Less common etiologies• radiation injury,• chronic bile reflux,• mechanical injury, and• systemic diseasesuch 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 intrinsicfactor• Reduced serum pepsinogen Iconcentration• Antral endocrine cell hyperplAsiA• Vitamin B12 deficiency• Defective gastric acid secretion(achlorhydria)
PathogenesisAutoimmune gastritis is associated withloss of parietal cells,which are responsible for secretion of gastricacid and intrinsic factor. The absence of acidproduction stimulates gastrin release,resulting in hypergastrinemia andhyperplAsiA of antral gastrin-producingG cells.
• Lack of intrinsic factor disables ilealvitamin B12 absorption, leading to B12deficiency and a slow-onset megaloblasticanemia (perniciousAnemiA).• The reduced serum pepsinogen Iconcentration results from chief celldestruction.
clinicAl feAtures• Chronic gastritis usually causes few or nosymptoms;1.Upper abdominal discomfort2.Nausea3.Vomiting4.symptoms of anemia5.atrophic glossitis,6. diarrhea.7.peripheral neuropathy, spinal cord lesions, andcerebral dysfunction.
The median age atdiagnosis is 60 years.Slightly more womenthan men are affected.
EpidemiologyAssociAted with :Poverty,Household crowding,Llimited education,African-American or Mexican-American ethnicity,Residence in rural areas.
• the mode of h. pyloritrAnsmissionis not well defined, but humans are the onlyknown host, making oral-oral, fecal-oral, and environmentalspread the most likely routes of infection.
Pathogenesis• The most import cause is infection byH. pylori.Gastritis develops as a result of the combinedinfluence of• bacterial enzymes and• toxins and release of• noxious chemicals by the recruitedneutrophils.
• After initial exposure to H.pylori, gastritis maydevelop in two patterns:• 1. antral- tyPe with high acidproduction and higher risk for thedevelopment of duodenal ulcer, and• 2. Pangastritis with multifocalmucosal atrophy, with low acid secretion andincreased risk for carcinoma.
Four features are linked to H. pylori virulence:1. Flagella, which allow the bacteria to bemotile in viscous mucus2.urease, which generates ammonia fromendogenous urea and thereby elevates localgastric pH3.adhesins that enhance their bacterialadherence to surface foveolar cells4. toxins, such as cytotoxin-associated gene A(CagA), that may be involved in ulcer or cancerdevelopment by poorly defined mechanisms
Clinical Features/Diagnosis.Histologic identification of the organism,Serologic test for antibodies to H. pylori,Fecal bacterial detection, andThe urea breath test based on the generationof ammonia by the bacterial urease.
• Gastric biopsy specimens can alsobe analyzed by• the rapid urease test,• bacterial culture, or• bacterial DNA detection by PCR.
treatment• Combinations of antibiotics and protonpump inhibitors.• Individuals with H. pylori gastritis usuallyimprove after treatment, although relapsescan occur after incomplete eradication or re-infection.• Prophylactic and therapeutic vaccinedevelopment is still at an early stage ofdevelopment.
UNCOMMON FORMS OF GASTRITISReactive GastropathyEosinophilicgastritisLymphocyticgastritis
Complications of Chronic Gastritis• PEPTIC ULCER DISEASE• MUCOSAL ATROPHY AND INTESTINALMETAPLASIA• DYSPLASIA• GASTRITIS CYSTICA
CanCer risk• The long-term risk of gastriCCarCinoma for persons with H. pylori-associated chronic gastritis is increased aboutfivefold relative to the normal population.• For autoimmune gastritis, the risk for cancer isin the range of 2% to 4% of affectedindividuals, which is well above that of thenormal population.
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