biochemistry doubt

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this concept has really got me into a confusin if any onehas an idea pls help..

when bile is relased frm the live3r it contains h2o/bile acids/bile salts/ buliburin and lecithin.
whn it reaches the intestine it is acted by intestinal bacteria to form a mixture of secondary bile acids/bile salts and primary bile acids. most of this bile acid mixture is resorbed in the ILEUM, with only .5mg begin excreated perday in feces which is compensated by the liver by DENOVA synthesisOF JUST .5MG OG BILE ACID FROM ITS CHOLESTROL POOL.

NOW DRUGS LIKE CHOLESTRYMINE AND DITERAY FIBRE GIVEN IN PATEINTS WITH HYPERCHOLESTERIMA REDUCE THE RESORBTION OF BILE ACIDS AND AID THEIR EXCREATION IN TO FECES.. HENCE MORE CHOLESTROL USED BY THE LIVER TO SYNTHESIS THE BILEACIDS AND MOBILIZATION OF CHOLESTROL LEADS TO LOSS OF WIEGHT IN SUCH PATIENTS.. THIS FAR I M CLEAR..

NXT ABOUT GALLSTONE CHOLELITHESIS,

IT IS SAID THT IF THERE IS A DEFICIENCY OF BILE SALTS/ACIDS IT LEADS TO ACUMALATION OF CH IN GALLBLADDER..
NO OF CONDITION CAN LEAD TO THIS CHOLELITHESIS LIKE LIVERDYSFUNCTION, INABILITY TO CNJUGATE BACIDS/ETC.. BUT HERE IT IS ALSO METIONED THAT PT WITH ILEAL DYSFUNCTION , IE WHO CANNOT RESORB BILE ACIDS HAVE GALL STONES??? WHY SHOULD THAT BE, IF ILEUM IS DYSFUNCTIONAL, THE LIVER IS STILL FUNCTIONAL, RIGHT!!(ISNT THIS THE SAME MECHANISM OF ACTION FOR ANTI HYPERCHOLESTROL DRUGS LIKE FIBRE JUST MENTIONED ) IT SHOULD USE UP ALL ITS CHOLESTROL POOL TO SYNTHESIZE BILEACIDS.. AND THE PT S SHOULD BE IN NEGATIVE CHOLESTROL POOL INSTED OF CH ACCUMATION IN GALL BLEDDER??? PLS EXPALIN...

 

[chipotle]

this concept has really got me into a confusin if any onehas an idea pls help..

when bile is relased frm the live3r it contains h2o/bile acids/bile salts/ buliburin and lecithin.
whn it reaches the intestine it is acted by intestinal bacteria to form a mixture of secondary bile acids/bile salts and primary bile acids. most of this bile acid mixture is resorbed in the ILEUM, with only .5mg begin excreated perday in feces which is compensated by the liver by DENOVA synthesisOF JUST .5MG OG BILE ACID FROM ITS CHOLESTROL POOL.

NOW DRUGS LIKE CHOLESTRYMINE AND DITERAY FIBRE GIVEN IN PATEINTS WITH HYPERCHOLESTERIMA REDUCE THE RESORBTION OF BILE ACIDS AND AID THEIR EXCREATION IN TO FECES.. HENCE MORE CHOLESTROL USED BY THE LIVER TO SYNTHESIS THE BILEACIDS AND MOBILIZATION OF CHOLESTROL LEADS TO LOSS OF WIEGHT IN SUCH PATIENTS.. THIS FAR I M CLEAR..

NXT ABOUT GALLSTONE CHOLELITHESIS,

IT IS SAID THT IF THERE IS A DEFICIENCY OF BILE SALTS/ACIDS IT LEADS TO ACUMALATION OF CH IN GALLBLADDER..
NO OF CONDITION CAN LEAD TO THIS CHOLELITHESIS LIKE LIVERDYSFUNCTION, INABILITY TO CNJUGATE BACIDS/ETC.. BUT HERE IT IS ALSO METIONED THAT PT WITH ILEAL DYSFUNCTION , IE WHO CANNOT RESORB BILE ACIDS HAVE GALL STONES??? WHY SHOULD THAT BE, IF ILEUM IS DYSFUNCTIONAL, THE LIVER IS STILL FUNCTIONAL, RIGHT!!(ISNT THIS THE SAME MECHANISM OF ACTION FOR ANTI HYPERCHOLESTROL DRUGS LIKE FIBRE JUST MENTIONED ) IT SHOULD USE UP ALL ITS CHOLESTROL POOL TO SYNTHESIZE BILEACIDS.. AND THE PT S SHOULD BE IN NEGATIVE CHOLESTROL POOL INSTED OF CH ACCUMATION IN GALL BLEDDER??? PLS EXPALIN...

Read this a couple of times and trying to figure out what exactlly is the question here ...u mean how cud a pt with ileal dysfunction who cannot absorb bile acid have gall stones ?keeping in mind the role of cholesterol here ....well Ileal disease or resection causes bile salt malabsorption and a reduction in the bile salt content of bile....... Since cholesterol solubility requires adequate bile salt concentrations, depletion of the bile salt content of bile might, therefore, jeopardize cholesterol solubility and predispose to cholesterol gallstone formation. And also bile acids are not recirculated until they reach the the terminal ileum, bile acids are present for maximal absorption of lipids throughout the upper small intestine.And after ileal resection/dysfunction, bile acids are not recirculated to the liver but are excrected in feces. The acid pool is therby depleted and fat absorption is impaired , resulting in Steatorrhea.

 

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read this a couple of times and trying to figure out what exactlly is the question here ...u mean how cud a pt with ileal dysfunction who cannot absorb bile acid have gall stones ?keeping in mind the role of cholesterol here ....well ileal disease or resection causes bile salt malabsorption and a reduction in the bile salt content of bile....... Since cholesterol solubility requires adequate bile salt concentrations, depletion of the bile salt content of bile might, therefore, jeopardize cholesterol solubility and predispose to cholesterol gallstone formation. and also bile acids are not recirculated until they reach the the terminal ileum, bile acids are present for maximal absorption of lipids throughout the upper small intestine.and after ileal resection/dysfunction, bile acids are not recirculated to the liver but are excrected in feces. The acid pool is therby depleted and fat absorption is impaired , resulting in steatorrhea.

thanks for making an attempt to answer my doubt, sorry if i didnt sound clear here.

My doubt was the basis for use of dietary fibre for hypercholsetremia pateints is inhibiton of resorbtion at ileum so that bile acids are lost in feces n new cholestrol is mobilised by liver for more synethisis of bile acids to keep the choelstrol solublized n keep a check of cholestrol level.

But pts with ileal resection have the same problem i mean no absorbtion of bile acids ----> excreation in feces of ba.why do thy suffer frm gall stones, why isnt the liver mobilizing its cholestrol pool for lost ba.

I guess the answer gcould be the severity of malabsorbtions, drugs could probably to adjusted to such levels tht it prevent only excess ba/bs frm resorption to keep a tab....

Thnks for u r effort though