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20 Cards in this Set
- Front
- Back
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What is atherosclerosis?
What is the speed of plaque development? What is another name for the plaques? |
inflammatory cells, SMCs, lipid, and connective tissue progressively accumulate in the intima of large and medium-sized elastic and muscular arteries.
Slowly, over decades. atheromas |
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What is necessary but not sufficient for atheroma formation?
How might LDL get into the wall? Do mural thrombi initiate atheroma formation? How might smooth muscle cells accumulate in atheromas? |
lipid accumulation in the vessel wall.
too big for endothelial junctions, probably transported across the endothelial cells by "foamy" macrophages which then undergo necrosis --> releasing lipid No, but they play an important role later in progression. growth factors like FGF, TGF-B, thrombin, LDL (all of which can be released by macrophages)..... platelet-derived polypeptides like PDGF are released once mural thrombi form --> further SMC prolif |
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Some theories hold that atheromas have commonalities with leimyomas. why?
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Some research seems to show that the SMCs capping the atheroma are monoclonal.
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In humans atheromas tend to arise at sites where shear stresses are low, but fluctuate rapidly like _____ and ______.
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branch points and bifurcations.
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HTN ______ the severity of atheromas.
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increases
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walk through atheroma initiation and formation.
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1. @ site of favorable hemodynamics, "foamy macroP" get into the walls and lyse, releasing lipids.
2. MacroP also stim SMC prolif w/ gfs 3. mural thrombi form, and PDGF is released --> more SMC prolif 4. deep intima undergoes necrosis --> angiogenesis is initiated and forms new vasovasorum in the plaque. 5. fibroinflamm lipid plaque is formed, w/ a central necrotic core and a fibrous cap. |
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Once the atheroma protrudes ____ into the lumen, the vessel cannot compensate w/ remodeling any longer. Result?
What eventually happens that has clinical significance? |
halfway, stenosis
plaques rupture --> thrombosis, occlusion, etc. |
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Two distinct lesions have been seen as precursors of atherosclerotic plaques.
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Fatty streak
Intimal cell mass.(SMC and connective tissue, but no lipid) |
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Foam cells are...
What is a common mechanism of atheroma expansion? |
... either macrophages or SMCs that have taken up tons'o'lipid
neovascularization --> rupture --> intraplaque hemorrhage --> expansion |
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Where does calcification occur in atherosclerotic plaques? How?
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in areas of necrosis
depends on mineral deposition and resorption |
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When a plaque ruptures, what comes into contact with the blood that is *extremely* thrombogenic?
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TF
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When mural thrombi on the plaque suddenly occlude a vessel, result?
What effect does the chronic narrowing of the lumen have in less acute situations? |
acute infarction
whatever is supplied by that blood --> atrophy, e.g., renal atrophy, intestinal stricture, ischemic atrophy of skin in diabetics |
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Can plaques cause aneurysms? Where?
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yes, typically in the abdominal aorta (AAA).
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HTN
Blood cholesterol lvls smoking diabetes being a guy increasing age physical inactivity elevated homocyteine elevated CRP .... all are what? |
risk factors for atherosclerosis.
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What are the three forms of arteriosclerosis?
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1. Atherosclerosis, the dominant pattern with intimal fibrous plaques often with central grumous lipid-rich cores; luminal narrowing can cause ischemic damage
2. Monckeberg medial calcific sclerosis, with calcific deposits in tunica media of medium-sized muscular arteries, usu in persons >50 yo 3. Arteriosclerosis and arteriolosclerosis, a disease of small arteries and arterioles featuring hyaline or hyperplastic features; luminal narrowing can cause ischemic damage; arteriolosclerosis most frequently assoc with hypertension and diabetes |
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Two most commonly affects areas in atherosclerosis?
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Abdominal Aorta (most frequent)
Coronary arteries |
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Aortic fatty streaks are seen in _____ children by age ____.
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all by age 10
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do fatty streaks disturb blood flow?
What are fatty streaks? |
No
possible precursors of atheroma, lipid-filled flam cells w/ T-lymphocytes and extracellular lipid w/i intima |
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Intermediate lesions are called _____ and characterized by what?
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fibrofatty plaque
Focal raised lesions with disturbance of blood flow Fibrous cap Smooth muscle, monocytes, lymphocytes, foam cells, connective tissue Lipid core Necrotic debris, cholesterol, foam cells |
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What is the most feared complication of complicated atheromas? Where does it usually occur?
How are complicated lesions characterized? |
Superimposed thrombosis, usually occurs on disrupted lesions
Patchy or massive calcification Focal rupture or ulceration of luminal surface Exposure of thrombogenic constituents Atheroembolization Hemorrhage May induce plaque rupture |
