histopathology

1. BENIGN AND MALIGNANT
LESIONS OF INTESTINES.
Presenter: Dr Tashi Dolma
Guide: Dr Pallavi Agrawal.
Dated: 25th Feb 2016

2. INTRODUCTION.
 The small intestine and colon account for the
majority of GI tract length .
 The intestines are also the principal site where
the immune system interfaces with a diverse array
of antigens present in food and gut microbes.
 Intestinal bacteria outnumber eukaryotic cells in
our bodies by tenfold. Thus, it is not surprising
that the small intestine and colon are frequently
involved by infectious and inflammatory
processes.

3. CANCER BURDEN.
 Colorectal cancer (CRC) is a formidable health problem
worldwide.
 Small intestinal neoplasm are relatively rare.
 It is the third most common cancer in men (10.0% of
all cancer cases)
 the second most common in women ( 9.4% of all
cancer cases)
 60% of cases are encountered in developed countries.
 account for 8% of all cancer deaths and.
 In India, Colon cancer ranks 8th and rectal cancer
ranks 9th among men.
 For women, rectal cancer does not figure in the top 10
cancers, whereas colon cancer ranks 9th.

4. GUT tube development.

8. Duodenum:
● 25 cm long, from pyloric sphincter to
ligament of Treitz, mostly retroperitoneal,
fixed in position
● Common bile duct (CBD) and pancreatic
duct enter second part of duodenum
posteromedially at ampulla of vater

11. LARGE INTESTINE.

14. Small bowel mucosal biopsy
 Important step in evaluating patients with
malabsorption.
 Standard gastroscope for duodenal biopsy.
 1 or two from doudenal bulp and min 4 from distal
duodenum.
 Proper orientation most critical.
 H and E stained section , one Alcian blue PAS with
hematoxillin counter stain.
 Alcian blue PAS stain– Whipple disease and MAIC
infection.
 Trichrome stain– collagen deposition.
 Iron hematoxillin--- Giardia Lamblia identification.

15. NORMAL SMALL-INTESTINAL
HISTOLOGY

16. PATTERNS OF ABNORMAL SMALL-
BOWEL ARCHITECTURE
 The small-bowel mucosal responses to injury are
limited, and recognition of a response pattern can
be useful in differential diagnosis
SEVERE VILLOUS ABNORMALITY:
 Flat intestinal mucosa in which no villi are seen.
 Usually, diffuse, accompanied by epithelial lymphocytosis (at
least 30 to 40 intraepithelial lymphocytes per 100 enterocytes) .
 Crypt hyperplasia, evidenced by numerous mitotic figures.
VARIABLE VILLOUS ABNORMALITY
 The villi either are only focally flat or are less than flat (mild or
moderate villous shortening).
 May show increased intraepithelial lymphocytes.
 May be associated with features that suggest a specific
diagnosis (e.g., numerous eosinophils, granulomas, parasites),
or they may be nonspecific.

19. CELIAC SPRUE (Gluten-induced
Enteropathy, Gluten-sensitive Enteropathy,
and Nontropical sprue)
 Major cause of malabsorpton.
 The pathogenesis of CS involves immunologic injury to
the enterocyte associated with the ingestion of gluten .
 human leukocyte antigen (HLA)–associated condition
that is primarily associated with the MHC class II
alleles DQA1*0501 and DQB1*0201.
 rapid and dramatic clinical, serologic, and histologic
improvement with the removal of gluten from the diet,
and relapse following its reintroduction .

20. Pathogenesis of CS.

21. DEFINITIVE DIAGNOSIS OF CELIAC
SPRUE
 A pathologist does not make the diagnosis of CS.
 All that can be said is that the specimens contain a
severe villous abnormality that is consistent with CS.
 DEFINITIVE DIAGNOSIS depends on the
demonstration of
 a suitable clinical presentation,
 compatible serologic tests (e.g., immunoglobulin [Ig]
A antiendomysial antibodies, IgA anti-tissue
transglutaminase antibodies),
 appropriate small-bowel histology, and
 clinical and serologic response to gluten withdrawal

22. Mucosal lesions of CS
 Classified into five types (Marsh-Oberhuber scheme).
 Type 0: The preinfiltrative lesion, is essentially normal.
 Type 1: The infiltrative lesion, with intraepithelial lymphocytosis
(at least 40 per 100 enterocytes),
 Type 2: hyperplastic lesion, variable villous abnormality with
epithelial lymphocytosis.
 The type 3: Destructive lesion represents the classic CS lesion.
type 3a with partial villous shortening, type 3b with a more
severe villous change, and a type 3c that is flat
 The hypoplastic type 4: An atrophic end-stage lesion that is
seen in a minority of patients unresponsive to gluten
withdrawal; it includes the lesion of collagenous sprue

23. Differential diagnosis of celiac sprue
Includes all entities that may cause at least a
focal severe villous abnormality
 Common variable immunodeficiency,
 Protein allergies other than gluten,
 Some cases of infectious gastroenteritis
 Zollinger-Ellison syndrome
 Chronic ischemic bowel.
 Inflammatory bowel disease (IBD) .
Clinicopathologic correlation is essential for
proper diagnosis.
Numerous neutrophils, cryptitis, and crypt
abscess formation are usually not part of CS.

24. Entities Associated with a Variable Villous
Abnormality and Crypt Hypoplasia
 MARASMUS AND/OR KWASHIORKOR:
 MEGALOBLASTIC ANEMIA: impaired epithelial cell
replacement because of decreased DNA synthesis.
Consequently, a variable villous abnormality with or without
megaloblastic epithelial changes. the villous abnormality is
not severe and associated with decreased mitoses in the
crypts; and no increase in inflammatory cells
 RADIATION AND CHEMOTHERAPY EFFECT: changes are
similar to those in megaloblastic anaemia, are associated
with decreased mitotic activity in the crypts. There may also
cause focal necrosis of epithelial cells (apoptosis) and
increased numbers of chronic inflammatory cells within the
mucosa and submucosa
 MICROVILLOUS INCLUSION DISEASE

26. TROPICAL SPRUE
 Chronic diarrheal process associated with steatorrhea .
 Prevalent in South and Southeast Asia, West Africa, parts of
south America.
 Patients show dramatic response to folate, vitamin B12,
and tetracycline or other broad-spectrum antibiotics,
suggesting an infectious etiology.
 Small-bowel biopsy specimens show a variable villous
abnormality.
 Histologic appearance: mild to moderate villous shortening,
increased numbers of chronic inflammatory cells in the
lamina propria and epithelium, and crypt hyperplasia
 On occasion, a severe histologic lesion indistinguishable
from CS

27.  STASIS SYNDROMES
 Occur in surgical blind loops, bowel obstruction, small-
intestinal diverticulosis, and intestinal pseudo-obstruction.
 With stasis, bacteria multiply.
 Associated with malabsorption of fat and vitamin B12,
resulting primarily from the bacterial degradation of bile
salts and intestinal mucosal injury
 Patchy variable villous abnormality associated with
increased chronic inflammatory cells in the lamina propria
and epithelium
 Few neutrophils may be seen within the lamina and
epithelium.
 INFECTIOUS GASTROENTERITIS
 Typically patchy with a variable villous abnormality; rarely,
the villous abnormality can be severe, closely mimicking CS.
 Increased chronic inflammatory cells, acute inflammatory
cells are often seen both within epithelial cells and in the
lamina.
 The acute onset of the symptoms, with the acute
inflammatory changes in biopsy specimens, usually help in
the distinction from CS.

28. SYSTEMIC MASTOCYTOSIS
 Rare disorder with infiltration of mast cells in the skin
(urticaria pigmentosa), bones, lymph nodes, and other
parenchymal organs .
 90% demonstrate a D816V KIT mutation
 The gut, almost half of the affected patients
 present as mucosal nodule or nodularity, erosion,
friability, thickening ,loss of folds
 variable villous abnormality associated with increased
numbers of mast cells, or increased numbers of
eosinophils.
 The neoplastic mast cells occur in aggregates & sheets,
pericryptal below the luminal surface.
 cells are round, centrally placed nuclei, eosinophilic or
clear cytoplasm. Some can be spindled, elongated.
 Immunohistochemistry: CD117 and mast cell tryptase
for mast cells, and these cells coexpress CD2 and/or
CD25.

30. Entities Associated with Variable Villous
Abnormalities Illustrating Specific
Diagnostic Changes
 COLLAGENOUS SPRUE
 The excessive subepithelial deposition of collagen associated
with severe villous abnormalityin small-bowel with
malabsorption unresponsive to a gluten-free diet .
 Most pts have had a max subepithelial collagen deposit
(exceeding 10 μm). The collagen distribution is typically
patchy and it may not be present early in the disease..
 Can coexist with collagenous colitis/ileitis and/or
collagenous gastritis.
 T-cell receptor gene rearrangements in few suggesting
lymphoproliferative disorders.
 Antihypertensive drug olmesartan causing collagenous
sprue-like changes as well as lymphocytic and collagenous
gastritis and colitis .

31. Whipple disease, Tropheryma
whippeli
 A chronic systemic illness with gastrointestinal features such as
diarrhea and malabsorption.
 The diagnosis of Whipple disease is usually based on the
identification of PAS-positive, diastase-resistant inclusions in small-
intestinal biopsy specimens.
 The diagnosis can be confirmed by PCR for the bacterial 16S
ribosomal RNA, EM ad IHC.
 Infiltration of various organs with macrophages containing the
bacilli. (lamina of the small intestine, the mesenteric lymph nodes,
the cardiac valves, and the central nervous system).
 Mucosal biopsy demonstrate infiltration of the lamina propria;
muscularis mucosae; and, in some cases, submucosa by
macrophages with a foamy gray-blue cytoplasm .
 fat vacuoles are seen in the lamina propria. The macrophage
cytoplasm contains intensely PAS-positive material that is coarsely
granular.

38. Pattern of colonic inflammation.
 Chronic colitis
 Diffuse active colitis,
 Focal active colitis,
 Ischemic-type colitis,
 Trauma change,
 Apoptotic colopathy, and
 Intraepithelial lymphocytosis

40. Active Colitis
Describes an inflammatory condition in which
neutrophils are present in the lamina propria,
within the epithelial cells (cryptitis), or within
the crypt lumens (crypt abscesses).
 Included under this heading are:
(a) UC in an active phase,
(b) most examples of Crohn colitis, and
(c) infectious colitis and/or acute self-limited
colitis
Recognition of an inflammatory pattern,
coupled with clinical and endoscopic
correlation, allows a fairly specific diagnosis to
be made in many biopsy specimens.

45. EVALUATION OF RESECTION SPECIMENS
IN INFLAMMATORY BOWEL DISEASE
 After specific causes of enteritis and colitis have
been ruled out, a group of diseases referred to as
idiopathic IBD is left.
 IBD describes at least the following three entities:
CD, UC, and colitis of indeterminate type.
 Despite their nonspecific nature, the pathologic
features of CD and UC are sufficiently distinctive
that they can usually be distinguished from each
other and from other kinds of bowel inflammation

46. INFLAMMATORY BOWEL
DISEASE.
 Chronic condition resulting from inappropriate mucosal
response.
 Ulcerative colitis: severe ulcerating inflammatory disease
that is limited to the colon and rectum and extends only into
the mucosa and submucosa
 Crohn disease: referred to as regional enteritis. It may
involve any area of the GI tract and is typically transmural.

47. EPIDEMIOLOGY
 More frequently present in teens and early 20s.
 More in females.
 Caucasians and eastern jews.
 IBD worldwide is on the rise.
 Hygiene hypothesis.

48. PATHOGENESIS
Both UC and CD develops due to defects in
host interactions with intestinal microbiota,
intestinal epithelial dysfunction and
aberrant mucosal immune responses.
Genetics

50. Crohn disease.
A. Small intestinal
stricture
B. Linear mucosal ulcers
and thickened
intestinal wall.
C. Perforation and
associated serositis
D. Creeping fat.

51. Ulcerative colitis
A. Total colectomy with pancolitis showing active disease.
B. Sharp demarcation between active UC and normal mucosa
C. Inflammatory polyps
Mucosal bridging.

54. COLONIC DIVERTICULA
 Colonic diverticula are small, flask-like outpouchings that
occur in a regular distribution alongside the taeniae. 0.5 to 1
cm in diameter,
 most common in the sigmoid colon
 Colonic diverticula have a thin wall composed of a flattened
or atrophic mucosa, compressed submucosa, and attenuated
or, totally absent muscularis propria
 Hypertrophy of the circular layer of the muscularis propria
 Obstruction of diverticulae leads to inflammatory changes,
producing diverticulitis and peri-diverticulitis and perforation.
 Diverticulitis may cause segmental diverticular disease–
associated colitis, fibrotic thickening in and around the
colonic wall, or stricture formation.
 Perforation can result in pericolonic abscesses, sinus tracts,
and, occasionally, peritonitis.

55. Sigmoid diverticulitis.
A. Stool filled diverticula arranged regularly.
B. Cross section showing out pouchings of mucosa beneath the
muscularis propria

56. FOLICULAR PROCTITIS demonstrating
prominent lymphoid follicle formation with
cryptitis and superficial erosions

57. Acute Ischemic-Type Change
 Hemorrhage into the lamina propria with superficial epithelial
coagulative necrosis with sparing of deep portions of the
crypts.
 Extensive necrosis of the superficial epithelium with
inflammatory pseudomembrane formation.
 acute and chronic inflammatory cells (e.g., plasma cells) are
typically few.
 The differential diagnosis: inadequate perfusion, narrowing
of blood vessels for any reason, trauma/prolapse and
obstructing lesions of the bowel, and bowel distention.
 Associated with a wide variety of drugs, including
vasopressors, oral contraceptives, NSAIDs, cocaine, and
glutaraldehyde
 Some infectious agents, such as cytomegalovirus (CMV),
Clostridium difficile, Clostridium septicum, and the
enterohemorrhagic Escherichia coli,

58. Pseudomembranous colitis. An inflammatory pseudomembrane exudes
from the dilated degenerating crypt in an eruptive fashion. The
karyorrhectic debris and neutrophils within the pseudomembrane tend
to align in a linear configuration within the mucin.

59. Collagenous colitis.
Thickened subepithelial collagen layer accompanied by chronic
inflammatory cells in the lamina propria and the surface
epithelium. The surface epithelial degenerative changes are
accompanied by epithelial lymphocytosis.

60. Lymphocytic colitis.
(A) Chronic inflammatory cells are increased within the
lamina propria, and they are not associated with
architectural distortion. (B) Higher magnification reveals a
striking epithelial lymphocytosis.

61. Acute graft-versus-host disease..
Numerous apoptotic bodies (eosinophilic globules and nuclear
debris) are present

62. Biopsy specimen of the mucosa adjacent to an ulcer from a
patient with solitary rectal ulcer syndrome. The normal lamina
propria has been replaced by fibrosis and smooth muscle. The
mucosal capillaries are ectatic.

63. Follicular proctitis
prominent lymphoid follicle formation
associated with cryptitis and superficial
erosion

65. defunctionalized rectum
Lymphoid follicle formation accompanied by cryptitis and crypt
abscess formation, and it appears similar to follicular proctitis.

75. Tumours of intestines
 Polyps
 Carcinoma
 Carcinoid
 Lymphoma.

78. polyp
 Clinical term or gross description of any circumscribed tumour or
growth that projects above the surrounding mucosa.
 A polyp can be neoplastic, inflammatory, or hamartomatous.
 Only by histologic examination one can be certain of the nature
and clinical significance.


79. Types of polyps
Non neoplastic polyps: 90%
Hyperplastic polyp
Hamartomatous (juvenile and Peutz Jhegers
polyps)
Inflammatory polyp
lymphoid Polyp.
Neoplastic polyps: 10%
Adenoma

80. Serrated polyps:
 Hyperplastic polyp:
 distal colon/rectum. <5mm size
 Sessile serrated polyps/ adenoma with/without dysplasia: proximal
colon. 6-10 mm size. Premalignant.
 Traditional serrated adenoma.
 Distal colon. >10 mm size. premalignant
 Serrated polyposis syndrome. Previously called hyperplastic
polyposis

81. WHO definition of SPS.
 At least 5 histologically diagnosed serrated polyp prox. to sigmoid
colon, two>10cm size.
 Any no of polyps occurring prox. To sigmoid colon wih F/o SPS.
 > 30 serrated polyps of any size throughout colorectum.

82. Polyps Hyperplastic Polyp
 Asymtomatic
 > 50% are located in the rectosigmoid
 Sawtooth surface
 Star shaped crypts Composed of well-formed glands and crypts
lined by differentiated goblet or absorptive cells.

85. Types of hyperplastic polyp.
Microscopically, three types.
 Microvesicular hyperplastic polyp (MVHP)
 goblet cell hyperplastic polyp ( GCHP)
 Mucin poor hyperplastic polyp (MPHP)
They are molecular difference between
diff subtypes.
mutation GCHP MVHP
K-ras mutation 43% 13%
BRAF(V600E)
mutation
21% 76%
CIMP-H mutation 14% 47%

90. Serrated sessile adenoma/polyp.
 Flat and sessile lesion.
 Diagnosis is based on architectural features .
 Branching and dilatation of the base of crypts
 Inverted T or L shaped

92. Traditional serrated adenoma
pedunculated/ polypoid in nature
Complex serrated architecture misdiagnosed as villous adenoma.
Cells are uniform, pencilate cells with bright eosinophilic cytoplasm.
Pseudostratified nuclei, increased NC ratio, hyperchromatism and
mitosis mild.

94. SESSILE SERRATED ADENOMA/POLYP
WITH DYSPLASIA.

95. Hamartomatous polyp Juvenile Polyps
(retention polyp
 Developmental malformations affecting the glands and lamina
propria.
 Commonly occur in children under 5 years old in the rectum.
 In adult called retention polyp.

97. Junenile polyp.
 Mainly occurs in first two decades of life.
 Localised chiefly in rectum, usually solitary.
 Bleeding is most common symptom.
 Criteria of juvenile polyposis
 >5 polyps of the colon and rectum.
 Juvenile polyps in pt with a F/O.
 Juvenile polyp through entire length of GI tract.
 Any no. polyp in pts with F/o.

98. JUVENILE POLYP

100. Peutz-Jehgers syndrome
 Non-Neoplastic Hamartomatous Polyps.
 Rare, autosomal dominant
 hamartomatous polyps accompanied by mucosal
and cutaneous pigmentation around the lips, oral
mucosa, face and genitalia.
 Polyps tend to be large and pedunculated.
Increased risk of developing carcinoma of the
pancreas, breast, lung, ovary and uterus.

101.  Non-Neoplastic Polyps Inflammatory
Polyps longstanding IBD, especially in
chronic ulcerative colitis. Represent an
exuberant reparative response to
longstanding mucosal injury called
pseudopolyps

104. GANGLIONEUROMA

106. Inflammatory polyp.
A. Bizarre stromal changes.
B. High power view shows cells with enlarged bizarre nuclei.

109. Lymphoid polyp
A. Low power view showing polyp secondary to lymphoid tissue
with germinal centre.
B. High power view showing a lymphoid nodule with a reactive
germinal centre.

110. Neoplastic polyp (adenoma)
 Tubular
 Tubulovillous
 Villous.
 Polypoid or non polypoid.
 Clinically important: premalignant lesions
 Common in large intestine, and rare in small intestine.
 Small intestine: tubular or villous and sessile.
 90% pt with FAP coli hav small intestinal adenoma.

111. Small intestinal adenoma
A. Familial adenomatous polyposis.
B. High power view showing a villus half of which has adenomatous
change.

112. Large intestine adenoma
Prevelance Invasive
cancer
tubular 95% 2-3%
tubulovilous 2-4% 6-8%
villous 1-3% 10-18%

115. Villous adenoma
A. Whole mount view showing adenomatous epithelium in villous
arrangement.
B. High power view showing elongated nuclei with palisading. Nuclei do
not reach cell surface with mucin production at the apical portion.

124. Examples of reporting malignant polyps
 Example 1: sigmoid colon, polypectomy:
 grade III adenocarcinoma arising within an adenoma. The cancer
extends to the transected margin of resection. No evidence of
lymphatic or venous invasion.
 Example 2: Rectum, polypectomy: grade II adenocarcinoma arising
within adenoma. Cancer is 2.5cm from transected margin (the
margin is negative for cancer). No evidence of lymphatic or venous
invasion.

125. Adenoma with pseudoinvasion.

126. Familial adenomatous polyposis
 Autosomal dominant disorder.
 Colon is carpeted with adenomas (100-1000)
 Diagnostic criteria:
100 or more colorectal polyps.
Germline mutation in APC gene.
F/o APC.
At least one of the following: epidermal
cyst, osteoma, desmoid tumour.
ALL patient of FAP develop colonic adenocarcinoma if disorder is left
untreated.

127. Familial adenomatous poyposis.

128. Attenuated FAP
 Less severe form of polyposis with lower number of polyps (<100)
 Higher risk of developing colorectal cancer.

129. CARCINOMA
 Small intestine: adenocarcinomas account for 40% small intestinal
malignant tumours.
 As compared to colonic adenoca they are rare.
 Duodenum: 48.4%
 Jejunum: 32.5%
 Ileum: 19.2%
 Grossly: flat, stenising, ulcerative, infiltrative or polypoid.
 Morphologically similar to adenoca else where in GIT. More often
papillary.

131. ADENOCARCINOMA
grade % out of
colorectal
adenoca
morphology
I 20% Low grade/well
diff
Simple tubules
nuclear polarity
maintained.unifor
m sized.
II 60-70% Average/
moderately diff
Tubules may be
simple or comlex
or irregular. Loss
of nuclear polatiry.
III 15-20% Poorly diff Absence of
glandular pattern
solid , with loss of
nuclear polarity.

136. Low power view: signet cell carcinoma in association with an adenoma.
High power view: mucicarmine stain showing sheets of signet ring cells.
SIGNET RING CELL CARCINOMA

137. Small cell carcinoma
A. Whole mount section:
B. High power view showing proliferation of small cells .

139. Serrated adenocarcinoma
A. Low power: serrated high grade dysplasia.
B. High power: high grade vesicular nuclei with prominent nucleoli.
C. Low power: invasive cancer with serrated pattern.
D. High power: serrated cancer with nuclear atypia.
E. Mucinous component
F. High power view: papillry rods floating in mucin.
SERRATED
ADENOCARCINOMA

141. Tumour budding
 Denotes the detachment and migration of
neoplastic cells into the stroma at the advancing
edge of the tumour.
 Histologically, a tumour buds have five or less cells
located at the advancing edge. And/or
 Cytoplasmic pseudofragments seen as anucleated
globules when stained with anti cytokeratins
 Does not influence the over all grading of the
tumour.
 Grade1 and II have higher degree of tumour
budding.

143. Rectal cancer staging. 1932

145. TNM classification 2002

148. Carcinoid tumours (well diff NET)
 Located through out the GIT.
 Types: foregut (stomach and duodenum)
 midgut (small intestine and proximal colon)
 hindgut (distal colon and rectum.
 WHO categorisation: well diff and poorly diff NET.
 Grading is based on: no of mitosis and or Ki67 index.
Tumour grade Mitoses/10hpf Ki67 index
Grade 1 <2 <2%
Grade 2 2-20 3-20%
Grade 3 >20 >20%

149. SMALL INTESTINAL CARCINOID
A. Whole mount: no neoplastic change in the surface epithelium,
tumour is extensively involving submucosa.
B. Solid pattern of tumour growth.
C. High power view: round regular nuclei and faint idistinct cellular
borders.
D. Infiltrative pattern

150. Carcinoid tumour appendix.
Goblet cell carcinoid of the appendix.
A. Low power view: infiltrative pattern of tumour cells at the base of the
crepts through muscularis mucosae and submucosa.
B. High power view: bland benign appearing glands with prominent goblet
cells.

151. TUBULAR CARCINOID
A. Low power view, infiltrative pattern of tumour and extension into
submucosa.
B. High power view: showing bland appearing cells forming well
defined tubules.

152. CARCINOID OF THE RECTUM
A. Whole mount view: tomour limited to submucosa.
B. High power view: tight small glands with uniform bland nuclei.
C. Ribbon pattern of tumour.

153. Immunohistochemistry
MARKERS FOR NETS
 Synaptophysin
 NSE
 Chromogranin
 CD57
 CD56.
 CDX ( determining primary of metastatic NET).

154. LYMPHOMA
 GI tract most common site for extranodal lymphoma.
 30-40% of extranodal lymphoma

158. A. Plasma cells of the mocosa strongly express IgA heavy
chain
B. Negative staining of plasma cells for k and Llight chain
C. High power view: lymphomatous component stained with
AB against IgA heavy chain.

159. ENTEROPATHY ASSOCIATED T CELL
LYMPHOMA
A. Whole mount view: focal ulceration with non ulcerated mucosa
flattened.
B. Low power view: mocosa is flattened
C. High power view of the ulcer showing malignant cells with
inflammatory cells.

160. Malignant lymphomatous polyposis
A. whole mount view: numerous tumour nodules forming polyps
B. Low power view: tumour nodules stradding the muscularis mucosae
and involving deep mucosa and upper submucosa
C. High power view: showing small lymphocytes with cleaved irregular
nuclei.

161. FOLLICULAR CENTER CELL
LYMPHOMA OF THE SMALL
INTESTINE.
A. Low power view showing follicular proliferation
B. High power view: monotonous population of small cleaved
lymphocytes.

162. GASTROINTESTINAL STROMAL
CELL TUMOURS
 Mesenchymal neoplasms of GI tract.
 2/3 – stomach, 1/4-small intestine.
 Colorectal GIST 10%
 Most GIST express ckit (CD117)
 PDGFRA mutation

163. Gross appearance
Circumscribed, solitary, rounded or ovoid masses
Pinkish white appearance with areas of haemorrhage and
necrosis with myxoid changes or cavitory degeneration.

164. histologically
 Three categories
 Spindle cell type (duodenum and rest of small intestines)
 Epithelial type (stomach and omentum)
 Mixed type

165. GIST with spindle cells and bland uniform
nuclei. Cells appear as short fascicles or
whorls with pinkish cytoplasm.

166. Epitheliod GIST: clear eosinophillic
cytoplasm. Nuclei are vesicular, round and
regular.

167. GIST: with organoid pattern. Capillaries
separate tumour cells into groups.

168. Immunohistochemistry
 95% GIST express Ckit (CD117)
 95% express DOG1 (clone K9)
 80% Bcl 2,
 60-70% CD34
 30% SMA
 10 % S100

169. Strong diffuse expression of
CD117 (c-kit) GIST.

171. METASTATIC TUMOURS
Carcinoma metastasising to intestines are:
Breast, Stomach, and Ovaries
Lesions are usually multiple, extends from
serosal surface inwards.
Lack ca in situ or mucosal cancers

172. Biopsy from sigmoid colon: metastatic
ovarian papillary serous tumour.
A. Low power view:
colonic mucosa with
juxtaposed papillary
serous tumour.
Psammoma bodies
are also seen.
B. High power view:
characteristic
papillary serous
tumour of low
malignant potential
with psammoma
bodies.

173. Malignant melanoma
A. grossly, 2 large polypoid tumour nodules
B. High power view: spindle cells with mitotic figures.
IHC: S100,HMB45, CD34, CD117 help with the diagnosis.

174. Benign conditions mimicking
neoplasm.
ENDOMTRIOSIS OF THE RECTUM:
A. Low power view rectal mucosa and endometrial glands and
stroma.
B. High power view inactive endometrial glands and decidualized
stroma.

175. malakoplakia
A. Low power view: infiltration of limina propria by histiocytes
admixed with lymphocytes and plasma cells.
B. High power view: michaelis gutmann bodies, concentric
laminated bodies with targetoid appearance .

176. Signet ring changes associated with
pseudomembranous colitis.
A. Low power view: dilated crypts with vocanic eruption of
pseudomembranes.
B. High power view: signet ring cell canges limited to the
crypts.

179. BIBLIOGRAPHY
 Sternberg’s diagnostic surgical pathology. 6th
Edition
 Robbins and cotran pathlogic basis of disease. 8th
edition
 WHO classification of GI tumours
 Fletchers

180. THANK YOU…