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Physiology Block 5- Gastrointestinal Physiology > GI Motility > Flashcards

GI Motility Flashcards

1
Q

What are the pacemaker cells of the GI tract?

A

Interstitial cells of Cajal

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2
Q

What are the four phase of the GI ‘cycle’? What are the types of stimuli that regulate them?

A

Cephalic (neural-anticipatory), gastric (mechanical-distension), intestinal (chemical-mechanical), interdigestive (neural-hormonal)

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3
Q

What serves as the extrinsic neural regulator of GI motility?

A

Parasympathetics transmitted through the Vagus n.

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4
Q

What serves as the intrinsic nervous regulator of GI motility?

A

The enteric nervous system

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5
Q

What are the effects of the myenteric plexus on GI motility?

A

Increased intensity of rhythm of contraction, increased tone, increased rhythm rate, increased velocity of contraction

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6
Q

What are the functions of the submucosal plexus?

A

Regulation of GI blood flow, controls epithelial function

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7
Q

What are the two types of smooth muscle in the GI tract and where are they found?

A

Unitary (circular and longitudinal muscle layers), and multi-unit (sphincters)

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8
Q

What type of smooth muscle has a more rapid response time? Why?

A

Multi-unit smooth muscle in sphincters– every smooth muscle cell has a variscosity associated with it

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9
Q

How are action potentials transmitted through multi-unit smooth muscle?

A

Gap junctions

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10
Q

What are the two types of movement activated by the enteric nervous system? What muscles are responsible for each

A

Segmental contractions (mostly circular) and peristalsis (circular and longitudinal)

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11
Q

What is the typical stimulus for peristalsis?

A

Distension

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12
Q

True or False: Peristalsis requires an intact ENS but not an intact ANS.

A

True

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13
Q

What is GI segementation?

A

Mixing of contents to promote digestion and absorption

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14
Q

How is peristalsis achieved?

A

Circular muscle contracts behind the bolus and relaxes ahead of it and longitudinal muscle relaxes behind the bolus and contracts ahead of it

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15
Q

What maintains the tonic contraction of GI sphincters?

A

Prostaglandins

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16
Q

What compounds relax sphincters?

A

NO and VIP

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17
Q

What is aerophagia?

A

Swallowed air

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18
Q

What are the local neural pathways for smooth muscle activity?

A

Stimulation of a stretch, mechano-, or chemo-receptor activates an excitatory, ascending orad pathway to stimulate contraction behind the bolus, and inhibitory, descending aborad pathway to stimulate relaxation ahead of the bolus

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19
Q

How is myogenic control of smooth muscle actiity mediated?

A

Basic electrical rhythm

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20
Q

What is basic electrical rhythm in regards to GI motility?

A

Cyclical depolarization/ repolarization of smooth muscle cell membranes

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21
Q

How is BER propagated and in what direction?

A

Through gap junctions aborally (caudad)

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22
Q

How does the rate of BER change down the GI tract?

A

Decreases

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23
Q

What determines the strength of smooth muscle contractions in the GI tract?

A

Frequency of action potentials

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24
Q

What are the functions of the interstitial cells of Cajal?

A

Serve as electrical pacemakers and generate spontaneous electrical slow waves in the GI tract

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25
Q

How do motor neurons interact with the ICCs?

A

Excitatory motor neurons release ACh or Substance P onto ICC resulting in excitation or inhibitory motor neurons release NO or VIP, resulting in inhibition

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26
Q

True or False: Slow wave cyclical depolarization/ repolarization is sufficient to stimulate contraction?

A

False: have to superimpose action potentials to get membrane potential above threshold

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27
Q

In which GI motility phase do migrating motility complexes occur?

A

Interdigestive phase

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28
Q

Which MMC phase has them most slow waves superimposed with action potentials? Which pahse lasts the longest?

A

Phase 3; Phase 1`

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29
Q

What compound regulates the MMCs?

A

Motilin

30
Q

In which MMC phase is there BER with no MMCs?

A

I

31
Q

Which GI cells release motilin?

A

Enterochromaffin cells

32
Q

On what area of the brain does motilin act? What does it stimulate?

A

Area postrema– production of serotonin

33
Q

How does motilin-induced production of serotonin induce MMCs?

A

Serotonin binds to 5-HT3 receptors in the dorsal vagal complex, vagal efferents release ACh within the GI, stimulating MMCs

34
Q

How is MMC phase III generated?

A

Motilin stimulates release of 5HT from duodenal enterocytes which activates 5HT3 receptors on afferent vagal nerves which stimulates a massive production of 5HT in the brain

35
Q

What is mastication?

A

Chewing- complex series of movements designed to convert large chunks of food into discrete boli

36
Q

Where is the swallowing center in the brain?

A

Medulla

37
Q

What are the three phases of swallowing? Which are voluntary?

A

Oral (voluntary), pharyngeal, and esophageal

38
Q

How is esophageal peristalsis stimulated?

A

Bolus distension detected by mechanorecpeotrs stimulate vagal afferents to the dorsal vagal complex ultimately stimulating the release of ACh above the bolus and NO below

39
Q

What is the importance of 2ndary peristalsis in the esophagus?

A

Important for clearing the bolus or responding to gastric reflux

40
Q

What innervates the upper and lower esophageal sphincters?

A

UES- CN IX, X, ansa cervicalis and SNS from cervical ganglion (pharyngeal plexus); LES- Branches of vagus and ENS

41
Q

What common factors increase the LES tone?

A

Protein, increased intra-abdominal pressure, elevated gastric pH

42
Q

What common factors decrease the LES tone?

A

Fat, chocolate, peppermint, alcohol, smoking, gastric distension

43
Q

What processes occur during the gastric phase of digestion?

A

Filling, mixing/grinding, secretion of gastric juices, digestive processes, gastric emptying

44
Q

What is the effect of swallowing on the LES and proximal stomach?

A

Relaxation

45
Q

What is receptive relaxation?

A

Swallowing relaxes gastric smooth muscle making it compliant to incoming material

46
Q

What stimulates the force of gastric contraction? Inhibits?

A

Gastric distention via long/ short reflexes and gastrin; Inhibited by duodenal distension, fat, acid, hypertonic chyme and SNS stimulation

47
Q

What is the impact of a vagotomy on receptive relaxation?

A

With a vagotomy the stomach is less compliant such that the intraluminal pressure increases steadily with volume

48
Q

What is the function of the fundus?

A

Acts as a food store

49
Q

Which parts of the stomach mix food?

A

Body and antrum

50
Q

What limits the exit of chyme from the stomach?

A

Pyloric contraction

51
Q

What initiates the electrical activity in the stomach?

A

Band of interstitial cells initiate nerve impulses

52
Q

What part of the stomach has the strongest peristaltic contractions

A

Pylorus

53
Q

Where do peristaltic contractions originate in the stomach?

A

Upper fundus

54
Q

What happens with peristaltic contractions reach the pyloric sphincter?

A

It closes tightly

55
Q

What factors increase gastric emptying?

A

Gastric distension, gastrin, parasympathetic stimulation

56
Q

What factors inhibit gastric emptying

A

Chyme moving into the duodenum, carbs, fats, and protein within the duodenum, acidity, hypo-/hyper-osmotic chyme inhibitory, duodenal distension

57
Q

What is the enterogastric reflex?

A

The distension of duodenum by chyme and fatty acids leads to deceased PSNS and increased secretion of CCK, resulting in decreased gastric motility, increased intestinal motility, and inhibition of gastric emptying

58
Q

What is the relative capability of carbs, fats, and proteins to stimulate the the enterogastric reflex?

A

Carbs > proteins > fats

59
Q

What is gastric dumping? What could cause this?

A

Gastric dumping is the rapid emptying of fluids and large amounts of acidic chyme into the duodenum due to loss of vagal innervation and lack of pyloric sphincter contraction

60
Q

What is the junction of the small and large intestines?

A

Ileo-cecal sphincter

61
Q

What are the two types of small intestinal movement? Which is responsible for propulsion of the chyme forward?

A

Segmentations and migrating motility complexes (propulsive)

62
Q

What are the actions of CCK within the GI system?

A

Stimulates gall bladder contraction, acinar secretion in the pancreas; reduced gastric emptying; relaxation of sphincter of Oddi

63
Q

Through what kind of receptor does CCK mediate contraction of the gall bladder?

A

CCKA receptor on smooth muscle

64
Q

What is the ‘ileocecal brake’? What stimulates it?

A

Peptide YY- production stimulated by lipids in the proximal colon/ terminal ileum

65
Q

How does chyme pass through the ileo-cecal sphincter?

A

After a meal, the gastro-ileal reflex intensifies ileum peristalsis and forces chyme into the cecum; also gastrin causes distension

66
Q

What are the types of movement within the colon?

A

Haustration and mass movements

67
Q

What stimulates and controls haustration?

A

Stimulated by distension and controlled by the intrinsic plexus and arrangement of interstitial cells of Cajal

68
Q

In which parts of the colon do mass movements take place?

A

Ascending and transverse colon

69
Q

What triggers mass movements of the colon?

A

Gastrocolic and duodenocolic reflexes, irritation, intense PSNS stimulation

70
Q

What innervates the external anal sphincter?

A

Pudendal n.

71
Q

What is the defecation reflex?

A

Mass movement results in rectal distension which activates stretch receptors and signals the desire to defecate and relaxation of the internal anal sphincter through parasympathetic pelvic nerve

Physiology Block 5- Gastrointestinal Physiology (11 decks)

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