PATHOPHYSIOLOGY
This inhibitory neurotransmitter is deficient due to loss of ganglion cells in the myenteric (Auerbach's) plexus of the distal esophagus and LES.
NITRIC OXIDE
Barium esophagogram finding in achalasia
dilated esophagus tapering to a smooth, narrow point at the GE junction (bird beak)
During laparoscopic Heller myotomy, this nerve, running along the anterior esophagus, must be identified and preserved to protect gastric motility.
Left/anterior vagus nerve
This validated symptom score, incorporating dysphagia, regurgitation, chest pain, and weight loss, is used to grade achalasia severity and treatment response.
Eckardt score
Achalasia Patient-Reported Outcomes (APRO) scale, the Achalasia Quality of Life (ASQ) questionnaire, CARS score
On high-resolution manometry, this value — residual LES pressure during swallow-induced relaxation — must be elevated to diagnose achalasia.
Integrated relaxation pressure (IRP)?
This type of myenteric plexus neuron, which normally relaxes the LES, is selectively destroyed in achalasia.
inhibitory neurons
This procedure is mandatory before diagnosing achalasia, to exclude tumor causing pseudoachalasia.
Endoscopy (EGD) with retroflexion at the cardia
In a patient with achalasia and a prior failed Heller myotomy, this salvage option can be used.
pneumatic dilatation
This intraoperative complication of Heller myotomy, requires intra-op identification and management
Esophageal/gastric mucosal perforation
This Chicago Classification subtype shows minimal esophageal pressurization with 100% failed peristalsis and elevated IRP.
Type 1 (classic achalasia)
This achalasia mimicker should be ruled out in patients over 60 with rapid weight loss and short symptom duration.
Pseudoachalasia
This catheter-based functional test measures cross-sectional area and distensibility of the EG junction using impedance planimetry, and is increasingly used when manometry is equivocal or unobtainable.
FLIP (functional lumen imaging probe / EndoFLIP)
This partial fundoplication is most commonly paired with Heller myotomy.
Dor fundoplication
This is the most common complication after endoscopic treatment of achalasia
Gastroesophageal reflux disease
This Chicago Classification diagnosis shares achalasia's elevated IRP but, unlike achalasia, retains some preserved or weak peristalsis; its natural history is debated, as some cases evolve into true achalasia.
Esophagogastric junction outflow obstruction (EGJOO)
This parasite, responsible for Chagas disease, can cause a secondary achalasia identical in presentation to the idiopathic form.
Trypanosoma cruzi
This imaging modality can help unmask pseudoachalasia by showing a mass or wall thickening at the GE junction not apparent on endoscopy.
EUS
These two oral medication classes are used for medical treatment for achalasia.
nitrates and calcium channel blockers
This endoscopic modality is used for treating esophageal motility disorder involving long segment of esophagus.
POEM
This subtype features premature/spastic contractions and carries the worst outcomes with Heller myotomy alone.
Type III (spastic achalasia)
This virus has been proposed, alongside an autoimmune mechanism, as a possible inciting trigger for destruction of myenteric neurons in idiopathic achalasia.
Herpes simplex virus
On timed barium esophagram, this measurement taken 5 minutes after the contrast swallow objectively assesses esophageal emptying and treatment response.
height of the retained barium column at 5 minutes
In a patient with end stage achalasia, with sigmoid esophagus, this is the definitive salvage operation despite its higher morbidity and mortality.
Esophagectomy (with gastric or colonic interposition)
A missed or incomplete myotomy — failing to extend adequately onto this structure — is a common cause of persistent dysphagia after Heller myotomy.
gastric cardia (myotomy should extend 2–3 cm onto the stomach)
This subtype shows panesophageal pressurization in at least 20% of swallows and has the best response to treatment.
Type II achalasia