Pathology of the esophagus

Question 1

Tracheoesophageal fistula

Answer 1

• Most common congenital anomaly of esophagus, results from incomplete separation of the two structures
• Most common is type is type C (atresia of esophagus and fistula btwn trachea and distal esophagus)
• Complication is aspiration and PNA

Question 2

Esophageal diverticula

Answer 2

• Outpouching of the lumen of the esophagus
• Can result in dysphagia, regurgitation and aspiration during sleep
• Can lead to infection, perforation, hemorrhage, inflammation
• Pulsion diverticula: increased intraluminal pressure pushing thru area of weakened muscle (cricopharyngeus)
• Traction diverticula: external inflammation resulting in fibrosis (usually LN from TB) and eventually pulls the esophagus out

Question 3

Esophageal varices

Answer 3

• Dilated submucosal veins due to portal HTN
• ASx until rupture, then massive hemorrhage, hematemesis
• Complications: 50% die from first bleed, those who survive have 50% chance of re-bleeding w/in next year w/ similar mortality rate
• Rx: balloon tamponade, endoscopic ligation

Question 4

Plummer-Vinson syndrome

Answer 4

• Triad: microcytic hypochromic (Fe-def) anemia, koilonychia (malformed spoon-like nails), atrophic glossitis w/ dysphagia
• Dysphagia due to atrophy of pharyngeal mucosa (from anemia) and web-like mucosal folds
• Fe def due to menstrual blood loss
• Usually in women >40 from scandinavian countries
• Complications: increased risk of squamous cell CA in upper GI

Question 5

Gastroesophageal reflux disease (GERD) 1

Answer 5

• 95% of all esophageal inflammatory cases, usually due to incompetent lower esophageal sphincter
• Hyperemia and hemorrhage of esophagus mucosa
• Micro: hyperplasia of basal cells of mucosa/thickened mucosa, elongation of papillary height (>70% of mucosal thickness), presence of intraepithelial eosinophils and PMNs, no infectious etiology ID’d

Question 6

Gastroesophageal reflux disease (GERD) 2

Answer 6

• Can lead to reflux carditis: metaplasia of the cardiac region of esophagus produces more goblet cells in the esophageal mucosa (beginnings of barrett esophagus)
• Complications: ulceration and stricture formation, dental caries, pulmonary fibrosis, barrett esophagus, adenoCA

Question 7

Infectious esophagitis 1

Answer 7

• Almost always in immune compromised hosts (AIDS, etc), 3 main causes: candida, HSV, CMV
• Candida: causes odynophagia (pain on swallowing), seen on endoscopy as white plaques that are brushed off
• Histo: budding yeasts and pseudohyphae invading superficial mucosa
• HSV: causes odynophagia, dysphagia, hematemesis, endoscopically seen as discrete vesicles or aphthous lesions
• Histo: benign, reactive squamous mucosa w/ ulceration, giant cells w/ cowdry type A inclusions (ground glass, owl’s eyes), only affecting squamous mucosa (not submucosa)

Question 8

Infectious esophagitis 2

Answer 8

• CMV: same Sxs as HSV, looks like HSV on endoscopy
• Histo: large cells w/ cowdry type A inclusions often surrounded by halo, basophilic granular cytoplasmic inclusion bodies
• CMV does not infect squamous cells, just endothelial and mesenchymal cells
• May have CMV inclusion disease (no host response) or CMV esophagitis (must be treated) characterized by inflammation +/- ulceration

Question 9

Barret esophagus (preneoplastic)

Answer 9

• Replacement of normal distal squamous mucosa by metaplastic columnar epithelium + goblet cells
• Clinical: GERD is risk factor, “salmon-colored tongues”
• Must have biopsy for Dx to be made
• Histo: goblet cells (contain mucin, + staining for alcian blue) and columnar absorptive cells
• Complications: 5-10% will develop adenoCA, once diagnosed w/ barretts pt must undergo surveillance for dysplastic changes
• High grade dysplasia: absent goblet cells/mucin and loss of polarity, requires endoscopic mucosal resection
• Low grade dysplasia: decreased goblet cells/mucin

Question 10

Squamous cell CA of esophagus 1

Answer 10

• Usually >50, 3:1 M, Dx is endoscopy w/ biopsy
• Clinical: dysphagia, weight loss, pain (pts can sometimes point to tumor site)
• Causes: diet (aspergillus in food), esophageal d/o (plummer-vinson, achalasia- failure of relaxation of SmM and constitutively closed sphincter), ETOH/smoking, lye ingestion, genetics
• Location: 50% in middle 1/3rd, 30% in lower 1/3rd, 20% in upper 1/3rd

Question 11

Squamous cell CA of esophagus 2

Answer 11

• Histo: early lesion is plaque-like thickening of mucosa (typical squamous appearance: keratin pearls and intracellular bridges)
• Late lesions may be fungating (60%, protrudes into lumen), ulcerating (25%, hemorrhagic base that extends into submucosa), infiltrating (15%, grows into wall)
• Complications: local spread into adjacent cervical/mediastinal structures, lymphatic spread may occur early, hematogenous spread to lungs, liver, adrenals, kidneys

Question 12

AdenoCA of esophagus

Answer 12

• Now most common esophageal neoplasm
• Primary adenoCA most commonly due to complications from barretts esophagus
• Secondary adenoCA may arise elsewhere (e.g. stomach) and invade esophagus
• Risk factors: european ancestry, male, obesity, alcohol, smoking, barrett esophagus
• Histo: similar to high grade dysplasia in barrett but now has invaded lamina propria
• May be well, moderately, and poorly differentiate based on amount of gland formation (more gland formation the more differentiated)
• Poorly differentiated CAs do not form glands and instead are arranged in solid sheets