Gastritis

1. Gastritis

4. Gastritis
• Definition:
Gastric mucosal inflammation caused by any
reasons.
Usually accompanied with epithelial damage
and cellular regeneration.
damage-inflammation-regeneration.
• Classification:
acute gastritis and chronic gastritis according to
the course of disease.

5. Classification
Acute Gastritis
 Simple
 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

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

7. Acute Gastritis
7

8. Acute gastritis
• Definition
Acute gastric mucosal inflammation.
Accompanied with hyperemia、edema、
erosion、superficial ulcer or hemorrhage
The lesions are transient.
• Erosion: mucosal damage is not beyond
muscularis mucosae.
• Histological characters: the main cells in lamina
propria of mucosa is neutrophils.

9. Etiology and Pathogenesis
 Stress
 Shock ;
 Sepsis ;
 Burn;
 CNS Trauma or Surgery
 Renal, Hepatic or Respiratory Failure
NOTE: The ulcer casued by Burn or CNS disease are
named Curling or Cushing.
 Bacteria and Toxin (Helicobacter pylori)
 Alcohol
 NSAIDs (non-steroidal anti-inflammatory drugs)

10. Stress can cause ischemia and hypoxia of
gastric mucous, and there will be a decline in the
function of gastric mucosal barrier.
 Mucosa ischemia ; thromboxane A2 , leukotriene C4
 Inhibition of epithelial renewal ;
 Impairment of gastric mucosa barrier ;
 Hydrogen ion back-diffusion ;
 Free radicals
Stress Related Gastric Mucosa Damage

11.  Alcohol and Gastritis
Alcohol is lipid-soluble, high concentration
of ethanol transverses gastric mucosa and damage
gastric mucous directly by dissolving fat.
 NSAIDs and Gastritis
APC and naproxen, etc,.
Inhibiting synthesis of
prostaglandinsand cause the
damage of gastric mucosa.

12. Clinical manifestation
Mild erosive gastritis have no symptoms
Some patients have abdominal pain or distension
About 20％ have hematemesis and (or) melena.
There are epigastric tenderness on palpation.
• Acute Erosive-Hemorrhagic Gastritis
• Upper GI Bleeding Hematemesis; Melena;
Occult Blood in Stool.

13. Definite Diagnosis: Emergency Endoscopy
(24－48 hrs)

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

15. 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

16. Gastroscopy
demonstrates of
acute erosive
gastritis

17. Measures should be taken according to the primary diseases
and etiology.
 Remove offending agents
 Suspend or reduce the dosage of NSAID
 Refuse ethanol
 Treat predisposing conditions
 Application of acid-inhibition drugs and sucralfate or misoprostol
 Symptomatic treatment
 Hemostasis measures should be taken to patients with hemorrhage
Treatment

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

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

20. Chronic Gastritis

21. Chronic Gastritis
• Definition: Chronic inflammation of gastric
mucous, main infiltrating cells are lymphocyte
and plasmacyte.
• Categories: various
(Update Sydney system, 2006)
Non-atrophic gastritis (Superficial gastritis)
Atrophic gastritis
Specific gastritis

22. Categories of atrophic gastritis
• Multiple atrophic gastritis
The main damage is in gastric antrum
The main reason is HP infection
• Autoimmune gastritis
The main damage is in gastric body
The main reasons is autoimmunity

23. 1. Whitehead (1972)
Superficial
Chronic Gastritis
Atrophic
Evolution of the Classification

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

25. 25

26. 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 90% 10%
 Frequency in 90% 10%
pernicious anemia
 proposed etiological autoimmunity mucosa
factors genetic component irritants

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

28. 28

29. 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）
5.National consensus

30. Etiology and Pathogenesis

31. 1. Helicobacter pylori Infection—proof
(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.

32. • Helicobacter pylori infection—mechanism
The main etiology of chronic gastritis
HP increasing acid secretion
HP disrupting mucosal integrity
HP has a strong adhesion ability. It can produce
ammonia and induce immune response.

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

37. 2. Immunological Factors
 Parietal cell antibody (PCA)and intrinsic factor
antibody (IFA) are in 90% of patients with type
A atrophic gastritis, which cause the
reduction of parietal cell and gastric acid, the
reduction of VitB12 will cause malignant anemia.
 Pernicious anemia is also associated with other
autoimmune diseases:
 Hashimoto’s thyroiditis;
 Diabetes mellitus;
 Vitiligo 白癫风

38. 3. Duodenal-Gastric Reflux
(a) Dysfunction of pyloric sphincter (b) After Partial Gastrectomy
Bile、pancreatic secretion weakened the function
of gastric mucosal barrier.

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

40. Asymptomatic in majority of patients;
Most patients have no specific symptoms;
 Some have dyspeptic symptoms:
 Epigastric pain, discomfort or distension, after meal
 Belching, heartburn, regurgitation
 Loss of appetite
 Nausea and vomiting
 Others: emaciation, anorexia anemia, atrophy
tongue , perineural disease
 Some may develop symptomatic complication:
 Anemia;  Peptic ulcer;
 Gastric polyp;  Gastric carcinoma
Clinical Manifestation

41. Pathology—concept
• Inflammation：the main infiltrating cells in
mucous are lymphocyte and plasmacyte
• Atrophy：gastric mucosal glands are
damaged, then they are atrophic and
vanished. Fibrogenesis can happened and the
mucous become thin.
• Intestinal metaplasia：gastric glands turn
into intestinal glands, including small
intestine-type and colon-type.

42. Pathology—concept
• Dysplasia：the usual regeneration of
epithelium in hyperplasia gastric pit and
metaplasia intestine will develop to abnormal
cells, the structure of glands will be in a state
of chaos, they are precancerous lesion.
• HP can be seen in mucus、epithelial surface
and gastric pit.

43. Superficial Gastritis:
 Infiltration of plasma cell, lymphocytes and
neutrophils in lamina propria.
 Activity when neutrophils infiltration.
 Lymphoid follicle formed when HP existed.
 Surface cells damage
Histology and Pathology

44. chronic superficial gastritis
HE stain

45. Atrophic Gastritis:
 Inflammatory cells infiltration
 Atrophy of gastric glands
 Metaplasia:
 Intestinal Metaplasia
 Pseudopyloric Metaplasia
 Dysplasia (precancerous lesions of gastric cancer)
 Cell pleomorphism
 Tissue pleomorphism
Histology and Pathology

46. chronic atrophic gastritis with intestinal metaplasia

49. Two Types of Metaplasia in Gastric Mucosa
Lined by intestinal-type absorptive cells, goblet
cells and Peneth cells — Intestinal Metaplasia
Lined by mucus-secreting
cells similar to those in antral
mucosa —
Pseudopylori Metaplasia

50. 50

51. Laboratory Examinations
 Detection of H. pylori infection
 Gastric Secretory Test
Low acid or no acid in type A gastritis
 Serology Tests
Gastrin
A:IFA(intrinsic factor Ab)
A:PCA (parietal cell Ab)
Vitamin B12 level (300-900ng/L)
 Gastroscopy
 Histology

52. HP testing
Invasive method
• biopsy
• culture
• rapid urease test
• protein chip
Non-invasive method
• urea breash testing (13C/14C)
• stool HP antigen
• HP IgG antigen in blood
Laboratory examinations

53. Rapid urease test Histology Culture
Direct smear PCR 13C- Breath test
Detection of H. pylori Infection

54. H&E Stain Cresyl violet stain
Warthin -Starry Stain Acridine orange stain

56. Serum examination
 Autoimmune gastritis
 Anti-parietal cell antibody (90％)
 Anti-intrinsic factor antibody (75%)
 VitB12 and gastric acid are decreased
 Gastrin increased obviously
 Multiple atrophic gastritis
 Gastrin and acid level are normal or decreased
Laboratory examinations

57. Diagnosis
• Illness disease is not the most important because
of no any symptom in most of patients and
symptoms are non-specific
• Definitive diagnosis is made only by endoscopy
and biopsy
• Hp testing
• Serum anti-parietal cell antibody、anti-intrinsic
factor antibody、vitB12

58. Diagnostic process
Gastroscopy ﹠ Hp﹠ biopsy
Indispensable

59. Superficial gastritis：
 Edema
 Hyperemia
 Exudate
 Erosion in mucous
 Red speckle
 spot bleeding
The definitive diagnosis is made only by
gastroscopy and biopsy of gastric mucosa

60. Chronic superficial gastritis

61. Atrophic gastritis
 Visible blood vessels
 Mucous is pale and thinning
 Fold become slender and
flat
 Mucus lake become
wizened.
 If epithelial hyperplasia
there will be nodules.
 Erosions and hemorrhage
will be seen in some patients

62. Chronic atrophic gastritis

63.  Remove offending agents;
 Diet;
 Eradication of Hp;
 Prevention of Duodenal-gastric reflux;
 Symptomatic treatment;
 Supplement with anti-oxidants for CAG;
 Follow-up for CAG with high risk of gastric
cancer
Treatment

64.  Etiologic treatment
 Quit smoking and restriction drinking
 Stop or reduce the using of NSAID
Take magnesium carbonate to adsorption bile
 Take vitB12 to treat malignant anemia caused by
autoimmune gastritis.

65.  Diet (Supplement with Anti-
oxidants)
 More fruits and vegetables
 Less spicy food
 Less smoked and salted food
 High antioxidation vitamin C, E
 -carotene,
 Selenium
•

66.  Hp Eradication—indication
 Active gastritis
 Atrophy with dysplasia
 The family history of gastric carcinoma
 Remnant stomach with gastritis

67.  Prevention of Duodenal-gastric Reflux
 Prokinetic:
– Metoclopromide
– Domperidone
– Mosapride
 Bile-binding agents:
– Cholestyramine

68.  Symptomatic treatment
 Antacids、acid-inhibitory drugs
Sodium bicarbonate
H2 receptor antagonist: cimetidine, ranitidine
Proton Pump Inhibitor (PPI ): omeprazole( Losec),
pantoprazole
 Mucosal protective agents
Bismuth
Sucralfate
 Gastricdynamic agents
Domperidone
Mosapride

70. Role of Anti-oxidants in Prevention
of Gastric Cancer
Anti-oxidants
Nitrate
Nitrite
Nitroso Compounds
Inflammation
Free Radicals
Damage of epithelium
DNA mutation
(–) (–)

71.  Intestinal metaplasia or dysplasia
 Put away psychological fear of cancer
 Taking anti-oxidation vitamin
 Moderate dysplasia: Endoscopy surveillance
should be taken regularly
 Severe dysplasia: operation should be taken

72.  Follow-up
 Atrophic gastritis is one of precancerous
conditions, the annual risk for gastric cancer
is about 0.5%.
 Patients with severe atrophic gastritis or
dysplasia should be closely followed up by
endoscopy.

73. Gastric Precancerous Changes
Precancerous lesion
(Dysplasia)
Precancerous Conditions
 Atrophic Gastritis
 Gastric Polyp
 Gastric Ulcer
 Gastric Stump
 Menetrier’s Disease
WHO, 1978

74. Specific gastritis
• Infection gastritis: It intend to occur in
underdeveloped area, perforation often happened to
acute phlegmonous gastritis, so operation should be
take in time.
• Menetrier disease: gastric mucous、fold become
hypertrophy, parietal cell and principal cell reduced,
hypoproteinemia may be detected.
• Others: portal hypertensive gastropathy

75. Hypertrophic Gastritis
 Characterized by large mucosa folds
in stomach
 Two entities
 Menetrier’s disease
 Hypersecretory gastropathy

77. Menetrier’s Hypersecretory
Disease Gastropathy
Histology Hyperplasia of Enlarged fundic
pits mucus cells glands
Acid secretion Normal or low High
Loss of protein Yes No
Therapy High protein diet; Anti-secretory;
Eradication of Hp; Eradication of Hp;
Gastrectomy; Gastrectomy;

78. Summury
• Definition: A wide variety of inflammatory
or hemorrhagic conditions of gastric
mucosa.
• Classification: Acute Gastritis
Chronic gastritis

79. Acute Gastritis
• Etiology: Stress
Bacteria and Toxin
Alcohol; NSAIDs;
• Clinical Manifestations:
Acute Erosive &Hemorrhagic Gastritis
• Special Terms : Cushing Ulcer
Curling Ulcer
• Treatment
• Prevention

80. Chronic gastritis
• Classification: Gastritis of Corpus (Type A)
Gastritis of Antrum (Type B);
Updated Sydney System (1996)
• Etiology and Pathogenesis: Hp Infection;
Duodenal-Gastric Reflux;
Immunological Factors
• Clinical Manifestation: Asymptomatic

81. Chronic gastritis
•Histology: Inflammatory cells infiltration;
Atrophy;
Metaplasia (Pseudopylori; Intestinal)
Dyspepsia
•Diagnosis: endoscopy and biopsy
•Treatment: Eradication of Hp
• Gastric Precancerous Changes:
precancerous lesion
Precancerous Conditions

82. Thank you