Cholelithiaisis

Cholelithiaisis

1. Cholelithiasis

2. Cholelithiasis (Gallstones) Cholelithiasis -Stone in gallbladder. Two main types of gallstones. Cholesterol stones Pigment stones

3. Risk Factors for Gallstones 1) Cholesterol Stones: Demography: Northern Europe, US Advancing age Female sex hormones   -Female gender   -Oral contraceptives   -Pregnancy Obesity

4. Rapid weight reduction Gallbladder stasis Inborn disorders of bile acid metabolism Hyperlipidemia syndromes

5. 2) Pigment Stones: Demography: Asian more than Western, rural more than urban. Chronic hemolytic syndromes Biliary infection Gl disorders: ileal disease ( Crohn disease), ileal resection or bypass, cystic fibrosis with pancreatic insufficiency

6. However, 80% of individuals have no identifying risk factors other than age and gender. Heredity: Family history increases risk.

7. Age and gender differences- Major role of h ypersecretion of biliary of cholesterol. Estrogen exposure- OCP use and during pregnancy increases expression of hepatic lipoprotein receptors and stimulates hepatic HMG-CoA reductase activity, enhancing both cholesterol uptake and biosynthesis  E xcess biliary secretion of cholesterol. Obesity-increase biliary cholesterol secretion .

8. Rapid weight reduction- Cholesterol level ↑& amount of bile salts ↓. Long periods of starvation ↓ gallbladder contractions- not enough to empty out bile  gallstones form Gallbladder stasis-favorable for both cholesterol and pigment gallstone formation. Hereditary factors

9. Pathogenesis of Cholesterol Stones Cholesterol is rendered soluble in bile by aggregation with water-soluble bile salts and water-insoluble lecithins , both of which act as detergents. When cholesterol concentrations exceed solubilizing capacity of bile ( supersaturation ), cholesterol can no longer remain dispersed and nucleates into solid cholesterol monohydrate crystals.

10. Four conditions contribute to formation of cholesterol gallstones (1) supersaturation of bile with cholesterol (2) hypomotility of gallbladder (3) accelerated cholesterol crystal nucleation (4) hypersecretion of mucus in gallbladder  traps nucleated crystals  accretion of more cholesterol and appearance of macroscopic stones.

11. Pathogenesis of Pigment Stones Disorders that are associated with elevated levels of unconjugated bilirubin in bile, such as chronic hemolytic anemias , severe ileal dysfunction or bypass, and bacterial contamination of biliary tree, increase risk of developing pigment stones.

12. Unconjugated bilirubin is normally a minor component of bile, but increases when infection of biliary tract leads to release of microbial β- glucuronidases , which hydrolyze bilirubin glucuronides . Thus, infection of biliary tract with Escherichia coli, Ascaris lumbricoides , or liver fuke C. sinensis , increases risk of pigment stone formation.

13. In hemolytic anemias secretion of conjugated bilirubin into bile increases. About 1% of bilirubin glucuronides are deconjugated in biliary tree, and in setting of chronically increased secretion of conjugated bilirubin, there is sufficiently large amount of deconjugated bilirubin left to allow pigment stones to form.

14.   MORPHOLOGY Cholesterol stones- Arise  exclusively  in  gallbladder. 100%  pure  (rare)  to  around  50% cholesterol.  Pure cholesterol stones- pale yellow,  round  to ovoid,  have  a  finely  granular,  hard  external  surface which on  transection  reveals a glistening radiating crystalline palisade. 

15. With increasing proportions of calcium carbonate, phosphates, and  bilirubin , stones take on a gray-white to  black  color, may  be  lamellated .  Usually multiple stones present.  Rarely, a very large stone  fill  fundus. 

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17. Surfaces of multiple stones may be rounded or faceted, because of tight apposition.  Stones composed  largely of cholesterol- radiolucent; sufficient calcium carbonate found in 10-20% of cholesterol stones- radiopaque .

18. Pigment gallstones Brown  to black.  Black pigment stones are  found  in sterile gallbladder bile and brown stones   in  infected  large  bile  ducts.  Black  stones contain oxidized polymers of calcium salts of  unconjugated   bilirubin ,  small  amounts  of  calcium  carbonate,  calcium  phosphate, and  mucin  glycoprotein, and some cholesterol monohydrate crystals.

19. Brown stones contain similar compounds along with some cholesterol and calcium salts of  palmitate  and  stearate .  Black stones-rarely greater than 1.5 cm  in diameter,  present  in  great  number; are  quite  friable.

20. Their  contours  are  usually  spiculated   and molded.  Brown stones- laminated and soft and may have a  soaplike  or greasy consistency.  50-75% of black stones are  radiopaque  due to calcium salts while brown stones, containing calcium soaps, are radiolucent. 

21. Clinical features 70-80% asymptomatic throughout life. Remainder symptomatic. Pain- constant or "colicky" (spasmodic) from an obstructed gallbladder or when small gallstones move down-stream and lodge in biliary tree.

22. Inflammation of gallbladder with stones also generates pain. Pain is localized to right upper quadrant or epigastrium that may radiate to right shoulder or back.

23. COMPLICATIONS Infammation of gallbladder ( cholecystitis ) More severe complications- empyema perforation fistulas infammation of biliary tree ( cholangitis ) obstructive cholestasis and pancreatitis.

24. Occasionally a large stone may erode directly into an adjacent loop of small bowel, generating intestinal obstruction (“gallstone ileus ”). I ncreased risk of gallbladder carcinoma.