Classification.
1.Acute gastritis
2.Chronic gastritis
Acute gastritis (acutegastritis)
Definition: acute inflammation of the gastric mucosa.
Endoscopy: congestion, edema, erosion, bleeding, superficial ulceration.
Pathology: erosion not exceeding the mucosal muscle layer; bleeding in the submucosa (intra-mucosa), no mucosal epithelial destruction.
Clinical features and diagnosis.
In mild cases, only indigestion is present.
Bleeding: usually small, intermittent and self-limiting.
Massive bleeding: vomiting blood and black stools.
Endoscopy is performed within 24-48 hours after hemorrhage.
Concepts related to the pathology of chronic gastritis (chronicgastritis).
Superficial gastritis ~ glandular integrity
atrophic gastritis ~ glandular atrophy
intestinal metaplasia ~ transformation of gastric glands into intestinal glands
Pseudopyloric glandular metaplasia ~ transformation of the gastric body glands into sinus pyloric glands seen in atrophic gastritis and the elderly
atypical hyperplasia dysplasia ~ precancerous lesions above moderate level
Etiology and pathogenesis
1, Hp-helicobacterpylori the most important etiology: urease decomposition of urea to produce NH3, maintaining a neutral environment and damage to epithelial cells; vacuolar toxin VagA protein – damage to epithelial cells; cytotoxin-related genes CagA protein – strong inflammatory reaction; bacteriophage cell wall as antigen to produce immune response.
2, autoimmunity.
3, other factors (degenerative, NSAID, smoking, alcoholism).
Pathology
Classification and clinical manifestations.
Chronic gastric sinusitis (type B gastritis): manifestations of dyspepsia (acid-related and power-related).
Chronic gastric body infection (type A gastritis): anorexia, wasting, anemia, vitamin deficiency and peripheral neuropathy (immune-related).
Laboratory tests and diagnosis.
Gastric fluid analysis (pentagastrin method).
Type A Gastrin-free serology.
Type A ~ Gastrin, anti-mural cell Ab, endoglin, Ab, B12.
Type B ~ may have anti-mural cell Ab gastroscopy and biopsy- most reliable diagnostic method.
Hp testing.
Invasive: rapid urease test (preferred), histology (direct observation), mucosal smear staining microscopy (easy to miss), microoxygenated environmental culture and polymerase chain reaction (PCR, for scientific research).
Non-invasive: 13C/14C-UBT (preferred method for review), antibody IgG (not suitable as a confirmatory test for eradication) X-ray testing, Vit-B12 uptake test
Treatment
1.Treatment for Hp eradication.
2.Non-Hp gastritis even if the cause and causative factors are looked for.
3.Dietary modification.
4.Treatment of acid-related and dysmotic-related gastritis.
5.B12 supplementation for B gastritis.
6.Vitamins and trace elements for those with intestinalization and atypical hyperplasia.