NURS 350 patho CV Word Scramble
|
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
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
Popular Nursing sets