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Hepatic disease jaundice

Chronic hepatitis (disease lasting longer than 6 months) is usually associated with hepatitis B, C, and D. Chronic viral hepatitis may lead to the development of cirrhosis, which may induce end-stage liver disease (ESLD). Complications of ESLD include ascites, edema, jaundice, hepatic encephalopathy, infections, and bleeding esophageal varices. Therefore, prevention and treatment of viral hepatitis may prevent ESLD. [Pg.345]

Hepatic diseases do not change the serum levels of G-6-PDH (B15, K6, LI). In malignant occlusion jaundice, elevated levels of G-6-PDH have been reported (LI). [Pg.270]

As would be expected, khat overuse produces symptoms similar to those of other monoamine stimulants, such as cocaine or amphetamine, including signs of sympathetic overarousal. In the extreme this can involve a toxic psychosis. Disorders more frequently associated with chronic khat use in males are headaches, anorexia, insomnia, constipation, and respiratory illnesses (Kennedy et al. 1983). Females report higher incidences of acute gastritis, jaundice, bronchitis and hepatic diseases. Also, cathinone has toxic reproductive effects in humans and experimental animals (Islam et al. 1990). It decreases sperm count and motility, and increases the number of abnormal sperm cells. It also decreases plasma testosterone in rats. [Pg.143]

Occupational exposure of 12 male workers, whose hands were in contact with MDA several hours per day, caused toxic hepatitis. The clinical pattern of the cases included right upper quadrant pain, high fever, and chills with subsequent jaundice. A skin rash was seen in five of the cases. Percutaneous absorption was considered to be the major route of exposure because workers in the same occupational setting who did not have direct skin contact with MDA were not affected. All patients recovered within 7 weeks, and follow-up more than 5 years later showed no biochemical or clinical evidence of chronic hepatic disease. [Pg.474]

Contraindications Dehydration, jaundice, narrow-angle glaucoma, severe hepatic disease... [Pg.103]

Rare react ions with long-term use include peptic ulcer disease, G1 bleeding, gastritis, a severe hepatic reaction (jaundice), nephrotoxicity (hematuria, dysuria, proteinuria), and a severe hypersensitivity reaction (bronchospasm or angioedema). [Pg.357]

Estrogens should be avoided in individuals with current thrombophlebitis or thromboembolism, estrogen-depen-dent tumors, abnormal genital bleeding without a diagnosis, and pregnancy. They are also contraindicated in apparently healthy women if they have an earlier history of jaundice in pregnancy, hepatic disease, thromboembolism, or porphyria. [Pg.191]

Decompensated hepatic disease (e.g., active alcoholism, ascites, coagulopathy, hypoalbuminemia, or jaundice) should not be treated with PEG-interferon a-2b... [Pg.93]

Elevations of LD activity are observed in liver disease, but these elevations are not as great as the increases in aminotransferase activity. Elevations are especially high (10 times normal) in toxic hepatitis with jaundice. Shghtly lower values are observed in viral hepatitis and in infectious mononucleosis, the latter often associated with elevations of LD-3. LD activity is normal or at most twice the upper reference limit in cirrhosis and obstructive jaundice. Serum LD-5 is often notably elevated in patients with either primary fiver disease or fiver anoxia secondary to decreased oxygen perfusion. [Pg.602]

Typical signs and symptoms of hepatitis include jaundice (yellow discoloration of the skin and sclera of the eyes, dark urine and pale stools), anorexia (loss of appetite), an enlarged, tender liver (hepatomegaly), abdominal pain and tenderness, nausea and vomiting, and fever, although the disease may range in severity from subclinical to fulminant. [Pg.267]

It is used for eye and hepatic diseases, treatment of jaundic, inflammation, metrorhagia, gonorrhoea, healing of wounds and injvuies. [Pg.169]

Knowledge of the biochemistry of the porphyrins and of heme is basic to understanding the varied functions of hemoproteins (see below) in the body. The porphyrias are a group of diseases caused by abnormalities in the pathway of biosynthesis of the various porphyrins. Although porphyrias are not very prevalent, physicians must be aware of them. A much more prevalent clinical condition is jaundice, due to elevation of bilirubin in the plasma. This elevation is due to overproduction of bilirubin or to failure of its excretion and is seen in numerous diseases ranging from hemolytic anemias to viral hepatitis and to cancer of the pancreas. [Pg.270]

Type I Crigler-Najjar syndrome is a rare autosomal recessive disorder. It is characterized by severe congenital jaundice (serum bilirubin usually exceeds 20 mg/dL) due to mutations in the gene encoding bilirubin-UGT activity in hepatic tissues. The disease is often fatal within the first 15 months of life. Children with this condition have been treated with phototherapy, resulting in some reduction in plasma bilirubin levels. Phenobarbital has no effect on the formation of bilirubin glucuronides in patients with type I Crigler-Najjar syndrome. A liver transplant may be curative. [Pg.283]

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. [Pg.284]

Hepatomegaly, jaundice, and altered liver function tests have been reported in accidental poisonings with DME An outbreak of toxic liver disease was associated with DME exposure at a fabric coating factory. Thirty-six of 58 workers had elevations of either aspartate aminotransferase or alanine aminotransferase. Serological tests excluded known infectious causes of hepatitis in all but two cases. After modification of work practices and removal of the most severely affected from exposure, improvement in liver enzyme abnormalities and symptoms occurred in most patients. Medical surveillance of the working population for 14 months revealed no further cases of toxic liver... [Pg.265]

Enhanced anticoagulant effects Endogenous factors that may be responsible for increased PT/INR response include the following Blood dyscrasias cancer collagen vascular disease CHF diarrhea elevated temperature hepatic disorders (eg, infectious hepatitis, jaundice) hyperthyroidism poor nutritional state steatorrhea vitamin K deficiency. [Pg.142]

Hepatic function impairment In patients with preexisting severe liver disease, hepatic encephalopathy (manifested by tremors, confusion, and coma, and increased jaundice) may occur. Because amiloride is not metabolized by the liver, drug accumulation is not anticipated in patients with hepatic dysfunction, but accumulation can occur if hepatorenal syndrome develops. [Pg.695]


See other pages where Hepatic disease jaundice is mentioned: [Pg.277]    [Pg.165]    [Pg.7]    [Pg.532]    [Pg.565]    [Pg.1925]    [Pg.3584]    [Pg.551]    [Pg.1379]    [Pg.1806]    [Pg.1808]    [Pg.715]    [Pg.290]    [Pg.276]    [Pg.1397]    [Pg.1397]    [Pg.392]    [Pg.334]    [Pg.921]    [Pg.551]    [Pg.456]    [Pg.277]    [Pg.1242]    [Pg.172]    [Pg.198]    [Pg.270]    [Pg.49]    [Pg.276]    [Pg.214]   
See also in sourсe #XX -- [ Pg.1792 ]




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