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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Jaundice = clinical sign of hyperbilirubinaemia (>40 µmol/L for visible jaundice). First seen in sclerae
- Pre-hepatic (haemolytic): raised unconjugated bilirubin, normal LFTs, raised reticulocytes, raised LDH. Dark urine = absent
- Hepatic (hepatocellular): raised conjugated + unconjugated bilirubin, raised ALT/AST, ± low albumin. Causes: hepatitis, cirrhosis, drugs
- Post-hepatic (obstructive): raised conjugated bilirubin, raised ALP/GGT >> ALT/AST, dark urine, pale stools, pruritus
- First-line investigation for obstructive jaundice: USS abdomen (dilated ducts?). If obstructed → MRCP/ERCP
Overview
Jaundice is the yellow discolouration of the skin, sclerae, and mucous membranes caused by elevated circulating bilirubin. Bilirubin is a breakdown product of haem, primarily from senescent red blood cells. It is transported to the liver (unconjugated, bound to albumin), conjugated with glucuronic acid by hepatocytes (making it water-soluble), excreted into bile, and metabolised by gut bacteria to urobilinogen and stercobilin (giving stool its brown colour). Jaundice is classified by the site of the problem: pre-hepatic (excess bilirubin production from haemolysis), hepatic (impaired hepatocyte uptake, conjugation, or excretion), or post-hepatic/obstructive (blocked bile drainage into the duodenum).
Epidemiology
Jaundice is a clinical sign rather than a diagnosis, and its epidemiology depends on the underlying cause. The commonest causes in UK adults are gallstone-related obstruction (choledocholithiasis), alcoholic liver disease, viral hepatitis, drug-induced liver injury (paracetamol, antibiotics, statins), and malignancy (pancreatic head cancer, cholangiocarcinoma). Gilbert syndrome (benign unconjugated hyperbilirubinaemia) is extremely common, affecting ~5–10% of the population, and is the commonest cause of isolated mildly raised bilirubin found incidentally.
Clinical Features
Symptoms
Yellow skin and eyes (sclerae affected first — bilirubin has high affinity for elastic tissue)
Dark urine ("coca-cola" or "tea-coloured" — conjugated bilirubin is water-soluble and excreted renally)
Pale/clay-coloured stools (acholic — absent stercobilin in obstructive jaundice)
Pruritus (bile salt deposition in skin — prominent in obstructive jaundice)
Abdominal pain (RUQ — gallstones, hepatitis; painless = think malignancy)
Weight loss (malignancy)
Fever and rigors (cholangitis)
Signs
Scleral icterus (clinically visible at bilirubin >40 µmol/L)
Hepatomegaly (hepatitis, malignancy, fatty liver)
Palpable non-tender gallbladder (Courvoisier law — malignant distal CBD obstruction)
Splenomegaly (haemolysis, portal hypertension, lymphoproliferative disease)
Stigmata of chronic liver disease (if hepatic cause: spider naevi, palmar erythema, ascites)
Excoriation marks (severe pruritus from cholestasis)
Pallor (haemolytic anaemia)
Investigations
First-line
LFTs (liver function tests)Bilirubin (total and conjugated/unconjugated split if requested), ALT, AST, ALP, GGT, albumin. Obstructive: ALP/GGT >> ALT. Hepatocellular: ALT/AST >> ALP
FBC and blood filmAnaemia + reticulocytosis + raised LDH + low haptoglobin = haemolysis. Blood film may show spherocytes, schistocytes, sickle cells
Coagulation (INR/PT)Prolonged in liver failure (impaired synthesis) and obstructive jaundice (impaired vitamin K absorption — corrects with IV vitamin K in obstruction but NOT in hepatocellular failure)
UrinalysisConjugated hyperbilirubinaemia: bilirubin in urine (dark). Unconjugated: absent from urine (not water-soluble). Urobilinogen raised in haemolysis, absent in complete obstruction
Second-line
Abdominal ultrasoundFirst-line imaging for jaundice — assess for dilated bile ducts (obstruction), gallstones, liver parenchyma, pancreatic mass
Liver screenHepatitis B/C serology, autoantibodies (ANA, SMA, AMA, LKM), immunoglobulins, ferritin/transferrin saturation, caeruloplasmin (if <50 years)
Haemolysis screenIf pre-hepatic suspected: direct Coombs test (autoimmune), reticulocyte count, haptoglobin, LDH, blood film
Specialist
MRCPNon-invasive biliary imaging if USS shows dilated ducts — identifies CBD stones, strictures, mass lesions
ERCPTherapeutic: stone extraction, stenting. Not first-line diagnostic due to procedure risks (pancreatitis, perforation)
CT abdomen/pelvisIf malignancy suspected — staging of pancreatic, biliary, or hepatic tumours
Liver biopsyIf hepatic cause unclear after non-invasive work-up
1
Pre-hepatic (haemolytic)
- Treat underlying cause (autoimmune haemolysis → steroids; sickle cell → supportive; malaria → antimalarials)
- Folate supplementation (increased red cell turnover)
- Transfusion if severe anaemia
- Splenectomy in select cases (e.g. hereditary spherocytosis)
2
Hepatic (hepatocellular)
- Identify and treat cause: viral hepatitis (DAAs for HCV, antivirals for HBV), drug-induced (stop offending drug), alcoholic hepatitis (abstinence ± steroids), autoimmune hepatitis (steroids + azathioprine)
- Supportive care: avoid hepatotoxic drugs, adequate nutrition
- Consider liver transplant if acute liver failure or decompensated cirrhosis
3
Post-hepatic (obstructive)
- Gallstone obstruction (choledocholithiasis): ERCP + sphincterotomy + stone extraction → cholecystectomy
- Malignant obstruction: biliary stenting (ERCP or PTC) for symptom relief ± oncological management
- Correct coagulopathy: IV vitamin K 10 mg (response in obstruction confirms vitamin K malabsorption; no response suggests hepatocellular failure)
- Cholestyramine for pruritus (bile acid sequestrant)
4
Gilbert syndrome
- Reassurance — benign condition, no treatment required
- Unconjugated hyperbilirubinaemia triggered by fasting, stress, illness, or exercise
- Normal LFTs, no haemolysis, no liver disease. Genetically: UGT1A1 gene polymorphism
- Important to document in medical records to avoid future unnecessary investigation
Complications
- Biliary sepsis (cholangitis): Obstructive jaundice + infection → life-threatening. Charcot's triad: pain, jaundice, fever
- Coagulopathy: Vitamin K malabsorption (obstructive) or impaired synthesis (hepatocellular) → bleeding risk
- Hepatorenal syndrome: In advanced hepatic jaundice
- Kernicterus: Neonatal complication — unconjugated bilirubin crosses the blood-brain barrier → brain damage (not relevant in adults)
UKMLA Exam Tips
- 1Obstructive: ALP/GGT >> ALT, dark urine, pale stools, pruritus. Hepatocellular: ALT/AST >> ALP. Pre-hepatic: normal LFTs, raised LDH/reticulocytes
- 2Unconjugated bilirubin is NOT water-soluble → NOT excreted in urine → urine is normal colour in haemolysis
- 3IV vitamin K corrects INR in obstructive jaundice (bile salt deficiency) but NOT in hepatocellular failure (parenchymal damage) — important differentiator
- 4Gilbert syndrome: isolated mild unconjugated hyperbilirubinaemia, normal LFTs, worse with fasting. ~5–10% of population. BENIGN — no treatment needed
- 5Painless progressive jaundice + palpable gallbladder = Courvoisier law → think pancreatic/periampullary cancer (NOT gallstones)
- 6First investigation for jaundice: LFTs to classify, then USS to assess for obstruction (dilated ducts)
- 7Conjugated bilirubin in urine (dark urine) = hepatic or post-hepatic cause. No bilirubin in urine = pre-hepatic (unconjugated)
practicetest your knowledge on jaundiceApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — gastroenterology and beyond.
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