Friday, May 20, 2016

Pathophysiology of achalasia mnemonic


This post is about the pathophysiology of achalasia!

In achalasia, there is loss of NO and VIP releasing inhibitory neurons. Thus, the loss of the inhibitory innervation in achalasia results in the manometric consequence of failure of LES relaxation as well as loss of esophageal peristalsis.

Mnemonic: In achalasia, the LES allows NO entry of VIP food particles :D

Anticholinergic medications decrease the LES pressure, while cholinergic medications increase it confirming that the cholinergic neurons in achalasia are preserved. This is the same mechanism through which botulinum toxin reduces the LES pressure and is shown to be efficacious in treating achalasia.

Revision: Botulinum toxin is a protease that cleaves the SNARE protein to prevent fusion and release of Ach containing vesicles.

CCK test: CCK has a dual effect on the lower esophageal sphincter (LES): it stimulates smooth muscle contraction and the release of inhibitory neurotransmitters. Administration of CCK normally causes the LES pressure to fall because the effect on inhibitory neurotransmitters is greater. In patients with achalasia, CCK causes the lower esophageal sphincter pressure to rise. (Confirming the loss of inhibitory neurons theory!)

That's all!

Related post: Achalasia surgery mnemonic

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