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Gall bladder disease

Gall bladder disease. Harrison 2012 Baghbanian M. MD . Bile Secretion and Composition. Hepatic bile : isotonic fluid with an electrolyte composition resembling blood plasma. Gallbladder : water reabsorption → concentration of bile increases. components of bile .

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Gall bladder disease

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  1. Gall bladder disease Harrison 2012 Baghbanian M. MD

  2. Bile Secretion and Composition • Hepatic bile : • isotonicfluid with an electrolyte composition resembling blood plasma. • Gallbladder: • water reabsorption → concentration of bile increases

  3. components of bile • bile acids (80%), • lecithin and phospholipids (16%) • cholesterol (4.0%). • In the lithogenic state, the cholesterol value can be as high as 8–10%.

  4. components of bile • conjugated bilirubin • proteins (all immunoglobulins, albumin, metabolites of hormones) • Electrolytes • Mucus • drugs and their metabolites.

  5. daily basal secretion • 500–600 mL. • Many substances taken up or synthesized by the hepatocyte are secreted into the bile

  6. primary bile acids • cholic acid • chenodeoxycholicacid • are synthesized from cholesterol in the liver, • conjugated with glycine or taurine • secreted into the bile.

  7. Secondary bile acids • deoxycholate • lithocholate • ursodeoxycholicacid (UDCA). • formed in colon as bacterial metabolites of the primary bile acids.

  8. Bile acids are detergent-likemolecules • Cholesterol solubility in bile depends on: • lipid concentration • percentages of bile acids and lecithin. • Normal ratios of these →formation of solubilizingmixed micelles • abnormal ratios → cholesterol crystals

  9. Bile acids • major physiologic force for hepatic bile flow • aid in water and electrolyte transport in the small bowel and colon.

  10. Enterohepatic Circulation • normal bile acid pool: 2–4 g. • During digestion of a meal, one or more enterohepatic cycles • Normally: 5–10 times daily. • 95% efficient; fecal loss of bile acids is in the range of 0.2–0.4 g/d.

  11. Enterohepatic Circulation • fecal loss =daily synthesis of bile acids • bile acid pool is maintained. • the maximum rate of synthesis is 5 g/d

  12. Gallbladder and Sphincteric Functions • capacity of gallbladder is 30 mL • In the fasting state, the sphincter of Oddi →resistance to bile flow • prevent reflux of duodenal contents into the pancreatic and bile ducts • filling of the gallbladder.

  13. cholecystokinin(CCK) • major factor for : GB evacuation • released from : duodenal mucosa • In response to: fats and amino acids. • CCK produces • (1) powerful contraction of the gallbladder, • (2) decreased resistance of the sphincter of Oddi, • (3) enhanced flow of bile into duodenum.

  14. Phrygian cap • partial or complete septum (or fold) separates the fundus from the body.

  15. Anomalies of position or suspension • are not uncommon : • left-sided • intrahepatic • retrodisplacement • "floating" gallbladder • predisposes to acute torsion, volvulus, or herniation

  16. GallstonesEpidemiology and Pathogenesis • prevalent in most western countries. • USA : 7.9% in men and 16.6% in women. • high in Mexican Americans • low in African Americans

  17. gallstones • two major types: • cholesterol stones : > 80% • pigment stone < 20%.

  18. gallstones • Cholesterol gallstones : >50% cholesterol + calcium salts, bile pigments, and proteins. • Pigment stones : calcium bilirubinate; <20% cholesterol : • "black" • "brown" (chronic biliaryinfection.)

  19. Cholesterol Stones and Biliary Sludge • Cholesterol : water insoluble • excess of cholesterol in relation to phospholipids and bile acids→ unstable, cholesterol-rich vesicles → aggregate into large vesicles → cholesterol crystals

  20. mechanisms in the formation of lithogenic bile • The most important : increased biliary secretion of cholesterol. • This occur in : • obesity • metabolic syndrome • high-caloric and cholesterol-rich diets • drugs (e.g., clofibrate) • increased hepatic uptake of cholesterol from blood. (e.g., estrogen)

  21. genetic • In patients with gallstones, dietary cholesterol increasesbiliary cholesterol secretion. • This does not occur in non-gallstone patients on high-cholesterol diets. • In addition to environmental factors such as high-caloric and cholesterol-rich diets, genetic factors play an important role in gallstone disease.

  22. pronucleating factors • Mucin • non-mucinglycoproteins • immunoglobulins

  23. antinucleating factors • apolipoproteins A-I and A-II • other glycoproteins.

  24. Vesicle fusion leads to liquid crystals→ nucleate into solid cholesterol crystals. • direct nucleation of cholesterol from supersaturated biliary vesicles → growth of the crystals

  25. gallbladder hypomotility • If the gallbladder emptied all supersaturated or crystal-containing bile completely, stones would not be able to grow. • patients with gallstones : ↓gallbladder emptying. ↑gallbladder volume in fasting and after meal • Gallbladder fractional emptying is decreased.

  26. Biliary sludge • Thick • mucous material and • cholesterol monohydrate crystals • calcium bilirubinate, and mucin gels. • crescent-like in the most dependent portion of the gallbladder • recognized by ultrasonography

  27. biliary sludge • precursor for gallstone • 14%, gallstones developed • gallbladder hypomotility and gallstone formation ; • surgery, burns, total parenteral nutrition, pregnancy, and oral contraceptives

  28. pregnancy • →cholesterol-stone or sludge • pregnancy ="cholelithogenic state": • (1) ↑cholesterol saturation of bile in3th trimester • (2) ↓gallbladder contraction • reversal of these abnormalities quite rapidly after delivery.

  29. gallbladder sludge in pregnancy • 20–30% of women • asymptomatic • often resolves after delivery.

  30. gallstones in pregnancy • 5–12%. • less common than sludge • frequently associated with biliary colic • may disappear after delivery

  31. rapid weight reduction • 10–20% of persons with rapid weight reduction develop gallstones. • UDCA in a dosage of 600 mg/d effective in preventing gallstone formation

  32. cholesterol gallstone disease occurs because of several defects: (1) bile supersaturation with cholesterol (2) nucleation of cholesterol with crystal retention and stone growth (3) abnormal gallbladder motor function with delayed emptying and stasis.

  33. Increasing age→ cholesterol gallstone • → Increased biliary secretion of cholesterol • → decreased size of bile acid pool • → decreased secretion of bile salts

  34. Obesity→ cholesterol gallstone • Normal bile acid pool and secretion • increased biliary secretion of cholesterol

  35. Weight loss → cholesterol gallstone • Mobilization of tissue cholesterol leads to increased biliary cholesterol secretion

  36. Female sex hormones → cholesterol gallstone •  Estrogens → increase hepatic uptake of dietary cholesterol → increase biliary cholesterol secretion   • Natural estrogens, other estrogens, and OCP→ decreased bile salt secretion

  37. Gallbladder hypomotility→ cholesterol gallstone • Prolonged parenteral nutrition • Pregnancy    • Fasting    • octreotide

  38. Clofibrate therapy → cholesterol gallstone → Increased biliary secretion of cholesterol

  39. Decreased bile acid secretion→ cholesterol gallstone • Primary biliary cirrhosis

  40. High-calorie, high-fat diet → cholesterol gallstone    • Spinal cord injury → cholesterol gallstone

  41. Pigment Stones ethiology •  Asia, rural setting • Chronic hemolysis • Alcoholic cirrhosis • Pernicious anemia • Cystic fibrosis • Chronic biliary tract infection, parasite • Increasing age • Ileal disease, ileal resection or bypass

  42. Pigment Stones • Black : pure calcium bilirubinate with calcium and mucinglycoproteins. • more common in : • chronic hemolytic states • liver cirrhosis, • Gilbert's syndrome • cystic fibrosis.

  43. ilealdiseases→blackstones • ileal diseases , • ileal resection, • ileal bypass. • Enterohepatic recycling of bilirubin in ileal disease states

  44. Brown pigment stones • calcium salts of unconjugatedbilirubinwith cholesterol and protein. • in Asians and is often associated with infections in the gallbladder and biliary tree

  45. Diagnosis _Ultrasonography • Gallstone • emptying function of the gallbladder • Biliary sludge

  46. Diagnosis _Ultrasonography • very accurate in cholelithiasis • Stones as small as 1.5 mm may be identified • false-negative and false-positive rates for ultrasound in gallstone patients are 2–4%.

  47. Biliary sludge Ultrasonography • low echogenic • a layer in the most dependent position of the gallbladder • distinguish sludges from gallstones: • This layer shifts with postural changes • noacoustic shadowing;

  48. Gallbladder Ultrasound • Rapid • Accurate in gallstones (>95%) • Simultaneous scanning of GB, liver, bile ducts, pancreas • assessment of GB volume, contractility • Not limited by pregnancy • May detect very small stones(1.5 mm) • Procedure of choice for detection of stones

  49. Ultrasound Limitations • Bowel gas • Massive obesity • Ascites

  50. Plain Abdominal x-ray • Low cost • low yield • Pathognomonic in: calcified gallstones • Readily available • Contraindicated in pregnancy • porcelain GB • Emphysematous cholecystitis •  Gallstone ileus

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