Gastrointestinal Physiology: Motility I Flashcards

1
Q

The only exception to the net mouth to anus (aboral) movement

A

Vomiting

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2
Q

Generate the force to move material along the GI tract

A

Phasic contractions

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3
Q

Create resistance to movement

-normally in the sphincters or pathologically elsewhere

A

Tonic contractions

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4
Q

What are the three primary functions of mastication?

A
  1. ) Reduction in particle size
  2. ) Mixing
  3. ) Enhance stimulation of taste buds and other receptors
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5
Q

Mixing of the food with saliva is needed to libricate the mass and increase the exposure to which two things?

A
  1. ) Salivary amylase (carbohydrate digestion)

2. ) Lingual lipase (lipid digestion)

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6
Q

Mastication enhances stimulation of taste buds and other receptors in the oral cavity to increase salivation and appreciation of the food. Some of these receptors initiate the

A

Cephalic phase of digestion

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7
Q

Control of mastication is primarily

A

Reflexive

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8
Q

Plays a much larger role in indigestion than most people realize

A

Impaired chewing

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9
Q

Moving food and liquid from the mouth into the stomach, is an example of integration within the neural system. This is referred to as

A

Swallowing

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10
Q

Swallowing is divided into which 3 phases?

A
  1. ) Oral
  2. ) Pharyngeal
  3. ) Esophageal
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11
Q

When not swallowing (i.e. at rest), the upper esophageal sphincter (UES) and the lower esophageal sphincter (LES) are

A

Contracted

-effectively isolates the esophagus

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12
Q

The esophageal muscles do not maintain any tonic contractions, thus the esophagus is

A

Flaccid

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13
Q

The pressures in the upper and lower esophagus reflect the pressure in the

A

Thoracic and abdominal cavities respectively

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14
Q

The buccal or oral phase of swallowing is under

A

Voluntary control

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15
Q

A bolus, approx. 5-15 cm3, is moved to the back of the mouth by elevating the front of the tongue against the surface of the hard palate in the

A

Buccal (oral) phase

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16
Q

In the buccal (oral) phase of swallowing, the bolus is moved into the oropharynx by

A

Retraction and depression of the tongue

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17
Q

The driving force for movement of the bolus in the buccal phase is a pressure gradient of approximately

A

4-10 mmHg

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18
Q

An involuntary reflex coupled to the primary esophageal peristaltic wave

A

Pharyngeal phase of swallowing

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19
Q

Pharyngeal phase is an involuntary reflex coupled to the primary esophageal peristaltic wave. Both are controlled by the

A

Swallowing center

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20
Q

The pharyngeal phase is initiated by the bolus touching the pillars of fauces, tonsils, soft palate, base of tongue and

A

Posterior wall of the pharynx

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21
Q

When this happens, afferent impulses go to the swallowing center. Efferent fibers convey impulses back to the

A

Pharyngeal muscles, UES, esophageal muscles, LES, and orad portion of the stomach

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22
Q

The swallowing center also interacts with other centers controlling

A

Respiration and speech

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23
Q

Relaxes as the pharyngeal peristaltic wave starts (pressure gradient up to 100 mm Hg), and the bolus is propelled into the esophagus

A

UES

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24
Q

At the end of the pharyngeal contraction, the UES contracts to a level above resting tone. This prevents

A

Reflux

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25
Q

The air passages close simultaneously with the onset of the

A

Pharyngeal wave

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26
Q

The soft palate presses against the posterior pharyngeal wall sealing the

A

Nasopharynx

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27
Q

In the pharyngeal phase, the vocal cords come together, the epiglottis deflects horizontally and the larynx moves forward and upward under the base of the tongue closing the

A

Larynx

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28
Q

A primary peristaltic wave is initiated by the swallowing center, and mediated by the vagus to the striated circular and longitudinal muscles in the

A

Esophageal phase

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29
Q

This peristaltic wave goes to the myenteric plexus in the smooth muscle, thus, activating the

A

Enteric System

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30
Q

The primary peristaltic wave starts just below the sphincter and spreads downwards pushing the bolus toward the stomach when the

A

UES pressure is high

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31
Q

Almost simultaneously, a wave of inhibition starts in the

A

Proximal LES (LES relaxes)

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32
Q

The likely neurotransmitters for this LES inhibition are

A

VIP and NO

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33
Q

This continues into the stomach (receptive

relaxation), and is mediated by

A

Vagal inhibitory fibers acting on ENS

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34
Q

The temporary inhibition of resting tone in the fundus and orad area

A

Receptive Relaxation

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35
Q

This maintains the esophageal-gastric pressure gradient to prevent

A

Reflux during swallowing

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36
Q

After the peristaltic wave passes the LES, the LES contracts to a level above resting tone. This is mediated by

-prevents reflux

A

ACh and enkephalins

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37
Q

May move through the LES before the peristaltic wave in response to gravity

A

Liquids

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38
Q

Air in the pharynx at the start of a swallow passes into the

A

Trachea

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39
Q

Air trapped in saliva and food, or voluntarily swallowed, passes into the stomach. This results in

A

Burping

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40
Q

A peristaltic wave not preceded by pharyngeal activity or relaxation of the UES

A

Secondary Peristalsis

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41
Q

Functions to clear the esophagus of retained food and/or refluxed gastric contents

A

Secondary peristalsis

42
Q

Initiated by distention in the body of the esophagus that stimulates stretch receptors in the wall

A

Secondary peristalsis

43
Q

What is secondary peristalsis mediated by in

  1. ) Striated muscle?
  2. ) Smooth muscle
A
  1. ) Vagus

2. ) Vagus and ENS

44
Q

Is there any sensation associated with secondary peristaltic contractions?

A

No (little to none)

45
Q

Normally maintains a pressure that is 20-40 mmHg higher than the stomach which prevents reflux

A

LES

46
Q

This anti-reflux mechanism is particularly important during the third-trimester pregnancy as other mechanisms are weakened

A

Secondary peristalsis

47
Q

Another anti-reflux mechanism is the pinching action of the diaphragm on the

A

Esophagus

48
Q

Infants rely primarily on this anti-reflux mechanism, while awaiting other mechanisms to develop

A

Pinching of diaphragm on esophagus

49
Q

Another anti-reflux mechanism is that increases in intra-gastric and intra abdominal pressures lead to increased

A

LES pressure

50
Q

Occur in humans and are centrally controlled (does not occur in rats)

A

Retching and Vomiting

51
Q

However, reverse esophageal peristalsis does not usually occur in

A

Humans

52
Q

Starts with orally directed peristalsis in the small intestine that leads to movement of intestinal
contents into the stomach

A

Retching and Vomiting

53
Q

Then forceful contractions of duodenal and gastric antral muscles, coupled with deep inspiration and decreased LES tone leads to

A

Retching

54
Q

Movement of contents into the esophagus but with inadequate force to move contents through UES

A

Retching

55
Q

Subsequent additional contraction of the\ diaphragm and abdominal muscles (increases intraabdominal pressure), coupled with further decreases in LES and UES tone leads to

A

Vomiting

56
Q

Storage in the stomach is accomplished by both

A
  1. ) Receptive relaxation

2. ) Accommodation

57
Q

Muscle relaxation in response to stretching or distension by food

A

Accommodation

58
Q

Gastric filling leads to changes in volume with little to no change in

A

Wall pressure

59
Q

Increasing gastric volume with 1.6L of air increases intragastric pressure by

A

10mmHG or less

60
Q

Allows digestion of foo by salivary and gastric enzymes, as well as controlled gastric emptying

A

Gastric storage

61
Q

The storage site in the stomach

A

Upper stomach

62
Q

Causes the mixing of food, salivary secretions and gastric secretions

A

Antral muscle contraction

63
Q

Mixing facilitates gastric

A

Digestion

64
Q

The antrum grinds the solid food into small particles which the pylorus allows to pass into the

A

Duodenum

65
Q

The rate of gastric emptying is controlled to deliver chyme to the small intestine for optimized

A

Digestion and absorption

66
Q

Sweep luminal contents (e.g. undigestible materials) out of the stomach, down through the small intestine and into the large intestine

A

Migrating Myoelectric Complexes (MMCs)

67
Q

MMCs are only active during the

A

Interdigestive period

68
Q

At the onset of eating, shallow and slow peristaltic contractions start over the corpus, and increase in strength and velocity as they move into the

A

Antrum

69
Q

With increased time after eating, contractions start higher up in the corpus and are

A

Stronger

70
Q

The simultaneous contraction of the terminal antrum and pylorus

A

Antral Systole

71
Q

Results in 1) retrograde movement of chyme back into the stomach, leading to effective mixing, and 2) shearing forces, which reduces particle size

A

Antral systole

72
Q

Leave the stomach prior to antral systole

A

Chyme and liquids

73
Q

During the interdigestive period, when the stomach and small intestine empty, they generate

A

Strong peristaltic waves (MMCs)

74
Q

Results in semi-liquid chyme or liquids passing through the pylorus prior to antral systole and closure of pyloric sphincter

A

Gastric Emptying

75
Q

The emptying rate is controlled by the interactions of gastric and duodenal motilities, and pyloric sphincter tone, which are modified by

A

Enteric, spinal, and vago-vagal reflexes and GI peptides

76
Q

Increased gastric volume increases gastric emptying rate via

A

Gastric stretch receptors

77
Q

Particle size: 0.25 mm3 empty faster than 10 mm3 due to the

A

Pyloric lumenal diameter

78
Q

What empties faster, carbohydrates or proteins?

A

Carbohydrates

79
Q

What empties faster, proteins or fats?

A

Proteins

80
Q

Duodenal chemo-receptors, CCK, GIP and secretin, all have what effect on the rate of gastric emptying?

A

Decrease rate

81
Q

What empties faster, acidic or neutral species?

A

Neutral

82
Q

What empties faster, hypotonic, isotonic, or hypertonic solutions?

A

Isotonic faster than hypotonic

Hypotonic faster than hypertonic

83
Q

The duodenogastric reflex i.e. excessive duodenal distention activates duodenal stretch receptors, leading to

A

Reduced gastric contraction and emptying rate

84
Q

Ileal distension decreases

A

Gastric emptying

85
Q

Functions in gastric and small intestine interdigestive motility

A

Migrating myoelectric complex (MMC)

86
Q

The strongest peristaltic contractions observed in healthy individuals are from

A

MMCs

87
Q

“Clean out” residual material from the stomach and small intestine and moves it into the large intestine

A

MMCs

88
Q

MMCs require an intact

A

Enteric nervous system

89
Q

The beginning of the MMC is associated with rising blood levels of

A

Motilin

90
Q

Stop with rising blood gastrin levels and feeding

A

MMCs

91
Q

Not related to ‘hunger pangs’ but could contribute to the discomfort and pain of ulcers

A

MMCs

92
Q

Slow movement of the chyme through the intestine maximizes

A

Absorption of nutrients

93
Q

Mixing in the small intestine facilitates intraluminal digestion by mixing chyme with secretions and facilitates absorption by increasing exposure of the chyme to the

A

Epithelial surface

94
Q

In the small intestine, functions to empty unabsorbed residue and secreted material into the large bowel

A

MMCs

95
Q

Muscularis mucosae and villus muscle activity is responsible for movement of the

A

Mucosa and Villi of small intestine

96
Q

Muscularis mucosae and villus muscle contractions are independent of contractions in the

A

Muscularis externa

97
Q

Activity in these muscles serves to increase absorption and aids

A

Lymph flow

98
Q

Sympathetic stimulation and chyme stimulating touch receptors on the epithelial surface of the small intestine induces

A

Rapid shifts in mucosal surface

99
Q

This can be seen in X-rays after administering

A

Barium salts

100
Q

Responsible for intraluminal mixing and propulsion

A

Muscularis externa