Chronic gastritis can be caused by H. pylori infection or autoimmune disorders. H. pylori infection leads to antral predominant gastritis and is associated with peptic ulcers. Untreated, it can progress to complications like MALToma or intestinal metaplasia, increasing cancer risk. Autoimmune gastritis affects the body and fundus, and may be associated with pernicious anemia or gastric carcinoid tumors due to loss of parietal cells. Both can result in atrophy, dysplasia, and intestinal metaplasia predisposing to gastric cancer. Peptic ulcers are chronic mucosal ulcers in the stomach or duodenum caused by an imbalance

1. Chronic gastritis and Peptic ulcer
15-04-2020

2. Outlines
• Gastritis
• Chronic gastritis
• Types, etiopathogenesis and microscopic
findings.
• Peptic ulcer

5. • Gastritis
Mucosal inflammatory process
Acute and chronic

6. Acute & Chronic
 1. Acute refers to short term
inflammation.
 Acute refering to neurophilic infiltrate
 2. Chronic referring to long standing
forms
 Chronic referring to mononuclear cell
infiltrate especially lymphocyte and
macrophages

7. • Chronic Gastritis: ( 2 important causes )
• Helicobacter pylori infection.
• Auto-immune gastritis

8. Chronic
Gastritis
Type B
Antral
Gastritis
Type A
Autoimmune
gastritis

9. H.pylori infection
Helicobacter pylori aka (Campylobacter
pyloridis)
Gram-negative bacterium found in the
stomach.
70% to 90% of patients with duodenal
ulcers and in about 70% of those with
gastric ulcers.
Antral predominant inflammation.
Contaminated food and feco-oral
transmission

10. Intense inflammatory and immune response. There is increased
production of proinflammatory cytokines such as interleukin (IL)-1, IL-
6, tumor necrosis factor (TNF), and, most notably, IL-8
H. pylori secretes a urease that breaks down urea to form toxic
compounds such as ammonium chloride and monochloramine.
Adhesins and Flagellin
Phospholipases that damage surface epithelial cells.
Toxin encoding genes : vacuolating toxin (VacA), cytotoxin-
associated gene A (CagA)

12. • Complications:
• Long standing inflammation – MALToma.
• Long standing injury – Intestinal metaplasia
and risk of Adenocarcinoma

13. • Direct method : Endoscopic biopsy
• Indirect method;
• Stool fecal antigen test (sensitive)
• Anti H.pylori antibodies in the saliva

14.  Autoimmune gastritis
1) Antibodies to parietal cells, gastrin
receptor, intrinsic factor, and H+,K+
ATPase.
2) <10% of cases of chronic gastritis
3) Cardia and Body region affected

15. 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

16.  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)

17.  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

19. Autoimmune Gastritis -Morphology
Diffuse mucosal damage of the body and fundic
mucosa. Antrum less involved.

20. Peptic Ulcer
• Chronic mucosal ulceration.
• (Break in the continuity of the epithelium)
• Involves distal part of the stomach and /or
duodenum.

22. DEFENSIVE FORCES
Secretion of mucus and Bicarbonate by surface epithelial cells.
Rapid gastric epithelial regeneration.
Mucosal blood flow, to sweep away hydrogen ions that have back-
diffused into the mucosa from the lumen and to sustain the high cellular
metabolic and regenerative activity.
Prostaglandins, which help maintain mucosal blood flow.

23. IMPAIRED
DEFENCE
ISCHAEMIA,
SHOCK,
DELAYED GASRIC
EMPTYING,
GASRO-
OESOPHAGEAL
REFLUX
•INCREASED
AGGRESSION
•H.Pylori INFECTION,
NSAIDs (ASPIRIN),
SMOKING, ALCOHOL,
•IMPAIRED REGULATION
OF ACID-PEPSIN
SECRETION,
•BILE ACIDS

24. NSAIDS
 NSAIDs and aspirin also interfere with the
protective mucus layer by inhibiting
mucosal cyclooxygenase activity, reducing
levels of mucosal prostaglandins

25. Smoking
 Stimulate gastric acid secretion
 Causes alteration in mucosal blood flow
 Decrease mucus secretion
 Reduces prostaglandin synthesis
 Decrease pancreatic bicarbonate secretion

28. • Chronic and recurring epigastric pain,
• Burning occuring 1-3 hours after having food,
• Relieves with antacids.

30. Complications

32. • Q1) Which type of gastritis will lead to
MALToma?
• Q2) Which type of gastritis will lead to well
differentiated neuroendocrine tumour?

33. •THANK YOU