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LOWER G I T REVIEW
DR. PRASANNA N KUMAR
OMC
CONGENITAL ANOMALIES - MECKEL
DIVERTICULUM
 Failure of involution of vitelline
duct (omphalomesenteric duct)
 Antimesenteric side of bowel, within 2 feet
from ileocaecal valve
 True diverticulum – contains mucosa,
submucosa, muscularis propria
MECKEL DIVERTICULUM
 Bacterial overgrowth
– B12 deficiency –
megaloblastic
anemia
 Heterotopic rests
may be seen –
gastric mucosa,
pancreatic tissue
 Intestinal bleeding,
perforation
HIRSCHSPRUNG DISEASE-CONGENITAL
AGANGLIONIC MEGACOLON
 Mic – absence of
ganglion cells in muscle
wall & submucosa of
nondistended bowel
 Rectum and sigmoid
colon usually involved
 Proximal to aganglionic
segment –
MEGACOLON
 Failure to pass
meconium
INTESTINAL ULCERS - ORGANISMS
 TYPHOID ULCERS
longitudinal
 TUBERCULOSIS–
transverse ulcers
and strictures
 AMOEBIASIS
large intestine
E. histolytica
discrete, oval flaskshaped ulcers
 GIARDIASIS
A 23-year-old man presents with complaints
of diarrhea for 4 weeks. He describes his
stools as soft, pale, large and greasy. He
also says that he has lost 5 kgs of weight
over the last one month.
MALABSORPTION SYNDROMES
CELIAC DISEASE
 Sensitivity to gluten
 Caucasian disease
 Proximal small int.
 Atrophy of villi
 Responds to
gluten-free diet
TROPICAL SPRUE
? Infectious
Tropical disease
All levels of small int.
Severe diffuse enteritis
with villous flattening
Responds to antibiotics
NORMAL MUCOSA
CELIAC
DISEASE
IDIOPATHIC INFLAMMATORY
BOWEL DISEASE
 CD – autoimmune, esophagus – anus,




more in distal small intestine & colon
UC – chronic inflammatory disease limited
to colon and rectum
CD and UC – extraintestinal inflammatory
manifestations
HLA associations – HLA –DR1 (CD),
HLA-DR2 (UC)
CD – mutations in NOD2 gene
COMPARISON OF UC AND CD
MACROSCOPIC
FEATURES
CD
UC
Bowel region
Ileum + colon
Colon only
Distribution
Skip lesions,
serpentine ulcers
Diffuse, pancolitis
Stricture
Early – fissures,
fistulae, sinuses
No fissures,
fistulae, sinuses
Wall appearance
Thickened
Thin – toxic
megacolon
Dilation
No
Yes
CROHN DISEASE - GROSS
 “Skip lesions”
 “Cobblestone”
appearance of
mucosa
 Intestinal wall –
rubbery, thick
due to edema,
inflammation,
fibrosis, hypertrophy
of muscularis
propria
GROSS – CD AND UC
CD
UC
Toxic megacolon
COMPARISON OF UC AND CD
MICROSCOPIC
FEATURE
CD
UC
Inflammation
Transmural
Limited to mucosa
Pseudopolyps
No
Yes
Ulcers
Deep, linear
Superficial
Lymphoid reaction
Marked
Mild
Fibrosis
Marked
Mild
Serositis
Marked
Mild to nil
Granulomas
Yes(50%)
No
MICROSCOPY – CD
UC
COMPARISON OF UC AND CD
CLINICAL
CD
UC
Fat/vitamin
malabsorption
Yes
No
Malignant
potential
Yes, less than in
UC
Yes
Extraintestinal
involvement
Migratory
polyarthritis,
ankylosing
spondylitis etc.
Response to
surgery
Poor
Migratory
polyarthritis,
ankylosing
spondylitis etc.
Good
COMPARISON
OF
CD AND UC
TUMORS OF SMALL INTESTINE &
COLON
NON-NEOPLASTIC (BENIGN) POLYPS
 Hyperplastic polyps, hamartomatous polyps juvenile polyps, Peutz-Jeghers polyps
 Inflammatory polyps, lymphoid polyps
NEOPLASTIC EPITHELIAL LESIONS
 Benign – adenomas, adenomatous polyps
 Malignant – adenocarcinoma, carcinoid tumor
 Gastrointestinal stromal tumor (GIST) – benign to
malignant, LYMPHOMAS
NON-NEOPLASTIC POLYPS
 Hyperplastic polyps
 Hamartomatous polyps
Juvenile polyps
Peutz-Jeghers polyps
 Inflammatory polyps
 Lymphoid polyps
No malignant potential
POLYPS WITH MALIGNANT POTENTIAL
Tubular adenoma
Glands
with mild
to
severe
dysplasia
Villous adenoma
FAP
FAMILIAL ADENOMATOUS
POLYPOSIS SYNDROME (FAP)
 Mutations of the
adenomatous
polyposis coli gene
(APC gene –
gatekeeper gene) on
chromosome 5q21
 AD
 500-2500 colonic
adenomas
 Carpet the mucosal
surface
Early detection,
prophylactic colectomy in first-degree relatives
CA COLON – ETIOPATHOGENESIS
 Excess dietary caloric intake
 High fat intake, red meat
 Low content of vegetable fibre in diet –
toxic byproducts – contact with colonic
mucosa for long time
 Molecular carcinogenesis - mutations in
oncogenes, tumor suppressor genes, DNA
repair genes
 Adenoma – carcinoma sequence
CA COLON –
GROSS
Distal colon lesion - annular
Proximal colon lesion - exophytic
CA COLON – CLINICAL
 Asymptomatic
 Iron-deficiency
anemia
 Left sided lesions
detected earlier
than right sided
lesions
 Extension into
adjacent structures
 Metastasis –
lymphatics, blood
vessels
ACUTE APPENDICITIS
 Appendiceal inflammation associated with
obstruction in 50 – 80 % of cases
Lymphoid hyperplasia, fecoliths
Tumor, worms - less common
 Gross: normal glistening mucosa – dull,
granular, later fibrinopurulent reaction
over mucosa