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17 Cards in this Set

  • Front
  • Back
components of chylomicrons
high: TGs
low: cholesterol and protein
Apolipoproteins: B48, CII, E
functions of chylomicrons
carry dietary TGs to peripheral tissues
carry dietary cholesterol to liver
how VLDL is made
chylomicron + apoB-100
components of VLDL
moderate: TGs, cholesterol
low: proteins
Apolipoproteins: B-100, CII, E
components of LDL
low: TGs
moderate: protein
high: cholesterol
apolipoproteins: B-100
components of HDL
low: TG
moderate: cholesterol
high: protein
apolipoproteins: AI, CII, E
VLDL function
take liver TGs to peripheral tissues
fate of VLDL
made by liver, converted to LDL by capillary lipoprotein lipase (remember the fibs inhibit lipoprotin lipase...telling a FIB will stop the LIe)
function of LDL
takes liver cholesterol to peripheral tissues
fate of LDL
made from VLDL, endocytosed by target cells with LDL receptors, degraded causing cholesterol release which stops further cholesterol uptake
function of HDL
activates LCAT to form cholesteryl esters, transfers apoCII and apoE to chylomicrons and VLDL
type I hyperlipoproteinemia (most common form)
no lipoprotein lipase = increased chylomicrons and TGs
type I hyperlipoproteinemia (less common form)
no CII = increased chylomicrons and TGs
type II hyperlipoproteinemia
no/defunct LDL receptor

IIa = increased LDL and cholesterol
IIb = increased LDL, cholesterol and TGs

Look for Achilles xanthomas
type III hyperlipoproteinemia
no ApoE; "remnant disease"

increased cholesterol, TGs and IDL/chylomicron remnants
type IV hyperlipoproteinemia
decreased catabolism/increased synthesis of VLDL

increased TGs (familial hypertrigylceridemia)

Begins at puberty; acquired with ETOH-ism, diuretics, beta blockers, renal failure
type V hyperlipoproteinemia
type I + type IV