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27 Cards in this Set
- Front
- Back
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Q. HDL Origin?
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liver or intestine
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Q. HDL apolipoproteins?
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A1, E, C2
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Q. HDL functions?
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Gathers cholesterol from peripheral cells using LCAT
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Q. Where HDL degraded at?
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Liver
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Q. Where is A1 degraded at?
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Kidney
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Q. Where is VLDL made/nascent at?
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Liver
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Q. Where is VLDL active at?
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blood
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Q. VLDL apolipoproteins?
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B100, E, C2
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Q. VLDL function?
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Package triglycerides, recieve cholest from HDL via CETP, and delivers triglycerides & cholest to cells via LPL
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Q. IDL origin?
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VLDL
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Q. IDL apolipoproteins?
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B100, E
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Q. IDL function?
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Remnant VLDL (important)
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Q. LDL Origin?
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IDL
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Q. LDL apolipoproteins?
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B100
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Q. LDL Function?
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Engulfed by peripheral cells, clatharin coated pits endocytose, Curl releases FFA and cholest, cholest inhibits HMG
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Q. Where does LDL get degraded at?
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Peripheral Cells
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Q. LCAT purpose?
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Binds SRB-1 or ABC to transfer cholest
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Q. CETP function?
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Facilitates exchange of cholesterol from HDLs and Triglycer from VLDL
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Q. LPL function?
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Breaks open VLDL to absorb contents and removes C2
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Q. HMG(3 hydroxy 3 methyl reductase) function?
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Regulates cholest production in cells
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Q. Type 2 hyperlipidemia has trouble making?
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clatharin
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Q. HMG is not inhibited in Type 2 hyperlipidemia ? T or F
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True
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Q. Type 2 hyperlipidemia results in hypercholesteremia? T or F
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True
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Q. E3 Type?
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Wild type (normal)
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Q. E2 type?
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Leads to a build up of remnant chylomicron and increase in total cholesterol. Problem with E2 protein
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Q. E4 type?
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May be associated with increased incidence of dementia or alzheimers
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Q. peripheral cells release?
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LPL
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