Gastritis

Department of Gastroenterology
General Hospital of Ningxia Medical University
Si Cen MD.
 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.
 Classification
Acute Gastritis Chronic gastritis
 Simple
 Superficial
 Erosive & Hemorrhagic
 Atrophic
 Phlegmonous
 (Hypertrophic)
 Corrosive

•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
 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
Acute Gastritis

7
 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.
 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)
Stress Related Gastric Mucosa Damage
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
 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.
 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.
Definite Diagnosis: Emergency Endoscopy
(24－48 hrs)
ACUTE GASTRITIS - MORPHOLOGY

Mucosal congestion,
oedema, inflammation &
ulceration
 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
Gastroscopy
demonstrates of
acute erosive
gastritis
 Treatment
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-Antacids
 Inhibit or neutralize gastric acid :
 H2-receptor antagonists (H2-RAs)
Cimetidine, Ranitidine , Famotidine
 Proton pump Inhibitors (PPIs)
Omaprazole, Lansoprazole,
Pantoprazole, Rabeprazole,
Esoprazole
 Prevention
 Avoid offending agents
 Prophylactic use of acid-inhibiting
or mucosa-protecting drugs:
 Sucralfate;
 H2-RAs;
 PPIs
Chronic Gastritis
 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
 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
 Evolution of the Classification

1. Whitehead (1972)

Superficial

Chronic Gastritis
Atrophic
2. Strickland (1973)

Type A
Atrophic Gastritis
Type B
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 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
3. Sydney System (1990)

4. Updated Sydney System (1996)

28
 5. National consensus
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）
Etiology and Pathogenesis
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.

• 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.
 Antigenic Mimicry

Lipopolysaccharide
Heat Shock Protein

Gastric Epithelium,
G cells,
Antibody Canaliculi of Parietal Cells,
H+, K+-ATPase
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
 3. Duodenal-Gastric Reflux

(a) Dysfunction of pyloric sphincter (b) After Partial Gastrectomy

Bile、pancreatic secretion weakened the function
of gastric mucosal barrier.
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

 Clinical Manifestation
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
 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.
 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.
 Histology and Pathology
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
chronic superficial gastritis
HE stain
 Histology and Pathology
Atrophic Gastritis:
 Inflammatory cells infiltration
 Atrophy of gastric glands
 Metaplasia:
 Intestinal Metaplasia
 Pseudopyloric Metaplasia
 Dysplasia (precancerous lesions of gastric cancer)
 Cell pleomorphism
 Tissue pleomorphism
chronic atrophic gastritis with intestinal metaplasia
Two Types of Metaplasia in Gastric Mucosa

Lined by mucus-secreting
cells similar to those in antral
mucosa —
Pseudopylori Metaplasia

Lined by intestinal-type absorptive cells, goblet

cells and Peneth cells — Intestinal Metaplasia
50
 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
Laboratory examinations

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
 Detection of H. pylori Infection

Rapid urease test Histology Culture

Direct smear PCR 13C- Breath test

H&E Stain Cresyl violet stain

Warthin -Starry Stain Acridine orange stain

Laboratory examinations

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
 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
 Diagnostic process
Gastroscopy ﹠ Hp﹠ biopsy

Indispensable
The definitive diagnosis is made only by
gastroscopy and biopsy of gastric mucosa

Superficial gastritis：
 Edema
 Hyperemia
 Exudate
 Erosion in mucous
 Red speckle
 spot bleeding
Chronic superficial gastritis
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
Chronic atrophic gastritis
 Treatment
 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
 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.
 Diet (Supplement with Anti-
oxidants)
 More fruits and vegetables
 Less spicy food
 Less smoked and salted food
 High antioxidation vitamin C, E
 -carotene,
 Selenium
•
 Hp Eradication—indication
 Active gastritis
 Atrophy with dysplasia
 The family history of gastric carcinoma
 Remnant stomach with gastritis
 Prevention of Duodenal-gastric Reflux
 Prokinetic:
– Metoclopromide
– Domperidone
– Mosapride
 Bile-binding agents:
– Cholestyramine
 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
 Role of Anti-oxidants in Prevention
of Gastric Cancer
Anti-oxidants
Nitrate
Inflammation

Free Radicals (–) (–) Nitrite

Damage of epithelium
Nitroso Compounds
DNA mutation
 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
 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.
 Gastric Precancerous Changes

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

 Characterized by large mucosa folds

in stomach
 Two entities
 Menetrier’s disease
 Hypersecretory gastropathy
 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;
 Summury
• Definition: A wide variety of inflammatory
or hemorrhagic conditions of gastric
mucosa.

• Classification: Acute Gastritis

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

• Prevention
 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

 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
Thank You!

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