Obstructive Jaundice — Written Clinical Reasoning

Part A — Diagnosis and the mechanism of obstructive jaundice

Diagnosis

The diagnosis is obstructive (surgical) jaundice from a pancreatic head mass, with the clinical and biochemical features of complete biliary obstruction: painless progressive jaundice, pale stools (acholic, from absence of intestinal stercobilin), dark urine (from conjugated bilirubin excreted by the kidney), pruritus, weight loss, and a markedly elevated CA 19-9. The cholestatic liver function pattern (conjugated hyperbilirubinaemia, ALP five times normal, elevated GGT, mildly raised transaminases) and the Courvoisier sign (palpable, non-tender gallbladder in a jaundiced patient) are both consistent with a malignant distal biliary obstruction ^[5].

The CT finding of a pancreatic head mass makes pancreatic ductal adenocarcinoma the leading diagnosis. Courvoisier sign has a low sensitivity but a moderate-to-high specificity for malignancy — its presence strongly suggests a malignant rather than a stone obstruction ^[5].

Pathophysiology — why the pattern arises

The obstruction prevents conjugated bilirubin from reaching the gut, so it refluxes into the bloodstream (conjugated hyperbilirubinaemia) and is filtered by the kidney (dark urine). The absence of intestinal stercobilin produces pale stools. The elevated ALP and GGT reflect the cholestatic injury to the hepatocytes and canaliculi. The GGT confirms the hepatic (rather than bone) origin of the ALP. ^[1]