Lecture 19

INFLAMMATORY CONDITIONS
The two important inflammatory conditions of the stomach are gastritis and peptic ulcer. Rarely, stom-
ach may be involved in tuberculosis, sarcoidosis and Crohn's disease.
GASTRITIS. Acute Gastritis
Acute gastritis is a transient acute inflammatory involvement of the stomach, mainly mucosa.
ETIOPATHOGENESIS. A variety of etiologic agents have been implicated in the causation of acute
gastritis. These are as under:
1. Diet and personal habits: highly spiced food, excessive alcohol consumption, malnutrition, heavy
smoking.
2. Infections: Bacterial infections e.g. in diphtheria, salmonellosis, pneumonia, staphylococcal food
poisoning, Viral infections e.g. viral hepatitis, influenza, infectious mononucleosis.
3. Drugs: Intake of drugs like aspirin, cortisone, phenylbutazone, indomethacin, preparations of iron,
chemotherapeutic agents.
4. Chemical and physical agents: Intake of corrosive chemicals such as caustic soda, phenol.
5. Severe stress: Emotional factors like shock, anger, resentment etc., extensive burns.
PATHOLOGIC CHANGES. Grossly, the gastric mucosa is oedematous with abundant mucus and
haemorrhagic spots.
Microscopically, depending upon the stage, there is variable amount of oedema and infiltration by
neutrophils in the lamina propria. In acute haemorrhagic and erosive gastritis, the mucosa is sloughed
off and there are haemorrhages on the surface.
Chronic Gastritis
Chronic gastritis is the commonest histological change observed in biopsies from the stomach.
The mechanism of chronic gastric injury by any of the etiologic agents is by cytotoxic effect of the
injurious agent on the gastric mucosal epithelium, thus breaking the barrier and then inciting the
inflammatory response.
CLASSIFICATION. Based on the type of mucosa affected (i.e. cardiac, body, pyloric, antral or transi-
tional) the following clinicopathologic classification has been proposed:
1. Type A gastritis (Autoimmune gastritis)
2. Type B gastritis (Hypersecretory gastritis)
3. Type AB gastritis Fundic and antral (Environmental, mucosa chronic atrophic gastritis)
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.
2. Type B Gastritis (Hypersecretory gastritis).
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. These patients may have associated
duodenal or gastric ulcer.
3. Type AB 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. It is also called environmental gastritis because a number of as yet
unidentified environmental factors have been implicated in its etiopathogenesis. Chronic atrophic
gastritis is also used synonymously with type AB gastritis, because in advanced stage, there is progres-
sion from chronic superficial gastritis to chronic atrophic gastritis, characterised by mucosal atrophy
and metaplasia of intestinal or pseudopyloric type. PATHOLOGIC CHANGES. Macroscopically the
features of all forms of gastritis are inconclusive. The gastric mucosa may be normal, atrophied, or
oedematous. Chronic gastritis is essentially a histological diagnosis.
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Histologically, based on (i) the extent of inflammatory changes in the mucosa (i.e. superficial or deep),
(ii) the activity of inflammation (i.e. quiscent or active; acute or chronic), and (iii) the presence of and
type of metaplasia (i.e. intestinal or pseudopyloric), the following simple classification has emerged:
1, Chronic superficial gastritis. 2. Chronic atrophic gastritis. 3. Gastric atrophy
4. Chronic hypertrophic gastritis (Menetrier's disease)
5. Special varieties of chronic gastritis
6. Granulomatous gastritis
1. CHRONIC SUPERFICIAL GASTRITIS. As the name suggests (here 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 gas-
tritis may resolve completely or may progress to chronic atrophic gastritis.
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 histological feature is the presence of intestinal type mucus-goblet cells;
Paneth cells and endocrine cells may also be present. Parietal cells are very few or absent. Intestinal
metaplasia, focal or extensive, in atrophic gastritis is significant because its incidence is high in
populations having high prevalence rate of gastric cancer like in Japan.
(ii) Pseudopyloric metaplasia. It involves the body glands which are replaced by proliferated mucous
neck cells, conforming in appearance to normal pyloric glands. Its significance is not known.
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.
4. CHRONIC HYPERTROPHIC GASTRITIS (MENETERIER'S DISEASE). This is an uncom-
mon condition characterised pathologically by enormous thickening of gastric rugal folds resembling
cerebral convolutions, affecting mainly the region of fundic-body mucosa and characteristically spar-
ing 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 mucosa 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. The condition is considered significant in view of the risk of developing cancer.
5. SPECIAL VARIETIES OF CHRONIC GASTRITIS. A few other types of gastritis which do not
fit into the description of the types of gastritis described above are listed below:
Campylobacter gastritis. This is a recently described entity caused by Campylobacter pylori. The
organism appears to have affinity for gastric epithelial cells because the organisms are absent from
areas of intestinal metaplasia in the stomach which is heavily colonised by the organism and are seen in
areas of gastric metaplasia in duodenal ulcer. The organism acts by depleting protective mucus 'barrier'
in areas colonised by it. The microscopic appearance is initially of acute gastritis but later leads to
active chronic superficial gastritis with demonstrable C. pylori. The occurrence rate in duodenal ulcer is
very high (85-100%), though about 10% of normal healthy individuals may also have Campylobacter
gastritis.
PEPTIC ULCERS
Peptic ulcers are the areas of degeneration and necrosis of gastrointestinal mucosa exposed to acid-
peptic secretions.
Acute Peptic (Stress) Ulcers. Acute peptic ulcers or stress ulcers are multiple, small mucosal erosions,
seen most commonly in the stomach but occasionally involving the duodenum.
ETIOLOGY. These ulcers occur following severe stress. The causes are
(i) Psychological stress, (ii) Physiological stress as in: shock, severe trauma, septicaemia, extensive
burns (Curling's ulcers in the posterior aspect of the first part of the duodenum).
Intracranial lesions (Cushing's ulcers developing from hyperacidity following excessive vagal
stimulation). Drug intake (e.g. aspirin, steroids, butazolidine, indomethacin). Local irritants (e.g.
alcohol, smoking, coffee etc).
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 PATHOGENESIS.
1. Ischaemic hypoxic injury to the mucosal cells.
2. Depletion of the gastric mucus 'barrier' rendering the mucosa susceptible to attack by acid-peptic
secretions.
PATHOLOGIC CHANGES. Grossly, acute stress ulcers are multiple (more than three ulcers in 75% of
cases). They are more commonly seen anywhere in the stomach, followed in decreasing frequency ' by
occurrence in the first part of duodenum. They may be oval or circular in shape, usually less than 1 cm
in diameter.
Microscopically, the stress ulcers are shallow and do not invade the muscular layer. The margins and
base may show some inflammatory reaction depending upon the duration of the ulcers. These ulcers
commonly heal by complete re-epithelialisation without leaving any scars. Complications such as
haemorrhage and perforation may occur.
Chronic Peptic Ulcers (Gastric and Duodenal Ulcers)
Gastric and duodenal ulcers represent two distinct diseases as far as their etiology, pathogenesis
and clinical features are concerned. However, pathological findings in both are similar and quite diag-
nostic.
ETIOLOGY. The immediate cause of peptic ulcer disease is disturbance in normal protective mucosal
'barrier' by acid-pepsin, resulting in digestion of the mucosa. However, in contrast to duodenal ulcers,
the patients of gastric ulcer have low-to-normal gastric acid secretions, though true achlorhydria in
response to stimulants never occurs in benign gastric ulcer. Besides, 10-20% patients of gastric ulcer
may have coexistent duodenal ulcer as well. Thus, the etiology of peptic ulcers possibly may not be ex-
plained on the basis of a single factor but is multi-factorial.
PATHOGENESIS. Although the role of various etiologic factors just described is well known in
ulcerogenesis, there are distinct differences in the pathogenetic mechanisms involved in duodenal and
gastric ulcers.
PATHOLOGIC CHANGES. Gross and microscopic changes in gastric and duodenal ulcers are similar
and quite characteristic. Gastric ulcers are found predominantly along the lesser curvature in the region
of pyloric antrum, more commonly on the posterior than the anterior wall. Most duodenal ulcers are
found in the first part of the duodenum, usually immediately post-pyloric, more commonly on the
anterior than the posterior wall.
Grossly, typical peptic ulcers are commonly solitary (80%), small (1-2.5 cm in diameter), round to oval
and characteristically 'punched out'. Benign ulcers usually have flat margins in level with the surround-
ing mucosa. The mucosal folds converge towards the ulcer. The ulcers may vary in depth from being
superficial (confined to mucosa) to deep ulcers (penetrating into the muscular layer). In about 10-20%
of cases, gastric and duodenal ulcers are coexistent. Vast majority of the peptic ulcers are benign.
Chronic duodenal ulcer never turns malignant, while chronic gastric ulcer may develop carcinoma in
less than 1% of cases. Malignant gastric ulcers are larger;' bowl-shaped with elevated and indurated
mucosa at the margin.
Microscopically, chronic peptic ulcers have 4 histological zones. From within outside, these are as
under: 1. Necrotic zone - lies in the floor of the ulcer and is composed of fibrinous exudates containing
necrotic debris and a few leucocytes. 2. Superficial exudative zone lies underneath the necrotic zone.
The tissue elements here show coagulative necrosis giving eosinophilic, smudgy appearance with
nuclear debris. 3. Granulation tissue zoneis seen merging into the necrotic zone. It is composed of
nonspecific inflammatory infiltrate and proliferating capillaries.4. Zone of cicatrisationis seen
merging into thick layer of granulation tissue. It is composed of dense fibrocollagenic scar tissue over
which granulation tissue rests. Thrombosed or sclerotic arteries may cross the ulcer which on erosion
may result in haemorrhage.
COMPLICATIONS. Acute and subacute peptic ulcers usually heal without leaving any visible scar.
However, healing of chronic, larger and deeper ulcers may result in complications. These are as fol-
lows:
1. Obstruction. Development of fibrous scar at or near the pylorus results in pyloric stenosis. In the
case of healed duodenal ulcer, it causes duodenal stenosis. Healed ulcers along the lesser curvatures
may produce 'hour glass' deformity due to fibrosis and contraction.
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2. Haemorrhage. Minor bleeding by erosion of small blood vessels in the base of ulcer occurs in all
the ulcers and can be detected by testing the stool for occult blood. Chronic blood loss may result in
iron deficiency anaemia. Severe bleeding may cause 'coffee ground' vomitus or melaena. A penetrating
chronic ulcer may erode a major artery (e.g. left gastric, gastroduodenal or splenic artery) and cause a
massive and severe hematemesis and sometimes death.
3. Perforation. A perforated peptic ulcer is an acute abdominal emergency. Perforation occurs more
commonly in chronic duodenal ulcers than chronic gastric ulcers. Following sequelae may result:
(i) On perforation the contents escape into the lesser sac or into the peritoneal cavity, causing acute
peritonitis.
(ii) Air escapes from the stomach and lies between the liver and the diaphragm giving the characteris tic
radiological appearance of air under the diaphragm.
(iii) Subphrenic abscess between the liver and the diaphragm may develop due to infection.
(iv) Perforation may extend to involve the adjacent organs e.g. the liver and pancreas.
4. Malignant transformation. The dictum 'cancers ulcerate but ulcers rarely cancerate is true for
most peptic ulcers. A chronic duodenal ulcer never turns malignant, while less than 1% of chronic
gastric ulcers may transform into carcinoma.
INFLAMMATORY BOWEL DISEASE (CROHN'S DISEASE AND ULCERATIVE COLITIS)
DEFINITION. The term 'inflammatory bowel disease (IBD)' is commonly used to include 2 idiopathic
bowel diseases having many similarities but the conditions usually have distinctive morphological
appearance. These 2 conditions are Crohn's disease (regional enteritis) and ulcerative colitis.
1. Crohn's disease or Regional enteritis is an idiopathic chronic ulcerative IBD, characterised by
transmural, non-caseating granulomatous inflammation, affecting most commonly the segment of
terminal ileum and/or colon, though any part of the gastrointesrinal tract may be involved.
2. Ulcerative colitis is an idiopathic form of acute and chronic ulcero-inflammatory colitis affecting
chiefly the mucosa and submucosa of the rectum and descending colon, though sometimes it may
involve the entire length of large bowel.
Both these disorders primarily affect the bowel but may have systemic involvement in the form of
polyarthritis, uveitis, ankylosing spondylitis, skin lesions and hepatic involvement. Both diseases can
occur at any age but are more common in 2nd and 3rd decades of life. Females are affected slightly
more often.
CROHN'S DISEASE. Crohn's disease may involve any portion of the gastrointestinal tract but affects
most commonly 15-25 cm of the terminal ileum which may extend into the caecum and sometimes into
the ascending colon.
Grossly, characteristic feature is the multiple, well-demarcated segmental bowel involvement with in-
tervening uninvolved 'skip areas'. The wall of the affected bowel segment is thick and hard, resembling
a 'hose pipe'. Serosa may be scudded with minute granulomas. The lumen of the affected segment is
markedly narrowed. The mucosa shows 'serpigenous ulcers, while intervening surviving mucosa is
swollen giving 'cobblestone appearance'. There may be deep fissuring into the bowel wall.
Histologically, the characteristic features are as follows:
1. Transmural inflammatory cell infiltrate consisting of chronic inflammatory cells (lymphocytes,
plasma cells and macrophages) is the classical microscopic feature.
2. Non-caseating, sarcoid-like granulomas are present in all the layers of the affected bowel wall in
60% of cases and may even be seen in the regional lymphnodes.
3. There is patchy ulceration of the mucosa which may take the form of deep fissures, accompanied by
inflammatory infiltrate of lymphocytes and plasma cells.
4. There is widening of the submucosa due to oedema and foci of lymphoid aggregates.
5. In more chronic cases, fibrosis becomes increasingly prominent in all the layers disrupting muscular
layer.
APPENDICITIS
Acute inflammation of the appendix, acute appendicitis, is the most common acute abdominal con-
dition confronting the surgeon. The condition is seen more commonly in older children and young
adults, and is uncommon at the extremes of age. The disease is seen more frequently in the West and in

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affluent societies which may be due to variation in dieta diet with low bulk of cellulose and high
protein intake more often causes appendicitis.
ETIOPATHOGENESIS. The most common etiological factor is obstruction of the lumen that leads to
increased intraluminal pressure. This presses upon the blood vessels to produce ischemic injury which
in turn favours the bacterial proliferation and hence acute appendicitis. The common causes of
appendicitis are as under:
A. Obstructive: 1. Faecolith. 2. Calculi. 3. Foreign body. 4. Tumour. 5. Worms (especially Enterobius
vermicularis). 6. Diffuse lymphoid hyperplasia, especially in children
B. Non-obstructive: 1. Haematogenous spread of generalised infection
2. Vascular 'occlusion
3. Inappropriate diet lacking roughage.
PATHOLOGIC CHANGES. Macroscopically, the appearance depends upon the stage at which the
acutely-inflamed appendix is examined. In early:
acute appendicitis, the organ is swollen and serosa shows hyperaemia. In well-developed acute inflam-
mation called acute suppurative appendicitis, the serosa is coated with fibrinopurulent exudates and
engorged vessels on the surface. In further advanced cases called acute gangrenous appendicitis, there
is necrosis and ulcerations of mucosa which extend through the wall so that the appendix becomes soft
and friable and the surface is coated with greenish-black gangrenous necrosis.
Microscopically, the most important diagnostic histological criteria is the neutrophilic infiltration of
the muscularis. In early stage, the other changes besides acute inflammatory changes, are congestion
and oedema of the appendix wall. In later stages, the mucosa is sloughed off, the wall becomes
necrotic, the blood vessels may get thrombosed and there may be neutrophilic abscesses in the wall. In
either case, an impacted foreign body, faecolith, or concretion may be seen in the lumen. Thus, there is
good correlation between macroscopic and microscopic findings in acute appendicitis.
COMPLICATIONS. 1. Peritonitis. A perforated appendix as occurs in gangrenous appendicitis may
cause localised or generalised peritonitis.
2. Appendix abscess. This is due to rupture of an appendix giving rise to localised abscess in the right
iliac fossa. This abscess may spread to other sites such as between the liver and diaphragm (subphrenic
abscess), into the pelvis between the urinary bladder and rectum, and in the females may involve uterus
and fallopian tubes.
3. Adhesions. Late complications of acute appendicitis are fibrous adhesions to the greater omentum,
small intestine and other abdominal structures.
4. Portal pylephlebitis. Spread of infection into mesenteric veins may produce septic phlebitis and
liver abscess.
5. Mucocele. Distension of distal appendix by mucus following recovery from an attack of acute
appendicitis is referred to as mucocele. It occurs generally due to proximal obstruction but sometimes
may be due to a benign or malignant neoplasm in the appendix. Extravasation of the mucus following
rupture of mucocele gives rise to pseudomyxoma peritonei. An infected mucocele may result in
formation of empyema of the appendix.