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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
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
Which type of PSS is shown here?
Extrahepatic PSS
26
Clinical signs of PSS
* 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
Treatment of PSS
* Start by managing medically * Surgical treatment offers greater survival; various techniques available
28
Clinical signs of hepatic neoplasia
* 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
Diagnosis of hepatic neoplasia
* 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
Treatment for hepatic neoplasia
* 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
Signalment and cause of **neutrophilic cholangitis**
Signalment * Uncommon in dogs. More common in cats Cause * Ascending infection/ haematogenous spread * Organisms: Streps, *E. coli*, *Klebsiella, Proteus* spp.
32
Clinical signs associated with **neutrophilic cholangitis**
Variable * Pyrexia * Vomiting * Jaundice
33
Clinical pathology associated with **neutrophilic cholangitis**
* Variable liver enzyme elevations, increased bilirubin * Neutrophilia with/ without left shift * (Bacterial infection hence neutrophilia ±left shift)
34
Diagnosis of **neutrophilic cholangitis**
* Bile centesis * ± liver biopsy
35
Treatment for **neutrophilic cholangitis**
* Antibiotic treatment based on culture results * Treat for 8 weeks minimum
36
Potential causes of extrahepatic bile duct obstruction
* 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
Clinical signs of extrahepatic bile duct obstruction
* 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
Diagnosis of extrahepatic bile duct obstruction
* 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
Causes of bile duct rupture
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
Management of extrahepatic bile duct obstruction
* Medical management for pancreatitis * Other causes often require surgical mangement
41
Consequences and clinical signs of bile duct rupture
* 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
Treatment of bile duct rupture
* Manage underlying cause * Cholecystectomy: histopath and culture of gallbladder wall for followup treatment decisions
43
Indications for cholecystectomy
* Ruptured gallbladder * Primary neoplasia of the gallbladder - very rare * Cholecystitis that is unresponsive to medical management * Gallbladder mucocoele * Cholelithiasis
44
Diagnosis of cholelithiasis
Ultrasound
45
**Gallbladder mucocoele**
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
What should you do before a liver biopsy?
Run a clotting profile (assess coagulation factors to make sure your patient is stable enough to have the biopsy done)
47
What is the most specific marker of hepatocellular injury in the dog?
ALT

SMALL ANIMAL (90 decks)

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