Esophageal Motility and Slow Waves Flashcards
2 Types of visceral smooth muscle contraction
phasic and tonic contractions
phasic contraction
rhythmic contractions and relaxations in seconds (single-unit of SM)
tonic contractions
sustained contraction lasting minutes to hours (multi-unit SM or sphincters)
Which contraction occurs depends on
myogenic properties of the SM (single unit vs multi), NOT neuronal/hormonal control
The strength of the contraction depends on
neuronal/hormonal control
Tone
baseline tension maintained between phasic contractions above 0
What allows for single unit SM to have coordinated contractions?
GAP junctions
What is the effect of ACh on visceral SM?
Contraction
ACh binds what receptor to cause visceral SM contraction
Muscarinic
Peristalsis is an example of what type of contraction?
phasic contractions
All GI smooth muscle has basal tone except
smooth muscle of the lower 2/3 of the esophageal body
striated muscle of the esophageal body contracts when
excitatory NT is released
striated muscle of the esophageal body relaxes when
excitatory NT is NOT released
visceral smooth muscle contracts when
excitatory NT is released
visceral smooth muscle relaxes when
inhibitory NT is released
3 functional parts of the esophagus
Upper esophagus sphincter (UES), Body, Lower esophageal sphincter (LES)
UES
junction of pharynx and esophageal body; striated muscle, normally closed (vagal LMNs)
Body
located between 2 sphincters, upper 1/3 is striated, lower 2/3 is smooth muscle, no slow waves or basal tone
LES
junction of esophagus and stomach, under intra-thoracic and intra-abdominal pressure; multi-unit circular smooth muscle, high tone, modulated by inhibitory and excitatory neurons
Contraction
increased intensity of tonic contractions
Relaxation
decreased intensity of tonic or phasic contractions
Oral Stage of deglutition
VOLUNTARY; inhibits respiration for 2 sec
Pharyngeal stage of deglutition
INVOLUTARY; bolus activates afferent sensory neurons in oropharynx and PRIMARY peristaltic contractions propel food through UES and into upper esophageal body
Esophageal stage of deglutition
INVOLUNTARY; PRIMARY peristaltic contraction propels food through lower esophageal sphincter and into stomach
What nerve innervates the esophagus?
Vagus
Striated muscle of the UES and esophageal body is innervated
DIRECTLY by the vagal LMNs, which form motor endplates
Vagal LMN endplates release ______ that binds striated muscle receptors to cause contraction
ACh binds Nicotinic muscle receptors on UES and upper 1/3 esophageal body to cause contraction
Smooth muscle of the esophagus is innervated
INDIRECTLY by vagal preganglionic neurons synapsing on myenteric neurons (inhibitory and excitatory pathways)
2 types of esophageal peristalsis
primary and secondary
Primary esophageal peristalsis
preceded by pharyngeal peristalsis, follows a swallow, LONG parasympathetic neural reflex
Secondary esophageal peristalsis
absence of pharyngeal peristalsis, initiated by distention, mediated by LONG and SHORT neural reflexes (clear esophagus)
Swallowing reflex coordinated by Vagus
Afferent nerve activation in oropharynx by bolus –> opening of UES, primary peristalsis, relaxation and rebound of LES, receptive relaxation of fundus
Opening of UES (has basal tone)
CNS Inhibition of vagal LMN
Primary Peristalsis (ACh)
striated muscle of esophageal body sequentially activated by vagal LMNs
<1 second after swallowing
ALL preganglionic VAGAL inhibitory pathways to smooth muscle of esophageal body, LES, and fundus are activated
Vagal Inhibitory pathways <1 s after swallowing causes _______ on lower 2/3 esophageal body smooth muscle
Deglutitive inhibition or hyperpolarization of esophageal smooth muscle (no basal tone), esophagus remains relaxed followed by NANC “off” depolarization resulting in primary peristaltic wave (phasic contraction)
Vagal Inhibitory pathways <1 s after swallowing causes _______ on LES
vagal inhibition immediately causes relaxation and opening of the LES (due to basal tone) followed by rebound contraction by NANC off depolarization
Vagal Inhibitory pathways <1 s after swallowing causes _______ on fundus
relaxation of fundus, decrease in intra-gastric pressure to receive food
Deglutitive inhibition
IMMEDIATE vagal inhibition (preganglionic to enteric inhibitory) of all smooth muscle of the esophageal body, LES, and funds
Receptive relaxation
fundus relaxes when vagal inhibitory pathway is activated
1-5 s following swallowing
vagal excitatory pathways activate smooth muscle of the esophageal body and LES
Vagal excitatory pathway causes _______ on esophageal smooth muscle
Cholinergic contraction and NANC off contraction produce 1 total peristaltic pressure wave
Vagal excitatory pathway causes _______ on LES
Rebound contraction (closing) timed with NANC contraction
rostral dorsal motor nucleus
excitatory vagal response
caudal dorsal motor nucleus
inhibitory vagal response
Dysphagia definition
sensation of obstruction of food through the mouth, pharynx, or esophagus
Mechanical dysphagia
large food bolus or luminal narrowing of the esophageal body
Motor dysphagia
uncoordinated or weak primary peristaltic contractions
- initiating peristalsis (afferent neurons)
- Striated muscle (skeletal muscle weakness)
- Smooth muscle (paralysis or enteric NS disorder)
Upstroke of the peristaltic wave
seals the lumen and moves the bolus
Opening of the striated muscle sphincter UES is completed by
vagal LMN inhibition reducing ACh and causing relaxation
Swallowing center
Nucleus Ambiguus
movement of food through the upper 1/3 esophageal body (striated) is completed by
vagal LMN activation, increased ACh and causing contraction after food passes, propelling it
Movement of food through lower 2/3 esophageal body
immediate activation of vagus nerve to inhibitory enteric neurons (NO), followed by activation of excitatory enteric neurons (ACh) causing contraction (in addition to off contraction)
Movement of food through LES
normally closed due to basal tone, inhibitory input (NO) causes relaxation followed by excitatory input + off contraction to push food through
Receptive relaxation
fundus relaxes due to inhibitory input (NO), no rebound contraction
Vagal excitation
SEQUENTIAL activation of vagal excitatory pathways
- striated muscle of pharynx
- striated muscle of esophageal body
- smooth muscle of esophageal body
- smooth muscle of LES
Esophageal stricture due to chronic reflux esophagitis
scarring of the esophageal mucosa due to acid reflux causes a narrowing of the esophagus with a dilation above
GERD treatment
antacids, proton pump inhibitors, histamine receptor antagonists
Primary achalasia
dysfunctional NANC inhibitory enteric neurons and failure to relax LES and cause primary peristalsis in lower esophageal smooth muscle (incomplete opening of LES)
Causes of GERD
- transient, intermittent LES relaxations (long neural pathway), LES pressure < intragastric pressure
- Cholinergic (excitatory) enteric neuron damage resulting in decreased LES resting pressure
- hiatal hernia: contents of hernia reflux into esophagus when LES is open
- incomplete or defective primary peristalsis
Secondary Peristalsis
can be short or long neural reflex, caused by distention of esophagus in order to clear the esophagus
Slow Wave
Continuous and spontaneous oscillations of the RMP (-40 - -80) in the gastric antrum and sm intestine
Slow Waves limit
maximum frequency of phasic contractions, because APs can only occur during the slow wave depolarization NOT during hyperpolarization
Slow waves of smooth muscle do not cause
enough depolarization for Ca entry and APs to occur to generate a contraction
The likelihood of phasic contractions in the gastric antrum and small intestine can be increased or decreased by
modulating enteric or extrinsic AN activity or by hormone concentration
Substances that increase phasic contraction frequency
ACh, motilin, gastrin
Substances that decrease phasic contraction frequency
NE, secretin, opioids, NO
Interstitial Cells of Cajal
slow wave pacemaker cells
Location of Interstitial Cells of Cajal
wall of GIT
What determines Interstitial Cells of Cajal ability to generate slow waves
Calcium handling by ICC mitochondria
What alters ICC slow wave frequency?
thyroid hormone; it alters metabolism of Ca by the ICC mitochondria
Disruption of ICC network results in
disorder of GI motility
What segments of the GIT do not have slow waves
body of esophagus, orad stomach, GI sphincters
Imodium’s effect on phasic contraction frequency
opioid agonist to treat diarrhea
Opioids for pain may cause
constipation
ELECTRICAL SYNCYTIUM ICC networks of gut segments coordinate slow waves by
gap junctions between, smooth muscle cells, smooth muscle cells and ICC, and ICC’s
Discrete ICC networks for each portion of the gut - Small intestine
decrease in slow waves from duodenum (12/min) to ileum (8/min) to move chyme toward the colon
Colon and slow waves
No continuous slow waves, activated by distention or neural activity, increase in wave frequency from the ascending colon (11/min) to rectum (17/min) to retain fecal material in colon
Control of smooth muscle motility is due to
ICC and smooth muscle properties (slow waves), enteric neurons, extrinsic autonomic neurons, hormones