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However, if achalasia is not treated at all, the esophagus will expand more and more (the so-called dilation, this is already a disease, not a procedure) - up to the so-called megaesophagus with a complete loss of esophageal function. In addition, in the late stage (due to typical belching), complications with the lungs or inflammation of the esophagus (due to food remaining in the esophagus for a long time) can occur, which in turn can lead to ulcers or bleeding.

Another advantage of the operation compared to endoscopic procedures is its long-term effect, up to 10 years.

Achalasia is usually associated with an increased risk of developing cancer: about 4-6 percent of patients develop cancer of the esophagus (esophageal carcinoma) many years later.

Thus, the risk of developing esophageal cancer with achalasia is about 30 times higher. Therefore, regular endoscopic examinations are important in follow-up care.
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Prevention and recommendations. You cannot prevent achalasia because the exact cause of esophageal dysfunction is unknown. However, if you are one of those affected, you can reduce your risk of some common comorbidities (such as esophagitis) by avoiding alcohol and nicotine, for example.

In addition, in the case of achalasia, regular endoscopic examination of the esophagus for follow-up is recommended to detect possible late complications (especially esophageal cancer) at an early stage. General practitioner, gastroenterologist, hepatologist, infectious disease specialist. I carry out preventive measures for complications from the digestive system after long-term therapy with NSAIDs and blood-thinning drugs.

Achalasia cardia is a disease of the esophagus, in which the opening of the lower esophageal sphincter is disrupted, and peristaltic contractions are replaced by non-propulsive ones. Depending on the changes in the esophagus, two types of lisinopril pills are distinguished. With classic achalasia of the cardia, low-amplitude contractions of the esophagus are noted, with tonic - high-amplitude repetitive contractions, as in esophagospasm.

The disease is based on the absence or death of intramural neurons in the body of the esophagus and the lower esophageal sphincter. First of all, inhibitory neurons containing VIP and NO-synthase suffer. In the United States, the majority of patients with achalasia of the cardia is primary.


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The causes of secondary achalasia of the cardia can be gastric cancer growing into the esophagus, lymphomas and lymphogranulomatosis, Chagas disease, chronic intestinal pseudo-obstruction. An isolated increase in the tone of the lower esophageal sphincter can be considered as a variant of achalasia of the cardia.

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The disease occurs in both men and women at any age. The main symptoms are dysphagia, chest pain, and regurgitation. Dysphagia appears in the early stages of the disease, is noted when taking both solid and liquid food, and is aggravated by emotional overload and eating hastily. Pushing the food bolus into the stomach is facilitated by various techniques aimed at increasing intraesophageal pressure, including the Valsalva test.

 With tonic achalasia of the cardia, chest pain is more pronounced than with classical achalasia. The retention of large amounts of food and saliva in the esophagus leads to regurgitation and aspiration. The presence of gastroesophageal reflux is evidence against achalasia of the cardia.

The pressure in the esophagus outside the act of swallowing is increased. When swallowing, instead of peristalsis, simultaneous contractions are recorded. With classical achalasia of the cardia, the amplitude of contractions is reduced, with tonic - contractions are high-amplitude and long. The introduction of the M-cholinostimulator methacholine leads to a significant increase in basal pressure in the esophagus, chest pain and regurgitation of the contents of the esophagus (test with methacholine).

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There are no peristaltic contractions in the lower two-thirds of the esophagus. With tonic achalasia of the cardia, high-amplitude non-propulsive contractions are possible. With esophageal manometry, basal pressure in the area of lisinopril esophageal sphincter is normal or increased. Relaxation of the sphincter during swallowing does not occur, or it is short-lived or not sufficiently pronounced.

An X-ray examination with a barium suspension reveals an expansion, and in the later stages of the disease, an S-shaped deformity of the esophagus. The distal coracoid is narrowed due to the closed lower esophageal sphincter.