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20 Cards in this Set
- Front
- Back
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What are the fixed risk factors for atherosclerosis?
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inc. aging
genetic abnormalities family hx of MI (1st deg. relatives) male gender (>45) |
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What are the two categories of risk factors for atherosclerosis?
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Fixed (non-modifiable) and potentially controllable/acquired
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What are the controllable risk factors of atherosclerosis?
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hyperlipidemia
hypertension cigarette smoking diabetes mellitus |
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What are other risk factors for atherosclerosis?
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obesity, physical inactivity, stress, postmenopausal estrogen deficiency, high carb intake, elevated levels of lipoprotein A, saturated and trans-unsaturated fats, infections
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What are the 5 basic steps in plaque formation?
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1. Endothelial injury/dysfunction
2. Macrophage activation 3. smooth mm cell migration 4. lipid uptake by macrophages and smooth mm cells 5. organization of fibrous cap |
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What are the most important determinants of endothelial alterations?
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Hemodymanic disturbance (high BP, branch points)
Hypercholesterolemia |
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What causes hemodynamic disturbances?
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sheer stress
turbulent flow plaques |
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Where are the most common sites for plaques to occur?
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ostia of exiting vessels
branch points along post wall of abdominal aorta (hits the vertebrae as it pulses) |
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What are the possible ways that hyperlipidemia initiates endothelial dysfunction?
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1. inc. production of O2 free radicals deactivate nitric oxide (major endothelial-relaxing factor)
2. Lipoproteins accumulate in intima at sites of inc. permeability allowing for modification of lipid in arterial wall |
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What are the occurs in the vessels as a result of endothelial DYSFUNCTION?
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1. resultant inc permeability
2. WBC adhesion 3. platelets stick to endothelium 4. monocyte adhesion, migration, localize in intima (change into macrophages and engulf LDL) |
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What are foam cells in relation to atherosclerotic plaques?
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Macrophages with scavenger receptors that readily ingest oxidized LDL.
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Describe the process of macrophage activation
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activated--> release cytokines and growth factors--> attract monocytes and SMC to plaque--> produce toxic O2 species--> oxidation of LDL--> ingested by foam cells
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Describe smooth mm cell migration
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SMC regulate BP in media--> migrate to intima--> now produce proteins--> engulf oxidized LDL's
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Describe the transition of fatty streaks to atheromatous plaques
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fatty streak--> proliferation of SMC's about a foam cell--> fibrofatty atheroma--> modified w/ more deposition of collagen, elastin and proteoglycans--> fibrous cap--> more cellular proliferation and CT formations--> plaques
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What happens to the media of an underlying cap?
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advanced atherosclerotic lesion causes atrophy and fibrosis, impairing elasticity and wall strength
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When is an atherosclerotic lesion considered complicated?
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When any of these are preset: thrombosis, new blood vessel formation, medial layer atrophy, calcification w/in intima, ulceration of fibrous cap
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When does a mature atheroma develop?
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When the fibrous cap is formed over the plaque by extracellular matrix deposition.
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What are some complication of atherosclerosis?
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thrombus formation
microemboli hemorrhage into a plaque plaque rupture occluded lumen (angina/ischemia) |
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If there is lumen occlusion in small arteries what occurs?
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ischemia
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If there is lumen occlusion in large arteries what occurs?
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medial weakening which may lead to dilation/aneurysms
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