gastrointestinal motility jeffrey mccurdy md, phd, frcpc assistant professor division of...
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Gastrointestinal Motility
Jeffrey McCurdy MD, PhD, FRCPC
Assistant Professor
Division of Gastroenterology
The Ottawa Hospital
September 2015
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Objectives Summarize the process of normal gastric contractility and
emptying.
Outline the normal mechanism of swallowing.
Outline the mechanisms behind esophageal persistalsis and their coordination with esophageal sphincter tone, at rest and in response to swallowing.
Explain normal contractility of the intestines in the fed and fasting states.
Outline the mechanisms underlying the maintenance of fecal continence
Describe the normal process of defecation.
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Swallowing
Three phases Oral “preparatory phase”
Form food into bolus
Pharyngeal transfer of bolus to oropharnyx
Beginning of swallowing
Esophageal
1 second
10-15 seconds
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Oropharynx Oral cavity
Saliva production Mastication Lingual involvement
Pharynx Hollow cavity separated into the
nasopharynx, oropharynx and hypopharynx
Process requires pharyngeal paristalisis Protection from aspiration & nasal
regurgitation
Food bolus formation suitable for transfer to the pharynx
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Oropharynx
Oral phase Largely voluntary
CN V (trigeminal), VII (facial) and XII
(hypoglossal)
Pharyngeal phase Involuntary (reflexive response)
CN V (trigeminal), IX (glossopharyngeal), X
(vagus) and XII (hypoglossal)
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Upper Esophageal Sphincter
Muscle groups: cricopharyngeus, inferior
constrictor muscles and adjacent esophagus
Innervation: Vagus
Tonically closed at rest (continuous neural
excitation)
Relaxation: cessation motor neuron firing
(swallowing/burping, general
anesthetic/meds)
Relaxes w/in 0.2-0.3 sec after swallow
initiation
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Esophagus Motility
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Upper 1/3 esophagus
Lower 2/3 esophagus
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Lower Esophageal Sphincter
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High Resolution Manometry
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Dysphagia Symptomatic difficulties in passage of
food from the mouth into the stomach
Oropharyngeal dysphagia
Esophageal dysphagia
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Evaluation
History and physical
Video fluoroscopy (modified barium
swallow)
Barium swallow assessment
Upper endoscopy
Esophageal manometry
Additional depending on clinical picture
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Abnormality Causes of Oropharyngeal dysphagia
Reduced Saliva Production
Sjogrens, H&N radiation, medications (anticholinergics, antihistamines)
CNS Trauma, tumors, ALS, Parkinson, Multiple Sclerosis, Stroke, Hunting Disease, cerebral palsy, Alzheimer, infectious
PNS/muscular Myasthina Gravis, polymyositis, dermatomyositis, sarcoidosis, paraneoplastic syndromes
Structural Cricopaharyngeal bars, cervical vertebral body osteophytes, malignancy, Zenker’s diverticulum
Iatrogenic Radiation, caustic ingestion, surgery
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Abnormality Causes of Esophageal Dysphagia
Structural Schatski’s rings, webs, peptic strictures, caustic strictures
Malignant Gastric and esophageal cancers (adenocarcinoma or squameous cell carcinoma)
Motility Disorders
Achalasia, diffuse esophageal spasm, nutcracker esophagus…
Inflammatory Scleroderma, dermatomyositis, polymyositis, inflammatory bowel disease
Infectious Candida, HSV, CMV, chagas (pseudoachalasia)
Misc. Eosinophilic esophagitis
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Gastric Motility
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Gastric Motility Function
Gastric Function
1) Accommodation
2) Trituration
3) Regulated emptying
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Process of Gastric Emptying
1) Gastric peristalsis 2) Vigorous antral contraction3) Antral peristalsis 4) Relaxation of pylorus
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Regulation of Gastric Emptying
Controlled by central and local neurohormonal control
Neuronal control includes: Intrinsic myenteric plexus ICC cells Postganglionic sympathetic fibers of the celiac
plexus Preganglionic parasympathetic fibers of the
vagus nerve
Hormonal control via CCK Relaxes fundic tone, decreases antral contraction
and increase pyloric tone Also other hormones (glucagon like polypeptide,
peptide YY) can control gastric emptying
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Neurologic Control
1) Parasympathetic 2) Sympathetic3) ENS 4) Smooth muscles
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Promote Motility Inhibit Motility
Food LiquidsIso-osmolar Carbohydrates
SolidsHyperosmolar High fat content Cold,large mealETOH
Hormones Motilin, Serotonin, Substance P
CCK, Somatostatin, Progesterone
Medications
Beta blockers, Metaclopromide, Erythromycin, Domperideone
NarcoticsTricyclic antidepressantsBeta agonists
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Liquids & SolidsLiquids: linear emptying (no lag phase) Rate depends on volume, nutrient content
and osmolarity
Solids: Two phases required
Initial lag phase Linear emptying phase
Rate depends on size and consistency
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Liquid MealTotal stomach emptying time
Proximal stomach emptying time
Distal stomach emptying time
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Abnormal Gastric Motility Gastroparesis
Syndrome of objectively delayed gastric emptying
Dumping Syndrome Rapid release of hyperosmolar gastric
contents into the small intestine resulting in fluid shifts (hypotension) and hyperglycemia with rebound hypoglycemia
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Evaluation History and Physical
Exclude mechanical obstruction EGD, xray and/or CT/MRI
Assess gastric motility Gastric Scintigraphy
Wireless motility capsule
Gastroduodenal manometry
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Abnormality Specific Causes of Gastroparesis
Surgical Vagotomy, fundoplication, partial gastric resection
CNS Multiple Sclerosis, Stroke, Parkinson disease….
Metabolic Hyper/hypothyroid and Diabetes
Inflammatory Scleroderma, dermatomyositis, lupus
Structural* Peptic ulcer disease, inflammatory bowel disease, tumors (*cause similar features as gastroparesis)
Medications Narcotics, tricyclic antidepressants, calcium channel blockers, dopamine agonists
Misc. Infectious, AIDs, post-viral gastroparesis, paraneoplastic syndromes, Amyloidosis, sarcoidosis
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Small Bowel Motility
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Function Efficient absorption of nutrients
Mixing intestinal contents
Maximize contact with epithelium
Effective forward propagation
Maintenance of aboral movement of chyme along the small intestines Prevention of small intestinal bacterial
overgrowth
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Small Intestine Motility Motor function - entirely smooth
muscle
Can occur exclusively w ENS
Autonomic nervous system can modulate
Interstitial cells of Cajal: pacemaker cells (generate slow waves) and transduce both excitatory and inhibitory signals to myocytes for contractile activity
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Fed State
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Fasting State
Migratory motor complex (MMC)
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Large Bowel Motility
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Large Bowel
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Colonic motility Nonpropagating motor patterns
Random activity makes up majority of colonic motor activity
Presumed for mixing function Propagating motor patterns
Occur when excitatory motor neurons are active
Results in lumen occlusive contractions Send contents over considerable distances
along the colon (both retrograde & antegrade)
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Motor Activity Two types of rhythmic myoelectrical activity Myenteric potential oscillations (MPO)
Small amplitude Rapid oscillation (frequency 12-20 per minute) Originate from myenteric plexus Can cause both circular and longitudinal muscle
contractions for propulsion Slow Waves
Large amplitude Slower oscillation (2-4 per minute) Short distance for mixing of contents with little
propulsion
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Motor Activity Direct neuronal control via the ENS Modulated by sympathetic &
parasympathetic
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Sympathetic Parasympathetic
CNS Control
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Summary of Transit Time Esophagus
Stomach
Small Bowel
Large Bowel
15 secs
1-2 hrs
1-2 hrs
1-2 days
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Defecation & Continence
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Evaluation
History and Physical
Rectal examination
Balloon expulsion testing
MRI defecography
Anal rectal manometry
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Disorders of rectum
Dyssynergic defecation Difficulties passing stool
Pelvic/abdominal pain
Hemorrhoids, rectocele etc….
Incontinence