Type 1 Familial Dyslipidemia (pg. 94 FA 19 )

increased TG ---> pancreatitis Eruptice / pruritis Xanthomas and HSM

Can be caused by Lipoprotien lipase or Apoprotien CII deficiency

they said that LPL is fine so its APO CII

Heparin seperates LPL from Herparin Sulfate Moeity on Vasc Endothelium allowing us to test its function in the lab.

I got it wrong too - Stupid Rote memorization recall Question.

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