Non-neoplastic Diseases of the Esophagus
Non-neoplastic Diseases of the Esophagus
Normal esophagus
Squamous esophagus
Glandular stomach
Normal esophageal squamous mucosa
Normal GE
junction;
squamous
mucosa on the
right, and gastric
cardiac glandular
mucosa on the
left
Symptoms of Esophageal Disorders
Dysphagia: difficulty swallowing
Odynophagia: pain upon swallowing
Heartburn: retrosternal burning pain
Hematemesis: vomiting of blood
Melena: blood in stools
May be of upper GI origin
Anatomic Disorders
Hiatal hernia
Stenosis: narrowing
Usually secondary to reflux
Progressive intolerance to solid and then all foods
Atresia: absence of lumen
Usually newborns with aspiration, pneumonia, and feeding
problems; often occurs with fistula
Fistula: abnormal connection to another organ
Webs: partially occluding abnormal membrane
Hiatal Hernias
Caused by widening of space between esophagus and diaphragm
Portion of stomach protrudes above diaphragm
1-20% of adults
Significant because they may contribute to reflux
Sliding
95% of cases
Rolling or Paraesophageal
Motor DisordersAchalasia
Failure of the lower esophageal sphincter to relax following
swallowing
Functional obstruction
Dilation of upper esophagus
Primary vs. secondary
Dysphagia, nocturnal regurgitation, aspiration
Increased risk of squamous cell carcinoma
Disorder of innervation, not muscle
May have absent myenteric plexi
Esophageal AtresiaTracheo-esophageal Fistula
esophagus
stomach
trachea
Vascular Disorders: Mallory -Weiss Tears
Longitudinal tears at the G-E junction
Inadequate relaxation of muscles of LES following retching
Usually in chronic alcoholics
May be superficial or transmural
Infection
Upper GI bleeding or massive hemorrhage
Vascular Disorders: Varices
Collateral bypass channels where the portal and systemic
circulation communicate
Dilated tortuous veins in the submucosa
In 2/3 of all cirrhotic patients
Asymptomatic until rupture, when massive bleeding occurs
40% mortality, most survivors rebleed within one year
Esophagitis
Reflux
Uremia
Corrosives/irritants
Radiation/Chemotherapy
Infection
Viral
Fungal
Bacterial
Herpetic
Esophagitis
note marked
ulceration
and
hemorrhage
Herpetic
Esophagitis
Herpetic
Inclusions
Reflux Esophagitis
10-20% percent of adults in Western countries
Children and adults
Heartburn, regurgitation, chest pain
Severity of symptoms does not correlate with anatomic
findings
Sequelae
Bleeding, stricture, Barretts esophagus
Pathogenesis (usually multifactorial)
Incompetent LES, hiatal hernia, increased gastric volume
Reflux esophagitis
Gross
Mucosal redness
Erosions and/or ulceration
Microscopic
Elongation of papillae
Basal layer hyperplasia
Eosinophils +/- other inflammatory cells
Linear erosions
Typical of reflux
esophagitis
Reflux esophagitis. Note rete peg elongation and basal
layer hyperplasia.
Eosinophils in reflux
esophagitis
Esophageal
Stenosis
Markedly narrowed lumen
Barretts Esophagus
Probable complication of longstanding reflux (up to 11% reflux
patients)
Replacement of normal distal stratified squamous mucosal by
intestinal-type glandular mucosa
Possible pathogenesis
Reflux induces inflammation and mucosal injury
Healing occurs by ingrowth of stem cells and
re-epithelialization
Cells differentiate into abnormal intestinal mucosa that may be
more injury-resistant
Barretts esophagus-pathology
Irregular band of dark pink, velvety mucosa extending upward as
tongues of mucosa
May be very patchy or focal
Histology
Metaplastic columnar epithelium with goblet cells
Barretts esophagus
Normal white
Squamous
mucosa
Pink abnormal
Glandular
mucosa
Barretts esophagus
Note goblet cell metaplasia
Barretts esophagus-sequelae
Ulceration
Bleeding
Stricture
Adenocarcinoma
Dysplasia/Carcinoma Sequence
Barretts
Dysplasia
Carcinoma
Barretts esophagus with dysplasia. Note lack of mucin, nuclear
hyperchromasia,, and variation in size and shape.
High power
view of dysplasia in Barretts esophagus.. Note
nuclear variation, prominent nucleoli, and increased
mitoses.
Squamous mucosa
Carcinoma arising in Barretts
esophagus
