Motility of GI System Flashcards

1
Q

What involves the contraction and relaxation of the walls and sphincters of the GI tract?

A

Motility

–>regulated along GI tract

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2
Q

What are the functional layers of the GI tract?

A
Mucosal layer
-->muscularis mucosae
Submucosa
Muscle layers
Serosa
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3
Q

What is another name for serosa?

A

visceral peritoneum

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4
Q

What are the muscle layers of the GI tract?

A

Oblique
Circular
Longitudinal

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5
Q

What SM changes the shape and surface area of epithelium when it is contracted?

A

Muscularis Mucosae

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6
Q

Where is the submucosal plexus located?

A

Between submucosa and muscle layer

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7
Q

Where is the myenteric plexus?

A

between circular and longitudinal muscle layers

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8
Q

Circular M contraction ________ the diameter of the segment

A

decreases

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9
Q

Longitudinal M contraction _______the length of the segment

A

decreases

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10
Q

Are slow waves action potentials?

A

NO

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11
Q

What modulates the generation of AP and strength of contractions?

A

neural activity and hormonal activity

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12
Q

When do action potentials occur in the GI tract?

A

when the depolarization via slow waves moves the membrane potential goes above threshold

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13
Q

What contractions are periodic and followed by relaxation?

A

phasic

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14
Q

Where are phasic contractions located?

A
  • esophagus
  • stomach (antrum)
  • SI
  • tissues mixing and propulsion
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15
Q

What contractions are maintained at a constant level WITHOUT regular periods of relaxation?

A

tonic contractions

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16
Q

Where are tonic contractions?

A
  • stomach (orad)
  • lower esophageal
  • ileocecal
  • internal anal sphincters
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17
Q

What is the relation of strength of contractions with AP and slow waves?

A

Greater number of AP on top of slow waves–>larger contraction

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18
Q

What increases ampitude of slow waves?

A

ACh

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19
Q

What increases the number of AP in GI tract?

A

ACh

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20
Q

What decreases the amplitude of slow waves?

A

NE

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21
Q

Movements of GI are controlled by what plexus?

A

Myenteric

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22
Q

What plexus controls GI secretions and local blood flow?

A

Submucosal

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23
Q

What part of the ENS generates spontaneous slow wave activity?

A

Pacemaker regions in both plexuses

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24
Q

What cells are the pacemaker for GI smooth muscle?

A

Interstitial cells of Cajal (ICC)

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25
Q

What do ICC do in GI smooth muscle?

A

generate and propagate slow waves

–>spontaneous slow waves generated and spread via gap jxns

–>electrical activity in them drive frequency of contractions

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26
Q

What innervaets the muscles of mastication?

A

trigeminal N

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27
Q

What is caused by a chewing reflex?

A

mastication

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28
Q

What part of the swallowing phase is voluntary?

A

oral phase (initiates swallowing process)

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29
Q

Describe the pharyngeal phase of swallowing

A

Involuntary

soft palate goes up–>moves epiglottis–>relaxes UES–> peristaltic wave initiated in pharynx–>food propelled through open UES

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30
Q

What controls the esophageal phase of swallowing?

A

swallowing reflex and ENS

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31
Q

What controls the involuntary swallowing reflex?

A

Medulla via vagus/glossopharyngeal input

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32
Q

What wave of the esophageal phase cannot occur after vagotomy?

A

primary peristaltic wave

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33
Q

Compare control of primary vs secondary peristaltic waves in swallowing pathway

A

Primary controlled by medulla only

Secondary controlled by medulla and ENS

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34
Q

What occurs if primary peristaltic wave fails to empty esophagus or d/t gastric reflux into esophagus?

A

secondary peristaltic wave

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35
Q

Can the secondary peristaltic wave occur after vagotomy?

A

Yes

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36
Q

The secondary peristaltic wave can occur in absence of _________

A

oral and pharyngeal phases

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37
Q

What occurs in achalasia?

A

impaired peristalsis, incomplete LES relaxation during swallowing or elevation of LES resting pressure

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38
Q

What are the consequences of achalasia?

A

backflow of food in esophagus (regurg)

difficulty swallowing liquids and solids (dysphagia)

heartburn

chest pain

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39
Q

Why does achalasia occur?

A

Decreased ganglion cells in myenteric plexus d/t incomplete migration of NCC

–>damages inhibitory neurons that produce NO/VIP in esophagus so it can’t squeeze food into stomach

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40
Q

What causes GERD?

A

changes in barrier between esophagus and stomach

–>LES weakens or relaxes abnormally

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41
Q

What conditions can cause GERD?

A

Pregnancy
following large meal
heavy lifting

–>any increase in intragastric pressure (lowers LES pressure)

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42
Q

Intragastric pressure increases cause ______that ultimately lead to GERD

A

persistent reflex and inflammation

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43
Q

What are complications of GERD?

A
  • GI bleeding
  • Esophagitis
  • Stricture of esophagus
  • Barrett’s esophagus
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44
Q

Backwash of ______occurs in GERD

A

bile, pepsin, acid

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45
Q

What are the extrinsic innervations of the stomach?

A

PNS, SNS

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46
Q

What are the intrinsic innervations of the stomach?

A

ENS

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47
Q

What region of the stomach does receptive relaxation occur in?

A

orad region–>minimal contractile activity

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48
Q

Define receptive relaxation

A

decreased pressure d/t increased volume of orad region

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49
Q

What reflex causes receptive relaxation

A

vagovagal reflex

50
Q

What is the role of CCK in receptive relaxation?

A

CCK decreases contractions and increases gastric distensibility

51
Q

Where do mixing and digestion occur in the stomach?

A

caudad region

52
Q

What is max frequency of stomach contractions?

A

3-5 waves/min

53
Q

Contractions ______ in force and velocity as they approach the pylorus

A

increase

54
Q

Why does retropulsion occur in the caudad region of the stomach?

A

propelled back into stomach for further mixing and reduction of particle size

55
Q

What stimuli increase AP and force of contractions?

A

PNS
Gastrin
Motilin

56
Q

What stimule decrease AP and force of contractions?

A

SNS
Secretin
GIP

57
Q

How long does gastric emptying take?

A

3 hours

58
Q

What increases the rate of gastric emptying?

A
  • Decreased distensibility of orad
  • Increased force of contractions in caudad
  • Decreased tone of pylorus
  • Increased diameter and inhibition of proximal duodenum contractions
59
Q

Why is gastric emptying closely regulated?

A

provide adequate time for digestion, absorption and neutralization of H+ in duodenum

60
Q

What inhibits gastric emptying?

A

relaxation of orad (increased distensibility)

decreased force of contractions

increased tone of pyloric sphincter

segmental contractions in intestine

61
Q

What is the entero-gastric reflex?

A

Negative feedback from duodenum will slow rate of gastric emptying

62
Q

What is the role of secretin in the entero-gastric reflex?

A

acid in duodenum stimulates secretin release—> inhibts gastrin which inhibtis stomach motility

63
Q

What is the role of CCK and GIP in the entero-gastric reflex?

A

fats in duodenum–>stimulates CCK and GIP–> inhibits stomach motility

64
Q

What is the most common problem associated with disorders of gastric motility?

A

slow gastric emptying

65
Q

What are the causes of slow gastric emptying?

A

gastric ulcer
cancer
eating disorders
vagotomy

66
Q

What are sx of slow gastric emptying?

A

fullness
loss of appetite
N
V

67
Q

What treatments exist for slow gastric emptying?

A

pyloroplasty

balloon dilation

68
Q

Define gastroparesis

A

Slow emptying of stomach or paralysis of stomach in absence of mechanical obstruction

69
Q

What is a common cause of gastroparesis?

A

DM and injury to vagus N

70
Q

What fxns to empty the stomach of undigested residue?

A

Migrating motor complex (MMC)

71
Q

How are MMCs mediated?

A

motilin

72
Q

What is inhibited during feeding, occur at 90 minute intervals and during fasting, and are periodic bursing peristaltic contractions?

A

MMCs

73
Q

What is important for preventing small intestinal bacterial overgrowth?

A

MMCs

74
Q

What can bacterial overgrowth cause?

A

disturbance in smal bowel motility–>N, anorexia, bloating

75
Q

What does motility in the SI key for?

A

digestion and absorption

–>mix chyme with pancreatic secretions

–>expose nutrients to SI for absorption

–>propel unabsorbed chyme to LI

76
Q

What type of contractions generate back and foth movements but no propulsive or forward movements?

A

segmental contractions

77
Q

Where are segmental contractions primarily?

A

SI

78
Q

What is the difference between stomach and SI contractions?

A

Stomach–>peristaltic contractions

SI—>segmental contractions

79
Q

Why are stomach muscles reciprocally innervated?

A

So peristaltic contractions can propel food toward duodenum

–>if circular M +, longitudinal M -

80
Q

What is always present whether contractions are occurring or not?

A

slow waves

81
Q

Do slow waves themselves initiate contractions in the stomach?

A

YES

82
Q

Do slow waves themselves initiate contractions in the SI?

A

NO

–>spike AP necessary for contraction

83
Q

What sets up maximum frequency of contractions in the SI?

A

slow wave frequency

84
Q

What is the slow wave frequency in the duodenum?

A

12 cycles/min

85
Q

What is the slow wave frequency in the jejunum?

A

10 cycles/min

86
Q

What is the slow wave frequency in the ileum?

A

8 cycles/min

87
Q

What is released by enterochromaffin cells that initiate peristaltic reflexes?

A

Serotonin

bind to intrinsic primary afferent neurons

88
Q

What plexus regulate sthe relaxation and contraction of the intestinal wall?

A

myenteric plexus

89
Q

What neural inputs control SI contractions?

A

ENS

PNS, SNS

90
Q

How does serotonin control SI contractions?

A

stimulates contractions

91
Q

How does prostaglandins control SI contractions?

A

stimulates contractions

92
Q

How does epinephrine control SI contractions?

A

inhibits contractions

93
Q

How do gastrin, CCK, motilin and insullin control SI contractions?

A

Stimulate contractions

94
Q

How does secretin and glucagon control SI contractions?

A

Inhibit contractions

95
Q

What coordinates the vomiting reflex?

A

medulla

96
Q

Describe the vomiting reflex

A

Reverse peristalsis in SI–> stomach and pylorus relaxation–> forces inspiraiton increases abd pressure–> movement of the larynx–> LES relaxation–> glottis closes–>forceful expulsion of gastric contents

97
Q

Where do nerve pulses travel to reach the medulla in the vomiting reflex>

A

vagus N

98
Q

What is regulated at the ileocecal jxn?

A

Distention of ileum–> relaxation of sphincter

Distention of colon–>contraction of sphincter

99
Q

What are the muscular layers of the large intestine?

A

Longitudinal (taenia coli)

Circular

100
Q

What are haustras?

A

small pouches that give the intestine its segmented appearance—>not fixed

101
Q

Where are the ENS concentrated in the large intestine?

A

beneath teneae

102
Q

What portions of the large intestine does the vagus N innervate?

A

cecum, asc and trans colon

103
Q

What portions of the large intestine do the pelvic nerves innervate?

A

descending and sigmoid colon, rectum

104
Q

What regions of the large intestine do the superior mesenteric ganglion innervate?

A

proximal

105
Q

What regions of the large intestine do the inferior mesenteric ganglion innervate?

A

distal

106
Q

What regions of the large intestine does the hypogastric plexus innervate?

A

distal rectum, anal canal

107
Q

What innervates the internal anal sphincter?

A

pelvic splanchnic N

108
Q

What innervates the external anal sphincter?

A

pudendal N

109
Q

What is the motility of the large intestine?

A

mass movements, 1-3x/day

110
Q

Motility in the large intestine is key for?

A

absorption of water and vitamins

conversion of digested food into feces

111
Q

How does the rectum fill?

A

intermittently via mass movements and segmental contractions

112
Q

Describe the rectosphincteric reflex

A

sm in walls of rectum contract–>internal anal sphincter relaxes

113
Q

Which anal sphincter is under voluntary control?

A

external anal sphincter

114
Q

What reinforces rectosphincteric reflex with ENS?

A

neurons within spinal cord

–>destruction causes loss of voluntary defecation

115
Q

Define Hirschsprung disease

A

Absent ganglion cells from colon–> low VIP levels–> SM contriction–> accumulation of colon contents–> megacolon

116
Q

What characterizes hirschsprung disease in newborns?

A

failure to pass meconium

117
Q

What reflex initiates mass movements via distention of stomach/duodenum?

A

gastro-colic and duodeno-colic reflexes

118
Q

What is the defecation reflex?

A

rectosphincteric

rectum distended–>relaxes IAS

119
Q

What reflex slows down the rate of gastric emptying via negative feedback from duodenum?

A

enterogastric reflex

120
Q

What reflex relaxes ileocecal sphincter via gastric distention?

A

gastroileal/gastroenteric reflex

121
Q

What reflex inhibits contractions in one part of intestine when proximal part is distended?

A

intestino-intestinal reflex