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MCQ on antihyperlipidemics: Page-1

The drug that inhibits the absorption of cholesterol by  forming a complex with bile acids is

(A) Simvastatin

(B) Ezetimibe

(C) Gemfibrozil

(D) Colestipol

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.

Atherogenesis is mainly initiated by

(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.

Select the lipoproteins that are not involved in the endogenous pathway
LDL and VLDL

(A) Q

(B) R

(C) S

(D) Q and R

Endogenous pathway involves the transport of lipids by VLDL, LDL and HDL.

During atherogenesis foam cells are formed in endothelium. These cells are mainly composed of

(A) Chylomicrons

(B) HDL

(C) VLDL

(D) LDL

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.

The fatty acids are absorbed from the lumen in the form of

(A) Cholesterol

(B) Triglycerides

(C) Bile salts

(D) HDL

Fatty acids are converted in to their triglycerides and absorbed from the intestine as chylomicrons.