Oesphageal Problems

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From its origin at the cricoid cartilage to its termination at the oesophagogastric junction,
the oesophagus is normally lined by stratified non-keratinizing squamous epithelium.
The oesophageal wall contains both striated muscle (in its upper portion) and smooth muscle
(in the lower portion).
A competent lower oesophageal sphincter is essential to prevent the reflux of
gastric contents back into the oesophagus.
Reflux oesophagitis is the most common abnormality of the oesophagus encountered by the family practitioner.
Reflux of gastric acid into the lower oesophagus produces a burning pain in the centre of the
lower chest or hypochondrium, commonly known as heartburn. Predisposing factors to acid reflux
include those that increase intra-abdominal pressure, e.g. over-eating, pregnancy, and poor
posture; and those that render the lower oesophageal sphincter lax or incompetent, e.g. hiatus hernia,
smoking, and alcohol ingestion.

The normal squamous epithelium of the lower oesophagus is sensitive to the effects of the
acid and is frequently damaged.
Several complications may arise:
Reflux oesophagitis. The oesophageal mucosa becomes acutely inflamed.
Peptic ulceration of lower oesophagus. Small ulcers usually develop, which become chronic, with fibrosis.
Lower oesophageal stricture. Chronic peptic ulceration causes progressive fibrous thickening of the
lower oesophagus wall. The resultant narrowing causes difficulty in swallowing.
Barrett's oesophagus. Persistent oesophageal reflux causes metaplasia
of the lower oesophageal mucosa, the squamous epithelium being replaced by glandular epithelium
composed of tall columnar cells

This is also termed columnar epithelial-lined oesophagus (CELO).

Barrett's oesophagus

Barrett's oesophagus predisposes to the development of adenocarcinoma
Barrett's oesophagus can progress from metaplastic glandular epithelium to epithelial
dysplasia (with nuclear pleomorphism and hyperchromicity), and then to frank adenocarcinoma.
Patients with Barrett's oesophagus are kept under surveillance through repeated endoscopy
and biopsy to detect early neoplastic changes.
Treatment by oesophageal surgery is then possible before development of invasion.

The lower oesophageal mucosa is replaced by darker columnar epithelium, with an area of ulceration
at the oesophagogastric junction. The arrow marks the abnormally high squamocolumnar junction.

Any oesophageal obstruction causes difficulty In swallowing, known as dysphagia
Four main types of lesion cause obstruction:
Lesions in the lumen. Swallowed foreign bodies.
Lesions in the wall. Neoplasm or carcinoma of the oesophagus, fibrosis caused by chronic inflammation.
Lesions outside the wall.
Lesions affecting function. Achalasia, motor neuron disease
Oesophageal obstruction may be complicated by reflux of food into the airways, resulting in
aspiration pneumonia, and by malnutrition due to the inability to maintain adequate intake.


Achalasia of the oesophagus is due to abnormal innervation

In achalasia, lack of co-ordinated muscle contraction and relaxation at the lower end
of the oesophagus leads to retention of the food bolus, the result of peristaltic spasms
combined with sluggish relaxation at the oesophagogastric sphincter. The condition
is mainly seen in middle age.
Over a period of time the oesophagus becomes markedly dilated (megaoesophagus).
Its cause is unknown, but reduced numbers of ganglion cells in the muscle plexus have been
noted in long-standing cases. This condition also predisposes to development of carcinoma of the oesophagus.
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