Flashcards in Chap 5 + 6 Atherosclerosis & Intimal Hyperplasia Deck (11):
What component sod the vessel wall contribute to atherosclerosis?
Name products secreted by the endothelium.
Describe the formation of an athersclerotic plaque.
1. LDL migrates into subendothelium
2. LDL becomes oxidize
This is one of the chemoattractants of monocytes to the site
3. Inflamm response to LDL and the oxidized LDL itself causes monocyte binding to ahteroma.
4. Monocytes migrate into sub endothelium, become MAC, take up oxidize LDL and become foam cells.
5. SMC and connective tissue form fibrous cap with a core of cholesterol esters, free cholesterol all forming the fibrous plaque.
6. fibrous plaque can become complicated by calcification, ulceration, hemorrhage, necrosis.
How does the faso vasorum contribute to athersclerosis development?
Increase in VV with plaque formation
Increase leukocyte traffic and promote inflamm process
What are the hypothesis of at hero devel.
response to injury hypothesis
Describe the process of intimal hyperplasia.
1. biochemical/mechanical insult leads to activation of SMC. They switch from contractile/quiescent to synthetic/proliferative.
2. Inflam cells migrate and release proteases (MMPs). these break down extracellular matrix.
3. SMC then liberated and migrate to intima where the proliferate and deposit matrix proteins.
4.SMC in intima cannot organize cellular and matrix components so histologically disordered.
5. De novo intimal layer accumulates over time.
What are causes of lumen loss after vascular procedures.
Wall remodelling (arteries enlarge cross sectional area to accommodate athero lesion, but can get wall shrinkage)
Vascular tone and recoil (HTN can lead to permanent increased tone, balloon angio destroys wall integrity loosing recoil property)
What are inciting factors for IH?
List the cellular effectors of IH.
PLT and leukocytes
List biochemical effectors of IH.
Inflammatory mediators (cytokines)
Growth and Migration Factors (VEGF, TGF)
Matrix Metabolism (MMP)