Specific Liver Diseases Flashcards

1
Q

Acute hepatitis

  • causes and therapy (4)
  • more specific therapies (4)
A
  • 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
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2
Q

Chronic hepatitis

  • Facts (3)
  • Therapy (2)
A
  • 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)

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3
Q

Idiopathic chronic hepatitis

  • causes (4)
  • Dx (3)
A
  • 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
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4
Q

monitoring efficacy of steroids (3)

A
  • ALKP will increase as a side effect
  • ALT should decrease if therapy is effective
  • normally 4-6 week tapering dose
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5
Q

Copper associated hepatopathy

  • predisposition
  • pathogenesis
  • disease
  • Tests
A
  • 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
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6
Q

Copper analysis

A
  • 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
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7
Q

Progression of copper hepatopathy (4)

A
  • 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
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8
Q

beddligton terriers (5)

A
  • 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
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9
Q

Copper hepatopathy Treatment (4 + facts)

A

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

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10
Q

Feline Inflammatory Liver Disease

A
  • Neutrophilic cholangitis
  • Lymphocytic cholangitis
  • Mixed cell cholangitis
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11
Q

Neutrophilic cholangitis

  • definition
  • test
  • where
  • predisposition? (2)
A
  • 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
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12
Q

Neutrophilic Cholangitis CS (8)

A
  • 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
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13
Q

Neutrophilic cholangitis Dx (5)

A
  • 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
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14
Q

Neutrophilic cholangitis

  • treatment (3)
  • prognosis (2)
A
- 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
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15
Q

Lymphocytic Cholangitis

A
  • Lymphocytic inflammation around portal triads (not bile ducts)
  • Variable fibrosis – can be very severe
  • Immune mediated disease
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16
Q

Lymphocytic Cholangitis

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

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
17
Q

Mixed Cell Cholangitis

  • what
  • CS (4)
  • Tx (3)
A
  • Chronic neutrophilic cholangitis
  • Neutrophils, lymphocytes and fibrosis
  • systemically unwell

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

18
Q

Hepatic lipidosis pathogenesis (5)

A
  • 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.
19
Q

Hepatic lipidosis

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

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

20
Q

Hepatic Lipidosis Tx (3)

A

Food!:

  • high protein stops breakdown
  • deliver gradually

fluids

carnitine supplementation