Page 563 - Textbook of Pathology, 6th Edition

Viral infections e.g. viral hepatitis, influenza, infectious 3. Associated disease of the stomach and duodenum, such as 547
mononucleosis. gastric or duodenal ulcer, gastric carcinoma.
4. Chronic hypochromic anaemia, especially associated with
3. Drugs: atrophic gastritis.
Intake of drugs like non-steroidal anti-inflammatory
drugs (NSAIDs), aspirin, cortisone, phenylbutazone, 5. Immunological factors such as autoantibodies to gastric
parietal cells in atrophic gastritis and autoantibodies against
indomethacin, preparations of iron, chemotherapeutic intrinsic factor.
agents.
The mechanism of chronic gastric injury by any of the
4. Chemical and physical agents: etiologic agents is by cytotoxic effect of the injurious agent
Intake of corrosive chemicals such as caustic soda, phenol, on the gastric mucosal epithelium, thus breaking the barrier
lysol and then inciting the inflammatory response.
Gastric irradiation
Freezing. CLASSIFICATION. Based on the type of mucosa affected
(i.e. cardiac, body, pyloric, antral or transitional), a
5. Severe stress: clinicopathologic classification has been proposed
Emotional factors like shock, anger, resentment etc. (Table 20.2).
Extensive burns 1. Type A gastritis (Autoimmune gastritis). Type A gas-
Trauma tritis involves mainly the body-fundic mucosa. It is also called
Surgery.
autoimmune gastritis due to the presence of circulating
The mucosal injury and subsequent acute inflammation antibodies and is sometimes associated with other
in acute gastritis occurs by one of the following mechanisms: autoimmune diseases such as Hashimoto’s thyroiditis and
1. Reduced blood flow, resulting in mucosal hypoperfusion Addison’s disease. As a result of the antibodies against
due to ischaemia. parietal cells and intrinsic factor, there is depletion of parietal
cells and impaired secretion of intrinsic factor. These changes
2. Increased acid secretion and its accumulation due to H.
pylori infection resulting in damage to epithelial barrier. may lead to significant gastric atrophy where intestinal
metaplasia may occur, and a small proportion of these CHAPTER 20
3. Decreased production of bicarbonate buffer.
patients may develop pernicious anaemia. Due to depletion
MORPHOLOGIC FEATURES. Grossly, the gastric of gastric acid-producing mucosal area, there is hypo- or
mucosa is oedematous with abundant mucus and achlorhydria, and hyperplasia of gastrin-producing G cells
haemorrhagic spots. in the antrum resulting in hypergastrinaemia.
Microscopically, depending upon the stage, there is 2. Type B gastritis (H. pylori-related). Type B gastritis
variable amount of oedema and infiltration by neutrophils mainly involves the region of antral mucosa and is more
in the lamina propria. In acute haemorrhagic and erosive common. It is also called hypersecretory gastritis due to
gastritis, the mucosa is sloughed off and there are excessive secretion of acid, commonly due to infection with
haemorrhages on the surface. H. pylori. These patients may have associated peptic ulcer.
Unlike type A gastritis, this form of gastritis has no
Chronic Gastritis autoimmune basis nor has association with other The Gastrointestinal Tract
autoimmune diseases.
Chronic gastritis is the commonest histological change 3. Type AB gastritis (Mixed gastritis, Environmental
observed in biopsies from the stomach. The microscopic gastritis, Chronic atrophic gastritis). Type AB gastritis affects
change is usually poorly correlated to the symptomatology, the mucosal region of A as well as B types (body-fundic and
as the change is observed in about 35% of endoscopically antral mucosa). This is the most common type of gastritis in
normal mucosal biopsies. The condition occurs more all age groups. It is also called environmental gastritis
frequently with advancing age; average age for symptomatic because a number of unidentified environmental factors have
chronic gastritis being 45 years which corresponds well with been implicated in its etiopathogenesis. Chronic atrophic
the age incidence of gastric ulcer. gastritis is also used synonymously with type AB gastritis
because in advanced stage, there is progression from chronic
ETIOPATHOGENESIS. In the absence of clear etiology of superficial gastritis to chronic atrophic gastritis, characterised
chronic gastritis, a number of etiologic factors have been by mucosal atrophy and metaplasia of intestinal or
implicated. All the causative factors of acute gastritis pseudopyloric type.
described above may result in chronic gastritis too. Recurrent
attacks of acute gastritis may result in chronic gastritis. Some MORPHOLOGIC FEATURES. Grossly, the features of all
additional causes are as under: forms of gastritis are inconclusive. The gastric mucosa may
1. Reflux of duodenal contents into the stomach, especially in be normal, atrophied, or oedematous.
cases which have undergone surgical intervention in the Histologically, criteria for categorisation are based on the
region of pylorus. following:
2. Infection with H. pylori is strongly implicated in the i) Extent of inflammatory changes in the mucosa (i.e.
etiology of chronic gastritis and is more common. superficial or deep).