Sandbox:Madhu: Difference between revisions
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=== Pathogenesis === | === Pathogenesis === | ||
* The exact pathogenesis of DES is not fully understood. However, current high-resolution manometric studies suggest impairment of inhibitory myenteric plexus neuron. These neurons use nitric oxide (NO) as neurotransmitter. Hence, these patients may also have dysregulation of endogenous NO synthesis or/and degradation. The final result being premature and rapidly propagated or simultaneous contraction of smooth muscles of distal esophagus. | * The exact pathogenesis of DES is not fully understood. However, current high-resolution manometric studies suggest impairment of inhibitory myenteric plexus neuron. These neurons use nitric oxide (NO) as neurotransmitter. Hence, these patients may also have dysregulation of endogenous NO synthesis or/and degradation. The final result being premature and rapidly propagated or simultaneous contraction of smooth muscles of distal esophagus. | ||
Revision as of 18:27, 28 October 2017
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Madhu Sigdel
Classification of DES
- There is no established system for the classification of DES although it is categorized as one of the major disorders of Peristalsis according to The Chicago Classification v.3.0
Risk Factors
- Common risk factors in the development of Diffuse Esophageal Spasm include Age (60-80 years), presence of GERD, Hypertension, anxiety or depression, and drinks (eg. red wine, very hot or cold liquid or fluid).
Pathophysiology
Pathogenesis
- The exact pathogenesis of DES is not fully understood. However, current high-resolution manometric studies suggest impairment of inhibitory myenteric plexus neuron. These neurons use nitric oxide (NO) as neurotransmitter. Hence, these patients may also have dysregulation of endogenous NO synthesis or/and degradation. The final result being premature and rapidly propagated or simultaneous contraction of smooth muscles of distal esophagus.