Gastritis: Palangka Raya University Faculty of Medicine
Gastritis: Palangka Raya University Faculty of Medicine
Gastritis: Palangka Raya University Faculty of Medicine
Lecture
2
Classification
Acute Gastritis Chronic gastritis
Simple
Superficial
Erosive & Hemorrhagic
Atrophic
Phlegmonous
(Hypertrophic)
Corrosive
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
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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.
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Clinical Manifestations
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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)
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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
25
1. Helicobacter pylori Infection:
(Koch’s postulates)
High prevalence of Hp infection in patients
with chronic active gastritis (80-95%).
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27
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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
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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