Atherosclerosis (Corbett) - 11/2/16

Question 1

Clinical consequences of Atherosclerosis

Answer 1

• Coronary Artery Disease
  
  • Myocardial ischemia
  • Unstable angina
  • Myocardial infarction
• Stroke
• Renal Artery Disease
  
  • Atheroembolic renal disease
  • Renal artery stenosis
• Aneurysms
• Peripheral Artery Disease
  
  • Limb claudication
  • Limb ischemia

Question 2

Elastic artery vs. Muscular artery

Answer 2

• Largest arteries (closest to the heart) - aorta/pulmonic arteries
• Elastic artery has a lot of collagen and elastin in tunica media
• Give rise to medium vessels –> muscular arteries

Question 3

Endothelial cells participate in structural and functional integrity of vascular wall (align in direction of blood flow).

Properties of normal endothelium (4)

Answer 3

1. Endothelium-dependent vasodilatation
   
   1. ​NO
   2. Prostacyclin
2. Modulation of Immune Response
   
   1. ​Resist WBC adhesion and attachment
3. Anti-hypertrophic properties
   
   1. Inhibition of VSMC (Vascular smooth muscle cells)
   2. Proliferation and migration
4. Anticoagulant, anti-thrombotic, and pro-fibrinolytic function
   
   1. ​Heparan sulfate
   2. Thrombomodulin

Question 4

Atherosclerosis

Answer 4

Very common.

Disease of elastic arteries and large- and medium-sized muscular arteries; a form of arteriosclerosis caused by buildup of cholesterol plaques

Intimal plaque that obstructs blood flow

Question 5

Location

Answer 5

Abdominal aorta > coronary artery > popliteal artery > carotid artery

Most common at bifurcation points

Question 6

Risk factors: modifiable and non-modifiable

Answer 6

Modifiable:

• Smoking
• HTN
• Hyperlipidemia (inc. LDL)
• Diabetes

Non-modifiable:

• Age
• Sex (inc. in men and postmenopausal women)
• Family hx

Question 7

Symptoms

Answer 7

• Angina
• Claudication, but can be asymptomatic

Question 8

Progression/pathogenesis

Answer 8

Endothelial cell dysfunction (disturbed shear) /injury (dyslipidemia) →

Lipids leak into intima → Lipids oxidized and consumed by macrophages (Macrophage and LDL accumulate) via scavenger receptors→ Foam cell forms

→ Fatty Streaks → Smooth muscle cell migration (involves PDGF and FGF) → Proliferation + ECM deposition → Fibrous plaque → complex atheromas (degeneration of walls of arteries)