Portal-systemic encephalopathy and hepatic coma.
Decompensation in the cirrhotic patient is typically manifested as hepatic encephalopathy or coma. This may be precipitated by azotemia, gastrointestinal bleeding, infection, hypokalemic alkalosis, excess dietary protein, or the use of sedative, tranquilizer, or analgesic medications. The pathogenesis of hepatic encephalopathy associated with portal-systemic shunting is unknown, but theories purporting major roles for ammonia, AAAs, false neurotransmitters, and GABA have been advanced. Treatment is aimed at removing precipitating factors and eliminating nitrogenous substances from the gastrointestinal tract.
D000596:Amino Acids / Q000378:metabolism; D000641:Ammonia / Q000378:metabolism; D004044:Dietary Proteins / Q000008:administration & dosage; D006501:Hepatic Encephalopathy / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism / Q000628:therapy; D006801:Humans; D007792:Lactulose / Q000627:therapeutic use; D009355:Neomycin / Q000627:therapeutic use; D018377:Neurotransmitter Agents / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D000596:Amino Acids; D004044:Dietary Proteins; D018377:Neurotransmitter Agents; D007792:Lactulose; D005680:gamma-Aminobutyric Acid; D000641:Ammonia; D009355:Neomycin