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The gallbladder, a pear-shaped, hollow, saclike organ, 7.5 to 10 cm (3 to 4 in) long, lies in a shallow depression on the inferior sur-face of the liver, to which it is attached by loose connective tissue. The capacity of the gallbladder is 30 to 50 mL of bile. Its wall is composed largely of smooth muscle. The gallbladder is connected to the common bile duct by the cystic duct (Fig. 40-1).
The gallbladder functions as a storage depot for bile. Between meals, when the sphincter of Oddi is closed, bile produced by the hepatocytes enters the gallbladder. During storage, a large portion of the water in bile is absorbed through the walls of the gall-bladder, so that gallbladder bile is five to ten times more concen-trated than that originally secreted by the liver. When food enters the duodenum, the gallbladder contracts and the sphincter of Oddi (located at the junction where the common bile duct en-ters the duodenum) relaxes. Relaxation of the sphincter of Oddi allows the bile to enter the intestine. This response is mediated by secretion of the hormone cholecystokinin–pancreozymin(CCK-PZ) from the intestinal wall. Bile is composed of waterand electrolytes (sodium, potassium, calcium, chloride, and bi-carbonate) and significant amounts of lecithin, fatty acids, cho-lesterol, bilirubin, and bile salts. The bile salts, together with cholesterol, assist in emulsification of fats in the distal ileum. They then are reabsorbed into the portal blood for return to the liver and again excreted into the bile. This pathway from hepatocytes to bile to intestine and back to the hepatocytes is called the enterohepatic circulation. Because of the enterohepatic cir-culation, only a small fraction of the bile salts that enter the in-testine are excreted in the feces. This decreases the need for active synthesis of bile salts by the liver cells.
If the flow of bile is impeded (ie, with gallstones in the bile ducts), bilirubin, a pigment derived from the breakdown of red blood cells, does not enter the intestine. As a result, bilirubin levels in the blood increase. This results, in turn, in increased renal excretion of urobilinogen, which results from conversion of bilirubin in the small intestine, and decreased excretion in the stool. These changes produce many of the signs and symptoms seen in gallbladder disorders.
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