Term
| Major Steps of Pathogenisis |
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Definition
| Injury, Increased permeability, inflammation, proliferation, fatty streak, necrosis, repair, fibrous plaque, complication lesion |
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Term
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Definition
| Caused by high shear forces, hypertension, nicotine, oxidized LDL, and hyperglycemia |
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Term
| Step 2: Increased Permability |
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Definition
| Leads to Impaired vasodilation, increased permeability, increased platelet aggregation, loss of ability to produce nitric oxide (inactivates plates, inhibits cell adhesion, inhibits smooth muscle cell migration and proliferation, promotes vasodilation) |
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Term
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Definition
Platelets release PDGF or
a. “platelet derived growth factor”
PDGF enhances monocyte binding
a. Monocytes differentiate into macrophages
b. Macrophages are phagocytic and oxidize LDL
c. LDL can more easily enter the endothelium
PDGF increases growth and migration of smooth muscle cells from the media to the intima which becomes an important part of plaque |
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Term
| Step 4: Proliferation and Fatty Streaks |
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Definition
Smooth muscle cell
migration to intima
Smooth muscle and
macrophage accumulate
oxidized LDL-C
Forming “Foam Cells”
Foam cells release cholesterol into the cell and surround areas around the cell
Forming “Fatty Streaks” – the earliest detectable sign of atherosclerosis |
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Term
| Step 5: Necrosis, Repair, Fibrous Plaque |
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Definition
Plaque formation leads to
1. Cell death or necrosis
Necrosis leads to repair
Repair initiates “vascular
remodeling”
1. Lumen diameter is reduced
2. When diameter is reduced by 40% complete compensation is reached and impairment of blood flow occurs
Fibrous cap and plaque
formed |
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