Warning:
JavaScript is turned OFF. None of the links on this page will work until it is reactivated.
If you need help turning JavaScript On, click here.
The Concept Map you are trying to access has information related to:
Atherosclerosis, Atherosclerosis 3 Variations of Arteriosclerosis -thickened, less elastic aa walls Arteriolosclerosis -dz of small aa, a'oles -Hyaline, Hyperplastic ->downstream ischemia -via HTN, DM, Atherosclerosis 3 Variations of Arteriosclerosis -thickened, less elastic aa walls Monckeberg Medial Calcific Sclerosis -Ca deposits in med mm aa. ᡪyo -can ossify-look like medial plates, transverse rings -nodular on palpation -DO NOT ENCROACH ON LUMEN, Atherosclerosis Pathogenesis Response to Injury Hypothesis -chronic inflam due to injury to endoth Via: Chronic Endoth Injury->endoth dysfcn -inc. perm, adhesion -cigarette smoke, toxins, hypoxia, homocys -esp HEMODYNAMIC PROBLEMS, HIGH CHOL Lipoproteins into wall, esp LDL, VLDL -modification by oxidation->scavenged by macs -chemotactic for macs, inc adhesion -antioxidants help lower athero dzs Blood Monocyte adhesion->to intima ->become macs/foam cells->TNF, IL-1->adhesion Platelet adhesion to focal denudation areas -or to WBCs Release of factors from plts, macs, vasc cells ->migration of cells from media to intima Proliferation of sm. mm cells in intima ->elaborate ECM (collagen, PGs) -fatty streak->fibrofatty atheroma->fibrous cap -via PDGF, FGF, TGF-a (beta inhibits) Enhanced lipid accumulation -extracellularly and in macs, sm. mm. Other Fx-Oligoclonality (tumorous?), Infx (herpes, CMV, Chlamydia pneumo), Atherosclerosis Prevention Thrombosis, Calcification, Aneurysm ->heart, brain, LL ischemic events Primary and Secondary (after MI) Prevention -stop smoking -control HTN -weight loss via diet, exercise -moderation of EtOH MOST IMP'T-lower LDL, raise HDL Secondary-antiplatelet drugs, aspirin, Atherosclerosis 3 Variations of Arteriosclerosis -thickened, less elastic aa walls Atherosclerosis-dominant, Atherosclerosis Risk Factors UNCHANGEABLE Age-mortality rises w/ each decade Sex-MEN, women's nears men after menopause -same MI freq at 60-70yo -protection via HRT-better lipids, endoth fcn Genetics-cluster w/ DM, HTN, lipoprotein metabolism IRREVERSIBLE Hyperlipidemia-esp chol-lipid not as imp't -esp high LDL, low HDL (reverse xport) -homozy fam hyperchol(liver LDL-R)->MI ងyo -DM, hypothyroidism->high chol -omega-3 FAs lower chol, less thrombosis, dilation HTN ᡥyo greater risk, inc death rate w/ /70 -control w/ anti-hypertensives, diet Cigarette smoking DM->hypercholesterolemia->athero -2x greater incidence in DM than non ->strokes, LL gangrene Elevated Plasma Homocysteine-endoth dysfcn -from elevated ROS -increase folate, B6, B12 intake to improve Hemostasis/Thrombosis- Fibrinolysis-elevated PAI-1, CRP (aspirin lowers) increased Lipoprotein Lp(a)->cor, CVD Others-stress, Type A, weight gain, sedentary RISK FACTORS ARE SYNERGISTIC Protective-moderate EtOH, exercise->raise HDL, Atherosclerosis NL Intimal Thickening In response to hemodynamic stimuli -in adult coronary aa. -lipid-free, width similar to media, Atherosclerosis Clinical ->more mortality than anything else Plaques obstructive alone in sm aa. -but destructive in larger aa->encroach on media ->aneurysm, rupture, thrombosis Distribution-mostly elastic aa., large-med mm. aa. -Ao (esp abd), carotid, iliac, coronary, pop -begins in kids, (-)Sx til adulthood -Sx-heart, brain, kidneys, legs, sm intestine -esp MI, STROKE, Ao ANEURYSM MORPHOLOGY-intimal thickening, lipid accum Atheromatous Plaque-chol/CE core, fibrous cap -firm, whitish-yellow plaques -Lesions at Ostia of branches -coronary>pop>desc thor Ao>int. carotid>Willis -patchy, eccentric around wall 3 components- 1)cells-sm. mm, macs, leukocytes 2)CT ECM-collagen, elastic fibers, PGs 3)intra/extracellular lipid deposits Anatomy-shoulder-macs, sm.mm, T-cells -deeper necrotic core w/ lipid, chol clefts, foam cells, fibrin, thrombus -foam cells=sm. mm. or macs that eat lipid -neovascularization around periph Fibrous plaques can ->scar even w/ fat Complicated plaque- Calcification (adv dz)-brittle Rupture, ulceration-thrombogenic -can discharge debris (chol emboli, atheroemboli) Hemorrhage into plaque-esp cor aa->rupture -from cap or neovasc vessels Superimposed thrombosis-in rupture/ulcerated/ eroded/hemorrhaged -MOST FEARED COMPLICATION->occlusions Atrophy of media w/ elastic tissue loss->weakness -aneurysmal dilation, Atherosclerosis Clinical Fatty Streak -not raised, but could precede -multiple flat yellow spots -coalesce into streaks -composed of foam, T cells, extracell lipid -can be in əyo, all ᡂyo Ao -less common in cor aa (start in teens) -some evolution into plaques, not all -same risk factors as plaques