1. Esophagitis
Lecture3

3. Esophagitis
• Inflammation of esophagus (after injury to
esophageal mucosa).
Predisposing factors/Origins/Causes:
• Prolonged gastric intubation,
• Ureamia
• Ingestion of corrosive or Irritant substances
• Radiation
• Chemotherapy

4. Epidemiology
• In Iran (more than80%) and China the prevalence is
extremely high due to unknown reason.
• In Western countries high prevalence is due to
reflux of gastric contents (reflux esophagitis).
• In USA o.5% due to gastro esophageal disease

5. Types/causes of esophagitis
Reflux esophagitis
CHEMICAL AND INFECTIOUS ESOPHAGITIS
EOSINOPHILIC ESOPHAGITIS
Herpes simplex esophagitis
Cytomegalovirus (CMV) esophagitis
Candida esophagitis
Crohn’s disease
Idiopathic eosinophilic esophagitis
Other types of esophagitis include those caused by tuberculosis,
blastomycosis, drugs, allergic reactions, irradiation and ingestion of
corrosive chemicals.

6. 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.

7. GERD
• constant lower esophageal sphincter tone
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 esophagitis .The
associated clinical condition is termed
gastroesophageal reflux disease (GERD).

8. Pathogenesis.
• Reflux of gastric juices is central to the
development of mucosal injury in GERD.
• In severe cases, reflux of bile from the duodenum
may exacerbate the damage.

9. • Conditions that decrease lower esophageal
sphincter tone or increase abdominal
pressure contribute to GERD and include
alcohol and tobacco use, obesity, central
nervous system depressants, pregnancy,
hiatal hernia ,delayed gastric emptying, and
increased gastric volume.
• In many cases, no definitive cause is
identified.

10. Morphology.
•
Simple hyperemia, evident to the endoscopist
as redness, may be the only alteration.
• In mild GERD the mucosal histology is often
unremarkable. t.

11. • With more significant disease,
eosinophilsare recruited into the
squamous mucosa followed by neutrophils,
which are usually associated with more
severe injury.

12. • Basal zone hyperplasia exceeding 20% of the
total epithelial thickness and elongation of
lamina propria papillae, such that they
extend into the upper third of the
epithelium, may also be present.

13. Clinical Features
• GERD is most common in adults over age 40
but also occurs in infants and children. The
most common clinical symptoms are
dysphagia, heartburn, and, less frequently,
noticeable regurgitation of sour-tasting
gastric contents.
• Rarely, chronic GERD is punctuated by
attacks of severe chest pain that may be
mistaken for heart disease.

14. Treatment
• Treatment with proton pump inhibitors or H2
histamine receptor antagonists, which reduce
gastric acidity, typically provides
symptomatic relief.

15. Complications
• esophageal ulceration,
• hematemesis,
• melena,
• stricture development, and
• Barrett esophagus.

16. Barrett’s Esophagus
• Defined as occurrence of a
specialized columnar epithelium
lining a segment of distal
esophagus above the level of
lower esophageal sphincter.

17. MOTOR DISORDERS
• Achalasia
• Hiatal Hernia (sliding [95%],
paraesophageal)
• “ZENKER” diverticulum (pharyngoesophageal diverticulum)
• Esophagophrenic diverticulum
• Mallory-Weiss tear

18. Hiatal hernia
• is characterized by separation of the
diaphragmatic crura and protrusion of the
stomach into the thorax through the resulting gap.
Congenital hiatal hernias are recognized in infants
and children, but many are acquired in later life.
Hiatal hernia is symptomatic in fewer than 10% of
adults, and these cases are generally associated
with other causes of LES incompetence.
Symptoms, including heartburn and regurgitation
of gastric juices, are similar to GERD.

19. ACHALASIA
• Increased tone of the lower esophageal
sphincter (LES), as a result of impaired
smooth muscle relaxation, is an important
cause of esophageal obstruction. Achalasia is
characterized by the triad of incomplete LES
relaxation, increased LES tone, and
aperistalsis of the esophagus.

20. Mallory-Weiss tears
• Longitudinal tears in the esophagus near the
gastroesophageal junction are termed
Mallory-Weiss tears, and are most often
associated with severe retching or vomiting
secondary to acute alcohol intoxication.

21. Esophagus
• Normal Anatomy
– Muscular tube, 25 cm in
length in adults.
– Extending from the upper
esophageal sphincter at 15-
18 cm from the incisors to
lower esophageal sphincter
at 40 cm (variable).

22. • Histology
– Lined by stratified
squamous non-keratinized
epithelium.
– Basal layer 4 cell thick; not
more than 15% of total
epithelial thickness.
Melanocytes &
neuroendocrine cells
maybe found.

23. ESOPHAGUS
– Lamina propria: Loose connective tissue, mucous glands in
distal portion (cardiac glands)
– Muscularis Mucosae: Thicker than other parts of GI tract.
– Submucosa: Submucosal glands.
– Muscularis propria: Admixture of striated & smooth muscle in
the upper quarter, only smooth muscle in the rest of the organ.
– No serosal layer, except for the most distal portion.
– Autonomic nervous system: Meissner’s plexus in submucosa
(sparse); Auerbach (Myenteric) plexus in muscularis propria
(denser in the distal portion).
– Lymphatics: Upper third drains into the cervical nodes, the
middle third into the paraesophageal and paratracheal nodes,
and lower third into nodes around aorta and celiac axis.