A. Esophagus

1. Congenital and mechanical disorders a. Tracheoesophageal fistula i. Definition: congenital connection between the esophagus and trachea ii. Often associated with esophageal atresia iii. Often discovered soon after birth because of aspiration b. Esophageal webs i. Definition: weblike protrusions of the esophageal mucosa into the lumen ji. Presentation: dysphagia iii. Plummer- Vinson syndrome

• Middle-aged women

• Esophageal webs

■ Iron deficiency anemia

• Increased risk of carcinoma iv. Schatzki ring: weblike narrowing at gastroesophageal junction c. Achalasia i. Definition: failure of the lower esophageal sphincter (LES) to relax with swallowing ii. Etiology

■ Unknown in most cases

• South America; —> Chagas disease Presentation: progressive dysphagia Gross: esophageal dilation proximal to the LES Barium swallow: "bird-beak" sign Micro: loss of ganglion cells in the myenteric plexus vii. Treatment: LES balloon dilation or myotomy viii. Increased risk of esophageal carcinoma

2. Hematemesis and esophageal bleeding a. Mallory-Weiss syndrome i. Definition: laceration at the gastroesophageal junction produced by severe prolonged vomiting

Most common cause: alcoholism

Presentation: hematemesis

Gross: linear lacerations at the gastroesophageal junction Complications: Boerhaave syndrome: esophageal rupture (rare)

Clinical Correlate m.

The most common type of tracheoesophageal fistula:




Tracheoesophageal fistula

In a Nutshell

Mallory-Weiss tears versus esophageal varices:

Although both are associated with alcohol abuse and can present with hematemesis, Mallory-Weiss tears typically occur acutely as a result of retching/

vomiting. Esophageal varices result from portal hypertension and will usually present with a more significant bleeding episode.

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b. Esophageal varices i. Definition: dilated submucosal veins in the lower third of the esophagus, usually secondary to portal hypertension ii. Most common cause: cirrhosis iii. Presentation

• Asymptomatic

• Massive hematemesis when ruptured iv. Complication: potentially fatal hemorrhage v. Treatment: band Ligation, sclerotherapy, or balloon tamponade

3. Esophagitis a. Gastroesophageal reflux disease (reflux esophagitis)

i. Definition: esophageal irritation and inflammation due to reflux of gastric secretions into the esophagus ii. Presentation: heartburn and regurgitation iii. Complications

Bronchospasm and asthma

• Barrett esophagus b. Barrett esophagus i. Definition: metaplasia of the squamous esophageal mucosa to a more protective columnar type because of chronic exposure to gastric secretions ii. Incidence is increasing iii. Cause: gastroesophageal reflux disease (GERD)

jv. Gross: irregular gastroesophageal (GE) junction with tongues of red granular mucosa extending up into the esophagus v. Increased risk of dysplasia and esophageal adenocarcinoma

4. Esophageal carcinoma a. Squamous cell carcinoma (SCC) of the esophagus i. Epidemiology

■ SCC is the most common type of esophageal cancer in the world, but not in the United States.

• African Americans > Caucasians ii. Risk factors

■ Heavy smoking and alcohol use

• Plummer-Vinson syndrome

• Prior lye ingestion iii. Presentation

■ Often asymptomatic until late in the course

■ Progressive dysphagia

• Weight loss and anorexia

■ Hoarseness or cough (advanced cancers)

iv. Diagnosis: endoscopy and biopsy v. Treatment: surgery vi. Prognosis: poor b. Adenocarcinoma of the esophagus i. More common than SCC in the United States ii. Caucasians > African Americans iii. Arises in the distal esophagus iv. Associated with Barrett esophagus and dysplasia v. Prognosis: poor B. Stomach

1. Congenital disorders a. Pyloric stenosis i. Definition: congenital stenosis of the pylorus due to marked muscular hypertrophy of the pyloric sphincter, resulting in gastric outlet obstruction ii. Males > females iii. Associated with Turner and Edwards syndromes iv. Presentation

• Onset of regurgitation and vomiting in the second week of life

■ Waves of peristalsis are visible on the abdomen

■ Palpable oval abdominal mass v. Treatment: surgery b. Congenital diaphragmatic hernia i. Definition: congenital defect in the diaphragm, resulting in herniation of the abdominal organs into the thoracic cavity ii. The stomach is the most commonly herniated organ iii. Often associated with intestinal malrotation iv. Complications: respiratory compromise

2. Hypertrophic gastropathy a. Ménétrier disease i. Middle-aged men ii. Gross: enlarged rugal folds in the body and fundus iii. Micro: massive foveolar hyperplasia with replacement of the parietal and chief cells iv. Decreased acid production v. Protein losing enteropathy vi. Increased risk of gastric cancer b. Zollinger-EIlison syndrome i. Pancreatic gastrinoma producing gastrin ii. Gross: enlarged rugal folds iii. Increased acid secretion iv. Presentation: multiple intractable peptic ulcers

Clinical Correlate

Pyloric stenosis is congenital hypertrophy of the pylori, which presents with projectile vomiting and a palpable abdominal "olive."

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Acute inflammation and stress ulcers a. Acute hemorrhagic gastritis i. Definition: acute inflammation, erosion, and hemorrhage of the gastric mucosa due to a breakdown of the mucosal barrier and acid-induced injury ii. Etiology

• Chronic aspirin or NSAID use

• Postsurgery

Chemotherapy iii. Presentation

• Epigastric abdominal pain

■ Gastric hemorrhage, hematemesis, and melena b. Gastric stress ulcers i. Gross: multiple, small, round, superficial ulcers of the stomach and duodenum ii. ■ Etiology

• Severe stress

■ Severe burns or trauma (Curling ulcers)

• Elevated intracranial pressure (Cushing ulcers)

iii. High incidence in intensive care unit (ICU) patients iv. Complication: bleeding Chronic gastritis a. Definition: chronic inflammation of the gastric mucosa eventually leading to atrophy (chronic atrophic gastritis)

■ Autoimmune atrophic gastritis

■ Involves the body and the fundus

• Autoantibodies to parietal cells an d/o r intrinsic factor ' Loss of parietal cells

• Decreased acid secretion

• Increased serum gastrin (G-ceU hyperplasia)

■ Pernicious anemia: megaloblastic anemia due to lack of intrinsic factor and B12 malabsorption ii. Gross: loss of rugal folds in the body and fundus iii. Micro:

■ Mucosa] atrophy with loss of glands and parietal cells

• Chronic lymphoplasmacytic inflammation

• Intestinal metaplasia iv. Increased risk of gastric carcinoma c. Antral type (type B)

i. Helicobacter pylori gastritis ii. Most common form of chronic gastritis in the United States iii. Helicobacter pylori

• Curved, gram-negative rods

■ Urease producing

■ Risk of infection increases with age

• Associated with chronic gastritis (type B)

• Associated with duodenal and gastric peptic ulcers

• Associated with gastric carcinoma iv. Micro

• H. pylori organisms are visible in the mucous layer of the surface epithelium

■ Foci of acute inflammation

• Chronic inflammation with lymphoid follicles

• Intestinal metaplasia v. Increased risk of gastric carcinoma 5. Chronic peptic ulcer (benign ulcer)

a. Peptic ulcer i. Definition: ulcers of the distal stomach and proximal duodenum caused by gastric secretions (hydrochloric acid and pepsin) and impaired mucosal defenses ii. Etiology

• Chronic NSAID and aspirin use

• H. pylori infection iii. Two major locations (see b and c below)

iv. Diagnosis: endoscopy ± biopsy v. Treatment

■ Acid suppression: H2 blocker, proton pump inhibitor, etc.

■ Eradication of H. pylori vi. Complications

• Hemorrhage

» Iron deficiency anemia

• Penetration into adjacent organs

■ Perforation (x-ray shows free air under the diaphragm) « Pyloric obstruction b. Duodenal peptic ulcer i. More common than gastric ulcers ii. Associations

• Increased gastric acid secretion

Clinical Correlate

Ability of H, pylori to produce urease is clinically used for detection by the [13Q-urea breath test and clofazimine (CLO) tests. Other methods of detection include biopsy (histologic identification is the gold standard) and serology.

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