EqMed Q2, Liver Dz I

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EqMed Q2, Liver Dz I
2013-04-11 17:43:37
EqMed Q2 Liver Dz

EqMed Q2, Liver Dz I
Show Answers:

  1. How much of the liver is damaged before C/S?
  2. what are some of the classic c/s of liver Dz? 6
    • Icterus
    • Depression/neurologic disease
    • Anorexia/wt loss
    • Photosensitization
    • Colic/diarrhea
    • Hemorrhage (end stage)
  3. Liver enzymes suggestive of hepatocellular injury?
    • SDH
    • AST
    • (ALT not reliable in large animals)
  4. Liver specific enzyme with short 1/2 life?
    SDH (sorbitol dehydrogenase)
  5. Where else does AST come from?
    • Liver
    • Muscle
    • RBCs
  6. What enzymes are suggestive of cholestasis?
    • GGT
    • ALP
  7. What liver enzyme is elevated in healthy young horses due to bone isoform?
  8. what are liver functions indicators?
    • *Albumin*
    • *Glucose*
    • *BUN*
    • *Bilirubin*
    • Bile acids
    • Ammonia
    • Coagulation tests
  9. If bilirubin is elevated due to inappetance, will elevation be due to conjugated/direct or unconjugated/indirect form?


    Liganden, which conjugates bilirubin, has short 1/2 life in face of anorexia
  10. does direct or indirect bilirubin increase with cholestasis?


    Its conjugated in liver but cholestasis impedes elimination
  11. Why is it unnecessary to fast a horse before bile acid?
    • No gall bladder
    • (steady release regardless)
  12. Is it helpful to do bile acids test if the horse is icteric?
    Yes, in horses it is still indicated
  13. Where is US probe placed to visualize liver?
    • L: 7-9th ICS
    • R: 6-15th ICS
    • Ventral to lung margins
    • Within costrochondral jx
  14. where should liver biopsy be taken from (anatomical land marks)?
    • R: 11-14 ICS
    • Angle from point of hip down to elbow
    • Aim cranio-ventral
  15. What is first step for treating hepatic encephalopathy?
    • Sedation
    • *detomidine* alpha 2 agonist
    • (Self Trauma or injury to others)
  16. Why are benzodiazepines a poor choice for sedation in a horse with HE?
    Elevated ammonia already upregulates GABA;

    Benzo's have same MOA so can worsen the condition
  17. Although controversial what are some options for reducing ammonia formation in the gut? 3
    • oral neomycin
    • oral lactulose
    • acetic acid/vinegar
  18. Benefits of dextrose CRI in a hypoglycemic horse with liver Dz?
    • Decr. [Ammonia]¬†
    • Reduc catabolic gluconeogenesis (Work load on liver)
    • Decr. protein catabolism
  19. Glucose should be maintained between 80-120. what is a non-invasive way to monitor?
    U/A - renal threshold = 180
  20. Do appropriate liver diets have more aromatic or branch chain AA?
    • avoid aromatics
    • more Branch chain AA
  21. what are some good choices for feeding horse with liver disease?
    • Oats
    • Grass hay

    • Supplements:
    • Beet pulp
    • Milo
    • Sorghum
    • (avoid alfalfa)
    • *feed something, even if not ideal diet*
  22. When are ABx indicated for liver Dz? 4
    • Biopsy = inflammatory infiltrates
    • Positive culture/sensitivity
    • Chronic active hepatitis
    • Cholangiohepatitis
  23. What Abx concentrate in the liver and biliary tract? 5
    • Penicllin/Gentamicin
    • Enrofloxacin
    • Chloramphenicol
    • TMS
    • +/- metronidazole
  24. Benefits of pentoxyfilline to horse with liver Dz?

    What other drug may be helpful?
    • Cheap
    • Anti-fibrotic¬†
    • Anti-oxidant
    • Anti-inflammatory

    Flunixin meglumine
  25. Benefits of SAMe?
    • Antioxidant
    • Hepatoprotectant
  26. What is another drug option that acts as free radical scavenger and can potentially dissolve biliary stones/sludge?
    DMSO - dimethyl sulfoxide
  27. Why is Actigall (ursodeoxycholic acid) not used in horses?
    • Toxic effects in rabbits/Hind gut fermenters
    • Used to Tx choleresis in SA Med
  28. Sx can be performed when biliary stones are located where?
    When is Sx not an option?
    • Distal bile duct
    • No fibrosis
  29. What is the most common cause of acute hepatitis in the horse?

    Idiopathic Acute Hepatitis Disease

    • aka:
    • Theiler's disease
    • Serum sickness
    • Post-vx hepatitis
  30. What part of the hepatocyte is most affected by acute hepatitis?

    How long after giving biologics (vx, plasma, etc) can signs be seen?
    Centrilobar necrosis (most O2 dependent part)

    30-70 days post administration