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GI Final Exam > motility of the GI tract > Flashcards

motility of the GI tract Flashcards

1
Q

What is the function of tissues involved with phasic contractions?

A

mixing and propulsion

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2
Q

What usually has tonic contractions?

A

sphincters

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3
Q

What are slow waves not?

A

AP’s!

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4
Q

What is key to remember about the timing b/w the electrical and chemical responses?

A

mechanical comes shortly after electrical

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5
Q

What are slow waves?

A

de and repolarization of the membrane potential

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6
Q

What is the relationship between the number of AP’s on top of the slowave and the phasic contraction?

A

more AP’s leads to large phasic contraction

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7
Q

What does Ach do to slow waves?

A

increases their amplitude

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8
Q

What does NE do to slow waves?

A

decreases amplitude

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9
Q

What changes the shape and surace areal of the epithelium?

A

muscularis mucosae (not propria)

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10
Q

What is the order of layers starting at the epithelium?

A

Epithelium, lamina propria, muscularis mucosae, submucosa, circular muscle, longitudinal muscle, and serosa

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11
Q

What generates spontaneous slow wave activity?

A

the pacemaker regions in the myenteric and submucosal plexuses

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12
Q

Where is the myenteric plexus?

A

between the longitudinal and circular layers

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13
Q

What does the myenteric plexus control?

A

movements of the GI tract

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14
Q

Where is the submucsoal plexus and what dioes it mainly control?

A

the secretions and local blood flow of the GI tract

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15
Q

What is the pacemaker for GI smooth muscle?

A

interstitial cells of Cajal

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16
Q

How do smooth muscle cells respond to slow wave depolarizations?

A

with increased Ca2+ channel open probability

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17
Q

What is the oral phase of swallowing?

A

volutnary

-initiates the swallowing process

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18
Q

What is the pharyngeal phase of swallowing?

A

involuntary

  • passage of food through pharynx into esophagus
  • soft palate pulled upward, epiglotis moves, ues relaxes, perstaltic wave of contractions is initiated in pharnyx, food is propelled through open UES
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19
Q

What is the esophageal phase of swallowing?

A

involuntary

  • passage of food from pharynx to stomach
  • control by the swallowing reflex and the ENS (primary and secondary peristaltic wave)
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20
Q

Where is the swallowing center located?

A

the medulla

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21
Q

What does the swallowing center inhibit during the pharyngeal stage?

A

the respiratory center! we can either eat or breath but not both at the same time

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22
Q

What are the afferent nerves when swallowing?

A

afferent and glossopharyngeal N.

-go to the swallowing center in medulla and that goes to brain stem nuclei and then to efferent input to the pharynx

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23
Q

What is the primary peristaltic wave?

A

a continuation of pharyngeal peristalsis

-controlled by the medulla (swallowing center)

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24
Q

What cannot occur after a vagotomy?

A

a primary peristaltic wave

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25
Q

What is the secondary peristaltic wave?

A
  • happens when the primary wave fails to clear the esophagus or when gastric contents reflux into the esophagus
  • repeats until bolus is clears
  • both swallowing center and ENS are involved
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26
Q

Which persitaltic wave int he esophagus can occur even after a vagotomy?

A

the secondary one (because of the ENS involvement)

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27
Q

How long does it take to get strong secondary peristaltic waves after the vagus nerve gets cut?

A

several days

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28
Q

in the esophagus, what 2 places are normally above atmospheric pressure in the lumen at rest?

A

the UES and the LES… They’re sphincters so they are normally closed

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29
Q

Which part of the esohpagus never actually increases in pressure?

A

the LES… it just kinda opens. it doesn’t have to push anything else through

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30
Q

What are the pressure levels in the thorax?

A

below atmospheric

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31
Q

What might be important about intraluminal esophageal pressure?

A

it reflects the intra-abdomial pressure

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32
Q

In gastroesophageal reflux, where might the pressure be increased?

A

in the intra-abdominal area in pregnancy or morbid obesity

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33
Q

What is the input of the Vagus N. on the LES?

A

inhibitory

  • release of VIP relaxes it
  • could be NO?
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34
Q

what is GERD?

A

backwask of acid, pepsin, and bile into the esophagus

-abnormal relaxation of the LES

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35
Q

What is achlasia?

A

Neurogenic esophageal motility disorder

  • impaired peristalsis
  • no LES relaxation… food get’s backed up
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36
Q

What is the cause of Achlasia?

A

lasck of VIP or enteric system has been knocked out

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37
Q

How many layers does the stomach have?

A

3 layers, circular, longitudinal, and oblique

38
Q

What kind of reflex is receptive relaxation of the orad?

A

a vagovagal reflex

-VIP

39
Q

What does CCK do to contractions and distensibility of the stomach?

A

lowers contractions and raises distensibility

40
Q

Where does mixing and digestion occur in the stomach?

A

the caudad region

41
Q

Where do most of the gastric contests go in the caudad region?

A

they get propelled back into the stomach for further mixing and further reduction of particle size
retropulsion

42
Q

What increases the AP and force of contractions in the stomach?

A

PSymp, gastrin, and motilin

43
Q

What decreases the AP and force of contractions in the stomach?

A

Symp, secretin, and GIP

44
Q

How long does gastric emptying take?

A

about 3 hrs

45
Q

What factors increase the rate of gastric emptying?

A
  • low distensibility of the orad
  • increased force of peristaltic contractions of the caudad stomach
  • decreased tone of the pyorus
  • increased diameter and inhibition of segmenting contractions of the proximal duodenum
46
Q

What factors inhibit gastric emptying?

A
  • relaxation of the orad
  • decreased force of peristaltic contractions
  • increased tone of pyloric sphincter
  • segmentation contractions in intestine
47
Q

What do fat and proteins induce in the duodenum?

A

release of CCK which increases gastric distensibility

48
Q

What mediates the H+ inhibitory effects?

A

the ENS involving interneurons in the myenteric plexus

49
Q

What does acid in the duodenum stimulate?

A

secretin release

-this inhibits stomach motility via gastrin inhibition

50
Q

What does fats in the duodenum stimulate?

A

CCK and GIP

-inhibits stomach motility

51
Q

What does hypertonicity in the duodenum do?

A

inhibits gastric emptying

-unknown hormone

52
Q

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

A

slow gastric emptying

53
Q

What is Gastroparesis?

A

Slow emptying of the stomach

54
Q

What is the cause of Gastroparesis?

A

damage to the vagus nerve

  • may get high blood glucose as well
  • the goal is to lower the blood glucose
55
Q

What are MMC’s

A

Migrating myoelectric complexes

  • peristaltic contractions occuring during fasting, in both the stomach and small intestine
  • 90 minute intervals
  • mediated by motilin
56
Q

What inhibits MMC’s

A

feeding

57
Q

What about MMC’s is associated with gastroparesis?

A

the abscence of them

58
Q

What are the 2 movements that happen in the small intestine?

A

segmentation and peristaltic contractions

59
Q

What happens during segmentation contractions?

A

back and forth movement

*NO FORWARD PROPULSIVE MOVEMENT ALONG THE SMALL INTESTINE

60
Q

What happens during peristaltic contractions?

A

circular m. contracts BEHIND the bolus and longitudinal m. relaxes

  • in FRONT of the bolus, it’s the opposite
  • circular and longitudinal m.’s are reciprocally innervated
61
Q

In the small intestine, do slow waves initiate contraction?

A

no

-but in the stomach they do apparently

62
Q

What is the frequency gradient like for the contractions along the GI tract?

A

it decreases as we go towards the ileocecal junction

63
Q

What initates the peristaltic reflex in the SI?

A

serotonin released from ECCs that bind to receptors in IPANs

64
Q

What does serotonin do?

A

stimulates contractions

65
Q

What doe PG’s do?

A

stimulate contractions

66
Q

What does epinephrine do?

A

inhibits contractions

67
Q

What does gastrin, CCK, motilin, and insulin do?

A

tend to stimulate contractions

68
Q

What does secretin and glucagon do?

A

inhibit contractions (tend to)

69
Q

What coordinates the comiting reflex?

A

the medulla

70
Q

What is the order of events in the vomiting reflex?

A
  • reverse persitalsis in SI
  • relaxation of the stomach and pylorus
  • force inspiration to increase ab pressure
  • movement of larynx
  • relax the LES
  • close the glottis
  • forceful expulsion of gastric contents
71
Q

What lets stuff from the small to the large intestine?

A

the ileocecal sphinctorer

72
Q

What are the main functions of the large intestine?

A

absorption of water and vitamins as well as conversion of digested food into feces

73
Q

How far do the Taeniae coli run?

A

from the cecum to the rectum

74
Q

How far do the circular muscle of the large intestine run?

A

from the cecum all the way to the anal canal

75
Q

Are haustrae fixed?

A

no, they disappear and come back again

76
Q

What psymp innervates the cecum, ascending and transverse colon?

A

the Vagus N.

77
Q

What psymp innervates the descending and sigmoid colon and rectum?

A

pelvic Nerves (S2-4)

78
Q

What is the symp innervation to the large intestine like?

A

superior mesenteric ganglion gets prox regions

  • inferior gets distal
  • hypogastric plexus gets distal rectum and anal canal
  • and the somatic pudendal nerves get the external anal sphincter
79
Q

What are the major exitatory mediators?

A

AcH and substance P

80
Q

What are the major inhibitory mediators?

A

NO and VIP

81
Q

Where do segmentation contraction happen?

A

int he cecum and ascending colon

82
Q

What is the purpose of segmentation contractions?

A

to mix the contents of the large intestine

83
Q

What propels the fecal content into the rectum?

A

a final mass movement

84
Q

What is the result of poor motility in the large intestine?

A

greater absorption, hard feces in the transverse colon cause constipation

85
Q

What is the result of excess motility in the large intestine?

A

less absorption and diarrhea or loose feces

86
Q

Where does the volutnary control and the sensation of rectal distention come from

A

within the spinal cord that lead to the cerebral cortex

-destruction of these pathways causes a loss of voluntary control of defecation

87
Q

What is Diverticulitis?

A

small sacs of intestinal lining that bulge outward at weak spots

88
Q

Where does diverticulitis normally occur?

A

on the left side

89
Q

What is the cause of hirschsprung disease?

A

ganglion cells absent from segment of colon

90
Q

What is the result of no ganglion cells in colon?

A

VIP levels low, SM constriction. loss of coordinated movement, colon contents accumulate (it’s like achalasia but for the colon)

GI Final Exam (10 decks)

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