1. Gastritis Department of Digestive Disease
Shanghai Institute of Digestive Disease
Zheng Qing

2. Gastritis Definition: A wide variety of inflammatory or hemorrhagic
conditions of gastric mucosa.
Gastritis is mostly a histological term that needs
biopsy to be confirmed

3. Classification Acute Gastritis Chronic gastritis Simple Superficial
Erosive & Hemorrhagic
Phlegmonous
Corrosive
Chronic gastritis
Superficial
Atrophic
(Hypertrophic)
Acute vs. chronic
Acute referring to short term inflammation
Acute referring to neurophilic infiltrate
Chronic referring to long standing forms
Chronic referring to mononuclear cell infiltrate especially lymphocyte and macrophages

4. Anatomical site CARDIA 贲门 MUCOUS SECRETING ENDOCRINE BODY 胃体
SPECIALISED SECRETORY PARIETAL – ACID
CHIEF - PEPSINOGEN ENDOCRINE HIST, SOMASTATIN
ANTRUM 胃窦
MUCOUS SECRETING ENDOCRINE GASTRIN, 5HT

5. Acute Gastritis Developing shortly exposure to various
injurious substances or following
depression in mucosal blood flow

6. Etiology and Pathogenesis
Stress
 Shock ;
 Sepsis ;
 Burn;
 CNS Trauma or Surgery
 Renal, Hepatic or Respiratory Failure
Alcohol
NSAIDs (non-steroidal anti-inflammatory drugs)
Bacteria and Toxin (Helicobacter pylori)

7. Stress Related Gastric Mucosa Damage
Mucosa ischemia ;
thromboxane A2 , leukotriene C4
Inhibition of epithelial renewal ;
Impairment of gastric mucosa barrier ;
Hydrogen ion back-diffusion ;
Free radicals

8. Alcohol is lipid-soluble, high concentration
Alcohol and Gastritis
Alcohol is lipid-soluble, high concentration
of ethanol transverses gastric mucosa and results in mucosa damage.
NSAIDs and Gastritis
Inhibiting synthesis of
prostaglandins

9. Clinical Manifestations
Acute Simple Gastritis
Epigastric Pain or discomfort
Anorexia
Nausea and Vomiting

10. Clinical Manifestations
Acute Erosive & Hemorrhagic Gastritis
Upper GI Bleeding
 Hematemesis;
 Melena;
 Occult Blood in Stool

11. Definite Diagnosis: Emergency Endoscopy

12. ACUTE GASTRITIS - MORPHOLOGY
Mucosal congestion, oedema, inflammation & ulceration

13. Two Special Terms in Acute Erosive & Hemorrhagic Gastritis
Cushing Ulcer
Erosions and ulcers associated with CNS
trauma or surgery
Curling Ulcer
Erosions and ulcers associated with burn

14. Treatment Remove offending agents Treat predisposing conditions
Symptomatic treatment
Protect gastric mucosa: Sucralfate

15. Treatment Inhibit or neutralize gastric acid :  Antacids
 H2-receptor antagonists (H2-RAs)
Cimetidine, Ranitidine , Famotidine
 Proton pump Inhibitors (PPIs)
Omaprazole, Lansoprazole,
Pantoprazole, Rabeprazole,
Esoprazole

16. Prevention Avoid offending agents Prophylactic use of acid-inhibiting
or mucosa-protecting drugs:
 Sucralfate;
 H2-RAs;
 PPIs

17. Chronic Gastritis

18. Classification 1. Whitehead (1972) Superficial Chronic Gastritis
Atrophic

19. 2. Strickland (1973)
Type A
Atrophic Gastritis
Type B

21. Classification of CAG by Strickland
Features Type A Type B
Morphology
antrum normal atrophy
corpus diffuse multifocal
Serum gastrin
Gastric acid secretion anacidity hypoacidity
Gastric autoantibodies % %
Frequency in % %
pernicious anemia
proposed etiological autoimmunity mucosa
factors genetic component irritants

22. 3. Sydney System (1990)
4. Updated Sydney System (1996)

24. National consensus Superficial Atrophic (Hypertrophic)
重庆共识 （1982）
Superficial
Atrophic
(Hypertrophic)
Location: antrum, corpus or pan-;
Severity: mild, moderate, severe;
Activity: active, quiescent;
Metaplasia: intestinal, pseudopyloric
井冈山共识 （2000）
上海共识 （2006）

25. Etiology and Pathogenesis

26. 1. Helicobacter pylori Infection:
(Koch’s postulates)
High prevalence of Hp infection in patients
with chronic active gastritis (80-95%).
Hp infection is associated with gastric mucosal inflammation.
 Distribution
 Inflammation subsides after eradication of Hp
Studies in volunteer and animal models.

29. Antigenic Mimicry Antibody Lipopolysaccharide Heat Shock Protein
Gastric Epithelium,
G cells,
Canaliculi of Parietal Cells,
H+, K+-ATPase
Antibody

30. 2. Immunological Factors
Parietal cell antibody (PCA)and intrinsic factor
antibody (IFA) are in 90% of patients with type
A atrophic gastritis and pernicious anemia.
Pernicious anemia is also associated with other
autoimmune diseases:
 Hashimoto’s thyroiditis;
 Diabetes mellitus;
 Vitiligo 白癫风

31. 3. Duodenal-Gastric Reflux
(a) Dysfunction of pyloric sphincter (b) After Partial Gastrectomy

32. Mechanisms of Gastric Mucosal Damage
by Duodenal Contents
Bile Pancreatic
Enzymes
Lecithin
卵磷脂
Lysolecithin
溶血卵磷脂
Damage of Gastric Mucosal Barrier