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PA23.5-7 | Intestinal TB, Appendicitis, IBD & Malabsorption — SDL Guide

Learning Objectives

Describe the etiology, pathogenesis, and pathological forms of intestinal tuberculosis, and distinguish it from Crohn disease
Explain the pathogenesis and morphological stages of acute appendicitis, including complications
Compare Crohn disease and ulcerative colitis across distribution, gross morphology, microscopy, complications, and extraintestinal manifestations
Enumerate the causes of malabsorption syndrome and describe the laboratory approach to its diagnosis

INSTRUCTIONS

Gastrointestinal pathology is a high-yield area in Indian clinical medicine — intestinal tuberculosis mimics Crohn disease on endoscopy, appendicitis is the commonest surgical emergency, and tropical sprue is a diagnosis you will make in your own patient population. This module links pathological mechanisms directly to clinical presentations and investigations you will order as a doctor.

References

Robbins & Kumar Basic Pathology, 11th ed., Ch 14 (textbook)
Harsh Mohan Textbook of Pathology, 8th ed., Ch 17 (textbook)

Version 2.0 | NMC CBUC 2024

CLINICAL SCENARIO

A 24-year-old woman from rural Tamil Nadu presents with 3 months of right iliac fossa pain, weight loss, and a palpable mass. Colonoscopy shows ulceration and narrowing at the ileocaecal junction. The gastroenterologist and the surgeon are debating: is this Crohn disease or intestinal tuberculosis? The biopsy report arrives — and the pathologist's words will determine whether she gets steroids or anti-TB therapy. One wrong call is life-threatening. By the end of this module, you will know exactly what to look for on that biopsy.

WHY THIS MATTERS

India carries the world's highest burden of intestinal tuberculosis. Appendicitis is the most common acute surgical abdomen you will manage as a house officer. Inflammatory bowel disease is rising in urban India. Coeliac disease and tropical sprue cause preventable nutritional failure. These four conditions together underlie a large fraction of the gastrointestinal surgery and medicine admissions in any Indian tertiary hospital.

RECALL

Before you start, recall from Year-1:
• Mycobacterium tuberculosis — acid-fast bacillus, caseating granuloma as the hallmark lesion.
• The appendix — a blind-ended diverticulum of the caecum; lymphoid tissue is prominent in childhood.
• Autoimmune disease concept — immune response targeting self or luminal antigens.
• Malabsorption — failure to absorb nutrients in the small intestine; leads to steatorrhoea and nutritional deficiencies.

Hold these in mind as we build on them.

Intestinal Tuberculosis — Forms and Pathogenesis

Diagram showing routes of intestinal tuberculosis infection, ileocaecal predilection, pathogenesis through Peyer's patches and granulomas, and ulcerative versus fibrotic morphological outcomes. — **Panel A:** GI tract overview showing mouth, lungs, stomach, small intestine, terminal ileum, caecum, primary ingestion route, secondary swallowed sputum route, haematogenous spread, and direct extension.. **Panel B:** Magnified ileocaecal junction showing terminal ileum, caecum, Peyer's patches, lymphoid tissue, physiological stasis, and increased mucosal permeability.. **Panel C:** Pathogenesis flow showing Mycobacterium tuberculosis bacilli, Peyer's patch entry, macrophage uptake, caseating granuloma formation, ulceration, and fibrosis.. **Panel D:** Gross morphological outcomes showing transverse circumferential girdle ulcers with undermined edges and caseating base, contrasted with hyperplastic or fibrotic thickening and luminal narrowing..

Intestinal tuberculosis (ITB) is caused by Mycobacterium tuberculosis (occasionally M. bovis from unpasteurised milk). It reaches the gut by one of three routes:
1. Primary ITB — ingestion of bacilli in childhood; no lung focus; Peyer's patches in the terminal ileum are the entry point.
2. Secondary ITB — swallowing infected sputum from pulmonary TB (most common in adults).
3. Haematogenous spread or direct extension from adjacent organs (less common).

Why the ileocaecal region? The terminal ileum and caecum are the preferred sites because of abundant lymphoid tissue (Peyer's patches), physiological stasis, and increased mucosal permeability at this junction — providing ideal conditions for mycobacterial implantation.

Pathogenesis: Bacilli enter Peyer's patches → macrophage uptake → caseating granuloma formation → ulceration or fibrosis depending on host immunity.

Four-panel medical diagram showing primary and secondary routes of intestinal tuberculosis to the ileocaecal region, with ulcerative, hyperplastic, microscopic, and complication features. — **Panel A:** Primary ingestion route, secondary pulmonary/systemic routes, swallowed infected sputum, hematogenous spread, lymphatic spread, terminal ileum, ileocaecal valve, caecum, Peyer's patches, ileocaecal predilection. **Panel B:** Ulcerative form, transverse circumferential girdle ulcers, ulcers perpendicular to long axis, undermined edges, caseous ulcer base, fibrosis, stricture formation. **Panel C:** Hyperplastic form, thickened contracted caecum, mural fibrosis, napkin-ring stricture, ileocaecal mass, cocoon caecum, inverted umbrella sign. **Panel D:** Caseating granulomas, central caseous necrosis, Langhans giant cells, submucosa, muscularis propria, serosa, stricture obstruction, rare perforation, rare fistula, malabsorption, rare hemorrhage.

Intestinal Tuberculosis — Morphological Forms

Diagram of intestinal tuberculosis showing ulcerative transverse girdle ulcers, hyperplastic ileocaecal thickening, caseating granulomas across bowel wall layers, and major complications. — **Panel A:** Opened terminal ileum showing transverse circumferential girdle or belt ulcers, perpendicular orientation to bowel long axis, undermined ulcer edges, caseous ulcer bases, and scale bar.. **Panel B:** Hyperplastic intestinal tuberculosis showing thickened contracted caecum, mural fibrosis, napkin-ring stricture, ileocaecal mass or cocoon caecum, and inverted umbrella sign inset.. **Panel C:** Microscopy showing caseating granulomas in submucosa, muscularis propria, and serosa, with central caseous necrosis, epithelioid cells, confluent granulomas, and Langhans giant cells.. **Panel D:** Complications strip showing fibrotic stricture with obstruction, uncommon perforation, rare fistula, malabsorption from mucosal damage, and TB transverse ulcers contrasted with Crohn longitudinal fissures..

Ulcerative form (more common, ~60%):
• Transverse ulcers that run around the circumference — hence called 'girdle' or 'belt' ulcers. This is the pathognomonic gross feature.
• Ulcers are perpendicular to the long axis of the bowel (contrast with Crohn's longitudinal fissures).
• Base shows caseating granulomas; edges are undermined.
• Heals with fibrosis → stricture.

Hyperplastic (hypertrophic) form (~40%):
• Marked fibrosis and mural thickening produce a napkin-ring stricture or a palpable ileocaecal mass (the 'cocoon' caecum).
• The caecum is thickened and contracted — radiologically the 'inverted umbrella' sign.
• More commonly confused with carcinoma or Crohn disease clinically.

Microscopy (both forms): Caseating granulomas in all layers — submucosa, muscularis, serosa. Granulomas are larger, more numerous, and confluent compared with Crohn disease. Langhans giant cells are characteristic.

Complications: Stricture and obstruction (commonest), perforation (uncommon — fibrosis protects), fistulae (rare vs Crohn), malabsorption from mucosal damage, and rarely haemorrhage.

Medical illustration comparing intestinal tuberculosis and Crohn disease, emphasizing transverse girdle ulcers in the terminal ileum and key gross and microscopic distinguishing clues. — **Panel A:** Opened terminal ileum specimen showing transverse circumferential girdle ulcers, ulcer base with necrotic slough, thickened bowel wall, callout arrows, and 2 cm scale bar.. **Panel B:** Comparison of intestinal TB with transverse circumferential ulcers and continuous ileocaecal involvement versus Crohn disease with longitudinal fissures, aphthous ulcers, cobblestone mucosa, and skip lesions.. **Panel C:** Pathology clues comparing intestinal TB with fibrinous serosa, caseating granuloma, central caseous necrosis, and AFB positivity versus Crohn disease with creeping fat, transmural inflammation, non-caseating granulomas, fistula tract, and AFB negativity..

Intestinal TB vs Crohn Disease — The India-Critical Distinction

Side-by-side medical diagram comparing intestinal tuberculosis and Crohn disease in ileocaecal involvement, ulcer orientation, granulomas, serosal changes, fistulae, skip lesions, and AFB status. — **Panel A:** Terminal ileum, caecum, ileocaecal valve, ascending colon, ileocaecal disease focus, Intestinal TB, Crohn Disease. **Panel B:** Transverse circumferential girdle ulcer, longitudinal fissure, aphthous ulcer, cobblestone mucosa, skip lesion, continuous disease at ileocaecal site. **Panel C:** Thickened fibrinous serosa, large confluent caseating granuloma, central caseous necrosis, AFB positive, creeping fat, transmural inflammation, small scattered non-caseating granuloma, fistula tract, AFB negative.

This comparison is tested in exams and saves lives in practice. Both cause ileocaecal disease with granulomas.

Feature	Intestinal TB	Crohn Disease
Ulcer orientation	Transverse (girdle)	Longitudinal fissures + aphthous
Granulomas	Caseating, large, confluent	Non-caseating, small, scattered
Serosa	Thickened, fibrinous	Creeping fat wrapping
Fistulae	Rare	Very common
Skip lesions	No (usually continuous at site)	Yes
AFB smear/PCR	Positive (or culture)	Negative
Mantoux/IGRA	Usually positive	Negative
Response to steroids	Worsens (or masks)	Improves

Clinical pearl: In India, NEVER start steroids for presumed Crohn disease without first excluding TB by Mantoux, IGRA, and biopsy PCR. Steroid immunosuppression converts latent TB to disseminated disease.

Side-by-side diagram comparing intestinal tuberculosis with transverse girdle ulcers and caseating granulomas against Crohn disease with longitudinal fissures, cobblestoning, and non-caseating granulomas. — **Panel A:** Intestinal tuberculosis: transverse girdle ulcers, ileocaecal stricture, thickened bowel wall, transmural granulomatous inflammation, caseating granuloma, central caseous necrosis, Langhans giant cell, lymphocytic rim.. **Panel B:** Crohn disease: longitudinal fissures, cobblestone mucosa, skip lesion pattern, deep fissuring ulcer, transmural inflammation, creeping fat, non-caseating granuloma, no central necrosis, epithelioid histiocytes..

SELF-CHECK

A biopsy from an ileocaecal stricture in a 28-year-old shows large, confluent granulomas with central caseous necrosis involving all bowel wall layers. Which single feature most definitively distinguishes intestinal tuberculosis from Crohn disease on histology?

A. Caseating necrosis within granulomas

B. Transmural inflammation

C. Presence of Langhans giant cells

D. Mucosal ulceration

Reveal Answer

Answer: A. Caseating necrosis within granulomas

Caseating necrosis is the histological hallmark of TB granulomas and is absent in Crohn disease. Both conditions show transmural inflammation and giant cells. Ulceration occurs in both. Caseous necrosis on biopsy, confirmed by AFB stain or PCR, drives the decision to treat as TB rather than IBD.