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PA23.9 | GI Morphology — Practical — SDL Guide (Part 2)

Intestinal Ulcers — A Comparative Framework

A four-panel comparison diagram contrasts tuberculous, Crohn disease, ulcerative colitis, and typhoid intestinal ulcers using gross bowel morphology and histology insets.

Comparative Framework of Intestinal Ulcers

Panel A: A. Tuberculous ulcer: ileocaecal region; transverse ulcers crossing bowel axis; multiple irregular ulcers; healed stricture; caseating granuloma; central caseous necrosis; Langhans giant cell; transmural inflammation.. Panel B: B. Crohn disease: skip lesions; cobblestone mucosa; linear fissuring ulcers; creeping fat; pipe-stem stricture; non-caseating granuloma; lymphoid aggregates; transmural inflammation; no caseous necrosis.. Panel C: C. Ulcerative colitis: rectum upward continuous involvement; superficial mucosal ulcers; pseudopolyps; mucosa and superficial submucosa only; crypt abscess; crypt distortion; goblet cell depletion; no granulomas.. Panel D: D. Typhoid ulcer: terminal ileum; Peyer's patches; longitudinal ulcers parallel to bowel axis; lymphoid tissue necrosis; macrophage infiltrate; typhoid cells with engulfed red blood cells and bacteria..

Four inflammatory ulcers of the intestine appear regularly in Pathology practicals. Read them as a comparison group, not as isolated facts.

Tuberculous (TB) ulcer (small bowel, ileocaecal region most common):
- Gross: transverse orientation (crosses the bowel axis), multiple, irregular; healed lesions form strictures
- Micro: caseating granulomas in the submucosa and deeper layers; Langhans giant cells present; central caseous necrosis; transmural inflammation

Crohn disease (ileocaecal most common, skip lesions anywhere):
- Gross: cobblestone mucosa (linear/fissuring ulcers between oedematous islands), skip lesions, creeping fat, pipe-stem strictures
- Micro: non-caseating granulomas (the key negative: no caseous centre); transmural inflammation; lymphoid aggregates in all layers; fissure ulcers; no crypt abscesses (in contrast to UC)

Ulcerative colitis (UC) (rectum upward, continuous):
- Gross: continuous mucosal involvement; pseudopolyps (islands of surviving inflamed mucosa between ulcers)
- Micro: ulceration confined to mucosa and superficial submucosa; crypt abscesses (neutrophils within crypts); crypt architectural distortion; goblet cell depletion; no granulomas; no transmural involvement

Typhoid ulcer (terminal ileum, Peyer's patches):
- Gross: longitudinal ulcers along the axis; located over Peyer's patches
- Micro: macrophage infiltration with engulfed red blood cells and bacteria (typhoid cells); necrosis of lymphoid tissue; Salmonella-specific picture

Side-by-side labeled H&E-style histology comparison of tuberculous intestinal ulcer with caseating granuloma and Langhans giant cell versus Crohn disease with non-caseating granuloma and transmural lymphoid aggregates.

TB Ulcer vs Crohn Disease: Granuloma Histology

Panel A: Tuberculous intestinal ulcer mucosa showing ulcerated mucosa, caseating granuloma, central caseous necrosis, Langhans giant cell, and transmural inflammation.. Panel B: Crohn disease mucosa showing fissuring ulcer, non-caseating granuloma without caseous necrosis, transmural chronic inflammation, and lymphoid aggregates..

SELF-CHECK

A section from the terminal ileum shows transmural inflammation, non-caseating granulomas in the submucosa, and fissure ulcers penetrating toward the muscularis propria. Crypt abscesses are absent. The most likely diagnosis is:

A. Ulcerative colitis

B. Crohn disease

C. Tuberculous enteritis

D. Typhoid ulcer

Reveal Answer

Answer: B. Crohn disease

The combination of transmural inflammation + non-caseating granulomas + fissure ulcers + absence of crypt abscesses is the diagnostic fingerprint of Crohn disease. TB granulomas are caseating (central caseous necrosis). UC is mucosal only and characterised by crypt abscesses without granulomas. Typhoid shows macrophage-rich infiltrate (typhoid cells) over Peyer's patches, not granulomas.

CLINICAL PEARL

Granuloma type is the fastest discriminator between TB and Crohn. In the exam hall: look under medium power for the granuloma centre — if it is pink, amorphous, and structureless, it is caseation (TB). If the granuloma has a neat lymphocytic rim but a clear centre or just epithelioid histiocytes with no necrosis, it is non-caseating (Crohn). A common trap is mistaking the central eosinophilic material in a reactive/foreign-body granuloma for caseation — the distinction is sharpness: caseous necrosis is ghost-cell debris without nuclei, not refractile material.

GI Tumours — Systematic Microscopic Recognition

Six-panel histology diagram comparing key microscopic recognition patterns of squamous cell carcinoma, gastric adenocarcinoma intestinal type, gastric diffuse signet-ring carcinoma, and colorectal adenocarcinoma.

Microscopic Recognition of Common GI Tumours

Panel A: Squamous cell carcinoma with invasive nests, sheets of atypical squamous cells, central keratin pearls, and desmoplastic stroma.. Panel B: High-power squamous cell carcinoma showing individual cell keratinisation, glassy eosinophilic cytoplasm, pyknotic nuclei, prickle cells, and intercellular bridges.. Panel C: Gastric adenocarcinoma intestinal type with irregular back-to-back glands, tubular or papillary gland formation, cytological atypia, inflammatory stroma, and submucosal invasion.. Panel D: Gastric adenocarcinoma diffuse type with scattered signet-ring cells, intracytoplasmic mucin vacuoles, peripheral nuclei, stromal infiltration without gland formation, and linitis plastica inset.. Panel E: Colorectal adenocarcinoma with irregular confluent malignant glands, luminal dirty necrosis, moderate-to-severe atypia, invasion through muscularis propria, and possible vascular or perineural invasion.. Panel F: Exam recognition anchors: keratin pearl, back-to-back glands, signet-ring cells, and dirty necrosis within gland lumina..

The practical exam presents tumour slides in groups. Anchor each tumour to its characteristic micro pattern.

Oesophageal / Oral squamous cell carcinoma (SCC):
- Pattern: sheets and nests of squamous cells with central keratin pearls (concentric whorls of pink, keratinised cells)
- Individual cell keratinisation (glassy pink cytoplasm, pyknotic nucleus) and intercellular bridges (prickle cells) on high power
- Stromal desmoplasia around invasive nests

Gastric adenocarcinoma — intestinal type:
- Pattern: irregular, back-to-back glands with moderate-to-severe cytological atypia; glandular architecture is recognisable (tubular or papillary)
- Invasion into the submucosa or deeper
- Inflammatory stroma; intestinal metaplasia often present in adjacent mucosa

Gastric adenocarcinoma — diffuse (signet-ring cell) type:
- Pattern: individual cells infiltrating the stroma, no gland formation
- Signet-ring cells: large intracytoplasmic mucin vacuole pushes the nucleus to the periphery, giving a 'signet ring' appearance on H&E
- Infiltrates diffusely through all layers; may cause linitis plastica (leather-bottle stomach) grossly

Colorectal adenocarcinoma:
- Pattern: irregular, confluent glands with moderate-to-severe atypia; luminal dirty necrosis (dark, granular, necrotic cell debris within gland lumina) is a classic clue
- Invasion through the muscularis propria; perineural or vascular invasion may be visible
- Tumour budding at the invasive front on low power

Adenomatous polyp (tubular vs villous):
- Tubular adenoma: branching tubular glands lined by dysplastic columnar epithelium; stalk present; low-grade dysplasia most common
- Villous adenoma: finger-like villi projecting from the surface; higher dysplasia risk; larger size
- Both are intramucosal dysplastic lesions — malignant transformation requires invasion through the muscularis mucosae

Side-by-side H&E-style histology comparison of tubular adenoma with branching tubular glands and villous adenoma with elongated finger-like villi, both showing dysplastic epithelium.

Tubular Adenoma versus Villous Adenoma

Panel A: Tubular adenoma showing preserved stalk, branching tubular glands, crowded dysplastic epithelium, hyperchromatic pseudostratified nuclei, and lamina propria.. Panel B: Villous adenoma showing elongated finger-like villi, fibrovascular cores, surface dysplasia, crowded hyperchromatic epithelial nuclei, and mucin depletion..

Four-Panel Composite: GI Specimen Identification Activity

A four-panel H&E-style histology composite showing peptic ulcer zones, colorectal adenocarcinoma with dirty necrosis, diffuse gastric adenocarcinoma with signet-ring cells, and Crohn disease versus ulcerative colitis.

GI Specimen Identification: Key Histologic Lesions

Panel A: Peptic ulcer floor showing fibrinopurulent exudate, necrotic debris, granulation tissue, and fibrotic scar base.. Panel B: Colorectal adenocarcinoma showing irregular malignant glands, invasive growth, desmoplastic stroma, and dirty necrosis in gland lumina.. Panel C: Diffuse gastric adenocarcinoma showing signet-ring cells infiltrating lamina propria, mucin vacuoles, peripheral nuclei, and absent gland formation.. Panel D: Crohn disease versus ulcerative colitis comparison showing non-caseating granuloma and transmural inflammation on the left, crypt abscess and mucosal disease on the right..

Use the image below as an H5P Image Hotspots identification exercise. For each panel, identify the lesion and its key diagnostic feature before expanding the hotspot.

A four-panel H&E-style pathology teaching grid comparing peptic ulcer floor, colorectal adenocarcinoma, diffuse gastric adenocarcinoma, and Crohn disease versus ulcerative colitis.

GI Histopathology: Ulcers and Adenocarcinoma Patterns

Panel A: Peptic ulcer floor showing fibrinopurulent exudate, necrotic zone, granulation tissue, and deepest fibrotic base.. Panel B: Colorectal adenocarcinoma showing irregular invasive glands, dirty necrosis in gland lumina, desmoplastic stroma, and pleomorphic malignant epithelium.. Panel C: Diffuse gastric adenocarcinoma showing signet-ring cells infiltrating lamina propria, mucin vacuoles, peripheral nuclei, and absence of gland formation.. Panel D: Crohn disease versus ulcerative colitis comparison showing non-caseating granuloma and transmural inflammation on the left, with mucosal inflammation and crypt abscess on the right..

SELF-CHECK

A colorectal resection slide shows irregular malignant glands with central dark granular material filling the gland lumina. This finding is referred to as:

A. Caseous necrosis

B. Dirty necrosis

C. Comedonecrosis

D. Colliquative necrosis

Reveal Answer

Answer: B. Dirty necrosis

Dirty necrosis — dark, granular, necrotic tumour cell debris within malignant gland lumina — is a hallmark of colorectal adenocarcinoma on H&E. It contrasts with caseous necrosis (amorphous, pale, ghost-cell debris in TB granulomas) and comedonecrosis (central necrosis in cribriform ducts, classically DCIS of the breast). Dirty necrosis in a gland-forming tumour of the colorectum is essentially pathognomonic in the exam context.

SELF-CHECK

A gastric biopsy shows individually scattered cells with a large, clear intracytoplasmic vacuole displacing the nucleus to the cell periphery. These cells infiltrate the lamina propria without forming recognisable glands. Which tumour type and subtype does this describe?

A. Intestinal-type gastric adenocarcinoma

B. Diffuse-type gastric adenocarcinoma (signet-ring cell)

C. Gastric MALT lymphoma

D. Metastatic lobular breast carcinoma

Reveal Answer

Answer: B. Diffuse-type gastric adenocarcinoma (signet-ring cell)

The description — solitary cells with mucin vacuole pushing nucleus to periphery, no gland formation, diffuse infiltration — is the classic signet-ring cell pattern of diffuse-type gastric adenocarcinoma. Intestinal-type forms recognisable glands. MALT lymphoma shows lymphoid cells with lymphoepithelial lesions. Metastatic lobular carcinoma from the breast can produce an identical picture (both are signet-ring patterns) — clinical context and immunohistochemistry (CDX2, CK20 for gastric; ER, GATA3 for breast) distinguish them.