GI Motility - Fan 2/18/16 Flashcards

(57 cards)

1
Q

role of organ in digestion/motility:

mouth

A

chewing/mastication

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2
Q

role of organ in digestion/motility:

esophagus

A

swallowing

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3
Q

role of organ in digestion/motility:

stomach

A

digestive period: receptive relaxation, accomodation, gastric emptying

interdigestive period: MMC (migrating myoelectric complexes)

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4
Q

role of organ in digestion/motility:

small intestine

A

digestive period: segmentation (for optimal digestion/abs)

interdigestive period: peristalsis (MMC)

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5
Q

role of organ in digestion/motility:

large intestine

A

haustral shuttling (storage of feces)

mass movement (defecation)

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6
Q

role of organ in digestion/motility:

rectum

A

defecation

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7
Q

organs involved in function:

mechanical digestion/breaking food down into smaller particles

A

mouth

stomach

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8
Q

organs involved in function:

storage

A

stomach

small intestine

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9
Q

organs involved in function:

mixing of luminal contents

A

mouth

stomach

small intestine

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10
Q

organs involved in function:

housekeeping

A

stomach, small intestine: MMC

large intestine: defecation

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11
Q

“aboral”

A

downward

onward

orthograde

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12
Q

resident and transit time through GI tract

A
  • mouth/esoph: seconds
  • stomach/sm int: DIGESTIVE PERIODS
    • ​stomach: 2-4h
    • sm intestine: 2-4h
  • stomach/sm int: INTERDIGESTIVE PERIOD
    • ​empty stomach/sm int: migrating myoelectric complex cycles (approx 1.5h/cycle) for 10-18 hours
  • large intestine: 42-52 hours (8-12h min)
    • defecation: seconds-minutes
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13
Q

SWALLOWING

phases

organs involved

A
  1. oral phase: involuntary or voluntary control
  2. pharyngeal phase: involuntary reflex
  3. esophageal phase: involuntary reflex

mouth, pharynx, esophagus, stomach, resp system - actions coordinated by CNS

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14
Q

key events of swallowing

A
  • pharynx rapid sequential contraction
  • upper eso sphincter relaxes, then contracts
  • esophageal slow peristaltic wave
  • lower eso sphincter relaxes, then contracts
  • fundus and body of stomach relax: happens early on in swallowing, in prep to receive bolus
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15
Q

what happens when primary eso peristalsis fails?

A

if something gets stuck in esophagus, secondary eso peristalsis takes over, starting a contractile/peristaltic wave just above the stuck bolus (not all the way up at the upper eso sphincter!)

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16
Q

LES overshooting

A

lower eso sphincter contraction aims to prevent reflux

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17
Q

general mechanisms to prevent reflux

A
  • high tone of lower eso sphincter
  • secondary eso peristalsis (acitvation of chemoreceptors)
  • pinching of LES by diaphragm
  • 2 reflexes
    • LES contracts in response to gastric pressue increase and abd pressure increase

*

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18
Q

mechanisms to prevent reflux: infants

A

only have pinching of LES by diaphragm as anti-reflux mechanism

  • have to be careful squeezing babies, also have to burp them to decrease the pressure/volume of stomach post meal
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19
Q

mechanisms to prevent reflux: pregnant women

A

only have secondary peristalsis as anti-reflux mechanism

  • LES tone knocked out by hormonal changes
  • diaphragm elevated due to pregnancy
  • gastric/abd pressure constantly elevated due to preg: hard to activate the pressure reflexes
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20
Q

problems with LES contraction

A

insufficient/weak: GERD

  • heartburn

excessive/strong: esophageal achalasia

  • overactive, excitatory neurons
  • abnormal muscle overgrowth
  • difficulty swallowing
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21
Q

roles of stomach (and its parts) in gastric motility

A

DIGESTIVE PERIOD

  • proximal stomach: storage
    • receptive relaxation (during swallowing)
    • accomodation (significant increase in volume without huge wall tension increase due to elasticity of sm muscle)
  • distal stomach: mixing/grinding
    • mixing, size reduction, emptying via contraction

INTERDIGESTIVE PERIOD

  • housekeeping
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22
Q

gastric contractions during digestive period

A

serve the function of mixing, size reduction, and emptying via…

  • propulsion: mixing/size red, emptying 0-3.7x/min
  • antral systole: grinding, shearing, retropulsion for net effect of mixing/size red
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23
Q

control of gastric emptying

A

promoted by

  • proximal stomach tone
  • distal stomach peristalsis

inhibited by

  • pyloric sphincter tone
  • duodenal contraction
24
Q

gastric emptying: stomach

A
  • food enters stomach, triggers stomach distension, stretch receptors hit vagal afferent-CNS-vagal efferents which come through and release Ach and gastrin
  • also, peptides/a.a.s trigger gastrin secretion
  • in total, stomach contraction triggered
25
gastric emptying: duodenum
* presence of acid → secretin production * presence of FAs, a.a.s/peptides → CCK production * presence of glucose → GIP production all three of these neuroendrocine secretions will have joint effect of... 1. duodenal contraction 2. inhibition of gastrin secretion [either directly or through somatostatin] contraction of the duodenum, in turn, triggers stretch receptors in duodenum for joint effect of... 1. duodenal contraction 2. inhibition of stomach contraction
26
interdigestive period: "housekeeping"
**migrating myoelectric complexes** [as compared to digestive motility] * stronger * intermittent/in waves [vs. constant] * pylorus is open [vs. closed or close to it] * sm intestine undergoes peristalsis [vs segmentation - slow, nonperistaltic] * fx: remove undigestible material and prevent bacterial growth [vs. optimize digestions/abs] * mediated by **motilin**
27
pyloric contraction
pylorus kept small during digestive period because you **don't want everything emptying into small intestine all at once** * ​clinically: dumping syndrome
28
small intestinal motility | (muscles and functions)
1. **muscularis externa:** intraluminal mixing and propulsion via _segmentation_ to optimize digestion/abs. also _housekeeping via MMC_ 2. **muscularis mucosae, villus muscle:** facilitate _absorption_ and _lymph flow_
29
segmentation
aka slow movement main fx: **separation and recombo of chyme boluses** _​effects two means of digestion_ * **luminal digestion:** mixing of chyme with secretions (enzymes, alkaline fluid, bile) * **membrane digestion:** moving chyme to cell membranes toward... * digestive enzymes: membrane digestion * transporters/carriers: **absorption**
30
ECA
**electrical control activity** (unique to gut smooth muscle) * aka: slow waves, basal electric rhythm * origin: pacemaker cells (interstitial cells of Cajal, ICC) * made spontaneously, constantly * conducted to smooth muscle cells via gap jx * modulated (not originated) by motor neurons in muscle and by endocrine secretions
31
frequency of ECAs in GI tract
stomach: 3.7 x/min duodenum: 12 x/min ileum: 10 x/min colon: 3 x/min
32
ECA action potential events
1. **depolarization:** Na, Ca influx 2. **plateau phase:** Na, Ca influx; K efflux 3. **repolarization:** K efflux large ECAs with spike potentials cause muscle contraction = **ERA: electric response activities** * excitatory neuroendocrine factors can lead to higher levels of Ca, spike potentials
33
modulation of ECAs by neuroendocrine factors
**excitatory factors:** Ach, gastin **inhibitory factors:** norepi, nitric oxide
34
relationship between ECAs and ERAs
and ERA is an ECA that is strong/spiked enough to actually initiate contraction * excitatory mediators increase ERA/ECA ratio * inhibitory mediates decrease ERA/ECA ratio
35
neuroendocrine control of peristalsis
peristalsis involves circular and longitudinal muscle layers oppositely relaxing/contracting * **constricted** part of tract * inhibitory neuroendocrine activity/**relaxation of longitudinal m** * excitatory neuroendocrine activity/**contraction of circular m** * **relaxed** part of tract * inhibitory neuroendocrine activity/**relaxation of circular m** * excitatory neuroendocrine activity/**contraction of longitudinal m**
36
how is peristaltic motility coordinated?
**interneurons** * presence of bolus triggers receptors that communicate with interneurons * distension triggers baroreceptors * content might also trigger osmoreceptors, chemoreceptors * interneurons communicate with motor neurons * proximal motor neurons: excitatory neuroendo: **contraction** * distal motor neurons: inhibitory neuroendo: **relaxation** generates a pressure gradient for the bolus to move down
37
describe the various contractile behaviors associated with physiological states of * segmentation * MMC * diarrhea/vomiting
* _segmentation_: short distance propulsion * _MMC_: intermed distance propulsion * _diarrhea/vomiting_: long distance propulsion (opposite directions)
38
reflexive relaxation/contraction of ileocecal sphincter
relaxes/contracts based on distention of regions immediately proximal and distal * distention in distal ileum leads to sphincter relaxation * movement of chyme into cecum * distention in proximal cecum leads to sphincter constriction * prevents reflux
39
overview of large intestinal motility
1. **haustral shuttling** (segmenting, nonperistaltic contractions) to slow fecal stream 2. **reabs** of water and electrolytes (700mL water into cecum, all but 100-300 reabs) 3. periodic **peristalsis** to move feces along 4. rare **mass movement** to move stool into rectum 5. **defecation** (100-300mL) if defecation does NOT occur - get retrograde propulsion!
40
reflexes involved in defecation
1. **involuntary:** stool distends rectum 2. **involuntary:** reflexive contraction of rectum, relaxation of int anal sph, contraction of ext anal sph: movement of stool into anal canal 3. brain receives signals of awareness, which then makes it your **voluntary** call to hold off (contract EAS) or defecate (relax EAS)
41
constipation factors and mechanisms: ## Footnote **diet low in insoluble fiber**
* insufficient stim of baroceptors * loss of benefical microbes that come with a high fiber diet
42
constipation factors and mechanisms: ## Footnote **insufficient fluid intake**
* lack of baroceptor stimulation [low volume] * dry feces
43
constipation factors and mechanisms: excessive delay of defecation
* dry feces (excessive reabs?) * low stim of baroceptors [low volume]
44
constipation factors and mechanisms: ## Footnote **narcotics**
* inhibition of fluid secretion, leading to low stim of baroceptors [low vol] * increased sphincter tone
45
constipation factors and mechanisms: ## Footnote **physical inactivity**
* decreased baroceptor stim due to decreased food intake * decreased GI neuroendo secretion (associated with exercise)
46
constipation factors and mechanisms: ## Footnote **antibiotics**
* disruption of microbiome and associated ENS activities
47
constipation factors and mechanisms: ## Footnote **old age**
combination of * reduced food intake * reduced ENS neuroendo activity, physical activity
48
gastroileal reflex
stimulatory * entry of food into stomach → relaxation of ileocecal sph, emptying of ileum
49
gastrocolic reflex duodenalcolic reflex
stimulatory * entry of food into empty stomach **or** chyme into duodenum → increases aboral propulsive movement in colon
50
colonocolonic reflex
stimulatory * distention in one part of colon → relaxation of another part * ultimately favors aboral movement
51
duodenogastric reflex
inhibitory, physiological * duodenal distension → delayed gastric emptying
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ileogastric reflex
inhibitory, physiological * distention of ileum → delayed gastric emptying
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intestinointestinal reflex
inhibitory * overdistention of one part of intestine → general inhibition of instestinal muscle activity
54
colonic-intestinal reflex
inhibitory * overdistention of colon → general inhibition of intestinal muscle activity
55
peritoneo-intestinal reflex
inhibitory * handling of GI tract during surgeries and/or intestinal irrigation → general inhibition of intestinal muscle activity
56
adynamic ileus
occurs due to * obstruction * bacterial overgrowth * abdominal surgery results in triggering of **intestino-intestinal reflex, colonic-intestinal reflex, peritoneo-intestinal reflex** which is why you ask patients to fast until GI motility is regained!
57