Esophageal Motility and Slow Waves Flashcards Preview

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Flashcards in Esophageal Motility and Slow Waves Deck (79)
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1
Q

2 Types of visceral smooth muscle contraction

A

phasic and tonic contractions

2
Q

phasic contraction

A

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

3
Q

tonic contractions

A

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

4
Q

Which contraction occurs depends on

A

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

5
Q

The strength of the contraction depends on

A

neuronal/hormonal control

6
Q

Tone

A

baseline tension maintained between phasic contractions above 0

7
Q

What allows for single unit SM to have coordinated contractions?

A

GAP junctions

8
Q

What is the effect of ACh on visceral SM?

A

Contraction

9
Q

ACh binds what receptor to cause visceral SM contraction

A

Muscarinic

10
Q

Peristalsis is an example of what type of contraction?

A

phasic contractions

11
Q

All GI smooth muscle has basal tone except

A

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

12
Q

striated muscle of the esophageal body contracts when

A

excitatory NT is released

13
Q

striated muscle of the esophageal body relaxes when

A

excitatory NT is NOT released

14
Q

visceral smooth muscle contracts when

A

excitatory NT is released

15
Q

visceral smooth muscle relaxes when

A

inhibitory NT is released

16
Q

3 functional parts of the esophagus

A

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

17
Q

UES

A

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

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

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

20
Q

Contraction

A

increased intensity of tonic contractions

21
Q

Relaxation

A

decreased intensity of tonic or phasic contractions

22
Q

Oral Stage of deglutition

A

VOLUNTARY; inhibits respiration for 2 sec

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

24
Q

Esophageal stage of deglutition

A

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

25
Q

What nerve innervates the esophagus?

A

Vagus

26
Q

Striated muscle of the UES and esophageal body is innervated

A

DIRECTLY by the vagal LMNs, which form motor endplates

27
Q

Vagal LMN endplates release ______ that binds striated muscle receptors to cause contraction

A

ACh binds Nicotinic muscle receptors on UES and upper 1/3 esophageal body to cause contraction

28
Q

Smooth muscle of the esophagus is innervated

A

INDIRECTLY by vagal preganglionic neurons synapsing on myenteric neurons (inhibitory and excitatory pathways)

29
Q

2 types of esophageal peristalsis

A

primary and secondary

30
Q

Primary esophageal peristalsis

A

preceded by pharyngeal peristalsis, follows a swallow, LONG parasympathetic neural reflex

31
Q

Secondary esophageal peristalsis

A

absence of pharyngeal peristalsis, initiated by distention, mediated by LONG and SHORT neural reflexes (clear esophagus)

32
Q

Swallowing reflex coordinated by Vagus

A

Afferent nerve activation in oropharynx by bolus –> opening of UES, primary peristalsis, relaxation and rebound of LES, receptive relaxation of fundus

33
Q

Opening of UES (has basal tone)

A

CNS Inhibition of vagal LMN

34
Q

Primary Peristalsis (ACh)

A

striated muscle of esophageal body sequentially activated by vagal LMNs

35
Q

<1 second after swallowing

A

ALL preganglionic VAGAL inhibitory pathways to smooth muscle of esophageal body, LES, and fundus are activated

36
Q

Vagal Inhibitory pathways <1 s after swallowing causes _______ on lower 2/3 esophageal body smooth muscle

A

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
Q

Vagal Inhibitory pathways <1 s after swallowing causes _______ on LES

A

vagal inhibition immediately causes relaxation and opening of the LES (due to basal tone) followed by rebound contraction by NANC off depolarization

38
Q

Vagal Inhibitory pathways <1 s after swallowing causes _______ on fundus

A

relaxation of fundus, decrease in intra-gastric pressure to receive food

39
Q

Deglutitive inhibition

A

IMMEDIATE vagal inhibition (preganglionic to enteric inhibitory) of all smooth muscle of the esophageal body, LES, and funds

40
Q

Receptive relaxation

A

fundus relaxes when vagal inhibitory pathway is activated

41
Q

1-5 s following swallowing

A

vagal excitatory pathways activate smooth muscle of the esophageal body and LES

42
Q

Vagal excitatory pathway causes _______ on esophageal smooth muscle

A

Cholinergic contraction and NANC off contraction produce 1 total peristaltic pressure wave

43
Q

Vagal excitatory pathway causes _______ on LES

A

Rebound contraction (closing) timed with NANC contraction

44
Q

rostral dorsal motor nucleus

A

excitatory vagal response

45
Q

caudal dorsal motor nucleus

A

inhibitory vagal response

46
Q

Dysphagia definition

A

sensation of obstruction of food through the mouth, pharynx, or esophagus

47
Q

Mechanical dysphagia

A

large food bolus or luminal narrowing of the esophageal body

48
Q

Motor dysphagia

A

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
Q

Upstroke of the peristaltic wave

A

seals the lumen and moves the bolus

50
Q

Opening of the striated muscle sphincter UES is completed by

A

vagal LMN inhibition reducing ACh and causing relaxation

51
Q

Swallowing center

A

Nucleus Ambiguus

52
Q

movement of food through the upper 1/3 esophageal body (striated) is completed by

A

vagal LMN activation, increased ACh and causing contraction after food passes, propelling it

53
Q

Movement of food through lower 2/3 esophageal body

A

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
Q

Movement of food through LES

A

normally closed due to basal tone, inhibitory input (NO) causes relaxation followed by excitatory input + off contraction to push food through

55
Q

Receptive relaxation

A

fundus relaxes due to inhibitory input (NO), no rebound contraction

56
Q

Vagal excitation

A

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
Q

Esophageal stricture due to chronic reflux esophagitis

A

scarring of the esophageal mucosa due to acid reflux causes a narrowing of the esophagus with a dilation above

58
Q

GERD treatment

A

antacids, proton pump inhibitors, histamine receptor antagonists

59
Q

Primary achalasia

A

dysfunctional NANC inhibitory enteric neurons and failure to relax LES and cause primary peristalsis in lower esophageal smooth muscle (incomplete opening of LES)

60
Q

Causes of GERD

A
  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
Q

Secondary Peristalsis

A

can be short or long neural reflex, caused by distention of esophagus in order to clear the esophagus

62
Q

Slow Wave

A

Continuous and spontaneous oscillations of the RMP (-40 - -80) in the gastric antrum and sm intestine

63
Q

Slow Waves limit

A

maximum frequency of phasic contractions, because APs can only occur during the slow wave depolarization NOT during hyperpolarization

64
Q

Slow waves of smooth muscle do not cause

A

enough depolarization for Ca entry and APs to occur to generate a contraction

65
Q

The likelihood of phasic contractions in the gastric antrum and small intestine can be increased or decreased by

A

modulating enteric or extrinsic AN activity or by hormone concentration

66
Q

Substances that increase phasic contraction frequency

A

ACh, motilin, gastrin

67
Q

Substances that decrease phasic contraction frequency

A

NE, secretin, opioids, NO

68
Q

Interstitial Cells of Cajal

A

slow wave pacemaker cells

69
Q

Location of Interstitial Cells of Cajal

A

wall of GIT

70
Q

What determines Interstitial Cells of Cajal ability to generate slow waves

A

Calcium handling by ICC mitochondria

71
Q

What alters ICC slow wave frequency?

A

thyroid hormone; it alters metabolism of Ca by the ICC mitochondria

72
Q

Disruption of ICC network results in

A

disorder of GI motility

73
Q

What segments of the GIT do not have slow waves

A

body of esophagus, orad stomach, GI sphincters

74
Q

Imodium’s effect on phasic contraction frequency

A

opioid agonist to treat diarrhea

75
Q

Opioids for pain may cause

A

constipation

76
Q

ELECTRICAL SYNCYTIUM ICC networks of gut segments coordinate slow waves by

A

gap junctions between, smooth muscle cells, smooth muscle cells and ICC, and ICC’s

77
Q

Discrete ICC networks for each portion of the gut - Small intestine

A

decrease in slow waves from duodenum (12/min) to ileum (8/min) to move chyme toward the colon

78
Q

Colon and slow waves

A

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
Q

Control of smooth muscle motility is due to

A

ICC and smooth muscle properties (slow waves), enteric neurons, extrinsic autonomic neurons, hormones