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GI II > Swallowing, gastric emptying and intestinal motility > Flashcards

Swallowing, gastric emptying and intestinal motility Flashcards

1
Q

Where are the Touch R for swallowing

A

near opening of pharynx

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2
Q

Where is the integration center for swallowing

A

medulla oblongata (lower pons)

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3
Q

What n control the upper esophagus and pharynx

A

cranial nn

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4
Q

what n innervates the lower esophagus

A

vagus n

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5
Q

what mm are inn by the cranial and vagus nn

A

pharyngeal and esophageal striated and smooth m

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6
Q

What are the three phases of swallowing

A

oral phase
pharyngeal phase
esophageal phase

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7
Q

Which phase is voluntary in swallowing

A

oral. tongue to pharynx

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8
Q

describe the pharyngeal phase of swallowing

A

involuntary, reflex-respiration inhibited- epiglottis blocks trachea
soft palate blocks nasopharynx entry-way
pressure R in pharynx trigger
bolus directed into esophagus via relaxed upper esophageal sphincter

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9
Q

describe the esophageal phase of swallowing

A

involuntary

bolus from upper esophageal sphincter via peristalsis through lower esophageal sphincter–> stomach

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10
Q

What are the prtective effects of the upper esophageal sphincter

A

protect airway from swallowed material

protect airway from gastric reflux

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11
Q

What are the protective effects of the lower esophageal sphincter

A

protects esophagus from gastric reflux

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12
Q

During what phases of swallowing is the larynx elevated

A

end of oral all of pharyngeal and begining of esophageal

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13
Q

What initiates esophageal phase

A

peristaltic wave initiated by swallowing center.

secondary peristalsis is initiated by distention (only if primary wave not sufficient)

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14
Q

What nn are involved with esophageal phase

A

input from esophageal fibers to CNS and ENS modulate primary and secondary esophageal peristalsis

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15
Q

Swallowing induces relaxation of lower esophageal sphincter and?

A

proximal stomach

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16
Q

How do sphincters manage antegrade and retrograde movement

A

high resting pressure

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17
Q

Differentiate proximal stimuli and distal for sphincters

A

proximal cause relaxation, distal cause contraction

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18
Q

What needs to be coordinated for unidirectional movement of GI

A

smooth m contractions
neural stimulation
humoral stimulation

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19
Q

Describe structure upper esophageal sphincter

A

striated m
regulated by cranial nn
highest resting pressure
closed during inspiration

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20
Q

desribe structure lower esophageal sphincter

A

smooth muscle regulated by cholinergic stimuli and vagus n

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21
Q

What is the primary function of lower esophageal sphincter

A

allows coordinated movement

prevents reflux of gastric contents into esophagus

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22
Q

Describe the LES resting tone

A

Intrinsic myogenic properties

cholinergic regulation

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23
Q

Describe LES relaxation

A

intrinsic smooth m
vagus n
occurs after UES returns to high resting pressure

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24
Q

What inhibits the LES relaxation

A

VIP and NO

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25
Q

what allows for entry of food into the stomach

A

the distention or swallowing decreases LES pressure and makes it less than intragastric pressure

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26
Q

What is dysphagia

A

difficulty swallowing

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27
Q

What are some structural abnormalities to dysphagia

A

tongue
esophageal or pharyngeal wall out pouching
stomach protruding above diaphragm (hiatal hernia)
esophageal tumors

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28
Q

What are some functional abnormalities that can cause dysphagia

A

neurological defects, PD, Myasthenia Gravis

muscular layer defect

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29
Q

What are Tx for dysphagia

A

surgery- cut tight muscle
remove obstructing tumors
increase salivary function

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30
Q

What is Achlasia

A

special form of dysphagia from a dilated esophagus proximal to LES so that it fails to relax, peristalsis is impaired

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31
Q

What is the Tx for achlasia

A

wiring defect cannot be corrected

symptomatic relief to reduce LES pressure, gravity

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32
Q

What is GERD

A

LES resting pressure prevents reflux from esophagus usually but with GERD reduce LES resting pressure

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33
Q

What is it that refluxes in GERD, and what can it cause

A

gastric juice, causing esophagitis or erosion of esophageal mucosa

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34
Q

What is Tx for GERD

A

control gastric acid secretion
less R of esophageal mucus
Less HCO3 secretion from saliva
commonest disease

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35
Q

Where is the orad region of the stomach

A

fundus and proximal body

receives and stores food

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36
Q

Where is the caudad region

A

distal body and antrum

mixing and propeling

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37
Q

What is secreted in gastric lumen near LES/cardia

A

mucus and HCO3

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38
Q

What is secreted in gastric lumen near funds/body

A

H+, IF, mucus, HCO3, pepsinogens, lipase

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39
Q

What is secreted in gastric lumen near antrum and pylorus

A

mucus and HCO3

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40
Q

What is receptive relaxation

A

LES and stomach relax, vagovagal reflex of VIP, pressure in stomach does not increase with increased V

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41
Q

What can cause a rapid pressure increase in the stomach

A

disruption of vagus n- vagotomy

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42
Q

What is gastric accommodation

A

relaxation in response to gastric filling, dilate fundus

allows increased volume to keep P consistent

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43
Q

What n controls gastric accommodation

A

vagus and ENS

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44
Q

Where does gastric mixing happen

A

antrum

45
Q

what occurs during gastric mixing

A

increased gastric contractility

the stomach contents of chyme is a positive stimuli for contractility

46
Q

What substances can increase gastric mixing

A

ENS: Ach and Substance P

Gastrin

47
Q

What stimuli are inhibitory to gastric emptying

A

duodenum contents: fatty acids, monoglycerides, acidic pH, volume/distention, hypertonicity, AA and peptides

48
Q

What hormones can inhibit gastric emptying

A

CCK, secretin, GIP

49
Q

what neural control is there over gastric emptying

A

intrinsic and extrinsic

50
Q

Increased fluidity of stomach causes more or less contraction

A

more motility

51
Q

Intense pain has what effect on stomach

A

inhibits motility and emptying

52
Q

emotion has what effect on stomach

A

stimulates or inhibits motility and emptying

53
Q

Where is the pacemaker zone of stomach and role

A

in body of stomach, sets rate of gastric peristalsis (3-5 slow waves/min)

54
Q

What determines contraction force of stomach

A

degree od depolarization

duration of membrane depolarization

55
Q

What affect do gastrin and Ach have on gastric contractions

A

increase amplitude and duration

increase contractility

56
Q

what affect does norepinephrine have on gastric contractions

A

decreases contractility

57
Q

What are the 3 mechanisms of gastric mixing

A

propulsion
grinding
retropulsion

58
Q

what is stomach trituration

A

reduction of solid particle size
has to me less than 2 mm
emptying does not happen until solids are broken down

59
Q

what molecules are emptied from stomach in order of greatest amount to least

A

liquid, carbs, protein, fat

60
Q

Is gastric emptying carrying isotonic, hypertonic or hypotonic fluid

A

isotonic usually

61
Q

What R are in the duodenum

A

pH, osmole, FA/monoglycerides, aa/peptides

62
Q

what stimulus from duodenum slows gastric emptying

A

byproducts of fat and protein digestion
hypertonic chyme
<3.5 pH

63
Q

Why is coordination of stomach with duodenum important

A

so chyme can be effectively processed by duodenum and not regurgitated

64
Q

What are the neural and humoral events in duodenum that inhibit gastric emptying

A

relaxation fundus
inhibit antral contraction
stimulate pyloric contraction

65
Q

What stimulates secretin release and its effects

A

acidic chyme

results in dec contractility of antrum, increased constriction of pylorus

66
Q

What simtulates CCK and GIP and what are the effects

A

FA and monoglycerides
results in relaxation of gastric smooth m
increased constriction of pylorus

67
Q

What stimulates gastrin and what are the effects

A

purely hormonal from peptides and aa
causes increased contractility in antrum
constriction of pylorus

68
Q

What hormones cause increased constriciton of pyloric sphincter

A

CCK, GIP, secretin and gastrin

69
Q

Describe the neural regulation of pyloric sphincter

A

SAN–>constriction
PAN–>vagus
constriction is Ach, relaxation is VIP

70
Q

Approx when does the fasting state occur in regard to a meal

A

2 hours after a meal,

migrating myoelectri complex

71
Q

What is Emesis

A

reflex vomiting, integration in medulla

72
Q

What stimulates vomiting

A

gastric and duodenal distention and irritants
dizziness, inner ear dysfunction, moiton sickness
drugs
genitourinary injury
emetics: chem that cause vomiting

73
Q

What is an emetic and where is the response center

A

ipecac- gastric/duodenal R that rigger chemo receptor in 4th ventricle of brain

74
Q

What occurs in the vomit reflex

A 
reverse peristalsis from SI->pylorus
pyloric sphincter relaxes and stomach
abs contract
pylorus and antrum contract
LES releaxes, gastric contents enter, UES relaxes
75
Q

What are the 3 types of SI mobility

A

segmentation(mixing)
peristalsis(propulsion)
migrating myoelectric complex(sweeping of undigested contents during fasting state

76
Q

What is the postprandial period of segmentation

A

part of segmentation when there are alternating contractions of circular sm m

77
Q

Why is segmentation a slow process of propulsion and retropulsion

A

time for digestion and absorption
mixes chyme with digestive secretions
maximizes contact with mucosal layer

78
Q

What is the postprandial phase of peristalsis

A

coordinated propulsive contractions of circular sm m

79
Q

What causes the releaxation in front of bolus and contraction behind during perstalsis

A

relaxation in front: VIP and NO

contraction: ACh and Substance P

80
Q

Describe the migrating myoelectric complex

A

new wave starts in stomach once previous wave passes distal ileum to move undigested material

81
Q

What are the 3 phases of migrating myoelectric complex

A

quiescence, small disorganized contractions, strong propagating contractions

82
Q

circulating motilin usually correlates to what

A

migrating myoelectric complex

83
Q

What protective mech is the migrating myoelectric complex

A

prevent backflow of bacteria from colon to ileum

84
Q

What part of SI has highest electrical rhythym

A

duodenum

85
Q

What increases the burst of APs on slow waves

A

hormones, ENS, PAN and SAN via ENS

86
Q

The contraction behind and relaxation in front of bolus is intrinsic or extrinsic

A

intrinsic ENS

87
Q

What is intestinointestinal reflex

A

distention in one segment, relaxation in the rest of SI

88
Q

What coordinates tone of ileocecal sphincter

A

normally contracted

ENS reflexes, long range extrinsic ENS and hormones

89
Q

distention and ileum causes what in ileocecal sphincter? distension in ascending colon?

A

ileum->relaxation

ascending colon->constriction

90
Q

What is the gastroleal reflex

A

increased gastric activity increases ileal motility and releaxation of the ileocecal sphincter

91
Q

what is the purpose of the ileocecal sphincter

A

control rate of chyme entering colon so can absorb water and salts

92
Q

What are the 3 primary types of colonic motility

A

Haustrations
Long duration contractions
mass movements

93
Q

describe haustrations of colon

A

short duraction contrations, circular m–>mixing

94
Q

describe long duration contractions

A

taeniae coli, mixing contractions that may cause propagation short distances in either direction
(not in proximal colon so can retain chyme)

95
Q

describe mass movements of colon

A

high amplitude propagating contractions, sweep length of colon
1-3/day
high variability in colonic motility per person

96
Q

Describe the control of colonic motility

A

primarily neural regulation via ENS, PNS, SNS via intrinsic control and extrinsic modulation
local reflexes from colonic distention
long range reflex from gastric distention- gastrocolic reflex

97
Q

What is the effect of PAN on colon

A

vagus via ENS increases mixing in proximal colon

pelvic splanchnic nn via ENS cause increased contractions and propulsive movements in distal colon

98
Q

What is the effect of SAN on colon

A

inhibits motility

postganglionics via abdominal sympathetic ganglia

99
Q

Describe the internal anal sphincter

A

smooth m
involuntary control
majority of tone

100
Q

describe the external anal sphincter

A

striated m

voluntary and involuntary control

101
Q

defectaiton requires what stimulus

A

extrinsix neural input-> higher CNS

102
Q

What results from distention in rectum

A

relaxation IAS reflex
rectosphincteric reflex: VIP and NO
reflex to constrict EAS

103
Q

Is defectaion voluntary or no

A

coordinated volunatary and involuntary events
voluntary relaxation of EAS
contraction ABs
relaxation pelvic mm

104
Q

What is Hirschsprungs disease

A 
congenital megacolon
fialure of ENS development
impairs motility
Aganaglionic segment
rectosphincteric reflex impaired
105
Q

Tx for hirschsprungs

A

surgical excision of diseased or aganglionic segment

106
Q

Irritable bowel syndrome or disease is what

A

group of inflammatory conditions of colon and SI

107
Q

What causes IBS/IBD

A

visceral hypersensitivity due to sensitization of afferent neural pathways
respond abnoramaly to stimuli
idiopathic, distention, inflammation, GI infections
partial dysmotility

108
Q

What are the major types of IBD

A

Crohn’s disease and ulcerative colitis

109
Q

How do you Dx IBD

A

assessment of inflammatory markers in stool then colonoscopy with biopsy of pathological lesions

GI II (12 decks)

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