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SMALL ANIMAL > 9.5.4: Approach to jaundice > Flashcards

9.5.4: Approach to jaundice Flashcards

1
Q

Jaundice/ icterus is caused by

A

hyperbilirubinaemia (>50 umol/l)

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2
Q

What is bilirubin?

A
  • Poduct of haemoglobin metabolism
  • Much of this metabolism occurs in the liver, where bilirubin is conjugated and excreted into bile
  • Conjugated bilirubin enters the biliary tree and the GIT at the duodenal papilla
  • On reaching the colon, colonic bacteria deconjugate bilirubin into urobilinogen, which then oxidises into urobilin (urine) and stercobilin (faeces)
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3
Q

Where in the body can bilirubin build up?

A
  • Pre-hepatic - haemoglobin
  • Hepatic - liver and intrahepatic biliary tract
  • Post-hepatic - biliary excretion (extrahepatic)
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4
Q

Differentials for pre-hepatic jaundice

A

(Primarily consider this as an oversupply of precursors i.e. haem into the system, overwhelming excretion mechanisms).
* Haemolytic anaemia
* Internal haemorrhage - would likely have other signs before jaundice!
* Severe myolysis (myoglobin e.g. racing greyhounds)

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5
Q

Diagnostics when suspicious of pre-hepatic jaundice

A

Initially look for haemolysis, then look for the underlying cause.
* Haematology: look for anaemia
* Blood smear: look for spherocytosis, auto-agglutination, concurrent thrombocytopaenia
* Further IMHA testing: e.g. Coombe’s test
* Consider infectious disease screening
* Further history re toxin/ drug risk
* Could look for neoplastic causes of IMHA using advanced imaging

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6
Q

What could a microcytic, hypochromic anaemia suggest?

A

Chronic blood loss e.g. fleas or a GI bleed

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7
Q

What could a macrocytic, hypochromic, regenerative anaemia suggest?

A

Classic for haemolysis

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8
Q

What could a microcytic normochromic non-regenerative anaemia suggest?

A

Maybe chronic disease e.g. of the liver

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9
Q

How do you diagnose primary IMHA?

A

Primary IMHA is a diagnosis of exclusion once you have ruled everything else

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10
Q

Pathogenesis for hepatic jaundice

A

Metabolism/ delivery of haem into the system is normal, but the ability of the liver to process the bilirubin and excrete it is poor. The liver is failing somehow OR the intrahepatic biliary tree is damaged/ compressed by the liver around it.

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11
Q

Differentials for hepatic jaundice

A

The liver is failing somehow OR the intrahepatic biliary tree is damaged/ compressed by the liver around it.
* Hepatitis: bacterial, fungal, viral infection
* Inflammatory cause e.g. cholangiohepatitis
* Neoplasia: lymphoma, MCT, adenocarcinoma
* Drugs/ toxins: paracetamol, NSAIDs
* Degenerative disease: amyloidosis, lipidosis (cats), cirrhosis
* Proximal biliary disease: cholangitis/ cholangiohepatitis

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12
Q

What are some viral infections that could cause hepatic jaundice in dogs and cats?

A

Cats:
* FIV
* FIP
* FeLV

Dogs
* CAV
* Lepto (can get even though vaccinated, and zoonotic!)

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13
Q

What is a good marker of hepatocellular damage?

A

ALT (predominantly found inside liver cells)
* Remember that even with cirrhosis / shunt the animal may have normal ALT because the cells are not damaged enough to trigger marked increase.

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14
Q

What are some markers of liver damage?

A
  • ALT
  • AST (also muscle)
  • ALP (cholestatic marker)
  • GGT (cholestatic marker)
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15
Q

What are some possible reasons for elevations in ALP?

A
  • Cholestatic marker = biliary tree damage

Other causes of small increases
* Bone (osteosarcoma)
* Gut (GI disease)
* Steroid induced
* Phenobarbitone

Also:
* Reactive hepatopathies: hyperadrenocorticism, diabetes mellitus, thyroid disease

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16
Q

How could you differentiate between AST elevation due to liver disease or muscle damage?

A
  • If muscle damaged, would expect concurrent CK elevation
17
Q

What are some markers / tests of liver function?

A
  • Urea - low in liver disease as liver not making as much
  • Ammonia - high in liver disease
  • Albumin - low in severe liver disease
  • Clotting factors - most produced by liver
  • Bile acid stim test
18
Q

What would happen to urea levels in liver disease and what else could lead to this result?

A

Urea = low in liver disease
* Anorexia will also decrease urea
* Eating high protein meals and renal disease elevate urea

19
Q

What would happen to ammonia levels in liver disease and what happens as a consequence of this?

A

Ammonia = high in liver disease
* High ammonia -> hepatic encephalopathy

20
Q

True/false: bile acid stim test is poorly sensitive for differentiating between hepatic and post-hepatic jaundice.

A

True

21
Q

Describe how a bile acid stim test works

A
22
Q

What imaging modalities can you use to assess the liver?

A

Ultrasound or CT preferably; radiography limited to just assessing size
* To make a diagnosis, may need FNA or more likely biopsy
* Consider clotting factors before you take a biopsy
* Culture and sensitivity on samples (e.g. lepto)

23
Q

Pathogenesis of post-hepatic jaundice

A
  • Delivery and metabolism of heme is normal
  • Excretion of bilirubin by the liver is normal
  • Bile duct is no longer transporting it, leading to back pressure and exudation back into the system
  • Most likely due to obstruction (EHBDO)
  • An obstruction can be intraluminal, mural or extramural
24
Q

Examples of intraluminal obstructions? What type of jaundice would they lead to?

A

Obstruction -> post-hepatic jaundice
Intraluminal obstructions:
* Cholelithiasis (stones)
* Gallbladder mucocoele (Border Terriers)
* Inspissated bile (dry bile)
* Gallbladder polyps
* Cysts (cats)

25
Q

Examples of mural obstructions? What type of jaundice would they lead to?

A

Obstruction -> post hepatic jaundice

Mural obstructions:
* Inflammatory swelling: cholangitis, cholecystitis, choledochitis = most common
* Neoplasia

26
Q

Example of extramural obstructions? What type of jaundice would they lead to?

A

Obstruction -> post hepatic jaundice

Extramural obstructions can happen anywhere along the path of the biliary tract.

Pancreatic disease
* Pancreatitis (common reason for elevated ALP)
* Pancreatic neoplasia (head of pancreas)

Duodenal disease: infectious, inflammatory, neoplastic

Porta hepatis stricture: local inflammatory/ infectious/ neoplastic disease.

27
Q

Diagnostics for suspected post-hepatic jaundice

A
  • Biochemistry: ALP, GGT, ALT, cholesterol
  • Imaging: ultrasound of gallbladder and biliary tree, pancreas, surrounding mesentery and LNs
  • CT
  • Gallbladder FNA for C&S (experienced vet / referral procedure)
  • cPLI / fPLI for pancreatitis
28
Q

What level of ALP would you expect in post hepatic jaundice?

A

ALP = cholestatic marker
* Increased in post-hepatic jaundice
* Biliary damage will lead to release into serum

29
Q

What level of ALT would you expect in post hepatic jaundice? What would this be in relation to ALP?

A

ALT will probably be elevated to a degree, also through ascending damage to the liver.
However, proportionally, ALP elevation will be larger than ALT elevation in post-hepatic jaundice.

30
Q

In hepatic jaundice, what would you expect ALT and ALP levels to be relative to one another?

A

In hepatic disease, ALT and ALP are likely to rise to a similar degree OR ALT will be higher than ALP.

31
Q

What colour urine is consistent with bilirubin being present?

A

Orange

32
Q

What colour faeces is consistent with bilirubin being absent?

A

White faeces = lack of bilirubin in it

33
Q

If liver disease leading to loss of clotting factors and therefore a disorder of secondary haemostasis, what clinical signs would you expect?

A

Clotting factor loss -> secondary haemostasis not working -> big bleeds and bruising
* NOT looking for petechiae - this is associated with primary clotting disorder i.e. defective platelet function

34
Q

Cranial abdominal pain suggests you should look at which organs?

A

Liver and pancreas

35
Q

What history questions should you ask / factors should you consider in the animal with suspected hepatic disease?

A
36
Q

What clinical exam findings might suggest hepatic disease?

A

SMALL ANIMAL (90 decks)

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