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Biliary Pathophysiology (1).
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Biliary Pathophysiology (1).
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Biliary PathophysiologyWhat causes gallstones? - ANS-- disequilibrium and GB stasis
- cholesterol kept soluble in bile by bile salts and PLs; if concs. change, gallstones form
- too much cholesterol—> supersaturation—> solid
- too little BS or PLs—> can't keep cholesterol solubilized
Most common elective operation in US - ANS-cholecystectomy
Prevalence of gallstones - ANS-variable, high in US
Genetic risk of gallstones - ANS-- first-degree 4.5x more likely
- high risk: Pima Indians (70% women by 25); Scandinavians (50% by 50)
- low risk: SS Africa, Asia, African American
Gallstone RFs - ANS-Age: inc. cholesterol and dec. BA synthesis
Female: inc. cholesterol related to estrogen?
Obesity: cholesterol hypersecretion into bile and inc. cholesterol synthesis
Weight loss: cholesterol hyper secretion into bile, reduced BA synthesis, GB hypo motility
Total parenteral nutrition: GB hypomotility
Pregnancy: inc. cholesterol secretion, GB hypomotility
Resection or severe disease of terminal ileum: dec. SA for BA reabsorption—> dec. BA in bile
Meds that inc. gallstones risk (5) - ANS-Oral contraceptives: inc. cholesterol secretion
Fibrates: suppression cholesterol 7a-hydroxylase activity—> inc. free cholesterol secretion in
bile
Progesterone: dec. GB motility
Ceftriaxone: precipitation of salt
Octreotide (somatostatin): dec. GB motility
Cholesterol stones - ANS-- yellow, >75%
- cholesterol with variable Ca carbonate
- large and yellow-white
Bilirubin stones - ANS-- black, 10%
- Ca bilirubinate and mucin glycoproteins
- Occur with greater frequency in chronic hemolytic states (unconjugated BR precipitates)
Brown stones - ANS-- rare
- Ca salts of unconjugated BR, varying amounts of cholesterol and protein
- usually associated with biliary infection
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