Subject: Practice of Medicine and Pathology

1. GASTRITIS
Subject: Practice Of Medicine
Prepared by Dr. Suman Chaudhary MD (Hom.)

2.  The term ‘gastritis’ is commonly employed for
any clinical condition with upper abdominal
discomfort like indigestion or dyspepsia in which
the specific clinical signs and radiological
abnormalities are absent.
 The condition is of great importance due to its
relationship with peptic ulcer and gastric cancer.
Broadly speaking, gastritis may be of 2 types—
acute and chronic. Chronic gastritis can further
be of various types.

4. ACUTE GASTRITIS
 Acute gastritis is a transient acute inflammatory
involvement of the stomach, mainly mucosa

5. ETIOPATHOGENESIS
 A variety of etiologic agents have been implicated
in the causation of acute gastritis. These are as
follows:
 1. Diet and personal habits:
 Highly spiced food
 Excessive alcohol consumption
 Malnutrition
 Heavy smoking.
 2. Infections:
 Bacterial infections e.g. Helicobacter pylori,
diphtheria, salmonellosis, pneumonia,
staphylococcal food poisoning.

6.  Viral infections e.g. viral hepatitis, influenza,
infectious mononucleosis.
 3. Drugs: Intake of drugs like non-steroidal anti-
inflammatory drugs (NSAIDs), aspirin, cortisone,
phenylbutazone, indomethacin, preparations of iron,
chemotherapeutic agents.
 4. Chemical and physical agents: Intake of
corrosive chemicals such as caustic soda, phenol, lysol
Gastric irradiation Freezing.
 5. Severe stress:
 Emotional factors like shock, anger, resentment etc.
 Extensive burns
 Trauma
 Surgery.

7.  The mucosal injury and subsequent acute
inflammation in acute gastritis occurs by one of
the following mechanisms:
 1. Reduced blood flow, resulting in mucosal
hypoperfusion due to ischaemia.
 2. Increased acid secretion and its accumulation
due to H. pylori infection resulting in damage to
epithelial barrier.
 3. Decreased production of bicarbonate buffer.

8. MANIFESTATION
 Epigastric discomfort
 Abdominal tenderness
 Cramping
 Belching
 Reflux
 Severe nausea and vomiting
 Hematemesis
 Sometimes GI bleeding is the only manifestation
 When contaminated food is the cause of gastritis,
diarrhea usually develops within 5 hours of
ingestion

9. DIAGNOSIS
 Diagnosis is based on a detailed history of food
intake, medications taken, and any disorder
related to gastritis.
 The physician may also perform a gastroscopic
examination with endoscopy.
 Histological examination by biopsy of a sample.

10. MANAGEMENT
 Anti – emetic drugs like Inj. Perinorm or Tab.
Domperidone are frequently effective in vomiting.
 Antacids like cimetidine, Ranitidine, or
Famotidine are effective to reduce the pain.
 If ingestion of NSAIDs is a problem, a
prostaglandin E1 (PGE1) analog may be
prescribed to protect the stomach mucosa and
inhibit gastric acid secretion.

11.  Initially foods and fluids are withheld until
nausea and vomiting subside.
 Once the client tolerates food, the diet includes
decaffeinated tea, gelatin, toast, and simple
bland foods.
 The client should avoid spicy foods, caffeine and
large, heavy meals.
 In the continued absence of nausea, vomiting
and bloating, the client can slowly return to a
normal diet.

12. CHRONIC GASTRITIS
 The condition occurs more frequently with
advancing age; average age for symptomatic
chronic gastritis being 45 years which
corresponds well with the age incidence of gastric
ulcer.

13. ETIOPATHOGENESIS
 All the causative factors of acute gastritis
described above may result in chronic gastritis
too. Recurrent attacks of acute gastritis may
result in chronic gastritis. Some additional
causes are as under:
 1. Reflux of duodenal contents into the stomach,
especially in cases which have undergone surgical
intervention in the region of pylorus.
 2. Infection with H. pylori is strongly implicated
in the etiology of chronic gastritis and is more
common.

14.  3. Associated disease of the stomach and
duodenum, such as gastric or duodenal ulcer,
gastric carcinoma.
 4. Chronic hypochromic anaemia, especially
associated with atrophic gastritis.
 5. Immunological factors such as autoantibodies
to gastric parietal cells in atrophic gastritis and
autoantibodies against intrinsic factor.

15. CLASSIFICATION
 1. Type A gastritis (Autoimmune gastritis)
 Type A gastritis involves mainly the body-fundic mucosa. It
is also called autoimmune gastritis due to the presence of
circulating antibodies and is sometimes associated with
other autoimmune diseases such as Hashimoto’s thyroiditis
and Addison’s disease.
 As a result of the antibodies against parietal cells and
intrinsic factor, there is depletion of parietal cells and
impaired secretion of intrinsic factor. These changes may
lead to significant gastric atrophy where intestinal
metaplasia may occur, and a small proportion of these
patients may develop pernicious anaemia.
 Due to depletion of gastric acid-producing mucosal area,
there is hypo- or achlorhydria, and hyperplasia of gastrin-
producing G cells in the antrum resulting in
hypergastrinaemia.

16.  2. Type B gastritis (H. pylori-related). Type
B gastritis mainly involves the region of antral
mucosa and is more common.
 It is also called hypersecretory gastritis due to
excessive secretion of acid, commonly due to
infection with H. pylori. These patients may have
associated peptic ulcer.

17.  3. Type AB gastritis (Mixed gastritis,
Environmental gastritis, Chronic atrophic
gastritis). Type AB gastritis affects the
mucosal region of A as well as B types (body-
fundic and antral mucosa). This is the most
common type of gastritis in all age groups.

18.  following simple morphologic classification has
been proposed:
 1. Chronic superficial gastritis
 2. Chronic atrophic gastritis
 3. Gastric atrophy
 4. Chronic hypertrophic gastritis (Ménétrier’s
disease)
 5. Uncommon forms of chronic gastritis.

19. 1. CHRONIC SUPERFICIAL
GASTRITIS
 As the name suggests there is inflammatory
infiltrate consisting of plasma cells and
lymphocytes in the superficial layer of the gastric
mucosa, but there are no histological changes in
the deep layer of mucosa containing gastric
glands. Chronic superficial gastritis may resolve
completely or may progress to chronic gastric
atrophy.

20.  Although most patients of chronic superficial
gastritis due to H. pylori remain asymptomatic,
they may develop chronic atrophic gastritis,
gastric atrophy, peptic ulcer disease.
 H. pylori infection is now considered an
independent risk factor for gastric cancer: 3-6
fold increased risk for gastric adenocarcinoma
and 6-50 times risk of MALT lymphoma

21. 2. CHRONIC ATROPHIC
GASTRITIS
 In this stage, there is inflammatory cell infiltrate
in the deeper layer of the mucosa and atrophy of
the epithelial elements including destruction of
the glands. Two types of metaplasia are
commonly associated with atrophic gastritis:
 i) Intestinal metaplasia. Intestinal
metaplasia is more common and involves
antral mucosa more frequently. Characteristic
histologic feature is the presence of intestinal
type mucus-goblet cells; Paneth cells and
endocrine cells may also be present.

22. A, Chronic atrophic gastritis (right) contrasted with normal pyloric
mucosa (left). There is marked gastric atrophy with disappearance
of gastric glands and appearance of goblet cells (intestinal metaplasia).
B, Photomicrograph showing chronic atrophic gastritis with intestinal
metaplasia.

23.  ii) Pseudopyloric metaplasia. It involves the
body glands which are replaced by proliferated
mucus neck cells, conforming in appearance to
normal pyloric glands. Its significance is not
known.

24.  3. GASTRIC ATROPHY. In this, there is
thinning of the gastric mucosa with loss of
glands but no inflammation though lymphoid
aggregates may be present.

25. 4. CHRONIC HYPERTROPHIC
GASTRITIS (MÉNÉ-
TRIER’S DISEASE).
 This is an uncommon condition characterised
pathologically by enormous thickening of gastric
rugal folds resembling cerebral convolutions, affecting
mainly the region of fundic-body mucosa and
characteristically sparing antral mucosa.
 The patients present with dyspepsia, haematemesis,
melaena or protein-losing enteropathy.
 Histologically, the gastric pits are elongated
and are tortuous. The mucosa is markedly thickened
and parts of muscularis mucosae may extend into the
thickened folds. Epithelium-lined cysts are commonly
seen in the glandular layer. Inflammatory infiltrate is
usually mild but lymphoid follicles may be present.

26. 5. MISCELLANEOUS FORMS OF
CHRONIC GASTRITIS
 i) Eosinophilic gastritis. This condition is
characterised by diffuse thickening of the
pyloric antrum due to oedema and extensive
infiltration by eosinophils in all the layers of the
wall of antrum. Eosinophilic gastritis probabl has
an allergic basis.
 iii) Chronic follicular gastritis. This is a
variant of chronic atrophic gastritis in which
numerous lymphoid follicles are present in the
mucosa and submucosa of the stomach.

27.  iv) Haemorrhagic (Erosive) gastritis. In this
condition, there are superficial erosions and
mucosal haemorrhages, usually following severe
haematemesis.
 The causes for such erosions and haemorrhages
are duodenal-gastric reflux, administration of
non-steroidal anti-inflammatory drugs (NSAIDs),
portal hypertension.
 v) Granulomatous gastritis. Rarely,
granulomas may be present in the gastric
mucosa such as in tuberculosis, sarcoidosis,
Crohn’s disease, syphilis, various mycoses, and as
a reaction to endogenous substance or foreign
material.

28. MANIFESTATIONS
 Manifestations are vague and may be absent
because the problem does not cause an increase
in hydrochloric acid.
 Assessment may reveal
 Anorexia
 Feeling of fullness
 Dyspepsia
 Belching
 Vague epigastric pain
 Nausea
 Vomiting
 Intolerance of spicy and fatty foods

29. COMPLICATIONS
 Bleeding
 Pernicious anemia
 Gastric cancer

30. TREATMENT
 Discomfort may lessen with a bland diet, small
frequent meals, antacids, H2 receptor
antagonists, proton pump inhibitors, and
avoidance of food that cause manifestations.
 If H.pylori bacteria are present, anti-biotics and
other medications are administered to eliminate
the bacteria.
 If 1 week of this regimen does not succeed in
eliminating the bacteria, the regimen may be
repeated for an additional week.
 If pernicious anemia develops, intramuscular
injections of vitamin B12 may be administered
monthly for the remainder of the client’s life.

31.  Thank you