PATHOLOGY
GASTROINTESTINAL TRACT
, GASTROINTESTINAL TRACT
(RS)(5M)(3M) PRECANCEROUS LESIONS OF THE GASTROINTESTINAL SYSTEM/ BARETT’S
ESOPHAGUS/ PRECANCEROUS CONDITION OF ESOPHAGUS
Barrett esophagus is characterized by intestinal metaplasia within the squamous mucosa of
esophagus occurring as a complication to chronic gastroesophageal reflux (GERD).
Incidence: Occur in 10% of patients with symptomatic GERD.
Gender and age: Males, usually between 40 and 60 years of age.
MORPHOLOGY
GROSS
Appears as one or several tongues or patches of red, velvety mucosa extending from
gastroesophageal junction upwards into esophagus.
MICROSCOPY
1. Intestinal metaplasia: Normal squamous lining of the lower esophagus is replaced by columnar
mucosa. Goblet cells with distinct mucous vacuoles are seen in the region of intestinal metaplasia,
are necessary for diagnosis. Intestinal metaplasia is an important risk factor for the development
of adenocarcinoma.
2. Dysplasia (low grade or high grade): It may be seen in the metaplastic epithelium.
(RS)(10M)(5M)(3M) DEFINE PEPTIC ULCER. DISCUSS ETIOPATHOGENESIS/CAUSES, SITES,
PATHOLOGY (MORPHOLOGY) AND COMPLICATIONS OF (CHRONIC) PEPTIC/GASTRIC ULCER
DISEASE.
(RS)(5M)(3M) HELICOBACTER PYLORI (ROLE IN GASTRIC ULCER)
(RS)(5M)(3M) PEPTIC (GASTRIC/DUODENAL) ULCER- CAUSES, GROSS, MICROSCOPY,
COMPLICATIONS
,PEPTIC ULCER
-
DEFINITION: Peptic ulcer is defined as a chronic mucosal ulceration/defect that penetrates the
muscularis mucosae. It usually affects the duodenum (duodenal ulcer) or stomach (gastric ulcer).
PATHOGENESIS AND CAUSES OF PUD/ ACUTE OR CHRONIC GASTRITIS
Q. Discuss the role of H. pylori in gastric ulcer.
The imbalances between MUCOSAL DEFENCES and DAMAGING FORCES cause chronic gastritis and
also PUD.
Risk factors for peptic ulcer disease
H. pylori infection: Risk factors
x Cigarette smoking
x NSAIDs (non-steroidal anti-inflammatory drugs)
x Chronic obstructive pulmonary disease (COPD)
x Alcoholic cirrhosis
x Psychological stress
x Zollinger-Ellison Syndrome
DIRECT MUCOSAL INJURY/ INCREASED DAMAGE:
1. H. pylori infection is one of the most important, common, primary cause of PUD. H. pylori is
detected from the gastric antrum in almost all patients with duodenal ulcers. It is associated with
increased secretion of gastric acid and reduced duodenal secretion of bicarbonate.
2. Nonsteroidal anti-inflammatory drugs (NSAIDs) and aspirin: It causes 1) direct chemical
irritation of mucosa, 2) suppresses mucosal prostaglandin synthesis and 3) reduces the bicarbonate
secretion.
3. Cigarette smoking: Impairs blood flow to the mucosa and healing of mucosal damage.
4. Alcohol, radiation therapy and chemotherapy: They cause direct injury to mucosal cells.
5. Ingestion of chemicals: These include acids or bases and cause direct injury.
6. Gastric hyperacidity: The causes of hyperacidity include H. pylori infection, parietal cell
hyperplasia and Zollinger-Ellison syndrome
IMPAIRED DEFENCE:
1. Ischemia: Decreased oxygen delivery (e.g. at high altitudes and shock)
2. Shock
3. Delayed gastric emptying
4. Host factors: Reduced mucin synthesis in the elderly leads to increased susceptibility to
gastritis.
, MORPHOLOGY
GROSS
Sites of peptic ulcer:
1. Duodenum
2. Stomach
3. Esophagus
4. Jejunum
5. Gastric mucosa in Meckel diverticulum
Peptic ulcer: Most common sites—
1. Duodenal ulcer: First part of duodenum
2. Gastric ulcer: Lesser curvature along the incisive angularis
1. Number: Solitary in more than 80% of patients, but may be more than one.
2. Size: Lesions less than 0.3 cm in diameter are shallow and those larger than 0.6 cm are likely
to be deeper ulcers.
3. Shape: Round to oval
4. Margin: Usually in level with the surrounding mucosa. The gastric mucosal folds can be traced
up to the margins of ulcer and the radiating folds of mucosa from ulcer appear like a spoke wheel.
In contrast, heaped-up margins are more characteristic of gastric cancers.
5. Depth: Varies.
6. Base: It is smooth and clean as a result of peptic digestion of exudate.
MICROSCOPY
Gastric and duodenal ulcers are microscopically similar. From the lumen outward four layers can be
identified and are known as Askanazy zones.
1. Necrotic zone: It is the most superficial zone.
2. Superficial exudative zone: It consists of fibrinopurulent exudates with predominantly
neutrophilic inflammatory infiltrate.
3. Granulation tissue zone: It consists of granulation tissue infiltrated with mononuclear
leukocytes.
4. Zone of cicatrization: It consists of fibrous tissue or collagenous scar which forms the base of
the ulcer and may show chronic inflammatory cells.
GASTROINTESTINAL TRACT
, GASTROINTESTINAL TRACT
(RS)(5M)(3M) PRECANCEROUS LESIONS OF THE GASTROINTESTINAL SYSTEM/ BARETT’S
ESOPHAGUS/ PRECANCEROUS CONDITION OF ESOPHAGUS
Barrett esophagus is characterized by intestinal metaplasia within the squamous mucosa of
esophagus occurring as a complication to chronic gastroesophageal reflux (GERD).
Incidence: Occur in 10% of patients with symptomatic GERD.
Gender and age: Males, usually between 40 and 60 years of age.
MORPHOLOGY
GROSS
Appears as one or several tongues or patches of red, velvety mucosa extending from
gastroesophageal junction upwards into esophagus.
MICROSCOPY
1. Intestinal metaplasia: Normal squamous lining of the lower esophagus is replaced by columnar
mucosa. Goblet cells with distinct mucous vacuoles are seen in the region of intestinal metaplasia,
are necessary for diagnosis. Intestinal metaplasia is an important risk factor for the development
of adenocarcinoma.
2. Dysplasia (low grade or high grade): It may be seen in the metaplastic epithelium.
(RS)(10M)(5M)(3M) DEFINE PEPTIC ULCER. DISCUSS ETIOPATHOGENESIS/CAUSES, SITES,
PATHOLOGY (MORPHOLOGY) AND COMPLICATIONS OF (CHRONIC) PEPTIC/GASTRIC ULCER
DISEASE.
(RS)(5M)(3M) HELICOBACTER PYLORI (ROLE IN GASTRIC ULCER)
(RS)(5M)(3M) PEPTIC (GASTRIC/DUODENAL) ULCER- CAUSES, GROSS, MICROSCOPY,
COMPLICATIONS
,PEPTIC ULCER
-
DEFINITION: Peptic ulcer is defined as a chronic mucosal ulceration/defect that penetrates the
muscularis mucosae. It usually affects the duodenum (duodenal ulcer) or stomach (gastric ulcer).
PATHOGENESIS AND CAUSES OF PUD/ ACUTE OR CHRONIC GASTRITIS
Q. Discuss the role of H. pylori in gastric ulcer.
The imbalances between MUCOSAL DEFENCES and DAMAGING FORCES cause chronic gastritis and
also PUD.
Risk factors for peptic ulcer disease
H. pylori infection: Risk factors
x Cigarette smoking
x NSAIDs (non-steroidal anti-inflammatory drugs)
x Chronic obstructive pulmonary disease (COPD)
x Alcoholic cirrhosis
x Psychological stress
x Zollinger-Ellison Syndrome
DIRECT MUCOSAL INJURY/ INCREASED DAMAGE:
1. H. pylori infection is one of the most important, common, primary cause of PUD. H. pylori is
detected from the gastric antrum in almost all patients with duodenal ulcers. It is associated with
increased secretion of gastric acid and reduced duodenal secretion of bicarbonate.
2. Nonsteroidal anti-inflammatory drugs (NSAIDs) and aspirin: It causes 1) direct chemical
irritation of mucosa, 2) suppresses mucosal prostaglandin synthesis and 3) reduces the bicarbonate
secretion.
3. Cigarette smoking: Impairs blood flow to the mucosa and healing of mucosal damage.
4. Alcohol, radiation therapy and chemotherapy: They cause direct injury to mucosal cells.
5. Ingestion of chemicals: These include acids or bases and cause direct injury.
6. Gastric hyperacidity: The causes of hyperacidity include H. pylori infection, parietal cell
hyperplasia and Zollinger-Ellison syndrome
IMPAIRED DEFENCE:
1. Ischemia: Decreased oxygen delivery (e.g. at high altitudes and shock)
2. Shock
3. Delayed gastric emptying
4. Host factors: Reduced mucin synthesis in the elderly leads to increased susceptibility to
gastritis.
, MORPHOLOGY
GROSS
Sites of peptic ulcer:
1. Duodenum
2. Stomach
3. Esophagus
4. Jejunum
5. Gastric mucosa in Meckel diverticulum
Peptic ulcer: Most common sites—
1. Duodenal ulcer: First part of duodenum
2. Gastric ulcer: Lesser curvature along the incisive angularis
1. Number: Solitary in more than 80% of patients, but may be more than one.
2. Size: Lesions less than 0.3 cm in diameter are shallow and those larger than 0.6 cm are likely
to be deeper ulcers.
3. Shape: Round to oval
4. Margin: Usually in level with the surrounding mucosa. The gastric mucosal folds can be traced
up to the margins of ulcer and the radiating folds of mucosa from ulcer appear like a spoke wheel.
In contrast, heaped-up margins are more characteristic of gastric cancers.
5. Depth: Varies.
6. Base: It is smooth and clean as a result of peptic digestion of exudate.
MICROSCOPY
Gastric and duodenal ulcers are microscopically similar. From the lumen outward four layers can be
identified and are known as Askanazy zones.
1. Necrotic zone: It is the most superficial zone.
2. Superficial exudative zone: It consists of fibrinopurulent exudates with predominantly
neutrophilic inflammatory infiltrate.
3. Granulation tissue zone: It consists of granulation tissue infiltrated with mononuclear
leukocytes.
4. Zone of cicatrization: It consists of fibrous tissue or collagenous scar which forms the base of
the ulcer and may show chronic inflammatory cells.
