L8 peptic ulcer


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L8 peptic ulcer

  1. 1. H Pylori HELICOBACTER Campylobacter Pylori PYLORI 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. H Pylori PePtic ulcer Lecture 8
  2. 2. Definition • Ulcer of the GIT (Peptic ulcer) is defined histologically as a breach in the mucosa that extends through the muscularis mucosea into the submucosa or deeper. The areas of degeneration & necrosis of gastrointestinal mucosa exposed to acid-peptic secretions.
  3. 3. Acid peptic digestion is the ultimate cause for Ulceration. DU: GU= 4:1
  4. 4. Hurry, worry & Curry Genetic Factors: Blood group: O & A Monozygotic twins,association with HLA-B5 gene Work, worry, weather Reflux of Bile & Pancreatic Juices
  5. 5. Bile Reflux
  6. 6. L Ulcers are caused by loss of balance Between protective & Hostile factors. Loss of balance between Attack& Defence
  7. 7. Damagin g Forces Defensive Forces Ulcers are caused by loss of balance between Mucosal defence & acid attack Loss of balance between Attack& Defence Ulcers are caused by loss of balance Between protective & Hostile factors.
  8. 8. Ulcers are caused by loss of balance between Mucosal defence & acid attack. Loss of balance between Attack& Defence H.pylori NSAIDs Ulcers are caused by loss of balance Between protective & Hostile factors.
  9. 9. Ulcers are caused by loss of balance Between protective & Hostile factors. Loss of balance between Attack& Defence
  10. 10. Pathogenesis • H. Pylori plays crucial role in pathogenesis. • 10-fold higher risk (antral atrophy 12-fold higher risk) • Corpus atrophy decreases the risk when complete atrophy) (to zero
  11. 11. Pathogenesis of DU Duodenal Ulcer: High acid-pepsin secretions • 1. Hypersecretion of gastric acid into the fasting stomach at night (vagal stimulation). • 2. Rapid emptying of the stomach exposing the duodenal mucosa to the aggressive action of HCl. • 3. H. pylori: • i) Mucosal defence is broken by bacterial elaboration of urease, protease,& phospholipase. • ii) Host factors: H. pylori infected mucosal epithelium releases proinflammatory cytokines such as IL-1, IL-6, IL-8 & TNF-incite inflammatory reaction. • iii) Bacterial factors: Epithelial injury is also induced by cytotoxic-associated gene protein (Cag A), while vacuolating cytotoxin (Vac A) induces elaboration of cytokines.
  12. 12. Pathogenesis of gastric ulcer GU: Impaired gastric mucosal defences against acid-pepsin secretions. Other features in pathogenesis: • 1. Hyperacidity due to increased serum gastrin levels in response to ingested food in an atonic stomach. • 2.In case of Low to Normal HCl: Damaging influence of gastritis, bile reflux, smoking. • 3. Disorder of protective gastric mucus ‘barrier’ by H. pylori.
  13. 13. DU & GU • Gastric & duodenal ulcers represent two diseases as far as their etiology, pathogenesis & clinical features are concerned • but morphological findings in both are similar.
  14. 14. Acute Peptic(Stress) Ulcer • Multiple, small mucosal erosions, seen most commonly in the stomach but may occur in the duodenum. Mucosal erosion (loss of continuity of the epithelial lining) is a common feature of acute gastritis. • Etiology: • I. Psychological Stress • II. Physiological stress: Shock, trauma, septicaemia, Extensive burns • • • (curling’s ulcer ) Intracranial lesions (Cushing’s ulcers developing from hyperacidity following excessive vagal stimulation). Drug intake (Aspirin, steroids) Local irritants (alcohol, smocking, coffee).
  15. 15. ACID ? Pathogenesis Hyperacidity? Role of hyperacidity in acute gastritis? • 1. Ischaemic hypoxic injury to the mucosal cells. • 2. Depletion of the gastric mucus barrier rendering the mucosa susceptible to attack by acid-peptic secretions. Mucosal erosion (loss of continuity of the epithelial lining) is a common feature of acute gastritis. If the defect is severe enough to penetrate the muscularis mucosae to involve the submucosa, this becomes—by definition—an ulcer. Acute ulcers can be distinguished morphologically from chronic gastritis by the lack of fibrosis in the former.
  16. 16. Morphology of Acute Peptic Ulcer • Gross: Multiple, more common in stomach, oval or circular, small (<1cm). • Microscopically, shallow, do not invade the muscular layer. The margins & base may show some inflammatory reaction. Heal without any scar. • Complications: Hemorrhage, Perforation. Mucosal erosion (loss of continuity of the epithelial lining) is a common feature of
  17. 17. Chronic Peptic Ulcer • Always occurs in an achlorhydric zone of mucosa ( an area of stomach lined by pyloric type mucosa). Up to 95% of the ulcers are located on the lesser curvature (Magenstrasse) near the incisura angularis. • Can be found anywhere in the stomach. Pyloric antrum & lesser curvature of the stomach are the sites most exposed for longer periods to local irritants & thus are the common sites for occurrence of gastric ulcers. Local Irritants: Heavily spiced foods, alcohol, smoking &
  18. 18. Remitting & relapsing lesions Once a peptic ulcer patient, always a peptic ulcer patient . Age: DU- 5th decade, GU- 6th decade People at risk: DU-StressExecutives, leaders GU—Labouring groups Vomiting, Hematemesis, melena, Appetite, Diet, Weight loss ,deep tenderness Periodicity: attacks—2-6 weeks, Interval of freedom-1-6 weeks Attacks worsened by Indigestion ‘work, worry, weather
  19. 19. Morphology of Chronic gastritis • Morphology of GU & Du are similar. • Location: GU –along the Lesser curvature in the the pyloric antrum on the posterior wall. • Du: in the first part of the duodenum, immediately post pyloric on the anterior wall. • Number: Solitary (80%) • Size: Small (1-2.5cm) • Shape: Round to oval • Punched out: Rounded, sharply circumscribed, with sharply demarcated vertical margins.
  20. 20. >3 cm
  21. 21. A, Typical gross appearance of chronic peptic ulcer of stomach. B, Sharply delimited chronic peptic ulcer with converging folds of mucosa in the upper half. The ulcer bed is covered by fibrinopurulent exudate. Punched Out Ulcer: rounded, sharply circumscribed, often multiple lesions with sharply demarcated vertical margins.
  22. 22. Morphology of Chronic Gastritis • Benign ulcers usually have flat margins in level with the surrounding mucosa. The mucosal folds converge towards the ulcer. • Depth: The ulcers may vary in depth from being superficial (confined to mucosa) to deep ulcers ( penetrating into the muscular layer). • Coexistence: GU+DU in 10-20% cases • Malignant transformation: DU never GU 1%-carcinoma • Malignant GU are larger, bowl-shaped with elevated & indurated mucosa at the margins
  23. 23. Gross Morphology • The proximal margin tends to have overhanging edges, whereas the distal margin usually has sloping borders.
  24. 24. Whole mount view of chronic peptic ulcer. The external muscle layer has been totally destroyed. Note the overhanging mucosa on one edge and the sloping mucosa on the other.
  25. 25. • On section, there is undermining of the edges (especially on the proximal side) and complete replacement of the muscle wall by grayish white fibrous tissue.
  26. 26. Morphology On the serosal side, there may be subserosal fibrosis and inflammatory enlargement of the regional lymph nodes.
  27. 27. Morphology • Prominent marginal nodularity about the ulcer should suggest the presence of carcinoma; however, it should be remembered that it may be impossible to distinguish grossly a peptic ulcer from an ulcerated carcinoma. As a matter of fact, approximately 10–15% of gastric carcinomas appear, grossly, to be benign ulcers.
  28. 28. MICROSCOPY • Four histological zones Chr. Peptic ulcer have 4 histological zones. From within outside, these are as under: • 1. Nicrotic zone— lies in the floor of the ulcer & is composed of fibrinous exudate containing necrotic debris & a few leukocytes. • 2. Superficial exudative zone –lies underneath the necrotic zone. The tissue elements here show coagulative necrosis giving eosinophilic, smudgy appearance with nuclear debris. • 3. Granulation tissue zone– is seen merging into the necrotic zone. It is composed of nonspecific inflammatory infiltrate & proliferative capillaries.
  29. 29. • 4. Zone of Cicatrization– is seen merging into thick layer of granulation tissue. It is composed of dense fibrocollagenic scar tissue over which granulation tissue rests. Thrombosed or sclerotic arteries may cross the ulcer which on erosion may result in haemorrhage.
  30. 30. • Other common features in the ulcer bed include: 1)Thickening of vessels (caused by subendothelial fibrous proliferation) and 2)Hypertrophy of nerve bundles; both of these changes are probably secondary events. • The necrotic surface may show superimposed infection by Candida albicans.
  31. 31. • The mucosa surrounding the ulcer is of pyloric type, including a component of gastrin (and somatostatin) immunoreactive cells. • In cases infected with H. pylori, a typical constellation of morphologic changes • (loss of the apical portion and dropout of epithelial cells, epithelial pits, erosions, and cellular tufts) is seen at the ulcer edge.
  32. 32. Classification of Peptic Ulcer • DU & GU • Acute, Subacute & Chronic Peptic ulcers can be classified according to their • shape and size (round-oval, giant, linear), • activity (open ulcers or ulcer scars), • depth of penetration (submucosa, muscularis externa, or beyond), or • a combination of these criteria.
  33. 33. Fiberoptic gastroscopy The radiographic diagnosis is approximately 95% Endoscopic gastric biopsy multiple (about 10) biopsies are recommended for the standard-size ulcer.
  34. 34. 80% 19% Seems to be decreasing Seems to be decreasing secrete either low normal or below normal amounts of acid. Associated with acid Hypersecretion Mucosal Injury
  35. 35. Chronic, larger & deeper ulcers cause complications. Duodenal stenosis,’hour glass’ deformity. Cancers ulcerate but ulcers rarely cancerate
  36. 36. Zollinger–Ellison Syndrome (ZES) caused by a non–beta islet cell, gastrin-secreting tumor of the pancreas that stimulates the acidsecreting cells of the stomach to maximal activity, with consequent gastrointestinal mucosal ulceration. ZES may occur sporadically or as part of an autosomal dominant familial syndrome called multiple endocrine neoplasia type 1 (MEN 1). The primary tumor is usually located in the pancreas, duodenum or abdominal lymph nodes, but ectopic locations have also been described (e.g., heart, ovary, gallbladder, liver, kidney).