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Liver encephalopathy

Fatty liver, encephalopathy, and sudden unexpected death in early childhood due to medium-chain acyl-coenzyme A dehydrogenase deficiency. [Pg.11]

The separation of methionine into methanethiol and hydrogen sulfide by microbes was shown in patients with alcoholic liver cirrhosis to cause liver encephalopathy (McClain et al. 1980). Methanethiol reduced oxygen consumption in the liver and in brain mitochondria, inhibited the Na/K-ATPase of the brain, and had a deleterious effect on cytochrome c oxidase (Waller 1977, Vahlkamp et al. 1979, Quaforth et al. 1976). [Pg.1312]

Reye syndrome is a rare disorder in children, characterized by a combination of severe liver disorder and encephalopathy (central nervous system (CNS) disturbances) that can follow an acute viral illness and which has a relatively high mortality. It has been found to be... [Pg.1079]

O Portal hypertension is the precipitating factor for the complications of cirrhotic liver disease—ascites, spontaneous bacterial peritonitis (SBP), variceal bleeding, and hepatic encephalopathy. Lowering portal pressure can reduce the complications of cirrhosis and decrease morbidity and mortality. [Pg.323]

Cirrhosis is the progressive replacement of normal hepatic cells by fibrous scar tissue. This scarring is accompanied by the loss of viable hepatocytes, which are the functional cells of the liver. Progressive cirrhosis is irreversible and leads to portal hypertension that is in turn responsible for many of the complications of advanced liver disease. These consequences include (but are not limited to) spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, and variceal bleeding.1... [Pg.323]

Ammonia (NH3) is just one of the toxins implicated in HE. It is a metabolic by-product of protein catabolism and is also generated by bacteria in the GI tract. In a normally functioning liver, hepatocytes take up ammonia and degrade it to form urea, which is then renally excreted. In patients with cirrhosis, the conversion of ammonia to urea is retarded and ammonia accumulates, resulting in encephalopathy. This decrease in urea formation is manifest on laboratory assessment as decreased blood urea nitrogen (BUN), but BUN levels do not correlate with degree of HE. Patients with HE commonly have elevated serum ammonia concentrations, but the levels do not correlate well with the degree of central nervous system impairment.20... [Pg.327]

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]

Managing viral hepatitis involves both prevention and treatment. Prevention of hepatitis A and B (and indirectly for hepatitis D) can be achieved with immune globulin or vaccines. There is no specific pharmacologic treatment for acute viral hepatitis A, B, C, D, or E only supportive care is available. Individuals with mild to moderate symptoms rarely require hospitalization. Occasionally, hospitalization is required in individuals experiencing significant nausea, vomiting, diarrhea, and encephalopathy. Liver transplantation may be required in rare instances if fulminant hepatitis develops. [Pg.350]

Liver Fever, lethargy, change in color or quantity of bile in patients w/ biliary T-tube, graft tenderness and swelling, back pain, anorexia, ileus, tachycardia, jaundice, ascites, encephalopathy Abnormal LFTs, increased bilirubin, alkaline phosphatase, transaminases, biopsy positive for mononuclear cell infiltrate with evidence of tissue damage... [Pg.834]

Crystalline amino acid bulk solutions are supplied by various manufacturers in various concentrations (e.g., 3.5%, 5%, 7%, 8.5%, 10%, 15%, and 20%). Different formulations are tailored for specific age groups (e.g., adults and infants) and disease states (e.g., renal and liver disease). Specialized formulations for patients with renal failure contain higher proportions of essential amino acids. Formulas for patients with hepatic encephalopathy contain higher amounts of branched-chain and lower amounts of aromatic amino acids. However, these specialized formulations should not be used routinely in clinical practice because their efficacy has not been clearly demonstrated. Crystalline amino acid solutions have an acidic pH (pH = 5-7) and may contain inherent electrolytes (e.g., sodium, potassium, acetate, and phosphate). [Pg.1494]

End-stage liver disease Liver failure that is usually accompanied by complications such as ascites or hepatic encephalopathy. [Pg.1565]

Hepatic encephalopathy Change in mental or neurologic status secondary to progressive liver disease or confusion and disorientation that a patient with advanced liver disease experiences due to accumulation of ammonia. [Pg.1567]

Reye s syndrome A sudden, sometimes fatal, syndrome characterized by encephalopathy and liver degeneration it occurs in children after viral infection and may be associated with aspirin use. [Pg.1576]

Ammonia Bacterial flora Benzodiazepines, endogenous Encephalopathy, hepatic Liver cirrhosis Rifaximin... [Pg.90]

NBZDs are present in trace amounts in the blood of normal subjects but they may rise severalfold in the blood of patients with liver cirrhosis, with or without encephalopathy [2, 38]. Increased levels of these compounds are inconstantly present in cirrhotic patients. A significant albeit week correlation [38] between circulating NBZDs... [Pg.91]

Avallone R, Zeneroli ML, Venturini I, Corsi L, Schreier P, Kleinschnitz M, Ferrarese C, Farina F, Baraldi C, Pecora N, Frigo M, Baraldi M Endogenous benzodiazepine-like compounds and diazepam binding inhibitor in serum of liver cirrhosis patients with and without encephalopathy. Gut 1998 42 860-867. [Pg.94]

L The answer is a. (Hardman, p 922) Lactulose is a synthetic disaccharide (galactose-fructose) that is not absorbed. In moderate doses, it acts as a laxative. In higher doses, it is capable of binding ammonia and other toxins that form in the intestine in severe liver deficiency and that are believed to cause the encephalopathy. Loperamide is an antidiarrheal opioid lorazepam is a CNS depressant loxapine is a heterocyclic antipsychotic. [Pg.233]

The metabolic encephalopathies comprise a series of neurological disorders not caused by primary structural abnormalities rather, they result from systemic illness, such as diabetes, liver disease and renal failure. Metabolic encephalopathies usually develop acutely or subacutely and are reversible if the systemic disorder is treated. If left... [Pg.594]

FIGURE 34-3 Positron emission tomography using 13NH3 showing increased brain ammonia uptake in a patient with liver cirrhosis and mild hepatic encephalopathy. CMRA, cerebral metabolic ratio for ammonia HE, hepatic encephalopathy PS, permeability/surface area product. (With permission from reference [9].)... [Pg.598]

Lockwood, A. H., Yap, E. W. H. and Wong, W. H. Cerebral ammonia metabolism in patients with severe liver disease and minimal hepatic encephalopathy. /. Cereb. Blood Flow Metab. 11 337-341,1991. [Pg.602]

Ascites, jaundice, variceal bleeding, and hepatic encephalopathy can manifest with liver decompensation. [Pg.289]

Paracetamol overdose is most likely to cause hepatic necrosis and to a lesser extent renal necrosis. Hepatic necrosis is maximal within 3-4 hours of ingestion and may lead to encephalopathy, haemorrhage, hypoglycaemia, cerebral oedema and death. Acetylcysteine tends to protect the liver if given within 10-12 hours of paracetamol poisoning. The maximum adult dose of paracetamol is 4 g in 24 hours. [Pg.294]

Inhalation exposure of rats and mice (10-25ppm over 2 weeks or 5-50ppm over 13 weeks) caused methemoglobinemia, encephalopathy, and lesions in the liver (hepatocyte necrosis and hepatomegaly), kidney (hyalin nephrosis), and spleen (extramedullary... [Pg.517]


See other pages where Liver encephalopathy is mentioned: [Pg.113]    [Pg.148]    [Pg.874]    [Pg.301]    [Pg.306]    [Pg.331]    [Pg.598]    [Pg.271]    [Pg.36]    [Pg.90]    [Pg.90]    [Pg.91]    [Pg.95]    [Pg.162]    [Pg.262]    [Pg.593]    [Pg.596]    [Pg.596]    [Pg.597]    [Pg.597]    [Pg.597]    [Pg.786]    [Pg.357]    [Pg.357]    [Pg.75]    [Pg.98]    [Pg.58]   


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Encephalopathies

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