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Esophageal MotilityEsophageal Motility
David Markowitz, MDColumbia University, College ofColumbia University, College of
Physicians and Surgeons
Alimentary Tract Motility
• Propulsion– Movement of food and endogenousMovement of food and endogenous
secretions• MixingMixing
– Allows for greater contact of food with digestive enzymes and absorptive surfacedigestive enzymes and absorptive surface
• Reservoir
Determinants of GI TractDeterminants of GI Tract Motility
• Myogenic controlMyogenic control
• Neurogenic controlg
• Endocrine factors
Myogenic Control
• Basic Electrical Rythym:– intrinsic rhythmic fluctuation of smoothintrinsic rhythmic fluctuation of smooth
muscle membrane potential• Pacemaker Cells:Pacemaker Cells:
– set BER for the entire organ• Slow waves:• Slow waves:
– spread from cell to cell via gap junctions
Enteric Nervous System
• Afferent and efferent arms• Numerous interneurons in the ENS are highly g y
integrated and receive input from:– CNS– efferent arm of ENS
• Afferent neurons receive input from ENS i t d th ff tinterneurons and these affect:– smooth muscle
blood vessels– blood vessels– secretory cells
Swallowing
• Oropharyngeal Phase– Involuntary & Voluntary PhasesInvoluntary & Voluntary Phases– Extremely rapid– Dx test: Video esophagramDx test: Video esophagram
• Esophageal PhaseSlow– Slow
– StereotypedD t t E h l M t– Dx test: Esophageal Manometry
Oropharyngeal Phase ofOropharyngeal Phase of Swallowing
• Moves ingested food and fluid into upper esophaguspp p g
• Prevents aspiration or regurgitation of the bolusthe bolus
• Voluntary movement by the tongue of the bolus into the pharynx triggers thethe bolus into the pharynx triggers the involuntary phase of swallowing
Esophageal DiseaseEsophageal Disease Symtpoms
• Dysphagia– Oropharyngeal DysphagiaOropharyngeal Dysphagia– Esophageal Dysphagia
• Pain• Pain– Odynophagia
Atypical Chest pain– Atypical Chest pain• GE Reflux disease (GERD)
Dyspahgia
• Oropharyngeal– Difficulty transferring bolus out of mouthDifficulty transferring bolus out of mouth– Associated w/ coughing & aspiration
• Esophageal• Esophageal– Sense of bolus “sticking in chest”
Mechanical causes– Mechanical causes– Motility disorders
Esophageal DysphagiaEsophageal DysphagiaMechanical Causes
• Typically occurs with solid foods• Frequently progressive especially withFrequently progressive, especially with
malignancy• Food impaction (w/ forced regurgitation)• Food impaction (w/ forced regurgitation)
commonP i t i ht l l /• Prominent weight loss only w/ malignancy
Schiatzki Ringg
Schiatzki RingSchiatzki Ring
Esophageal Strictures
Esophageal StrictureEsophageal Stricture
Esophageal Dilators
TTS Ballons
Esophageal Carcinoma
Esophageal CarcinomaEsophageal Carcinoma
Esophageal CarcinomaEsophageal Carcinoma
Esophageal Stents
Esophageal StentsEsophageal Stents
Barrett’s Esophagus
Barrett’s esophagus –d fi itidefinition
• “A change in the esophageal epithelium of any length that can g p g p y gbe recognized at endoscopy and is confirmed to have intestinal
metaplasia by biopsy”
Sampliner. Am J Gastroenterol 1998
Barrett’s EsophagusBarrett s Esophagus
Barrett’s esophagus is a premalignant l i f h l d i
Normal
lesion for esophageal adenocarcinoma
Endoscopy-negative reflux disease
Erosive esophagitis
?
Barrett’s esophagus
?
?
Dysplasia
?
Esophageal adenocarcinoma
Esophageal DysphagiaEsophageal Dysphagia
Motor Disorders
Esophageal ManometryNormal Study
Achalasia
Achalasia
Achalasia
AchalasiaAchalasia
Achalasia
Achalasia
SclerodermaScleroderma
S l dScleroderma
SclerodermaScleroderma
Esophageal DysphagiaEsophageal Dysphagia
E h l D h iEsophageal Dysphagia
Mechanical Motor
Benign Malignant AchalasiaScleroderma
WebsRings
Adeno ca.Sq cell caRings
StricturesSq. cell ca.
Spastic Motility Disorders
Diffuse Esophageal Spasmp g p
Atypical Chest Pain
Candida Esophagitis
GE RefluxNormal PhysiologyNormal Physiology
GERDGERD
The sequellae of prolonged exposure of esophageal mucosa g
to caustic gastric refluxate
GERD: PathogenesisGERD: Pathogenesis
Defective Esophageal ClearanceDefective Esophageal Clearance
• Ineffective peristalsis
• Reduced salivary secretionsecretion
• Reduced secretion from esophageal submucosal glands
LES ‘dysfunction’
• Inappropriate and prolongedand prolonged transient relaxationsrelaxations
• Reduction in basal LES pressure/tone
Hiatal hernia
• May trap a reservoir of gastric contentsof gastric contents above the diaphragm, increasing refluxincreasing reflux
M i• May compromise LES function
Delayed gastric emptying• May result in an
y g p y g
increase in the volume of gastric contents available for reflux into the esophagus
• Exact role in GERD remains toGERD remains to be clarified
Bravo Capsule
Bravo CapsuleBravo Capsule
Nissen FundoplicationNissen Fundoplication
Stretta procedureStretta procedure
St 1Step 1
Step 2
Step 3
Mechanism of action of refluxate in GERD
Acid-peptic attack weakens cell junctions
leading to a widening of cell gaps
and thus allowing acid penetration
GERD
weakens cell junctions cell gaps penetration
AcidTight cell WidenedPepsinBicarbonate
Nerve endingTight celljunction
Widened cell
junctionOrlando. Am J Gastroenterol 1996
Mechanism of action of refluxate in GERD
Penetration of acid and pepsin allows contact of acid with nerve
endings
and disrupts intracellular mechanisms leading to cell rupture
and damage
refluxate in GERDg g
Acidc dPepsinBicarbonate
Nerveending
Orlando. Am J Gastroenterol 1996