Esophageal Motility And Slow Waves Flashcards
(28 cards)
Upper esophageal sphincter (UES)
. Junction of pharynx and esophageal body
. Composed of striated muscle
Esophagus body
. Located btw 2 sphincters
. Composed of both striated muscles (upper 1/3) and smooth mm.
. Body has no slow waves and no tone (flaccid)
Lower esophageal sphincter (LES)
. Junction of esophageal body and stomach
. Sphincter is 4 cm long
. Upper portion is subject to intra-thoracic pressure and lower portion is subject to intra-abdominal pressure
. Composed of multi-unit circular smooth muscle w/ high myogenic tone
. Both inhibitory and excitatory neurons modulate the tone of the LES
. Along w/ crural diaphragm the LES is component of high pressure barrier btw esophageal body and stomach (esophagastric junction)
Deglutition
. Swallowing
. Oral stage: voluntary, bonus food moved into oropharynx by tongue, resp. Inhibited for approx. 2 sec
. Pharyngeal stage: involuntary, begins when sensory afferent nn. Innervating oropharynx activated by bolus of food, primary peristaltic contractions of pharynx propel food through UES and into upper esophageal body
. Esophageal stage: begins as primary peristaltic wave of contraction occurs in body of esophagus and propels bolus of food through LES and into stomach
Striated mm. Of UES
. Innervated directly by vagal LMNs
. Form motor endplates on striated mm.
. Release ACh
Smooth muscle of esophagus
. Innervated indirectly by the vagal preganglionic neurons through myenteric neurons
. Both vagal inhibitory and vagal excitatory pathways innervate smooth m. Of esophagus
Primary peristalsis
. Esophageal peristalsis is preceded by pharyngeal peristalsis
. Always follows a swallow
. Mediated by long parasympathetic neural reflex
Secondary peristalsis
. Esophageal peristalsis in absence of pharyngeal peristalsis
. Initiated by distension of esophageal body by reflexes chyme
. Mediated by short and long neural reflexes
. Secondary peristalsis clears the esophageal contents
Swallowing reflex
. Sensory afferent CNs innervating the oropharynx are activated by bolus of food pushed by tongue to back of mouth
. Airway closes and respiration is inhibited
. In swallowing center in brainstem, activity of efferent CNs is modulated
. Opening of UES, primary peristalsis in pharynx and striated and smooth mm. Of the body, relaxation and rebound contraction of LES
. Receptive relaxation of the fungus are all coordinated in the brainstem and mediated through efferent CN X
How UES opens during swallowing
. CNS inhibition of vagal LMNs to striated m. Of UES
Primary peristalsis due to swallowing
. Striated m. Of esophageal body
. CNS coordinates sequential activation of vagal LMNs to progressively distal regions of striated m.
. CNS activates parallel vagal inhibitory (NANC) and excitatory (ACh) pathways innervating all smooth mm. Regions of esophagus and fungus
. Occurs in body of esophagus (contraction), the LES opens (relaxation) and the fundic pressure drops (receptive relaxation)
Vagal pathways after swallowing
. Less than 1 sec. after: All vagal inhibitory pathways innervating all smooth m. Of esophageal body, LES, and fungus are simultaneously activated
. 1-5 sec. after: vagal excitatory pathways innervating the smooth m. Of the body and the LES are sequentially activated
. Vagal preganglionic nn. That innervate progressively distal regions of the esophagus have inc. slower conduction velocities
Esophageal body after swallow
. Prompt inhibition of all smooth m. Of esophageal body (deglutitive inhibition)
. Duration and magnitude of deglutitive inhibition inc. in progressively distal regions of the body due to inc. proportion of enteric inhibitory motor neurons
. Smooth m. Of body is hyperpolarzied but bc it has no basal tone there is no change in pressure
. NANC “off” depolarization participates in primary peristaltic contraction
. Cholinergic contraction and NANC “off” contraction are timed to overlap producing the total peristaltic pressure wave
LES after swallow
. Opens when vagal inhibitory pathway is activated
. LES has basal tone, the prompt hyperpolarization of smooth m. Causes relaxation (opening) of sphincter
. NANS “off” depolarization participates in the rebound contraction of LES
. Rebound contraction of the :ES is timed to coincide w/ the NANC “off” contraction
Fundus after swallow
. Fundus relaxes when vagal inhibitory pathway is. Activated (receptive relaxation)
. Intra-gastric pressure drops to receive swallowed food
Mechanical dysphagia
. Caused by a large food bolus or luminal narrowing of esophageal body
Motor dysphagia
. Caused by uncoordination or weakness of primary peristaltic contractions of esophageal body
. Difficulty initiating peristaltic reflex: damage to afferent sensory nn. Innervating the oropharynx
. Disorders of pharyngeal and/or esophageal striated m. (Skeletal m. Weakness and non-peristaltic contractions)
. Disorders of esophageal smooth m. (Paralysis of esophageal body or non-peristaltic contractions, disorders of enteric nervous system activity)
Gastroesophageal reflux disease (GERD)
. Gastric contents are reflexes into esophageal body causing bothersome symptoms and/or complications
. Symptoms: due to visceral hypersensitivity to refluxed gastric contents or damage to esophageal mucosa
. Treatment: antacids, histamine receptor antagonists, proton pump inhibitors
Gastric contents reflux into esophagus because of ____
. Inc. number of transient, intermittent LES relaxations that occur independent of a swallow
. Dec. LES resting pressure (damage to cholinergic enteric motor neurons)
. Hiatal hernia (portion stomach protrudes rough diaphragm into thoracic cavity
. Swallow-induced LES relaxations (assoc. w/ incomplete or defective primary peristalsis)
How inc. number of transient intermittent LES relaxations that occur independent of swallow
. LES resting pressure might be normal, but LES pressure is lower than gastric pressure during long-lasting relaxations permitting reflux
. Afferents: CN X, activated by prox. Stomach distension
. Efferent: CN X inhibitory pathway to esophagus
Slow waves
. Smooth mm. Of gastric antrum and SI exhibit continuous, spontaneous oscillations of resting membrane potential (slow wave) or basic electrical rhythm
. Always occurring regardless of presence or absence of smooth m. Phasic contractions or presence/absence of chyme in lumen
. Does not cause smooth m. Phasic contractions but sets frequency that AP bursts can occur in smooth m. (Phasic contractions can’t occur at higher frequency than slow wave)
. As slow wave depolarizes AP bursts can occur and smooth m. Contracts
Likelihood that AP burst will occur in smooth m. Can be increased or decreased by ____
Modulating enteric or extrinsic autonomic n. Activity
. Modulating conc. Of circulating hormone or of local paracrines
Substances that alter frequency of phasic contractions of smooth m.
. ACh
. Gastrin
. Motilin: exists only during interdigestive periods
Substances that dec. frequency of phasic contractions
. NE/E
. Secretin
. NO
. Opioids