5. Acute Gastritis
● Most common causes of acute gastritis
are infectious (H. pylori )
● Sudden onset of epigastric pain, nausea,
and vomiting
● If not treated, this picture will evolve into
one of chronic gastritis
● Phlegmonous gastritis is a rare (Elderly
individuals, alcoholics, and AIDS )
● Failure of supportive measures and
antibiotics may result in gastrectomy
● Herpes simplex or CMV gastritis in AIDS
6. Chronic Gastritis
● Inflammatory cell infiltrate consisting
primarily of lymphocytes and plasma cells
● Distribution of the inflammation may be
patchy, initially involving superficial and
glandular portions of the gastric mucosa.
● This picture may progress to more severe
glandular destruction, with atrophy and
metaplasia
7. Superficial gastritis
● The early phase of chronic gastritis
● Inflammatory changes are limited to the
lamina propria of the surface mucosa, with
edema and cellular infiltrates separating
intact gastric glands
● Decreased mucus in the mucous cells and
decreased mitotic figures in the glandular
cells
8. Atrophic gastritis
● Inflammatory infiltrate extends deeper into
the mucosa, with progressive distortion
and destruction of the glands
● Final stage of chronic gastritis is gastric
atrophy
● Endoscopically, the mucosa may be
substantially thin, permitting clear
visualization of the underlying blood
vessels
9. ● Gastric glands may undergo morphologic
transformation in chronic gastritis.
● Intestinal metaplasia denotes the
conversion of gastric glands to a small
intestinal phenotype with small-bowel
mucosal glands containing goblet cells.
● The metaplastic changes may vary in
distribution from patchy to fairly extensive
gastric involvement.
● Intestinal metaplasia is an important
predisposing factor for gastric cancer
10. ● Chronic gastritis is also classified
according to the predominant site of
involvement:
● Type A refers to the body-predominant
form (autoimmune)
● Type B is the antral-predominant form (H.
pylori–related).
11. Type A Gastritis
● less common
● Involves primarily the fundus and body
● Antral sparing
● Associated with pernicious anemia
● Antibodies against parietal cells and IF
(autoimmune gastritis)
● H. pylori infection can lead to a similar
distribution of gastritis
●
12. ● Antibodies to parietal cells have been
detected in >90% of patients with
pernicious anemia
● in up to 50% of patients with type A
gastritis
● Parietal cell antibodies and atrophic
gastritis are observed in family members
● half of patients with pernicious anemia
have antibodies to thyroid antigens
● ~ 30% of patients with thyroid disease
have circulating antiparietal cell antibodies
13. ● Anti-IF antibodies are more specific than
parietal cell antibodies
● HLA-B8 and -DR3
● Achlorhydria & vitamin B12 deficiency
results
● Sparing of the antral mucosa (site of G
cells), leads to hypergastrinemia
● Development of gastric carcinoid tumors
14. Type B Gastritis
● The more common form
● H. pylori is the cause
● Improves after H. pylori eradication
● antral-predominant, gastritis
● Progression of the inflammatory process
toward the body and fundus
● Conversion to a pan-gastritis is
time-dependent–estimated to require
15–20 years
15. ● Number of H. pylori organisms decreases
dramatically with progression to gastric atrophy,
● Degree of inflammation correlates with the level
of these organisms
● Multifocal atrophic gastritis, gastric atrophy with
subsequent metaplasia
● lead to development of gastric adenocarcinoma
or low-grade B cell lymphoma (gastric MALT
lymphoma)
● Eradication of H. pylori as a general preventative
measure for gastric cancer is being evaluated
but is not yet recommended
16. Treatment
● Patients with pernicious anemia will
require parenteral vitamin B12
supplementation on a long-term basis.
●
● Eradication of H. pylori is not routinely
recommended unless PUD or a low-grade
MALT lymphoma is present
