Mecanism of action Lipid lower drugs

Question 1

Statins :

Answer 1

They inhibits the action of HMG-CoA reductase which is a rate-controlling enzyme of the mevalonate pathway of synthesizing of cholesterol by competitively blocking the active site of the first and key rate-limiting enzyme (HMA-CoA reductase), inhibition of this site prevents substrate access, thereby blocking the conversion of HMG-CoA to mevalonic acid or mevalonate, hence inhibiting the cholesterol synthesis.

Question 2

Nicotinic acid drugs :

Answer 2

Reduces the release of fatty acids from adipose tissue into the blood and increases the size of LDL particles (impedes intimal infiltration). This leads to a decrease in liver synthesis and release of cholesterol, TG and LDL into the blood.

Question 3

Fibrates :

Answer 3

Fibrates activate PPAR (peroxisome proliferator-activated receptors), especially PPARα.(the PPARs are a class of intracellular receptors that modulate carbohydrate and fat metabolism and adipose tissue differentiation). Activating PPARs induces the transcription of a number of genes that facilitate lipid metabolism.

Question 4

Probucol :

Answer 4

Included in the LDL and accelerates their elimination from the blood to the liver, reduces the ability of LDL to penetrate the intima and oxidize there.

Question 5

Bile acid sequestrants :

Answer 5

Bile acid sequestrants exchange anions such as chloride ions for bile acids. By doing so, they bind bile acids and set them apart from the enterohepatic circulation. The liver then produces more bile acids to replace those that have been lost. Because the body uses cholesterol to make bile acids, this reduces the level of LDL cholesterol circulating in the blood. Bile acid sequestrants are large polymeric structures, and they are not significantly absorbed from the gut into the bloodstream. Thus, bile acid sequestrants, along with the bile acids bound to the it, are excreted through the feces after passage through the gastrointestinal tract.