Gastrointestinal Motility

Jeffrey McCurdy MD, PhD, FRCPC

Assistant Professor

Division of Gastroenterology

The Ottawa Hospital

September 2015

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.

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

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

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)

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

Esophagus Motility

Upper 1/3 esophagus

Lower 2/3 esophagus

Lower Esophageal Sphincter

High Resolution Manometry

Dysphagia Symptomatic difficulties in passage of

food from the mouth into the stomach

Oropharyngeal dysphagia

Esophageal dysphagia

Evaluation

History and physical

Video fluoroscopy (modified barium

swallow)

Barium swallow assessment

Upper endoscopy

Esophageal manometry

Additional depending on clinical picture

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

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

Gastric Motility

Gastric Motility Function

Gastric Function

1) Accommodation

2) Trituration

3) Regulated emptying

Process of Gastric Emptying

1) Gastric peristalsis 2) Vigorous antral contraction3) Antral peristalsis 4) Relaxation of pylorus

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

Neurologic Control

1) Parasympathetic 2) Sympathetic3) ENS 4) Smooth muscles

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

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

Liquid MealTotal stomach emptying time

Proximal stomach emptying time

Distal stomach emptying time

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

Evaluation History and Physical

Exclude mechanical obstruction EGD, xray and/or CT/MRI

Assess gastric motility Gastric Scintigraphy

Wireless motility capsule

Gastroduodenal manometry

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

Small Bowel Motility

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

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

Fed State

Fasting State

Migratory motor complex (MMC)

Large Bowel Motility

Large Bowel

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)

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

Motor Activity Direct neuronal control via the ENS Modulated by sympathetic &

parasympathetic

Sympathetic Parasympathetic

CNS Control

Summary of Transit Time Esophagus

Stomach

Small Bowel

Large Bowel

15 secs

1-2 hrs

1-2 hrs

1-2 days

Defecation & Continence

Evaluation

History and Physical

Rectal examination

Balloon expulsion testing

MRI defecography

Anal rectal manometry

Questions

Interested in GI Research?

jmccurdy@toh.on.ca

Disorders of rectum

Dyssynergic defecation Difficulties passing stool

Pelvic/abdominal pain

Hemorrhoids, rectocele etc….

Incontinence