PATHOLOGY OF NON NEOPLASTIC LESIONS OF THE UPPER GASTROINTESTINAL TRACT.

PATHOLOGY OF NON NEOPLASTIC LESIONS OF THE UPPER GASTROINTESTINAL TRACT.

OESOPHAGEAL LESIONS

OESOPHAGITIS AND OTHER NON NEOPLASTIC DISORDERS Corrosive Gastroesophageal reflux (GERD), Pills, Acid intake, Irradiation. Infections like Candida, Herpes simplex, CMV, Tuberculosis. Eosinophilic oesophagitis. Barrett Oesophagus. Achalasia Cardia

GERD

GERD Histology 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

GERD

TB Oesophagus

Candida

Herpes Oesophagitis

CMV Oesophagitis.

Eosinophilic oesophagitis Endoscopy ringed Oeso, Furrows, narrow Oeso,Strictures or normal. Mostly Males. Eosinophils in epithelium with microabscess.

Barrett Oesophagus - A Premalignant condition A change in the Oesophageal epithelium of any length recognised by endoscopy and confirmed to have intestinal metaplasia in the form of Goblet cells by biopsy

BARRETT OESOPHAGUS

Differential Diagnosis of Oesophageal Glandular epithelium Inadvertently sampled Gastric mucosa or wrongly labeled bottle. GE junction mucosa located in distal 2cms difficult to judge precise location on endoscopy. Hence incidental Goblet cells do not fulfill the criteria. Important as intestinal metaplasia of the cardia is less likely to progress to carcinoma. Hetrotropic Gastric fundic or cardiac mucosa usually in upper 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

Barret oesophagus with severe dysplasia progressing to Carcinoma

Achalasia cardia with T cell reaction around Myenteric plexus

NON NEOPLASTIC LESIONS OF THE STOMACH

Inflammatory lesions of the stomach 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 CHRONIC GASTRITIS AND PEPTIC ULCERATION WITH CO-RELATION TO HELICO BACTER INFECTION AND OTHER CAUSES

Modified Sydney system of chronic gastritis based on Topography, morphology and etiology

Type of Gastritis Etiology Synonyms Non Atrophic Helico bacter Type B: Superficial: Diffuse antral: Chronic Superficial: Interstitial Follicular: Atrophic - Autoimmune Auto immune reaction Type A : Perniceous anemia associated Atrophic Multofocal atrophic Helico bacter, Dietary, Environmental Type B: Special - Chemical Chemicals, Bile, drugs NSAID Type C Special -Radiation Radiation injury Special Lymphocytic Helicobacter : Gluten Special - Granuloma Crohn s, TB, Sarcoidosis, FB Eosinophilic Allergy Celiac associated

Non Atrophic Helicobacter induced Chronic Gastritis Chronic Active Superficial gastritis Chronic Superficial Gastritis Chronic Superficial Gastritis with Lymphoid hyperplasia 1 to 3 grades Chronic multifocal atrophic gastritis

Neutrophils in chronic active gastritis

Chronic superficial gastritis with grade 3 lymphoid infiltrates

Helicobacter Heilmannii

Lymphocytic Gastritis

Granulomatous gastritis

Eosinophilic gastritis

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 Autoimmune gastritis and Helico Bacter infection Many patients of Helicobacter infection develop autoantibodies like Anticanalicular Antibody Antifoveolar Antibody Antiparietal Antibody. Hence when H.Pylori are present either with AG or suspicious AG, treatment of H. Pylori is important. Result 1. Serum Gastrin levels reduce 2. Regression of ECL Hyperplasia 3. 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 in the bulb. Biopsy should be sent for pathology with proper orientation on paper. ie Luminal side uppermost on filter paper

Histology Architecture of the mucosa with shape of villous thin,leaf like, broad, blunt,flat Villous/ crypt ratio-vc ratio -3:1 to 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 in relation to malabsorption syndrome A. Severe diffuse villous atrophy Eg. Celiac sprue, Protein allergies, Lymphocytic enterocolitis B. Partial atrophy 1. Hypoplasia- eg Kwashiorkar disease, Megaloblastic anemia, Radiation damage. 2. Without hypoplasia eg. Tropical sprue, infections, Drug induced, IBD, T cell enteropathy, 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 mucosa Lymphocyte and plasma cell infiltrate Intraepithelial lymphoctes mostly T8 Definitive diagnosis only with serological studies: IgA Antiendomysial Antibodies IgA Anti tissue transglutaminase antibodies

Giardiasis

Thank you