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GI System Final I > Motility of the GI tract > Flashcards

Motility of the GI tract Flashcards

1
Q

Why is motility used

A

preparation of ingested food for digestion and absorption, propelling food from mouth to rectum

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2
Q

Circular muscle function

A

decreases diameter of the segment

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3
Q

Longitudinal muscle function

A

decreases the length of the segment

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4
Q

Two types of contractions for motility

A

phasic and tonic

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5
Q

Phasic contraction process

A

periodic contractions followed by relaxation

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6
Q

Where do phasic contractions occur

A

esophagus stomach, small intestine, all tissues involved in mixing and propulsion

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7
Q

Tonic contractions

A

constant level of contraction without regular relaxation usually under basic conditions

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8
Q

Where do tonic contractions occur?

A

stomach (orad), lower esophageal, ileocecal, internal anal sphincter

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9
Q

T/F Slow was are unique to the GI smooth muscle

A

T

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10
Q

What are slow waves

A

depolarization and repolarization of the membrane potential due to electroconductivity to initiate contraction

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11
Q

T/F Slow waves are the same as action potentials

A

F- slow waves are NOT action potentials

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12
Q

How does slow wave invoke a action potential

A

slow wave has to touch the threshold for particular membrane

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13
Q

Tension and slow wave relation

A

if there is slow wave activity - tension (contraction) will follow

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14
Q

What does tension determine

A

the strength of the contraction

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15
Q

Normal frequency of slow waves

A

3-12 waves/min

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16
Q

What changes the frequency of slow waves

A

where the organ is located

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17
Q

T/F Subthreshold depolarization can not produce contraction

A

F- subthreshold depolarization can produce weak contraction

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18
Q

What are basal contractions

A

weak contractions produced by subthreshold depolarization

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19
Q

What happens with there is a greater number of action potentials on top of the slow wave

A

larger phasic contraction

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20
Q

What increases the amplitude of slow waves?

A

Stretch, Ach, Parasympathetics

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21
Q

What decreases the amplitude of slow waves?

A

Norepinephrine, Sympathetics

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22
Q

Decreased amplitude of slow waves _____ the number of action potentials

A

decreases

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23
Q

Where is Ach released from

A

Vagus nerve

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24
Q

Increased action potentials is caused by ______ amplitude

A

increase

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25
Q

Pacemaker for GI smooth muscle

A

Interstitial cells of Cajal

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26
Q

Where do slow waves originate

A

Interstitial cells of Cajal

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27
Q

Where are the interstitial cells of Cajal located?

A

myenteric plexus

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28
Q

How do slow waves travel in ICC to smooth muscle

A

spontaneously and spread rapidly via gap junctions

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29
Q

Calcium channels and GI system smooth muscle

A

circular and longitudinal muscle increases permeability to calcium and they are important for contraction

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30
Q

What happens with increase in Ca+ channel to open

A

bigger contraction

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31
Q

What initiates swallowing?

A

voluntarily in the mouth

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32
Q

What reflex controls swallowing after the mouth

A

involuntary reflex

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33
Q

What are the 3 phases of swallowing

A
  • Oral phase (voluntary), - Pharyngeal phase, - Esophageal phase
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34
Q

What happen in oral phase

A

initiation of swallowing

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35
Q

What happens in the pharyngeal phase

A

passage of food through pharynx into esophagus

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36
Q

Process during pharyngeal phase

A

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

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37
Q

Which part of the swallowing components is striated muscle

A

Pharynx and UES

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38
Q

Which part of the swallowing components is smooth muscle

A

Esophagus and LES and stomach (& rest of GI)

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39
Q

What happens during esophageal phase

A

passage of food from pharynx to stomach

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40
Q

What controls esophageal phase?

A

swallowing reflex and ENS

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41
Q

Importance of pharynx in respiration and propelling food

A

pharynx makes switch from respiration for short time to help propel food and swallow

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42
Q

What swallowing reflex is controlled by the medulla

A

involuntary

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43
Q

What types of receptors are in the pharynx

A

somtosensory receptors - mechanoreceptors and chemoreceptors

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44
Q

Swallowing process after stimulation

A

afferent info end to medulla by vagus and glossopharyngeal nerves –> efferent input to pharynx to swallow

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45
Q

Two types of peristaltic waves

A

primary and secondary

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46
Q

Primary peristaltic wave

A

continuation of pharyngeal peristalsis

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47
Q

What controls primary peristaltic wave

A

swallowing center in the medulla

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48
Q

Secondary peristaltic wave

A

occurs if primary contraction fails to empty esophagus or when there is gastric reflux into the esophagus

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49
Q

What controls secondary peristaltic wave

A

swallowing center and ENS

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50
Q

T/F Secondary peristaltic wave needs stimulation from vagus nerve

A

F- secondary peristaltic waves can occur even without stimulation from vagus nerve

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51
Q

What if vagus nerve is cut?

A

myenteric plexus becomes excitable enough after several days to cause strong 2ndary peristaltic waves

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52
Q

What state are the sphincters in between swallows?

A

closed

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53
Q

What state is the esophagus in betweens swallows?

A

flaccid

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54
Q

Which pressure is higher between swallows?

A

pressure in upper esophageal sphincter is greater than the pharynx and body of esophagus

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55
Q

What is the pressure like in the thorax

A

subatmospheric

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56
Q

When is the UES open?

A

when food bolus going from pharynx to esophagus

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57
Q

When is LES open?

A

when food bolus going from esophagus to stomach

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58
Q

What pressure change occurs during gastroesophageal reflux?

A

intra-abdominal pressure increased

59
Q

When can the intra-abdominal pressure be increased?

A

pregnancy and obesity

60
Q

What is the opening of the LES mediated by?

A

vagal nerve

61
Q

What are two other substances released by vagus nerve?

A

vasointestinal peptide (VIP), and nitric oxide (NO)

62
Q

Function of nitric oxide

A

involved in relaxation of LES

63
Q

What happens to pressure of LES after bolus enter stomach?

A

increase in pressure and LES contracts

64
Q

Gastroesophageal Reflux disease (GERD)

A

heartburn/acid indigestion

65
Q

How does GERD occur?

A

backwash of acid, pepsin, bile into esophagus

66
Q

What can cause GERD?

A

scar tissue in esophagus, barret’s esophagus, asthma, chronic sinus infection

67
Q

Achalasia

A

damage to nerves in esophagus preventing it from squeezing food into stomach

68
Q

Symptoms of achalasia

A

backflow of food in the throat, chest pain, and weight loss

69
Q

Extrinsic innervation

A

ANS

70
Q

Intrinsic Innervation

A

myenteric and submucosal plexus

71
Q

3 layers of muscle in the stomach

A

circular, longitudinal, oblique

72
Q

What occurs in the orad region of the stomach

A

receptive relaxation

73
Q

Function of receptive relaxation

A

receive food bolus

74
Q

What is the receptive relaxation

A

decrease in pressure and increase in volume of orad region

75
Q

T/F Receptive relaxation is a vagovagal reflex

A

T

76
Q

CCK in orad region

A

CCK decreases contraction and increase gastric distensibility

77
Q

What occurs in the caudad region of the stomach

A

mix, digest, and propel gastric contents

78
Q

Primary contractive event in caudad region

A

peristaltic contraction from mid stomach to pylorus

79
Q

What happens as contractions approach the pylorus

A

increase both force and velocity

80
Q

Retrorepulsion

A

as weight comes down, it closes the pylous so some goes through but most goes back into antrum of stomahc

81
Q

Parasymp stimulation, gastrin, and motilin during gastric contrations

A

increase AP and force of contractions

82
Q

Sympathetic stimulation, secretin, and GIP during gastric contractions

A

decrease AP and force of contraction

83
Q

How to increase gastric emptying

A
  • decrease distensibility of orad
  • increase force of peristaltic contraction of caudad
  • decrease tone of pylorus
  • increase diameter and inhibiton of segmenting contractions of proximal duodenum
84
Q

How long does gastric emptying take

A

3 hours

85
Q

Factors that inhibit gastric emptying

A
  • relaxation of orad
  • decrease force of peristaltic contraction
  • increase tone of pyloric sphincter
  • segmentation contractions in intestine
86
Q

What triggers enterogastric reflexes

A

intestinal mucosal receptors

87
Q

What kind of responses does receptor activation trigger

A
  1. inhibit gastric emptying, 2. increase gastric distensibility by CCK
88
Q

Slow gastric emptying causes

A

ulcer, cancer, eating disorder, vagotomy

89
Q

S/S of gastric emptying

A

fullness, loss of appetite, nausea

90
Q

Gastroparesis

A

slow emptying of stomach/paralysis of stomach

91
Q

Cause of Gatroparesis

A

high blood pressure (diabetes), idiopathic

92
Q

S/S of gastroparesis

A

nausea, vomiting, early feeling of fullness, weight loss, abdominal bloating

93
Q

Migrating myoelectric complexes occur when…

A

emptying of large undigested particles remaining in stomach

94
Q

What are migrating myoelectric complexes

A

periodic bursting peristaltic contractions that occurs during FASTING

95
Q

What mediates MMC

A

motilin

96
Q

What inhibits MMCs

A

feeding

97
Q

Motility in small intestine function

A

mix cyme with digestive enzyme and pancreatic secretions, expose nutrients for absorption, propel unabsorbed chyme along small intestine

98
Q

Two types of contraction in small intestine

A
  1. Segmentation contractions, 2. Peristaltic contractions
99
Q

Segmentation contractions

A

mix chyme and expose it to pancreatic enzymes and secretions

no forward movement

100
Q

Peristaltic contractions

A

propel chyme toward large intestine through circular muscle contraction and longitudinal muscle relaxation

101
Q

What controls contraction of the intestine

A

ICC and smooth muscle cells

102
Q

What is electrical activity?

A

Slow wave activity is always present whether contractions are occurring or not

103
Q

Difference between slow waves in stomach and small intestine

A

Slow waves in intestine DO NOT initiate contractions in small intestine

104
Q

What is necessary for muscle contraction in the intestine

A

spike potentials

105
Q

What determines frequency of contractions in intestine

A

slow wave frequency

106
Q

Where in the small intestine is the frequency of contraction the least?

A

ileum (toward ileocecal junction)

107
Q

Frequency of slow waves in duodenum

A

numerous (12 cycles)

108
Q

What initiates contraction of small intestine

A

Ach, Substance P

109
Q

What initiates inhibitory motor neuron in small intestine

A

VIP, NO

110
Q

What does submucosal plexus sense in the small itnestine

A

environment of the lumen

111
Q

Neural input to intestine contractions

A
  • peristaltic reflex mediated by ENS

- PNS and SNS inhibit contractions

112
Q

Serotonin on intestine contractions

A

stimuates

113
Q

Prostaglandins on intestine contractions

A

stimualte

114
Q

Epinephrine on intestine contractions

A

inhibit

115
Q

Gastrin, CCK, insulin on intestine contractions

A

stimulate

116
Q

Secretin and glucagon on intestine contractions

A

inhibit

117
Q

Where is the vomitting reflex found

A

medulla

118
Q

How are impulses sent to brain for vomiting reflex

A

vagal and sympathetic afferent nerve fibers

119
Q

Reverse peristalsis for vomiting

A

relaxation of stomach and pylorus, forced inspiration to increase abdominal pressure, movement of larynx, relaxation of LES, closure of glottis, forceful expulsion of gastric contents

120
Q

What regulates flow of contents from small intestine to large intestine

A

ileocecal sphincter relaxing periodically

121
Q

Longitudinal muscle layers of large intestine

A

taenia coli

122
Q

What are the two sphincters of large inestine

A

internal anal sphincter and external anal sphincter

123
Q

Cells of internal anal sphincter

A

smooth muscle

124
Q

Cells of external anal sphincter

A

striated muscle

125
Q

Distinguishing characteristic of large intestine

A

haustras

126
Q

ENS (myenteric plexus) of large intestine

A

beneath taenia, innervate muscle laters

127
Q

Parasymp of large intestine

A

Vagus (up to transverse colon), Pelvic nerves (descending to rectum)

128
Q

Symp of large intestine

A

superior mesenteric, inferior mesenterix, hypogastric, somatic pudendal

129
Q

Superior mesenteric location for large intestine

A

proximal region

130
Q

Inferior mesenteric location for large intestine

A

distal region

131
Q

Hypogastric plexus location for large intestine

A

distal rectum and anal canal

132
Q

Somatic pudendal nerve location for large intestine

A

external anal sphincter

133
Q

Major excitatory mediators

A

Ach, Substance P

134
Q

Major inhibitory mediators

A

NO, VIP

135
Q

Mass movements of colon

A

Moves content of large intestine over long distances and stimulate defecation reflex

136
Q

Final mass movement

A

propel fecal content into rectum

137
Q

What ultimately prevents and controls the defecation reflex

A

external anal sphincter

138
Q

What controls rectosphincteric reflex and act of defecation

A

CNS neurons

139
Q

What happens if a patient is paraplegic

A

rectosphincteric reflex results in defecation

140
Q

Hirschsprung Disease

A

megacolon

141
Q

Cause of Hirschsprung Disease

A

ganglion cells absent from segment of colon

142
Q

Result of Hirschsprung Disease

A

low VIP levels, smooth muscle constriction and loss of coordinated movement –> result: colon contents accumulates

143
Q

Diverticulitis

A

small sacs of intestinal lining that bulge at weak spots

GI System Final I (7 decks)

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