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Physio U4 > Esophageal Motility and Slow Waves > Flashcards

Esophageal Motility and Slow Waves Flashcards

1
Q

2 Types of visceral smooth muscle contraction

A

phasic and tonic contractions

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2
Q

phasic contraction

A

rhythmic contractions and relaxations in seconds (single-unit of SM)

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3
Q

tonic contractions

A

sustained contraction lasting minutes to hours (multi-unit SM or sphincters)

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4
Q

Which contraction occurs depends on

A

myogenic properties of the SM (single unit vs multi), NOT neuronal/hormonal control

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5
Q

The strength of the contraction depends on

A

neuronal/hormonal control

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6
Q

Tone

A

baseline tension maintained between phasic contractions above 0

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7
Q

What allows for single unit SM to have coordinated contractions?

A

GAP junctions

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8
Q

What is the effect of ACh on visceral SM?

A

Contraction

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9
Q

ACh binds what receptor to cause visceral SM contraction

A

Muscarinic

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10
Q

Peristalsis is an example of what type of contraction?

A

phasic contractions

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11
Q

All GI smooth muscle has basal tone except

A

smooth muscle of the lower 2/3 of the esophageal body

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12
Q

striated muscle of the esophageal body contracts when

A

excitatory NT is released

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13
Q

striated muscle of the esophageal body relaxes when

A

excitatory NT is NOT released

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14
Q

visceral smooth muscle contracts when

A

excitatory NT is released

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15
Q

visceral smooth muscle relaxes when

A

inhibitory NT is released

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16
Q

3 functional parts of the esophagus

A

Upper esophagus sphincter (UES), Body, Lower esophageal sphincter (LES)

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17
Q

UES

A

junction of pharynx and esophageal body; striated muscle, normally closed (vagal LMNs)

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18
Q

Body

A

located between 2 sphincters, upper 1/3 is striated, lower 2/3 is smooth muscle, no slow waves or basal tone

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19
Q

LES

A

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

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20
Q

Contraction

A

increased intensity of tonic contractions

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21
Q

Relaxation

A

decreased intensity of tonic or phasic contractions

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22
Q

Oral Stage of deglutition

A

VOLUNTARY; inhibits respiration for 2 sec

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23
Q

Pharyngeal stage of deglutition

A

INVOLUTARY; bolus activates afferent sensory neurons in oropharynx and PRIMARY peristaltic contractions propel food through UES and into upper esophageal body

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24
Q

Esophageal stage of deglutition

A

INVOLUNTARY; PRIMARY peristaltic contraction propels food through lower esophageal sphincter and into stomach

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25
What nerve innervates the esophagus?
Vagus
26
Striated muscle of the UES and esophageal body is innervated
DIRECTLY by the vagal LMNs, which form motor endplates
27
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
28
Smooth muscle of the esophagus is innervated
INDIRECTLY by vagal preganglionic neurons synapsing on myenteric neurons (inhibitory and excitatory pathways)
29
2 types of esophageal peristalsis
primary and secondary
30
Primary esophageal peristalsis
preceded by pharyngeal peristalsis, follows a swallow, LONG parasympathetic neural reflex
31
Secondary esophageal peristalsis
absence of pharyngeal peristalsis, initiated by distention, mediated by LONG and SHORT neural reflexes (clear esophagus)
32
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
33
Opening of UES (has basal tone)
CNS Inhibition of vagal LMN
34
Primary Peristalsis (ACh)
striated muscle of esophageal body sequentially activated by vagal LMNs
35
<1 second after swallowing
ALL preganglionic VAGAL inhibitory pathways to smooth muscle of esophageal body, LES, and fundus are activated
36
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)
37
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
38
Vagal Inhibitory pathways <1 s after swallowing causes _______ on fundus
relaxation of fundus, decrease in intra-gastric pressure to receive food
39
Deglutitive inhibition
IMMEDIATE vagal inhibition (preganglionic to enteric inhibitory) of all smooth muscle of the esophageal body, LES, and funds
40
Receptive relaxation
fundus relaxes when vagal inhibitory pathway is activated
41
1-5 s following swallowing
vagal excitatory pathways activate smooth muscle of the esophageal body and LES
42
Vagal excitatory pathway causes _______ on esophageal smooth muscle
Cholinergic contraction and NANC off contraction produce 1 total peristaltic pressure wave
43
Vagal excitatory pathway causes _______ on LES
Rebound contraction (closing) timed with NANC contraction
44
rostral dorsal motor nucleus
excitatory vagal response
45
caudal dorsal motor nucleus
inhibitory vagal response
46
Dysphagia definition
sensation of obstruction of food through the mouth, pharynx, or esophagus
47
Mechanical dysphagia
large food bolus or luminal narrowing of the esophageal body
48
Motor dysphagia
uncoordinated or weak primary peristaltic contractions 1. initiating peristalsis (afferent neurons) 2. Striated muscle (skeletal muscle weakness) 3. Smooth muscle (paralysis or enteric NS disorder)
49
Upstroke of the peristaltic wave
seals the lumen and moves the bolus
50
Opening of the striated muscle sphincter UES is completed by
vagal LMN inhibition reducing ACh and causing relaxation
51
Swallowing center
Nucleus Ambiguus
52
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
53
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)
54
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
55
Receptive relaxation
fundus relaxes due to inhibitory input (NO), no rebound contraction
56
Vagal excitation
SEQUENTIAL activation of vagal excitatory pathways 1. striated muscle of pharynx 2. striated muscle of esophageal body 3. smooth muscle of esophageal body 4. smooth muscle of LES
57
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
58
GERD treatment
antacids, proton pump inhibitors, histamine receptor antagonists
59
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)
60
Causes of GERD
1. transient, intermittent LES relaxations (long neural pathway), LES pressure < intragastric pressure 2. Cholinergic (excitatory) enteric neuron damage resulting in decreased LES resting pressure 3. hiatal hernia: contents of hernia reflux into esophagus when LES is open 4. incomplete or defective primary peristalsis
61
Secondary Peristalsis
can be short or long neural reflex, caused by distention of esophagus in order to clear the esophagus
62
Slow Wave
Continuous and spontaneous oscillations of the RMP (-40 - -80) in the gastric antrum and sm intestine
63
Slow Waves limit
maximum frequency of phasic contractions, because APs can only occur during the slow wave depolarization NOT during hyperpolarization
64
Slow waves of smooth muscle do not cause
enough depolarization for Ca entry and APs to occur to generate a contraction
65
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
66
Substances that increase phasic contraction frequency
ACh, motilin, gastrin
67
Substances that decrease phasic contraction frequency
NE, secretin, opioids, NO
68
Interstitial Cells of Cajal
slow wave pacemaker cells
69
Location of Interstitial Cells of Cajal
wall of GIT
70
What determines Interstitial Cells of Cajal ability to generate slow waves
Calcium handling by ICC mitochondria
71
What alters ICC slow wave frequency?
thyroid hormone; it alters metabolism of Ca by the ICC mitochondria
72
Disruption of ICC network results in
disorder of GI motility
73
What segments of the GIT do not have slow waves
body of esophagus, orad stomach, GI sphincters
74
Imodium's effect on phasic contraction frequency
opioid agonist to treat diarrhea
75
Opioids for pain may cause
constipation
76
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
77
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
78
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
79
Control of smooth muscle motility is due to
ICC and smooth muscle properties (slow waves), enteric neurons, extrinsic autonomic neurons, hormones

Physio U4 (9 decks)

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