Hepatic obstruction

These drug are used cautiously in patients with renal or hepatic disease, bladder obstruction, seizure disorders, sick sinus syndrome, gastrointestinal bleeding, and asthma Individuals with a history of ulcer disease may have a recurrence of the bleeding. 

Antiemetics and antivertigo drag s are used cautiously in patients with glaucoma or obstructive disease of the gastrointestinal or genitourinary system, those with renal or hepatic dysfunction, and in older men with possible prostatic hypertrophy. Piromethazine is used cautiously in patients with hypertension, sleep apnea, or epilepsy. Trimethobenzamide is used cautiously in children with a viral illness because it may increase the risk of Reye s syndrome... 

Laxatives are contraindicated in patients with known hypersensitivity and those with persistent abdominal pain, nausea, or vomiting of unknown cause or signs of acute appendicitis, fecal impaction, intestinal obstruction, or acute hepatitis. These dragp are used only as directed because excessive or prolonged use may cause dependence. Magnesium hydroxide is used cautiously in patients with any degree of renal impairment. Laxatives... 

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 term cholestatic jaundice is used to include all cases of extrahepatic obstructive jaundice. It also covers those cases of jaundice that exhibit conjugated hyperbilirubinemia due to micro-obstruction of intrahepatic biliary ductules by swollen, damaged hepatocytes (eg, as may occur in infectious hepatitis). 

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. 

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). 

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... 

Superior mesenteric artery syndrome Enteric infections Inflammatory bowel diseases Pancreatitis Appendicitis Cholecystitis Biliary colic Gastroparesis Postvagotomy syndrome Intestinal pseudo-obstruction Functional dyspepsia Gastroesophageal reflux Peptic ulcer disease Hepatitis Peritonitis Gastric malignancy Liver failure... 

Portal hypertension is a consequence of increased resistance to blood flow through the portal vein. Increased resistance is usually due to restructuring of intrahepatic tissue (sinusoidal damage) but may also be caused by presinusoidal damage such as portal vein occlusion from trauma, malignancy, or thrombosis. A third (and the least common) mechanism is outflow obstruction of the hepatic vein. This latter damage is posthepatic, and normal liver structure is maintained. This chapter will focus on portal hypertension caused by intrahepatic damage from cirrhosis. 

The pathophysiologic mechanisms of portal hypertension and of cirrhosis itself are entwined with the mechanisms of ascites (Fig. 19-3). Cirrhotic changes and the subsequent decrease in synthetic function lead to a decrease in production of albumin (hypoalbuminemia). Albumin is the major intravascular protein involved in maintaining oncotic pressure in the vascular system low serum albumin levels and increased capillary permeability allow fluid to leak from the vascular space into body tissues. This can result in peripheral edema, ascites, and fluid in the pulmonary system. The obstruction of hepatic sinusoids and... 

Enhanced bilirubin level may suggest drug toxicity, bile-tract obstruction, hepatitis and hepatic dysfunction,... 

Conditicms that increase direct bilirubin Hepatic damage Bile duct obstruction... 

Death. Chloroform levels of 40,000 ppm cause death in patients under chloroform anesthesia (Featherstone 1947 Whitaker and Jones 1965). Death is usually due to severe respiratory depression/ failure or disturbances in cardiac rhythm. Accidental or intentional ingestion of large doses of chloroform may lead to death (Piersol et al. 1933). Death in humans after oral exposure to chloroform is usually caused by respiratory obstruction by the tongue due to jaw relaxation, central respiratory paralysis, acute cardiac failure, or severe hepatic injury (Piersol et al. 1933 Schroeder 1965). 

Cholestyramine (Cuemid, Dowex 1-X2-C1, Questran) is a quaternary ammonium cationic resin used primarily to bind, in the gut, bile salts which appear to be the main cause of pruritis in obstructive hepatic disease. Again, many unexpected facets of steroid and lipid metabolism are becoming clear following studies of the drug s effects [451.452]. 

Speciai risk patients Patients on dialysis may develop orthostatic hypotension monitor blood pressure closely. Initiate treatment under close medical supervision for patients with biliary obstructive disorders or hepatic insufficiency. Correct the condition of patients with depletion of intravascular volume before initiating therapy and monitor closely. 

Telmisartan- As the majority of telmisartan is eliminated by biliary excretion, patients with biliary obstructive disorders or hepatic insufficiency can be expected to have reduced clearance. Use telmisartan with caution in these patients. 

Urinary retention Administer ER tablets with caution to patients with clinically significant bladder outflow obstruction because of the risk of urinary retention. Renal/Hepatic function impairment Use ER tablets with caution in patients with hepatic or renal impairment. 

Gl Obstructive disease (eg, achalasia, pyloroduodenal stenosis or pyloric obstruction, cardiospasm) paralytic ileus intestinal atony of the elderly or debilitated severe ulcerative colitis toxic megacolon complicating ulcerative colitis hepatic disease. 

Severe renal impairment moderate or severe hepatic impairment history of bowel obstruction, symptomatic gallbladder disease, suspected sphincter of Oddi dysfunction, or abdominal adhesions known hypersensitivity to the drug or any of its excipients. 

Hepatic disease or biliary obstruction - In general, total daily dosage greater than 4 g should not be necessary. 

Renal function impairment Cephalosporins may be nephrotoxic use with caution in the presence of markedly impaired renal function (Ccr less than 50 mL/min/1.73 m ). Hepatic function impairment Cefoperazone is extensively excreted in bile. Serum half-life increases 2-fold to 4-fold in patients with hepatic disease or biliary obstruction. 

The rate of resectability is only 15-20% for proximal bile duct carcinomas but up to 70% for distal lesions. In addition, there is little benefit to preoperative decompression of the biliary tree in patients having obstructive jaundice (65,66). However, this procedure is frequently practiced. For proximal cancers, local excision is often possible. In particular, hepatic resection is indicated for upper bile duct cancers with quadrate lobe invasion or unilateral intrahepatic ductal or vascular involvement, and distal and midductal lesions may require pancreatoduodenectomy. Also, biliary-enteric continuity... 

Evidence of increased serum total bilirubin (>2x ULN) with no evidence of intra- or extra-hepatic bilirubin obstruction (elevated serum ALP) or Gilberts syndrome. 

Contraindication are myasthenia gravis, chronic obstructive pulmonary disease and severe hepatic disease. Both in the elderly and in children paradoxical reactions were described. In the elderly the use of benzodiazepines is strongly correlated with falls and hip fractures. 

Sodium retention and hypo albumin aemi a are constant features. The former appears consequent on disturbed blood volume distribution, withslanch-nic dilatation and reduced effective central arterial blood volume leads to sodium retention. Hypoalbu-minaemia associated with reduced hepatic albumin synthesis, and raised portal pressure associated with obstruction to flow, as well as active sodium retention all predispose to ascites. Hypoalbuminaemia is associated with reduced hepatic synthesis. 

Accessory measures insertion of a peritoneo-venous shunt to allow transfer of ascitic fluid to the venous compartment has largely been abandoned due to frequent shunt obstruction, peritoneal infection and the occurrence of encephalopathy. TIPS is as effective in relieving ascites as paracentesis with albumin replacement, but shunts can quickly become obstructed, and hepatic encephalopathy is a common complication. 

Propafenone is contraindicated in the presence of severe or uncontrolled congestive heart failure cardiogenic shock sinoatrial, A-V, and intraventricular disorders of conduction and sinus node dysfunction, such as sick sinus syndrome. Other contraindications include severe bradycardia, hypotension, obstructive pulmonary disease, and hepatic and renal failure. Because of its weak (3-blocking action, propafenone may cause possible dose-related bronchospasm. This problem is greatest in patients who are slow metaboUzers. 

Urinary excretion is the major elimination path for most cephalosporins. When prescribing cephalosporins to patients with renal failure, practitioners must consider dose reduction or dose interval extension (Table 45.2). Renal tubular secretion contributes to the elimination of some cephalosporins, and an increase in cephalosporin plasma concentrations may occur when probenecid blocks renal tubular secretion of cephalosporins. Biliary elimination is important for some cephalosporins. Cefmetazole, cefoperazone (Cefobid), cefoxitin, and ceftriaxone achieve biliary concentrations greater than those in plasma. After parenteral administration of cefoperazone, 70% of the dose appears in the bile within 24 hours. Practitioners should decrease the dose of cefoperazone when prescribing for patients with hepatic failure or biliary obstruction. Metabolism is not a major elimination path for most cephalosporins. Cefotaxime is one of the few cephalosporins having an active metabolite, desacetyl cefotaxime. 

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