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NURS 350 patho CV

Patho - cardio - atherosclerosis

QuestionAnswer
very abbriviated drill - see lecture guide see lecture guide for specifics
arteriosclerosis (broad term) chronic disease of arterial system characterized by abnormal THICKENING and HARDENING of coronary arteries
atherosclerosois - is a form of arteriorsclerosis a form of arteriosclerosis - thickening/hardening is caused by soft depositsof INTRA arterial fat and fibrin that harden over time
CAD any disorder --> narrowing/occlusion of coronary artery
atherosclerosis is main contributor to these diseases CAD---MI---CVA---gangreen of extremities ----50% of deaths in US, Europe, Japan
atherosclerosis is more than a disease is a process over a lifetime - even kids have beginning stages of atherosclerosis
atherosclerosis is wound healing gone awry bwo excessive inflammatory-fibroproliferative responses to injury--> occlusion of arteries
3 sources of injury -->atherosclerosis altered hemodynamic forces/HTN----chemicals that vasoCON/nicotine, catecholamines----bacterial infections/c.pneumoniae
3 other sources of injury-->atherosclerosis hyperlipidemia---mechanical trauma/angioplasty----inflamm cells/mediators/oxidative stress/inj
major hypothesis for atherosclerosis response-to-injury hypothesis ---focus on inflamm and role of oxidative mechanisms
3 types of atherosclerotic lesions fatty streak---intermediate---fibrous plaque
fatty streak characteristics (found in 1/2 of autopsies of 10-14 year olds in England) first recognizable lesion as fat deposits---macrophages ingest fat-->dysfunctional foam cells-->inflamm response---aggregation of foam cells/Tcells in tunica intima.
intermediate lesion characteristics progressive stage where inflamm cells, foam cells, fat cells invade into sub-intima/media------layers of phages/sm muscle cells-----DYSFUNCTIONAL ENDOTHELIUM CAN'T MAKE NO-----can't vasodil----glycoprotiens make vessel sticky/THROMBOGENIC
Fibrous plaque characeteristics complex lesions protrude into lumen---covered wtih fibrous cap of CT embedded with SMOOTH MUSCLE---fibrous cap overlays core of lipid/necrotic debris
what is contained in the fibrous plaque? macrophages, smooth muscle cells, activated Tcells
how do fibrous plaques contribute to deaths they rupture/crack which causes bleeding ---thrombosis---occccclusion
key concept in response to injury hypothesis injured endothelium becomes dysfunctional
MOA dysfunctional endothelium lipoproteins trapped---glycopro expression on endothelial surface---sticky/thrombogenic endothel---phage/Tcell attachement, move btw endotheial cells
MOA dysfunctional endothelium once inflamm cells move betw endothelial cells enjured endothelium release growth factors/cytokines---migrating cells move deeper into artery wall---phages to foam cells---foam cells+WBCs = fatty streak
evens of lesion progression sm muscle/phages/Tcells proliferate---smooth muscle cells form CT matrix (elastic fibers, collagen, proteoglycans)----lipid/chol accumulate in matrix----LUMENAL SURFACE OCCLUDED
Lesion progression marked by alternating layers of smooth muscle/foam cells---endothelial cell retraction occurs---foam cells exposed---now sites for platelet interactions---may lead to clot formation
what is source of CT in WOUND HEALING fibroblasts form CTin traditional wound healing
source of CT in atherosclerotic lesions smooth muscle cells - which transform, become migratory and more like fibroblasts
in wound healing, the source of injury ultimately removed. Not so in atherosclerosis. why because the sources of injury are chronic - we need bp and cholesterol to survive ----so progression from fatty streak to fibrous plaque is UNLIKELY TO BE INTERRUPTED
there are many molecules in network - major players are NO can't be made by dysfunctional endothelium-------growth factors upregulated in lesions (PDGF, FGF, IL-1, TNFalpha, etc)-----chemotaxis factors (CSF, PDGF, IGF-1)----inflamm modulators respond to injury (IL1, TNFalpha, INF)
important areas of research C-Reactive Protein---inflammation---obesity---NIDDM-type2------adipocytes make inflamm cytokines contributing to athero
C-reactive protein role marker of inflammation, indicates high risk of athero
Created by: lorrelaws