Gastritis

Lecture

Palangka Raya University

Faculty of Medicine 1
 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

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 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
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 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 4
 Acute Gastritis
Developing shortly exposure to various

injurious substances or following

depression in mucosal blood flow

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 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)

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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

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 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
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 Clinical Manifestations

Acute Simple Gastritis

 Epigastric Pain or discomfort

 Anorexia
 Nausea and Vomiting

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 Clinical Manifestations

Acute Erosive & Hemorrhagic Gastritis

 Upper GI Bleeding
 Hematemesis;
 Melena;
 Occult Blood in Stool

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Definite Diagnosis: Emergency Endoscopy

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ACUTE GASTRITIS - MORPHOLOGY

Mucosal congestion,
oedema, inflammation &
ulceration

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 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

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

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 Treatment
 Inhibit or neutralize gastric acid :
 Antacids
 H2-receptor antagonists (H2-RAs)
Cimetidine, Ranitidine , Famotidine
 Proton pump Inhibitors (PPIs)
Omaprazole, Lansoprazole,
Pantoprazole, Rabeprazole,
Esoprazole
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 Prevention
 Avoid offending agents
 Prophylactic use of acid-inhibiting
or mucosa-protecting drugs:
 Sucralfate;
 H2-RAs;
 PPIs
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Chronic Gastritis

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 Classification
1. Whitehead (1972)

Superficial

Chronic Gastritis
Atrophic

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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 irritants21
3. Sydney System (1990)

4. Updated Sydney System (1996)

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 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）
上海共识 （2006） 24
Etiology and Pathogenesis

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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.

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 Antigenic Mimicry

Lipopolysaccharide
Heat Shock Protein

Gastric Epithelium,
G cells,
Antibody Canaliculi of Parietal Cells,
H+, K+-ATPase
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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

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 3. Duodenal-Gastric Reflux

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

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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

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