Encephalopathy is a metabolic disorder arising in the CNS of patients with liver failure. It is always associated with increased circulating levels of ammonia (NH3). Patients present with altered mental status, asterixis with flapping tremor, confusion, circadian rhythm disturbances, and decreased motor ability. The cause of hepatic encephalopathy is not known but is probably multifactorial:
- Increased uptake of ammonia from the GI tract.
- Increased dietary protein intake
- Absorption of blood from bleeding oesophageal varices
- Decreased conversion of ammonia into urea in the liver. Normally, ammonia is converted into urea by the liver and then excreted by the kidneys. This process is inhibited by decreased liver function.
- High circulating ammonia levels interfere in the CNS with normal metabolic pathways, resulting in encephalopathy.
Which of the following factors is unlikely to cause hepatic encephalopathy:
Extra info: Hepatic encephalopathy is associated with increased circulating ammonia. Benzodiazepines, hypokalaemia, and high protein intake all contribute to increase of ammonia. Only anticoagulants do not. Long-acting benzodiazepines increase the already high circulating levels of endogenous GABA agonists, leading to confusion; hypokalaemia promotes metabolic alkalosis and stimulates the dissociation of ammonium into ammonia and hydrogen ions in the blood; a steak dinner provides a high protein load in the GI tract a