• Can be acquired (eg, liver disease) or hereditary (eg, urea cycle enzyme deficiencies).
  • Excess NH3 depletes glutamate and increases GABA inhibition
    • Astrocytes take up glutamate, reacts with ammonia to form glutamine (a non-neuroactive compound). Glutamine is released by astrocytes and is converted in neurons to glutamate. Excess ammonia → ↑ glutamine production → increased intracellular osmolarity, astrocyte swelling → impaired glutamine release → decreased glutamate decreased glutamate in neurons → disruption in excitatory neurotransmission.
    • NH3 depletes α-ketoglutarate → inhibition of TCA cycle.
    • Hepatic encephalopathy
      • Precipitating factors
        • Drugs – sedatives, narcotics
        • Hypovolemia – diarrhea
        • Electrolyte changes – hypokalemia
        • ↑ Nitrogen load – GI bleeding
        • Infection – pneumonia, UTI, spontaneous bacterial peritonitis
        • Portosystemic shunting (TIPS)
      • Clinical presentation
        • Sleep pattern changes
        • Altered mental status
        • Slurring of speech
        • Vomiting
        • Cerebral edema
        • Blurring of vision
        • Ataxia
        • Asterixis (flapping tremor)
    • Treatment: limit protein in diet.
    • May be given to ↓ ammonia levels:
      • Lactulose to acidify the GI tract and trap NH4+ for excretion.
      • Antibiotics (eg, rifaximin, neomycin) to ↓ colonic ammoniagenic bacteria.
      • Benzoate, phenylacetate, or phenylbutyrate react with glycine or glutamine,  products that are renally excreted.
      • Correct precipitating causes

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