Flashcards in 60. Hepatic encephalopathy Deck (13):
cirrhosis --> portosystemic shunts --> decreased NH3 metabolism --> neuropsychiatric dysfunction
spectrum from disorientation/ asterixis ( mild ) to difficult arousal or coma
mechanism of trigger
1. increased NH3 production and absorption
2. decreasd NH3 removal
1. increased NH3 production and absorption --> dietary protein, GI bleed, constipation, infection
2. decreased Nh3 removal --> renal failure , diuretics, bypassed hepatic flow post-TIPS
treatment ( and mechanism )
1. lactulose --> increases NH4++ generation
2. rifamixin or neomycin --> decreases NH4+ producing gut bacteria
GI bleeding increases ammonia - mechanism
RBCs contain proteins significant bleeding ( esp upper GI) --> increases the protein load in the intestine and the production of ammonia
Diuretic therapy ammonia
decreased serum potassium levels and alkalosis may facilitate the conversion of ammonium ( NH4) to ammonia ( +NH3)
Constipation - ammonia
constipation increases intestinal production and absorption of ammonia
• A non-alcoholic patient with portosystemic shunt has asterixis. He has eaten only protein powder for the past month. How do you treat him?
Treat with lactulose and rifaximin (he is suffering from hepatic encephalopathy), & he should eat less protein (decreases NH3 production)
• A patient with decreased NH3 metabolism and neuropsychiatric dysfunction presents with profound delirium. How do you treat him?
Treat with lactulose and rifaximin (he is suffering from hepatic encephalopathy
• What are some triggers of hepatic encephalopathy?
Increased NH3 production (protein intake, GI bleeding, constipation, infection), decreased NH3 removal (renal failure, diuretics, TIPS)
• A patient with hepatic encephalopathy is prescribed lactulose. He is also a medical student who wonders what lactulose does. You say?
Lactulose increases NH4+ generation, which decreases NH3 that can contribute to hepatic encephalopathy