Specific Liver Diseases

Question 1

Acute hepatitis

• causes and therapy (4)
• more specific therapies (4)

Answer 1

• infectious/drug/toxin induced
• symptomatic therapy
• correct fluid and electrolyte imbalance (do NOT use hartmanns!)
• K supplementation
• monitor K and glucose levels
• hepatic encephalopathy: lactulose, IV ABs, keppra
• portal hypertension: PPI, H2 blockers, gastric protectants
• ascites: spirinolactone
• anti-oxidant therapy: NAC, SAM-e

Question 2

Chronic hepatitis

• Facts (3)
• Therapy (2)

Answer 2

• non specific CS
• waxing and waning, eventually leads to fibrosis and cirrhosis
• biopsy required

Therapy:
- same as acute + prednisilone at anti-inflammatory dose (only AFTER hepatic encephalopathy has resolved)

Question 3

Idiopathic chronic hepatitis

• causes (4)
• Dx (3)

Answer 3

• Genetic influences
• Metabolic defects: Copper associated disease
• Autoimmune disease
• Infectious causes: Cholangiohepatitis(bacteria)/ Leptospirosis / adenovirus
• Drugs and toxins

Dx:

• haemogram: mild anaemia (normocytic, normochromic), decrease in platelets, increats in PT/APTT
• biochem: increase in ALT, ALKP, bilirubin, hypoalbuminaemia, urea
• Biopsy: true cut are best

Question 4

monitoring efficacy of steroids (3)

Answer 4

• ALKP will increase as a side effect
• ALT should decrease if therapy is effective
• normally 4-6 week tapering dose

Question 5

Copper associated hepatopathy

• predisposition
• pathogenesis
• disease
• Tests

Answer 5

• beddlington, dalmation, WHWT
• Usually stored in hepatic lysosymes and then excreted via biliary tree
• Excess copper accumulates in cytosol –> oxidative damage

Disease can be primary disease or secondary disease due to choleostasis

Tests:

• Quantitative analysis*
• Histology and zonal distribution

Question 6

Copper analysis

Answer 6

• 1 gram of tissue required (Not formalin fixed)
• Primary copper disease likely if > 2000 ppm
• Rubeanicacid staining of biopsy to look at distribution and qualitative accumulation

Question 7

Progression of copper hepatopathy (4)

Answer 7

• Copper accumulation initially subclinical –> Therapy works
• Hepatocyte death – ALT increases –> Therapy works
• Progression and development of chronic hepatitis –>Therapy unlikely to be effective
• Massive Cu release – anaemia and renal failure

Question 8

beddligton terriers (5)

Answer 8

• Mutation in COMMD-1 gene
• Commercial test available
• Will detect 95% of affected / carriers
• Early screening and low copper diets can prevent disease progression
• N.B Copper restricted diets should only be fed to fully grown dogs as also low in protein

Question 9

Copper hepatopathy Treatment (4 + facts)

Answer 9

D-penicillamine

• Chelating agent
• Binds extravascular copper
• Effective over many months (4-6)
• 30% have vomiting – give with food

Once hepatic copper levels reduced switch to zinc:

• chelating agent
• stops Cu absorption across GI tract
• DON’T use with D penicillamine: since decreases the efficacy of it!

Copper restricted diet (L/d)
Anti-oxidant therapy

Question 10

Feline Inflammatory Liver Disease

Answer 10

• Neutrophilic cholangitis
• Lymphocytic cholangitis
• Mixed cell cholangitis

Question 11

Neutrophilic cholangitis

• definition
• test
• where
• predisposition? (2)

Answer 11

• Ascending infection from intestines via the biliary tree – anatomical problem in cats! (E.coli most common)
• Suppurative inflammation on histology
• Cannot differentiate on FNA
• occurs in bile ducts +/- parenchyma involved
• Underlying inflammatory bowel disease may predispose
• Triaditis: Concurrent IBD and pancreatitis & Common opening between CBD and pancreatic duct

Question 12

Neutrophilic Cholangitis CS (8)

Answer 12

• Usually middle aged to older cats
• Acute onset can be seen but typically more insidious
• Systemically unwell
• Jaundice, anorexia and pyrexia most common (due to choleostasis)
• Intrahepatic choleostasis
• Vomiting / lip smacking

Question 13

Neutrophilic cholangitis Dx (5)

Answer 13

• Bloods: anaemia, liver enzymes, bilirubin, neutrophilia*
• Feline PLI for pancreatic assessment
• Imaging
  Mottled / hypoechoic parenchyma
  Distended bile duct and thickened gall bladder wall
  Possible cholelithiasis
• FNA not useful
• biopsy: tru cut: allows surgical inspection of viscera and feeding tube to be placed at the same time

Question 14

Neutrophilic cholangitis

• treatment (3)
• prognosis (2)

Answer 14

- Antibiotics
	Amoxycillin-clavulonate +/- fluoroquinolones
- Hepatic support therapy
- Diet modification to control IBD?
- Prognosis good if early intervention
	Mean survival 29 months
	5/6 alive at 12 months

Question 15

Lymphocytic Cholangitis

Answer 15

• Lymphocytic inflammation around portal triads (not bile ducts)
• Variable fibrosis – can be very severe
• Immune mediated disease

Question 16

Lymphocytic Cholangitis

• CS
• Dx (2)
• DDx
• Tx (2)
• prognosis

Answer 16

CS:

• Normally systemically well with good / increased appetite
• Chronic history
• Hepatomegaly
• Often have ascites and jaundice
• Normothermic

Dx:

• Bloods:
• -> Anaemia and lymphopaenia
• -> Hyperglobulinaemia
• -> Increased liver parameters and bilirubin

DDx – Feline Infectious Peritonitis

Imaging

• Free abdominal fluid (transudate)
• Mixed echogenicity to liver

Tx:

• supportive
• corticosteroids (prednisilone)
• fair prognosis

Question 17

Mixed Cell Cholangitis

• what
• CS (4)
• Tx (3)

Answer 17

• Chronic neutrophilic cholangitis
• Neutrophils, lymphocytes and fibrosis
• systemically unwell

Treatment
Hepatic support
Culture negative – steroids (+/- antibiotics)
Culture positive – antibiotics (+/- steroids)

Question 18

Hepatic lipidosis pathogenesis (5)

Answer 18

• normally fat is taken form the GIT adn metabollised in the liver (also from adipose tissue)
• metabolised into lipoproteins
• also oxidised by carnitine to give energy
• with another illness you can get a massive breakdown of fat –> massive release of hormone sensitive lipase –> conteracts insulin
• liver is overwhelmed, becomes inflamed and gets a build up of fat.

Question 19

Hepatic lipidosis

• CS (5)
• check (4)
• clin path (3)
• imaging
• tissue samping

Answer 19

CS:

• Dull
• Anorexia
• Weigh loss
• Jaundice
• Underlying dz - PUPD

Check:

• Clotting
• B vitamins
• Ammonia
• PLI and fructosamine

Clin path:

• liver enzymes: GGT
• bilirubin
• bile acids

Imaging:
- larger and hyperechoic liver

Tissue sampling:
- FNA: vaculoisation

Question 20

Hepatic Lipidosis Tx (3)

Answer 20

Food!:

• high protein stops breakdown
• deliver gradually

fluids

carnitine supplementation