skip to main content

Anti-EGFR GI Toxicity — SCE Medical Oncology MCQ

Instant feedback + full explanation. One question, done properly.

HardGI CancersAnti-EGFR GI ToxicitySCE Medical Oncology

A 72-year-old man with metastatic CRC develops chronic diarrhoea on long-term cetuximab. He has no colitis symptoms and stool cultures are negative. The diarrhoea correlates with the severity of his acneiform rash. What is the mechanism?

Educational content. Not a substitute for clinical judgement or local policy.

Reveal the answer and explanation

Correct answer: C — Loss of EGFR-dependent intestinal epithelial repair and secretory control

EGFR supports intestinal epithelial renewal and fluid regulation; its blockade can produce chronic secretory diarrhoea alongside the parallel acneiform skin effect. Loss of EGFR-dependent pancreatic acinar repair causing exocrine insufficiency: cetuximab diarrhoea is principally an intestinal epithelial effect rather than pancreatic failure. Loss of EGFR-dependent bile-duct repair causing bile-acid malabsorption: the drug does not selectively injure terminal ileal bile-acid transport via this mechanism. Loss of EGFR-dependent enteric-neuron repair causing autonomic hypermotility: enteric neuronal injury is not the established class mechanism. Loss of EGFR-dependent mucosal immunity causing opportunistic enteric infection: negative cultures and chronic non-neutropenic presentation favour direct epithelial toxicity.

Reference: Clinical management of diarrhoea in patients treated with targeted agents (Published June 2021): https://pmc.ncbi.nlm.nih.gov/articles/PMC8201561/; Erbitux UK summary of product characteristics (Updated September 2025): https://www.medicines.org.uk/emc/product/317/smpc