Gastritis final


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I m a student of BEMS 4th Professional at University of Poonch.
Sir Asif teach us Pathology.

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Gastritis final

  1. 1. Aamir Sharif, BEMS 4th ProfessionalDepartment of Eastern Medicine & Surgery
  2. 2. Stomach 3 muscle layers  Oblique  Circular  Longitudinal Regions  Cardiac sphincter  Fundus  Antrum (pylorus)  Pyloric sphincter Vascular Inner surface thrown into folds – Rugae Contains enzymes that work best at pH 1-2 3
  3. 3. Normal Stomach Anatomy
  4. 4. Stomach - Normal
  5. 5. Stomach - Normal
  6. 6. Stomach Functions  Absorbs  Mix food  Alcohol  Reservoir  Water  Start digestion of  Lipophilic acid  Protein  B 12  Nucleic acids  Fats  Activates some enzymes  Destroy some bacteria  Makes intrinsic factor – B 12 absorption  Destroys some bacteria 7
  7. 7. InflammatoryDisease of Stomach
  8. 8. Definition The term gastritis is used to denote inflammation associated with mucosal injury. Gastritis is mostly a histological term that needs biopsy to be confirmed. Gastritis is usually due to infectious agents (such as Helicobacter pylori) and autoimmune and hypersensitivity reactions.
  9. 9. Definition Epithelial cell damage and regeneration without associated inflammation is properly referred to as "gastropathy.― Gastropathy may be referred without histological evidence and just according to gross appearance in endoscopy or radiology Gastropathy is usually caused by irritants such as drugs (e.g., nonsteroidal anti-inflammatory agents and alcohol), bile reflux, hypovolemia, and chronic congestion.
  10. 10. Sex: Male-to-female ratio of gastritis is approximately1:1 Male-to-female ratio of PUD is approximately 2:1
  11. 11. Pathophysiology The mechanisms of mucosal injury in gastritis is thought to be an imbalance of aggressive factors acid production or pepsinand defensive factors mucus production bicarbonate and blood flow
  12. 12. Protective factors vs. hostile factors
  13. 13. GastritisAcute Chronic
  14. 14. Acute & Chronic Difference Acute refers to short term inflammation Acute refering to neurophilic infiltrate Chronic referring to long standing forms Chronic referring to mononuclear cell infiltrate especially lymphocyte and macrophages
  15. 15. Acute Gastritis Definition  An acute mucosal inflammatory process, with neutrophilic infiltrate, that is usually transient.  There may be hemorrhage into the mucosa or sloughing of the mucosa.  Severe erosive form is an important cause of severe GI bleeding
  16. 16.  Etiology  Frequently associated with, among others: heavy use of NSAIDS, especially aspirin excessive alcohol consumption heavy smoking severe stress e.g. trauma, burns, surgery Ischemia Systemic infection  Often, idiopathic
  17. 17. NSAIDs NSAIDs and aspirin also interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity, reducing levels of mucosal prostaglandins
  18. 18. Smoking Promotes gastritis & ulcer occurrence Increases the likelihood of ulcer complications Mechanisms  Stimulate gastric acid secretion  Stimulate bile salt reflux  Causes alteration in mucosal blood flow  Decrease mucus secretion  Reduces prostaglandin synthesis  Decrease pancreatic bicarbonate secretion
  19. 19. Effects of Diet and Stress Diet and Stress ActionDiet Dyspepsia, may pain - not believed to cause ulcer or assist healingPhysiologic ↓ mucosal blood flow, tissue hypoxia,stress mucosal lining degradation; e.g. ICU, sepsis, burn, trauma. Associated with multiple erosions & significant bleeding
  20. 20. Etiology ofGastritisA) NormalB) IncreasedAttack*Hcl*Pepsin.*NSAIDs.C) Weak defense*Helicobacter pylori*Stress, drugs, smoking
  21. 21. Acute Gastritis - Pathogenesis Acid secretion + BicarbonateAll above Factor + back diffusion buffer + Direct Disruption Mucosal + of Blood flow Injury Mucus layer Acute Gastritis
  22. 22. Stages of Acute Gastritis Acute superficial  Acute erosive gastritis gastritis Inflammation of Destruction of multiple superficial gastric small zones of mucosa. superficial mucosa. Acute Gastric Ulceration  Destruction of full thickness of mucosa
  23. 23. ACUTE GASTRITIS - MORPHOLOGYMucosal congestion ,edema inflammation & ulceration
  24. 24. Acute Gastritis - MorphologyRanges from edema with neutrophil infiltration, vascular congestion,&an intact epithelium, to erosion (mucosal defect that does not crossthe muscularis mucosa) and hemorrhage.
  25. 25. Acute Gastritis Gastric mucosa demonstrates infiltration by Neutrophils
  26. 26. Acute Gastritis diffusely hyperemic gastric mucosa causes for acute gastritis  alcoholism  drugs  infections, etc.
  27. 27. Acute Gastritis Clinical Features  broad range of signs and symptoms that depend on the severity of the condition  Asymptomatic  Epigastric pain, nausea & vomiting  Hemorrhage, massive hematemesis, melena, or fatal blood loss  One of the major causes of massive hematemesis, particularly in alcoholics.  ~25% patients taking aspirin for rheumatoid arthritis will develop acute gastritis, and some will bleed
  28. 28. Complications: Malignancy Hemorrhage Perforation Obstruction
  29. 29. Chronic Gastritis Definition  Chronic mucosal inflammatory changes leading to atrophy and metaplasia (usually without erosions) Dysplasia and ultimate neoplasia are complications.
  30. 30. Chronic GastritisType B Type A Antral AutoimmuneGastritis gastritis
  31. 31. Type B (Antral Gastritis)  90% of patients with antral chronic gastritis: Helicobacter pylori infected  Motile, gram negative curvilinear rods that elaborate urease (buffers gastric acid) & toxins and have adhesins to bind to the epithelium. Pathogenesis  H. pylori (urease NH4+ + toxins) + Host (acid + peptic enzymes) Chronic Inflammation  Antibodies Gland destruction + Mucosal atrophy acid intrinsic factor (which can lead to pernicious anemia)
  32. 32. Helicobacter gastritis 2 patterns of infection  Diffuse involvement of body and antrum (―pan gastritis‖ associated with diminishing acid output)  Infection confined to antrum (antral gastritis, associate with increased acid output)
  33. 33. Helicobacter pylori Adapted to live in association with surface epithelium beneath mucus barrier Causes cell damage and inflammatory cell infiltration In most countries the majority of adults are infected
  34. 34. H. pylori Gastritis - Morphology H. pylori organisms along superficial mucus layer of antral biopsy Web Path
  35. 35. Bile reflux gastropathy Bile reflux gastropathy typically results from the regurgitation of bile into the stomach because of an operative stomach, an incompetent pyloric sphincter, or abnormal duodenal motility. The effect of bile salts on gastric mucosa is comparable to that seen after chronic NSAID use
  36. 36. Chemical gastritis Commonly seen with bile reflux (toxic to cells) Prominent hyperplastic response (inflammatory cells scanty) With time – intestinal metaplasia
  37. 37. Clinical FeaturesUsually only a few symptoms: nausea, vomiting, upper abdominal discomfort  Most infected person have gastritis, but are asymptomatic  Hypochlorhydria, but NOT achlorhydria and pernicious anemia (parietal cells never completely destroyed)  Gastrin normal to slightly elevated  Antibiotics are treatment of choice
  38. 38. Clinical Complications H. pylori H. pylori predisposes to peptic ulcers in duodenum and stomach—Most patients with a peptic ulcer are infected. Risk of gastric carcinoma and lymphoma
  39. 39. Type A (Auto immune) Etiology  Autoimmune - antibodies to parietal cells, gastrin receptor, intrinsic factor, and H+,K+ ATPase <10% of cases of chronic gastritis Possible autosomal dominant inheritance
  40. 40. Morphology of chronic gastritis Chronic inflammatory cell infiltration Mucosal atrophy Intestinal (goblet cell) metaplasiaSeen in Helicobacter and autoimmune gastritis (not chemical)
  41. 41. Autoimmune gastritis Autoimmune gastritis - pernicious anemia Chronic atrophic gastritis is associated with Ab’s - intrinsic factor - patietal cell bright green IF- in the parietal cells of the gastric mucosa.
  42. 42. Autoimmune Gastritis -MorphologyDiffuse mucosal damage of the body and fundicmucosa. Antrum less involved. PJ Goldblatt, MD
  43. 43. Chronic Gastritis Clinical Features  Usually only a few symptoms: nausea, vomiting, upper abdominal discomfort  Autoimmune Hypo to achlorhydria (severe loss of parietal glands) Hypergastrinemia 10% have pernicious anemia
  44. 44. Clinical Complications Autoimmune: Often seen in association with other autoimmune disorders (Hashimoto thyroiditis, Addison disease, and type I diabetes) Significant risk for the development of gastric carcinoma (2-4%) and endocrine tumors (carcinoid tumor)
  45. 45. Chronic Gastritis Morphology  Varying degrees of mucosal damage possible  Mucosal lesions are reddened, with thickened rugae  Atrophied rugae in long-standing cases  Lymphocytes and plasma cell infiltrate; neutrophils indicate ―active‖ inflammation (may or may not be present)
  46. 46.  Regeneration - constant feature Metaplasia - mucosa of antral and body-fundic regions converts to columnar absorptive cells and goblet cells (intestinal metaplasia) Atrophy - marked loss of glands Dysplasia – precursor lesion to gastric cancer in atrophic gastritis
  47. 47. Hypertrophic gastritis Three variants are recognized Menetrier’s disease Hypersecretory gastropathy Gastric gland hyperplasia [the Zollinger-Ellison syndrome]
  48. 48. Hyperplastic gastropathiesproliferative,inflammatory, andinfiltrativeconditions areassociated withlarge folds due toexcessive numberof mucosalepithelial cells
  49. 49. Ménétriers disease Epithelial hyperplasia involving the surface and foveolar mucous cells (i.e., foveolar hyperplasia); the oxyntic glands can be normal or atrophic.
  50. 50. Zollinger-Ellison syndromeIncreased numbersof parietal cellswith no change insurface andfoveolar mucouscells.
  51. 51. Hyperplastic gastropathiesmixed-type in whichboth mucous andoxyntic glandularcells showhyperplasia, may beseen in aslymphocytic and H.pylori gastritis.
  52. 52.  Stomach Acute Gastritis= inflammation of gastric mucosa  acute – presence of neutrophils  Chronic –lymphocytes and plasma cells Caused by ingestion of strong acids or alkalies, NSAIDs, cancer chemotherapy, irradiation, alcohol, uremia, severe stress & shock states Proposed mechanisms: ↑ acid production with ↓ surface bicarbonate buffer Morphology: Mucosal edema, hyperemia, PML infiltration, erosions (not deeper than muscularis mucosa) & hemorrhages
  53. 53.  Stomach Chronic Gastritis = Chronic mucosal inflammation Leading to mucosal atrophy, intestinal metaplasia & dysplasia. Pathogenesis: Chronic infection by Helicobacter pylori (90%): MCC of chronic gastritis, Elaboration of urease  produces ammonia that buffers gastric acid, protecting organism from acid Other diseases associated with H. pylori Infection  Peptic ulcer disease  Gastric carcinoma  Gastric lymphoma Autoimmunity (>10%): Antibodies to parietal cells cause parietal cell destruction (HCl & intrinsic factor)
  54. 54.  Stomach Chronic Gastritis Morphology:  Autoimmune diffuse mucosal damage of the body-fundic mucosa  H. pylori affect antral mucosa Histology: Lymphocytic & plasma cell infiltrate of the lamina propria  atrophy, regeneration, metaplasia (to intestinal type mucosa) & dysplasia.  H. pylori detected on the mucosal surface Clinically:  Mild abdominal discomfort, nausea, vomiting; hypochlorhydria, hypergastrinemia & rarely  Overt pernicious anemia (in autoimmune) gastritis). Long-term risk of cancer is 2-4%