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SMALL ANIMAL > 9.5.5: Chronic hepatobiliary disease > Flashcards

9.5.5: Chronic hepatobiliary disease Flashcards

1
Q

Causes chronic hepatitis

A
  • Idiopathic chronic hepatitis
  • Copper-associated liver disease
  • True copper storage disease
  • Congenital vascular disease
  • Neoplasia
  • Biliary tract disease
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2
Q

What is the most common liver disease in dogs?

A

Idiopathic chronic hepatitis

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3
Q

Breed predisposition for idiopathic chronic hepatitis

A
  • Cocker spaniels
  • Labs
  • Bedlington terrier
  • Springers
  • Standard Poodles
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4
Q

Breed predisposition for copper-associated storage disease

A
  • Labds
  • Dalmatians
  • Skye terries
  • Dobermanns
  • WHWT
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5
Q

Breed predisposition for true copper storage disease

A

Bedlington terriers

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6
Q

Examples of primary hepatic neoplasia

A
  • Hepatocellular carcinoma
  • Haemangiosarcoma
  • Biliary carcinoma
  • Biliary adenoma
  • Neuroendocrine tumours
  • Leiomyosarcoma
  • (Lymphoma)
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7
Q

Prevalence and presentation of secondary hepatic neoplasia

A
  • Liver = very common site for metastases
  • Can be clinically silent
  • Can haemorrhage e.g. met from splenic haemangiosarcoma
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8
Q

Examples of biliary tract disease

A
  • Biliary mucoceles
  • Neutrophilic cholangitis
  • Extrahepatic bile duct obstruction
  • Bile duct rupture
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9
Q

Signalment of canine chronic hepatitis

A
  • Breed predispositions: Cairn terriers, Dalmatians, Dobermanns, American and English Cocker Spaniels, English Springer Spaniels, Labs, Great Danes, Samoyeds
  • Most common in middle-aged and older animals ~8 y.o.
  • Seen younger in Springers and Dobermanns
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10
Q

Clinical signs of canine chronic hepatitis

A
  • Waxing and waning clinical signs
  • Inappetance
  • Weight loss
  • Vomiting ± haematemesis if GI ulceration
  • Diarrhoea ± melaenia
  • PUPD
  • Lethargy/ depression -> true neuro signs / hepatic encephalopathy
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11
Q

Presentation and significant clinical exam findings of canine chronic hepatitis

A

May present as a case not responding to conventional treatment e.g. repeat V+/D+ that is not responding to diet; OR dog with variable appetite that is now showing weight loss/ abdo distension

Significant clinical exam findings
* Poor BCS
* Jaundice
* Ascites

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12
Q

What does chronic liver injury result in?

A

Activation of ito cells and extracellular matrix production

-> formation of fibrosis

-> portal hypertension and loss of hepatocyte function

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13
Q

How to definitively diagnose canine chronic hepatitis

A

Take biopsy
Will see:
* Variable mononuclear or mixed inflammatory infiltrate
* Hepatocellular apoptosis or necrosis
* Regeneration and fibrosis

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14
Q

Treatment options for chronic liver disease

A
  • Ursodeoxycholic acid (UDA)
  • Antioxidants: SAMe, silybin/ silymarin, Vitamin E
  • Corticosteroids
  • Antibiotics
  • Diuretics
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15
Q

What is UDA and when is is useful? What must you remember when prescribing it?

A
  • Useful in liver diseases where cholestasis is present or suspected
  • Used under cascade in dogs and cats as no licensed options -> obtain owner consent for use
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16
Q

When are corticosteroids contraindicated in treatment of liver disease?

A
  • If it is end-stage/ there is cirrhosis / there is bridging fibrosis
  • If there is ascites / GI ulceration (= portal hypertension)
  • In there is a risk of undiagnosed infection (bacterial, viral or fungal)
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17
Q

Potential adverse effects of corticosteroids used to treat liver disease

A
  • Increased protein catabolism -> can cause or worsen hepatic encephalopathy
  • Fluid retention can cause or worsen ascites
  • Ulcerogenic effects -> can lead to GI ulceration (dexamethasone more so than prednisolone)
  • Increased risk of infection/ could exacerbate existing infection

Use with caution!

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18
Q

Justification of antibiotic use in liver disease

A
  • Management of hepatic encephalopathy - decreased ammonia formation by decreasing the bacterial load in the colon
  • If histopathology changes suggest ascending cholangitis/ significant neutrophilic component to any inflammation
  • Commonly appropriate choices: ampicillin, metronidazole; avoid fluoroquinolones unless culture and sensitivity
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19
Q

Management of ascites

A
  • Furosemide - monitor potassium as this is not potassium sparing
  • Spironolactone
  • Peritoneal drainage - only if life threatening because ascites reforms rapidly, and this contributes to dehydration and worsens hypoalbuminaemia
20
Q

Dietary management of chronic liver disease

A
  • High quality, highly digestible and palatable protein sources - avoid white fish
  • Complex carbohydrates preferred e.g. rice, pasta, potato
  • Fat - only restrict if steatorrhiea develops
  • Fibre - soluble and insoluble both good
  • Commercial liver diets are protein and copper restricted - best reserved for dogs with copper accumulation or evidence of protein intolerance (e.g. hepatic encephalopathy, urate urolithiasis)
21
Q

Prognosis and prognostic indicators for chronic liver disease

A

Prognosis very variable
* Might do well for years with supportive care
* Might have rapid deterioration despite good care

Negative prognostic indicators
* Ascites
* Jaundice

22
Q
A

Ascites

23
Q

Which type of PSS is shown here?

A

This is a normal liver

24
Q

Which type of PSS is shown here?

A

Intrahepatic PSS

25
Q

Which type of PSS is shown here?

A

Extrahepatic PSS

26
Q

Clinical signs of PSS

A
  • Neuro: lethargy, ataxia, obtundation, pacing, circling, blindness, seizures, coma
  • GI: vomiting, diarrhoea, anorexia, pica, melaena, haematemesis
  • Urinary: ammonium urate crystals -> haematuria, stranguria, pollakuria, urethral obstruction
27
Q

Treatment of PSS

A
  • Start by managing medically
  • Surgical treatment offers greater survival; various techniques available
28
Q

Clinical signs of hepatic neoplasia

A
  • Often non-specific clinical signs: lethargy, poor appetite
  • Signs may be associated with a complication e.g. abdo bleed if ruptured mass
  • Palpable mass may be the only sign e.g. abdo distension, discomfort
  • Signs often similar to chronic hepatitis
29
Q

Diagnosis of hepatic neoplasia

A
  • Lab findings may be similar to chronic hepatitis e.g. markers of hepatocellular damage, findings related to abdo bleed
  • Diagnostic imaging: radiography, ultrasonography
  • Definitive diagnosis: FNA for cytology, biopsy for histopath
30
Q

Treatment for hepatic neoplasia

A
  • Surgery = treatment of choice but assess for mets beforehand - take thoracic R, L lateral and DV rads with image taken on inflation (i.e. under GA) or consider CT
  • Chemotherapy only effective for lymphoma
31
Q

Signalment and cause of neutrophilic cholangitis

A

Signalment
* Uncommon in dogs. More common in cats

Cause
* Ascending infection/ haematogenous spread
* Organisms: Streps, E. coli, Klebsiella, Proteus spp.

32
Q

Clinical signs associated with neutrophilic cholangitis

A

Variable
* Pyrexia
* Vomiting
* Jaundice

33
Q

Clinical pathology associated with neutrophilic cholangitis

A
  • Variable liver enzyme elevations, increased bilirubin
  • Neutrophilia with/ without left shift
  • (Bacterial infection hence neutrophilia ±left shift)
34
Q

Diagnosis of neutrophilic cholangitis

A
  • Bile centesis
  • ± liver biopsy
35
Q

Treatment for neutrophilic cholangitis

A
  • Antibiotic treatment based on culture results
  • Treat for 8 weeks minimum
36
Q

Potential causes of extrahepatic bile duct obstruction

A
  • Pancreatitis
  • Pancreatic tumour
  • Bile duct tumour
  • Duodenal tumour / FB
  • Gallbladder mucocoele
  • Cholelithiasis
  • Local trauma, inflammation
  • Most common cause: secondary to acute or chronic hepatitis. Happens due to extrinsic compression of common bile duct into duodenum
37
Q

Clinical signs of extrahepatic bile duct obstruction

A
  • Signs relate to underlying reason for obstruction
  • Very variable and non-specific in the early syages
  • Depends on whether partial or complete obstruction
  • May start with mild abdominal pain
38
Q

Diagnosis of extrahepatic bile duct obstruction

A
  • Clin path: ALP, bilirubin usually v high. Other abnormalities associated with underlying cause.
  • Ultrasound: determine if cause can be seen e.g. pancreatitis, cholelith
39
Q

Causes of bile duct rupture

A

Usually the same as extrahepatic bile duct obstruction (EHBDO):
* Pancreatitis
* Pancreatic tumour
* Bile duct tumour
* Duodenal tumour/ FB
* Gallbladder mucocoele
* Cholelithiasis
* Local trauma, inflammation
* Acute / chronic hepatitis

40
Q

Management of extrahepatic bile duct obstruction

A
  • Medical management for pancreatitis
  • Other causes often require surgical mangement
41
Q

Consequences and clinical signs of bile duct rupture

A
  • Bile peritonitis -> abdominal effusion (may be infected if secondary to ascending cholangitis; important to culture abdo fluid in these cases)
  • Profound jaundice is common
42
Q

Treatment of bile duct rupture

A
  • Manage underlying cause
  • Cholecystectomy: histopath and culture of gallbladder wall for followup treatment decisions
43
Q

Indications for cholecystectomy

A
  • Ruptured gallbladder
  • Primary neoplasia of the gallbladder - very rare
  • Cholecystitis that is unresponsive to medical management
  • Gallbladder mucocoele
  • Cholelithiasis
44
Q

Diagnosis of cholelithiasis

A

Ultrasound

45
Q

Gallbladder mucocoele

A

distension of the gallbladder by inappropriate amounts of mucus (mucocoele).
* Quite uncommon
* Diagnosed on ultrasound
* Possibly associaed with endocrine diseases e.g. hypoT4, hyperadrenocorticism, hyperlipidaemia

46
Q

What should you do before a liver biopsy?

A

Run a clotting profile (assess coagulation factors to make sure your patient is stable enough to have the biopsy done)

47
Q

What is the most specific marker of hepatocellular injury in the dog?

A

ALT

SMALL ANIMAL (90 decks)

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