chronicgastritis

Chronic Gastritis

DefinitionChronic gastritis is defined as the

presence of chronic inflammatory changes in the

mucosa leading eventually to mucosal atrophy and epithelial metaplasia.

Etiology/types/classification

90%

Less than 10%

Less common etiologies

• radiation injury, • chronic bile reflux, •mechanical injury, and • systemic disease such as Crohn disease, amyloidosis, or graft-

versus-host disease.

Autoimmune gastritis(Body predominant)

Type A Less than 10%

•The most common cause of atrophic gastritis,

• Spares the antrum• Hypergastrinemia

Autoimmune gastritis is characterized by:

• Antibodies to parietal cells and intrinsic factor

• Reduced serum pepsinogen I concentration

• Antral endocrine cell hyperplasia • Vitamin B12 deficiency

• Defective gastric acid secretion (achlorhydria)

Pathogenesis Autoimmune gastritis is associated with

loss of parietal cells, which are responsible for secretion of gastric acid and intrinsic factor. The absence of acid production stimulates gastrin release, resulting in hypergastrinemia and hyperplasia of antral gastrin-producing

G cells.

• Lack of intrinsic factor disables ileal vitamin B12 absorption, leading to B12 deficiency and a slow-onset megaloblastic

anemia (pernicious anemia).

• The reduced serum pepsinogen I

concentration results from chief cell destruction.

Clinical features• Chronic gastritis usually causes few or no

symptoms; 1.Upper abdominal discomfort 2.Nausea3.Vomiting 4.symptoms of anemia 5.atrophic glossitis,6. diarrhea. 7.peripheral neuropathy, spinal cord lesions, and

cerebral dysfunction.

The median age at diagnosis is 60 years. Slightly more women than men are affected.

>90%

EpidemiologyAssociated with :Poverty, Household crowding,Llimited education, African-American or Mexican-American

ethnicity, Residence in rural areas.

• The mode of H. pylori transmission

is not well defined, but humans are the only known host, making oral-oral, fecal-oral, and environmental spread the most likely routes of infection.

Pathogenesis• The most import cause is infection by H. pylori. Gastritis develops as a result of the combined

influence of• bacterial enzymes and • toxins and release of• noxious chemicals by the recruited

neutrophils.

• After initial exposure to H.pylori, gastritis may develop in two patterns:

• 1. antral- type with high acid production and higher risk for the development of duodenal ulcer, and

• 2. pangastritis with multifocal mucosal atrophy, with low acid secretion and increased risk for carcinoma.

Four features are linked to H. pylori virulence: 1. Flagella, which allow the bacteria to be motile

in viscous mucus

2.Urease, which generates ammonia from endogenous urea and thereby elevates local gastric pH

3.Adhesins that enhance their bacterial adherence to surface foveolar cells

4. Toxins, such as cytotoxin-associated gene A (CagA), that may be involved in ulcer or cancer development by poorly defined mechanisms

Autoimmune gastritis

Type B Type A

AntPan

Ant Pan

Clinical Features/Diagnosis. Histologic identification of the organism,

Serologic test for antibodies to H. pylori,Fecal bacterial detection, and The urea breath test based on the generation

of ammonia by the bacterial urease.

• Gastric biopsy specimens can also be analyzed by

• the rapid urease test, • bacterial culture, or• bacterial DNA detection by PCR.

Treatment• Combinations of antibiotics and proton pump

inhibitors. • Individuals with H. pylori gastritis usually

improve after treatment, although relapses can occur after incomplete eradication or re-infection.

• Prophylactic and therapeutic vaccine development is still at an early stage of development.

UNCOMMON FORMS OF GASTRITIS

Reactive GastropathyEosinophilic gastritisLymphocytic gastritis

Complications of Chronic Gastritis

• PEPTIC ULCER DISEASE• MUCOSAL ATROPHY AND INTESTINAL

METAPLASIA • DYSPLASIA• GASTRITIS CYSTICA

Cancer Risk• The long-term risk of gastric carcinoma

for persons with H. pylori-associated chronic gastritis is increased about fivefold relative to the normal population.

• For autoimmune gastritis, the risk for cancer is in the range of 2% to 4% of affected individuals, which is well above that of the normal population.