GI2- Equine Liver Dz

  1. Clinical signs associated with liver disease in horses. (11)
    icterus, anorexia, depression, weight loss, colic, diarrhea, fever, encephalopathy, ptyalism, photosensitization, death
  2. Where does each enzyme come from:
    • ALP- biliary tract
    • SDH-hepatic parenchyma
    • AST- hepatic parenchyma¬†
    • GGT- biliary tract
    • LDH- hepatic parenchyma
  3. What is the only enzyme that is specific to the liver in horses?
    sorbitol dehydrogenase (SDH)
  4. Hepatocellular disease markers. (4)
    increased SDH, AST, LDH, unconjugated bili> conjugated bili
  5. What are cholestatic disease markers? (3)
    increased GGT, ALP, conjugated bili
  6. What are the acute phase proteins of horses? (2)
    fibrinogen, serum amyloid A
  7. The hepatic functional residual capacity (FRC) is __________.
    high [ie. when an animal is showing clinical signs, the disease is advanced/severe]
  8. What are the species susceptibilities to pyrrolizidine alkaloid (PA) toxicity (most to least)?
    pigs> chickens> cattle/horses> sheep/goats
  9. Animals of __________ are more susceptible to PA toxicity; PA toxicity causes ______(2)______.
    poor nutrition; chronic fibrosing hepatopathy and hepatic failure
  10. Animals get chronic fibrosing hepatopathy associated with PA toxicity from... (2)
    chronic cumulative exposure and ingestion of 2-5% of body weight of toxic plant
  11. To become toxic, pyrrolizidine alkaloids must...
    be bioactivated by P450 to toxic pyrroles.
  12. PA alkaloids are __(2)__, causing disease.
    cytotoxic and antimitotic [mitotic spindle inhibition]
  13. How do you diagnose PA toxicity? (4)
    clinical findings, increased GGT, hyperbili, liver biopsy
  14. What are the 3 classic histologic findings on liver biopsy with PA toxicity?
    megalocytic hepatopathy, bridging periportal fibrosis, biliary duct hyperplasia
  15. How do you treat PA toxicity? (3)
    supportive/ non-specific, treat hepatic encephalopathy, keep out of direct sunlight (photosensitization)
  16. What is the prognosis of PA toxicity?
  17. How do you prevent PA toxicity? (3)
    remove from pasture, plant control, herd assessment of GGT
  18. What pathology is associated with acute cases of PA toxicity? (3)
    enlarged liver, hemorrhages, icterus
  19. What pathology is associated with chronic cases of PA toxicity? (2)
    atrophied, small liver, fibrous
  20. How can hepatic encephalopathy occur? (3)
    decreased synthesis of substances required for brain function (glucose), increased synthesis of encephalopathogenic products (ammonia), decreased metabolism of encephalopathogenic precursors [accumulation of toxic products]
  21. Hepatic encephalopathy is a(n) ____________; therefore, you must address...
    secondary disease; address the underlying disease.
  22. What are potential causes of hepatic encephalopathy? (10)
    PA toxicity, Theiler's dz, Tyzzer's dz, Cholangiohepatitis, Cholelithiasis, iron toxicity, neoplasia, PSS, lipidosis/ amyloidosis, necrosis
  23. What are the theories of how hepatic encephalopathy arises? (4)
    toxic metabolite, hyperammonemia, false neurotransmitter/AA imbalance, benzodiaepine-like substances (valium/diazepam, midazolam)
  24. What are the 3 parts of the toxic metabolite theory of hepatic encephalopathy?
    • accumulation of toxic products not metabolized first pass through the liver or bypass the liver
    • anatomic defects (PSS)
    • nitrogenous metabolites implicates
  25. With the hyperammonemia theory of HE, there is dysfunction of ___(2)__, leading to an increase in __(3)__, causing... (3)
    Na+K+ATPase pump and Kreb's cycle; CNS nitric oxide, free radicals, altered ion dynamics; cell swelling, abnormal ion gradient, demyelination.
  26. False neurotransmitters are produced from __________; they are thought to cause HE by... (3)
    aromatic amino acids; competing for binding sites, activating CNS receptors, altering neuronal function and mentation.
  27. Describe the benzodiazepine theory of HE.
    increased inhibitory GABA, increased production of endogenous GABA, increased inhibition, causing altered mentation, depression, head pressing, aggressive behavior, seizures.
  28. How do you treat/manage HE in horses? (8)
    lactulose (decreases pH and promotes ammonia trapping in the gut), mineral oil, sodium sulfate, activated charcoal, diuresis (decrease cerebral edema), antioxidants, neomycin, supportive therapy, +/- other antibiotics
  29. How is diagnosis of hepatic inflammatory disease achieved? (3)
    liver biopsy, histopathology, tissue culture (determine if bacterial etiology)
  30. Cholangitis is ______ in horses and is most often associated with ____________.
    rare; gram negative enteric organisms
  31. Tyzzer's disease occurs in __________ horses and is...
    young; severe, acute, fulimnant, necrotizing bacterial hepatitis caused by Clostridium piliformis [ingestion].
  32. Theiler's disease occurs in _________ horses with a....
    adult; history of biological products, like an antitoxin or blood transfusion.
  33. Clinical signs of Tyzzer's disease. (6)
    icterus, depression, encephalopathy, diarrhea, colic, acute death
  34. What is the prognosis for Tyzzer's disease?
  35. If you attempt treatment for Tyzzer's disease, what will you do? (5)
    penicillin, cephalosporins, metronidazole, oxytet, supportive care
  36. What is the etiology of Theiler's disease?
    equine adenovirus, gaining entry from administration of biological products
  37. What are clinical signs of Theiler's disease? (9)
    anorexia, icterus, pigmenturia, fever, edema, colic, photodermatitis, HE, 4-10 weeks after receiving biological products
  38. What is the prognosis for Theiler's disease?
  39. How do you diagnose Theiler's disease? (3)
    history, ultrasonography (small liver), histopath (centrilobular and midzonal necrosis/ hemorrhage)
  40. How do you treat Theiler's disease? (3)
    supportive care, minimize stress, treat HE
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GI2- Equine Liver Dz
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