increasing problem of swallowing food

[bharat]

A 49 year old female presents with increasing problwm of swallowing food( prograsive disphagia). X-ray studies with contrast revel that she has markedly dilated esophagus above the leval of lower esphageal spincture(LES). No Leisons are seen with in the lumen of esophagus.
The patient's symptoms are more likely caused by:-
a. Decreased LES resting pressure
b. Absence of myenteric plexus in the body of esophagus
c. Absence of myenteric plexus at the LES
d. Absence of submucosal plexus on the body of esophagus
e. Absence of submucoasl plexus at LES

[Oak]

bhara i would go for b I think its a case of Achalasia Cardia

The exact etiology of achalasia is not known. The most widely accepted current theories implicate autoimmune disorders, infectious diseases, or both. The last decade has witnessed much progress in the understanding of the cellular and molecular derangements in achalasia.

Degeneration of the esophageal myenteric plexus of Auerbach is the primary histologic finding. However, with early achalasia, a mixed inflammatory infiltrate of T cells, mast cells, and eosinophils is found in association with myenteric neural fibrosis and with a selective loss of inhibitory postganglionic neurons from the Auerbach plexus. In these patients with early achalasia, neurons of the myenteric plexus are relatively well preserved.

The inhibitory neurons produce nitric oxide (NO) and vasoactive intestinal peptide (VIP). NO and VIP are inhibitory neurotransmitters responsible for relaxation of the LES and for coordinated esophageal peristalsis. The loss of inhibitory neurons allows unopposed excitatory stimulation by postganglionic cholinergic neurons of the Auerbach plexus, which leads to a failure in LES relaxation and, eventually, to aperistalsis of the distal esophagus due to loss of the esophageal body latency gradient.

Essentially, this means that this portion of the esophagus is unable to relax and subsequently generate a proper, sequential peristaltic wave.

Clinically important features defined by this pathophysiology include the following:

• Peristalsis in the distal smooth muscle segment of the esophagus may be lost. Contractions occur, but they are weak; simultaneous; uncoordinated; and, therefore, nonpropulsive.
• The LES fails to relax, either partially or completely.
• LES pressure is elevated in some patients.
• The coordination of LES relaxation in response to swallowing and esophageal contraction is lost.

[bharat]

ya. Bro. u are correct answer is b.
Achalaisa -which can be also described as absence of normal LES relaxation, which may result from decreased or absent ganglionic cells in myenteric plexus of the body of the esophagus. The etiology of neuronal loss is unknown like u said in u're answer;
however ,some cases are secondary to other disease such as diabetes mellitus, amyloidosis, Sarcoidosis, and Chagas' Disease.
Becuse of increased LES pressure and absence of peristaltic waves in the lower esophagus, esophagus of these patients are dilated and tortuous above the leval of LES.