Pigmented gallstones from unconjugated or conjugated bilirubin?

[beatsbydre]

I'm a little confused on this? or does it not matter? My notes says that injured hepatocytes release beta-glucuronidase, which hydrolyzes bilirubin gluconurides, which leads to an increase in unconjugated bilirubin, causing gallstones. however, there should not be any way of the unconjugated bilirubin to end up in the gallbladder in the first place.

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[cage92]

I'm a little confused on this? or does it not matter? My notes says that injured hepatocytes release beta-glucuronidase, which hydrolyzes bilirubin gluconurides, which leads to an increase in unconjugated bilirubin, causing gallstones. however, there should not be any way of the unconjugated bilirubin to end up in the gallbladder in the first place.[/QUO
the pigmented stone lead to obstructive jaundice which lead to increase conjugated bilir
the color due to infection which release glucoronidase which give unconjugated bilirubine not in blood (in duct or gall bladder) this give the brown color

 

[beatsbydre]

I'm a little confused on this? or does it not matter? My notes says that injured hepatocytes release beta-glucuronidase, which hydrolyzes bilirubin gluconurides, which leads to an increase in unconjugated bilirubin, causing gallstones. however, there should not be any way of the unconjugated bilirubin to end up in the gallbladder in the first place.[/QUO
the pigmented stone lead to obstructive jaundice which lead to increase conjugated bilir
the color due to infection which release glucoronidase which give unconjugated bilirubine not in blood (in duct or gall bladder) this give the brown color

so after the conjugated bilirubin is in the bile duct/bladder, it gets unconjugated and turned into a different color?

 

[cage92]

so after the conjugated bilirubin is in the bile duct/bladder, it gets unconjugated and turned into a different color?

yes

 

[JRjcu08]

http://www.ncbi.nlm.nih.gov/pubmed/318581

"Pigment gallstones are defined as any dark brown-to-black stone, consisting of calcium salts of bilirubin, phosphate, carbonate and other anions, and can be separated into carbonate- and noncarbonate-containing groups. Pigment stones predominate in the rural Orient, in cirrhosis, and in elderly United States patients undergoing cholecystectomy. Clinical associations include bile duct obstruction, stasis, and possibly hemolysis. Of pigment stones, 50% are radioopaque and account for two-thirds of all opaque stones. The concentrations of bile salts, phospholipids,, cholesterol, and total bilirubin in bile are similar to normal levels, but the concentration of unconjugated bilirubin is increased in the bile of some patients. Increased unconjugated bilirubin in bile may be caused by increased hydrolysis of excreted conjugated bilirubin. Unconjugated bilirubin is solubilized by bile salts, but the interaction is primarily nonmicellar. Ionized calcium and pH are important determinants of solubility. Sulfated glycoproteins, excreted in increased amounts in patients with cholelithiasis, may be the site of pigment stone precipitation because these compounds bind calcium salts tightly. E coli is frequently cultured from pigment stones in Japan but not in the United States; thus, bacterial beta-glucuronidase may be important in stone formation in Japan but probably not in the West. Stasis leads to increased calcium secretion and to increases in the concentration of sparingly soluble compounds that may then precipitate. Incomplete emptying of the gallbladder may result in the same concentration process. Unsaturated fats and chronic vagal stimulation cause pigment stone formation in animals. At present, surgery is the only treatment for pigment lithiasis."