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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
What is the secondary peristaltic wave?
- 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
26
Which persitaltic wave int he esophagus can occur even after a vagotomy?
the secondary one (because of the ENS involvement)
27
How long does it take to get strong secondary peristaltic waves after the vagus nerve gets cut?
several days
28
in the esophagus, what 2 places are normally above atmospheric pressure in the lumen at rest?
the UES and the LES... They're sphincters so they are normally closed
29
Which part of the esohpagus never actually increases in pressure?
the LES... it just kinda opens. it doesn't have to push anything else through
30
What are the pressure levels in the thorax?
below atmospheric
31
What might be important about intraluminal esophageal pressure?
it reflects the intra-abdomial pressure
32
In gastroesophageal reflux, where might the pressure be increased?
in the intra-abdominal area in pregnancy or morbid obesity
33
What is the input of the Vagus N. on the LES?
inhibitory - release of VIP relaxes it - could be NO?
34
what is GERD?
backwask of acid, pepsin, and bile into the esophagus | -abnormal relaxation of the LES
35
What is achlasia?
Neurogenic esophageal motility disorder - impaired peristalsis - no LES relaxation... food get's backed up
36
What is the cause of Achlasia?
lasck of VIP or enteric system has been knocked out
37
How many layers does the stomach have?
3 layers, circular, longitudinal, and oblique
38
What kind of reflex is receptive relaxation of the orad?
a vagovagal reflex | -VIP
39
What does CCK do to contractions and distensibility of the stomach?
lowers contractions and raises distensibility
40
Where does mixing and digestion occur in the stomach?
the caudad region
41
Where do most of the gastric contests go in the caudad region?
they get propelled back into the stomach for further mixing and further reduction of particle size *retropulsion*
42
What increases the AP and force of contractions in the stomach?
PSymp, gastrin, and motilin
43
What decreases the AP and force of contractions in the stomach?
Symp, secretin, and GIP
44
How long does gastric emptying take?
about 3 hrs
45
What factors increase the rate of gastric emptying?
- 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
What factors inhibit gastric emptying?
- relaxation of the orad - decreased force of peristaltic contractions - increased tone of pyloric sphincter - segmentation contractions in intestine
47
What do fat and proteins induce in the duodenum?
release of CCK which increases gastric distensibility
48
What mediates the H+ inhibitory effects?
the ENS involving interneurons in the myenteric plexus
49
What does acid in the duodenum stimulate?
secretin release | -this inhibits stomach motility via gastrin inhibition
50
What does fats in the duodenum stimulate?
CCK and GIP | -inhibits stomach motility
51
What does hypertonicity in the duodenum do?
inhibits gastric emptying | -unknown hormone
52
What is the most common problem associated with disorders of gastric motility?
slow gastric emptying
53
What is Gastroparesis?
Slow emptying of the stomach
54
What is the cause of Gastroparesis?
damage to the vagus nerve - may get high blood glucose as well - the goal is to lower the blood glucose
55
What are MMC's
Migrating myoelectric complexes - peristaltic contractions occuring during fasting, in both the stomach and small intestine - 90 minute intervals - mediated by motilin
56
What inhibits MMC's
feeding
57
What about MMC's is associated with gastroparesis?
the abscence of them
58
What are the 2 movements that happen in the small intestine?
segmentation and peristaltic contractions
59
What happens during segmentation contractions?
back and forth movement | *NO FORWARD PROPULSIVE MOVEMENT ALONG THE SMALL INTESTINE
60
What happens during peristaltic contractions?
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
In the small intestine, do slow waves initiate contraction?
no | -but in the stomach they do apparently
62
What is the frequency gradient like for the contractions along the GI tract?
it decreases as we go towards the ileocecal junction
63
What initates the peristaltic reflex in the SI?
serotonin released from ECCs that bind to receptors in IPANs
64
What does serotonin do?
stimulates contractions
65
What doe PG's do?
stimulate contractions
66
What does epinephrine do?
inhibits contractions
67
What does gastrin, CCK, motilin, and insulin do?
tend to stimulate contractions
68
What does secretin and glucagon do?
inhibit contractions (tend to)
69
What coordinates the comiting reflex?
the medulla
70
What is the order of events in the vomiting reflex?
- 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
What lets stuff from the small to the large intestine?
the ileocecal sphinctorer
72
What are the main functions of the large intestine?
absorption of water and vitamins as well as conversion of digested food into feces
73
How far do the Taeniae coli run?
from the cecum to the rectum
74
How far do the circular muscle of the large intestine run?
from the cecum all the way to the anal canal
75
Are haustrae fixed?
no, they disappear and come back again
76
What psymp innervates the cecum, ascending and transverse colon?
the Vagus N.
77
What psymp innervates the descending and sigmoid colon and rectum?
pelvic Nerves (S2-4)
78
What is the symp innervation to the large intestine like?
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
What are the major exitatory mediators?
AcH and substance P
80
What are the major inhibitory mediators?
NO and VIP
81
Where do segmentation contraction happen?
int he cecum and ascending colon
82
What is the purpose of segmentation contractions?
to mix the contents of the large intestine
83
What propels the fecal content into the rectum?
a final mass movement
84
What is the result of poor motility in the large intestine?
greater absorption, hard feces in the transverse colon cause constipation
85
What is the result of excess motility in the large intestine?
less absorption and diarrhea or loose feces
86
Where does the volutnary control and the sensation of rectal distention come from
within the spinal cord that lead to the cerebral cortex | -destruction of these pathways causes a loss of voluntary control of defecation
87
What is Diverticulitis?
small sacs of intestinal lining that bulge outward at weak spots
88
Where does diverticulitis normally occur?
on the left side
89
What is the cause of hirschsprung disease?
ganglion cells absent from segment of colon
90
What is the result of no ganglion cells in colon?
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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