An undergraduate lecture on Congenital Anomalies, Inflammatory & Neoplastic Disorders of Esophagus for medical students delivered by Dr Muhammad Omair Riaz

1. Congenital Anomalies, Inflammatory
& Neoplastic Disorders of Esophagus
Dr Muhammad Omair Riaz

2. Esophagus - Pathology
 Congenital anomalies
 Inflammatory disorders
 Neoplastic disorders

3. Esophagus – Congenital Anomalies
 Tracheoesophageal fistula
 Esophageal atresia

7. Esophagus – Congenital Anomalies
Effects
 Either form of fistula can lead to aspiration,
suffocation, pneumonia, and severe fluid and
electrolyte imbalances.
 Developmental abnormalities of the esophagus are
associated with congenital heart defects,
genitourinary malformations, and neurologic disease.

8. Esophagus – Inflammatory disorders
 Lacerations
 Chemical and Infectious Esophagitis
 Reflux Esophagitis
 Eosinophilic Esophagitis
 Esophageal Varices
 Barrett Esophagus

9. Lacerations
 Longitudinal mucosal tears near the
gastroesophageal junction are termed Mallory-
Weiss tears
 Most often associated with severe retching or
vomiting secondary to acute alcohol intoxication.

10. Lacerations
 Mechanism
 Normally, a reflex relaxation of the gastroesophageal
musculature precedes the antiperistaltic contractile
wave associated with vomiting. It is speculated that
this relaxation fails during prolonged vomiting, with
the result that refluxing gastric contents overwhelm
the gastric inlet and cause the esophageal wall to
stretch and tear.
 These tears usually cross the gastroesophageal
junction and may also be located in the proximal
gastric mucosa.

12. Chemical and Infectious Esophagitis
 Stratified squamous mucosa of the esophagus may
be damaged by a variety of irritants including
alcohol, corrosive acids or alkalis, excessively hot
fluids, and heavy smoking.
 Symptoms range from self-limited pain, particularly
on swallowing, that is, odynophagia, to hemorrhage,
stricture, or perforation in severe cases

13. Chemical and Infectious Esophagitis
 Esophageal infections in otherwise healthy
individuals are uncommon
 Most often due to herpes simplex virus.
 Infections in patients who are debilitated or
immunosuppressed, as a result of disease or
therapy, is more common and can be caused by
herpes simplex virus, cytomegalovirus (CMV), or
fungal organisms. Among fungi, candidiasis is most
common, although mucormycosis and aspergillosis
are also seen.

16. Reflux Esophagitis
 The stratified squamous epithelium of the esophagus
is resistant to abrasion from foods but is sensitive to
acid.
 Submucosal glands, which are most abundant in the
proximal and distal esophagus, contribute to
mucosal protection by secreting mucin and
bicarbonate.
 The tone of the lower esophageal sphincter prevents
reflux of acidic gastric contents, which are under
positive pressure and would otherwise enter the
esophagus.
 Reflux of gastric contents into the lower
esophagus is the most frequent cause of

18. Esophageal Varices
 Venous blood from the GI tract passes through the
liver, via the portal vein, before returning to the heart.
 This circulatory pattern is responsible for the first-
pass effect in which drugs and other materials
absorbed in the intestines are processed by the liver
before entering the systemic circulation.
 Diseases that impede this flow cause portal
hypertension and can lead to the development of
esophageal varices

19. Pathogenesis
 Portal hypertension results in the development
of collateral channels at sites where the portal
and caval systems communicate.
 These collateral veins allow some drainage to occur,
but at the same time they lead to development of
congested subepithelial and submucosal venous
plexi within the distal esophagus and proximal
stomach.
 These vessels, termed varices, develop in the vast
majority of cirrhotic patients, most commonly in
association with alcoholic liver disease

20. Morphology
 Varices are tortuous dilated veins lying primarily within
the submucosa of the distal esophagus and proximal
stomach. Venous channels directly beneath the
esophageal epithelium may also become massively
dilated.
 Varices may not be grossly obvious in surgical or
postmortem specimens, because they collapse in the
absence of blood flow and are obscured by the overlying
mucosa.
 Variceal rupture results in hemorrhage into the lumen or
the esophageal wall, in which case the overlying mucosa
appears ulcerated and necrotic. If rupture has occurred in
the past, venous thrombosis, inflammation, and evidence
of prior therapy may also be present.

21. Clinical Features
 Gastroesophageal varices are present in nearly half
of the patients with cirrhosis, and 25-40% of patients
with cirrhosis develop variceal bleeding.
 Approximately 12% of previously asymptomatic
varices bleed each year.
 Variceal hemorrhage is an emergency.

23. Barret Esophagus
 A complication of chronic GERD that is
characterized by intestinal metaplasia within the
esophageal squamous mucosa.
 The incidence of Barrett esophagus is rising, and it is
estimated to occur in as many as 10% of individuals
with symptomatic GERD.
 Barrett esophagus is most common in white males
and typically presents between 40 and 60 years of
age.
 The greatest concern in Barrett esophagus is that it
confers an increased risk of esophageal
adenocarcinoma.

24. Morphology
 Diagnosis of Barrett esophagus requires endoscopic
evidence of metaplastic columnar mucosa above the
gastroesophageal junction.
 Microscopically, intestinal-type metaplasia is seen as
replacement of the squamous esophageal epithelium
with goblet cells.
 These are diagnostic of Barrett esophagus

27. Esophagus - Neoplastic disorders
 Esophageal Tumors
 Adenocarcinoma
 Squamous Cell Carcinoma

28. Esophagus - Neoplastic disorders
 The vast majority of esophageal cancers fall into one
of two types
 Adenocarcinoma
 Squamous cell carcinoma.

29. Esophagus - Adenocarcinoma
 Most esophageal adenocarcinomas arise from
Barrett esophagus.
 Increased rates of esophageal adenocarcinoma may
be partly due to the increased incidence of obesity-
related gastroesophageal reflux and Barrett
esophagus.
 Additional risk factors include tobacco use and
exposure to radiation.
 Conversely, risk is reduced by diets rich in fresh
fruits and vegetables. Some serotypes of
Helicobacter pylori are associated with decreased
risk of esophageal

30. Esophagus – Adenocarcinoma
Morphology
 Esophageal adenocarcinoma usually occurs in the
distal third of the esophagus and may invade the
adjacent gastric cardia.
 Initially appearing as flat or raised patches in
otherwise intact mucosa, large masses of 5 cm or
more in diameter may develop.
 Alternatively, tumors may infiltrate diffusely or
ulcerate and invade deeply. Microscopically, Barrett
esophagus is frequently present adjacent to the
tumor. Tumors most commonly produce mucin and
form glands often with intestinal-type morphology;

32. Esophagus – Squamous Cell Carcinoma
 Esophageal squamous cell carcinoma occurs in adults
older than age 45 and affects males four times more
frequently than females.
 Risk factors include alcohol and tobacco use, poverty,
caustic esophageal injury, achalasia, tylosis, Plummer-
Vinson syndrome, diets that are deficient in fruits or
vegetables, and frequent consumption of very hot
beverages.
 Previous radiation to the mediastinum also predisposes
individuals to esophageal carcinoma
 Esophageal squamous cell carcinoma is nearly eight-fold
more common in African Americans than Caucasians

33. Esophagus – Squamous Cell Carcinoma
Morphology
 Polypoid, or exophytic tumors, protrude into and
obstruct the lumen.
 Maybe either ulcerated or diffusely infiltrative lesions
that spread within the esophageal wall and cause
thickening, rigidity, and luminal narrowing.
 They may invade surrounding structures including
the respiratory tree, causing pneumonia; the aorta,
causing catastrophic exsanguination; or the
mediastinum and pericardium.
 Most squamous cell carcinomas are moderately to
welldifferentiated

35. THANK YOU
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