INTESTINAL TUBERCULOSIS,

APPENDIX
AND
COLORECTAL POLYPS
Competency
PA24.5 Describe etiology and pathogenesis and pathologic features of
Tuberculosis of the intestine
 Intestinal Tuberculosis

Primary Secondary
• Common in developing countries • occurs in a patient of active
including India pulmonary tuberculosis who
• Caused by swallows the coughed up
1. Mycobacterium bovis: ingestion sputum
of infected unpasteurized cow’s
milk
2. M. tuberculosis Hypertrophic/
Ulcerative
hyperplastic
Intestinal Tuberculosis

Ingestion of Entry of bacilli Granulomatous

infected milk into the mucosa inflammation in the
or sputum of the GI tract mucosa

Caseation necrosis

Spread in to deeper layers of the intestine

Ulceration of the
overlying mucosa
Spread into adjacent lymph nodes and
peritoneum
Primary Intestinal Tuberculosis
• changes are seen in mesenteric lymph nodes without any significant intestinal lesion

Gross:
• Affected lymph nodes are enlarged,
matted and caseous- Tabes
mesenterica
• Healing by fibrosis and
calcification
Microscopic:
• Initial stage- primary complex or Ghon’s focus in the intestinal mucosa
• Later stages- the mesenteric lymph nodes are affected which show typical
tuberculous granulomatous inflammatory reaction with caseation necrosis
• Tuberculous peritonitis may occur due to spread of the infection
Secondry Intestinal Tuberculosis
Cause: Swallowing of sputum in patients with active pulmonary tuberculosis
Common site: Terminal ileum and rarely in the colon
Gross:
• Intestinal lesions are prominent than the lesions in regional lymph nodes
• The lesions begin in the Peyer’s patches or the lymphoid follicles
• as a small ulcerative lesion which later enlarges to form a large transverse ulcer
 Ulcers are perpendicular to the long axis of the bowel
• This is because of the spread by lymphatics
• Serosa may be studded with visible tubercles
• Advanced cases- transverse fibrous strictures and intestinal obstruction are seen

Serosal surface- tubercles (small elevation or protuberance)

 Typhoid ulcers are longitudinal ulcers, i.e, they run parallel to the long axis of the
bowel
Microscopic:
• Char. by presence of tubercles
• Mucosa and submucosa show ulceration and the muscularis may be replaced by
variable degree of fibrosis
• Tuberculous peritonitis may be observed
Differential diagnosis:
• Typhoid (enteric fever) ulcer
Difference between Tuberculous and Typhoid Ulcers
Feature Tuberculous ulcer Typhoid ulcer
Etiology M. Tuberculosis Salmonella typi
M. Bovis
Common site Terminal ileum and caecum Terminal ileum (peyer’s patches)
Orientation Perpendicular to long axis Parallel to long axis
Gross appearance Transverse ulcers Longitudinal oval ulcers over Peyer’s
patches
Microscopy Caseating epithelioid cell Infiltrate of lymphocytes, plasma cells
granulomas and histiocytes; erythrophagocytosis in
some histiocytes
Fibrosis and Common, may present with Rare
stricture formation intestinal obstruction
Perforation May be present common
Bleeding Absent present
Hyperplastic Caecal Tuberculosis
• Occurs secondary to pulmonary tuberculosis
• Cecum is primarily involved, sometimes ascending colon
• Clinically, the lesion is palpable and may be mistaken for carcinoma
Gross:
• The wall of the cecum is thick and sometimes forms a mass lesion because
of tuberculous granulation tissue
• mucosal ulceration may be seen
Microscopic examination
• Mucosa shows ulceration
• Caseating granulomas are seen in the wall of the intestine
• Granulomas are composed of lymphocytes, plasma cells and Langhan’s type of giant
cells

Differential diagnosis
• Crohn’s disease:
 Granulomas are non-caseating (CD)
 ZN stain: acid fast bacilli positive in TB intestine
the sensitivity of AFB staining is very low (20%), yet a positive stain is
100% specific for intestinal tuberculosis
 Bacteriological evidence by culture or animal inoculation and Mantoux test are
helpful in differential diagnosis of the two conditions
APPENDIX
• vestigial organ
• diverticulum of the caecum
• lies behind the caecum
• length 4 to 20 cm (average 7 cm)
Histology:
• four layers—
• mucosa- patchy distribution
of crypts
• submucosa- abundant
lymphoid tissue
• muscularis
• serosa
• Argentaffin and non-
argentaffin endocrine cells are
present in the base of mucosal
glands just as in the small
intestine
Acute Appendicitis
Definition:
• Acute inflammation of appendix
Etiology:
Obstructive Non – obstructive

Faecolith Haematogenous spread of generalized

infection
Calculi Vascular occlusion

Foreign body Inappropriate diet lacking roughage

Tumour

Worms (E. Vermicularis)

Acute Appendicitis
Pathogenesis:
Increased Pressure
Etiological Obstruction
intraluminal on blood
factors of the lumen
pressure vessels

Ischemic
injury

Acute Bacterial
appendicitis proliferation
Gross features:
• Early acute appendicitis - appendix swollen
- serosa hyperemic
• Acute suppurative appendicitis - fibropurulent exudate on serosa
- blood vessels engorged
• Acute gangrenous appendicitis - necrosis & ulceration of mucosa
- appendix soft and friable
- surface is coated with greenish-black
gangrenous necrosis
Microscopic features:
Necrotic
• Neutrophilic infiltration in the mucosa
muscularis layer- characteristic feature
• early stage- acute inflammatory changes
- congestion and oedema of
the appendiceal wall
• late stages- mucosa sloughed off
- wall necrotic
- blood vessels thrombosed
- neutrophilic abscesses
• lumen- may be patent, impacted foreign
body, fecolith or concretion
Clinical Features:
• colicky pain
• nausea & vomiting
• fever
• abdominal pain
Complications:
• Peritonitis
• Abscess
• Adhesions
• Mucocele – distention of appendix distal to obstruction by mucus
• Portal pylephlebitis – spread of infection in mesenteric veins
Tumors of Appendix:
• quite rare
• include:
• carcinoid tumour (most common)
• adenocarcinoma
Neuroendocrine (Carcinoid tumour)
• Tumors originating from the endocrine cells
• endocrine cells are distributed throughout the mucosa of GI tract; have
secretory granules which stain positively with silver stains
• 3rd – 4th decade of life
•M=F
• Most common site- tip of the appendix
Gross features:
• small, button-like sub-mucosal elevations
with intact or ulcerated overlying mucosa
• circumscribed nodule of < 1 cm diameter
• cut section – bright yellow in colour
Microscopic featuress:
• tumour cells are arranged in variety of pattern – solid nests, sheets, cords,
trabeculae & clusters with characteristic palisading of the peripheral cells
• individual tumour cell – small, monotonous with uniform nuclei & poorly
defined cell borders
COLORECTAL POLYPS
Definition:
• any growth or mass protruding from the mucous membrane into the
lumen
• large intestine >> small intestine
• more common rectosigmoid colon

non-neoplastic neoplastic familial

 Colorectal Polyps

Non –Neoplastic Neoplastic Familial

Tubular Villous Tubulovillus

adenoma adenoma adenoma

Hyperplastic Hamartomatous Inflammatory Lymphoid

Peutz Juvenile Sessile serrated

Jeghers (Retention) adenoma
 Colorectal Polyps

Non –Neoplastic Neoplastic Familial

Familial Gardener’s Turcot’s Juvenile

Polyposis syndrome syndrome polyposis
Coli syndrome
 Non –Neoplastic

Hyperplastic Hamartomatous Inflammatory Lymphoid

Peutz Jeghers Juvenile( Retention)

Hyperplastic (Metaplastic) Polyps
• most common
• rectosigmoid colon
• ‘hyperplastic’ - epithelial hyperplasia at the
base of the crypts
• ‘metaplastic’ - areas of cystic metaplasia
• elderly (6th-7th decade)
Gross: multiple, sessile, smooth-surfaced and
small (less than 0.5 cm)
Microscopic: long and cystically dilated glands
and crypts lined by normal epithelial cells
lining epithelium is often serrated or saw-
toothed
• symptomless
• no malignant potential
Hamartomatous Polyps
Peutz Jegher’s Polyposis
• Autosomal dominant defect characterized
by
hamartomatous intestinal polyposis
melanotic pigmentation of lips, mouth and
genitalia
• jejunum and ileum
• adolescence and early childhood
Gross: large, multiple and pedunculated
Microscopic: tree like branching of
muscularis mucosae
• glands may show hyperplasia and cystic
change
Hamartomatous Polyps
Juvenile (Retention) Polyps
• children < 5 years of age
• solitary juvenile polyps- rectum
• multiple juvenile polyposis- anywhere
Gross: spherical, smooth-surfaced
2 cm in diameter
pedunculated
Microscopic: cystically dilated glands
containing mucus
• stroma inflammatory cell infiltrate
Inflammatory Polyps (Pseudopolyps)
• seen in UC
Gross: multiple, cylindrical to rounded overgrowths of mucosa
vary from minute nodules to several cm in size
Microscopic: the centre consists of connective tissue core showing
inflammatory cell infiltrate covered superficially by regenerating
epithelial cells and some cystically-dilated glands
• no malignant potential
Lymphoid Polyps
• more prominent in the rectum and terminal ileum
• localized form- rectum in elderly
• diffuse form- younger age
Gross: solitary or multiple, tiny elevated lesions
Microscopic: composed of prominent lymphoid follicles with germinal
centres located in the sub-mucosa and mucosa and covered by epithelium
that may be inflamed
• benign lesions
D/D: Lymphoma
 Neoplastic

Tubular Villous Tubulovillus

adenoma adenoma adenoma

Sessile serrated
adenoma
Tubular Adenoma (Adenomatous Polyp)
• most common neoplastic polyps (75%)
• 3rd decade of life
• M> F
• distal colon and rectum
• Singly- sporadic cases
• Multiple- familial polyposis syndrome with AD
inheritance pattern
• asymptomatic or may manifest by rectal bleeding
Gross: adenomatous polyps may be single or
multiple; sessile or pedunculated; vary in size from
less than 1 cm to large, spherical masses with an
irregular surface; larger lesions have stalks
Tubular Adenoma (Adenomatous Polyp)
Microscopic: branching tubules embedded in the lamina propria
lining epithelial cells are of large intestinal type with diminished mucus
secretion, large nuclei and increased mitotic activity, cytologic atypia
• malignant transformation is present in 5%
Villous Adenoma
• less common
• 6th decade
• M=F
• distal colon and rectum
Gross: round to oval exophytic masses
size 1-10 cm
Microscopic: slender, finger-like villi with fibrovascular stromal core
covered by epithelial cells varying from apparently benign to anaplastic
cells
• symptomatic; rectal bleeding and diarrhoea
• malignant transformation reported in 30% of villous adenomas
Tubulovillous Adenoma
• intermediate form of pattern between tubular adenoma and villous
adenoma
Gross: sessile or pedunculated
size from 0.5-5 cm
Microscopic: intermediate or mixed pattern; vertical villi and deeper part
showing tubular pattern
• behavior intermediate between tubular and villous adenomas
Sessile serrated adenomas:
• Overlap histologically with
hyperplastic polyps
• More commonly found in the right
colon
• Lack typical cytologic features of
dysplasia that are present in other
adenomas
• Have malignant potential
• Histologically, characterized by
the presence of serrated architecture
throughout the full length of the
glands including the crypt base
crypt dilation Sessile serrated adenoma lined by goblet cells without cytologic
lateral crypt growth features of dysplasia. This lesion is distinguished from a
hyperplastic polyp by extension of the neoplastic process to the
crypts, resulting in lateral growth
 Familial

Familial Gardener’s Turcot’s Juvenile

Polyposis syndrome syndrome polyposis
Coli syndrome
Familial Polyposis Coli (Adenomatosis)
• hereditary disease
• >> 100 neoplastic polyps (adenomas) on the
mucosal surface of the colon (average 1000)
• AD transmission
• germline mutations in APC gene
• progression to invasive cancer
• 2nd and 3rd decades
• M=F
Gross & microscopic: tubular adenoma
• malignant potential very high
• colorectal cancer develops virtually in
100% of cases
Gardner’s Syndrome
• combination of familial polyposis coli and certain extra-colonic lesions
such as multiple osteomas (mandible and maxilla), sebaceous cysts and
connective tissue tumors
• Number of polyps fewer than in the familial polyposis coli but clinical
behavior is identical

Turcot’s Syndrome
• combination of familial polyposis coli and malignant neoplasms of the
CNS
Juvenile Polyposis Syndrome
• multiple juvenile polyps in the colon, stomach and small intestine but
their number is not as high as in familial polyposis coli
• family history AD inheritance
• resemble the typical juvenile polyps as regards their age, sex, distribution
and morphology but lack the malignant potential
 Non-neoplastic polyps Neoplastic polyps (Adenomas)

Frequency More common Less common

Number Often sporadic Sporadic as well as multiple

Familial predisposition No Yes, in sporadic cases

Types Hyperplastic (90%), hamartomatous Tubular, villous and tubulovillous

(Peutz-Jeghers, juvenile), adenomas
inflammatory, lymphoid

Familial syndromes Juvenile polyposis syndrome Familial polyposis coli, Gardner’s,

Turcot’s

Biologic behavior Always benign Variable malignant potential:

Tubular adenoma 5%, villous 30%,
tubulovillous intermediate
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