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GI Final > Motility of the GI tract > Flashcards

Motility of the GI tract Flashcards

1
Q

What are the two types of contraction of smooth muscle that are key for motility along the GI tract?

A
  1. Phasic contraction

2. tonic contraction

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2
Q

What is phasic contractions?

A

Phasic contractions are periodic contractions followed by relaxation (like in phases)

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3
Q

Which parts of the GI are involved in phasic contractions?

A

Esophagus, stomach (antrum), small intestine and all tissues involved in mixing and propulsion

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4
Q

What is tonic contractions?

A

Tonic contractions maintain a constant level of contraction w/o regular periods of relaxation.

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5
Q

What parts of the GI are involved in tonic contractions?

A

Stomach (orad), lower esophageal, ileocecal, and internal anal sphincters.

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6
Q

What are slow waves of the GI smooth muscles electrical activity?

A

They’re slow undulating changes in the resting membrane potential which causes small depolarization and repolarization. They produce tension but do not produce AP.

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7
Q

How does Ach affect the amplitude of slow waves and number of APs?

A

Increases both amplitude and number of AP

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8
Q

How does NE decreases the amplitude of slow waves?

A

NE decreases the amplitude of slow waves.

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9
Q

What causes depolarization in the GI wall?

A
  1. Stretch
  2. ACh from vagas
  3. Parasympathetis
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10
Q

What causes hyperpolarization of membrane of the GI smooth muscle cell?

A
  1. NE

2. Sympathetics innervation.

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11
Q

What is the main function of the musculares mucosa?

A

Increase surface area for absorption.

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12
Q

What is the main function of the submucosal plexus?

A

Control GI secretion and local blood flow.

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13
Q

What is the main function of the Myenteric plexus?

A

Control GI movement.

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14
Q

Which regions of the myenteric and submucosal plexuses generate spontaneous slow wave activity?

A

Pacemaker region made of interstitial cells of Cajal.

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15
Q

Where do slow waves of the GI smooth muscle cell electrical activity originate?

A

In the interstitial cells of Cajal

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16
Q

How do the slow waves generated in the ICC spread to smooth muscle?

A

Via gap junctions

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17
Q

What are the three phases of swallowing?

A
  1. Oral phase
  2. Pharyngeal phase
  3. Esophageal phase
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18
Q

Which phases of swallowing are voluntary and which are involuntary?

A

Pharyngeal phase and esophageal phase. Only the oral phase is voluntary.

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19
Q

Which phase of swallowing initiates the swallowing process?

A

Oral phase.

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20
Q

What happens during pharyngeal phase?

A

Passage of food through pharynx into esophagus. Soft palate is pulled upward – epiglotis moves –> UES relaxes –> peristaltic wave of contractions is initiated in pharynx –> food is propelled through open UES.

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21
Q

Which phase of swallowing lasts the longest?

A

Esophageal phase

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22
Q

What controls the eosphageal phase?

A

Swallowing reflex and ENS

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23
Q

What controls the involuntary swallowing reflex?

A

By the swallowing center in the medulla in the brain.

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24
Q

Describe the swallowing reflex.

A

When you put something in your mouth, oral phase is initiated, and afferent signals that are generated by mechanosensitive or chemosenstiive signals, via afferent sensory neurons like Vagas or glossopharyngeal N to swallowing center in the medulla. From there it goes to the brain stem nuclei and efferent input is sent back to the pharynx via either vagas, trigenimal, or glossopharyngeal n.

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25
Q

What effects do the efferent fibers of the swallowing reflex have?

A

It allows for pharynx to open and the upper esophageal sphincter to open.

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26
Q

During which phase of swallowing is the respiratory center inhibited?

A

During pharyngeal phase.

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27
Q

The pharyngeal peristalsis continues in the eosphageal phase as what wave?

A

Primary peristaltic wave.

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28
Q

Which peristatltic wave of the esophageal phase cannot occur after vagotomy?

A

Primary peristaltic wave.

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29
Q

What controls the primary peristaltic wave?

A

Controlled by the swallowing center in the medulla.

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30
Q

Under what conditions do secondary peristaltic wave take place?

A

Occurs if primary contraction fails to empty the eosphagus or when gastric contents reflux into the esophagus

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31
Q

What induces secondary peristaltic wave?

A

induced by distention of the esophagus by retained food and repeats until bolus is cleared.

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32
Q

What controls the secondary peristaltic wave?

A

swallowing center in medulla and ENS.

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33
Q

Can secondary peristaltic wave be possible after a vagotomy?

A

Yes.

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34
Q

What innervates the pharynx and upper part of the esophagus?

A

Vagus and glossopharyngeal nerves.

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35
Q

Normally when you’re not swallowing things, are the UES and LES open or closed?

A

Closed.

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36
Q

What can be used to see changes in intraluminal pressure between swallows and during swallowing of esophagus and stomach?

A

manometric recordings

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37
Q

Prior to swallowing, are the intraluminal pressure of the UES and LES higher or lower than zero?

A

Higher.

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38
Q

After swallowing, are the intraluminal pressure of the esophagus higher or lower before the diaphgram?

A

higher. The portion after the diaphgram the lumen has lower pressure.

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39
Q

Between swallows, what is the status of the UES and LES, body of esophagus; pressure in the UES vs pharynx and body of esophagus.

A

UES and LES is closed. The body of the esophagus is flaccid. Pressure in the UES is greater than pharyx and body of esophagus

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40
Q

T or F. Pressures in the body of the esophagus are similar to those within the body cavity in which the esophagus lies.

A

True

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41
Q

What are two challenges that the intrathoracic esophagus pose?

A
  1. keeping air out of the esophagus at the upper end
  2. keeping acidic gastric contents out of hte lower end.
    this is solved by keeping the UES and LES closed at all times unless when youre swallowing.
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42
Q

With increased intra-abdominal pressure which can occur during pregancy, poses risk of _?

A

Gastroesophageal reflux.

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43
Q

Once you initiate swallowing, the upper one opens and once bolus passes the UES, it closes back up and then goes down throught he body of esophagus via peristaltic wave. What mediates the opening of the LES?

A

Mediated by peptidergic fibers in the vagal nerve, part of the vago-vagal reflex.

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44
Q

How does VIP effect the UES and LES?

A

induce relaxation

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45
Q

What are some symptoms of GERD?

A
  • heartburn
  • chest pain
  • difficulty swallowing (dysphagis)
  • regurgitation of food (acid reflu)
  • sensation of a lump in your thourg, dry cough.
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46
Q

What are some consequences of GERD?

A
  • stricture of esophagus (scar tisse)
  • astham (aspiration)
  • chronic sinus infection (reflux into throat)
  • Barrett’s esophagus
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47
Q

How do Achalasia present?

A

It’s a neuroenic esophageal motility disorder where peristalsis is impaired due to lack of LES relaxation during swallowing - LES stays closed during swallowing, resulting in the back up of food (regurgiation). Also presents with dysphasia (both solid and fluid), vomitting, chest pain, heartburn, weight loss.

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48
Q

What is the cause of achalasia?

A

Lack of VIP or enteric system has been knocked out. Results from damage to nerves in the esophagus, preventing it from squeezing food into the stomach. It can also be caused by an abnormal immune system response.

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49
Q

What are common treatments for achalasia?

A

Endoscropic therapy or surgery.

50
Q

What part of the stomach do receptive relaxation occur?

A

The orad region, where it’s receiving food from the esophagus.

51
Q

During receptive relaxation of the orad region of the stomach, how do the pressure and volume change?

A

Pressure decreased and volume increases.

52
Q

What nerve is responsible for the receptive relaxation of the orad part of the stomach?

A

Trigeminal n. Receptive relaxation is part of the vagovagal reflex.

53
Q

What neurotransmitter does trigeminal n use during the vagovagal reflex causing receptive relaxation?

A

VIP

54
Q

Contraction of what part of the stomach serve to both mix and propel gastric contents?

A

The caudad region which has thick muscular wall and contracts faster and stronger compared to orad region.

55
Q

As contraction approaches the pylorus, how do the force and velocity change?

A

Force and velocity increase at a max frequency of 3-5 waves per min.

56
Q

What is retropulsion?

A

It’s the propulsion of gastric contents back into the stomach from the caudad region for further mixing and further reduction of particle size.

57
Q

What increases AP and force of contractions in the stomach?

A
  1. parasympathetic stimulation
  2. gastrin
  3. motilin
58
Q

What decreases AP and force of contraction in the stomach?

A
  1. sympathetic stimulation
  2. secretin
  3. GIP
59
Q

What structures are involved in gastric emptying?

A

Coordinated contractile activity of the stomach, pylorus, and proximal small intestine.

60
Q

what are some factors that can increase the rate of gastric emptying?

A
  1. Decreased distensibility of the orad
  2. increased force of peristaltic contractions of the caudad stomach
  3. Decrease tone of the pylurus
  4. increased diameter and inhibition of segmenting contractions of the proximal duodenum.
61
Q

What are some factors that can inhibit gastric emptying?

A
  1. relaxation of orad
  2. decreased force of peristaltic contractions
  3. increased tone of pyloric sphincter
  4. segmentation contractions in intestine
  5. hormones that also decrease gastric emptying like CCK.
62
Q

Regulation of gastric emptying results from the presence of receptors that lie in the _.

A

small intestine

63
Q

Info from the duodenal receptors to the gastric smooth muscle is carried by what neurons and what stimuli do these neurons respond to?

A

Submucosal and myenteric plexuses. THey respond to the physical properties (e.g. osmotic presure) and chemical composition (e.g. H+, fat and protein) of the intestinal contents

64
Q

What is the entero-gastric reflex?

A

It’s the negative feedback from duodenum which slows down the rate of gastric emptying.

65
Q

describe the mechanisms involved in the entero-gastric reflex?

A
  1. Acid in duodenum –> stimulate secretin release –> inhibit stomach motility via gastrin inhibition
  2. Fats in duodenum –> stimulate CCK and GIP –> inhibit stomach motility
  3. Hypertonicity in duodenum –> (unknown hormone) –> inhibit gastric emptying
66
Q

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

A

Slow gastric emptying

67
Q

What are some symptoms associated with gastric motility disorders

A

fullness, loss of appetite, nausea, sometimes vomitting.

68
Q

What are some causes of gastric motility disorder?

A
  1. gastric ulcer (scar tissue),
  2. cancer (physical obstruction)
  3. eating disorders (anorexia nervosa, bulimia nervosa, obesity)
  4. vagotomy
69
Q

What are some common treatment options for gastric motility disorder?

A
  1. Pyloroplasty

2. ballon dilation

70
Q

What is gastroparesis?

A

Slow emptying of stomach/paralysis of stomach

71
Q

Gastroparesis is common (about 20%) in patients with what other endocrine disorder?

A

DM1 sometimes DM2

72
Q

What are the causes of Gastroparesis?

A

Damage to vagus nerve. Could be idiopathic or due to high blood glucose as seen in diabetic gastroparesis

73
Q

What are some symptoms of gastroparesis?

A

Nausea, vomitting, an early feeling of fullness when eating, weight loss, abdominal bloating, abdominal discomfort

74
Q

What are migrating myoelectric complexes?

A

They are also known as migrating motor complex and they are periodic, bursting peristaltic contractions occurring during fasting, in both stomach and small intestine.

75
Q

How does the stomach empty of large particle of undigested residue remaining in the stomach?

A

Via migrating myoelectric complexes

76
Q

What mediates migrating myoelectric complexes?

A

motilin

77
Q

How often do migrating myoelectric complexes occur?

A

at 90 min intervals

78
Q

Absence of MMC has been associated with what GI disorder?

A

gastroparesis

79
Q

What are two types of contraction in the small intestine and what are their function?

A
  1. Segmentation contraction (serve to mix the chyme and expose it to pancreatic enzyme and secretion)
  2. Peristaltic contraction (serve to propel the chyme down the large intestine)
80
Q

In peristaltic contraction, how do the circular and longitudinal msucles respond before and after the bolus?

A

Behind the bolus, the inner circular contract and longitudinal relax. After the bolus, Inner circular relax and longitudinal contract

81
Q

In the small intestine can slow wave produce AP?

A

NO they cannot. Spike potentials are necessary.

82
Q

In the small intestine, slow wave cannot produce an AP but they set the

A

maximum frequency of contractions

83
Q

What is the gradient of electrical activity and thus frequency of contraction along the small intestine as you go from duodenum to ileum?

A

There is a decrease in frequency toward the ileocecal junction. in the duodenum it’s 12 cycles/min; jejunum 10 cycles/min; ileum 8 cycles/min

84
Q

Describe the peristatltic reflex, what neuron is involved and what nt binds to it to initiate the reflex. and what information do these reflex relay?

A

Peristaltic reflex responds to luminal content of the tone of the mucles and relays these information via the intrinsic primary afferent neuron which uses serotonin as it’s neutransmitter.

85
Q

The _ plexus is located between the longitudinal and circular smooth muscle layers, mainly regulates the relaxation and contraction of the intestinal wall.

A

Myenteric plexus

86
Q

The _ plexus senses the lumen environment among other functions.

A

Submucosal.

87
Q

What are some example of excitatory motor neurons neurotransmitters causing peristaltic contraction in the small intestine?

A

ACh and substance P

88
Q

What are some examples of inhibitory motor neuron neurotransmitters causing relaxation of small intestine smooth muscle?

A

VIP and NO

89
Q

Of the following hormones indicate whether they cause contraction or relaxation of the small intestine smooth muscles:

  1. Serotonin
  2. Prostaglandins
  3. Gastrin
  4. CCK
  5. Motilin
  6. insulin
  7. Secretin
  8. glucagon
A
  1. Contraction
  2. contraction
  3. relaxation
  4. contraction
  5. Contraction
  6. Contraction
  7. Relaxation
  8. relaxation
90
Q

Where in the brain is the vomitting center for the vomitting reflex located?

A

Medulla

91
Q

Which afferent nerve fibers travel to multiple distrubuted nuclei in the brain stem as part of the vomitting reflex?

A

Vagal afferents and sympathetic afferents.

92
Q

What is the order of events for the vomiting reflex?

A
  1. reverse peristatlsis in the small intestine
  2. relaxation of the stomach and pylorus
  3. forced inspiration to increase abdominal pressure
  4. movement of the larynx
  5. relaxation of the LES
  6. Closure of the glottis
  7. Forceful expulsion of gastric contents
93
Q

What is the direct cause of the ileocecal sphincter to relax?

A

pressure and chemical iritation in the distal ileum.

fluidity of the contents of the ileum promotes emptying

94
Q

What effect will pressure or chemical irritaion in the cecum have on the peristalsis of ileum and ileocecal sphincter?

A

Inhibit peristalsis and excite sphincter.

95
Q

what is the main function of the large intestine?

A

Absorption of water and vitamins and conversion of digested food into feces.

96
Q

In the large intestine where are the myenteric plexus concentrated?

A

Beneath the taenia coli’s.

97
Q

What are the major excitatory neurotransmitters and inhibitory neurotransmitters of the large intestine?

A

Excitatory: ACh, substance P
Inhibitory: NO and VIP

98
Q

Where in the large intestine are segmentation contractions more common and what is the purpose of this segmentation?

A

Cecum and ascending colon. Serves to mix the contents of the large intestine.

99
Q

Movements of contents along the large intestine is usually occur over large distances such as from the transverse colon to sigmoid colon. What term/phrase does this idea describe.

A

Mass movement

100
Q

Describe the texture of poop and how it changes going from the cecum to the anus.

A 
Cecum = Fluid
Ascending colon = fluid
Right colic flexure = semifluid
Transverse colon = Mush
Left colic flexure = semi mush
Descending colon = semi solid
Anus = Solid
101
Q

Excessive motility of the large intestine will cause _.

A

Less absorption and diarrhea or loose feces.

102
Q

What is the rectosphincteric reflex?

A

As the rectum fills with poop, the distention causes the smooth muscles of the rectum wall to contract and the internal anal sphincter relaxes.

103
Q

Urge to defecate occurs when the rectum fills what percent of it’s capacity?

A

25%.

104
Q

For the act of defecation, where do the preganglionic fibers of the neural pathway originate and does it synapse? Where do the postganglionic neuron synapse?

A

Preganglionic fibers origainate in the cortex of the brain. The fibers travels down to the pelvic spinal cord and synapse. The postganglionic fibers travel to the external sphincters causing it to relax and defecation occurs.

105
Q

The vago-vagal reflex involves which neurons?

A

The vagus carries both the afferent (75%) and he efferent (25%)

106
Q

What is the common action of the vago-vagal reflex?

A

Generally stimulatory to increase motility, secretomotor, vasodilatory activities

107
Q

What is the intestino-intestinal reflex?

A

It’s a short reflex which is generally inhibitory and involves only the ENS (completely independent of ANS)

108
Q

Give an example of intestino-intestinal reflex.

A

ileocecal sphincter

109
Q

What is the enterogastric reflex?

A

It’s the negative feedback from the duodenum which slows down the rate of gastric emptying

110
Q

What is the gastroileal reflex?

A

Gastric distention relaxes the ileocecal sphincters

111
Q

What is the gastro and duodeneo-colic reflex?

A

Distention of the stomach/duodenum causes mass movements transmitted by ANS

112
Q

What ist eh rectosphincteric reflex?

A

Rectal distention initiates defecation

113
Q

what are the clinical signs and symptoms associated with diverticulitis?

A

Constipation, flatus, left-sided abdominal pain, tenderness, fever, tachycardia.

114
Q

What are diverticula?

A

Small sacs of intestinal lining that bulge outward at weak spots

115
Q

What causes diverticulosis and where are they usually found?

A

Caused by excess pressure in the colon that causes weak spots in colon to bulge out and become diverticula. It can happen anywhere in the colon but usually seen around distal end of descending colon and sigmoid colon.

116
Q

What is diverticulitis?

A

when the area around the diverticulum becomes swollen and infected.

117
Q

What are some common treatment options for diverticulosis?

A

Dietary and lifestyle interventions

118
Q

What is Hirshsprung diseaes?

A

AKA megacolon which is caused by absence of ganglion cells (myenteric pluxes) from segments of the colon. As a result VIP levels are low and contraction of muscle are lost and colon contents accumulates.

119
Q

What are some common symptoms and clinical findings in patients with Hirshsprung disease?

A

Usually diagnosed in newborn who can’t pass meconium shorterly after birth. Presents with poor feeding, jaundice, and vomitting. Older kids will present constipation swollen belly and malnutrition.

120
Q

What is a treatment option for Hirshsprung diseaes?

A

surgical resection of colon segment lacking the ganglia.

GI Final (11 decks)

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