Cholelithiasis & Choledocholithiasis



Cholelithiasis & Choledocholithiasis





CHOLELITHIASIS


Definition:



  • “Gallstones”


  • “Sludge” (microlithiasis): super-concentrated mixture of bile acids, bilirubin, cholesterol, mucus, and proteins



    • Discharge into cystic duct & CBD can cause Acalculous Cholecystitis or ‘Idiopathic Pancreatitis’; Often after feeding from being NPO


Epidemiology:



  • >10% adults in U.S. have gallstones, however only 20% of these persons develop symptoms (1-2% chance per year)


  • ↑ prevalence in women, Native Americans, and with increasing age, obesity and pregnancy


  • 500,000 cholecystectomies are performed each year in the United States


Etiologies:



  • Drug/Medical therapies associated:



    • Ceftriaxone, OCPs, Octreotide impairs emptying, TPN & fasting promote gallbladder atony and sludge formation


Pathophysiology:



  • Bile Physiology: Liver synthesizes 0.2-0.6 g/day; Pool of bile in body is about 3 grams



    • Biliary secretion = pool × (pool is 3 g, cycles occur 4-12 times/day, slowing during fasting, accelerating with meals)



      • Hence, there are 12-36 grams of bile secreted and absorbed per day


    • Bile composed of bile salts, phospholipids, cholesterol; ↑ cholesterol saturation in bile promotes gallstones


  • Enterohepatic circulation: Biliary secretion occurs, Ileal absorption returns 97% of intraluminal bile acid back into circulation via portal vein



    • (90% are extracted from portal circulation on their first pass through the liver)


    • Fecal excretion (0.2-0.6 g/day), Urinary excretion via systemic circulation (<0.5 mg/day)


    • In health, hepatic synthesis of bile acids is equivalent to enteric losses (0.2-0.6 g/day)


  • Gallbladder:



    • In health, the gallbladder concentrates bile 10-fold for efficient storage during fasting


    • Intraduodenal fat and protein release cholecystokinin (CCK) which stimulates gallbladder contraction, sphincter-of-Oddi relaxation


  • Principle factors involved in gallstone formation: cholesterol supersaturation, crystal nucleation, gallbladder hypomotility



    • Cholesterol supersaturation: result from deficient bile secretion or hypersecretion of cholesterol



      • Bile secretion reduced with age or liver disease, reduced enterohepatic circulation (TI disease)


      • Cholesterol secretion increased with hormones (female, sex, pregnancy, exogenous estrogens), obesity, liver disease


    • Nucleation: formation of insoluble deposits from supersaturated bile within biliary system


    • Gallbladder hypomotility: pregnancy, prolonged TPN, somatostatin therapy


    • Other influencing factors: bile transit time, gallbladder contraction, presence of bacteria, mucin, glycoproteins such as IgA


  • Types of gallstones; including color of stone



    • Mixed (80%): multiple stones, composed of 80% cholesterol and 20% unconjugated bilirubin, may calcify (15-20%); Yellow


    • Cholesterol (10%): usually single stone, large, uncalcified; Yellow


    • Pigment (10%): unconjugated bilirubin (hence seen in chronic hemolysis) and cirrhosis; Calcium too; Black & Radiopaque


    • Infectious: colonization of bile with enteric bacteria and/or parasites; Soft clay-like in ducts, not gallbladder; Asian population; Brown


Clinical Manifestations/Physical Exam:

Aug 24, 2016 | Posted by in GASTROENTEROLOGY | Comments Off on Cholelithiasis & Choledocholithiasis

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