Atherosclerosis is due to:
|A||HDL receptor defect|
|B||Apo protein E deficiency|
|C||Decreased LDL activity|
|D||Decreased lipoprotein lipase|
a. Due to Binding defect form of APo-E
b. Because Apo-E plays a crucial role in the catabolism of chylomicrons and VLDL remnants, affected individuals have elevations in both- VLDL triglyceride and VLDL cholesterol, and chylomicron remnants are present in fasting plasma.
c. LDL and HDL→usually low
d. C/F→Tuberous xanthomas and deposits of cholesterol in the palmar creases striaepalmaris, yellow colour, and this is specific for dys beta Lipoproteinemia.
e. Risk for Atherosclerosis and its complications is increased
Familial Lipoprotein lipase deficiency: - due to impairment or absent of LPL C/f:
a. ↑plasma chylomicrons massive ↑
b. Pancreatitis, eruptive xanthoma, hepatomegaly, splenomegaly, foam cells infiltration of the bone
c. marrow and lipemiaretinalis when >1000 mg/dL
d. Atherosclerosis is not accelerated
e. Diagnosis → A layer of cream at the top of plasma after overnight incubation at 4°C and; confirm by injecting heparin :→ plasma LPL level do not increase normally it increases plasma LPL level