A 35-year-old woman presents with a 2-year history of chronic rectal bleeding and incomplete evacuation. Sigmoidoscopy reveals a well-demarcated ulcer with heaped erythematous edges on the anterior rectal wall, 8 cm from the anal verge. Multiple biopsies show fibromuscular obliteration of the lamina propria with thickening of the muscularis mucosae. The structure marked **A** in the diagram represents this anterior rectal wall lesion. Which of the following is the PRIMARY PATHOPHYSIOLOGIC MECHANISM underlying the formation of this lesion?
A. Transmural inflammation from Crohn disease with secondary ulceration and fistulization
B. Repetitive mucosal trauma from paradoxical puborectalis contraction and internal rectal intussusception during straining
C. Ischemic injury to the rectal mucosa from atherosclerotic stenosis of the superior rectal artery
D. Malignant transformation of a tubulovillous adenoma with invasion of the muscularis propria
Explanation
Why "Repetitive mucosal trauma from paradoxical puborectalis contraction and internal rectal intussusception during straining" is right
The anterior rectal wall ulcer marked A is the hallmark of solitary rectal ulcer syndrome (SRUS), a benign chronic defecation disorder. The pathogenesis is well-established: dyssynergic defecation (anismus) causes the puborectalis to contract paradoxically during straining, leading to internal rectal intussusception. This repetitive mechanical trauma causes mucosal ischemia and prolapse against the contracted sphincter, producing the characteristic anterior wall ulcer with the pathognomonic histologic triad of fibromuscular obliteration of the lamina propria, muscularis mucosae thickening, and crypt distortion. This mechanism is the defining feature of SRUS per ACG Functional Bowel Guidelines and Felt-Bersma WJG 2009.
Why each distractor is wrong
Transmural inflammation from Crohn disease with secondary ulceration and fistulization: Crohn proctitis (marked C in the diagram) presents with transmural inflammation, skip lesions, and fistulization. The histology shows granulomatous inflammation, not fibromuscular obliteration. The lesion distribution and clinical context differ fundamentally from SRUS.
Malignant transformation of a tubulovillous adenoma with invasion of the muscularis propria: A tubulovillous adenoma (marked D) is a premalignant polyp that may undergo dysplastic change, but it does not produce the characteristic fibromuscular obliteration pattern seen in SRUS. The histology and location differ, and malignant lesions show dysplasia and invasion, not the benign muscularis mucosae thickening of SRUS.
Ischemic injury to the rectal mucosa from atherosclerotic stenosis of the superior rectal artery: Ischemic proctitis produces segmental ulceration from vascular insufficiency, but lacks the characteristic anterior wall location, the fibromuscular obliteration pattern, and the association with dyssynergic defecation. The pathophysiology is vascular, not mechanical.
High-YieldNEET PG
SRUS is a benign mechanical injury syndrome from anismus and internal rectal intussusception, NOT inflammatory or malignant—the fibromuscular obliteration of lamina propria is pathognomonic.
