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37 Cards in this Set
- Front
- Back
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What is meant by the "response to injury" hypothesis of atherosclerosis?
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Chronic inflammation response: Chronic or repetitive injury to Epithelium is cornerstone --> lesions develop into "dysfunction"
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what does endothelial dysfunction lead to? *details*
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Activated endothelial cells --> expression of adhesion molecules --> monocyte migration (macrophage maturity) --> platelets aggregate --> *lipoproteins* accumulate in intima at sites of increased permeability
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What occurs in the intima once macrophages and platelets secretory product is released?
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smooth muscle is recruited into intima (from media)
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What do the macrophages and smooth muscle now in the intima "do"? and what to they "become"?
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engulf lipids (mostly oxidized LDL); --> foam cells
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what two things happen to lipoproteins in the vessel walls?
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1. oxidized by free radicals --> oxidized LDL
2. engulfed by macrophages and smooth muscle --> foam cells |
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what effect does oxidized LDL have on endothelial cells and smooth muscle?
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cytotoxic
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what are some of the "chronic Injuries" that induce chronic inflammation in normal vessels?
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hyperlipidemia, HTN, smoking, homocysteine, viruses, toxins, immune rxn, etc.
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What is the initial lesion in atherosclerosis called? does it disrupt blood flow?
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Fatty streak
No! |
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do all fatty streaks progress into atheroscleromas?
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No. often occur in areas no susceptible. Also, evident in ALL people >10 years
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what is an intimal collection of foam cells?
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fatty streak
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where would you find a fatty streak? (vessel type)
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aorta/large/med arteries
recall, atherosclerosis occurs in the elastic large/med arteries |
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what is the longer result of smooth muscle moving into the intima?
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ECM components deposited --> mature atherosclerotic plaque formation
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what do lesions consist of?
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cells (macrophages, T cells, smooth muscle)
Connective Tissue ECM (collagen, proteoglycans, elastic fibers) Lipid deposits -- extracellular and intracellular (foam cells) |
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What are the three "component" in the structure of an atheromatous plaque?
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Fibrous cap - s.m. and connective tissue
Necrotic lipid core "shoulder" - everything else (prominent macrophages, collagen, etc.) |
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What are the clinical results of severe fixed coronary obstruction?
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chronic ischemic heart disease
heart failure |
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what results from an "acute plaque change" (plaque disruption) in a coronary artery?
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MI
Angina sudden death |
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What event can trigger an "acute plaque change"?
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Hemmorage
Ulceration of fibrous cap Thrombosis --> platelet aggregation --> thrombus --> blockage |
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what is the risk/result of a thinning underlying Media?
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aneurysm
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what is meant by a "vulnerable plaque"?
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- markedly eccentric configuration
- large, soft core of necrotic debris and lipid - high density of macrophages - only a thin fibrous cap |
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what is the most frequent location of atherosclerotic aneurysms?
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abdominal aorta
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what is the process that leads to an aneurysm?
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plaque weakens media --> necrosis; macrophages also release proteins that degrade ECM
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What are the “Complicated Lesions” of Atherosclerosis?
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aneurysms
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What type of cell death occurs during an infarction?
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Ischemic Coagulative Necrosis
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What are the time intervals and what is the result during an ischemic event?
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Within seconds: cessation of aerobic glycolysis (ATP depletion)
<20 minutes: reversible cell damage (swelling, etc.) 20-40 minutes: irreversible cell damage |
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Can an MI be visible pathologically early on? what confirms a diagnosis of MI?
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No, no gross changes visible early (~24 hours), TTC staining
enzyme release confirms |
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What enzymes are released from an MI?
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CPK-MB
Troponins (remain 7-10 days) LDH (peaks 3-6 days) none visible after 2 weeks |
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What are the histologic changes in a one-day old MI?
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wavy fibers &
eosinophilia |
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What are the histologic changes in a 2-3 day old MI?
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neutrophil presence
necrotic (plain looking) myocardium |
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What are the histologic changes in a 7-10 day old MI?
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macrophages
necrtotic myocytes have been removed (cannot see) ... only normal looking myocardium may be surrounding the area |
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what is a concern 3-7 days after an MI resulting from mechanical weakening from necrotic and subsequently inflamed myocardium?
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myocardial rupture (nearly always fatal)
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what is a gross morphological change evident 3-7 days post-MI that consists of acute inflammation?
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hyperemic rim (red zone)
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when is scarring post-MI complete?
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8 weeks
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what causes arteriolosclerosis?
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Hypertension
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In what patients would you see hyaline arteriosclerosis?
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elderly, htn, diabetes
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In what patients would you see "onion skinning"? (rings of smooth muscle around arteriole)
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malignant hypertension (rapid development of HTN)
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Is aortic dissection common among patients with substantial atherosclerosis?
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No.
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What are the two common causes behind aortic dissection?
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Men with hypertension
Connective tissue abnormality (Marfan's: abnormal elastin in media) |
