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Small Animal Medicine II > Feline Hepatobiliary Disease > Flashcards

Feline Hepatobiliary Disease Flashcards

1
Q

How is feline liver enzyme increase different compared to dogs?

A

elevations are more significant due to their shorter half-lives

  • ALT = leakage enzyme from damaged hepatocytes (T1/2 = 6 hr)
  • ALP = membrane-bound, cats lack cALP and contain overall less compared to dogs = increase is ALWAYS significant (T1/2 = 6 hr)
  • AST = in cytosol and mitochondria (T1/2 = 77 min)
  • GGT = on hepatocellular membrane (cholestasis)
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2
Q

What are the 5 most common liver diseases in cats?

A
  1. hepatic lipidosis
  2. feline inflammatory diseases
  3. lymphoma
  4. FIP
  5. Toxoplasma, fungal
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3
Q

What is the difference between cholangitis, choledochitis, cholecystitis, and cholangiohepatitis?

A

inflammation of the biliary tree

inflammation of the bile ducts

inflammation of the GB

hepatic inflammation centered on the biliary tract extending into adjacent hepatic parenchyma

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4
Q

What are the 4 major categories of cholangitis in cats?

A
  1. neutrophilic*
  2. lymphocytic (or lymphoplasmacytic)*
  3. destructive - bile ducts targeted and destroyed, end-stage lymphocytic
  4. chronic cholangitis associated with fluke infestation
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5
Q

What signalment is associated with feline neutrophilic cholangitis? What is thought to be the cause?

A

any age, breed, and sex –> acute form tends to occur in younger to middle-aged

ascending bacterial (E. coli most common) infection from the GIT (breach duodenal papilla) up the biliary tree +/- hematogenous spread

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6
Q

What clinical signs are associated with feline neutrophilic cholangitis?

A
  • abdominal pain
  • vomiting
  • diarrhea
  • anorexia
  • fever
  • dehydration
  • icterus
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7
Q

What is seen on clinicopathology and AUS in cases of feline neutrophilic cholangitis? What is diagnosis based on?

A

leukocytosis +/- left shift with variable increased liver enzyme activity (ALT, ALP, GGT) and hyperbilirubinemia

hyper/hypoechoic liver with bile duct dilation +/- GB debris –> 60% of cats are normal!

cholecystocentesis for bile analysis and culture and liver biopsies for evidence of neutrophilic inflammation

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8
Q

GB and liver, U/S

A
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9
Q

Bile culture and cytology:

A

neutrophilic –> inflammatory cells + bacteria

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10
Q

When is percutaneous cholecystocentesis performed? Complications are rare, but what are 3 possibilities?

A

cats with suspected hepatobiliary disease

  1. intraperitoneal bile leakage
  2. hemorrhage
  3. vasovagal reaction - respiratory arrest, severe bradycardia, death - have Atropine ready!
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11
Q

What 3 things are included in medical treatment of feline neutrophilic cholangitis? What are the most common bacterial etiologies?

A
  1. antimicrobials - E. coli, Enterococcus, anaerobes -potentiated penicillin for broad-spectrum coverage (Clavamox, Unasyn), add fluoroquinolones for G- coverage
  2. Ursodiol
  3. supportive care
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12
Q

What commonly concurrently occurs with chronic forms of feline neutrophilic cholangitis? What treatment is necessary?

A

IBD, pancreatitis (triaditis!), extrahepatic biliary obstruction

anti-inflammatories, antibiotics, Ursodiol, Prednisone –> can be cured!

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13
Q

How does feline lymphocytic cholangitis affect the liver? What concurrent diseases are associated? What are the most common clinical signs?

A

slowly progressive disease - lymphocytic inflammation +/- fibrosis and bile duct hyperplasia

IBD and pancreatitis

non-specific anorexia, vomiting, lethargy, or weight loss with icterus and hepatomegaly

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14
Q

How is feline lymphocytic cholangitis diagnosed? What 3 treatments are indicated?

A

liver biopsy and cholecystocentesis for bile culture

  1. antibiotics as indicate if bacteria are present or culture is positive
  2. Prednisone +/- additional immunosuppressive (Chlorambucil, Cyclosporine)
  3. Ursodiol
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15
Q

What are the 2 most flukes that can infect feline livers/

A
  1. Platynosomum concinnum (fatosum) - Florida, Hawaii, tropical areas
  2. Amphimerus pseudofelineus
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16
Q

How are liver flukes transmitted? How do they affect the hepatobiliary system?

A

ingestion by secondary host (slugs, mollusks, fish) containing the fluke

  • young flukes emerge in the intestines and migrate into the CBD, GB, or hepatic ducts
  • embryonated eggs pass from bile into the intestines
  • eggs shed in feces as early as 12 weeks after infection (fecal examination can fail to detect eggs!)
17
Q

What treatments are recommended for cases of liver flukes?

A
  • Praziquantel for 3-5 days
  • surgical removal
  • Prednisolone to reduce eosinophilic inflammation
  • broad-spectrum antibiotics
  • Ursodiol

(eggs can be detected in feces up to 2 months after successful treatment)

18
Q

What is the most common hepatobiliary disease in cats? What incited it?

A

hepatic lipidosis

negative energy balance –> anorexia (2 days to 2 weeks)

19
Q

What are 4 effects of negative energy balances?

A
  1. influx of NEFAs derived from peripheral fat stores
  2. de novo synthesis of fats
  3. increased rate of hepatic FA oxidation
  4. dispersal of hepatic triglycerides via excretion of VLDLs
20
Q

What causes primary and secondary hepatic lipidosis?

A

PRIMARY = decreased food availability, nonpalatable food, stress

SECONDARY = underlying disease, like DM, pancreatitis, inflammatory hepatobiliary disease, GI disease, renal failure, neoplasia

21
Q

What cats are most commonly affected by hepatic lipidosis?

A
  • middle-aged
  • higher BCS (more fat to metabolize when in a negative energy balance!)
  • history of anorexia and weight loss
22
Q

What is a characteristic sign of hepatic lipidosis in cats? What else is seen?

A

ptyalism - nausea, hepatic encephalopathy due to arginine deficiency impairing the urea cycle

  • icterus
  • vomiting
  • constipation, diarrhea
23
Q

What are 7 signs of hepatic lipidosis on bloodwork?

A
  1. increased ALP +/- ALT
  2. normal GGT
  3. hyperbilirubinemia
  4. decreased/increased glucose
  5. decreased albumin
  6. hypokalemia
  7. coagulation abnormalities –> check MBBT and give vitamin K if needed
24
Q

What are 3 parts to diagnosing hepatic lipidosis?

A
  1. AUS - enlarged and hyperechoic due to increased fat content
  2. FNA and cytology - hepatocytes full of fat
  3. histopathology - underlying liver disease
25
Q

What is the most important part of treating hepatic lipidosis?

A

feed a high protein, calorically dense diet through feeding tubes, starting with 1/3 to 1/4 RER and slowly increase to RER over 3-4 days

  • do NOT rely on appetite stimulants and AVOID syringe feeding
  • without nutrition, stomach will shrink and insulin release will further the hypokalemia and cause hypophosphatemia
26
Q

What are 3 options of feeding tubes used in cats with hepatic lipidosis?

A
  1. nasoesophageal feeding tube until stable
  2. esophagostomy tube - can be left in for months
  3. PEG tube - port in the stomach can be left for years

can remove 7 days past eating by itself

27
Q

What supportive care is recommended in cases of hepatic lipidosis? What is prognosis like?

A
  • antiemetics
  • vitamin K or plasma
  • antioxidants/fatty acid oxidation - B12, thiamine, SAMe, carnitine

good with early enteral nutrition

28
Q

What 3 hepatobiliary neoplasia are common in cats?

A
  1. biliary cystadenoma - benign, good prognosis with liver lobectomy, only clinical if it’s large enough to affect function of other organs or the liver
  2. biliary cystadenocarcinoma - malignant, lobectomy if focal to one lobe, poor prognosis if multifocal to diffuse
  3. lymphoma

Small Animal Medicine II (57 decks)

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