GI Motility Flashcards
(99 cards)
1
Q
what does motility involve?
A
contraction and relaxation of the walls and sphincters of the GI tract
2
Q
how is motility rate regulated along the GI tract?
A
neuro or endocrine regulated
3
Q
what specifically provides the motility to the GI tract?
A
the muscularis propria- circular muscle and longitudinal muscle
4
Q
what happens when the circular muscle contracts?
A
it decreases the diameter of the GI segment
5
Q
what happens when the longitudinal muscle contracts?
A
it decreases the length of the segment
6
Q
what are slow waves?
A
oscillations of depolarization and repolarization of the membrane potential
7
Q
what are the two types of contractions?
A
phasic and tonic contractions
8
Q
what are phasic contractions?
A
periodic contractions followed by relaxation
9
Q
where do phasic contractions take place?
A
the esophagus, stomach (antrum), small intestine
10
Q
what is the purpose of phasic contractions?
A
involved in mixing and propulsion
11
Q
what are tonic contractions?
A
they maintain a constant level of contraction without regular periods of relaxation
12
Q
where do tonic contractions take place?
A
stomach (orad), lower esophageal, ileocecal, and internal anal sphincters
13
Q
what is the purpose of tonic contractions?
A
they regulate the passage of foods
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
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
16
Q
what is the effect of NE on slow waves?
A
it decreases the amplitude of the slow waves/ causes hyperpolarization
17
Q
what makes up the enteric nervous system?
A
the submucosal plexus (meissner’s plexus) and the myenteric plexus of Auerbach’s
18
Q
where is the submucosal plexus found?
A
in the submucosa
19
Q
what does the submucosal plexus control?
A
GI secretions and local blood flow
20
Q
where is the myenteric plexus found?
A
between the circular and longitudinal muscle layers
21
Q
what does the myenteric plexus mainly control?
A
GI movements
22
Q
how are slow waves generated?
A
interstitial cells of Cajal (ICC) generate and propagate slow waves
23
Q
how do slow waves that occur spontaneously in the ICC spread rapidly to the adjacent smooth muscle?
A
via gap junctions
24
Q
what is considered to be the pacemaker for GI smooth muscle?
A
ICCs
25
where are ICCs found to be abundant?
in the myenteric plexus
26
What are most of the muscles of mastication innervated by?
the motor branch of the trigeminal nerve (CN V)
27
what is mastication caused by?
the chewing reflex
28
What are the phases of swallowing?
oral phase, pharyngeal phase, and then esophageal phase
29
which phase of swallowing initiates the process?
the oral phase
30
what happens in the pharyngeal phase of swallowing?
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
31
what is the esophageal phase of swallowing controlled by?
the swallowing reflex and the ENS
32
what occurs during the esophageal phase of swallowing?
a primary and then secondary peristaltic wave
33
What is the reflex portion of swallowing controlled by?
the swallowing center
34
where is the swallowing center located?
in the medulla
35
how is sensory information (food in the mouth) detected?
by somatosensory receptors located near the pharynx
36
how is the sensory (afferent) information from the mouth taken to the swallowing center in the medulla?
via the vagus and glossopharyngeal nerves
37
what is controlling the primary peristaltic wave?
the medulla
38
what is controlling the secondary peristaltic wave?
the medulla and the ENS are involved
39
which peristaltic wave requires vagal innervation?
primary peristaltic wave; it cannot occur after a vagotomy
40
at rest, what sphincters are contracted?
the UES, the LES, and the fundus of the stomach
41
what occurs during swallowing that allows the food bolus to keep moving?
there are changes in pressure along the esophagus as the food bolus passes through it
42
what is achalasia?
impaired peristalsis; incomplete LES relaxation during swallowing
43
what happens during achalasia?
the LES stays mostly closed during swallowing; results in the backup of food; there is an elevation of LES resting pressure
44
why does achalasia happen?
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
what happens in cases of GERD?
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
what can be said about the pressure of the esophagus at the levels of the sphincters and the fundus of the stomach at rest?
they are above the atmospheric pressure
47
what can be said about the pressure of the the thoracic parts of the esophagus at rest?
the pressure is going to be very low- below atmospheric pressure
48
what can be said about the esophageal pressure at the abdominal level at rest?
it is a little over the atmospheric pressure
49
in order to get the UES to relax, what happens to the pressure?
it drops to 0mmHg
50
what are the two regions of the stomach?
the orad and the caudad
51
what are the three layers of muscles in the stomach?
circular layer, longitudinal layer, and the oblique layer
52
what is the extrinsic innervation of the stomach?
the parasympathetic and the sympathetics
53
what is the intrinsic innervation of the stomach?
myenteric and submucosal plexuses (ENS)
54
what is receptive relaxation and where does it occur?
decreased pressure and increased volume in the orad region of the stomach
55
what mediates the receptive relaxation response?
the vagovagal reflex
56
what happens when CCK is released from the duodenum?
it signals back to the stomach to limit contractions and increase distensibility
57
where does the mixing and the digestion take place in the stomach?
in the caudad region of the stomach
58
How do the contractions in the stomach change as you reach the pylorus?
contractions increase in force and velocity as they approach the pylorus
59
what is retropulsion?
most of the gastric contents are propelled back into the stomach for further mixing and further reduction in particle size
60
how are the gastric contractions regulated?
the ANS (parasympathetics and sympathetics) and hormonal regulation
61
what hormones increase the action potentials that regulate the gastric contractions?
gastrin and motilin
62
what hormones decrease the APs that regulate the gastric contractions?
secretin and GIP
63
how is gastric emptying accomplished?
by the coordinated contractile activity of the stomach, pylorus, and proximal small intestine
64
what factors cause the rate of gastric emptying to increase?
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
why is gastric emptying closely regulated?
to provide adequate time for neutralization of gastric H+ in the duodenum and sufficient time for digestion and absorption
66
what are the factors that inhibit gastric emptying?
relaxation of the orad, decreased force of peristaltic contractions, increased tone of the pyloric sphincter, segmentation contractions in the intestine
67
what is the entero-gastric reflex?
negative feedback from the duodenum will slow down the rate of gastric emptying
68
what does acid in the duodenum stimulate?
secretin release
69
what is the result of secretin release?
inhibition of the stomach motility via gastrin inhibition
70
what does fat in the duodenum stimulate?
CCK and GIP secretion--> inhibits stomach motility
71
what does hypertonicity in the duodenum stimulate?
an unknown hormone that inhibits gastric emptying
72
what is the most common problem associated with disorders of gastric motility?
slow gastric emptying
73
what are some causes of slow gastric emptying?
gastric ulcer, cancer, eating disorders, vagotomy
74
how do you treat slow gastric emptying?
pyloroplasty or balloon dilation
75
what is gastroparesis?
slow emptying of the stomach/ paralysis of the stomach in the absence of mechanical obstruction
76
what is a common cause of gastroparesis?
diabetes mellitus or an injury to the vagus nerve
77
what are migrating myoelectric complexes?
periodic bursting peristaltic contractions that occur at 90 minute intervals during fasting
78
what mediates the MMCs?
motilin
79
what are MMCs used for?
housekeeping- large particles of undigested residue remaining in the stomach are emptied by this complex
80
what inhibits MMCs?
feeding
81
what do the MMCs prevent?
Small intestinal bacterial overgrowth (SIBO)
82
what is the purpose of the segmentation contractions in the SI?
they serve to mix the chyme and expose it to pancreatic enzymes and secretions
83
what kind of movements are the segmentation contractions?
back and forth movements; no forward, propulsive movement along the small intestine
84
what is the purpose of the peristaltic contractions?
they are designed to propel the chyme along the small intestine
85
what are necessary for muscle contraction to occur in the small intestine?
spike potentials (AP)
86
what sets the maximum frequency of contractions in the SI?
slow wave frequency
87
what happens to the slow wave frequency as you move towards the distal SI?
it decreases
88
once the food bolus in the intestinal lumen is sensed by enterochromaffin cells of the intestinal mucosa, what happens?
there is a release of serotonin
89
what happens when there is a release of serotonin by the enterochromaffin cells?
it binds to receptors on the intrinsic primary afferent neurons (IPANs) and initiates the peristaltic reflex
90
what is the perostaltic reflex mediated by?
the ENS
91
what affect does gastrin, CCK, motilin, and insulin have on the SI?
they stimulate contractions
92
what effect do secretin and glucagon have on the SI?
they inhibit contractions
93
what is the vomiting reflex mediated by?
the medulla
94
what causes relaxation of the ileocecal junction?
distention of the ileum
95
what innervates the internal anal sphincter?
the pelvic splanchnic nerve
96
what innervates the external anal sphincter?
the somatic nervous system through the pudendal nerve
97
what are mass movements?
they occur in the colon and function to move the contents of the large intestine over long distances; stimulate defecation reflex
98
as the rectum fills with feces, the smooth muscle wall of the rectum contracts and the internal anal sphincter relaxes in what reflex?
the rectosphincteric reflex
99
what causes a loss of voluntary control of defecation?
destruction of pathways within the spinal cord that lead to the cerebral cortex
