Approach to jaundice Flashcards

(29 cards)

1
Q

How can we best define the CS of jaundice?

A
  • hyperbilirubinaemia causing yellowing of body tissues
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2
Q

Fill in the blank: bilirubin is a product of … metabolism

A
  • haemoglobin
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3
Q

Fill in the blank: most of haemoglobin metabolism occurs in the …

A
  • liver
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4
Q

Fill in the blank: once conjugated in the liver, bilirubin enters the GIT at the …

A
  • biliary tree - into the duodenum - enters at the duodenal papilla
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5
Q

Fill in the blank: urobilin is excreted in …

A
  • urine
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6
Q

Fill in the blank: stercobilin is excreted in …

A
  • faeces
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7
Q

Why is hyperbilirubinaemia problematic?

A

-> renal tubular damage

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8
Q

At what concentration of bilirubin in the blood is jaundice/icterus seen?

A
  • hyperbilrubinaemia = >50µmol/l
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9
Q

Categories of jaundice

A

Pre-hepatic
- before the liver
- relates to increased haemoglobin destruction

Hepatic
- the liver doesn’t do its job
- reduced conjugation of bilirubin

Post-hepatic
- the conjugated bilirubin cannot exit via the biliary system

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10
Q

Cause of pre-hepatic jaundice

A

Oversupply of precursors (haemoglobin/haeme) into the system = increased destruction of RBCs.

Haemolytic anaemia

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11
Q

Causes of haemolytic anaemia

A

Acquired defects
- hypophosphataemia
- oxidative damage
– e.g. toxic insults (onion, garlic, paracetamol)
– metabolic dz e.g. hyperthyroidism, DM, renal dz

Genetic defects
- Abyssinian and somali cats: hereditary haemolysis
- non-spherocytic haemolytic anaemia in beagles
- phosphofructokinase deficiency in spaniels

Immune-mediated
- primary
- secondary
— drugs/toxins
— other immune dz e.g. systemic lupus erythematosus
— infectious e.g. FeLV, lepto, mycoplasma
— neoplasia e.g. lymphoma

Mechanical injury
- turbulent blood flow
— neoplasia e.g. haemangiosarcoma
— DIC

Internal haemorrhage
- look for other adverse effects

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12
Q

How do we tell if jaundice is pre-hepatic?

A

Haematology
- anaemia
— regenerative
— microcytic, hypochromic
- blood smear
— spherocytes
— auto-agglutination

Imaging
(primarily looking for neoplastic causes of IMHA)
- 3 view CXR, lung and abdo US
- advanced imaging: CT with contrast

Serum and urine discolouration
- haemoglobinaemia
- haemoglobinuria
– pink urine (haemoglobinuria) an indicator of intravascular haemolysis

Further bloods/infectious dz screening

Toxin/drug risk

Other clues e.g. pyrexia, pallor, haemic murmur

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13
Q

Causes of hepatic jaundice

A

Metabolism and delivery of heme into the system is normal.

The ability of the liver to process the bilirubin and excrete it is poor i.e. the liver is failing in some way, or the intrahepatic biliary tree is damaged/compressed by the liver around ot.

Infectious (hepatitis)
- bacterial
- fungal
- viral (CAV, FIV, FIP, FeLV)

Inflammatory
- cholangiohepatitis

Neoplasia
- lymphoma, MCT, adenocarcinoma

Drugs/toxins
- paracetamol, NSAIDs, etc

Degenerative
- amyloidosis
- lipidosis (cats)
- cirrhosis

Proximal biliary dz
- cholangitis/cholangiohepatitis

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14
Q

Liver enzymes

A
  • ALT
  • AST
  • GGT
  • ALP
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15
Q

ALT - what is it? when does it elevate?

A
  • part of the pyruvate cycle
  • inside liver cells
  • serum elevations are consistent with hepatocellular damage
    — dependent on numbers of liver cells present e.g. cirrhosis may be low/normal
    — depends on number of cells damaged e.g. focal neoplasia vs widespread infection
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16
Q

AST - what is it? when does it elevate?

A
  • found in liver and muscle (skeletal and cardiac)
  • often elevated through venipuncture
  • CK elevations often found concurrently if due to muscle damage
  • resultantly many people disregard AST elevations on biochem
17
Q

GGT - what is it? when does it elevate?

A
  • part of glutathione metabolism and present in biliary tract cells (and pancreas, spleen, heart, brain)
  • similar to ALP in terms of determining biliary tract dz and obstruction
  • probably more useful in combination as can give false positives alone (esp cats)
18
Q

ALP - what is it? when does it elevate?

A
  • widespread in the body but is found in concentrated amounts in the biliary tree
  • other: bone, gut, steroid induced
  • even small elevations in cats could be significant due to a shorter T1/2 cf dogs (6h vs 66h)
  • reactive hepatopathies: hyperadrenocorticism, DM, thyroid dz
  • elevation often reflects biliary dz, but can still reflect liver changes
  • animals with bigger skeletal turnover (young animals) will have increased ALP
19
Q

Liver function tests - examples

A
  • bile acid stimulation test (BAST)
  • clotting factors
  • albumin
  • urea
  • ammonia
20
Q

Use/accuracy of liver function tests

A

Up to 70% of the liver may be lost before affects on function are seen, due to large functional reserve

21
Q

Bile acid stimulation test (BAST) - what does it assess?

A

Will assess liver function and biliary flow -> bile acids are synthesised in the liver, secreted into the bile and moved in the duodenum. Reabsorbed from the GIT and return to the liver via the portal vein to be recycled and re-excreted into the gall bladder: entero-hepatic recycling
- this means these are an excellent test of liver function and/or biliary tract dz, but they are poor at differentiating between hepatic and post hepatic jaundice

Take a sample before and after eating

22
Q

Clotting factors - use, which ones?

A

All produced by the liver (except VIII and vWF) -> prolonged aPTT and PT

23
Q

Albumin - use

A
  • produced by the liver
  • low values may support liver dz (<15g/l -> oedema/ascites)
24
Q

Urea - use

A
  • urea is an end product of protein metabolism and ammonia production
  • low values support reduced liver function
25
Ammonia - use
- liver converts ammonia to urea - high values can support liver disease - very labile so need point of care testing to test quickly enough
26
How do we tell if jaundice is hepatic?
Liver function tests = proof the liver isn't functioning - urea - ammonia - albumin - clotting factors - BAST Biochemistry - ALT & ALP are often raised proportionally in liver dz Haematology - normal? - or inflammatory profile - or chronic anaemia - other? neoplasia? -- abnormal cells or high calcium indicates neoplasia Liver sampling - FNA - biopsy - histopath - C&ST Imaging - US - CT / contrast CT - radiographs only indicate hepatic size -- liver should go to the last rib, bigger than this is abnormal
27
Causes of post-hepatic jaundice
Delivery/metabolism of heme is normal. Conjugation and excretion of bilirubin by the liver is normal. The bile duct is no longer transporting it away -> back-pressure and exudation back into the system. Realistically this is most likely to be an obstruction = extrahpetic bile duct obstruction (EHBDO).
28
Causes of post-hepatic jaundice: EHBDO
Intraluminal obstruction - cholelithiasis (stones) - gall bladder mucocoele (border terriers) - insipissated bile - gall bladder polyps - cysts (cats) - FB stuck at duodenal papilla (rare) Extramural - pancreatic dz (pancreatitis, pancreatic neoplasia) - duodenal dz (infection, inflammatory, neoplastic) - porta hepatis stricture Mural - inflammatory swelling (cholangitis, cholecystitis, choledochitis) - neoplasia
29
How do we tell if jaundice is post-hepatic?
Liver function tests = largely normal Biochemistry - in post-hepatic dz, ALP & GGT are often raised disproportionally compared to ALT - ALT is raised secondarily due to 'back pressure' Haematology - normal? - or inflammatory profile - or chronic anaemia - other? neoplasia? Imaging - US: GB, biliary tree, pancreas, mesenteric LN - CT / contrast CT: gall bladder, biliary tree, pancreas, GIT Pancreatic screening tests - cPLI - fPLI Biliary tree sampling - FNA - biopsy of gall bladder/mass - pancreas - histopath - C&ST - exploratory sx to assess biliary tree