Esophageal achalasia

Esophageal achalasia is a motor state in which to relax the esophageal sphincter does not properly reduced. As a result of a functional obstruction (eg, obstruction by abnormal function in the absence of the visible mass or lesion), a list to swallow as the expression of dysphagia (inability), regurgitation and chest pain.

It is a progressive disease that develops through the heavy distortion of radiology of the esophagus. The underlying cause of achalasia of the esophagus, which occurswith an incidence of 0.5-1.0 per 100,000 population per year, is unknown. Degeneration of the myenteric plexus and loss of inhibitory neurons that extend the release of VIP and nitric oxide, reduced esophageal sphincter, could help.

Esophageal involvement in Chagas' disease, which carries out damage from the neural plexuses of the esophagus by the parasite Trypanosoma cruzi, a striking similarity with esophageal achalasia. A lot of other diseases, includingMalignancies could, with support pressure or radiological features, functions similar to this observed in idiopathic achalasia of the esophagus.

Although achalasia is manifested as an engine state of the smooth muscle of the esophagus, it is actually due to defective innervation of the smooth muscle of the esophagus in body composition and reduced esophageal sphincter. Lower esophageal sphincter tone is usually by tonic contraction with intermittent Relaxation is characterizeda neural reflex arc.

In achalasia, there is much more contracted fixed and can not relax properly in response to swallow because of partial loss of nerve cells in the wall of the esophagus. Therefore, achalasia, a condition that has to be thought by defective inhibitory webs of the esophagus, enteric nervous system triggered program. Interestingly takes injections of botulinum toxin, the reduced the excitatory esophageal webs and thereby improveSymptoms.

In addition to dysfunction of the lower esophageal sphincter, reduction of regular peristalsis in the esophageal body is often seen in achalasia, consistent with the hypothesis of the myenteric plexus degeneration. Variations of achalasia exist replaced by the regular peristalsis by simultaneous contraction of the large or small amplitude.

Over many months and years, the lower esophageal sphincter dysfunction results in an enormous expansion of theEsophagus. Normally intended as a direct connection to the stomach, the esophagus in advanced cases of achalasia hold as much as 1 L putrid, infected material, creating a high aspiration pneumonia.

Without treatment, patients display progressive extreme weight loss with worsening chest discomfort, mucosal ulcers, infection, rupture of the esophagus and, occasionally, culminating in death.

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