Week 1: Pathology of Esophagus Flashcards
1
Q
Hiatal Hernia
A
- 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
2
Q
Tracheoesophageal fistula
A
- 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
3
Q
Esophageal diverticuli
A
- 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.
4
Q
Esophageal varices
A
- 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
5
Q
Plummer-Vinson Syndrome
A
- 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
6
Q
Gastroesophageal Reflux disease (GERD): gross and histological features
A
- 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
7
Q
Complications of GERD
A
- 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
8
Q
Infectious esophagitis: Candida albicans
A
- 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.
9
Q
Infectious esophagitis: Herpes simplex virus
A
-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
10
Q
Infectious esophagitis: CMV
A
- 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
11
Q
Other causes of esophagitis
A
- 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
12
Q
Barrett Esophagus
A
- 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.
13
Q
Low grade vs. high grade dysplasia in barrett esophagus
A
- 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.
14
Q
SCC of esophagus: epidemiology and clinical
A
- 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
15
Q
Pathology of SCC of esophagus
A
- 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
