Biliary and chronic liver disease Flashcards
Biliary and chronic disease
What clinical signs are associated with chronic and biliary disease?
Long-standing, chronic, recurrent or waxing-waning signs
Non-specific clinical signs including
* Inappetence and weight loss; poor body condition
* Vomiting +/- haematemesis if GI ulceration
* Diarrhoea +/- melaena
* PU/PD
* Lethargy, depression -> true neuro signs/hepatic encephalopathy
Slightly more specific:
* Jaundice
* Ascites
What are common differentials when looking at chronic liver and biliary disease?
- idiopathic chronic hepatitis
- copper associated liver disease
- true copper storage disease
- congenital vascular disease
- neoplasia (primary or secondary)
- biliary tract disease
- biliary mucoceles
- neutrophilic cholangitis
- extrahepatic bile duct obstruction
- bile duct rupture
What clinical signs are associated with portosystemic shunts? How are they diagnosed? How is it treated?
Clinical signs:
* Neurological: Lethargy, ataxia, obtundation, pacing, circling, blindness, seizures, coma
* Gastrointestinal: Vomiting, diarrhoea, anorexia, pica, melaena, haematemesis
* Urinary – ammonium urate crystals; Haematuria, stranguria, pollakiuria, urethral obstruction
Diagnosis
* Laboratory clues: maybe low BUN; low albumin; low glucose
* Raised liver enzymes, but not always as liver is small
* Low USG +/- ammonium biurate crystals
* Raised fasting and post-prandial bile acids; increased ammonia
* Ultrasound; portogram (radiograph/ fluoroscopy); contrast CT
Treatment
Surgical treatment offers significantly greater survival times
- Surgical ligation
- Complete attenuation: 50-86% can not tolerate
- Partial attenuation -> Second surgery 3-6 months later
- Cellophane banding
- Clear non-medical grade cellophane
- Titanium clips used to hold in place
- Fibrous tissue reaction leading to gradual occlusion
- Ameroid ring
- Ring of casein surrounded by stainless steel
- Hygroscopic substance that swells after absorbing fluid
- Incites a fibrous tissue reaction
What different techniques are available to biopsy liver? What information do they tell us?
- FNA
- punch biopsy
- crush forceps
- core biopsy
Whether it is, inflammation (neutrophilic, lymphocytic or ganulomatous), neoplasia or infection
What clinical signs are associated with primary hepatic neoplasia? What laboratory findings would you expect? How can you reach a diagnosis? How can they be treated? What are the most common types?
Often non-specific clinical signs - lethargy, poor appetite
Signs may be associated with a complication
Abdominal bleed if ruptured mass
Palpable mass may be only sign
Abdominal distension/discomfort
Laboratory findings can be similar to chronic hepatitis - markers of hepatocellular damage
**Diagnostic imaging **- ultrasound
Definitive diagnosis - FNA for cytology or biopsy for histopathology
Surgery is often treatment of choice
Assess for metastatic disease first
Chemotherapy only effective for lymphoma
What causes chronic hepatitis? What are the treatment options for the different diseases processes occuring in chronic hepatitis?
Infectious, metabolic, toxic and immune
BUT most cases in the dog are classed as idiopathic.
- inflammation: corticosteroids and anti-oxidants
- infection: antibiotics
- slow biliary flow:destolit (ursodeoxycholic acid)
- ascites: diuretics
What is the main indication for steroids in chronic hepatitis? When should we avoid corticosteroids? What are the potential adverse effects of corticosteroids?
Main indication:
* Suspected autoimmune hepatitis
* marked lymphoplasmacytic inflammatory infiltrate on biopsy
* no other underlying cause found
* Prednisolone 1-2 mg/kg/SID (ie immune suppressive not just anti inflammatory)
Avoid in
* End-stage/cirrhosis/bridging fibrosis
* Ascites/GI ulceration (=portal hypertension)
* Risk of undiagnosed infection (bacterial, viral, fungal)
Adverse effects
* Increased protein catabolism can cause or worsen hepatic encephalopathy
* Fluid retention can cause (or worsen) ascites
* Ulcerogenic effects -> GI ulceration
* dexamethasone is more ulcerogenic than prednisolone
* Increased risk of infection or exacerbates existing infections
How does UDA work in chronic hepatitis?
Ursodeoxycholic Acid (UDA)
* Hydrophilic bile acid that displaces more toxic hydrophobic bile acids
* Draws water in to bile ie it has choleretic effects
* It is immune-modulating and prevents cells entering apoptosis pathway
* Increased production of glutathione
* Not licensed in dogs or cats but useful if any cholestasis
What is the justification for antibiotics in chronic hepatitis?
- Management of hepatic encephalopathy
- Decreased ammonia formation by reducing bacterial load in the colon
- If histopathology changes suggest:
- ascending cholangitis
- significant neutrophilic component to any inflammation
Choose appropriate antibiotics and at doses which are not hepatotoxic:
* ampicillin
* metronidazole
How can you manage ascites in chronic hepatitis?
Spironolactone
* Aldosterone receptor antagonist
* 2-3 day delay before effect
* might have anti fibrotic effects??
Furosemide
* with spironolactone if poor response
* monitor potassium
Peritoneal drainage?
* only if life threatening because reforms rapidly
* contributes to dehydration
* aggravates decreased albumin
What is liver failure and cirrhosis?
When the liver is damaged, extra cellular matrix or collagen is made which leads to remodelling and fibrosis within the liver. As a result, the portal blood flow is inhibited and portal hypertension can occur, then causing loss of hepatocyte function.
Cirrhosis = end stage CH, when architecture is very distorted, fibrosis and portal hypertension are present.
Liver failure is the point at which the liver can no longer compensate and function normally.
What is the prognosis for chronic hepatitis?
- Very variable
- Stable disease- might do well for years with supportive care
- Rapid deterioration despite good care
English Springers MST 6 months - This might improve for those given prednisolone.
Negative prognostic indicators:
* ascites
* jaundice
What causes neutrophilic cholangitis? What clinical signs are associated? How is it diagnosed? How is it treated?
Uncommonly reported in dogs (more common in cats)
Cause: ascending infection or haematogenous spread - Streps, E coli, Klebsiella, Proteus
Clinical signs variable but can include: lethargy, pyrexia, vomiting, jaundice
**Clinical pathology: **Variable liver enzyme elevations, increased bilirubin; neutrophilia with/without left shift
Diagnosis requires biliocentesis +/- liver biopsy
Treatment: antibiotic treatment based on culture results; treat for 8 weeks minimum - Supportive care
What causes extrahepatic bile duct obstruction (EHBDO)? What clinical signs are associated? How is it diagnosed? How is it managed?
Causes include
* Pancreatitis
* Pancreatic tumour
* Bile duct tumour
* Duodenal tumour….or less likely FB
* GB mucocoele
* Cholelithiasis
* Local trauma, inflammation
Clinical signs
* Signs can relate to underlying reason for obstruction
* Very variable, non specific in early stages and depends on whether partial or complete obstruction
Diagnosis –
* Supportive bloodwork - very high bilirubin and very high ALP and GGT, ALT and AST
* Ultrasound and CT
Management
* medical management for pancreatitis
* other causes -> surgical assessment
What causes bile duct rupture? What consequences and clinical signs are associated? How is it treated?
Causes:
Usually same causes as EHBDO
Consequences and clinical signs:
Bile peritonitis -> abdominal effusion
May be infectious if secondary to ascending cholangitis; important to culture abdominal fluid in these cases
Profound jaundice common
Treatment:
Surgery
Manage underlying cause
Cholecystectomy
histopath and culture of gall bladder wall for follow up treatment decisions
