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GIGU Midterm > GI Motility > Flashcards

GI Motility Flashcards

1
Q

what does motility involve?

A

contraction and relaxation of the walls and sphincters of the GI tract

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2
Q

how is motility rate regulated along the GI tract?

A

neuro or endocrine regulated

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3
Q

what specifically provides the motility to the GI tract?

A

the muscularis propria- circular muscle and longitudinal muscle

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4
Q

what happens when the circular muscle contracts?

A

it decreases the diameter of the GI segment

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5
Q

what happens when the longitudinal muscle contracts?

A

it decreases the length of the segment

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6
Q

what are slow waves?

A

oscillations of depolarization and repolarization of the membrane potential

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7
Q

what are the two types of contractions?

A

phasic and tonic contractions

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8
Q

what are phasic contractions?

A

periodic contractions followed by relaxation

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9
Q

where do phasic contractions take place?

A

the esophagus, stomach (antrum), small intestine

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10
Q

what is the purpose of phasic contractions?

A

involved in mixing and propulsion

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11
Q

what are tonic contractions?

A

they maintain a constant level of contraction without regular periods of relaxation

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12
Q

where do tonic contractions take place?

A

stomach (orad), lower esophageal, ileocecal, and internal anal sphincters

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13
Q

what is the purpose of tonic contractions?

A

they regulate the passage of foods

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14
Q

what is the relationship between slow waves, APs, and contractions in the smooth muscle?

A

the greater the number of APs on top of the slow wave, the larger the contraction

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15
Q

What is the effect of ACh on slow waves?

A

it increases the amplitude of the slow waves and the number of APs

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16
Q

what is the effect of NE on slow waves?

A

it decreases the amplitude of the slow waves/ causes hyperpolarization

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17
Q

what makes up the enteric nervous system?

A

the submucosal plexus (meissner’s plexus) and the myenteric plexus of Auerbach’s

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18
Q

where is the submucosal plexus found?

A

in the submucosa

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19
Q

what does the submucosal plexus control?

A

GI secretions and local blood flow

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20
Q

where is the myenteric plexus found?

A

between the circular and longitudinal muscle layers

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21
Q

what does the myenteric plexus mainly control?

A

GI movements

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22
Q

how are slow waves generated?

A

interstitial cells of Cajal (ICC) generate and propagate slow waves

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23
Q

how do slow waves that occur spontaneously in the ICC spread rapidly to the adjacent smooth muscle?

A

via gap junctions

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24
Q

what is considered to be the pacemaker for GI smooth muscle?

A

ICCs

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25
Q

where are ICCs found to be abundant?

A

in the myenteric plexus

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26
Q

What are most of the muscles of mastication innervated by?

A

the motor branch of the trigeminal nerve (CN V)

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27
Q

what is mastication caused by?

A

the chewing reflex

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28
Q

What are the phases of swallowing?

A

oral phase, pharyngeal phase, and then esophageal phase

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29
Q

which phase of swallowing initiates the process?

A

the oral phase

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30
Q

what happens in the pharyngeal phase of swallowing?

A

the soft palate is pulled upward–> the epiglottis moves–> the upper esophageal sphincter relaxes–> peristaltic wave of contractions is initiated in the pharynx –> food is propelled through the open UES

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31
Q

what is the esophageal phase of swallowing controlled by?

A

the swallowing reflex and the ENS

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32
Q

what occurs during the esophageal phase of swallowing?

A

a primary and then secondary peristaltic wave

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33
Q

What is the reflex portion of swallowing controlled by?

A

the swallowing center

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34
Q

where is the swallowing center located?

A

in the medulla

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35
Q

how is sensory information (food in the mouth) detected?

A

by somatosensory receptors located near the pharynx

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36
Q

how is the sensory (afferent) information from the mouth taken to the swallowing center in the medulla?

A

via the vagus and glossopharyngeal nerves

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37
Q

what is controlling the primary peristaltic wave?

A

the medulla

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38
Q

what is controlling the secondary peristaltic wave?

A

the medulla and the ENS are involved

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39
Q

which peristaltic wave requires vagal innervation?

A

primary peristaltic wave; it cannot occur after a vagotomy

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40
Q

at rest, what sphincters are contracted?

A

the UES, the LES, and the fundus of the stomach

41
Q

what occurs during swallowing that allows the food bolus to keep moving?

A

there are changes in pressure along the esophagus as the food bolus passes through it

42
Q

what is achalasia?

A

impaired peristalsis; incomplete LES relaxation during swallowing

43
Q

what happens during achalasia?

A

the LES stays mostly closed during swallowing; results in the backup of food; there is an elevation of LES resting pressure

44
Q

why does achalasia happen?

A

there are decreased numbers of ganglion cells in the myenteric plexus; degeneration of inhibitory neurons that produce NO/VIP (these normally cause relaxation); damage to nerves in the esophagus, preventing it from squeezing food into the stomach

45
Q

what happens in cases of GERD?

A

there are changes in the barrier between the esophagus and the stomach (e.g. the LES relaxes abnormally or weakens); abnormally low pressures in the LES

46
Q

what can be said about the pressure of the esophagus at the levels of the sphincters and the fundus of the stomach at rest?

A

they are above the atmospheric pressure

47
Q

what can be said about the pressure of the the thoracic parts of the esophagus at rest?

A

the pressure is going to be very low- below atmospheric pressure

48
Q

what can be said about the esophageal pressure at the abdominal level at rest?

A

it is a little over the atmospheric pressure

49
Q

in order to get the UES to relax, what happens to the pressure?

A

it drops to 0mmHg

50
Q

what are the two regions of the stomach?

A

the orad and the caudad

51
Q

what are the three layers of muscles in the stomach?

A

circular layer, longitudinal layer, and the oblique layer

52
Q

what is the extrinsic innervation of the stomach?

A

the parasympathetic and the sympathetics

53
Q

what is the intrinsic innervation of the stomach?

A

myenteric and submucosal plexuses (ENS)

54
Q

what is receptive relaxation and where does it occur?

A

decreased pressure and increased volume in the orad region of the stomach

55
Q

what mediates the receptive relaxation response?

A

the vagovagal reflex

56
Q

what happens when CCK is released from the duodenum?

A

it signals back to the stomach to limit contractions and increase distensibility

57
Q

where does the mixing and the digestion take place in the stomach?

A

in the caudad region of the stomach

58
Q

How do the contractions in the stomach change as you reach the pylorus?

A

contractions increase in force and velocity as they approach the pylorus

59
Q

what is retropulsion?

A

most of the gastric contents are propelled back into the stomach for further mixing and further reduction in particle size

60
Q

how are the gastric contractions regulated?

A

the ANS (parasympathetics and sympathetics) and hormonal regulation

61
Q

what hormones increase the action potentials that regulate the gastric contractions?

A

gastrin and motilin

62
Q

what hormones decrease the APs that regulate the gastric contractions?

A

secretin and GIP

63
Q

how is gastric emptying accomplished?

A

by the coordinated contractile activity of the stomach, pylorus, and proximal small intestine

64
Q

what factors cause the rate of gastric emptying to increase?

A

decreased distensibility of the orad stomach, increased force of peristaltic contractions of the caudad stomach, decreased tone of the pylorus (it becomes relaxed) and increased diameter and inhibition of segmenting contractions of the proximal duodenum

65
Q

why is gastric emptying closely regulated?

A

to provide adequate time for neutralization of gastric H+ in the duodenum and sufficient time for digestion and absorption

66
Q

what are the factors that inhibit gastric emptying?

A

relaxation of the orad, decreased force of peristaltic contractions, increased tone of the pyloric sphincter, segmentation contractions in the intestine

67
Q

what is the entero-gastric reflex?

A

negative feedback from the duodenum will slow down the rate of gastric emptying

68
Q

what does acid in the duodenum stimulate?

A

secretin release

69
Q

what is the result of secretin release?

A

inhibition of the stomach motility via gastrin inhibition

70
Q

what does fat in the duodenum stimulate?

A

CCK and GIP secretion–> inhibits stomach motility

71
Q

what does hypertonicity in the duodenum stimulate?

A

an unknown hormone that inhibits gastric emptying

72
Q

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

A

slow gastric emptying

73
Q

what are some causes of slow gastric emptying?

A

gastric ulcer, cancer, eating disorders, vagotomy

74
Q

how do you treat slow gastric emptying?

A

pyloroplasty or balloon dilation

75
Q

what is gastroparesis?

A

slow emptying of the stomach/ paralysis of the stomach in the absence of mechanical obstruction

76
Q

what is a common cause of gastroparesis?

A

diabetes mellitus or an injury to the vagus nerve

77
Q

what are migrating myoelectric complexes?

A

periodic bursting peristaltic contractions that occur at 90 minute intervals during fasting

78
Q

what mediates the MMCs?

A

motilin

79
Q

what are MMCs used for?

A

housekeeping- large particles of undigested residue remaining in the stomach are emptied by this complex

80
Q

what inhibits MMCs?

A

feeding

81
Q

what do the MMCs prevent?

A

Small intestinal bacterial overgrowth (SIBO)

82
Q

what is the purpose of the segmentation contractions in the SI?

A

they serve to mix the chyme and expose it to pancreatic enzymes and secretions

83
Q

what kind of movements are the segmentation contractions?

A

back and forth movements; no forward, propulsive movement along the small intestine

84
Q

what is the purpose of the peristaltic contractions?

A

they are designed to propel the chyme along the small intestine

85
Q

what are necessary for muscle contraction to occur in the small intestine?

A

spike potentials (AP)

86
Q

what sets the maximum frequency of contractions in the SI?

A

slow wave frequency

87
Q

what happens to the slow wave frequency as you move towards the distal SI?

A

it decreases

88
Q

once the food bolus in the intestinal lumen is sensed by enterochromaffin cells of the intestinal mucosa, what happens?

A

there is a release of serotonin

89
Q

what happens when there is a release of serotonin by the enterochromaffin cells?

A

it binds to receptors on the intrinsic primary afferent neurons (IPANs) and initiates the peristaltic reflex

90
Q

what is the perostaltic reflex mediated by?

A

the ENS

91
Q

what affect does gastrin, CCK, motilin, and insulin have on the SI?

A

they stimulate contractions

92
Q

what effect do secretin and glucagon have on the SI?

A

they inhibit contractions

93
Q

what is the vomiting reflex mediated by?

A

the medulla

94
Q

what causes relaxation of the ileocecal junction?

A

distention of the ileum

95
Q

what innervates the internal anal sphincter?

A

the pelvic splanchnic nerve

96
Q

what innervates the external anal sphincter?

A

the somatic nervous system through the pudendal nerve

97
Q

what are mass movements?

A

they occur in the colon and function to move the contents of the large intestine over long distances; stimulate defecation reflex

98
Q

as the rectum fills with feces, the smooth muscle wall of the rectum contracts and the internal anal sphincter relaxes in what reflex?

A

the rectosphincteric reflex

99
Q

what causes a loss of voluntary control of defecation?

A

destruction of pathways within the spinal cord that lead to the cerebral cortex

GIGU Midterm (19 decks)

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