yTep 1 aaFllmii iiDaidsymple g(p. 49 AF 91 )
reecsaind TG g---&t; santtraipcie Er itcpue / iirrutsp nmsah ndXoaat MSH
Can be aucdes yb irpiLpeonto spleia ro ippoAnotre CII iidyefcecn
ethy aids atht PLL is fien os sti PAO ICI
ipnaHre etrsespea PLL ofrm anieHrpr uSftale tyiMoe on scVa ouidmeElhnt ngoalilw us to etst tis oniftnuc in the a.lb
I tgo it worng too - diptSu Roet ooainitzrmem aclerl esino.Qut
Going over the other answer choices:
ApoC2 defect as already explained in the other comments is Type 1 hyperchylonmicronemia with increased TG and chylomicrons, creamy layer in the supernatant, and is associated with pancreatitis and eruptive xanthomas.
LDL receptors are defective in Type 2 which is associated with a MI before age
29 20, accelerated atherosclerosis and increased LDL levels.
Someone with a pancreatic lipase defect will probably have pancreatitis and have increased triglycerides in their stool because pancreatic lipase can break down the TG into FFA.
UW has a question on the familial dyslipidemia III which is a defective ApoE. ApoE is what mediates chylomicron remnant uptake into the liver and so if its defective the liver cant efficiently remove chylomicrons and VLDL from the circulation. You get an increase in those things causing premature atherosclerosis, palmar xanthomas.
this stuff is hard