INTERPRETATION OF ENDOSCOPIC

UPPER GASTROINTESTINAL
& SMALL INTESTINAL BIOPSIES

Dr. Reshama Nirmale

 ENDOSCOPY
Endo : within & skopein : to view
Introduced by Rudolf Schindler in 1880.
Rigid flexirigid (1920) flexible
optical axis (1980) fibreoptic
endoscopes
 ENDOSCOPY
Direct visualization of GIT
Taking photographs
Cytological specimens
Taking biopsies
Undertaking therapeutic procedures
sclerotherapy, band ligation, polypectomy,
stenting & dilatation of strictures, removal
of foreign bodies.
 ENDOSCOPES
Rigid endoscopes
Flexible endoscopes

1) Fiberoptic, 2) Electronic.
ENDOSCOPIC BIOPSY FORCEPS

2 cup shaped jaws,

round / elliptical, serrated / non
serrated,
Forcep with central spike - to fix
the mucosa
Other techniques for full thickness
biopsy specimen FNAB thr
endoscope, snare biopsy technique
- electrocoagulation
 BIOPSY PROCESSING
Careful handling
Proper orientation

1. Magnifying lens,
2. Orienting mucosal surface upward by
mounting biopsy on Filter paper / wire
mesh / plastic mesh/ frosted glass,
Fixation 10% buffered formalin for 2-3 hr
Alternative - Bouins fluid.
 BIOPSY PROCESSING
Automatic tissue processor or by hand processing in
short cycles
Ascending grades of Alcohol - 30 mins each
Xylene - 30 mins each
Paraffin bath - 60 min each
Orientation is imp while making the paraffin block
Step sections at 3-4 level
STAINS : H & E,
SPECIAL STAINS :- PAS, Alcian blue, Z N, Congo
red, Masson trichrome, etc.
INTERPRETATION OF BIOPSIES

Requires good communication bet endoscopist &

pathologist,
REAL CHALLENGE : as biopsy is very SMALL
Pathologist must know : clinical history, physical
findings, result of radiographic & lab studies, ind.
for scopy, endoscopic findings & site of Biopsy, etc
So complete endoscopy report is necessory.
 Patient preperation
Kept fasting for 4-6 hrs
Coagulation profile BT, CT, PT,platelet
count normal
Laft lateral position with slight elevation
of head
Local anasthesia, IV sedatives
 INDICATIONS OF
UPPER GI ENDOSCOPY
Dysphagia / odynophagia
Persistent nausea / vomitting > 48 hrs
Dyspepsia - > 45 yrs, wt. loss, anemia; < 45 yrs - +ve
diagnostic test for H. pylori, refractory to t/t
Acute bleeding varices, acute esophagitis & gastritis
Gastroesophageal reflux heartburn, acid
regurgitation
Portal hypertension
Duodenal biopsy chronic diarrhoea, celiac disease,
iron & folic acid deficiency,
ESOPHAGUS
 ESOPHAGUS

Biopsy 1-5 mm in diameter; Epithelium,

lamina propria, slip of muscularis mucosae occ.
Gastroesophageal reflux disease (GERD)
Infectious candida, HSV, CMV,
Others corrosive, radiation induced, associated
with transplantation, eosinophilic esophagitis,
crohns disease.
GASTROESOPHAGEAL REFLUX
DISEASE (GERD)
GERD
Epithelial hyperplasia
Basal zone expansion,
Elongated lamina
propria papillae,
Balloon cells
Basal dilated & congested
capillaries
Intraepithelial
eosinophils, lymphocytes
Severe - Neutrophils,
ulceration
GERD
CANDIDA
CMV & HSV ESOPHAGITIS
BARRETT ESOPHAGUS
Replacement of distal squamous
mucosa by metaplastic columnar
epithelium - prolonged injury.
(GERD)
Criteria for diagnosis
1. Endoscopic e/o columnar lining,
2. Histologic e/o intestinal
metaplasia.
Long segment > 3 cm, short < 3 cm,
Imp risk factor for adenoca.
 Three Essential Steps for Endoscopic
Diagnosis and Description

2. Recognize the
squamocolumnar junction

3.Describe extent of
metaplasia 1. Locate gastro-esophageal
consistently junction
BARRETT ESOPHAGUS

Incomplete intestinal
metaplasia - goblet +
foveolar type cells.
Complete goblet +
neuroendocrine + paneth
cells.
a/w foci of fundic &
cardiac type epithelium
BARRETT ESOPHAGUS
Alcian blue stain at
pH 2.5

Cells +ve for acidic mucin

DYSPLASIA in Barrett esophagus
DYSPLASIA in Barrett esophagus
 POLYPOIDAL LESIONS
Squmous papilloma
Leiomyoma
Fibrovascular polyps
Squamous cell carcinoma
Adenocarcinoma
SQUAMOUS PAPILLOMA

< 0.5 cm, solitory,

Exophytic, endophytic
Distal part
HPV 6,11,16,18
SQUAMOUS PAPILLOMA

Fibrovacular core

Acanthotic, parakeratotic
stratified squamous epi
SQUAMOUS CELL CARCINOMA

MC, >50 yrs, M > F

MC mid portion,
Polypoidal, flat,
ulcerative
SQUAMOUS CELL CARCINOMA

Dysplastic squamous epi

with kratin pearls
ADENOCARCINOMA

MC lower 1/3rd, >50yrs,

M > F,
Risk factors Barrett
esophagus, tobacco
exposure, obesity, H. pylori
infection,
Dysphagia, wt loss, chest
pain, vomiting.
Bad prognosis - < 20% 5 yr
survival.
ADENOCARCINOMA

Normal squamous epi

Malignant glands invading

stroma
STOMACH
 STOMACH
Ideal no. of biopsies
vary with disease;
minimum 5 -
2 - antral,
2 - fundic,
1 incisura
Ulcer rim involving all 4 quadrants, floor.
 Stomach

Chronic gastritis
Ulcers
Polyps
CHRONIC GASTRITIS
 CHRONIC GASTRITIS
Causes :-
H. pylori gastritis
Multifocal atrophic gastritis
Gastritis secondary to drug therapy
Autoimmune gastritis
Granulomatous gastritis
Gastritis in immunosuppressed patients.
HELICOBACTER PYLORI
GASTRITIS

MC cause of chronic gastritis,

Mechanism - Binding MHC class
II molecules Cag A protein
increased IL-8, TNF superficial
gastritis,
Up to 80% patients
autoantibodies against canalicular
membranes of parietal cells
parietal cell destruction,
Acute gastritis rare, pit abscesses,
neutrophils in surface epithelium.
HELICOBACTER PYLORI
GASTRITIS

Diffuse chronic gastritis

Pyloric antrum,- full
thickness infiltration
Corpus superficial layers
Lymphoid follicles with
germinal centers
pathognomic
Neutrphils in surface &
foveolar epithelium pit
abcesses - active gastritis
HELICOBACTER PYLORI
GASTRITIS

Multifocal atrophic gastritis :-

End stage of H. pylori gastritis
Pylorus & corpus in patchy
manner
Full thickness chronic
inflammation with atrophy of
glands
Intestinal metaplasia
diagnostic feature
Adjecent mucosa active
inflammation with pit abcess
formation & H. pylori infection.
HELICOBACTER PYLORI
GASTRITIS
 DRUG THERAPY
MC cause
Alcohol, aspirin, NSAIDS, proton pump inhibitors
Ulcers are deeper & larger direct irritation of mucosa
PPI exacerbation of H.pylori gastritis

- Hyperplasia of antral G & corpus ECL cells

- multiple fundic gland polyps.
GRANULOMATOUS GASTRITIS
MC antrum,
Early phases limited till
submucosa, late thickening,
fibrosis & pyloric stenosis
Immunocompromised patients
Tuberculosis, fungal
infections candida,
histoplasma, phycomycetes
Noninfectious diseases crohn
disaese, foreign body
granulomas, sarcoidosis, tumor
associates granulomas,
 AUTOIMMUNE GASTRITIS
80- 90 % cases a/w pernicious anemia
Causes :- Parietal cell Ab, H. pylori inf.,
Early - Inflammatory infiltrate in lamina propria around
glands, destruction, no inflammation in superficial mucosa,
parietal cell pseudohypertrophy,
Late mucosal thinning with intestinal metaplasia, glandular
atrophy.
Hypochlorhydria G cell stimulation hypergastrinemia
nodular ECL cell hyperplasia in corpus carcinoids
LYMPHOCYTIC GASTRITIS

Endoscopy :- Normal /
mucosal nodules with erosion,
prominent mucosal folds
Increased (>25 lymphocytes/
100 epithelial cells) in
superfical, foveolar + lamina
propria
Antral prominent a/w celiac
disease ,corpus prominent a/w
H. pylori infection
EOSINOPHILIC GASTRITIS
MAG, allergic
granulomatosis, crohns
disease, food allergy,
Eustoma rotundatum,
connective tissue disorders
scleroderma,
polymyositis,,
Patchy intense infiltration
by sheets of eosinophlis
displacing mucosal glands
producing crypt abcesses
 GASTRITIS IN
IMMUNOCOMPROMISED PATIENTS

CMV infection
HSV infection
MAI
Cryptosporidium
infection
 REACTIVE GASTROPATHY
Reflux or Chemical gastritis,
Aspirin, NSAIDS, bile reflux, mucosal prolapse,
Mucosal edema with Foveolar hyperplasia with loss of mucin
& hyperchromatic nuclei in uninflammed biopsy
Glandular compartment normal,
Prepyloric region bile reflux
ACUTE EROSIVE GASTRITIS

Alcohol, aspirin, NSAIDS,

stress- shock, sepsis, hypoxia
Acute hemorrhagic gastritis
multiple hemorrhagic erosions
superficial slough &
necrotic tissue with viable
basal epithelium; edges
capillary congestion &
extravasation of blood
PEPTIC ULCER

Acute peptic ulcer

Stress ulcers sepsis,
surgery, trauma
Curlings ulcers
Cushings ulcers
Steroid ulcers
PEPTIC ULCER
Chronic peptic ulcer :
1st portion of
duodenum, anterior
wall,
H.pylori, NSAIDS,
alcoholism, steroids,
hypercalcemia- CRF,
hyperparathyroidism
Malignant peptic
ulcers -
adenocarcinoma
PEPTIC ULCER
Chronic peptic ulcer

Necrotic debris

Inflammatory infiltrate

Granulation tissue
REGENERATIVE ATYPIA
OR DYSPLASIA ?
GASTRIC POLYPS
 GASTRIC POLYPS
Hamartomatous Hyperplastic &
Peutz - jeghers inflammatory polyps
syndrome Hyperplastic polyp
Juvenile polyp Fundic gland polyp
Cowden disease Inflammatory fibroid
polyp
Lymphoid hyperplasia
 GASTRIC POLYPS
Neoplastic polyps Mucosal folds
Adenoma Giant folds (normal variant)
Carcinoma Zollinger ellison syndrome
Carcinoid Menetrier disease
Lymphomatous polyposis Malignant infiltration
Mesenchymal tumors

Biopsy polyp ? Prominent mucosal fold

Polyp sessile / pedunculated? stalk sampled
Evidence of polyps in other parts of GIT?
Biopsy from surrounding mucosa.
HAMARTOMATOUS POLYPS

Peutz-Jeghars polyps
Childhood, adolescent
1-3 cm, coarsely
lobulated surface, short
& broad stalk

Smooth muscles

Surface & foveolar

epithelium
HAMARTOMATOUS POLYPS

Juvenile polyps
Rounded smooth
surface, 1-2 cm, short
narrow stalk

Cystically dilated glands

HYPERPLASTIC POLYPS

Similar to inflammatory
colonic polyps
Exaggerated response to
mucosal damage chronic
gastritis
at junction of pyloric &
corpus mucosa, GE junction
Multiple, sessile, broad base
small, 0.5 2.5 cm
>2 cm , a/w malignancy
FUNDIC GLAND POLYP
Multiple (> 10), a/w
drugs for acid
suppression, FAP
Small, 1-15 mm,
Multiple - dysplasia

cystically dilated fundic

glands lined by
attenuated epithelium
INFLAMMATORY FIBROID POLYP

MC in antrum, sessile
Mucosal trauma
Overgrowth of loose
connective tissue
stroma, ulcerates
mucosa
Thin walled blood
vessels
Inflamm. cells
 ENLARGED MUCOSAL FOLDS

Normal variant Menetrier disease

Zollinger ellison a/w low acid production,

syndrome protein loss, corpus

foveolar hyperplasia
Pancreatic & duodenal G
cell neoplasm gastrin
Mucosal folds of corpus
hyperplasia of parietal
cells, ECL cells
ADENOMAS

Sessile,
Tubulovillous & villous
type
Gastric & intestinal
differentiation
Two layers dysplastic
epithelium on top,
nondysplastic cystically
dilated glands below.
Malignancy intestinal
type, >2cm
CARCINOMA OF STOMACH

Nodular. Polypoid,
ulcerated, plaque
like- diffuse
Intestinal
adenocarcinoma &
diffuse type, signet
ring cell ca.
CARCINOMA OF STOMACH
 ENDOCRINE TUMORS
Type I pernicious anemia hypergastrinemia
ECL cell proliferation
Multiple mucosal nodules , (> 5 mm, invading submucosa -
neoplastic)
F>M; Body of stomach

Type II a/w zollinger ellison syndrome,

Body

Type III M>F

Solitary nodules, not a/w pernicious anemia, atrophic
gastritis
Anywhere in stomach (ECL, EC, G cells)
 ENDOCRINE TUMORS
Type IV poorly
differentiated, small
cell carcinomas
LYMPHOMAS
Mucosa associated lymphoid
tumor :-
Ulcers, enlarged mucosal folds, flat
Features of low grade MALT
1. Small lympho, small cleaved cells
2. Lymphoid follicles
3. Neoplastic plasma cells
4. Lymphoepithelial lesions cluster
of 3-4 lymphocytes destroying
glands (lymphocytic gastritis
single cells in epi)
5. Dutcher bodies pas +ve
intranuclear inclusions
High grade no LEL, large cells
vesicular nuclei, prominent nucleoli
 LYMPHOMAS
Non MALT type mantle cell lymphoma , Burkitt
lymphoma, follicular lymphoma
MESENCHYMAL TUMORS
GIST
Solitary, rounded,
lobulated,
MC in corpus,
Two types
Spindle cell
Epithelioid
Prognosis
Size - >5cm, mitotic
figures ->5/ 50 hpf
bad.
SMALL INTESTINAL BIOPSY
INTERPRETATION
 SMALL BOWEL BIOPSIES
COMMON INDICATIONS
Chronic Diarrhea malabsorption,
Chronic Abdominal pain
Occult GI Bleeding
Polyps

Biopsy specimens are mounted with mucosal

side up on filter paper or gelfoam
4- 6 biopsy specimens mandatory
Biopsy : The diagnostic test
(Diffuse lesions)

Whipples disease
Abetalipoproteinemia
Agammaglobinemia
Collagenous colitis
WHIPPLES DISEASE

Diarrhea, malabsorption
Tropheryma whippeli
Lamina propria,
muscularis mucosae,
submucosa foamy
macrophages PAS
positive diastase
resistant bacilli
DD- 1.histoplasmasis
2. MAIC
ABETALIPOPROTEINEMIA

Lack of apoprotein B
Accumulation of
triglycerides in
enterocytes
tips of villi show
intracytoplasmic lipid
droplets
DD megaloblastic
anemia, CS, TS
 AGAMMAGLOBULINEMIA
Absence of plasma cells
& lymphocytes,

COLLAGEN COLITIS
End stage of celiac sprue
Unresponsive to gluten free diet.
Total villous atrophy, subepithelial collagen
deposition
Uneven collagen distribution, multiple
biopsies
Biopsy: may have diagnostic value
(Patchy lesions)

Parasitic Crohns disease

infestation Tuberculosis
Lymphangiectasia IPSID
Eosinophilic Lymphoma
enteritis
PARASITIC INFESTATIONS

Giardia lamblia
MC duodenum
Patchy villous atrophy
Trophozoites along
surface epithelium
Giemsa / trichrome
red organism
Stool examination,
ELISA, direct IF,
PARASITIC INFESTATIONS

Strongyloides
stercoralis
In duodenum, jejunum
In Mucosa eggs
rhabditiform larvae
Stool examination for
larvae
LYMPHANGIECTASIA

Dilatation of mucosal
submucosal subserosal
lymphatics
Protein losing enteropathy,
hypoalbuminemia, edema
Primary congenital
obstructive defects
Secondary retroperitoneal
fibrosis,pancreatitis,
malignancies
 EOSINOPHILIC ENTERITIS
MC in children & young adults
Patchy Mucosal involvement malabsorption ,
diarrhoea; submucosa, muscularis propria
obstruction
1. Absence of associated other inflammatory cells
2. Focal mucosal architectural distortion crypt
abcesses,
3. Infiltration of muscularis mucosae
EOSINOPHILIC ENTERITIS

Causes
Parasites
IBD
NHL
a/w peripheral
eosinophilia
Never associated with
chronicity or
metaplastic changes
CROHN S DISEASE

Mc involves terminal ileum,

Immune response to luminal
flora / their products
Complications :-
Fibrosing strictures,
Fistulas,
Protein losing enteropathy,
Malabsorption,
Steatorrhoea,
 CROHN S DISEASE
1. Small apthoid ulcers / serpiginous ulcers
with
2. Skip areas,
3. Narrowing of lumen,
4. Transmural involvement,
5. Fissures &
6. Granulomas
CROHN S DISEASE
 TUBERCULOSIS
Primary or secondary,
MC ileocaecal
junctions,
Ulcerative /
Hyperplastic,
Narrowing with
obstruction,
MICRO :-
ICT Caseating granulomas
ICM Large areas of

caseation without
granulomas
LYMPHOMAS
IPSID (-chain dis.) :-
Special type of MALToma,
MC Ileum,
Solitory, polypoid,
ulcerative or infiltrative,
Thickened folds with small
nodules,
MC low grade,
Immune response to cont.
Ag stimulation
 LYMPHOMAS
MALT Lymphoma :-
MC Ileum,
Same as gastric MALToma,
Lympho-epithelial lesions less common

Burkitts lymphoma :-
Sporadic,
Ileo-caecal inv.,
Medium, non-cleaved, monomorphic sized cells,
Round nuclei, multiple nucleioli & abundant
basophilic cytoplasm,
Starry-sky app.
Biopsy : Abnormal but
Not diagnostic
Celiac sprue
Tropical sprue
Protein energy malnutrition
(Kwashiorkor)
Folate deficiency
Vitamin B12 deficiency
Bacterial over growth syndrome
 CELIAC SPRUE
Immunogenic injury d/t Gluten (wheat, rye, barley),
Type II adenovirus,
Severe in Proximal intestinal mucosa,
 II I
Marsh Scoring

Grade I: Inflammation in LP:

Lymphocytes & plasma cells
normal villi & crypts

Grade II: Hypertrophy of

Crypts, mild villous atrophy
III

Grade III: Villous atrophy

Partial / Subtotal / Total

Grade IV: Villous atrophy, Crypt

hypoplasia
 CELIAC SPRUE
Diagnosis

Clinical Presentation: Childhood,

Endoscopy: Flattened mucosal folds, scallops,
Biopsy diagnosis: Villous atrophy (partial / total)
Serology: Anti gliadin, Antiendomysial (AEA),
transglutaminase (TGA) Ab,
Response to gluten free diet
CELIAC DISEASE
 TROPICAL SPRUE

Chronic diarrhoeal dis,

Steatorrhoea
Bacterial inf. E. coli, Haemophilus,
Mild-mod villous shortening,
Increased no of chr inflam in LP & epithelium,
Crypt hyperplasia.
 POLYPS
Hyperplastic polyps :-
Sessile, small dome shaped,
MC Rectum,
Serrated app of glands,
Goblet + Absorptive cells
+nt,
Bland nuclei round to oval,
basally placed,
Thickened subepithelial
collagen
 ADENOMAS
Serrated adenoma :-
Pedunculated or sessile,
MC Rectum / Sigmoid
colon,
Dilated crypts, complex
branching,
Majority Absorptive
cells,
Nuclei elongated,
vesicular, prominent
nucleoli, focal
pseudostratification,
 POLYPS

Hamartomatous polyp :-
Stomach, SI, Colon,
Solitory, 1-3 cm,
Sessile / pedunculated,
Normal glandular
epithelium resting on
branching smooth msl
(christmas tree app.),
 POLYPS
Juvenile polyps :-
Children, adolescents,
MC Rectum,
Solitory,
Pedunculated, < 3 cm,
Glistening white, smooth,
With polyposis 15-30 %
dysplasia,
Cystic, tortuous, dilated
glands l/b mucin secreting
epi.
POLYPS

Inflammatory polyps :-
Amoebiasis, Adj to ulcers,
Anostomatic sites, UC, CD
raised mucosa,
Nodules of granulation
tissue,
Sec to mucosal prolapse in
ileum,
 POLYPS
Angiogenic polyp :-
d/t angiogenic growth
factors by carcinoid
tumours,
Exuberant mucosal
polyposis = Cobble
stoning
Expanded villi +
intramucosal capillary
& fibromuscular
proliferation,
 POLYPS
Inflammatory fibroid
polyp :-
Small intestine, stomach,
1.5 13 cm, broad based,
Polypoid,
Arises in submucosa,
extending to mucosa & MP,
Mesenchymal lesion =
inflam + vascular prolif.
 POLYPS

Lymphoid polyp :-
Ileum with FAP coli &
Gardeners synd.
Multiple,
Lymphoid follicles in
mucosa & submucosa,
ADENOMATOUS POLYPS

Tubular adenoma :-
Less common,
Periampullary region,
Small pedunculated,
Single or multiple,
 ADENOMATOUS POLYPS

Villous adenoma :-
Rectum & recto-sigmoid
colon,
Sessile, up to 10 cm,
Velvety cauliflower-like,

Tubulo-villous :-
Intermediate,
Intermixed pattern,
Risk of malignancy
villous component
NEOPLASTIC POLYPS
Adenocarcinoma :-
MC Duodenum (periampullary region),
a/w HNPCC, Crohns, Peutz-Jeghers synd.,
Polypoid, Napkin ring in distal tumours,
NEOPLASTIC POLYPS

CARCINOID :-
MC Ileum,
a/w Celiac dis, Crohns
dis, Inflammatory
polyps,
Multiple with intact
mucosa,
Bright yellow colored,
 Clinicopathological Correlation

Endoscopist Pathologist

Basic mucosal Basic disease process

pattern of the disease Recent developments in
endoscopy

Good clinicopathological correlation = accurate diagnosis

Advances Capsule endoscopy
THANK YOU