PATHOLOGY OF GASTROINTESTINAL TRACT: ESOPHAGUS AND
STOMACH: CONGENITAL ANOMALIES, INFLAMMATION, TUMORS.
PEPTIC ULCER DISEASE.
PATHOLOGY OF ESOPHAGUS
Clinical signs of esophageal lesions:
-dysphagia- means difficulties in swallowing. Most diseases of esophagus
cause dysphagia
-retrosternal pain = heartburn-commonly occurs when acidic gastric juice
refluxes into the esophagus
-hematemesis= vomiting of blood
1) CONGENITAL ESOPHAGEAL DISORDERS:
-tracheoesophageal fistula- is the commonest congenital anomaly of
esophagus
abnormal communication between the trachea and esophagus
2) INFLAMMATORY LESIONS OF THE ESOPHAGUS:
-reflux esophagitis ( peptic esophagitis)
caused by reflux of acid gastric juice into the lower part of esophagus
-symptomatic esophagitis occurs when normal mechanisms of clearing the
esophagus are impaired (even in normal individuals without clinical signs of
esophagitis- some reflux occurs, but in normal persons- any fluid regurgitated
into the esophagus is rapidly returned to stomach by peristalsis)
causes of reflux esophagitis
-impairment of peristalsis- may cause symptoms of reflux esophagitis
-composition of regurgitated gastric juice- higher levels of acids and enzymes,
as well as the presence of bile and pancreatic enzymes
-relation to hiatal hernia- is not clear, hernia is defined as protrusion of part of
stomach through the diaphragmatic hiatus
pathology: superficial erosions of the mucosa of lower esophagus- peptic ulcus
and fibrous narrowing of esophagus
histology: hyperplasia of the basal cells of the squamous epithelium and presence
of neutrophils in the epithelium
clinically: low retrosternal sensation of burning pain called "heartburn"
-in chronic cases- the pain may be constant and is accompanied by dysphagia
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-Barrett's esophagus
-intestinal metaplasia of the epithelium of lower part of esophagus,
presence of gastric mucosa of cardial type is normal within lowest 3 cm of
esophagus
-primary adenocarcinoma of esophagus may arise in Barrett's esophagus or
peptic ulcer may appear
-infectious esophagitis
infections of esophagus are rare, except of in immunocompromised patients
(AIDS, patients receiving anti-cancer therapy), esophagitis is most commonly of
fungal origin-candida albicans
-esophageal candidosis
caused by Candida albicans, it is most common opportunistic infection
morphology: the yeasts infect superficial layers of the epithelium- the surface
is covered by white plaques - grossly visible, composed of cellular debris,
inflammatory cells and fungi
-viral esophagitis
common in AIDS- intranuclear inclusions and occurrence of herpetic giant cellscaused by herpes virus, other type is cause by cytomegalovirus- infects
submucosal endothelial cells- necrosis, hemorrhage, inflammation
3) FUNCTIONAL DISORDERS OF ESOPHAGUS
-Plummer-Vinson syndrome
consists of severe iron-deficiency anemia, koilonychia, atrophic glossitis and
dysphagia-results from the atrophy of pharyngeal mucosa, increased risk of
development of squamous cell carcinoma of tongue, esophagus and pharynx
-more common in women, -dysphagia is corrected if the iron-deficiency is
treated
-achalasia of the cardia
achalasia means failure to relax- the cause od the disorders lies in the lack of
ganglia in the myenteric plexus- this results in failure of peristalsis- the cardiac
sphincter does not relax- the esophagus dilates massively and becomes
elongated
-the patients present with dysphagia
possible complications: reflux of the contents into the trachea- aspiration
pneumonia- lung abscess formation
treatment: myotomy and repeated dilatation of cardia
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-esophageal diverticula
diverticulum- outpouching of the lumen outside the wall
-pulsion diverticulum- occurs when internal pressure forces an epithelial sac out
through weakened muscle layer
-traction diverticulum- are due to external infiltrative processes- with fibrosis
-esophageal varices
occur in lower esophagus and in gastric fundus in patients with portal
hypertension- most common cause is liver cirrhosis
morphology: dilated veins in submucosa may rupture- severe hemorrhage
(hematemesis, melena) occurs
TUMORS OF ESOPHAGUS
1- Carcinoma -accounts for over 95% of all tumors of esophagus
-it is highly lethal-more common in old persons
etiologic factors: cigarette smoking and chronic alcoholism increase the risk of
carcinoma
premalignat
syndrome
conditions: include- Barrett's esophagus and Plummer-Vinson
gross appearance: plaque-like thickening of the mucosa with ulcerationstricture or narrowing of the lumen
microscopically: over 90% are squamous cell carcinoma
- adenocarcinoma is less common- arises in mucosal glands or in Barrett
esophagus
spread of carcinoma through the esophageal wall- invasion of bronchial walltracheoesophageal fistula, -invasion of the aorta may cause massive fatal
bleeding
-lymphatic spread-is very rapid, through the lymphatic capillaries in the
submucosa- lymph node metastases
-bloodstream spread- metastases to the liver and the lungs
clinically: most patients present with dysphagia and pain, severe weight loss,
anemia-due to chronic bleeding
prognosis is poor
Pathology of the stomach
Non - neoplastic disorders of the stomach
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1) Congenital pyloric stenosis
one of the most common congenital disorders of GIT,
-marked hypertrophy of pyloric sphincter results in obstruction of gastric
emptying
symptoms- 1-2 weeks after birth- projectile vomiting after feeding
treatment: surgical muscle splitting is curative
2) inflammatory lesions of stomach- gastritis
Gastritis is simply defined as inflammation of the gastric mucosa, inflammation
may be predominantly acute (neutrophilic leukocytes), or chronic (lymphocytes
and plasmacytes)
1- Acute gastritis
-is an acute mucosal inflammatory process of transient nature, may be
accompanied by hemorrhages- severe form of acute erosive gastritis may cause
acute GI bleeding
grossly: affected mucosa shows red colour, erosions, and hemorrhages
microscopically: hyperemia, edema, leukocytic infiltration of the lamina propria
etiologic factors: the pathogenesis is poorly understood, acute gastritis is
frequently associated with:

Heavy use of nonsteroid anti-inflammatory drugs, such as aspirin, excessive
alcohol consumtion, heavy smoking, treatment with anti-cancer drugs, uremia,
systemic infections, such as salmonelosis, viral infections,severe stress,
ischemia and shock, gastric irradiation, etc.

It must be emphasized that some patients have idiopathic acute gastritis
without any associated disorder
clinically: clinical course depends on the severity of anatomic changes-epigastric
pain, nausea, vomiting, anorrhexia occur in moderate degree of gastritis endoscopic and microscopic changes are minute
-in more severe types- massive hemorrhages, hematemesis, and potentially fatal
blood loss- in alcoholics
2- Chronic gastritis
chronic gastritis is defined as the presence of chronic mucosal inflammatory
changes leading possibly to mucosal atrophy and epithelial metaplasia, chronic
gastritis is notable for distinct causal subgroups with different location,
histology and clinical features.
Pathogenesis: the major etiologic associations of chronic gastritis are as folows
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Immunologic, associated with pernicious anemia,
chronic infection,caused by Helicobacter pylori,
toxic, as with heavy smoking and alcohol consumption
postsurgical, especially following antrectomy and gastrectomy with reflux of
bilious duodenal secretions
 granulomatous conditions, such as in Crohn disease
 miscellaneous- GVHD, uremia, etc.
Basically, three major types of chronic gastritis can be distinguished:
Type A gastritis -associated with pernicious anemia




-involves mainly fundus and body
-is of autoimmune origin- antibodies to parietal cells- decreased acid secretion
and lower production of intrinsic factor- failure of vitamin B12 absorption and
development of pernicious anemia
histologically gastric mucosa shows-chronic atrophy with decrease or absence of
parietal cells, there is lymphoplasmocytic infiltration in the mucosa
-intestinal metaplasia and dysplasia present - precancerous lesion
Type B gastritis -much more common than type A
-involves mainly antral region of the stomach
-is of non-immune origin, is caused by infection of the mucosa of the stomach by
H.pylori. This microorganism is a nonsporing, S-shaped gram negative rod
clinically: epigastric discomfort, pain, nausea
-patients with chronic g-itis caused by H.pylori usually improve when treated
with antimicrobial agents, and relapses are associated with reappearance of
H.pylori in the stomach
-very important is the relationship between chronic gastritis and peptic ulcer,
the patients are possibly in higher risk of development of gastric cancer
3) Peptic ulcer disease
-chronic, most often solitary ulcers in any portion of the alimentary tract
arising from exposure to acid-peptic juices- most occur in the duodenum and
stomach
epidemiology: most often in middle age, more common in men, no genetic
tendencies, duodenal ulcer is more frequent in patients with alcoholic cirrhosis,
chronic renal failure and hyperparathyroidism
morphology: grossly- sharply punched out defect with overhanging mucosal
borders, smooth and clean ulcer base
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microscopy: four layer can be identified-a thin superficial layer-necrotic debris,
zone of inflammation, which is underlaid by a layer of granulation tissue, beneath
which there is fibrous scar
-surrounding mucosa exhibits a chronic gastritis
Pathogenesis: peptic ulcers are produced by an imbalance between the
gastroduodenal mucosal defence mechanisms and damaging force of gastric juice
 mucosal defence mechanisms- include surface mucus secretion, bicarbonate
content in secretion, mucosal blood flow, apical epithelial cell transport
systems, epithelial regeneration, mucus defence is impaired by shock,
ischemia, delayed gastric emptying, and duodenal reflux
 damaging forces- include gastric acid and pepsin, H. pylori infection, aspirin,
cigarettes, alcohol, impaired regulation of acid secretion, stress-uncertain
Clinical features: typical symptoms are epigastric burning, aching pain that is
worse at night, or 1 to3 hours after meals, nausea, vomiting, belching, etc.
complications include anemia (because of occult bleeding), hemorrhage,
perforation, obstruction (edema and/or scar in a pyloric channel), malignant
transformation
TUMORS OF THE STOMACH
 Gastric polyps and Benign tumors
gastric polyps- are rare-there are two major types of epithelial polyps
the term polyp refers to any nodule or mass that projects above the level of the
surrounding mucosa, majority of gastric polyps are hyperplastic/inflammatory
(90%)
 -hyperplastic polyps -smooth-surfaced, sessile or pedunculated
-they represent non-neoplastic lesions- regenerative, inflammatory
 -adenomatous polyps -benign neoplastic lesions
histologically: consist of closely packed tubular epithelial structures with varying
degree of cellular atypia and polymorphism- called dysplasia
Multiple polyps are seen in polyposis syndromes, such as
 -familial adenomatous polyposis
is an autosomal dominant polyposis exhibiting numerous adenomatous polyps in
the colon, stomach and elsewhere, with high risk of progression to
adenocarcinoma
-treatment- prophylactic colectomy, adenomas elsewhere create continued
problems
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 -Peutz-Jeghers syndrome
is an autosomal dominant inherited disorder composed of melanotic pigmentation
of mucosal and skin surfaces, hamartomatous polyps of the small intestine and
colon, and increased risk of carcinoma of breast, pancreas, lung, ovary and
uterus
-hamartomatous polyp- is large pedunculated, with arborizing smooth muscle
surrounding normal abundant glands
 -Gardners syndrome
is an FAP variant exhibiting multiple osteomas (mandible, skull, long bones),
epidermal cysts, fibromatosis (desmoid tumor), and numerous adenomatous
polyps in GI
Mesenchymal tumors -uncommon, well-circumscribed benign tumors within the
wall of the stomach, covered by preserved mucosa, smooth surface
-epithelioid leiomyoma =leiomyoblastoma- is a variant of leiomyoma peculiar to
the stomach
-biologically benign, well circumscribed, may be large intramural mass
histologically: composed of large spindle or round pleomorphic cells with
features of smooth muscle cells
 Malignant tumors
1. Gastric carcinoma -accounts for over 90% of malignant tumors of the
stomach
-geographic differences in the incidence- 10 times higher in Japan than in the
U.S. for example- environmental factors play role
-precancerous lesions for gastric carcinoma include:
-chronic atrophic gastritis with dysplasia- its association with PA
-adenomatous polyps with dysplasia
-chronic peptic ulcers
grossly:-early cancer- =gastric carcinoma restricted to the mucosa and
submucosa
-recognized in Japan- diagnosis by endoscopic examination and biopsy
-advanced gastric cancer- =gastric carcinoma that invades the gastric wallpresents as- endoscopic gross morphology:
-fungating mass that protrudes into the lumen- polypoid
-as a malignant ulceration with raised edges
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-as an ulcer resembling the peptic ulcer
- as a diffusely infiltrating lesion that causes diffuse thickening of the
gastric wall
microscopically: all gastric carcinomas are adenocarcinomas of varying degree of
differentiation
-the most common -poorly differentiated so called diffuse carcinoma of signetring cell type
-well differentiated carcinoma resembling the tubular adenocarcinoma of the
intestine is less common = intestinal type of gastric cancer
spread: gastric carcinoma is locally aggressive- rapidly spreads through the
whole wall of the stomach -lymphatic spread- rapid, lymph node metastases spread along the surfaces of the peritoneum -bloodstream spread- to the liver
and lungs
prognosis: depends almost entirely on the depth of invasion of the tumor
early gastric cancer- 5-year survival rate of 85%
advanced cancer- only 30%
2. Malignant lymphoma
accounts for about 3 % of malignant tumors of the stomach
grossly: polypoid masses, ulcers or mucosal thickenings
diagnosis: only by endoscopic biopsy (histologic examination of the specimen)
primary gastrointestinal ML= MALT lymphoma -arises in mucosa-associated
lymphoid tissue
-majority of lymphomas are of B-cell type, derived from follicular-center cells
gastric lymphoma- responds well to chemotherapy- better prognosis than that
of carcinoma
MALT-lymphomas have better prognosis than nodal lymphomas of the same
type- lower tendency to disseminate
3. Gastric
malignancies
leiomyosarcoma
-accounts
for
about
2%
of
gastric
grossly: large masses that originates in the wall of the stomach -lower tendency
to metastasize than in carcinoma
microscopically: composed of malignant smooth muscle cells with high mitotic
activity, necroses and foci of hemorrhages
clinically: bleeding, blood loss, anemia, palpable mass
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tumor is often located deep in the wall- diagnosis by endoscopy usually
impossible- variant of this tumor- epithelioid leiomyosarcoma (mitotic activity,
necroses, aggressive growth )
4. Carcinoid -arises from neuroendocrine cells present within the mucosa
of the stomach- histological appearance and biological behavior - similar to
identical tumors of the intestine
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