SECODERY HYPERLIPIDIMIA
1. OBESITYin VLDL and/or LDL
in HDL
MECHANISM
adipose tissue mass accumulation
insulin-sensitivity of FA TG in
liver & adipose
tissue
note: LDL-C = total cholesterol – (TG/5+HDL)
2. D.MT1DM no hyperlipidaemia-when good
glycaemic-control
DKA hypertriglyceridaemia
hepatic influx of F.F.A from
adipose tissue
T2DM: dyslipidaemia even when good glycaemic- control
plasma TG ( VLDL + remnant )
dense LDL
HDL-C
MECHANISMS ARE :
1. LDL enzyme activity
2. F.F.A from adipose tissue
3. hepatic F.A synthesis
4. hepatic VLDL production
3. TYROID DISEASE :
a. hypothyroidism LDL-C
IDL
due to low clearence of LDL due to decrease
of LDL-receptor-function
b. hyperthyroidism LDL-C
4. RENAL DISEASE : mechanism
a. nephritic-syndrome LDL-C or hepatic productionT.G = clearance
both of VLDL
LDL production
b. E.S.R.D TG (mild) accumulation of VLDL
+remnant in circulation
c. kidney-transplants : hyperlipidaema statins
on cyclosporine & cautiously used
steroids
5. LIVER-DISEAES :
a. hepatic VLDL- synthesis principle
(infection , drugs :. TG (mild-moderate) site of
& alcohol) synthesis&
clearance of
lipoprotein
b. sever liver damage C & TG
c. cholestasis LDL-C (very sever) blockage ofcholesterol
excretion
with bile
6. ALCOHOL : TG ( VLDL) HDL-C
7. OESTROGEN:(contraceptive pills) TG( biosynthesis of VLDL)
LDL-C ( mild)
8. CUSHING’S SYNDROME
9. DRUG-INDUCED