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PH-GI22

Oesophagitis beyond reflux

How causes other than acid reflux inflame the oesophagus: an allergic type 2 response in eosinophilic oesophagitis, Candida and herpesviruses when immunity is weak, tablets that lodge, swallowed caustics and radiation.

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  • 5 steps · 10 questions
  • 3D normal anatomy

By the end, you can

  • Describe the defences of the oesophageal lining (squamous epithelium, saliva, peristalsis and cellular immunity) that each form of oesophagitis overcomes.
  • Explain how a type 2 immune response to food antigens causes eosinophilic oesophagitis and its rings, furrows and narrowing.
  • Explain why Candida, herpes simplex virus and cytomegalovirus infect the oesophagus mainly when immunity is weak, and how their lesions differ.
  • Explain how tablets, caustic substances and radiation injure the lining, and why alkali burns penetrate deeper than acid burns.
  • Tell these forms apart from reflux oesophagitis by site, endoscopy and biopsy, and explain how each main treatment acts on its mechanism.

What it is

Oesophagitis is inflammation of the lining of the oesophagus. Reflux of gastric acid is the commonest cause and has its own lesson; this one covers the others: eosinophilic oesophagitis, a chronic allergic (type 2) immune disease; infective oesophagitis from Candida, herpes simplex virus or cytomegalovirus; pill-induced injury from tablets that lodge; caustic (corrosive) injury from swallowed acids or alkalis; and radiation oesophagitis. Most cause painful swallowing (odynophagia) or difficulty swallowing (dysphagia), and endoscopy with biopsy usually tells them apart.

5 types to tell apart
Eosinophilic oesophagitis
A chronic, mostly non-IgE type 2 immune response to food antigens fills the whole length of the oesophageal epithelium with eosinophils; fibrosis narrows the lumen.
Infective oesophagitis
Candida, herpes simplex virus and cytomegalovirus, mainly when cellular immunity, saliva or motility fail: plaques, small punched-out ulcers or large deep ulcers.
Pill-induced oesophagitis
A tablet that sticks at a narrowing dissolves against the lining and releases a concentrated irritant, leaving a discrete ulcer.
Caustic injury
Swallowed alkalis cause deep liquefactive necrosis, acids coagulative necrosis with an eschar; severe burns can perforate and later scar into long strictures.
Radiation oesophagitis
Chest radiotherapy kills the dividing basal cells, so the lining thins and ulcerates within weeks; damage to small vessels and fibrosis can cause a stricture much later.

US spelling: oesophagitis → esophagitis, oesophagus → esophagus, oesophageal → esophageal.

Normal function

A squamous tube with layered defences

The runs from the pharynx behind the , through the posterior mediastinum and the to the stomach. It is not uniformly wide: it is narrowed at its upper sphincter, where the and cross it, and at the lower sphincter, and it lies directly behind the . These are the places where swallowed objects and tablets tend to stick.

It is lined by non-keratinised stratified squamous epithelium, renewed from its basal layer. Its defences come in layers: swallowed saliva and the secretions of submucosal glands wash and buffer the surface; tight junctions between the squamous cells keep irritants out; peristalsis clears anything swallowed or refluxed within seconds; and the blood supply removes acid that does get in and feeds repair. Cellular immunity, particularly T cells, keeps Candida and latent herpesviruses in check. Unlike the stomach and intestine, the healthy oesophageal epithelium contains almost no eosinophils.

Reflux oesophagitis, taught in its own lesson, injures the lower oesophagus with acid and pepsin when the barrier at the gastro-oesophageal junction fails. The forms in this lesson break other defences: the epithelial barrier and immune tolerance (eosinophilic oesophagitis), cellular immunity (infection), clearance past the narrowings (tablets), or the tissue itself (caustics and radiation).

Point to it on the model