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SA Gastro > Canine and Feline Liver Disease > Flashcards

Canine and Feline Liver Disease Flashcards

1
Q

what are the causes of acute hepatitis?

A
  • hepatotoxins (CCl4, mycotoxins, xylitol)
  • drugs (acetaminophen in cats, azathioprine, trimethoprim-sulfa)
  • mushrooms (Amanita)
  • viruses
  • sago palm (when ingested, esp in FL)
  • cause usually can’t be found so get histo diagnosis of just toxic hepatitis
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2
Q

how is acute hepatitis diagnosed?

A
  • increase in ALT and AST
  • ALP normal or mildly increased
  • increase in serum bilirubin if many hepatocytes affected
  • liver biopsy not helpful or essential
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3
Q

how is acute hepatitis managed?

A
  • good prognosis if cause found, stop any suspected drugs
  • supportive care w/ fluids
  • anti-emetics
  • nutritional support
  • antioxidants maybe, especially if amanita mushroom toxicity
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4
Q

what are the possible causes of chronic hepatitis in the dog?

A

leptospirosis

drugs (phenobarbital)

copper metabolism

idiopathic

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5
Q

which breeds are prone to chronic hepatitis?

A

Dobermans, Cocker Spaniels, Labrador Retrievers

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6
Q

which breeds are susceptible to copper-associated hepatopathy?

A

Dalmation, Bedlington terrier, West Highland white terrier, Labradors

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7
Q

how is chronic hepatitis managed?

A
  • remove the cause (drugs, copper)
  • anti-inflammatories (GCs usually)
  • antioxidants
  • supportive therapy
  • copper chelators for copper related disease, copper restricted diet
  • UCDA (bile acid to prevent apoptosis and mitochondrial damage, increase bile flow, immunodilating effects)
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8
Q

what are the two forms of cholangitis in the cat?

A

neutrophilic and lymphocytic

based on type of infiltrate in the bile duct lumen and/or biliary epithelium, need a liver biopsy and bile culture to diagnose

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9
Q

what are the signs of neutrophilic cholangitis?

A
  • fever, lethargy, vomiting, jaundice
  • may be acute or chronic
  • thought to be from ascending bacterial infection from intestine
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10
Q

what are the signs of lymphocytic cholangitis?

A
  • ascites and jaundice
  • may be from some initiating factors that triggers immune-mediated mechanisms that perpetuate liver pathology
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11
Q

what is triaditis?

A

cholangitis + pancreatitis + inflammatory bowel disease

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12
Q

what is the treatment for neutrophilic cholangitis?

A
  • antibiotic therapy (based on culture), E. coli usually the culprit
  • glucocorticoids for inflammation
  • cholecystectomy: in cases with inspissated bile and biliary duct obstruction
  • fluid therapy and nutritional support
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13
Q

what is the treatment for lymphocytic cholangitis (and chronic neutrophilic/mixed inflammatory)?

A
  • glucocorticoids at immunosuppressive doses
  • may treat with antibiotics if suspect chronic neutrophilic cholangitis
  • fluids, nutritional, antioxidant support
  • with ascites, give low Na+ diet and diuretics
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14
Q

what is the most common liver disease of the cat?

A

hepatic lipidosis

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15
Q

what are the causes of feline hepatic lipidosis?

A
  • may be primary idiopathic or secondary
  • no confirmed etiology
  • from formation of a metabolic disorder
  • believed to be related to pathogenesis of malnutrition
  • obesity = increased risk
  • increased risk from sudden rapid weight loss or decreased calorie intake
  • may be related to negative nitrogen balance
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16
Q

what are the lab findings with feline hepatic lipidosis?

A
  • dramatic increase in ALP (short half life so only see with disease)
  • increase in ALT (higher than ALP, may have lipidosis and another liver disease)
  • moderate increase in AST
  • normal or mildly increased GGT
  • normocytic, normochromic, non-regenerative anemia
17
Q

what are some additional ways to diagnose feline hepatic lipidosis?

A
  • history of anorexia, fat cat with muscle wasting, or increased ALP with normal GGT
  • hepatomegaly in x-ray with rounded margins
  • hyperechogenic ultrasound of liver
  • may make diagnosis off tissue aspiration, careful not to misinterpret normal fat vacuoles
18
Q

how is feline hepatic lipidosis managed?

A
  • nutritional support (60 kcal/kg/day at least)
  • treat any concurrent illness/underlying cause
  • usually place an E-tube
  • metoclopramide or cisapride for delayed gastric emptying
  • antiemetics if vomiting
19
Q

extrahepatic biliary obstruction

A

impairment of bile flow in biliary system between liver and duodenum

20
Q

what are the clinical signs of extrahepatic biliary obstruction?

A

very general, vomiting, lethargy, inappetance

21
Q

how is extrahepatic biliary obstruction diagnosed?

A

marked increase in ALP (always higher than ALT), can only confirm by laparotomy

22
Q

what are the causes of extrahepatic biliary obstruction?

A

pancreatitis in the dog

pancreatic and biliary neoplasia in the cat

23
Q

how is extrahepatic biliary obstruction managed?

A

medically, non-resolving may need surgical correction

24
Q

what is a congenital portosystemic shunt?

A

abnormal development of hepatic portal circulation

25
Q

what are the pre-dispositions for congenital portosystemic shunts?

A

young dogs that are “small” for their age and “don’t do well”

yorkies, miniature Schnauzers, and Maltese predisposed

Irish wolfhound increased frequency

26
Q

intrahepatic shunts are more common in which animals?

A

large breed dogs

27
Q

extrahepatic shunts are more common in which animals?

A

cats and small breed dogs

28
Q

what is the clinical presentation of portosystemic shunt and hepatic encephalopathy in cats?

A

small stature, ptyalism, copper irises

may see PU/PD and urate stones

29
Q

what are the lab findings with portosystemic shunt and hepatic encephalopathy?

A
  • biochemical profile may be normal
  • ALT, AST, ALP, and GGT may be normal or mildly increased
  • ammonium biurate crystals in urine
  • low urea nitrogen, albumin, and glucose, microcytic anemia from low iron (decreased synthesis)
  • one or more liver function tests abnormal (bile acids, ammonia)
30
Q

what are the diagnostic imaging techniques used to diagnose portosystemic shunt and hepatic encephalopathy?

A
  • ultrasound: may see small aortic to portal vein ratio, renomegaly, may visualize shunt
  • CT angiogram
  • transplenic scintigraphy: not used anymore
31
Q

How are portosystemic shunt and hepatic encephalopathy managed?

A
  • controversy over best tx
  • medical: restricted protein, high quality diet and lactulose, antibiotics (acute), stabilize medically before surgery
  • surgical ligation of shunt (through jug to CVC and block vessel, cellophane banding, ameroid constrictor)
32
Q

how does hepatology in cats differ from dogs?

A
  • common bile duct and pancreatic duct join before entering duodenal papilla
  • glucouronyltransferase deficiency (excrete NSAIDs and secrete bilirubin slower)
  • gluconeogenesis never shuts down when fasting
  • can’t synthesize arginine (encephalopathy with arg deficient diet)
  • need taurine to conjugate bile acids
  • AST increase less dramatic, associated with muscular dystrophy
  • ALP in response to epithelial stimulus, suggest hepatic disease
  • jaundice earlier than dogs b/c of reduced glutathione concentrations and decreased secretory ability
  • high renal threshold for bilirubin
  • bile acids sensitive for liver function
  • rare hypoalbuminemia in cats with liver disease
  • hyperglobulinemia can be concurrent with liver disease
33
Q

what is vacuolar hepatopathy?

A

glycogen accumulation in liver vacuoles due to steroids (endogenous or exogenous)

34
Q

what are the clinical signs of vacuolar hepatopathy?

A

PU/PD, polyphagia, panting, swollen abdomen, ALP increase with normal bilirubin (diagnosed by liver aspirate/biopsy)

SA Gastro (11 decks)

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