DISEASES OF THE COLON

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 CLASSIFICATION:
Congenital anomalies
Inflammatory Bowel Disease (IBD)
Vascular disorders (disease)
Tumours

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 CONGENITAL ANOMALIES.
 Congenital megacolon (Hirschsprung’s
disease)
• Definition.
 Is a congenital disease due to the absence
of ganglion cells and ganglia in muscle
wall (myenteric Auebach’s plexus) and
submucosa (Meisner’s plexus) in the
affected segment of the colon.

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 Aetiology
• Failure of migration of neuroblasts during
embryogenesis;
• There is arrest of neural crest cells during
migration to some point before reaching
the bowel wall and anus during
development
 The site.
• The rectum is the commonest site which is
affected, followed by sigmoid colon
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 Pathogenesis of HD
 Lack of both Meisner’s submucosal and
Auebach’s myenteric plexuses
 Loss of enteric neuronal coordination
 Functional obstruction and colonic dilatation
proximal to the affected segment
 Males have more short aganglionosis with
megacolon than females
 Females predominate with more long affected
segment than in males
 Overall M:F=4:1)

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 PATHOLOGY
Macroscopy:
 AGANGLIONIC ZONE:-
 Constricted and spastic distal segment

 PROXIMAL SEGMENT:-
 Progressive dilatation and hypertrophy (later)
 This occurs proximal to aganglionic segment
(Ascending colon)
 Mucosal inflammation with shallow stercoral
ulcers-produced by impacted, inspissated
faeces.
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 MICROSCOPY(Diagnosis):-
 Rectal full thickness biopsy;
 Includes mucosa, submucosa and muscle
to document the presence or absence of
ganglion cells
 Cholinergic fibres are increased strikingly
in submucosa and between muscle coats

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 CLINICAL PRESENTATION:-
• Failure to pass meconeum immediately
during neonatal period
• Obstructive constipation
• Intermittent bouts of diarrhoea in short
segment aganglionosis
• Associated diseases:-
 10% Down’s syndrome
 In 5% there is serious neurologic
abnormalities
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 COMPLICATIONS OF HD.
• Superimposed enterocolitis with formation
of stercoral ulcers-is one of the most
serious complications
• Fluid and electrolyte disturbances
• Perforation of the colon and appendix with
peritonitis

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HD

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HD-Barium enema

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HD-dilation of bowel (megacolon)-
proximal to affected bowel (sigmoid
colon)

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Inflammatory Bowel Disease

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 IBD
• There are 2 inflammatory disorders namely
CROHN’S DISEASE (CD) and ULCERATIVE
COLITIS (UC)
 Similarities:
 Both are of unknown aetiology (lack of proven
causal agent)
 Share many commom features are are thus
collectively known as IBD
 Have a pattern of familial occurrence
 Have systemic manifestation

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 CROHN’S DISEASE (CD).
 Aetiology and pathogenesis:
• Genetic predispostion.
 There is a familial aggregation
 In first degree relatives there is a 10 fold increase in the
risk
• Infectious causes.
 Certain infective agents are thought to play a role; these
include;
 Mycobacterium paratuberculosis
 Compaylobacter
 E. coli
 Pseudomonas etc

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 CD: aetiology and pathogenesis
cont--
• Structural changes in intestinal mucosa:
 Increased intestinal permeability to polythylene
glycol in patients with CD
 Alteration of mucin glycoprotein have been
demonstrated
• Abnormal Host Immunoreactivity:
 Immune-mediated injury is thought to play a role
 Inflammation acts as the final common pathway

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 CD: PATHOLOGY
• Macroscopic:
 Fistula and sinus tract formation
• Microscopy(characteristic histologic
feature)
 Mucosal inflammation– the earliest feature
- focal neutrophils
 Mucosal ulceration

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 CD: Microscopy cont--
 Transmural inflammation (+ lymphoid
aggregates)
 Discontinuous inflammation of intestine:
- “skip lesions” giving a cobble stone
appearance
 Non-caseating granulomas in submucosa
(descrete)

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CD: thickened wall and stenosis of
lumen of ileum

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CD:irregular ulcers separated by
normal colon (skip lesions)

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 ULCERATIVE COLITIS (UC)
• An ulceroinflammatory disease limited to
the colon
• Affects only the mucosa and submucosa
• It extends in a continuous fashion
proximally from rectum in contrast to CD
• Well formed granulomas are ABSENT

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Aetiology and pathogenesis of UC:
• The cause is unknown
• Other theories are as in CD

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 PATHOLOGY:
• 3 major pathological features characterize
ulcerative colitis and help differentiate from
other IBD
 A diffuse disease- from rectum, extends
proximally for a variable length
(PANCOLITIS)
 The inflammatory process is limited to the
colon
 It is essentially a disease of mucosa
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UC: hyperemic, friable, granular
mucosa of colon ceacum to anus

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 COMPLICATIONS OF UC:
Local:
 Toxic megacolon
 Perforation
 Peudopolyp (inflammatory polyp)
 Haemorrhage
 Colonic carcinoma

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 Complications of UC cont--
Systemic:
 Uveitis
 Erytherma nodosum
 Ankylosing spondylitis
 Arthritis
 Pyoderma gangrenosum

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 TUMOURS OF THE COLON
(Large intestine)
CLASSIFICATION:-
 Non-neoplastic polyps.
 Hyperplastic polyps (metaplastic)
 Harmatomatous polyps
• Juvenile (retention) polyps
• Peutz –Jegher polyps
 Inflammatory polyps (UC, CD)
 Lymphoid polyps

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 Classification cont--
 Neoplastic polyps:-
 Benign polyps
• Tubular adenoma
• Villous adenoma
• Tubulovillous adenoma
 Malignant tumours
 Those of epithelial origin.
• Adenocarcinoma
• Carcinoid tumours
• Anal zone carcinoma

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 Classification cont--
Those of mesechymal origin.
 Benign tumours:-
• Leiomyoma
• Lipoma
• Neuroma
• Angioma

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 Classification cont--
 Malignant mesenchymal tumours.
• Leiomyosarcoma
• Liposarcoma
• Kaposi’s sarcoma etc
Lymphoma (malignant)

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 ADENOMATOUS POLYPS
(Adenomas of colon)
• 50% are located in the rectosigmoid colon
Tubular adenoma.
 Constitute 2/3 of colon adenomas
 Neoplastic glands must remain superficial
to muscularis mucosa for the polyp be
considered benign
 The risk of invasive carcinomas correlates
with the SIZE of ≥2cm diameter (35% can
become malignant)
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Multiple adenomatous polyps

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 Adenomas of colon cont--
Villous adenona:-
 Constitutes 1/10 of colonic adenomas
 Are found predominantly in the
rectosigmoid region
 Typically are large, broad-based elevated
lesions
 SIZE ≥1/2 are 2cm in diameter
 Commonly contain foci of carcinoma
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 Adenomas of colon cont--
• NB: adenomas with ≥ 2cm-50% are
malignant
• 50% 0f villous adenomas measure more
than 2cm in greatest diameter, thus 1/3 of
the resected villous adenomas contain
invasive carcinoma
Tubulovillous adenoma:-
 ¼ of adenomatous polyps manifest both
tubular and villous features
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 Tubulovillous adenoma cont--
 Tend to be intermediate in distribution and
size between tubular and villous
adenomas in the risk of invasive
carcinoma

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 Malignant risk of adenomatous
polyps:-
• This is correlated with 3 interdependent features.
 Size of the polyp (≥ 2cm)
 Histology of the polyp (villous, tubular or tubulovillous )
 Severity (grade) of epithelial dysplasia (mild, moderate
or severe)
NB: the neoplastic gland must remain superficial to the
muscularis mucosae for a polyp to be considered
benign. Penetration of this muscle layer is considered
evidence of malignant transformation.

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 ADENOMATOUS POLYPOSIS
SYNDROMES:
 FAMILIAL Adenomatous polyposis(FAP)
- Also called Adenomatous Polyposis Coli (APC)
 Is inherited as autosomal dorminant trait
 Pregressive development of innumerable
adenomatous polyps of the colon- especially in
rectosigmoid region
 Mostly is of tubular variety,
 Carcinoma of the colon is inevitable nearly
always by the age of 40,
 APC gene, is responsible for FAP, has been
mapped to 5q21
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Adenomatous polyposis syndromes
cont--
Gardener’s syndrome:-
• Is an autosomal dorminant familial
disorder
• GIT polyps, particularly in the colon
• Osteomas of skull, mandible and long
bones
• Soft tissue tumours of the skin (epidermal
cysts, Fibromatosis)
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 Gardner’s syndrome cont----
• Ultimately it progresses to cancer of the
colon
• The gene has been located in 5q
(probably a variant of FAP)

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 Gardner’s syndrome-multiple
polyps covering colonic mucosa

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Adenomatous polyposis syndromes
cont--
Turcot’s syndrome:-
• Is inherited as autosomal recessive
• Is a combination of familial polyposis of
colon with malignant tumours of CNS,
mostly GLIOMAS.
• Can progress to cancer of the colon

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 COLORECTAL CARCINOMA:
AETIOLOGY.
 Age.
 Peak age of incidence in 7th decade
 Only 20% of cases occur prior to the age
of 50 years
 It is rare before 40 years without
associated polyposis syndrome

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 Colorectal carcinoma-aetiology
cont--
 Sex.
 Women with history of genital or breast
cancer are at increased risk
 Rectal carcinoma is more frequent in men,
whereas colon carcinomas are slightly
more common in women

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 Aetiology colorectal ca. cont--
 Enviromental factors.
 Immigrants from low risk countries to high
risk ones acquire risk of adopted country
 Dietary factors:- colon carcinoma is more
common where diet is;
• Higher in- animal fat, animal protein,
refined carbohydrates
• Lower in – fibre content (Western diet)
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 Dietary factors cont--
• Lower content in fibre increase the
anaerobic gut flora – leading to formation
of SECONDARY BILE ACIDS which may
be carcinogenic or cocarcinogens
• Decrease in fibre content causes low bulk
there by INCREASING the colonic
TRANSIT TIME that the carcinogens are
in contact with the epithelium

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 Dietary factors cont--
• High level of SELENIUM(in soil and
plants) has been correlated with low
prevalence of colon cancer.
• Vitamin E (exogenous antioxidant) and
Glutathion peroxidase (endogenous
antioxidant) which contain selenium and
vitamin C have protective effect in
experimental animals in development of
colon cancer

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Aetiology of colorectal cancer cont-
 Anaerobic bacteria:
 Faeces of persons in high risk population have high
content of anaerobic bacteria
 The bacteria convert bile acids into compounds that are
carcinogenic, thereby permitting longer exposure of the
mucosa to any chemical in the stool
 Fibre may bind potential carcinogens by increasing the
bulk of stool, DILUTE their concentration
 Dietary fibre may affect production of bile acids and their
potential cancer-causing compounds in the stool

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Aetiology of colorectal ca. cont--
 Genetic influences.
- Patients with significant heritable
predisposition of colon cancer include;
 Hereditary polyposis syndromes
 Non-polyposis syndromes
- In site-specific colon cancer found in
rectum
- In Hereditary Nonpolyposis colon cancer
syndrome (HNPCC)
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 HNPCC cont--
• Cancer family syndrome (Lynch syndrome
• Autosomal dorminant
• Inherited cancer of GIT, particularly colon
and rectum
• Have increased risk of colorectal cancer

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Aetiology of colorectal ca. cont--
 Pre-existing adenomatous polyps
- Evidence of adenoma-carcinoma
sequence:-
 Papulation with high prevalence of
adenomas have high incidence of
adenocarcinoms
 The disdribution of both is the same
 The risk of carcinoma is directly related to
number of adenomas
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 Adenoma-carcinoma sequence
cont--
 The peak incidence of adenomatous
polyps antedates some years the peak of
colorectal cancer

 As a complication of inflammatory bowel

diseases (IBD)- ulcerative colitis and
Crohn’s disease

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 MORPHOLOGY OF
COLORECTAL CANCER:
• MACROSCOPY.
 25% in caecum, 25% in rectosigmoid
colon, 25% in Descending/upper sigmoid
 LT –sided tumours are annular and
therefore cause earlier obstruction
 RT-sided tumours are polypoid and
therefore clinically silent for longer time

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Morphology colorectal cancer cont-
• MICROSCOPY.
 98% are adenocarcinomas +/-
extracellular mucin production
 Occasionally signet –ring type carcinoma
 Carcinomas of anorectal canal are most
commonly are squamous cell carcinoma

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Adenocarcinoma-rectosigmoid
coloc

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Adenocarcinoma sigmoid colon-
arising from villous adenoma

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 Clinical presentation:
• Depends on the site of tumour;
Right –sided lesions present with:-
 Iron deficiency anaemia due to occult
blood loss
 Weight loss
 Right iliac fossa mass
 Non-specific malaise

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 Clinical presentation cont--
Left-sided lesion present with:-
 Abdominal pain
 Alteration in bowel habits (change in bowel
habits)
 Rectal bleeding
 40% of patients present with surgical
emergency with either obstruction or
perforation
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 SPREAD:
• Local – direct extension to adjacent structures
• Metastases – to regional lymphnodes, liver, lung
and bones.
STAGING: (related to prognosis)
 Duke staging system:-
 A: confined to the wall (90%)
 B: through bowel wall to serosa
 C: lymphnode metastases
 D: distant metastases

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 INVESTIGATION:
• Sigmoidoscopy (rigid or flexible ) for
BIOPSY
• Colonoscopy –BIOPSY
• Double cantrast barium enema

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