2. Definition
Chronic gastritis is defined as the
presence of
chronic inflammatory changes in the
mucosa leading eventually to
mucosal atrophy and epithelial
metaplasia.
4. Less common etiologies
• radiation injury,
• chronic bile reflux,
• mechanical injury, and
• systemic disease
such as Crohn disease, amyloidosis, or graftversus-host disease.
9. 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 )
10. 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 gastrinproducing
G cells.
11. • Lack of intrinsic factor disables ileal
vitamin B12 absorption, leading to B12
deficiency and a slow-onset megaloblastic
pernicious
AnemiA ).
anemia (
• The reduced serum pepsinogen I
concentration results from chief
destruction.
cell
12. clinicAl feAtures
• Chronic gastritis usually causes few or no
symptoms;
1.Upper abdominal discomfort
2.Nausea
3.Vomiting
4.symptoms of anemia
5.atrophic glossitis,
6. diarrhea.
7.peripheral neuropathy, spinal cord lesions, and
cerebral dysfunction.
13. The median age at
diagnosis is 60 years.
Slightly more women
than men are affected.
16. • the mode of h. pylori
trAnsmission
is not well defined, but humans are the only
known host, making oral-oral, fecaloral, and environmental
spread the most likely routes of infection.
17. 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.
18. • 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.
19. 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
22. 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.
23. • Gastric biopsy specimens can also
be analyzed by
• the rapid urease test,
• bacterial culture, or
• bacterial DNA detection by PCR.
24. 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 reinfection.
• Prophylactic and therapeutic vaccine
development is still at an early stage of
development.
25.
26. UNCOMMON FORMS OF GASTRITIS
Reactive Gastropathy
Eosinophilic
gastritis
Lymphocytic
gastritis
27.
28. Complications of Chronic Gastritis
• PEPTIC ULCER DISEASE
• MUCOSAL ATROPHY AND INTESTINAL
METAPLASIA
• DYSPLASIA
• GASTRITIS CYSTICA
29. CanCer risk
• The long-term risk of gastriC
CarCinoma for persons with H. pyloriassociated 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.
