Page 422 - Concise Pathology for Exam Preparation ( PDFDrive )

14 The Oral Cavity and Gastrointestinal Tract 407

TABLE 14.5. Differences between tuberculous and typhoid ulcer

Features Tuberculous ulcer Typhoid ulcer
Causative organism Mycobacterium tuberculosis Salmonella typhi
Site Anywhere in small intestine; most com- Most common in terminal ileum (Peyer’s
mon in terminal ileum and caecum, patches); may occur in jejunum
rarely colon
Orientation of the ulcer Perpendicular to long axis of bowel Parallel to long axis of bowel (longitudinal
(transverse ulcer) due to spread by ulcer) due to involvement of Peyer’s
lacteals (lymphatics) patches
Microscopic features Epithelioid cell granulomas with or with- Lymphoplasmacytic infiltrate with
out caseous necrosis histiocytes some of which show
erythrophagocytosis
Fibrosis and stricture Common; intestinal tuberculosis may Rare
formation present with subacute or acute intesti-
nal obstruction
Perforation May be present Common
Bleeding Absent Present

Q. Define inflammatory bowel disease (IBD). Write briefly on its
aetiopathogenesis.

Ans. IBD is a chronic relapsing inflammatory disorder of unknown origin, which results
from an abnormal immune response to normal flora of gut/self-antigens, in genetically
susceptible individuals.
Pathogenesis of IBD involves genetic susceptibility, immune dysregulation and trigger-
ing by microbial flora.

Genetic Predisposition

• IBD is linked to specific HLA types; (ulcerative colitis with HLADRB1 and HLADR7 and
Crohn disease with HLADQ4).
• Association with non-HLA genes, namely, NOD2 (nucleotide-binding oligomerization
domain-2) and a mutant form of IL23, is well known.
• NOD2 is an intracellular receptor for muramyl dipeptidase, a component of the cell
wall in many bacteria, which plays an important role in host responses to these bacteria.
It is expressed in Paneth cells.
• The mutant form is defective in its response to the bacteria, thus allowing chronic infec-
tion to be established in the intestine and promoting inflammatory reactions.
• Alternately, the disease-associated mutant form may promote excessive host response to
the intestinal bacteria.
• IL-23 promotes production of IL17 by T cells and IL17 has been implicated in inflam-
matory reactions seen in IBD and other chronic diseases.

Immunological Reactions

• Immune reactions may be directed against self-antigens of the intestine or bacterial
antigens.
• Primary damaging cells appear to be CD41 T cells.
• Tissue inflammation may be the result of secretion of IL17 by a recently discovered
subset of CD41 T cells called T H 17 subset.
• TNF may play an important role in the pathogenesis of Crohn disease (proven by the
fact that TNF antagonists effectively control the disease).

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