Understanding Atherosclerosis Formation and Risks

Извадка от листа за преговор

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.

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Преглед на теста

1. Which process is primarily involved in the initiation of atherosclerosis related to endothelial dysfunction and LDL oxidation?

2. At what age do fatty streaks typically begin to form in arteries, according to the revision sheet?

3. What is the hallmark feature of foam cells in the development of fatty streaks in atherosclerosis?

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Преглед на флашкартите

Endothelial dysfunction — role?

Initiates atherosclerosis by increasing permeability.

Atherosclerosis — definition?

Fatty plaque formation in arteries.

LDL oxidation — location?

Occurs beneath the endothelium.

LDL cholesterol — role?

Main lipid in plaque deposits.

Foam cells — formation?

Macrophages ingest oxidized LDL.

Plaque rupture — consequence?

Thrombosis and vessel occlusion.

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