How do you assess esophageal motility?
What is achalasia?
What is the upper esophageal sphincter?
• (UES) The major elements of the analysis of upper esophageal sphincter are:
○ Degree of UES relaxation
§ Measured by the nadir UES pressure
○ Magnitude of the intrabolus pressure
§ As a measure of the resistance to flow across the UES
○ Presence or absence of pharyngeal peristalsis
How do you assess the function of the lower esophageal sphincter?
• Analysis of LES function involves determination of its location, basal pressure and degree of relaxation
How do you assess esophageal body motor function?
What are the esophageal manometry findings that establish the dx of achalasia?
• Incomplete relaxation of the LES aperistalsis in the smooth muscle esophagus
Why does scleroderma mess up GI motility?
• Multi-system disorder predominantly associated with skin and GI tract involvement
• Associated with alterations of the microvasculature, the autonomic nervous system and the immune system with a downstream consequence of fibrosis
• Initially small vessel vasculitis that leads to vascular derangement and resultant smooth muscle atrophy and finally fibrosis
• Enventually the entire smooth muscle section of GI tract is susceptible and 90% of patients with scleroderma have GI tract involvement
• In the esphagus - atrophy of the lower 2/3 of esophagus
• Also atrophy and hypotension of the LES
○ GERD and troubles swallowing
○ Eventually GERD creates strictures and makes swallowing even worse
How does esophageal manometry distinguish scleroderma from achalasia?
• Weakened LES in scleroderma vs. a hypertensive LES in achalasia
What is meant by spastic disorders of the esophagus?
What nervous system structures need to be coordinated to create proper gastric motility?
What happens in the proximal stomach when food first enters?
* Receptive relaxation - very little intragastric pressure increase when food first hits the fundus
What’s the major function of the distal stomach?
What mediates receptive relaxation in the proximal stomach?
Describe the peristaltic movements of the stomach
• Interstitial cells of Cajal are peristalsis pacemaker cells
○ Reside in the midportion of the gastric body and travel distally towards the pylorus at a frequency of about 3/min
• Contractions at proximal stomach are weak - mixing contents and secretions
• Waves are stronger in antrum where grinding occurs
• Early stages of antral contraction pylorus is open allowing a little chyme to leak out
• Followed by pyloric closure forcing intragastric contents back into antrum
○ Goal is 1-2mm size of globules
What do the interstitial cells of Cajal do to the stomach?
Can scleroderma affect the stomach too and not just the esophagus?
• Yes, there can be stomach-specific fibrosis of smooth muscle
What neurologic diseases can cause gastroparesis?
How do you make the definitive gastroparesis diagnosis?
time (between stomach and duodenum)
• Can be assessed several ways
• Most common - scintigraphic gastric emptying
○ Technetium labeled eff is eaten as part of a standardized meal and the percentage of radiotracer left in the stomach after 4 hours is measured
• Gastroparesis is described as mild, moderate or severe based on the percentage of meal remaining (over 35% is severe)
• Another way is WMC - wireless motility capsule
○ This simultaneously measures pressure, temp and pH as it goes down
○ Change in pH is the measure of emptying
What is meant by MMC in motility?
• MMC - migrating motor complex
• Normal people - present during states of fasting from birth to death
• One MMC cycle is made up of 3 phases, phase III being most easily recognized
• Phase III of MMC is a band of regular pressure waves lasting for about 5 min that migrates from proximal to distal small bowel
○ Intervals are 85-110min
• This requires enteric nervous system to be intact but the extrinsic nerve supply can be disconnected and it will still work
What happens in the postprandial period?
A patient has a chief complaint of pain, bloating, distension in a recurrent manner. The pain is reported as pretty bad. In the emergency room you note that they are in bad pain and distension. Imaging shows small bowel dilation, but no masses. What is going on?
What tests are performed to confirm CIPO diagnosis?
• Chronic intestinal pseudo-obstruction
• Wireless motility capsule
○ Fall in pH at ileocecal junction
• Manomoetry supports but lacks specificity
○ Myopathic - low amplitude contractions
○ Neuropathic - organization wrong but amplitude is fine
What is the treatment paradigm for CIPO?
• Treating resultant small intestinal bacterial overgrowth
○ SIBO
• Antibiotics and nutritional support
○ Parenteral or enteral
• Prokinetic medications
• Manometry can be prognostic in these conditions
Describe normal colonic motility
What is meant by HAPC in motility?
* These happen 6x/day and push poop to rectum