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what is most common cause of hepatic encephalopathy in dogs?
portosystemic shunt
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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)
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what are sources of ammonia from intestine?
- product from bacteria breakdown
- metabolism of glutamine
- breakdown of urea
- normal liver and circulation
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Do dogs with PSS have more branched or aromatic chains of amino acids?
more aromatic w/HE which more readily cross BBB
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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
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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
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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)
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Are dog or cats more likely to get HE without shunting?
cats
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Fasted cats may have arginine deficiency. How does this lead to HE?
arginine essential to hepatic urea cycle - deficiency causes inadequate detoxification
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how does HE lead to stranguria/hematuria?
ammonia biurate calculi
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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
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Is fasting ammonia levels more sensitive for chronic liver disease or PSS?
- *PSS*
- (100% have high levels; only 50% w/chronic liver dz)
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what are ways to get false positives when testing fasted ammonia levels?
inadequate centrifugation or hemolysis (false + due to recorded ammonia from RBCs)
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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
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What is goal of treating HE? how is this accomplished?
- restore neuro function
- diet + lactulose + Abs + control precipitating factors
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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
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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
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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
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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-)
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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
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Does acidosis or alkalosis facilitate NH3 crossing the BBB?
alkalosis worsens so want pt in mild acidosis
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How does hypoK precipitate HE?
hypoK leads to increased renal NH3 production
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why are enemas given in acute HE?
evacuate the colon so nothing else absorbed - lactulose enema or warm water
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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
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What is preferred long term seizure control for HE?
- potassium bromide
- (diazepam controversial bc needs hepatic metabolism)
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what other organ failure is seen in 40% cases with acute liver failure?
renal failure
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what are some factors that suggest poorer outcome?
- OSPT >100s
- very old/young
- idiosyncratic drug rxn or virus as cause
- markedly incr. bilirubin
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what is most important mechanism associated with ascites in dogs with HE?
- increased portal hypertension
- (ascites rare in cats)
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Ascites is typically only treated when associated with clinical signs. what is treatment?
Diet + diuretics + drain (abdominocentesis)
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what is most helpful aspect of diet for managing ascites?
restricted sodium
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If diet fails to control ascites, which diuretic is best for these patients?
- Spirinolactone (aldosterone antagonist)
- -monitor for hyperK
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what is most common location of ulcer in HE patient?
- duodenum
- (melena not always present)
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