motility disorders of the GI tract Flashcards
1) Understand that there are multiple underlying etiologies to GI motility disorders
CNS disorders (predominantly parasympathetic vagus), neuropathic (enteric nervous system disorders) and myopathic causes (genetic defect of acquired)
1) Understand that there are multiple underlying etiologies to GI motility disorders
CNS disorders (predominantly parasympathetic vagus), neuropathic (enteric nervous system disorders) and myopathic causes (genetic defect of acquired)
Spastic disorders of the esophagus
Symptoms are severe chest pain and dysphagia.
Peristalsis preserved but high pressures are generated due to overactivity of excitatory nerves or overactivity of smooth muscle response (neuropathic or myopathic).
There is a gradient of inhibitory nerves in the esophagus (proximally, there are few inhibitory nerves)
= “Jackhammer” Esophagus: peristalsis is present but disordered.
Scleroderma
fibrosis of multiple organs, especially the skin. GI manifestations common.
Smooth muscle atrophy (distal 2/3 of esophagus) and gut wall fibrosis.
Weak peristalsis (dysphagia), weak LES and esophagitis due to GERD.
On manometry, absence of peristalsis and low pressures of LES.
achalasia.
Dysphagia
No LES relaxation and an airball along the body due to absence of peristalsis =
Normal gastric motility
Not just a bag. A reservoir and a pump.
Mixing and churning with retropulsion (to convert an ingested solid into a fluid) and receptive relaxation to maintain low pressure.
Liquid emptying by tonic pressure gradient
Solid emptying by vagally-mediated contraction.
Residual solids emptied during non-fed state by MMC (migrating motor complexes) every 90-120 minutes.
As soon as you swallow, your stomach relaxes (swallowing-induced vagal response). It accommodates to the size of the meal (gastric mechanoreceptors and vagal).
Functional dyspepsia =
discomfort or pain in upper abdomen, plus postprandial heaviness and early satiety.
Organic causes include peptic ulcer disease, atypical GERD, cancer, etc.
It’s “functional” when there is no identifiable etiology. Prevalent is 20-25%. May be due to impaired gastric accommodation.
Gastroparesis =
stomach paralysis.
Impaired transit of food into duodenum (exclusing mechanical obstruction)
N/v, early satiety, and postprandial abdominal pain.
Causes: idiopathic, surgical vagal nerve injury, diabetic, due to meds, **scleroderma, etc. Neuropathic or myopathic.
Diagnosis via gastric emptying study/scintigraphy.
(Abnoral retention is >60% at 2 hours or >10% at 4 hours).
Management is difficult. Small and frequent meals. Low residue diet.
These can overlap. Up to 45% of Functional Dyspepsia patients have delayed gastric emptying.
CIPO =Chronic intestinal pseudo-obstruction.
Dilation on imaging. as a manifestation of small intestinal dysmotility
Complication is bacterial overgrowth that leads to fermentation/distention and malabsorption. Normally prevented with MMCs.
Etiologies include neuropathic (Parkinson’s, autoimmune, parasites, diabetic) or myopathic (infiltrative conditions like scleroderma or amyloidosis) or can be idiopathic or mixed.
Child and adult forms are different.
Kids – primary conditions, mostly congenital, absent MMC predicts need for IV nutrition. A third of infants born die in first year of life.
Altered small bowel motility with underlying neuropathic (DM, primary pediatric visceral neuropathy) or myopathic (scleroderma, amyloidosis, primary pediatric visceral myopathy) disorders
By length, makes up the majority of the GI tract.
Fed state – primary motility with segmentation for a total transit time 3-5 hours.
Fasted state – migratory motor complexes sweep the gut between meals.
Neuropathic disorders: normal amplitude of pressures but sustained bursts of uncoordinated phasic contraction. Impaired absorption with increased frequency of MMC and overwhelming the absorptive capacity of colon (lead to diarrhea).
Myopathic – decreased amplitude of contraction or complete lack of motor activity.
Some disease have features of both.
Normal colonic motility
.
Organ of luxury ☺
Function is to transport, store, and expel stool after absorbing majority of luminal fluid.
Low amplitude tonic and phasic contraction within haustra (mixing) and high amplitude propagated contractions (propelling).
Motility increases after meal and on awakening.
Altered colonic motility in chronic constipation, Hirschsprung’s disease and dyssynergic defecation
Constipation has many causes (drugs, mechanical, metabolic, myopathies like scleoderma, neurogenic like Hirschsprung’s, dyssynergic defecation, etc.)
Both smooth and skeletal muscle in rectal canal.
Internal anal sphincter is smooth – autonomic innervation by pelvic plexus.
External anal sphincter is skeletal – innervated by pudendal nerve.
Widening of anorectal angle is an important feature of normal defecation motality.
Inability to coordinate abdominal, rectoanal and pelvic floor muscles during defecation in pelvic floor dysfunction
Esophageal Manometry
Achalasia
Scleroderma
Gastric emptying study (Gastric scintigraphy)
Isotope in delayed-release capsule dissolves in alkaline pH of distal ileum and can be scanned.
Gastroparesis
Anal Manometry
Hirschsprung’s Disease-Congenital absence of myenteric neurons of the distal colon.
No reflex inhibition of the internal anal sphincter following rectal distention (no recto-anal inhibitory reflex is absent).
It’s difficult to amount enough pressure to bypass the internal sphincter.
Dyssynergic Defecation-Inability to coordinate abdominal, rectoanal and pelvic floor muscles during defecation in pelvic floor dysfunction.
Diagnosed by abnormal anorectal manometry showing paradoxical contraction of pelvic floor and external anal sphincters.
Teach someone how to defecate again through PT.
