A 28-year-old man presents with a 6-month history of chronic diarrhea, right lower quadrant abdominal pain, and a 4 kg weight loss. Ileocolonoscopy with biopsy reveals non-caseating granulomas and transmural inflammation. On contrast-enhanced CT enterography, the terminal ileum shows a markedly thickened, rigid wall with a severely narrowed lumen, creating the appearance shown as structure **A** in the diagram. Which of the following best explains why this morphological change occurs in Crohn disease but NOT in ulcerative colitis?
A. The transmural nature of inflammation in Crohn disease leads to fibrosis and smooth muscle hypertrophy throughout all layers of the bowel wall, causing wall thickening and luminal narrowing
B. Ulcerative colitis involves only the mucosa and submucosa, whereas Crohn disease causes inflammation extending through all layers of the bowel wall, resulting in fibrosis and stricture formation
C. Crohn disease is associated with caseating granulomas that destroy the muscularis propria, whereas ulcerative colitis spares the deeper layers
D. The presence of skip lesions in Crohn disease causes segmental wall thickening, whereas the continuous involvement in ulcerative colitis prevents localized stricture formation
Explanation
Why option 1 is correct
The structure marked A — the thickened, rigid terminal ileal wall with narrowed lumen (string sign) — is a hallmark gross feature of Crohn disease that results directly from its transmural inflammatory nature. Crohn disease is a chronic, transmural granulomatous inflammatory disease affecting all layers of the bowel wall (mucosa through serosa). This transmural inflammation triggers fibrosis, smooth muscle hypertrophy, and stricture formation, producing the characteristic thickened, rigid bowel wall with luminal narrowing visible on imaging. This pathological process is unique to Crohn disease because of its transmural depth, distinguishing it from ulcerative colitis, which is limited to the mucosa and submucosa and therefore does not produce transmural fibrosis or strictures. (Robbins Basic Pathology 11e; ECCO 2024 guidelines)
Why each distractor is wrong
Option 0: While this option is partially correct in naming fibrosis and smooth muscle hypertrophy, it fails to explicitly contrast the transmural nature of Crohn disease with the mucosal-only involvement of ulcerative colitis, which is the key mechanistic distinction required to answer the question.
Option 2: Crohn disease is characterized by non-caseating granulomas, not caseating granulomas. Caseating granulomas are seen in tuberculosis and fungal infections. This is a common distractor that tests whether students confuse the histological hallmark of Crohn disease.
Option 3: While skip lesions are indeed a feature of Crohn disease, they do not directly explain the thickened wall and luminal narrowing. The stricture formation is driven by transmural fibrosis, not by the presence of skip lesions. This distractor conflates a distribution pattern with a pathological mechanism.
High-YieldNEET PG
Crohn disease = transmural inflammation → fibrosis and strictures; Ulcerative colitis = mucosal inflammation → no strictures, only mucosal ulceration.
Robbins Basic Pathology 11e; ECCO 2024 guidelines
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