Week 1: Pathology of Esophagus

Question 1

Hiatal Hernia

Answer 1

• presents like GERD
• two types
  1. Sliding hiatal hernia 95%: portion of stomach herniates above the diaphragm upward (slides upward)
• associated with reflux symptoms
  2. Rolling or paraesophageal hernia 5%: portion of stomach herniates up in diaphragmatic crura and presses on lower esophageal spinchter- less assoc. with reflux

Question 2

Tracheoesophageal fistula

Answer 2

• most common congenital anomaly
• results from incomplete separation of trachea and esophagus
• different types, but most common is type C, with distal esophagus connected to trachea and proximal esophagus just ends
• complication: aspiration pneumonia

Question 3

Esophageal diverticuli

Answer 3

• pouch that protrudes outward in a weak part of the esophageal lining
• dysphagia and inflammation if large. Regurgitation and aspiration during sleep. Can cause halitosis.
  1. Zenker’s or pharyngeal diverticulum: increased intraluminal pressure pushes through weakness of cricopharynxgeus muscle. pulsion type.
  2. Traction diverticulum: distal esophagus, due to external inflammation resulting in fibrosis, e.g. TB lymph node.
  3. Epiphrenic: above the diarphagm. Pulsing type.

Question 4

Esophageal varices

Answer 4

• tortuous, dilated submucosal veins in distal esophagus and proximal stomach due to portal HTN
• asymptomatic until rupture
• massive hematemesis
• Rx: balloon tamponade, endoscopic ligation
• complications: 50% die at first bleeding episode, and others will rebleed within next year.
• also liver damage means can’t make coagulation factors, problems with hemostasis

Question 5

Plummer-Vinson Syndrome

Answer 5

• aka paterson-kelly syndrome
• Triad of Fe deficiency anemia, dysphagia, and esophageal web (mucosal fold that protrudes into lumen)
• dysphagia from web or atrophy of pharyngeal mucosa
• Fe deficiency from menstruation
• also see koilonychia, atrophic glossitis (smooth tongue, loss of papillae)
• associated with Norwegian women
• Complication: increased risk of SCC in upper esophagus, oropharynx and posterior tongue

Question 6

Gastroesophageal Reflux disease (GERD): gross and histological features

Answer 6

• from incompetent LES
• gross: hyperemia, hemorrhage, erythematous mucosa with exudate
• histology: hyperplasia of basal cells of squamous mucosa>20% thickness, elongation of papillae height>70% mucosal thickness, presence of Eos and PMNs, mucosal congestion and inflammation in cardiac mucosa
• reflux carditis: cardiac metaplasia with inflammation
• absence of a cause, e.g. candida

Question 7

Complications of GERD

Answer 7

• Ulceration: may cause stricture formation.
• dental caries: gastric content can get to oral cavity and causes breakdown of enamel
• pulmonary fibrosis from aspiration
• Barrett esophagus
• adenocarcinoma

Question 8

Infectious esophagitis: Candida albicans

Answer 8

• clinical: odynophagia (pain while swallowing)
• immunocompromised states: AIDs, cancer patients on chemo, diabetics, transplant patients on immunosuppressives, incidentally in elderly
• dx: endoscopy with biopsy or brushing and culture. Elevated shiny white plaques.
• histopath: PAS or GMS stains, budding yeast forms and pseudohyphae invading superficial layers of squamous mucosa.

Question 9

Infectious esophagitis: Herpes simplex virus

Answer 9

-can affect any part of GI, but esophagus most common (not counting oral)
-Clinical: odynophagia, dysphagia, hematemesis occasionally
-cause: HSVI and II
-immunocompromised hosts and immunocompetent
Dx: endoscopy and biopsy/brushing. Discrete vesicles or aphthous lesions
-histopath: biopsy at leading edge of ulcer is where viral inclusions are found. benign, reactive squamous mucosa with ulceration. Multi nucleated giant cells with ground glass Cowdry Type A intranuclear inclusions
-affects squamous mucosa not submucosa

Question 10

Infectious esophagitis: CMV

Answer 10

• immunocompromised hosts only
• clinically same as herpes esophagitis: odynophagia, dysphagia, hematemesis occasionally
• Dx: endoscopy with biopsy/brushing. Lesions may look like herpes
• histopath: cytomegaly, single cowdry type A inclusion, surrounded by halo “owl eyes”. Tends to infect endothelial cells and doesn’t effect squamous mucosa.
• CMV inclusion disease: no inflammatory response, no Rx needed
• CMV esophagitis: inflammation with or without ulceration. May give gangcyclovir

Question 11

Other causes of esophagitis

Answer 11

• caustic ingestion: lye
• causes stricture at level of bifurcation of trachea
• histopath: acanthosis, regenerative changes and marked fibrosis in muscular
• 100x increased risk of SCC after 40 years
• Rx: surgical removal

Question 12

Barrett Esophagus

Answer 12

• def: replacement of normal distal stratified squamous mucosa by metaplastic columnar epithelium containing goblet cells
• cause: occurs in 10% ppl with GERD
• Histopath: specialized columnar metaplastic epithelium above GEJ with goblet and columnar cells. goblet cells have acid mucin (stains positive with Alcian blue at pH 2.5).
• complications: 5-10% develop adenocarcinoma.
• patients must undergo surveillance for dysplastic change. High grade dysplasia is resected.

Question 13

Low grade vs. high grade dysplasia in barrett esophagus

Answer 13

• Low grade: granular architecture. more complex, nuclei enlarged, hyper chromatic, basophilic cytoplasm, decreased mucin
• high grade dysplasia: large nuclei with macro nucleoli. goblet cells and mucin absent. loss of polarity.

Question 14

SCC of esophagus: epidemiology and clinical

Answer 14

• 10% of GI cancers. Males more than females, over 50 years old.
• northern China, Iran, Russia, South Africa (silk road)
• clinical: dysphagia, weight loss, pain in 50%. anemia, hematemesis or melena less common.
• cause: multifactorial-diet with nitrites/aspergillus, esophageal disorders, chronic alcoholism, smoking, lye ingestion, genetic predisposition

Question 15

Pathology of SCC of esophagus

Answer 15

• 50% in middle third of esophagus
• early lesion: plaque like thickening of mucosa
• late: fungating (60%) protrudes into lumen, ulcerating, infiltrating
• histology: keratin pearls, desmosomes
• complications: submucosal spread insidious. local and lymphatic spread. hematogenous spread to liver, lungs, adrenals, kidneys.
• poor 5 year survival

Question 16

Adenocarcinoma of esophagus: causes, risks

Answer 16

• most common esophageal neoplasm
• Primary: 1) arising from cardiac glands of esophagus and esophageal glands proper. 2) arising from Barrett esophagus (most common)
• secondary: arising from elsewhere and invading esophagus
• risks: european, male, overweight, EtOH, smoking, Barrett esophagus

Question 17

adenocarcinoma of esophagus: pathology

Answer 17

• if well and moderately differentiated: gland like structures
• poorly differentiated: solid sheets of cells
• prognosis depends on stage