SA Med F, Liver Dz

  1. what is most common cause of hepatic encephalopathy in dogs?
    portosystemic shunt
  2. What is most important mediator in development of hepatic encephalopathy?
    • cerebral toxin accumulation of ammonia
    • (also glutamate toxicity, CSF amino acid alterans, hypoglycemia and fluid/e-lyte abnormalities)
  3. what are sources of ammonia from intestine?
    • product from bacteria breakdown
    • metabolism of glutamine
    • breakdown of urea
    • normal liver and circulation
  4. Do dogs with PSS have more branched or aromatic chains of amino acids?
    more aromatic w/HE which more readily cross BBB
  5. Congenital PSS is most common cause of HE, but what are some other causes?
    • acquired PSS
    • hepatic lipidosis
    • hepatic arteriovenous malformations
    • microvascular dysplasia
    • any cause of acute/chronic liver failure
  6. what should you know about ammonia and the urea cycle in the brain?
    there isn't urea cycle in the brain so ammonia removed by transamination
  7. transamination increases glutamine concentrations in CNS w/HE. It's then exchanged across BBB for tryptophan. What is effect of tryptophan in CNS?
    forms metabolites - serotonin (inhibitory) and quinolinic acid (excitatory)
  8. Are dog or cats more likely to get HE without shunting?
  9. Fasted cats may have arginine deficiency. How does this lead to HE?
    arginine essential to hepatic urea cycle - deficiency causes inadequate detoxification
  10. how does HE lead to stranguria/hematuria?
    ammonia biurate calculi
  11. what are clinical signs seen with HE?
    • cerebral signs - behavior changes, circling, head press, ataxia, seizure
    • cortical blindness
    • ventral neck flexion
    • ptyalism in cats (may be only sign)
    • may have mostly CNS depression
  12. Is fasting ammonia levels more sensitive for chronic liver disease or PSS?
    • *PSS*
    • (100% have high levels; only 50% w/chronic liver dz)
  13. what are ways to get false positives when testing fasted ammonia levels?
    inadequate centrifugation or hemolysis (false + due to recorded ammonia from RBCs)
  14. Fasted ammonia is the only toxin tested to determine HE. Is this test required? Can you rule out HE if levels are normal?
    • no, can treat based on clinical signs
    • no
  15. What is goal of treating HE? how is this accomplished?
    • restore neuro function
    • diet + lactulose + Abs + control precipitating factors
  16. What are considerations for diet given to HE patient?
    • *protein restriction*
    • high branched chain amino acids (low aromatic)
    • adequate arginine (for urea cycle)
    • low residue
  17. What does it mean to say lactulose acts as "catabolite repression"?
    it gives colon flora an energy source, thus reduces catabolism (proteolysis, deamination) so less NH3 produced
  18. T or F: Lactulose is often sufficient to manage chronic HE long term.
    true - lactulose can help when surgery not an option like microdysplasia or intrahepatic shunts
  19. Why are Abs given as part of tx? which Abs are effective at anaerobes for this purpose?
    • suppress bacteria that generate NH3/toxins
    • Amoxicillin/metro
    • (neomycin for G-)
  20. what are some precipitating factors that increase GI NH3 production which we should control?
    • hi protein diets (red meat)
    • GI bleeding
    • azotemia (recirculation of urea)
    • constipation
  21. Does acidosis or alkalosis facilitate NH3 crossing the BBB?
    alkalosis worsens so want pt in mild acidosis
  22. How does hypoK precipitate HE?
    hypoK leads to increased renal NH3 production
  23. why are enemas given in acute HE?
    evacuate the colon so nothing else absorbed - lactulose enema or warm water
  24. Should we give alkalinizing or acidifying IV fluids to acute HE patient? what is a good choice fluid to use?
    • give acidifying (avoid LRS)
    • 0.45% NaCl w/2.5% dextrose
  25. What is preferred long term seizure control for HE?
    • potassium bromide
    • (diazepam controversial bc needs hepatic metabolism)
  26. what other organ failure is seen in 40% cases with acute liver failure?
    renal failure
  27. what are some factors that suggest poorer outcome?
    • OSPT >100s
    • very old/young
    • idiosyncratic drug rxn or virus as cause
    • markedly incr. bilirubin
  28. what is most important mechanism associated with ascites in dogs with HE?
    • increased portal hypertension
    • (ascites rare in cats)
  29. Ascites is typically only treated when associated with clinical signs. what is treatment?
    Diet + diuretics + drain (abdominocentesis)
  30. what is most helpful aspect of diet for managing ascites?
    restricted sodium
  31. If diet fails to control ascites, which diuretic is best for these patients?
    • Spirinolactone (aldosterone antagonist)
    • -monitor for hyperK
  32. what is most common location of ulcer in HE patient?
    • duodenum
    • (melena not always present)
Card Set
SA Med F, Liver Dz
SA Med F, Liver Dz