Colestipol and cholestyramine are bile acid binding resins that for complex with bile acids and inhibit biliary reabsorption of cholesterol. These drugs as they are not specific to cholesterol inhibit the absorption of lipophilic drugs and lipophilic vitamins. They inhibit the absorption of digoxin. On the other hand, Ezetimibe inhibits the specific ion channels responsible for absorption of cholesterol from the brush border of the gut wall and hence free of these drug interactions.
(A) Endothelial dysfunction
(B) Altered NO synthesis
(C) Altered PG I2 synthesis
(D) All of the above
Endothelial dysfunction starts with altered biosynthesis of NO and PG I2 all cause atherogenesis.
(D) Q and R
Endogenous pathway involves the transport of lipids by VLDL, LDL and HDL.
Atherogenesis is a process in which LDL cholesterol it attached to the endothelium which is oxidized into fatty streaks forming atheroma. At the same time, cholesterol released from tissue breakdown is released in to blood stream as HDL leading less formation for atheroma. Therefore LDL cholesterol increases the atherogenesis whereas HDL cholesterol decreases atherogenesis. VLDL is rich in triglycerides hence poses less risk for atherogenesis.
(C) Bile salts
Fatty acids are converted in to their triglycerides and absorbed from the intestine as chylomicrons.