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What are the 2 main components of the vessel wall?
- 1. Endothelial cells (EC)
- 2. Smooth muscle cells (SMC)
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What are the 2 major mechanisms of clinical disease related to blood vessels?
- 1. The bv can NARROW or become totally obstructed
- 2. The bv can WEAKEN, leading to dilation or rupture
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If a change to EC is reversible and does not require new protein synthesis, like a response to histamine, what would this be classified as?
Rapid onset type of change
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If and endothelial dysfunction required a change in gene expression, what would this entail?
Need to make new or altered protein synthesis and may need hours or days to occur.
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What are the main things that could cause EC injury?
- 1. Cytokines and bacterial products: may lead to inflamm and/or septic shock
- 2. Hemodynamic stress and lipid products: may lead to atherosclerosis
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What things is a common possible cause of thrombus formation, atherosclerosis and vascular lesions of HTN?
EC injury
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What cells in a vessel are responsible for vasodilation and vasoconstriction due to physiologic stimuli?
SMC
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What cells in a vessel are responsible for synthesizing collagen, elastin, proteoglycans, growth factors and cytokines?
SMC
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What is the SMC response to EC injury?
- They migrate to subintima where they proliferate and lay dwn ECM.
- This forms neointima and may lead to exaggerated healing and intimal thickening, with lumen narrowing or occlusion of smaller vessels
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If there is a congenital anomaly such as an abnormal artery-vein connection, what is one at risk for?
- Rupture causing hemmorrhage b/c this abnormality may shunt blood from the arterial to venous side, overloading the heart.
- Of main concern for brain and GI
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What is "hardening of the arteries" called?
Atertiosclerosis. This refers to the thickening and loss of elasticity in the vessel walls.
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What are the 3 types of arteriosclerosis?
- 1. atherosclerosis- most important type
- 2. monckebergs medial calcific sclerosis
- 3. arterolosclerosis
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Atherosclerosis can involve what arteries?
- Large ones- supplying:
- heart
- brain
- kidney
- lower extremeties
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What are possible consequences of atherosclerosis?
Atheromas may occlude smaller lumens, they may also rupture and induce thrombus formation
in larger vessels atheromas may weaken the vessel wall produce and aneurysm and possibly rupture
atheromas are friable and may shed emboli which can occlude vessels
- mesenteric occlusion
- sudden cardiac death
- chronic ischemic heart disease
- ischemic encephalopathy
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Non-modifiable Risk factors for atherosclerosis include
age, gender, family history and genetic abnormalities
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modifiable risk factors for atherosclerosis include
- hyperlipidemia (LDL are the bad ones)
- HBP
- smoking and diabetes
- obesity, inactivity, stress, low estrogen post menopausal, infection
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Describe the chronic inflammatory steps that respond to endothelial injury leading to atherosclerosis
Increased EC permeability- leukocytes
lipoproteins seep into vessel wall and are oxidizes, Macrophages adhere and follow
platelets, smc from media to intima, intimal thickening
lipids accumulate
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Cells(smc, macrophages, WBCS); ECM; extra/intracellular lipid, new capillaries are all major components of what?
Atherosclerotic plaques
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