27. Hepatobillary Disease Flashcards

1
Q

Common diseases affecting the hepatobillary system?

A

Jaundice
Acute hepatopathy/hepatitis:
Canine chronic hepatitis:
Feline hepatic lipidosis:
Feline Inflammatory liver disease:
Hepatic encephalopathy

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2
Q

Jaundice Pathophysiology?

A

Jaundice;
Pathophysiology:
-Divided Into three types:
- Pre-hepatic:
> incr Production of haemoglobin due to haemolysis
- Hepatic:
> incr Uptake and conjugation due to hepatic failure
>Hepatic excretion
- Post-hepatic:
> Removal due to billary obstruction

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3
Q

Causes of Jaundice?

A

Causes:
- Pre-hepatic:
> Immune-mediated haemolytic anaemia
- Toxic: Snake, onions/garlic, paracetamol
> Bacterial: Mycoplasma haemofelis
“’ Hepatic:
» Hepatitis: Severe acute
• Toxic: Plants, mycotoxin
Inflammatory: Hepatitis, cholanglohepatitis, neoplasia
Infectious: Bacterial (leptospirosis), parasitic {migrating larvae, toxoplasma)
“’ Post-hepatic:
» BIiiary tract obstruction: Biliary stones or mucocele
> Duodenal foreign body: Blocking duodenal papillae)

-Pancreatitis

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4
Q

Clinical signs of Jaundice?

A

Clinical signs:”’ Icteric mucous membranes and sclera
“’ Clinical signs associated with underlying cause

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5
Q

Jaundice diagnostics?

A

Diagnostics:
“’ Pre-hepatic:
PCV/TP, lcteric serum
- Spherocytes
- Autoagglutination
“’ Hepatic:
Bilirubin, incr ALP, GGT, +/- incr ALT, AST
» Ultrasound: +/- Liver pathology
“’ Post-hepatic:
>Incr Bilirubin, Incr ALP, GGT
» Ultrasound: Biliary tract congestion, biliary stones, mucocele, pancreatitis

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6
Q

Jaundice treatment?

A

Treatment:
As per the underlying condition
Consider antibiotics for post-hepatic obstruction as biliary stasis is a high risk of infection

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7
Q

Acute hepatitis clinical signs?

A

Acute hepatopathy/hepatitis;
Clinical signs:
Acute onset,

  • anorexia,
  • vomiting,
  • cranial abdominal pain,
  • Jaundice,
  • bleeding,
  • hepatic encephalopathy,
    seizures
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8
Q

Acute hepatitis Diagnostics?

A

Diagnostics:
Biochemistry:
Elevated liver enzymes especially ALT and AST, ALP, bilirubin, bile acids, hypoproteinaemia,
hypoglycaemia
Haematology:
Anaemia, thrombocytopenia
Ultrasound: May not see any specific changes
Biopsy: May show non-specific changes

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9
Q

Acute hepatitis causes?

A

Causes:
Infectious (bacterial, viral, protozoal, parasitic, algae),

toxicity (paracetamol, cycad Ingestion),
neoplastic, pancreatitis, IBD etc.

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10
Q

Acute hepatitis treatment?

A

Treatment:
- Supportive therapy.
- IV fluids and electrolytes
- Antiemetic: Metoclopramide 0.5mg/kg TID, maropitant 1mg/kg SC SID for <5 days
- Gastric protectants: Proton pump Inhibitors, H2 antagonist (famotidine), sucralfate
- Antibiotics:
- Depending on cause
> Metronidazole 7 .5mg/kg Coagulopathy:
> Plasma for coagulopathy
> Vitamin K1 injection, single dose 5mg/kg SC, +/- continue with 2.5mg/kg PO BID
Adjunctive therapy:
> Antioxidants:
Vitamin E 400 IU PO SID and Vitamin C
• S-Adenosy·L·methlonlne (SAMe): Potent antioxidant 20mg/kg PO SID
)> Choleretic:
• Ursodeoxycholic acid (Actigall ®): 10-15mg/kg PO SID, only if no biliary tract obstruction ·
) Paracetamol toxicity:
• N-Acetylcystelrie: 140mg/kg IV initially (diluted In saline), then 70mg/kg IV or PO QID for 5 doses
Neurological signs:
avoid benzodiazepines, use propofol to stop seizures and begin
phenobarbitone or levetiracetam

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11
Q

Canine chronic hepatitis pathophysiology?

A

Canine chronic hepatitis:
Pathophysiology:
- Syndrome characterised by hepatic degeneration and necrosis leading to fibrosis, causes can Include:
Idiopathic: Most common
> Recurrent pancreatitis/lBD, biliary tract disease (obstruction, inflammation)
-Toxicity/drug: Chronic exposure
- Inflammation (lmmune mediated, fungal, bacterial, viral (adenovirus))
> Breed-specific copper accumulation disorders (Bedlington terriers, West Highland Terriers,
Dalmatians, Dobermans)

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12
Q

Canine chronic hepatitis clinical signs?

A

Clinical signs:
Anorexia, lethargy, vomiting, weight loss, jaundice, PU/PD, ascites (portal hypertension or
hypoalbuminaemia)
- Behaviour changes: Disorientation, head pressing, ataxia, pacing, seizures, circling

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13
Q

Diagnostics of chronic canine hepatitis?

A

Diagnostics:

  • Haematology and biochemistry:
  • Variable changes in haematology
  • Usually elevated ALT, bilirubin and paired serum bile acids
  • But signs of liver dysfunction: Low albumin, urea, glucose, coagulopathy
  • +/- Coagulopathy
  • Ultrasound
  • Biopsy: Definitive diagnosis, histopathology and culture and sensitivity
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14
Q

Treatment of canine chronic hepatitis?

A

Treatment:
- Treatment for specific disease according to diagnosis based on biopsy
- Supportive therapy:
» IV fluids and electrolytes
> Antiemetic: Metoclopramide O.5mg/kg TID, maropitant 1 mg/l<:g SC SID for <5 days
- Gastric protectants: Proton pump Inhibitors, H2 antagonist (famotidine), sucralfate
- Coagulopathies: Plasma and Vitamin K
- Adjunctive: Based on definitive diagnosis
- Diet as for “Hepatic encephalopathy”· protein restriction to minimise hepatic workload or protein
Intolerance
> lmmunosuppressive therapy:
• Prednisolone O.5mg/kg PO BID
• +/- Azathloprine 2mglkg PO SID until remission then O.5mg/kg PO EOD, monitor for bone
marrow suppression and hepatoxicity, also very toxic In cats
-Anti-fibrotic:
• Colchicine 0.03mg/kg PO BID
> Copper chelation:
D-penicillamine 10-15mg/kg PO 810
Zinc acetate 5mg/kg PO BID (max dose 100mg BID)
Anti-oxidants:
• Vitamin E 400 IU PO SID
S-Adenosy-L-methionine (SAMe): Potent anti-oxidant 20mg/kg PO SID
Milk thistle
> Choleretic:
Ursodeoxycholic acid (Acligall ®): 10· 1 5mg/kg PO SID
Only if there is no biliary tract obstruction
> Ascites:
SpIrolactone +/- FurosemIde
Abdominocentesis

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15
Q

Feline hepatic lipidosis Pathophysiology?

A

Feline hepatic lipidosis;
Pathophysiology:
-Increased hepatocellular accumulation of lipids and cholestasis leading to hepatic failure
- Typically seen In middle age obese cats that have experienced a period of prolonged anorexia resulting in rapid weight loss.
- Most commonly secondary to pancreatitis, inflammatory bowel disease, cholangiohepatitis and diabetes mellitus -
;. Other causes include hepatotoxins, other systemic Illnesses, surgery, severe prolonged stress

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16
Q

Clinical signs of feline hepatic lipidosis?

A

Clinical signs:
Weight loss and anorexia,

lethargy, vomiting, Jaundice, hypersalivation, hepatomegaly

17
Q

Diagnostics of feline hepatic lipidosis?

A
  • *Diagnostics:**
  • Haematology:
  • +/- Non-regenerative anaemia
  • Biochemistry:
  • Significant increases in ALP, GGT and bilirubin, also Increased ALT and AST
  • ALP Increase Is usually significantly higher than ALT
  • Cytology: Hepatocytes with cytoplasmic vacuolization
  • Biopsy: Definitive diagnosis
  • Ultrasound: Diffusely hyperechoic liver+/· hepatomegaly
18
Q

Treatment of feline hepatic lipidosis?

A

Treatment:
- Supportive therapy:
- IV fluids and electrolytes
- Antiemitics; Metoclopramide 0.5mg/kg TID, maropitant 1 mg/kg SC SID for <5 days
- Gastric protectants: Proton pump inhibitors, H2 antagonist {famotidine), sucralfate
- Antibiotics:
> +/- Amoxicillin or second generation cephalosporin +/- low dose metronidazole
- Change according to culture and sensitivity
- Nutrition:
- Very Important via nasoesophageal/gastric or oesophageal tubes

-Based on 60kcal/kg/day of ideal body weight (“” total caloric intake), using a high protein complete
and balanced diet ·
- Start at 25% and increase by 25% per day over 4 days
- Monitor electrolytes for refeeding syndrome: Hypophosphataemia, hypokalemia, hypomagnesaemia
- Adjunctive:
- Vitamin K1 2.5mg/kg SC BID for 2 days, then once weekly

Vitamin B12 250µg SC weekly ·
- S·Adenosy-L-methionine (SAMe): Potent anti-oxidant 20mg/kg PO SID

19
Q

Feline inflammatory liver disease pathophysiology suppuratative and non suppuratative?

A

Feline inflammatory liver disease:
Pathophysiology:
- Cholangitis is inflammation of the biliary tract and surrounding liver, common syndrome In cats, rare ln ·
dogs .
- Suppurative form:
- Acute neutrophilic cholangitis:
Neutrophilic inflammation of the portal triads and bile ductules
Ascending bacterial infection or biliary system pathology
Acute onset, severe pyrexia illness, usually younger males
- Chronic neutrophilic cholangitis:
Possible progression of acute neutrophilic form or possible Immune-mediated disease
- Often concurrent pancreatitis and IBD

Mixed Inflammation of the portal areas
• Chronic mild to moderate illness (weeks) occasionally pyrexic, usually middle-aged males
./ Non suppurative form:
» Lymphocytic portal hepatitis: Lymphocytic and plasmacytic
Nonspecific lymphocytic lnfiltration of the portal regions without concurrent cholangitis
common causing chronic mild illness (weeks}, rarely pyrexic, older aged cats
:> Lymphocytic cholangitis:
Lymphocytic Infiltration of the portal area with biliary hyperplasia and fibrosis
Less common, possible Immune-mediated pathogenesis

20
Q

Feline inflammatroy disease Clinical signs?

A

Clinical signs:
Vomiting, diarrhoea, anorexia, weight loss, jaundice, hepatomegaly, rarely ascites

20
Q

Feline inflammatroy disease Clinical signs?

A

Clinical signs:
Vomiting, diarrhoea, anorexia, weight loss, jaundice, hepatomegaly, rarely ascites

21
Q

Feline inflammatory disease diagnostics?

A

Diagnostics:
- Haematology:
- +/- Inflammatory leukogram, anaemia, thrombocytopenia
- Biochemistry:
- Increased bilirubin, bile acids and ALT
- ALP Increase is seen more with chronic forms; GGT is more sensitive In cats
- +/- Hypoproteinaemia, hypoglycaemia
> +/- Elevated feline pancreatic lipase immunoreactivity
- Ultrasound: May not see any specific changes
- Biopsy: Definitive diagnosis, histopathology and culture and sensitivity

22
Q

Feline inflammatory disease treatment?

A

Treatment:
- General:
» Suppurative form: Long-term antibiotics at least 5 weeks
> Non suppurative form: Long course of corticosteroids+/- antibiotics
- Supportive therapy:
> IV fluids and electrolytes
> Antiemitics: Metoclopramide O.5mg/kg TID, maropitant 1 mg/kg SC SID for <5 days
» Gastric protectants: Proton pump Inhibitors, H2 antagonist (famotidine), sucralfate
- Nutrition: Important via nasooesophageal/gastric or oesophageal lubes and feed as per “feline
hepatic lipidosis”
.; Antibiotics:
> Amoxicillin 22mg/kg TID or cephalothin 22mg/kg TID +/- metronidazole 7.5mg/kg BID
>Change according to culture and sensitivity
- Anti-inflammatories:
- If non-responsive to antibiotics, indicated with chronic neutrophilic cholangitis and lymphocytic
cholangitis
> Prednisolone 1 mg/kg PO BID, then tapered over 6 weeks to lowest EOD dose
> Chlorambucil: If cannot tolerate prednisolone can trial chlorambucil
- Adjunctive:
> Anti-oxidants:
• Vitamin E 400 IU PO SID and Vitamin C
• S·Adenosy-L-methionlne (SAMe): Potent anti-oxidant 20mg/kg PO SID
> Choleretic:
• Ursodeoxycholic acid (Actlgall ®) 10-15mg,’ kg PO SID
Only if no bilary tract obstruction
> Vitamin K 2.Smg/kg SC BID for 2 days, then once weekly

23
Q

Hepatic encephalopathy pathophysiology?

A
  • *Hepatic encephalopathy;**
  • *Pathophysiology:**
  • Can occur when >70% of hepatic function Is lost
  • Secondary to any hepatic disease process, most commonly portosystemic shunts
  • Younger animals most commonly shunt, older animals most commonly neoplasia
24
Q

Hepatic encephalopathy clinical signs?

A

Clinical signs:

  • Anorexia, vomiting, PU/PD, ascites
  • Behavioural changes: Disorientation, head pressing, ataxia, pacing, seizures, circling
25
Q

Hepatic encephalopathy causes?

A

Causes:
Acute or chronic hepatic failure, portosystemic shunts (congenital and acquired)

26
Q

Hepatic encephalopathy diagnostics?

A

Diagnostics:
- Haematology, biochemistry and urinalysis:
> Microcytic anaemia +/- target cells, acanthocytes, polkliocytes
> Variable changes in liver enzymes (ALT, AST, GGT, ALP) and billrubin
• Signs of liver dysfunction: Low albumin, urea, glucose, coagulopathy
> Paired serum bile acids (usually elevated)
> Blood ammonia levels may be elevated
> Urinalysls: Low USG and ammonia urate crystals
- Imaging:
> Ultrasound
> Scintigraphy, portography

27
Q

Treatment of acute hepatic encephalopathy?

A

Treatment of acute hepatic encephalopathy:
- IV fluids and electrolytes
- Reduce ammonia and urease-producing bacteria:
- Nil per os 12·24 hours
- Enema to remove toxins and reduce ammonia producing bacteria:
- Warm water to remove contents
Retention enema (5·10ml/kg) e.g. 3 parts lactulose to 7 parts water every 6 hours or until colon
Is empty in crisis states
~ +/- Gastric lavage If recent ingestion of hepatotoxic agent
> IV antibiotics: Metronidazole 7.5mg/kg IV BID or amoxicillin 20mg/kg IV TID
- Seizures:
> Treatment for seizures BUT avoid benzodiazepines, use propofol and begin phenobarbitone
> Cerebral oedema: Mannitol 1g/kg IV over 20 minutes
- Gastric protectants: Proton pump inhibitors, H2 antagonist {famotidlne), sucralfate
- Coagulopathies
> Vitamin K1 2.5mg/kg SC BID for 2 days then once weekly.

28
Q

Treatment of chronic hepatic encephalopathy?

A

Treatment of chronic hepatic encephalopathy:
- Treatment for underlying disease
- Reduce ammonia production
> Lactulose 0.5-2ml/kg PO BID· TIO OR psyllium (1·3 tsplday)
- Antibiotics:
- Used intermittently during relapse, metronidazole 7.5mg/kg PO BID
- Diet:
> Low protein but high biological value, high carbohydrate to reduce ammonia production e.g. Hilis
l/D®
> Small meals frequently
> Moderate fibre content to reduce ammonia production and constipatlon
> Vitamin B and C