GI2- SA Liver Dz Cont...

  1. What is the treatment of congenital PSS? (4)
    protein-restricted diet, lactulose, antibiotics, surgical coil
  2. Describe microvascular dysplasia.
    lab abnormalities and clinical signs similar to PSS but milder, probably doesn't need treatment
  3. Diagnostically, compare PSS to microvascular dysplasia.
    macroscopic imaging shows nothing for microvascular dysplasia (unlike PSS); histologically, both look the same (portal hypoperfusion)
  4. What is treatment for microvascular dysplasia?
    no treatment required (usually) +/- symptomatic therapy (medically manage hepatic encephalopathy)
  5. What are the most common disorders associated with metabolic dysfunction? (3)
    acute liver injury/failure, canine chronic hepatitis/cirrhosis, feline hepatic lipidosis
  6. What are the most common disorders associated with biliary tract dysfunction? (2)
    feline neutrophilic cholangitis, common bile duct obstruction
  7. What are the most common disorders associated with circulatory dysfunction? (2)
    congenital PSS, microvascular dysplasia
  8. 2 reasons that the liver is uniquely susceptible to toxins.
    • directly exposed to high concs of ingested drugs (portal blood flow)
    • central role in drug metabolism- P45- can generate unstable toxic metabolites
  9. Liver dysfunction occurring in the absence of known pre-existing liver disease.
    acute liver disease
  10. Liver dysfunction occurring in the absence of known pre-existing liver disease plus hepatic encephalopathy and coagulopathy.
    acute liver failure
  11. What are potential causes of acute liver injury? (6)
    drugs/toxins, infectious agents, systemic or metabolic disorders, traumatic, thermal, or hypoxic injury
  12. What drugs are often associated with acute liver injury? (6)
    Acetominophen, Carprofen, Diazepman, Itra-/Ketoconazole, Methimazole, Sulfonamides
  13. What are the 2 types of hepatic drug reactions?
    intrinsic (predictable), idiosyncratic (unpredictable)
  14. Describe predictable hepatotoxins. (5)
    dose-related, short latent period, affects all individuals, reproducible experimentally, parent drug or reliably generated toxic metabolite
  15. Describe idiosyncratic hepatotoxins. (5)
    +/- dose-related, variable latency, infrequent (a few individuals may have a reaction), hard to detect on pre-market screening, must discontinue drug
  16. What are potential factors for hepatic drug reactions? (4)
    genetic polymorphism in P450s, competition by other drugs (induction of P450), +/- breed predisposition, +/- pre-existing liver disease
  17. When should you suspect drug-induced liver disease? (4)
    asymptomatic liver enzyme elevations, acute hepatic injury, chronic hepatic disease, every patient with liver disease is suspect drug-induced
  18. How can you document drug-induced liver injury, and how is it treated?
    • Difficult to document- don't drug re-challenge (dangerous), liver biopsy not specific
    • Treat- discontinue suspect drug, +/-antidotes, supportive care
  19. What are potential hepatotoxins (other than drugs)? (5)
    aflatoxin (diet), amanita mushroom, blue-green algae, sago palms, xylitol
  20. What is a historical cause of acute liver injury?
    infectious canine hepatitis- "blue eye"
  21. Give an example of a systemic/metabolic disorder that causes acute liver injury.
    acute pancreatitis
  22. What historical questions should you ask when assessing acute liver injury? (4)
    • drugs or dietary supplements?
    • potential toxin exposure (diet, free-roaming)?
    • exposure to other sick animals (infectious)?
    • vaccination history?
  23. How do you diagnose acute liver injury? (5 categories)
    • history of exposure
    • acute liver failure- HE, coagulopathy, +/- icterus
    • necrosis- high ALT, AST
    • metabolic dysfunction- coagulopathy, hypoglycemia, increased ammonia, +/- hyperbili
    • variable imaging
  24. What signs are suggestive of acute hepatic injury (as opposed to chronic)? (5)
    sudden onset signs, good body condition, no ascites, no hypoalbuminemia, or no microhepatica
  25. What is the most common histopathological lesion associated with acute liver injury?
    hepatic necrosis
  26. Describe liver biopsy with respect to acute liver injury. (3)
    differentiate acute from chronic, lesions are almost never pathognomonic (usually "consistent with..."), +/- dx infectious causes
  27. An animal comes in and you decide it has acute liver injury, what are the first actions you should take? (3)
    discontinue suspect drugs (as long as they aren't necessary for life), treat Lepto off the bat w/ doxy or amoxi (takes too long to get definite dx), +/- antidotes
  28. Canine chronic hepatitis can progress to __________, which is irreversible; conversely, another sequelae, __________, is, to some degree, reversible.
    cirrhosis; fibrosis
  29. What are the 2 causes of canine chronic hepatitis that we can reliably identify (other causes are usually not identified)?
    copper toxicity, chronic phenobarb therapy
  30. What are the defining characteristics of hepatic cirrhosis? (4)
    irreversible, fibrosis, regenerative nodules, loss of architecture
  31. What are etiologies of canine chronic hepatitis? (5)
    • infectious- Lepto, Leishmania, +/- viral
    • familial- copper
    • drugs and toxins
    • +/- autoimmune
    • idiopathic
  32. What stain is used on liver biopsy samples to identify copper toxicity?
    rhodanine stain
  33. Describe copper metabolism.
    dietary intake--> intestinal absorption--> portal delivery to liver--> hepatic metabolism and storage--> secreted in bile--> feces
  34. What is the poster child of copper-associated chronic hepatitis?
    Other common breeds?
    Bedlington terrier; Doberman, Westies, Skye Terrier, Dalmation, Lab
  35. Hepatotoxic levels of copper are >_________, causing _________ injury.
    2000ppm; oxidant
  36. Describe pathogenesis of primary copper hepatopathy.
    primary copper retention centrolobularly--> hepatic copper accumulation--> chronic hepatitis--> cirrhosis
  37. Describe pathogenesis of secondary copper hepatopathy.
    chronic hepatitis--> cholestasis--> decreased copper excretion--> secondary hepatic copper accumulation periportally
  38. How do you diagnose copper-associated liver disease? (7)
    signalement, signs (variable), increased ALT, +/- cholestasis (if secondary), +/- metabolic dysfunction (if severe), +/- small liver if advanced), [definitive] liver biopsy and quantification of liver copper levels
  39. How do you treat/manage copper-associated liver disease? (4)
    low copper diet, penicillamine (get a definitive dx before you use this- expensive, risky, takes months to work), zinc (decreases copper absorption), Vit E (antioxidant)
  40. Describe the clinical presentation associated with idiopathic chronic hepatitis. (6)
    chronic liver disease, ask about drug therapy, lab indicative of hepatocellular injury +/- cholestasis, metabolic dysfunction, small liver on imaging
  41. How do you definitively diagnose idiopathic hepatitis?
    liver biopsy (fibrosis, most commonly lymphoplasmacytic) and rule out causes
  42. What are the goals of therapy of chronic hepatitis? (4)
    decrease inflammation (steroids), reduce hepatic copper (penacillamine, zinc), prevent oxidant injury (Vit E, SAMe), promote choleresis (Orsodiol)
  43. How do you monitor response to therapy with chronic idiopathic hepatitis?
    US guided needle biopsy
  44. What are the effects of phenobarbitol on the liver?
    • Almost all dogs: increased ALP +/- ALT 
    • Rarely: chronic hepatitis and cirrhosis, increased ALT, increased SBA, hyperbili, decreased albumin
  45. Phenobarb has caused chronic hepatitis and cirrhosis as serum levels >_________.
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GI2- SA Liver Dz Cont...
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