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                             Path Quiz Case- 79

Diagnosis: Gastric mucosa- Helicobacter-pylori

associated chronic gastritis with moderate activity

and  focal intestinal metaplasia.

               Atypical Fibroxanthoma

       Dr Sampurna Roy MD

            Case history and images:

 
   Gastrointestinal Stromal Tumour

   

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June 2009
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An outline of the anatomy and normal histology of the  stomach for pathologists.

Reporting of gastric biopsies (non-neoplastic gastric lesions).

Pathology and pathogenesis of peptic ulcer.

Acute Gastritis 

Chronic Gastritis

Helicobacter pylori  associated(TypeB) Gastritis 

Autoimmune Gastritis (Type A) 

Reactive /Reflux/ Chemical Gastritis (Type C)

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An approach to evaluation of small intestinal biopsy.

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- Normal Histology of the Large Intestine

- Interpretation of Large Intestinal Biopsies

- Assessment of abnormalities -1 (lumen, surface epithelium, subepithelial zone)

- Assessment of abnormalities - 2  (crypt density , architecture and epithelium)

- Assessment of abnormalities - 3 (changes in the lamina propria,muscularis mucosae and submucosa) 

Gross examination of colorectal resection specimens in  non-neoplastic diseases

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Juvenile polyp ; Peutz-Jeghers polyp ; Inflammatory fibroid polyp ; Multiple Lymphomatous polyposis ;  Lymphoid polyp   

Myxoid Tumours of Soft Tissue

               

Chronic gastritis is defined as  the presence of chronic mucosal inflammatory changes  leading eventually to mucosal atrophy and intestinal metaplasia.

The epithelial changes may become dysplastic and constitute a backround for the development of carcinoma.

30% of endoscopically normal biopsies may show chronic gastritis.

Classification:

Type A : Autoimmune gastritis- Associated with pernicious anaemia. Body of the stomach is usually affected.

Type B : Environmental gastritis- Result from dietary or intraluminal factors, specially Helicobacter pylori.  Usually localized in the antrum. In severe cases, the inflammation spreads to the proximal part of the stomach.

Type C :  Chemical gastritis- Associated with ingestion of non-steroidal  anti-inflammatory drugs or bile influx

What is Helicobacter pylori?

Small curved  gram negative bacillus that colonizes the mucus layer of the stomach.
The organisms adheres to the foveolar epithelium and in the crevices between foveolar cells.
Corkscrew-like  movement and production of enzymes play an important role in the pathogenesis.
Bacterial  adhesins identify cell surface proteins, glycoconjugates and helps in colonization.
H. pylori  move along  the lateral border of the foveolar cells and weaken the mucosal barrier.
The intracellular space is widened and there is invasion by neutrophil polymorphs.
Proteases produced by the H. pylori digest  gastric mucin and further damage the epithelium.

Helicobacter associated patterns of gastritis include:
(i) Antral-predominant  gastritis (principal cause of peptic ulcer)
(ii) Multifocal atrophic gastritis involving corpus, fundus and antrum ( may develop gastric ulcer and gastric carcinoma).
H pylori are  also associated with the  development of gastric lymphoma.
Cag A+strains of H. pylori (more ulcerogenic) are protective against development of gastroesophageal reflux disease.

What is Helicobacter heilmannii? IMAGE LINK (Dr Tsutsumi)

This bacteria has an elongated spiral appearance and are present only in small number of patients.
H. helmannii is a possible cause of gastric ulcer.

 

Morphological features: 

Histological responses to Helicobacter pylori infection: gastritis, atrophy and preneoplasia. Baillieres Clin Gastroenterol. 1995 Sep;9(3):467-86
 
-In the initial active phase there are features of acute gastritis characterised by neutrophil polymorphs in mucous neck region. In severe infection there is pit abscess formation.
-Cellular swelling and vacuolization, mucin loss and  desquamation of surface epithelium
-Erosion and frank ulceration.
-Degenerative and regenerative changes present.
-Regenerative changes - There are hyperplastic neck cells and elongated, distorted and tubular structures. The cells display cytoplasmic basophilia, increased mitoses and hyperchromatic nuclei, however the enlarged nuclei  show smooth regular nuclear membrane  (D/D dysplasia or ca-in situ)
- As the disease progresses there is superimposed chronic inflammation (Active chronic gastritis)
Neutrophils, eosinophils, basophils, macrophages, monocytes, plasma cells infiltrate the mucosa.
-Mucosa appears normal in thickness or slightly expanded by mononuclear cells.
-In early stage, lymphocytes and plasma cells are present in the superficial mucosa mostly along lesser curvature. (Chronic superficial gastritis)
-The inflammation extends into the glandular compartment.
- Focal epithelial cell dropout is noted.
-There is lymphoid follicle formation with or without germinal centres.  This is a marker for H pylori infection.
-Gradually develops pangastritis.
- There is glandular atrophy (Chronic atrophic gastritis)
IMAGE LINK
-Intestinal metaplasia replaces the gastric glands. H pylori is markedly decreased in the late stage as  intestinal metaplasia creates an unfavourable environment for H. pylori.
- Gastric atrophy is  the end stage of chronic gastritis and is characterized by thinning of gastric mucosa in the absence of inflammation. 
Parietal and chief cells are decreased in number in the body (autoimmune gastritis). Antrum shows loss of pyloric glands (type B gastritis).
[ 2 main causes of Atrophic gastritis - i ) H.pylori associated multifocal atrophic gastritis involving corpus and antrum.
ii) Autoimmune gastritis restricted to the corpus]

Note:
Following treatment of H. pylori infection the features of chronic gastritis with lymphoid follicles may persist .
These features are gradually resolve  after few years.
Following long term therapy with proton pump inhibitors there may be pseudo hypertrophy of parietal cells. Tiny fundic glands cysts lined by parietal and chief cells may be noted.

(AFIP)IMAGE LINK ; H. pylori IMAGE LINK ; IMAGE LINK

Metaplasia in chronic gastritis:

Pyloric metaplasia: Replacement of fundic type  glands by mucus secreting glands.

Intestinal metaplasia:  Begins at the antral corpus junction then spreads to the antrum and fundus.
(i) Small intestinal type  (ii) Large intestinal type
May be I - Complete : Mainly sialomucin  or
            II - Incomplete :  Neutral mucin (IIA) or
                                            Sulfomucin (IIB)

1- Initially there is epithelial type change 
2-Followed by villiform architecture of the mucosa
3- Enterocytes disappear and there is colonic metaplasia.

Colonic mucosa is more likely to be associated with dysplasia and carcinoma.
Pancreatic metaplasia: Associated with autoimmune gastritis.

               

Abstracts:

Evaluation of endoscopic and histological findings in Helicobacter pylori-positive Japanese young adults. J Gastroenterol Hepatol. 2006 Jan;21(1):258-61.

Increased rate of Helicobacter pylori infection detected by PCR in biopsies with chronic gastritis.Am J Surg Pathol. 2006 Feb;30(2):242-8.

Genetic alterations in benign lesions: Chronic gastritis and gastric ulcer.World J Gastroenterol. 2006;12(4): 625-9.

Effect of Helicobacter pylori Eradication on the Outcome of Reflux Esophagitis and Chronic Gastritis in the Elderly. A Randomized, Multicenter, Eight-Month Study.Gerontology. 2006 ;52(2):99-10

Comparison of Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients. World J Gastroenterol. 2005 Feb 21;11(7):976-81

Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer.World J Gastroenterol. 2005 Feb 14;11(6):791-6.

Histological changes in the gastric mucosa after Helicobacter pylori eradication.Eur J Gastroenterol Hepatol. 2004 Nov;16(11):1183-8.

Effect of Helicobacter pylori eradication on histological lesions of gastric mucosa. An 18-month follow-up study.Rev Clin Esp. 2000 ;200 (9):480-4.

Histopathology of Helicobacter pylori infections.Acta Med Austriaca. 2000;27(4):100-3.

Interobserver variation in the histopathological scoring of Helicobacter pylori related gastritis. J Clin Pathol. 1999 Aug;52(8):612-5.

Review article: Gastric atrophy and atrophic gastritis--nebulous concepts in search of a definition.Aliment Pharmacol Ther. 1998 Feb;12 Suppl 1:17-23.

Histological classification of gastritis and Helicobacter pylori infection: an agreement at last? The International Workshop on the Histopathology of Gastritis.Helicobacter. 1997 Jul;2 Suppl 1:S17-24.

Classification and grading of gastritis. The updated Sydney system. Am J Surg Pathol.1996; 20:1161-81

Recognizing atrophy: another step toward a classification of gastritis.Am J Surg Pathol. 1996;20 Suppl 1:S23-30.

           

 

  

      

      

      

       

        

         

 

NORMAL HISTOLOGY OF ESOPHAGUS

AN APPROACH TO THE  REPORTING  OF ESOPHAGEAL BIOPSIES

BARRETT'S   ESOPHAGUS   (INTESTINAL METAPLASIA  DYSPLASIA  &   ADENOCARCINOMA)

BENIGN TUMOURS AND  TUMOUR - LIKE CONDITIONS  OF  ESOPHAGUS

 1. SQUAMOUS PAPILLOMA OF THE ESOPHAGUS

 2. INFLAMMATORY FIBROID POLYP OF THE ESOPHAGUS

 3. LEIOMYOMA OF THE ESOPHAGUS

 4. GRANULAR CELL TUMOUR OF THE ESOPHAGUS

 5. ESOPHAGEAL CYSTS

 6. GLYCOGENIC ACANTHOSIS

 7.FIBROVASCULAR POLYPS

REPORTING  OF  ESOPHAGEAL  RESECTION SPECIMENS

SQUAMOUS  EPITHELIAL  DYSPLASIA INCLUDING SQUAMOUS CELL CARCINOMA IN-SITU OF THE ESOPHAGUS

SMALL CELL CARCINOMA OF THE ESOPHAGUS

DRUG  RELATED  LESIONS  OF  THE GASTRO-INTESTINAL TRACT

 
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