pathology of non neoplastic lesions of the upper...
TRANSCRIPT
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PATHOLOGY OF NONNEOPLASTIC LESIONS OF THE
UPPER GASTROINTESTINALTRACT.
PATHOLOGY OF NONNEOPLASTIC LESIONS OF THE
UPPER GASTROINTESTINALTRACT.
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OESOPHAGEAL LESIONS
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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
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GERD
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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
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GERD
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TB Oesophagus
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Candida
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Herpes Oesophagitis
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CMV Oesophagitis.
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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.
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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”
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BARRETT OESOPHAGUS
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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
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Barrett Oesophagus with Dysplasia
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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
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Barret oesophagus with severe dysplasiaprogressing to Carcinoma
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Achalasia cardia with T cell reaction aroundMyenteric plexus
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NON NEOPLASTIC LESIONSOF THE STOMACH
NON NEOPLASTIC LESIONSOF THE STOMACH
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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
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Acute and hemorrhagic erosive gastritis –Alcohol, Asprins, NSAID,Shock, Sepsis –
suppurative gastritis
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PATHOLOGY OF CHRONICGASTRITIS AND PEPTIC
ULCERATION WITH
PATHOLOGY OF CHRONICGASTRITIS AND PEPTIC
ULCERATION WITHCO-RELATION TO HELICOBACTER INFECTION AND
OTHER CAUSES
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Modified Sydney system ofchronic gastritis based on
Topography, morphology andetiology
Modified Sydney system ofchronic gastritis based on
Topography, morphology andetiology
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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
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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
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Neutrophils in chronic activegastritis
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Chronic superficial gastritis withgrade 3 lymphoid infiltrates
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Helicobacter Heilmannii
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Lymphocytic Gastritis
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Granulomatous gastritis
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Eosinophilic gastritis
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• 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.
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Serum antibodies in AG
• Anti parietal antibodies. 60% of patients• Intrinsic factor antibodies in 50%• Cross reacting anti canalicularantibody
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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.
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Crohn’s associated Gastritis
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Mucor in gastric ca
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cmv
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Apergillosois
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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
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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
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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
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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
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Giardiasis
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Thank you