-
Also
known as
Type A gastritis
is
limited to
corpus-fundus mucosa.
-
Patient usually presents with
pernicious anaemia.
-
Diffuse atrophy of parietal and chief cell mass.
-
Hypo
or achlorhydria , hypergastrinemia, decreased pepsinogen levels.
-
Associated with antibodies to parietal cells, intrinsic factor and
gastrin receptor.
-
Cobalamin deficiency eventually leads to pernicious anaemia.
-
May develop
gastric polyps.
- Increased risk of
developing gastric carcinoma.
Gross
appearance
: Pathology located in the gastric
corpus. Severe atrophy of the cell coats including muscle.Mucosa thinned
out with pebbled appearance.
Microscopic
features:
Early stage: Mononuclear cells consisting of lymphocytes
and plasma cells in the lamina propria. Usually located around fundic
glands and infiltration of the glands by lymphocytes. Glandular
destruction is present. Focal mucous neck cell hyperplasia
Florid stage: Parietal and chief cell atrophy. Increased
lymphocytic infiltration. Focal intestinal metaplasia.
End stage:
Fundic mucosa is completely replaced by
pyloric or intestinal glands.
-Other features:
In patients with pernicious anaemia the superficial gastric epithelium
may appear megaloblastic.
Focal pancreatic metaplasia is sometimes present.
G-cell hyperplasia in the antrum
Hypergastrinaemia leads to hyperplasia of corpus enterochromaffin
cells (ECL cells), causing first linear, then nodular lesions and
eventually multiple microcarcinoids and carcinoid tumours.
In cases of co-existing helicobacter pylori infection, histological
features of both Type A and Type B gastritis are present.
Visit :
Chronic gastritis
;
Acute Gastritis |