L7 chronic gastritis f

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L7 chronic gastritis f

  1. 1. This organism, formerly known as Campylobacter pylori , is a curved spirochete-like bacterium, of which two major genotypes exist.This organism colonizes the gastric mucosa (particularly the antrum and cardia) in a variety of ways: free in mucus, surface adhesion, and intercellularly. Chronic Gastritis f H. pylori has been found in 90% of patients with chronic gastritis, 95% with duodenal ulcer disease, 70% with gastric ulcer, and 50% with gastric carcinoma. Lecture 7
  2. 2. Stomach Anatomical Regions: Cardia, Fundus, Body, Pyloric antrum, Pylorus. Lesser curvature, Greater curvature. Histological Layers: Serosa, Muscularis m, Submucosa , Mucosa. Microscopic types of Gastric Mucosa: Cardiac, Fundic, Pyloric (antral). Glands of Stomach: Cardiac, Fundic, Pyloric. Cells of Fundic Epithelium: Mucous neck cells, Parietal cells, Chief cells, Enteroendocrine cells, Stem cells. Gastric gland are comprised of two major components: foveola (crypt, pit) and secretory portion (adenomere).
  3. 3. Definition Chronic gastritis is defined as the presence of chronic inflammatory changes in the mucosa leading eventually to mucosal atrophy & epithelial metaplasia. The two main features of this disease are infiltration of the lamina propria by inflammatory cells and atrophy of the glandular epithelium.
  4. 4. Etiology/types/classification B Body-predominant Less than 10% Antral-predominant 90% Nonimmune gastritis
  5. 5. Less common etiologies • RADIATION INJURY, • CHRONIC BILE REFLUX, • MECHANICAL INJURY, AND • SYSTEMIC DISEASE such as Crohn disease, amyloidosis, or graft-versushost disease.
  6. 6. Nonimmune Gastritis
  7. 7. Body Predominant Autoimmune gastritis is characterized by: • Antibodies to parietal cells (Oxyntic Cells) and intrinsic factor • Reduced serum pepsinogen I concentration • Antral endocrine cell hyperplAsiA • Vitamin B12 deficiency • Defective gastric acid secretion (achlorhydria )
  8. 8. Pathogenesis Autoimmune gastritis is associated with loss of parietal cells, which are responsible for secretion of gastric acid (HCl) and intrinsic factor. The absence of acid production stimulates gastrin release, resulting in hypergastrinemia and hyperplAsiA of antral gastrin-producing G cells.
  9. 9. • Lack of intrinsic factor disables ileal vitamin B12 absorption, leading to B12 deficiency and a slowonset megaloblastic anemia pernicious anemia ). ( • The reduced serum pepsinogen I concentration results from chief destruction. cell (Zymogenic cells or Peptic cells)
  10. 10. clinical features • Chronic gastritis usually causes few or no symptoms; 1.Upper abdominal discomfort 2.Nausea 3.Vomiting 4.symptoms of anemia 5.atrophic glossitis, 6. diarrhea. 7.peripheral neuropathy (B12 deficiency).
  11. 11. The median age at diagnosis is 60 years. Slightly more women than men are affected.
  12. 12. Antral-predominant >90% Pan-gastritis
  13. 13. Epidemiology associated with : Poverty, Household crowding, Llimited education, African-American or MexicanAmerican ethnicity, Residence in rural areas .
  14. 14. the mode of h. pylori transmission is not well defined, but humans are the only known host, making Oral-oral, Fecal-oral, and Environmental spread most likely routes of infection. the
  15. 15. pathogenesis • The most import cause is infection by H. pylori. Gastritis develops as a result of the combined influence of • bacterial enzymes (Urease,Protease,Phospholipase)and • toxins (cagA, VacA) and release of • noxious chemicals by the recruited neutrophils. Alcohol, tobacco, duodenal reflux (reflux gastritis), allergy to foods, and various drugs (particularly antiinflammatory agents).
  16. 16. • After initial exposure to H.pylori, gastritis may develop in two patterns: • 1. antral- type with high acid production and higher risk for the development of duodenal (Hypersecretory) ULCER, and • 2. pangastritis (Environmental with multifocal mucosal atrophy, with low acid secretion and increased risk for Gastritis)
  17. 17. Four features are linked to H. pylori virulence: 1. flagella , which allow the bacteria to be motile in viscous mucus 2.urease , which generates ammonia from endogenous urea and thereby elevates local gastric pH 3.adhesins that enhance their bacterial adherence to surface foveolar cells 4. toxins , such as cytotoxin-associated gene A (CagA), that may be involved in ulcer or cancer development by poorly defined mechanisms
  18. 18. • Chronic Inflammatory cell infiltration • Mucosal Atrophy • Intestinal metaplasia Neutrophils, plasma cells ( Autoimmune Gastritis) (Goblet Cell) Seen in H Pylori & Autoimmune gastritis not chemical. Intestinal metaplasia: Type I (complete), Type II (Incomplete) Pyloric Metaplasia Intestinal Metaplasia
  19. 19. Type B Ant Ant Pan Pan Type A
  20. 20. Clinical Features /Diagnosis Histologic identification of the organism, Serologic test for antibodies to H. pylori, Fecal bacterial detection, The urea breath test based on the generation of ammonia by the bacterial urease.
  21. 21. • Gastric biopsy specimens can also be analyzed by • the rapid UREASE test, • bacterial culture, or • bacterial DNA detection by PCR.
  22. 22. TreaTmenT • Combinations of antibiotics and proton pump inhibitors. Clarithromycin, Amoxicillin/ Flagyl, Omeprazole • Individuals with H. pylori gastritis usually improve after treatment, although RELAPSES can occur after incomplete eradication or reinfection. • Prophylactic and therapeutic vaccine development is still at an early stage of development.
  23. 23. Chronic superficial gastritis • If the inflammatory infiltrate is limited to the foveolar region and unaccompanied by glandular atrophy, the condition is designated as chronic superficial gastritis. • Subtle epithelial abnormalities seen in this form include a reduced amount of cytoplasmic mucin, nuclear and nucleolar enlargement, and some increase in foveolar mitoses.
  24. 24. UNCOMMON FORMS OF GASTRITIS Reactive Gastropathy Eosinophilic gastritis Lymphocytic gastritis
  25. 25. Chronic atrophic gastritis • When the inflammation is more extensive and accompanied by glandular atrophy, the condition is termed Chronic atrophic gastritis and is further categorized as mild, moderate, or severe by roughly estimating the thickness of the glandular portion in relation to the thickness of the whole mucosa.
  26. 26. Consequences of Chronic Gastritis • PEPTIC ULCER DISEASE • Adenocarcinomas
  27. 27. CanCer risk • The long-term risk of gastriC CarCinoma for persons with H. pylori-associated chronic five gastritis is increased about fold relative to the normal population. • For autoimmune gastritis, the risk for cancer is in the range of 2% to 4% of affected individuals, which is well above that of the normal population.
  28. 28. Other types of Gastritis • • • • • • • • • Nonspecific Gastritis Acute infectious nonbacterial gastroenteritis Hemorrhagic gastritis Collagenous gastritis Lymphocytic gastritis Allergic gastroenteritis Diffuse eosinophilic gastroenteritis Granulomatous gastritis Syphillis,, CMV, Cryptococcosis, Bacillary angiomatosis, Graft-versus-host disease

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