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Liver disease jaundice

Therapeutically, vitamin K is used in prophylaxis and treatment of deficiency of clotting factor due to dietary deficiency of vitamin K, chronic antimicrobial therapy, malabsorption syndrome, obstructive jaundice, liver diseases such as cirrhosis and hepatitis, in neonates to prevent or treat haemorrhagic disease of new born to counteract the overdosing of oral anticoagulants... [Pg.241]

Concern related to PCNs began in workplace settings with occurrences of chloracne, jaundice, liver disease, and death noted from prior to scale-up of production until PCN substitutes became popular (reviewed by Hayward (1998) [12]). Occupational exposures were reported as recently as 1989 [8]. Environmental contamination by PCNs was first observed in the 1970s in sediments near industrial sites [13], in air, water, and soil near sites of PCN manufacture and use [14,15], and in fish [16] and fish-eating birds [17,18]. [Pg.269]

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]

Another common liver disease, alcoholic liver damage produced by moderate to heavy alcoholic intake, is also reflected by an elevation of the serum GOT and GPT activities. The serim glutamyl transferase activity is reported to be a sensitive index of alcoholic intake and can serve to monitor persons on alcoholic withdrawal programs (60). The LD-5 isoenzyme arises mainly from liver tissue, but has a short half-life (61), which is about 1/5 and 1/2 of the half life of the transaminases, GPT and GOT respectively. Some authors consider that a normal LD-5 isoenzyme activity in a jaundiced patient is sufficient evidence to exclude primary liver disease and that obstruction is probably responsible for the jaundice (62). In hemolytic jaundice the LDH-1 and 2 isoenzymes are elevated. [Pg.208]

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]

Gram-negative bacteremia Hypoalbuminemia Increased age Liver disease Obstructive jaundice Preexisting kidney disease Poor nutrition... [Pg.985]

Cataracts in early childhood 1 1 Cataracts often within a few days of birth Vomiting and diarrhea after milk ingestion Jaundice and hyperbilirubinemia Hypoglycemia may be present Liver disease and cirrhosis Lethargy, hypotonia Mental retardation... [Pg.171]

Decompensated liver disease is complicated by jaundice, refractory ascites, bacterial peritonitis, coagulopathy, and variceal bleeding and may require liver transplantation. The number of liver transplants for decompensated cirrhosis doubled from 1990 to 2004, when 5845 cadaveric (orthotopic) liver transplants were performed (65). [Pg.402]

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]

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]

Hepatotoxicity There have been fatalities associated with jaundice in patients with liver disease or patients receiving rifampin concomitantly with other hepatotoxic agents. Carefully monitor liver function, especially AST and ALT, prior to therapy and then every 2 to 4 weeks during therapy. [Pg.1716]

Hepatocellular jaundice arises from liver disease, either inherited or acquired. [Pg.135]

Monitor for signs of liver disease (clay-colored stools, jaundice, dark urine, right upper quadrant tenderness, pruritus, fatigue, appetite loss, lethargy)... [Pg.1238]

Patients with liver disease may exhibit an increased sensitivity of many drugs. Patients with obstructive jaundice, hepatitis, cirrhosis shows reduce ability to synthesize glucuronide and sulfate conjugates. [Pg.33]

The deficiency of vitamin K occur due to liver disease, jaundice, malabsorption syndromes and chronic use of antimicrobial agents. [Pg.241]

Cholestatic jaundice has often been reported with oral estrogens and is probably related to an effect on the permeability of the canalicular membrane (SEDA-20, 381). Cholestatic jaundice induced by a subcutaneous estrogen implant has also been reported in the absence of any other cause of liver disease (SEDA-20, 381). After... [Pg.176]

A3. Amatuzio, D. S., Weber, L. J., and Nesbitt, S., Bilirubin and protein in the cerebrospinal fluid of jaundiced patients with severe liver disease with and without hepatic coma. /. Lab. Clin. Med. 41, 615-618 (1953). [Pg.293]

It is not advisable for people with a history of hepatitis, jaundice, or other serious liver disease to take [these] lysergic acid amides. Because several of the alkaloids in this family of sacraments have powerful uterus-stimulating properties we recommend that they not be taken by pregnant women. [Pg.192]

Adverse effects Adverse effects are a minor problem with rifampin, but can include nausea and vomiting, rash, and fever. The drug should be used judiciously in patients with hepatic failure because of the jaundice that occurs in patients with chronic liver disease, alcoholics, or in the elderly. [Pg.345]

Cirrhosis is often asymptomatic until complications of liver disease are present. Mrs MW may present with itching, jaundice, dark urine, pale fatty stools, abdominal pain, nausea, fatigue, bleeding - such as nose bleeds, hepatic encephalopathy, hepatomegaly, ascites, distended abdominal veins, spider angiomata, palmar erythema and asterixis. She may also present with the signs and symptoms of alcohol withdrawal, which include irritability, anxiety, tachycardia, tremor, sweating, confusion and hallucinations. [Pg.347]

Q3 Signs of jaundice jaundice gives a yellowish colour to the skin and mucous membranes, usually easiest to see in the cornea. The yellow colour is due to the presence of breakdown products of haemoglobin such as bilirubin in tissues, which the liver usually removes from the blood. Jaundice is indicative of liver disease, obstruction of the bile ducts or haemolytic disease. Bilirubin stains not only the tissues but also all body fluids, including plasma and urine, and the patient s urine can become really dark. [Pg.269]

This is an autosomal dominant hereditary disorder characterised by a progressive loss of the bile ducts within the liver and narrowing of the bile ducts outside the liver. It is also associated with congenital heart disease, and in particnlar pulmonary stenosis. Symptoms are related to chronic cholestasis and include jaundice, pruritus, pale loose stools and poor growth within the first three months of life. The majority of children have a benign course and many cases go undetected however, there is an overall mortality of 20-30% due to progressive liver disease with the development of cirrhosis, cardiac disease or intercnrrent infection. [Pg.61]

Organisms other than the viruses discussed earlier can cause acute liver infections, such as Leptospira icterohaemorrhagia, which causes Weil s disease, fungal infections caused by Candida species or aspergillosis, and schistosomiasis caused by trematodes. A number of systemic infections may also affect the liver, leading to jaundice, abnormal liver function tests or even acute liver failure. Table 3.6 lists some of the infective organisms that have been associated with liver disease. [Pg.71]

Before starting HRT patients should be assessed individually considering their risk of osteoporosis, the current status of their liver disease, and any other coexisting medical risks. They should also be assessed for any history, including family history, of jaundice. The risks and potential benefits of treatment should be carefully explained. [Pg.260]


See other pages where Liver disease jaundice is mentioned: [Pg.277]    [Pg.177]    [Pg.9]    [Pg.214]    [Pg.301]    [Pg.165]    [Pg.856]    [Pg.835]    [Pg.230]    [Pg.468]    [Pg.172]    [Pg.137]    [Pg.274]    [Pg.207]    [Pg.220]    [Pg.180]    [Pg.44]    [Pg.431]    [Pg.604]    [Pg.53]    [Pg.56]    [Pg.63]    [Pg.68]    [Pg.90]   
See also in sourсe #XX -- [ Pg.262 ]




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