Ch. 54 – Biliary System

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1550 Section X Abdomen Cystic artery Cystic duct Common duct The gallbladder is supplied by a single cystic artery, but in 12% of cases, a double cystic artery (anterior and posterior) may exist. The origin and course of the cystic artery is highly variable and is one of the most variable in the body. The cystic artery may originate from the left hepatic, common hepatic, gastroduodenal, or superior mesenteric arteries. The cystic artery divides into superfi cial and deep branches before entering the gallbladder. The cystic artery usually lies superior to the cystic duct and passes posterior to the common hepatic duct, but its course varies with its origin. The common hepatic duct, the liver, and the cystic duct defi ne the boundaries of Calot’s triangle (Fig. 54-4). Located within this triangle are important structures: the cystic artery, the right hepatic artery, and the cystic duct lymph node. The Calot node is the main route of lymphatic drainage of the gallbladder and is therefore commonly involved in infl ammatory or neoplastic diseases of the gallbladder. PHYSIOLOGY X Hepatic duct Portal vein Hepatic artery Figure 54-4 The triangle of Calot is bounded by the cystic duct, the common hepatic duct, and the inferior border of the liver. (From Gilchrist BF, Trunkey DD, Biliary Tract trauma. In Zuidema GD [ed]: Shackelford’s surgery of the alimentary tract, 3rd ed. WB Saunders, Philadelphia, 1991, pp 257.) Bile Ducts The bile ducts, gallbladder, and sphincter of Oddi modify, store, and regulate the fl ow of bile. The liver produces 500 to 1000 mL of bile per day and excretes it into the bile canaliculi. During its passage through the bile ductules and hepatic duct, canalicular bile is modifi ed by the absorption and secretion of electrolytes and water. The secretion of bile is responsive to neurogenic, humoral, and chemical stimuli. Vagal stimulation increases bile secretion, whereas splanchnic nerve stimulation results in decreased bile fl ow. The gastrointestinal hormone, secretin, stimulates bile fl ow primarily by increasing the active secretion of chloride-rich fl uid by the bile ducts and ductules. Secretin release is stimulated by hydrochloric acid, proteins, and fatty acids in the duodenum. Bile ductular secretion is also stimulated by cholecystokinin (CCK), gastrin, and other hormones. The bile duct epithelium is also capable of water and electrolyte absorption, which may be of primary importance in the storage of bile during fasting in patients who have previously undergone cholecystectomy. Bile is composed of water, electrolytes, bile salts, proteins, lipids, and bile pigments. Sodium, potassium, calcium, and chlorine have the same concentration in bile as in plasma or extracellular fl uid. The primary bile salts, cholate and chenodeoxycholate, are synthesized in the liver by cholesterol. They are conjugated there with taurine and glycine, and act within the bile as anions (bile acids) that are balanced by sodium. Bile salts are excreted into the bile by the hepatocyte and aid in the digestion and absorption of fats in the intestines. About 95% of the bile acid pool is reabsorbed and returned through the portal venous system to the liver, also known as the enterohepatic circulation (Fig. 54-5). The remaining 5% is excreted in the stool. Cholesterol and phospholipids synthesized in the liver are the principal lipids found in bile. The synthesis of phospholipid and cholesterol by the liver is regulated in part by bile acids. The color of bile is due to the presence of the pigment bilirubin diglucuronide, which is the metabolic product from the breakdown of hemoglobin, and is present in bile in concentrations 100 times greater than plasma. Once in the intestine, bacteria convert it into urobilinogen, a small fraction of which is absorbed and secreted into the bile. Gallbladder The gallbladder concentrates and stores hepatic bile during the fasting state and delivers bile into the duodenum in response to a meal. Since the usual capacity of the gallbladder is only about 30 to 60 mL, the remarkable absorptive capacity of the gallbladder accounts for its ability to store much of the 600 mL of bile produced each day. The gallbladder mucosa has the greatest absorptive capacity per unit area of any structure in the body. Bile is usually concentrated 5- to 10-fold by the absorption of water and electrolytes leading to a marked change in bile composition. Active NaCl transport by the gallbladder epithelium is the driving force for the concentration of bile. Water is passively absorbed in response to the osmotic force generated by solute absorption. The concentration of bile may affect the solubility of two important components of gallstones: calcium and cholesterol. Although the gallbladder mucosa absorbs calcium, this process is not nearly as effi cient as for sodium or water, leading to greater relative increase in calcium concentration. As the gallbladder bile becomes concentrated, several changes occur in the capacity of bile to solubilize cholesterol. The solubility in the micellar fraction is increased, but the stability of phospholipid-cholesterol vesicles is greatly decreased. Because cholesterol crystal precipitation occurs preferentially by vesicular rather than micellar mechanisms, the net effect of concentrating bile is an increased tendency for cholesterol nucleation. The gallbladder epithelial cell secretes at least two important products into the gallbladder lumen: glycopro-
Urinary excretion (95% of biliary secretion) Synthesis (0.2–0.6 g/d) teins and hydrogen ions. Secretion of mucus glycoprotein occurs primarily from the glands of the gallbladder neck and cystic duct. The resultant mucin gel is believed to constitute an important part of the unstirred layer (diffusion-resistant barrier) that separates the gallbladder cell membrane from the luminal bile. This mucus barrier may be very important in protecting the gallbladder epithelium from the strong detergent effect of the highly concentrated bile salts found in the gallbladder. However, considerable evidence also suggests that mucin glycoproteins play a role as a pronucleating agent for cholesterol crystallization. The transport of hydrogen ions by the gallbladder epithelium leads to a decrease in gallbladder bile pH through a sodium-exchange mechanism. Acidifi - cation of bile promotes calcium solubility, thereby preventing its precipitation as calcium salts. The gallbladder’s normal acidifi cation process lowers the pH of entering hepatic bile from 7.5 to 7.8 down to 7.1 to 7.3. The gallbladder fi lls from the continuous production of bile by the liver against the force of a contracted sphincter of Oddi. As the pressure within the common bile duct exceeds that within the gallbladder lumen, hepatic bile enters the gallbladder by retrograde fl ow through the cystic duct, wherein it is rapidly concentrated. Periods of fi lling are punctuated by brief episodes of partial emptying (∼10%-15% of its volume) of concentrated gallbladder bile that are coordinated through the duodenum of phase III of the migrating myoelectric complex (MMC). Fecal excretion (0.2–0.6 g/d) Biliary secretion = pool x cycles (12–36 g/d) (~3 g) x (4–12/d) Chapter 54 Biliary System 1551 Figure 54-5 Enterohepatic circulation. (From Arias IM, Popper H, Jakoby WB, et al: The liver: Biology and pathobiology. Philadelphia: Raven Press, 1988, p 576.) Following a meal, the gallbladder contracts in response to both a vagally mediated cephalic phase of activity and the release of CCK, the major regulator of gallbladder function. In the next 60 to 120 minutes, about 50% to 70% of gallbladder bile is steadily emptied into the intestinal tract. CCK is localized to the proximal small intestine, especially the duodenal epithelial cells, where its release is stimulated by intraluminal fat, amino acids, and gastric acid and inhibited by bile. In addition to stimulating gallbladder contractions, CCK also acts to functionally inhibit the normal phasic motor activity of the sphincter of Oddi. Gallbladder refi lling then occurs gradually over the next 60 to 90 minutes. Sphincter of Oddi The sphincter of Oddi is a complex structure that is functionally independent from the duodenal musculature. It creates a high-pressure zone between the bile duct and the duodenum. The sphincter regulates the fl ow of bile and pancreatic juice into the duodenum, prevents the regurgitation of duodenal contents into the biliary tract, and also diverts bile into the gallbladder. The sphincter of Oddi also has very high-pressure phasic contractions, which play a role in preventing the regurgitation of duodenal contents into the biliary tract. Both neural and hormonal factors infl uence the sphincter of Oddi. In response to CCK, both sphincter of Oddi pressure and phasic wave activity diminish. After a meal,
Page 1 and 2: Biliary System Ravi S. Chari, MD an
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Ch. 54 – Biliary System

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