eTpy 1 alFiamli siymiDilepda g(.p 94 AF 91 )
iedrcnesa TG --t;g-& cipsratteina uc rpeiEt / usrripit admatn Xohnas MSH
nCa eb saedcu by rnotiiLppoe lapsie or oeAriopnpt CII edyiicecfn
yeth disa htat PLL is nife os tis AOP ICI
eiarnHp arstpeese LLP ofrm apHenrri efSltua iMeoyt on aVsc ouldheimtEn aolnigwl us to stte tis foicnutn ni hte lab.
I tgo it wrnog oot - dutSpi oetR miemaoionztr eracll u.nietsoQ
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