Tpye 1 imlaliFa iaDmyspdelii (gp. 49 AF 91 )
reiasendc TG -&;tg-- aicasrittepn tiEerp uc / isrurtpi samatnXha nod SMH
naC eb cdeuas by iptorpneioL alipse ro tepoApinro CII cnfiiedcye
tyhe dsai atht LPL is einf os sti POA IIC
iHpenar earestesp LLP morf Hnpirare fetaSul oeiMyt on scaV tilnEdhumoe gniwlaol us to tset tsi cfnonitu in eht bal.
I tog ti onrwg oot - dtSpiu Rteo aionizrmteom lrealc tseu.oinQ
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