Helicobacter pylori plays a key role in both acute and chronic gastritis. It is the main cause of chronic gastritis and is associated with peptic ulcer disease. H. pylori infection leads to inflammation of the stomach lining through the actions of its virulence factors such as urease, adhesins, and toxins. This weakens the mucosal defenses and increases acid production, contributing to ulcer development. Autoimmune gastritis is characterized by antibodies against parietal cells, reduced acid and intrinsic factor secretion, and vitamin B12 deficiency.

1. Prepared by: Anish Dhakal (Aryan)
MBBS Student
Patan Academy of Health Sciences

2. Objectives
To discuss about acute and chronic
gastritis
To discuss the role of Helicobacter pylori
in peptic ulcer
2

3. ACUTE GASTRITIS
1. Excessive alcohol consumption
2. NSAIDs
3. Radiation therapy
4. Decreased oxygen delivery
3
Risk factors

4. 4
Gastritis is a mucosal inflammatory process

5. 5

6. Stress related mucosal disease
• Stress ulcers- shock, sepsis, or severe trauma
• Curling ulcers- severe burns or trauma
• Cushing ulcers- intracranial disease
Pathogenesis
-Stress induced splanchnic vasoconstriction
-Upregulation of NO synthase
-Increased release of vasoconstrictor endothelin-1
Ischemia
Gastric mucosal injury

7. CHRONIC GASTRITIS
Causes:
-H.pylori
-autoantibodies against parietal cells and intrinsic factor
-radiation injury
-chronic bile reflux
-mechanical injury
-systemic disease(Crohn disease,amyloidosis, graft-verses host disease)

8. H. PYLORI GASTRITIS
Spiral shaped bacilli
Mainly affects antrum with normal or increased acid
production
H. pylori ureases and proteases along with inflammation
weaken mucosal defenses
• Virulence Factors include:
1. Motility via flagella
2. Urease production buffering gastric acid
3. Bacterial adhesins to bind surface epithelial cells
4. Toxins (e.g. cagA)

9. PATHOGENESIS

10. MICROSCOPIC FEATURES

11. AUTOIMMUNE GASTRITIS
• Typically spares the antrum and is associated with
hypergastrinemia
• Characterized by:
-antibodies to parietal cells and intrinsic factor
-reduced serum pepsinogen I concentration
-endocrine cell hyperplasia
-vit B12 deficiency
-achlorhydria

12. PATHOGENESIS
• CD4+ T cells directed against parietal cell
components
• Loss of parietal cell which secrete gastric acid
and intrinsic factor

14. ROLE OF H. PYLORI IN
PEPTIC ULCER
• Increased expression of proinflamatory
cytokines, TNF, IL-1β
• Decreased expression of anti-inflammatory
cytokines(IL-10)
• Produces Urease
• Secrete phospholipase
• Damage proteoglycan of mucus
• Decreases bicarbonate secretion and increase HCl
production

15. 15