Motility of the GI Tract Flashcards

1
Q

circular m

A

contraction decreases the diameter of the segment

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2
Q

longitudinal m

A

contraction decreases the length of the segment

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3
Q

phasic contraction

A

periodic contractions followed by relaxation

esophagus, stomach, SI, and all tissues involved in mixing and propulsion

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4
Q

tonic contraction

A

maintain a constant level of contraction w/out regular periods of relaxation
stomach, lower esophageal, ileocecal, and internal anal sphincters

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5
Q

slow waves

A

unique feature of GI smooth m.
depolarization and repolarization of the membrane potential
AP leads to mechanical response
frequency of slow waves varies along the GI tract (3-12 waves/min)

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6
Q

basal contractions

A

GI smooth m even subthreshold depolarization can produce weak contraction

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7
Q

Ach effect on slow waves

A

increases the amplitude of slow waves and number of AP

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8
Q

NE effect on slow waves

A

decreases the amplitude of slow waves

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9
Q

Interstitial cells of Cajal

A

pacemaker for GI smooth m
slow waves originate here
slow waves occur spontaneously in ICC and spread rapidly to smooth m via gap junctions
electrical activity in the ICC drives the frequency of contractions

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10
Q

oral phase of swallowing (voluntary)

A

initiates swallowing process

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11
Q

pharyngeal phase

A

passage of food through pharynx into esophagus
soft palate is pulled upward which moves the epiglotis which causes the UES to relax leading to peristaltic waves of contractions through the pharynx which propels food through the open UES

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12
Q

esophageal phase

A

passage of food from pharynx to stomach
control by the swallowing reflex and the ENS
primary peristaltic wave
secondary peristaltic wave

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13
Q

control of involuntary swallowing

A

controlled by medulla
food in mouth is detected by somatosensory receptors near the pharynx
afferent info is carried to the medulla via the vagus and glossopharyngeal n
efferent input to pharynx

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14
Q

primary esophageal peristaltic waves

A

continuation of pharyngeal peristalsis
controlled by the medulla (swallowing center)
cannot occur after vagotomy

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15
Q

secondary esophageal peristaltic waves

A

occurs if primary contraction fails to empty the esophagus or when gastric contents reflux into the esophagus
induced by distention
repeats until bolus is cleared
both swallowing center and ENS are involved
can occur in the absence of oral and pharyngeal phases
occurs even after vagotomy

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16
Q

esophageal pressures between swallows

A

both UES and LES are closed
the body of the esophagus is flaccid
pressure in the UES is less than pharynx and body of esophagus
LES also exhibits elevated pressure

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17
Q

esophageal pressures during swallowing

A

UES relaxes (opens) - low pressure
UES closes after the bolus passes
peristaltic wave (high pressure)
LES and upper part of stomach relax - receptive relaxation (low pressure)
after bolus enters stomach, LES contracts (increase pressure)

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18
Q

Opening of LES

A

mediated by peptidergic fibers in the vagal n
vagal input is inhibitory
release of VIP
receptive relaxation decreases the pressure in the upper region of the stomach

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19
Q

GERD

A

heartburn/acid indigestion
backwash of acid, pepsin, and pile into esophagus
can lead to: stricture of esophagus, asthma, chronic sinus infection, Barrett’s esophagus

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20
Q

achalasia

A

results from damage to n in the esophagus, preventing it from squeezing food into the stomach
may be caused by an abnormal immune system response
symptoms: backflow of food in the throat, chest pain, weight loss
treatment: endoscopic therapy or surgery

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21
Q

stomach

A

three layers of m (circular, longitudinal, and oblique)
extrinsic innervation: ANS
intrinsic innervation: myenteric and submucosal plexus

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22
Q

orad region

A

proximal portion of the body
function of receptive relaxation is to receive the food bolus in the stomach
receptive relaxation: decrease in pressure and increase in volume of the orad region
exhibits minimal contractile activity therfore little mixing of ingested food occurs in this region of the stomach
CCK decreases contraction and increases gastric distensibility

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23
Q

caudad region

A

contractions serve to mix and propel gastric contents
primary contractile event is peristalitic contraction
as contractions approach the pylorus they increase in both force and velocity
max frequency is 3 to 5 waves per minute
most of the gastric contents are propelled back into the stomach for further mixing and further reduction of particle size

24
Q

Parasympathetic stimulation - regulation of gastric contractions

A

gastrin and motilin

increased AP and force of contractions

25
Sympathetic stimulation - regulation of gastric contractions
secretin and GIP | decrease AP and force of contractions
26
factors that increase rate of gastric emptying
decreased distensibility of orad increase force of perisaltic contractions of the caudad stomach decrease tone of pylurus increase diameter and inhibition of segmenting contractions of the proximal duodenum
27
factors that inhibit gastric emptying
relaxation of orad decrease force of peristaltic contractions increased tone of pyloric sphincter segmentation contractions in intestine
28
receptor activation that inhibit gastric emptying
fat and proteins induce release of CCK which in turn increase gastric distensibility H inhibitory effects are mediated by intrinsic neural reflex (ENS) involving interneurons in the myenteric plexus
29
gastroparesis
slow emptying of stomach/paralysis of stomach 20% Type I diabetics some type II high blood glucose damages vagus n. nausea, vomiting, an early feeling of fullness when eating, weight loos, abdominal bloating, abdominal discomfort goal is to lower blood glucose
30
migrating myoelectric complexes (MMC)
``` periodic, bursting peristaltic contractions occurring during fasting in both stomach and small intestines occur at 90 min intervals mediated by motilin feeding inhibits absence is associated with gastroparesis ```
31
function of motility in the small bowel
mix the chyme w/ digestive enzyme and pancreatic secretions expose nutrients to the intestinal mucosa for absorption propel the unabsorbed chyme along the small intestine to the LI
32
segmentation contractions
serve to mix the chyme and expose it to pancreatic enzyme and secretions generates back and forth movements produce no forward propulsive movement along the SI
33
peristaltic contractions
serve to propel the chyme toward the LI | behind the bolus, circular relaxes and longitudinal contracts
34
slow waves
always present DO NOT initiate contractions in SI set maximum frequency of contractions
35
spike potentials
needed for m contractions to occur
36
slow wave frequency duodenum
12 cycles/min
37
slow wave frequency jejunum
10 cycles/min
38
slow wave frequency ileum
8 cycles/min
39
neural input - contractions of SI
peristaltic reflex mediated by ENS | PNS stimulates and SNS inhibits contractions
40
hormonal control - contractions of SI
serotonin, prostaglandins stimulate contractions Epi inhibits contractions Gastrin, CCK, motilin and insulin stimulate contraction secretin and glucagon inhibit contraction
41
vomiting reflex
coordinated by medulla impulsed transmitted by vagal and sympathetic afferent n fibers to nuclei in the brain stem involves reverse peristalsis
42
order of events in vomiting reflex
``` reverse peristalsis in the SI relaxation of the stomach and pylorus force inspiration to increase abdominal pressure movement of the larynx relaxation of the LES closure of the glottis forceful expulsion of gastric contents ```
43
ileocecal junction
food is propelled into the LI when the ileocecal sphincter relaxes distention of ileum causes relaxation of sphincter distention of the colon causes contraction of sphincter
44
LI main functions
absorption of water and vitamins and conversion of digested food into feces
45
myenteric plexus innervation of LI
concentrated beneath taneia coli | innervated muscle layers
46
parasympathetic NS innervation of LI
vagus n - cecum, ascending and transverse colon | pelvic nerves - descending and sigmoid colon, rectum
47
sympathetic NS innervation of LI
superior mesenteric ganglion - proximal regions inferior mesenteric ganglion - distal regions hypogastric plexus - distal rectum and anal canal somatic pudendal n - external anal sphincter
48
major excitatory mediators of LI
Ach and Substance P
49
major inhibitory mediators of LI
NO and VIP
50
segmentation contractions of LI
occur in cecum and ascending colon appear disappear and form again at another location within the large intestine at adjacent sites contractions usually occur independently cause little propulsion server to mix the contents of the large intestine
51
mass moments of LI
occurs in the colon, over large distances, such as from the transverse colon to sigmoid colon occur 1 to 3 times/day move the content of the large intestine over long distances and stimulate defecation reflex a final mass movement propels the fecal content into the rectum
52
motility of the rectum and anal canal
as the rectum fills with feces smooth m wall of the rectum contracts and internal anal sphincter relaxes (retrosphincteric reflex) external anal sphincter is tonically closed (under voluntary control) urge to defecate occurs when the rectum fills 25%
53
retrosphincteric reflex
under neural control - ENS and is reinforced by neurons in spinal cord pathway leads to cerebral cortex
54
hirschsprungs disease
ganglion cells absent from segment of colon VIP levels low leads to SM constriction/loss of coordinated movement which leads to colon contents accumulate surgical resection of colon segment lacking ganglia
55
diverticulitis
small sacs of intestinal lining that bulge outward at weak spots caused by excess pressure in colon that cause weak spots in colon to bulge out and become diverticula increase with age dietary and lifestyle interventions