Bile ducts

Bile duct Bile pigments Biligram Bibrubin... 

In general, activation of alpha-1 adrenergic receptors causes a contraction of smooth muscle and of blood vessels, pilomotor muscles, dilator pupillae, vas deferens, nictitating membrane, splenic capsule, and sphincters of the intestine and urinary bladder and of the bile duct. An exception is the relaxation of the smooth muscle of the intestine. Prazosin [19216-56-9] indoramin [26844-12-2] and WB-4101 are relatively selective antagonists of these receptors. 

Crmlraindicalions Inflammation or occlusion of the bile duct intestinal occlusion. 

In addition to the described lipid pathways mainly operative in macrophages, two further ABC-transporteis, ABCG5 and ABCG8 have been implicated in the efflux of dietary sterols from intestinal cells back into the gut lumen and from liver to the bile duct (Fig 1). Both ABC-transporters form a functional heterodimer with highest expression levels in liver and intestine and are regulated... 

Supra-additivity This is a special case of cooperation where the blockade of a single receptor is not sufficient to reduce the overall response. Capsaicin-induced nonadrenergic, noncholinergic contraction in the guinea pig ileum or common bile duct can be inhibited only when at least two different TK receptors are blocked (e.g., NKX + NK2, NKX + NK3, NK2 + NK3)... 

Bile ducts Various intravenous cholegraphic agents, e.g., iodipamide Biligrafin Anion transport Lin SK et al (1977) Iodipamide kinetics Capacity-limited biliary excretion with simultaneous pseudo-first-order renal excretion. J Pharm Sci 66 1670-1674... 

Dibutyltin dichloride induced acute pancreatitis and bile duct lesions in rats, depending on dose (6 and 8 mg/kg body weight intravenously) and time (1-24 weeks) (Merkord Hennighausen, 1989 Merkord et al., 1997, 1999 Sparmann et al., 2001). The lesions in the pancreas developed into a pancreatic fibrosis, and the lesions in the liver into liver cirrhosis. A single intravenous administration of dibutyltin dichloride at 4 mg/kg body weight induced a mild interstitial pancreatitis after 2 days (Merkord et al., 2001). Repeated administration of dibutyltin dichloride (4 mg/kg body weight intravenously) to rats at intervals of 3 weeks induced acute interstitial pancreatitis and, after 9-12 weeks, a pancreatic fibrosis and liver lesions (intrahepatic bile duct hyperplasia) (Merkord et al, 2001). 

Conjugated hyperbilirubinemia commonly results from blockage of the hepatic or common bile ducts, most often due to a gallstone or to cancer of the head of the pancreas. Because of the obstruction, bilirubin diglu-curonide cannot be excreted. It thus regurgitates into the hepatic veins and lymphatics, and conjugated bilirubin appears in the blood and urine (choluric jaundice). 

The commonest causes of obstructive (posthepatic) jaundice are cancer of the head of the pancreas and a gallstone lodged in the common bile duct. The presence of bilirubin in the urine is sometimes referred to as choluria—therefore, hepatitis and obstruction of the common bile duct cause choluric Jaundice, whereas the Jaundice of hemolytic anemia is referred to as acholuric. The laboratory results in patients with hepatitis are variable, depending on the extent of damage to parenchymal cells and the extent of micro-obstruction to bile ductules. Serum levels of ALT and AST are usually markedly elevated in hepatitis, whereas serum levels of alkaline phosphatase are elevated in obstructive liver disease. 

Normally, there are mere traces of urobihnogen in the urine. In complete obstraction of the bile duct, no... 

Table 32-3 summarizes laboratory results obtained on patients with three different causes of jaundice—hemolytic anemia (a prehepatic cause), hepatitis (a hepatic cause), and obstruction of the common bile duct (a posthepatic cause). Laboratory tests on blood (evaluation of the possibihty of a hemolytic anemia and measurement of prothrombin time) and on semm (eg, electrophoresis of proteins activities of the enzymes ALT, AST, and alkahne phosphatase) are also important in helping to distinguish between prehepatic, hepatic, and posthepatic causes of jaundice. 

The Group II (biliary tract) enzymes are abnormal usually when the serum bilirubin concentration is also abnormal. Most commonly used is alkaline phosphatase which is a highly sensitive indicator of biliary tract obstruction, perhaps because the enzyme is synthesized as an induced response to obstruction of even small bile ducts. Most techniques used to identify the origin of an elevated serum alkaline phosphatase are not very useful from a clinical viewpoint (23). The simultaneous measurement of GMT activity has been found to be useful in differentiating between the hepatic and bony origin of alkaline phosphatase. An increased GMT activity in a patient with an increased ALP activity is a good indication that there is biliary biliary tract disease (62,63). 

Various conditions such as perforated peptic ulcer, cholecystitis, common bile duct and intestinal obstruction, trauma to the abdomen inducing pancreatitis and ruptured ectopic pregnancy may cause an elevated serum amylase but the levels are usually not as high as those found in acute pancreatitis. Mumps and bacterial parotitis, which block the secretion of salivary amylase are associated with mild elevations of serum amylase. 

In the bile-duct-ligated rat, hepatic mitochondrial lipid peroxides are increased and correlate with serum levels of alkaline phosphatase, bilirubin and alanine aminotransferase (Sokol et al., 1991). Dietary vitamin E deficiency resulted in relatively higher lipid peroxide and bilirubin... 

Babin, F., Lemonnier, F., Goguelin, A., AlagiUe, D. and Lemonnier, A. (1988). Plasma fatty acid composition and lipid peroxide levels in children with paucity of interlobular bile ducts. Annu. Rev. Metab. 32, 220-230. 

Singh, S., Shackelton, G., Ah-Sing, E., Chakraborty, J. and Bailey, M.E. (1992). Antioxidant defenses in the bile duct-ligated rat. Gastroenterology 103, 1625-1629. 

Sokol, R.J., Devereaux, M. and Khandwala, R,A. (1991). Effect of dietary lipid and vitamin E on mitochondrial lipid peroxidation and hepatic injury in the bile duct-ligated rat. J. Lipid Res. 32, 1349-1357. 

Hepatobiliary disease occurs due to bile duct obstruction from abnormal bile composition and flow. Hepatomegaly, splenomegaly, and cholecystitis may be present. Hepatic steatosis may also be present due to effects of malnutrition. The progression from cholestasis (impaired bile flow) to portal fibrosis and to focal and multilobar cirrhosis, esophageal varices, and portal hypertension takes several years. Many patients are compensated and asymptomatic but maybe susceptible to acute decompensation in the event of extrinsic hepatic insult from viruses, medications, or other factors.7... 

Primary biliary cirrhosis is characterized by progressive inflammatory destruction of the bile ducts. Immune-mediated inflammation of intrahepatic bile ducts results in remodeling and scarring, causing retention of bile within the liver and subsequent hepatocellular damage and cirrhosis. The number of patients affected with primary biliary cirrhosis is difficult to estimate because many people are asymptomatic and incidental diagnosis during routine health care visits is common. 

Chronic obstruction of the common bile duct by the inflamed pancreas can cause icterus, cholangitis, and biliary cirrhosis.36... 

The serum bilirubin or alkaline phosphatase may be elevated due to inflammation near the common bile duct. 

Neoplasms (e.g., hepatoma, cholangiocarcinoma, hepatoblastoma, and bile duct cancer)... 

Melanoma of the skin Liver intrahepatic bile duct Leukemia... 

Leukemia Kidney renal pelvis Liver intrahepatic bile duct... 

CBD Common bile duct DJD Degenerative joint disease... 

Gallstone (cholelithiasis) A solid formation in the gallbladder or bile duct composed of cholesterol and bile salts. 

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