PATHOLOGY OF NONNEOPLASTIC LESIONS OF THE

UPPER GASTROINTESTINALTRACT.

PATHOLOGY OF NONNEOPLASTIC LESIONS OF THE

UPPER GASTROINTESTINALTRACT.

OESOPHAGEAL LESIONS

OESOPHAGITIS AND OTHER NONNEOPLASTIC DISORDERS

• Corrosive – Gastroesophageal reflux (GERD),Pills, Acid intake, Irradiation.

• Infections like Candida, Herpes simplex, CMV,Tuberculosis.

• Eosinophilic oesophagitis.

• Barrett Oesophagus.

• Achalasia Cardia

• Corrosive – Gastroesophageal reflux (GERD),Pills, Acid intake, Irradiation.

• Infections like Candida, Herpes simplex, CMV,Tuberculosis.

• Eosinophilic oesophagitis.

• Barrett Oesophagus.

• Achalasia Cardia

GERD

GERDHistology in NERD on endoscopy

• Epithelial hyperplasia• Basal hyperplasia >15%• Papillary elongation.>2/3• Vascular congestion of

papilla• Intercellular spaces• Intraepithelial eosinophils• Neutrophils – on endoscopy

in GERD• Ulceration- Severe - on

endoscopy in GERD

• Epithelial hyperplasia• Basal hyperplasia >15%• Papillary elongation.>2/3• Vascular congestion of

papilla• Intercellular spaces• Intraepithelial eosinophils• Neutrophils – on endoscopy

in GERD• Ulceration- Severe - on

endoscopy in GERD

GERD

TB Oesophagus

Candida

Herpes Oesophagitis

CMV Oesophagitis.

Eosinophilic oesophagitis

• Endoscopy – ringedOeso, Furrows, narrowOeso ,Strictures ornormal. Mostly Males .

• Eosinophils in epitheliumwith microabscess.

• Endoscopy – ringedOeso, Furrows, narrowOeso ,Strictures ornormal. Mostly Males .

• Eosinophils in epitheliumwith microabscess.

Barrett Oesophagus - APremalignant condition

“A change in the Oesophagealepithelium of any length recognised by

endoscopy and confirmed to haveintestinal metaplasia in the form of

Goblet cells by biopsy”

“A change in the Oesophagealepithelium of any length recognised by

endoscopy and confirmed to haveintestinal metaplasia in the form of

Goblet cells by biopsy”

BARRETT OESOPHAGUS

Differential Diagnosis ofOesophageal Glandular epithelium

• Inadvertently sampled Gastric mucosa or wronglylabeled bottle.

• GE junction mucosa located in distal 2cms – difficultto judge precise location on endoscopy. Henceincidental Goblet cells do not fulfill the criteria.Important as intestinal metaplasia of the cardia isless likely to progress to carcinoma.

• Hetrotropic Gastric fundic or cardiac mucosa usually inupper Oesophagus.

• Infants – embryonal remnant• Rarely ectopic sebeceous glands

• Inadvertently sampled Gastric mucosa or wronglylabeled bottle.

• GE junction mucosa located in distal 2cms – difficultto judge precise location on endoscopy. Henceincidental Goblet cells do not fulfill the criteria.Important as intestinal metaplasia of the cardia isless likely to progress to carcinoma.

• Hetrotropic Gastric fundic or cardiac mucosa usually inupper Oesophagus.

• Infants – embryonal remnant• Rarely ectopic sebeceous glands

Barrett Oesophagus with Dysplasia

Dysplasia surveillance -4 quadrant biopsies– every 2cms

• Male patients• Endoscopically Abnormal –erosion, nodule

polyp• Endoscopically normal

• Male patients• Endoscopically Abnormal –erosion, nodule

polyp• Endoscopically normal

Barret oesophagus with severe dysplasiaprogressing to Carcinoma

Achalasia cardia with T cell reaction aroundMyenteric plexus

NON NEOPLASTIC LESIONSOF THE STOMACH

NON NEOPLASTIC LESIONSOF THE STOMACH

Inflammatory lesions of thestomach

• Acute haemorrhagic /erosive gastritis.• Helicobacter gastritis• Atrophic gastritis• Autoimmune gastritis.• Granulomatous gastritis.• Eosinophilic gastritis• Lymphocytic gastritis• Radiation gastritis• Gastritis in immunosupressed individuals• Gastritis in patients IBD.• Gastritis secondary to drug intake

• Acute haemorrhagic /erosive gastritis.• Helicobacter gastritis• Atrophic gastritis• Autoimmune gastritis.• Granulomatous gastritis.• Eosinophilic gastritis• Lymphocytic gastritis• Radiation gastritis• Gastritis in immunosupressed individuals• Gastritis in patients IBD.• Gastritis secondary to drug intake

Acute and hemorrhagic erosive gastritis –Alcohol, Asprins, NSAID,Shock, Sepsis –

suppurative gastritis

PATHOLOGY OF CHRONICGASTRITIS AND PEPTIC

ULCERATION WITH

PATHOLOGY OF CHRONICGASTRITIS AND PEPTIC

ULCERATION WITHCO-RELATION TO HELICOBACTER INFECTION AND

OTHER CAUSES

Modified Sydney system ofchronic gastritis based on

Topography, morphology andetiology

Modified Sydney system ofchronic gastritis based on

Topography, morphology andetiology

Type ofGastritis

Etiology Synonyms

Non Atrophic Helico bacter Type B: Superficial:Diffuse antral: ChronicSuperficial: Interstitial -Follicular:

Atrophic - Autoimmune Auto immune reaction Type A : Perniceousanemia associated

Atrophic – Multofocalatrophic

Helico bacter, Dietary ,Environmental

Type B:Atrophic – Multofocalatrophic

Helico bacter, Dietary ,Environmental

Special - Chemical Chemicals, Bile, drugsNSAID

Type C

Special -Radiation Radiation injury

Special – Lymphocytic Helicobacter : Gluten Celiac associated

Special - Granuloma Crohn’s, TB,Sarcoidosis, FB

Eosinophilic Allergy

Non Atrophic Helicobacter inducedChronic Gastritis

• Chronic Active Superficialgastritis

• Chronic SuperficialGastritis

• Chronic SuperficialGastritis with Lymphoidhyperplasia 1 to 3grades

• Chronic multifocalatrophic gastritis

• Chronic Active Superficialgastritis

• Chronic SuperficialGastritis

• Chronic SuperficialGastritis with Lymphoidhyperplasia 1 to 3grades

• Chronic multifocalatrophic gastritis

Neutrophils in chronic activegastritis

Chronic superficial gastritis withgrade 3 lymphoid infiltrates

Helicobacter Heilmannii

Lymphocytic Gastritis

Granulomatous gastritis

Eosinophilic gastritis

• Patchy to diffuse Lymphoplasmacytic infiltrate,often in deeper layers.

• Focal Lymphocytic infiltrate with destruction ofgland base

• Patchy atrophy of mucosa with intestinal/pyloricmetaplasia.

• Parietal cell pseudo hypertrophy.• ECL hyperplasia usually linear• Negative staining for Gastrin and positive for

Chromogranin.

AUTOIMMUNE GASTRITIS• Patchy to diffuse Lymphoplasmacytic infiltrate,

often in deeper layers.• Focal Lymphocytic infiltrate with destruction of

gland base• Patchy atrophy of mucosa with intestinal/pyloric

metaplasia.• Parietal cell pseudo hypertrophy.• ECL hyperplasia usually linear• Negative staining for Gastrin and positive for

Chromogranin.

Serum antibodies in AG

• Anti parietal antibodies. 60% of patients• Intrinsic factor antibodies in 50%• Cross reacting anti canalicularantibody

Relation ship between Autoimmunegastritis and Helico Bacter infection• Many patients of Helicobacter infection develop

autoantibodies likeAnticanalicular AntibodyAntifoveolar AntibodyAntiparietal Antibody.

Hence when H.Pylori are present either withAG or suspicious AG, treatment of H. Pyloriis important.

Result 1. Serum Gastrin levels reduce2. Regression of ECL Hyperplasia3. Atrophy persists.

• Many patients of Helicobacter infection developautoantibodies like

Anticanalicular AntibodyAntifoveolar AntibodyAntiparietal Antibody.

Hence when H.Pylori are present either withAG or suspicious AG, treatment of H. Pyloriis important.

Result 1. Serum Gastrin levels reduce2. Regression of ECL Hyperplasia3. Atrophy persists.

Crohn’s associated Gastritis

Mucor in gastric ca

cmv

Apergillosois

Duodenal biopsy• At least 3 sites to be biopsied so that patchy atrophy is

not missed.• At least one bit should be from Distal Duodenum as

pathology is more likely to start in distal end and not inthe bulb.

• Biopsy should be sent for pathology with properorientation on paper. ie Luminal side uppermost on filterpaper

• At least 3 sites to be biopsied so that patchy atrophy isnot missed.

• At least one bit should be from Distal Duodenum aspathology is more likely to start in distal end and not inthe bulb.

• Biopsy should be sent for pathology with properorientation on paper. ie Luminal side uppermost on filterpaper

Histology• Architecture of the mucosa

with shape of villous –thin,leaflike, broad, blunt,flat

• Villous/ crypt ratio-VC ratio -3:1to 5:1

• Crypt hyper and hypo plasia• Surface enterocytes• Brush border• IEL –intraepithelial

lymphocytes• Gastric metaplasia• Presence of Giardia, CMV,

Cryptococcus• Neoplasia

• Architecture of the mucosawith shape of villous –thin,leaflike, broad, blunt,flat

• Villous/ crypt ratio-VC ratio -3:1to 5:1

• Crypt hyper and hypo plasia• Surface enterocytes• Brush border• IEL –intraepithelial

lymphocytes• Gastric metaplasia• Presence of Giardia, CMV,

Cryptococcus• Neoplasia

Classification of Duodenal biopsy inrelation to malabsorption syndromeA. Severe diffuse villous atrophyEg . Celiac sprue, Protein allergies, Lymphocytic

enterocolitis

B. Partial atrophy1. Hypoplasia- eg Kwashiorkar disease,

Megaloblastic anemia, Radiation damage.2. Without hypoplasia eg. Tropical sprue,

infections, Drug induced, IBD , T cellenteropathy, Eoisinophilic enteritis,Autoimmune disorders, Tumours

A. Severe diffuse villous atrophyEg . Celiac sprue, Protein allergies, Lymphocytic

enterocolitis

B. Partial atrophy1. Hypoplasia- eg Kwashiorkar disease,

Megaloblastic anemia, Radiation damage.2. Without hypoplasia eg. Tropical sprue,

infections, Drug induced, IBD , T cellenteropathy, Eoisinophilic enteritis,Autoimmune disorders, Tumours

CELIAC SPRUE• Immunological injury to Enterocytes due to Gluten

Wheat (Gliadins )Rye (Secalins )Barley ( Hordeins)

• HLA associated – HLA DQ8• Histology .

Flat mucosaLymphocyte and plasma cell infiltrateIntraepithelial lymphoctes – mostly T8

• Definitive diagnosis only with serological studies:IgA – Antiendomysial AntibodiesIgA – Anti tissue transglutaminase antibodies

• Immunological injury to Enterocytes due to GlutenWheat (Gliadins )Rye (Secalins )Barley ( Hordeins)

• HLA associated – HLA DQ8• Histology .

Flat mucosaLymphocyte and plasma cell infiltrateIntraepithelial lymphoctes – mostly T8

• Definitive diagnosis only with serological studies:IgA – Antiendomysial AntibodiesIgA – Anti tissue transglutaminase antibodies

Giardiasis

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