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
Q

Sympathetic stimulation - regulation of gastric contractions

A

secretin and GIP

decrease AP and force of contractions

26
Q

factors that increase rate of gastric emptying

A

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
Q

factors that inhibit gastric emptying

A

relaxation of orad
decrease force of peristaltic contractions
increased tone of pyloric sphincter
segmentation contractions in intestine

28
Q

receptor activation that inhibit gastric emptying

A

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
Q

gastroparesis

A

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
Q

migrating myoelectric complexes (MMC)

A
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
Q

function of motility in the small bowel

A

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
Q

segmentation contractions

A

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
Q

peristaltic contractions

A

serve to propel the chyme toward the LI

behind the bolus, circular relaxes and longitudinal contracts

34
Q

slow waves

A

always present
DO NOT initiate contractions in SI
set maximum frequency of contractions

35
Q

spike potentials

A

needed for m contractions to occur

36
Q

slow wave frequency duodenum

A

12 cycles/min

37
Q

slow wave frequency jejunum

A

10 cycles/min

38
Q

slow wave frequency ileum

A

8 cycles/min

39
Q

neural input - contractions of SI

A

peristaltic reflex mediated by ENS

PNS stimulates and SNS inhibits contractions

40
Q

hormonal control - contractions of SI

A

serotonin, prostaglandins stimulate contractions
Epi inhibits contractions
Gastrin, CCK, motilin and insulin stimulate contraction
secretin and glucagon inhibit contraction

41
Q

vomiting reflex

A

coordinated by medulla
impulsed transmitted by vagal and sympathetic afferent n fibers to nuclei in the brain stem
involves reverse peristalsis

42
Q

order of events in vomiting reflex

A
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
Q

ileocecal junction

A

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
Q

LI main functions

A

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

45
Q

myenteric plexus innervation of LI

A

concentrated beneath taneia coli

innervated muscle layers

46
Q

parasympathetic NS innervation of LI

A

vagus n - cecum, ascending and transverse colon

pelvic nerves - descending and sigmoid colon, rectum

47
Q

sympathetic NS innervation of LI

A

superior mesenteric ganglion - proximal regions
inferior mesenteric ganglion - distal regions
hypogastric plexus - distal rectum and anal canal
somatic pudendal n - external anal sphincter

48
Q

major excitatory mediators of LI

A

Ach and Substance P

49
Q

major inhibitory mediators of LI

A

NO and VIP

50
Q

segmentation contractions of LI

A

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
Q

mass moments of LI

A

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
Q

motility of the rectum and anal canal

A

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
Q

retrosphincteric reflex

A

under neural control - ENS and is reinforced by neurons in spinal cord
pathway leads to cerebral cortex

54
Q

hirschsprungs disease

A

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
Q

diverticulitis

A

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