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NURS 350 patho CV
Patho - cardio - atherosclerosis
| Question | Answer |
|---|---|
| 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
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