PHYS Investigation of Jaundice - Week 5 Flashcards
Jaundice
Yellow appearance of skin, sclera, mucous membranes caused by excess bilirubin in blood.
When is jaundice detectable clinically?
Detectable clinically when serum bilirubin > 50umol or 3mg/dl (normal range < 17umol/L or 1 mg/dL).
Biliverdin colour
Green-yellow.
Unconjugated bilirubin colour & solubility.
Orange-yellow. Fat soluble.
Sources of bilirubin production and breakdown.
- 80% daily bilirubin production (250-400mg in adult) – derived from haemoglobin.
- 20% daily bilirubin production – derived from rapidly turning-over small pool of free haem.
Pathway of bilirubin production & circulation & excretion.
Haem -> unconjugated bilirubin [fat soluble] @ reticulo-endothelial system (RES) of the spleen -> bilirubin bound to albumin @ transported via blood to liver -> taken up by hepatocytes -> conjugated w sugar residues (glucoronic acid) -> conjugated bilirubin [water soluble] -> enters biliary system @ mid-duodenum.
-> 95% secreted bilirubin -> reabsorbed in the terminal ileum -> travels to the liver via portal circulation -> bile is re-secreted via liver into the small intestine… (enterohepatic circulation).
&
-> 5% secrete bilirubin -> hydrolysed by the intestinal flora -> reduced to form urobilinogen [water soluble]
-> oxidised by gut bacteria -> stercobilin [brown/stool colour].
OR -> reabsorbed via portal system -> recycled by the liver.
OR -> reabsorbed via portal system -> excreted in urine.
Urobilinogen colour
Colourless.
Causes of unconjugated hyperbilirubinaemia.
Haemolysis (faster than normal breakdown of RBCs), congenital defects in the liver’s uptake or transport system, physiological jaundice - babies develop in the first week of life (neonatal jaundice).
Biochemistry/tests for unconjugated hyperbilirubinaemia.
- For blood -> Total blood Br – conjugated Br = unconjugated Br increased
- For urine -> urinalysis urobilinogen increased (no increase w bilirubin)
Causes of conjugated hyperbilirubinaemia
Anything that causes obstruction in the excretion of bilirubin post-conjugation. E.g., gall stones, tumours (usually at the head of the pancreas), multiple small blockages within the liver itself (intrahepatic cholestasis), primary & secondary liver tumours causing intrahepatic cholestasis.
Signs/results of conjugated hyperbilirubinaemia - bloods, urine & stool samples
- For blood -> raised alk.phos & yGT
- For urine -> dark urine.
- For stools -> pale stools.
Causes of hepatocellular jaundice
Damage to the hepatocytes themselves. E.g., viral hepatitis, alcohol, non-alcoholic steotosis hepatitis (NASH).
HPC recurrent pain in RUQ may indicate
Gall stones
HPC painless, progressive jaundice & weight loss may indicate
Carcinoma of the head of the pancreas.
PMHx previous cancer, weight loss may indicate
Hepatic metastases.
PMHx acute onset jaundice, fever, travel, prodromal anorexia, shellfish ingestion may indicate
Viral Hep A
PMHx of blood transfusions may indicate
Viral hep B & C
SHx of recreational drugs, IVDU, tattoos, sexual promiscuity/unprotected sex may indicate
Viral hep B & C
MHx OTC paracetomol, alternative medicines (e.g., Chinese herbal medicines), ecstasy/amphetamines may indicate
Liver failure.
FHx jaundice may indicate
Wilson’s disease, haemochromatosis.
Investigations of jaundice
- Urinalysis
o Urobilinogen
o Bilirubin - LFT
o Alkaline phosphatase (alk.phos .) – produced by epithelial cells lining the bile canaliculi
o Gamma-glutamyl transferase (yGT ) – produced by epithelial cells lining the bile canaliculi
o ALT, AST – contained within the hepatocytes - Ab Ultrasound
- Ab CT
- Viral screen: hepatitis, leptospirosis, etc.
- Immunology: auto-antibodies
Increased presence/concentration of urobilinogen may indicate
Prehaptic or hepatic impairment.
Absence of urinary urobilinogen may indicate
Cholestasis.
Absence of bilirubin may indicate
Pre-hepatic jaundice.
Presence of bilirubin in the urine may indicate
Obstructive jaundice (due to leakage of conjugated bilirubin out of the hepatocytes).
Increased alk phos may indicate
Intrahepatic or extrahepatic obstruction.
Increased yGT may indicate
Intrahepatic obstruction, mixed enzyme induction by alcohol or drugs.
Raised ALT & AST may indicate
Hepatitis.
Alk. phos is produced by
Epithelial cells lining the bile canaliculi.
yGT is produced by
Epithelial cells lining the bile canaliculi.
ALT, AST is produced by
Contained within the hepatocytes.
Explain how conjugated hyperbilirubinaemia causes dark urine & pale stools
Conjugated bilirubin from the liver cannot enter gut.
Thus, spills into bloodstream. As water soluble, will pass via glomerulus -> urine (making urine dark).
Reduced Br in gut -> reduced urobilinogen -> no urobilinogen in the urine & little stercobilin.
In normal circumstances, how much urobilinogen is found in urine…
Only a trace.
If the skin appears yellow, but the sclera is not, can this be classified as jaundice?
No. Not jaundice.
Pathology of which part of the pancreas can cause jaundice?
Head.
What does a decrease in prothrombin time suggest?
Pathology of the liver - as liver is responsible for synthesis of coagulation factors (which incl. prothrombin).
