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DEMS > Motility Disorders > Flashcards

Motility Disorders Flashcards

1
Q

How do you assess esophageal motility?

A
  • Esophageal manometry
    • Currently termed high-resolution esophageal manometry
    • This test is performed using a transnasal, intraluminal manometry catheter containing pressure sensors spaced closely together
    • Once positioned from the nares into the stomach, assessment of esophageal motility is made as patient swallows repeated small boluses of water
    • This eval assesses the esophageal body peristalsis and upper and lower esophageal sphincter function
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2
Q

What is achalasia?

A
  • Prototypcial esophageal motility disorder
    • Results from inflammatory destruction of neurons in the myenteric plexuses of the esophagus
    • Destruction predominantly involves the nitric oxide-producing, inhibitory neurons that affect the relaxation of esophageal smooth muscle and spare the cholinergic neurons that contribute to the lower esophageal sphincter tone
    • Loss of inhibition at the LES leads to the cardinal defect = failure of appropriate LES relaxation after swallowing
    • In the esophageal body, this results in aperistalsis
    • Symptoms result from impairment of LES relaxation and resultant esophagogastric function outflow obstruction
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3
Q

What is the upper esophageal sphincter?

A

• (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

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4
Q

How do you assess the function of the lower esophageal sphincter?

A

• Analysis of LES function involves determination of its location, basal pressure and degree of relaxation

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5
Q

How do you assess esophageal body motor function?

A
  • Esophageal motor function is assessed by the amplitude and propagation of the pressure waves
    • These two parameters can be used to determine the presence and success rate of peristalsis
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6
Q

What are the esophageal manometry findings that establish the dx of achalasia?

A

• Incomplete relaxation of the LES aperistalsis in the smooth muscle esophagus

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7
Q

Why does scleroderma mess up GI motility?

A

• 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

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8
Q

What is meant by spastic disorders of the esophagus?

A
  • Uncoordinated peristalsis for some reason
    • Manometry shows inappropriate pressures for too long or too early
    • Patients report difficulty swallowing because the peristalsis isn’t pushing the bolus down properly
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9
Q

What nervous system structures need to be coordinated to create proper gastric motility?

A
  • Parasympathetic
    • Sympathetic
    • Enteric
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10
Q

What happens in the proximal stomach when food first enters?

A
  • Proximal stomach = cardia, fundus, body

* Receptive relaxation - very little intragastric pressure increase when food first hits the fundus

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11
Q

What’s the major function of the distal stomach?

A
  • Distal - gastric and antrum
    • Controls mechanical and some limited enzymatic digestion
    • Contraction in distal stomach also regulates gastric emptying into duodenum
    • Remember that delivery of chyme to duodenum is not to exceed the rate of small intestine digestion
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12
Q

What mediates receptive relaxation in the proximal stomach?

A
  • This facilitates the food storage role of the stomach
    • Occurs when a peristaltic wave reaches the lower esophageal sphincter and is largely mediated by vagal nerve fibers via stimulation of mechanoreceptors
    • Mechanoreceptors initiate a vaso-vagal reflex with is the basis for the decrease in gastric accommodation post-vagotomy
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13
Q

Describe the peristaltic movements of the stomach

A

• 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

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14
Q

What do the interstitial cells of Cajal do to the stomach?

A
  • Gastric peristalsis originates in the pacemaker cells
    • 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
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15
Q

Can scleroderma affect the stomach too and not just the esophagus?

A

• Yes, there can be stomach-specific fibrosis of smooth muscle

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16
Q

What neurologic diseases can cause gastroparesis?

A
  • Diabetic neuropathy (can affect autonomic nerves too)
    • MS
    • Brainstem stroke (vagal nerve injury)
    • Amyloidosis (vagal nerve injury)
    • AIDS neuropathy (myenteric plexus)
    • Parkinsons (myenteric plexus)
17
Q

How do you make the definitive gastroparesis diagnosis?

time (between stomach and duodenum)

A

• 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

18
Q

What is meant by MMC in motility?

A

• 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

19
Q

What happens in the postprandial period?

A
  • Food intake induces irregular pressure waves in the small bowel shortly after intake
    • After nutrients enter small bowel, transit is at first rapid and chyme is spread along bowel
    • Transit then slows and promotes absorption by increasing contact time
    • Pressure waves propogate short distances after a meal to promote grinding and mixing, not passage
20
Q

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?

A
  • CIPO
    • Chronic intestinal pseudo-obstruction
    • The symptoms and essentially disease state mimic a real obstruction (like by a tumor)
    • The causes are normally neuropathic but can be myopathic as well
    • Neuropathic causes - parkinsons, diabetic neuropathy, a couple inherited conditions (peds cases), paraneoplastic autoimmune neuropathy (various malignancies), Shy-Drager syndrome
    • The main infectious cause is Chagas disease
    • Slceroderma, amyloidosis and esosinophilic gastroenteritis is also a potential cause
21
Q

What tests are performed to confirm CIPO diagnosis?

A

• 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

22
Q

What is the treatment paradigm for CIPO?

A

• Treating resultant small intestinal bacterial overgrowth
○ SIBO
• Antibiotics and nutritional support
○ Parenteral or enteral
• Prokinetic medications
• Manometry can be prognostic in these conditions

23
Q

Describe normal colonic motility

A
  • Main purpose is reabsorption of water
    • Most contractions are non-peristaltic, but mix contents for better absorption
    • 6x/day there are peristaltic movements which trigger fecal urgency
24
Q

What is meant by HAPC in motility?

A
  • High amplitude propagating contractions

* These happen 6x/day and push poop to rectum

25
Q

What is a sitz marker study?

A

• Capsule containing 24 radioopaque markers is swallowed by the patient and an abdominal X-ray is obtained afer 5 days
• Less than 5 markers left in colon is normal
*used to study colonic motility disorder

26
Q

What is the reflex of stool causing distention of the rectum leading to internal anal sphincter relaxation called?

A
  • Recto-anal inhibitory reflex
    • This is absent in hirschsprungs disease
    • Congential absence of myenteric neurons of the distal colon
    • Results in lack of reflex inhibition of the interanal anal sphincter following rectal distention
27
Q

What is dyssynergic defecation?

A

• Disorder on coordination of pelvic floor musculature
• Anorectal manometry reveals paradoxical contraction of the pelvic floor and external anal sphincter with attempts at defecation
• Biofeedback is effective
○ Re-learning how to have a bowel movement

DEMS (30 decks)

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