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17 Cards in this Set
- Front
- Back
components of chylomicrons
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high: TGs
low: cholesterol and protein Apolipoproteins: B48, CII, E |
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functions of chylomicrons
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carry dietary TGs to peripheral tissues
carry dietary cholesterol to liver |
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how VLDL is made
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chylomicron + apoB-100
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components of VLDL
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moderate: TGs, cholesterol
low: proteins Apolipoproteins: B-100, CII, E |
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components of LDL
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low: TGs
moderate: protein high: cholesterol apolipoproteins: B-100 |
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components of HDL
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low: TG
moderate: cholesterol high: protein apolipoproteins: AI, CII, E |
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VLDL function
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take liver TGs to peripheral tissues
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fate of VLDL
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made by liver, converted to LDL by capillary lipoprotein lipase (remember the fibs inhibit lipoprotin lipase...telling a FIB will stop the LIe)
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function of LDL
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takes liver cholesterol to peripheral tissues
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fate of LDL
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made from VLDL, endocytosed by target cells with LDL receptors, degraded causing cholesterol release which stops further cholesterol uptake
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function of HDL
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activates LCAT to form cholesteryl esters, transfers apoCII and apoE to chylomicrons and VLDL
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type I hyperlipoproteinemia (most common form)
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no lipoprotein lipase = increased chylomicrons and TGs
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type I hyperlipoproteinemia (less common form)
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no CII = increased chylomicrons and TGs
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type II hyperlipoproteinemia
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no/defunct LDL receptor
IIa = increased LDL and cholesterol IIb = increased LDL, cholesterol and TGs Look for Achilles xanthomas |
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type III hyperlipoproteinemia
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no ApoE; "remnant disease"
increased cholesterol, TGs and IDL/chylomicron remnants |
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type IV hyperlipoproteinemia
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decreased catabolism/increased synthesis of VLDL
increased TGs (familial hypertrigylceridemia) Begins at puberty; acquired with ETOH-ism, diuretics, beta blockers, renal failure |
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type V hyperlipoproteinemia
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type I + type IV
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