This document summarizes different types of gastritis and gastric disorders. It defines gastritis as inflammation of the stomach lining and gastropathy as epithelial cell damage without inflammation. It then classifies gastritis as acute or chronic and discusses various causes including H. pylori infection, NSAIDs, stress, and autoimmune conditions. It also describes different metaplastic and hyperplastic gastropathies such as Menetrier's disease and Zollinger-Ellison syndrome.

1. Gastritis Dr.Mohammad Shaikhani Assistant professor Sulaimanyah College of Medicine.

2. Definition Inflammation associated with mucosal injury A histological term that needs biopsy to be confirmed. Usually due to infectious agents (As H pylori) , autoimmune & hypersensitivity reactions. Endoscopic mucosal changes of gastritis, 27% had a normal endoscopic biopsy specimen& a normal endoscopic appearance, 63 % had histological evidence of gastritis.

3. Definition “ Gastropathy “: Epithelial cell damage /regeneration without inflammation. Gastropathy may be referred without histological evidence, according to gross appearance in endoscopy or radiology. Gastropathy usually caused by irritants as drugs (eg, NSAIDs& alcohol), bile reflux, hypovolemia &chronic congestion.

4. Gross–histologic correlation?

5. Classification Acute: short term inflammation with neurophilic infiltrate Chronic:long standing with mononuclear cell infiltrate especially lymphocyte/maccrophages

6. Anatomical site ANTRUM CARDIA BODY MUCOUS SECRETING ENDOCRINE SPECIALISED SECRETORY: PARIETAL - ACID CHIEF - PEPSINOGEN ENDOCRINE HIST, SOMASTATIN MUCOUS SECRETING ENDOCRINE GASTRIN, 5HT

9. CLASSIFICATION GASTRITIS ACUTE COMMON CHRONIC EMAG AMAG BILE HP STRESS NSAID

10. CLASSIFICATION GASTRITIS ACUTE COMMON CHRONIC EMAG AMAG BILE HP STRESS NSAID

11. Acute hemorrhagic erosive (NSAIDs, alcohol, or bile acids) Mucosal hypoxia (trauma, burns [Curling's ulcers],sepsis) Combination of factors as antineoplastic chemotherapy Gastric/duodenal ulcers occurring during severe damage to CNS (Cushing's ulcers).

12. ACUTE GASTRITIS - MORPHOLOGY Mucosal congestion, oedema, inflammation, ulceration & Bleeding.

13. Acute hemorrhagic erosive NSAID-induced acute hemorrhagic& erosive gastropathy due to inhibition of prostaglandin production . Prostaglandins protect mucosa by several mechanisms, as stimulation of mucus / bicarbonate secretion&maintenance of mucosal blood flow Hemorrhagic or erosive gastropathy may be associated with the development of gastric or duodenal ulcers.

14. NSAID GI toxicity risk factor H/O adverse GI event (ulcer, hemorrhage) *5 increases. Age >60 increases risk *6. High (> twice normal) dosage of a NSAID increases risk *10. Concurrent use of glucocorticoids increases risk *5. Concurrent use of anticoagulants increases risk *10- 15.

15. HP/NSAID If H/O uncomplicated or complicated peptic ulcers (gastric, duodenal) should be tested for H. pylori prior to beginning a NSAID or low dose aspirin . If present, H. pylori should be treated with appropriate therapy, even if it is believed that the prior ulcer was due to NSAIDs.

16. NSAID-related GIT toxicity prophylaxis COX-2 selective inhibitor. Misoprostol PPI as lansoprazole .

17. Stress ulcer pathophysiology Hypersecretion of acid –head trauma. Defects in gastric glycoprotein mucus –In critically ill patients, increased refluxed bile salts or uremic toxins can denude the glycoprotein mucous barrier Ischemia – Shock, sepsis, trauma can lead to impaired perfusion of the gut.

18. Stress ulcer risk factors 2 major risk factors for clinically significant bleeding due to stress ulcers are: Mechanical ventilation for > 48 hours & coagulopathy . • Shock • Sepsis • Hepatic failure • Renal failure • Multiple trauma • Burns >35% total body surface area • Organ transplant recipients • Head or spinal trauma • H/O peptic ulcer disease or upper GI bleeding

19. Common type of gastritides

20. CLASSIFICATION GASTRITIS ACUTE COMMON CHRONIC EMAG AMAG BILE HP STRESS NSAID

21. H Pylori A spiral shaped, microaerophilic, gram negative bacterium measuring 3.5 length* 0.5 microns in width urease forms ammonia & bicarbonate that neutralize gastric acid& form a protective cloud around the organism Urease appears to be vital for its survival & colonization. Spiral shape, flagella facilitate its passage through the mucus layer Helicobacter pylori is the most common chronic bacterial infection in humans ;50% of the world's population is affected. The frequency of H.P for any age in any locality reflects rate of bacterial acquisition during childhood years &affected by: Density of housing. Overcrowding Number of siblings. Sharing a bed. Lack of running water.

24. The route by which infection occurs remains unknown. Person-to-person transmission by either fecal/oral or oral/oral exposure seems most likely Humans appear to be the major reservoir of infection Isolated from primates from domestic cats & in milk/ gastric tissue of sheep

25. Vac A & Cag A Vacuolating cytotoxin (VacA) causes cell injury in vitro & gastric tissue damage in vivo . All H. pylori contain the gene coding for VacA; but, only some strains have cytotoxin-associated gene A (cagA) Strains producing VacA & CagA cause more intense tissue inflammation&induce cytokine production

26. 85-100% with duodenal ulcers have CagA+ strains, compared to 30-60% of infected patients who do not develop ulcers CagA strains may be associated with a higher frequency of precancerous lesions.

27. Host polymorphism of IL-1 beta (&possibly IL-10) appears to determine the degree of inflammatory response to infection, resulting alteration in acid secretion (hyper or hypo secretion)&risk for subsequent gastric cancer

28. HP The inflammation usually superficial, located in the gastric pit & upper portion of the lamina propria, , consists of mononuclear cells & polymorphonuclear leukocytes, commonly termed chronic active inflammation . The antrum consistently is involved, whereas inflammation in the acid-secreting gastric body &fundus is more variable. H. pylori is causally associated with gastritis, duodenal &gastric ulcer, gastric adenocarcinoma&primary gastric B-cell lymphomas of mucosa-associated lymphoid tissue (MALT) Infected subjects have 1/6 lifetime risk of peptic ulcer; the lifetime risk of gastric cancer varies from 1-3% - > 12% in Japan. DISTRIBUTION & PROGRESSION: Antral- DU& Pangastritis-GASTRIC CA.

29. HP: diagnosis Serology with ELISA for IgG or IgA antibodies, 13C-urea or 14C-urea breath tests, or stool antigen testing. Tests requiring endoscopy&biopsy include histologic exam , urease testing of antral biopsy specimens, or culture. The optimal method depends on circumstances, local expertise, /availability. All tests have good sensitivity/specificity, but false-positive/false-negative determinations occur. In tests that depend on the No of organisms (breath &gastric biopsy specimens for urease activity, histology& culture), false-negative occur esp when the organism suppressed by antibiotics, PPI, or bismuth. Therapy may need to be discontinued for several weeks before these tests become positive.

30. HP:Trt H. pylori infection is typically latent. H. pylori gastritis is found more frequently, in patients with dyspepsia. Cure of the infection resolves symptoms in only 10% of patients with nonulcer dyspepsia. Antibiotic therapy for H. pylori is recommended because: Less expensive & safer than additional diagnostic studies & long-term continuous antacid therapy. Cure of the inf reduces the risk of subsequent PUD &gastric ca. Eliminates the individual as a carrier who can transmit the infection. H. pylori testing&treatment are appropriate for new-onset or previously undiagnosed dyspepsia without alarm features .

31. Bile reflux gastropathy Bile reflux gastropathy results from the regurgitation of bile into the stomach because of: An operative stoma. An incompetent pyloric sphincter Abnormal duodenal motility The effect of bile salts on gastric mucosa is comparable to that seen after chronic NSAID use

32. Chronic metaplastic gastritides

33. CLASSIFICATION GASTRITIS ACUTE COMMON CHRONIC EMAG AMAG BILE HP STRESS NSAID

34. Metaplastic atrophic gastritis Metaplasia, especially intestinal type, is virtually a universal feature of atrophic gastritis. Metaplasia is highly relevant to the pathogenesis of atrophic gastritis & to its complications (eg, pernicious anemia, gastric ulcer, gastric cancer).

35. metaplastic atrophic gastritis AUTOIMMUNE METAPLASTIC ATROPHIC GASTRITIS (AMAG) is an inherited form that is associated with an immune response in the oxyntic mucosa directed against parietal cells &intrinsic factor. AMAG is inherited as an autosomal dominant disorder

36. SYNONYMS OF AMAG TYPE A GASTRITIS AUTOIMMUNE GASTRITIS DIFFUSE CORPORAL GASTRITIS

37. Metaplastic atrophic gastritis The chronic inflammation, gland atrophy, epithelial metaplasia of AMAG are closely paralleled by elevated serum antibodies to parietal cells & intrinsic factor, reflecting its autoimmune origin.

39. Metaplastic atrophic gastritis The loss of parietal cell mass leads to profound hypochlorhydria, while the inadequate production of intrinsic factor leads to vitamin B12 malabsorption& pernicious anemia.

40. Metaplastic atrophic gastritis Patients with AMAG are at increased risk for the development of gastric carcinoid tumors& adenocarcinoma. CANCER

41. Metaplastic atrophic gastritis surveillance strategy for patients diagnosed with pernicious anemia • Upper endoscopy soon after diagnosis • Removal of gastric polyps if possible; most of these polyps will be benign • Frequent reinvestigation in patients whose polyps are not removed or who have severe mucosal dysplasia; in the remaining patients follow-up endoscopies should be performed at approximately five-year intervals.

42. metaplastic atrophic gastritis Patients with AMAG are less likely to be infected by H. pylori than aged-matched controls: Metaplastic epithelium is unsuitable for H. pylori colonization. The associated hypochlorhydria encourages overgrowth by other bacterial species

43. EMAG Environmental metaplastic atrophic gastritis (EMAG) is due to environmental factors, as diet (NITROSO COMPOUNDS) & H. pylori infection, on the gastric mucosa.

44. metaplastic atrophic gastritis Unlike AMAG, mucosal changes in patients with EMAG affect both the corpus & antrum in a multifocal distribution, but with heaviest involvement of the antrum.

45. Metaplastic atrophic gastritis EMAG vs AMAG • Gastric acid production does not disappear entirely • Serum gastrin is not elevated • Parietal cell & intrinsic factor autoantibodies & pernicious anemia are absent

46. Metaplastic atrophic gastritis There is an increased risk for gastric ulcer compared to AMAG, presumably due to the accompanying hypochlorhydria in the latter disorder CANCER

47. metaplastic atrophic gastritis Diagnosis of EMAG should not be made from biopsy specimens unless at least 20 % of the available antral or transitional mucosa is replaced by metaplastic glands, or there is unequivocal atrophy.

48. Hyperplastic gastropathies Proliferative, inflammatory, infiltrative conditions are associated with large folds due to excessive number of mucosal epithelial cells

49. Large gastric folds > 1.0 cm Chronic gastritis/lymphoid hyperplasia Benign tumors Gastric malignancy Zollinger-Ellison syndrome Menetrier's disease

50. Ménétrier's disease Epithelial hyperplasia involving the surface & foveolar mucous cells the oxyntic glands can be normal or atrophic. Surgery has been advocated for patients with intractable pain, hypoalbuminemia with edema, hemorrhage, pyloric obstruction, & in whom a malignancy cannot be excluded

51. Zollinger-Ellison syndrome Increased numbers of parietal cells with no change in surface &foveolar mucous cells. Signs: Multiple ulcers diarrhea ulcer in atypical site resistant ulcer enlarged folds severe esophagirtis FH of MEN1

52. Hyperplastic gastropathies mixed-type in which both mucous &oxyntic glandular cells show hyperplasia, may be seen in lymphocytic &H. pylori gastritis.

53. Portal hypertensive gastropathy Portal hypertensive gastropathy characteristically appears as a fine white reticular pattern separating areas of pinkish mucosa on endoscopy, giving the gastric mucosa a " snakeskin " appearance

54. Portal hypertensive gastropathy