cellular debris.
• Foam cells: Lipid-laden macrophages that ingest oxidized LDL.
• Smooth muscle cells: Migrate, proliferate, and produce collagen in plaques.
• Fibrous cap: Collagen-rich layer covering the lipid core.
• Calcifications: Hardened deposits in advanced lesions.
• Thrombus: Clot formed on ruptured plaque surface, occluding the vessel.

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3. 🔬 Functions, Mechanisms & Relationships

• Risk factors damage the endothelium, increasing permeability to LDL.
• LDL penetrates sub-endhelial space, oxidizes, and triggers inflammation.
• Monocytes adhere, migrate into intima, differentiate into macrophages, and ingest oxidized LDL → foam cells.
• Accumulation of foam cells forms fatty streaks.
• Smooth muscle cells migrate from media to intima, producing collagen to form a fibrous cap.
• Plaque progression involves lipid accumulation, smooth muscle proliferation, and extracellular matrix deposition.
• Plaque rupture exposes thrombogenic material, activating coagulation cascade → thrombosis.
• Stable plaques: abundant collagen, thick cap; unstable: lipid-rich, thin cap prone to rupture.
• Stenosis severity correlates with ischemia; symptoms typically manifest >70% stenosis.
• Rupture triggers acute ischemic events such as myocardial infarction.

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4. Summary Table

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5. Hierarchical Diagram (ASCII)

Atherosclerosis
 ├─ Endothelial Dysfunction
 │    └─ LDL infiltration & oxidation
 ├─ Fatty Streaks
 │    └─ Foam cells, monocytes, T-cells
 ├─ Fibrous Plaques
 │    ├─ Smooth muscle migration
 │    ├─ Collagen synthesis
 │    └─ Lipid core formation
 └─ Plaque Rupture
     ├─ Cap rupture or fissure
     └─ Thrombus formation → Vessel occlusion

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6. ⚠️ High-Yield Pitfalls & Confusions

• Confusing fatty streaks (benign, early lesion) with advanced plaques.
• Mistaking stable plaques for unstable due to thick fibrous caps.
• Overlooking the role of oxidized LDL rather than native LDL.
• Assuming all plaques cause symptoms; many are silent until severe stenosis.
• Conflating calcification (a feature of advanced plaques) with early lesions.
• Underestimating the importance of endothelial dysfunction as a trigger.
• Misidentifying rupture sites; not all ruptures cause clinical events.
• Not recognizing that size of stenosis (>70%) correlates with symptoms.

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7. ✅ Final Exam Checklist

• Understand the definition and pathogenesis of atherosclerosis.
• Identify the key steps: endothelial injury, LDL infiltration, foam cells, fatty streaks.
• Know the composition and features of fibroatheromas.
• Differentiate stable vs. unstable plaques.
• Recognize major risk factors and their mechanisms.
• Recall the affected arteries and typical clinical presentations.
• Describe the process leading to plaque rupture and thrombosis.
• Explain the significance of lumen narrowing (>70%) for symptoms.
• Distinguish early lesions (fatty streaks) from advanced, complicated plaques.
• Remember that oxidized LDL and inflammation are central to lesion progression.
• Be aware of common pitfalls and areas of confusion in interpretation.
• Link plaque stability with risk of rupture and clinical consequences.
• Know the primary regions affected: coronary, carotid, iliac, femoral.
• Recognize the importance of early management of risk factors to prevent progression.
• Comprehend the role of collagen and smooth muscle in plaque stability.

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Revise these points thoroughly to excel in exams on atherosclerosis!