Biliary obstruction caused

Stanley, N. F., and Joske, R. A., 1975, Animal model Chronic biliary obstruction caused by reovirus type 3, Am. J. Pathol. 80 185. 

Biliary cirrhosis, secondary disease this requires elimination of the obstructive cause. Itching associated with bile acid retention can respond to cholestyramine, a bile acid binding resin. 

Therapeutic uses The bile acid binding resins are the drugs of choice (often in combination with diet or niacin) in treating Type lla and lib hyperlipidemias. [Note In those rare individuals who are homozygous for Type lla, that is, for whom functional LDL receptors are totally lacking, these drugs have little effect on plasma LDL levels.] Cholestyramine can also relieve pruritus caused by accumulation of bile acids in patients with biliary obstruction. 

Pharmacokinetics Intravenous injection of vincristine or vinblastine leads to rapid cytotoxic effects and cell destruction. This in turn can cause hyperuricemia due to the oxidation of purines to uric acid. The hyperuricemia is ameliorated by administration of the xanthine oxidase inhibitor, allopurinol (see p. 417). The agents are concentrated and metabolized in the liver and are excreted into bile and feces. Doses must be modified in patients with impaired hepatic function or biliary obstruction. 

Dose-independent, drug-induced liver dysfunction (cholestatic jaundice) is not an unusual adverse reaction. Caused by a number of different, commonly used drugs, cholestasis is a hypersensitivity reaction that primarily affects the biliary canaliculi, causing an intrahepatic obstructive jaundice. An alteration in... 

In addition, biliary obstructive jaundice can also be caused by drug-induced toxicity, e.g. with Ciy-substi-tuted steroids, erythromycin estolate, chlorpromazine, chlorpropamide, ajmaline, halothane, methylthiouracil. 

Daniiewitz, M., Kotfila, R., Jensen, R Endoscopic diagnosis and management of Fasciola hepatica causing biliary obstruction. Amer. X... 

A 63-year-old man, who had taken amiloride and alfuzosin for 9 months for hypertension and benign prostatic hyperplasia, became jaundiced. His aspartate transaminase was 3013IU/1, alanine transaminase 2711 IU/1, alkaline phosphatase 500 IU/1, and total bilirubin 415 pmol/l. Viral causes, autoimmune hepatitis, and biliary obstruction were excluded. After withdrawal of alfuzosin, his liver function tests gradually returned to normal within 6 months. 

Hepatocellutar Disease. Most forms of acute or chronic hepatocellular disease, including acute viral hepatitis and cirrhosis with jaundice, are associated with decreased levels of Hp, possibly caused in part by altered estrogen metabolism. Increased red cell breakdown secondary to erythrocyte membrane lipid alterations may also play a role, although this has never been documented with turnover studies. In contrast, biliary obstruction is also associated with significant lipid alterations but with increased Hp levels, in the absence of severe hepatocellular disease. 

In practice, the plasma aminotransferases and ALP are the most useful tests as they allow differentiation of hepatocellular disease from cholestatic disease. The importance of this distinction cannot be overstated failure to recognize cholestatic disease caused by extrahepatic biliary obstruction will result in liver failure if the obstruction is not quickly corrected. It is also important to recognize that there may be a gray zone of mixed hepatocellular and cholestatic disease where the tests do not distinguish one disease from the other. In this case, it is wise to assume that the problem is cholestatic and rule out biliary obstruction. 

Hepatobiliary transporters are affected by both systemic inflammation (e.g., arising from an infection) and inflammation intrinsic to the liver (e.g., acute inflammatory cholestasis caused by drug or alcohol abuse). As described above, endotoxin or turpentine are used to trigger systemic inflammation in rodents. Other rodent models of cholangitis include ethinylestradiol (oral contraceptive-induced cholestasis/cholestasis of pregnancy), alpha-naphthylisocyanate (vanishing bile duct syndrome), and common bile duct ligation (extrahepatic biliary obstruction) [87, 88]. 

Biliary obstruction due to stone, tumor, or primary biliary cirrhosis Zollinger-Ellison syndrome (causes hyperacidity) bacterial overgrowth and stasis administration of drugs, neomycin, and cholestyramine Ileal disease or resection... 

In addition to nutritional inadequacy, vitamin deficiency may result from malabsorption, effects of pharmacological agents, and abnormalities of vitamin metabolism or utilization. Thus, in biliary obstruction or pancreatic disease, the fat-soluble vitamins are poorly absorbed despite adequate dietary intake because of steatorrhea. Absorption, transport, activation, and utilization of vitamins require the participation of enzymes or other proteins whose synthesis is under genetic control. Dysfunction or absence of one of these proteins can produce a disease that is clinically indistinguishable from one caused by dietary deficiency. In vitamin-dependent or vitamin-responsive... 

Cholestasis in the absence of demonstrable mechanical biliary obstruction is usually referred to as intrahepatic cholestasis, a term which implies that there is microscopic obstruction within the liver itself (P21). The condition occurs after the administration of various drugs, (see Table 10), in the presence of some infectious disorders (see Section 7.4), and during the last months of pregnancy. Mean serum alkaline phosphatase values in women with clinically overt cholestasis of pregnancy are higher than in matched controls (R13), although individual patients may have values appropriate to the last trimester of pregnancy (H2, R13). In some patients with intrahepatic cholestasis, no cause is identifiable (R35, S58). Serum alkaline phosphatase values in idiopathic cholestasis may be 7 times the upper reference limit (S75). 

BSP retention is usually increased in acute cholecystitis, but only occasionally is it increased in acute peritonitis and other acute abdominal conditions (B60, W21). The mechanism in these conditions is either partial biliary obstruction or alteration in hepatic blood flow. The effect of morphine in causing BSP retention by constriction of the sphincter of Oddi is relevant (see Section 7.12). Burnett (B60) found increased BSP retention ranging from 5 to 20% in 5 out of 6 patients with minor ailments given morphine, all of whom had shown normal BSP retention on the previous day. 

The place of dye tests in the investigation of the jaundiced patient is another aspect on which further studies are required. Biliary obstruction itself causes dye to be retained in plasma so that in a jaundiced patient it is not known to what extent a high dye retention value is due to biliary obstruction or to hepatocellular impairment. It is possible, however, that mathematical analysis of plasma dye disappearance curves may allow the two components to be separately assessed. With BSP, measurement of dye conjugates in plasma offer another means of separating the effects of biliary obstruction from those of hepatocellular failure, although results to date have not been promising in the assessment of individual patients. 

Chinese Liver Fluke. The adult worm of the Chinese liver fluke (Clonorchis sinensis) can grow to be 2 cm long. Worms infect the biliary tree where they cause local inflammation, diarrhea, and hepatomegaly in the acute infection. Progressive biliary obstruction and cirrhosis can occur in the more advanced disease state. The presence of 20—200 worms is common, but they may number over 20,000. Infection is the consequence of eating raw fish that contain viable parasites. Untreated worms can live for up to 30 years. Treatment is with praziquantil (1). 

Accumulated evidence suggests that liver disease is an important dinical risk factor for aminoglycoside nephrotoxicity [32]. This is particularly true of patients with biliary obstruction or cholangitis as distinct from other causes of liver disease such as alcoholic cirrhosis [33]. When hver disease is defined as any three of six criteria consisting of, AST > 2 times normal, total bi-hrubin > 2.5 pg/dl, albumin < 3 g/dl, elevated aUca-hne phosphatase, prothrombin time > 15 seconds or... 

Vitamin K is poorly absorbed in the absence of bile. Thus, hypoprothrombinemia may be associated with either intrahepatic or extrahepatic biliary obstruction or a severe defect in the intestinal absorption of fat from other causes. 

Medium-chain triglycerides (MCT) are important components of nutritional supplements used in patients with digestive disorders. They therefore can be employed as an easily absorbed source of calories in patients who have a gastrointestinal (Gl) disorder that may result in malabsorption of nutrients. These diseases include pancreatic insufficiency, intraluminal bile salt deficiency due to cholestatic liver disease, biliary obstruction, ileal disease or resection, and disease causing obstruction of intestinal lymphatics. Remember, however, that MCT do not contain polyunsaturated fatty acids that can be used for synthesis of eicosanoids (see Chapter 35). 

Bile acid sequestrants are indicated for the treatment of hypercholesterolemia in patients who do not adequately respond to dietary modifications. They may be used either alone or in combination with HMGRIs or niacin. These combinations often can achieve a 50% reduction in plasma LDL levels. Cholestyramine, but neither colestipol nor colesevelam, also is approved for the relief of pruritus associated with partial biliary obstruction. Bile acid sequestrants should not be used to treat hypertriglyceridemias or mixed hyperlipoproteinemias in which hypertriglyceridemia is the primary concern. These compounds also are contraindicated in patients with cholelithiasis or complete biliary obstruction because of the impaired secretion of bile acids caused by these conditions. Finally, cholestyramine and colestipol are contraindicated in patients with primary biliary cirrhosis, because this can further raise serum cholesterol (7,15,21). 

Chronic pancreatitis is a rare entity in children. Amongst the principal causes of chronic pancreatitis are hereditary pancreatitis, autoimmune conditions (sclerosing cholangitis), and CF. CT features of chronic pancreatitis include a focal or diffuse increase in pancreatic size, dilatation of the main pancreatic duct (almost always present), intraductal calcifications, or pseudocyst formation. ERCP can be used in children with unknown pancreatitis to identify and treat cases of biliary obstruction and structural cases of chronic pancreatitis. 

Clinical presentation. Bile duct complications develop within 2 months of chemoembolization but some may develop at a later stage [27]. Most patients with biliary strictures remain asymptomatic until the lumen of the bile duct is sufficiently narrowed to cause resistance to the flow of bile. Occasionally, patients may have intermittent episodes of RUQ (biliary colic), with or without laboratory features of biliary obstruction. 

Malabsorption. Steatorrhoea caused by exocrine pancreatic disease or biliary obstruction can cause vitamin D deficiency. 

An unsolved problem is the cause of cellular damage in biliary obstruction. The accumulation of bile acids is suspected. In man the normal cholic acid level is approximately 30 m moles/g this level is increased 7 times in biliary obstruction. Yet the extent of histological injury does not parallel the cholic acid level. In contrast, it parallels that of chenodeoxycholic acid. Although the levels of chenodeoxycholic acid are low at the onset of biliary obstruction, they increase gradually and may after weeks reach levels between 70 and 400 ng per g of liver. Chenodeoxycholic acid, but not the trihydroxylated cholic acid, is toxic for microsomes in vitro. Although it is likely that in vivo chenodeoxycholic acid is responsible for cellular damage, it is not known whether this results from damage to microsomes or cell membranes [110]. 

The inadequate intake of riboflavin seems to be the main cause for the deficiency of this vitamin, being common in populations whose diet lack dairy products and meat, and in anorexic individuals. Digestion and intestinal absorption disorders are other causes of disability, as observed in individuals with lactose intolerance, tropical sprue, coeliac disease and intestinal resection, as well as gastrointestinal and biliary obstruction. Other disorders such as diarrhoea, infectious enteritis and irritable bowel syndrome can cause poor absorption by increasing intestinal motility. Riboflavin deficiency also occurs in conditions such as chronic alcoholism, diabetes mellitus and inflammatory bowel diseases. 

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

If more cholesterol enters the bile than can be solubilized by the available bile salts and phosphatidylcholine, cholesterol gallstone disease (cholelithiasis) can occur. This is generally caused by gross malabsorption of bile acids from the intestine, obstruction of the biliary tract, or severe hepatic dysfunction, leading to abnormalities in bile or bile salt production. 

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