Motility of the GI Tract Flashcards

1
Q

Slow waves

A

Depolarization and repolarization of the membrane potential. Does not, on its own, equal an AP.

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2
Q

Phasic contraction definition:

Where does it occur?

A

Periodic contractions followed by relaxation.

Esophagus, antrum, SI.

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3
Q

Tonic contractions definition:

Where does it occur?

A

Constant contraction w/o regular periods of relaxation.

Orad of stomach, lower esophagus, ileocecal and anal sphincters.

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4
Q

What can stimulate an AP in the gut? (3)

A

Stretch
ACh
Parasympathetics

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5
Q

What can stimulate repolarization in the gut? (2)

A

NE

Sympathetics

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6
Q

What does the submcosal plexus control?

A

GI secretions and local blood flow.

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7
Q

What does the Myenteric plexus (Auerbach’s) control?

A

GI movement.

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8
Q

ICCs (Intestinal cells of Cajal)

A

Pacemaker cells of GI SM.

Propagate slow waves.

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9
Q

What nerve innervates most muscles of mastication?

A

CN 5, trigeminal n.

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10
Q

Oral phase of mastication is:

A

Voluntary.

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11
Q

Pharyngeal phase of mastication (5)

A
  1. Soft palate pulled upward.
  2. Epiglottis moves.
  3. UES relaxes.
  4. Peristaltic contractions initiated in pharynx.
  5. Food propelled thru UES.
    INVOLUNTARY
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12
Q

Esophageal phase is controlled by (2):

A

Swallowing reflex and ENS.

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13
Q

Who controls the involuntary swallowing reflex?

A

Medulla

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14
Q

Involuntary swallowing reflex (5)

A

Food in pharynx –> vagus/glossopharyngeal n. –> medulla –> brainstem nuclei –> motor output to pharynx

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15
Q

Primary peristaltic wave (3)

A

Continuation of pharyngeal peristalsis.
Controlled by medulla.
Cannot occur post vagotomy.

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16
Q

Secondary peristaltic wave (4)

A

Occurs if primary wave does not empty esophagus or if reflux occurs.
Medulla and ENS involved.
Can occur w/o oral and pharyngeal phases.
Can occur post vagotomy.

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17
Q

What occurs in achalasia?

A

The LES does not fully relax during swallowing, causing a buildup of food.
LES resting pressure is elevated.

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18
Q

What can cause achalasia?

A

Lack of VIP or ENS has been affected.

Damage for nerves in esophagus.

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19
Q

Physiology of GERD

A

LES has abnormally low pressure (it weakens) from lower motor problems. Acid, pepsin and bile can get into esophagus.

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20
Q

3 layers of muscle of the stomach

A

Circular
Longitudinal
Oblique

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21
Q

Where does receptive relaxation occur?

How does it affect pressure and volume of that region?

A

Orad region.
Decreases pressure and increases volume of orad region.
Vasovagal reflex.

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22
Q

What occurs does not occur in the orad region?

A

It does not have contractile ability; therefore, little mixing of food occurs.

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23
Q

What is the affect of CCK on contraction and gastric distensibility?

A

Decreases contractions

Increases gastric distensibility.

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24
Q

Peristalitic contraction of the stomach occurs at:

A

Mid-stomach to pylorus

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25
Q

What happens to the force/velocity of the contractions as the approach the pylorus?
What is the max. freq. of waves/min?

A

They increase.

3-5 waves/min

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26
Q

What happens to the gastric contents in caudad region?

A

“Retropulsion”

Most of it is propelled back into the stomach for further mixing and reduction of particle size.

27
Q

What is the affect of PSNS, gastrin and motilin on AP frequency on force of contractions?

A

Increases them

28
Q

What is the affect of SNS, secretin and GIP on AP frequency and force of contractions?

A

Decreases them

29
Q

How long does gastric emptying take?

A

3 hrs

30
Q

What increases the rate of gastric emptying? (5)

A

Decreased orad distensibility.
Increased force of peristaltic contractions of the caudad region.
Decrease tone of pylorus.
Increased diameter.
Inhibition of segmenting contractions of proximal duodenum.

31
Q

What inhibits the rate of gastric emptying? (4)

A

Relaxation of orad (increased in distensibility).
Decreased force of peristaltic contractions.
Increased tone of pyloric sphincter.
Segmentation contractions in intestine.

32
Q

Why is gastric emptying closely regulated?

A

To allow enough time for neutralization of gastric H+ in duodenum and enough time for absorption/digestion.

33
Q

Entero-Gastric reflex

A

Negative feedback from duodenum which slows the rate of gastric emptying.

34
Q

What happens when there is acid in the duodenum?

A

Stimulates secretin release and inhibitions stomach motility by gastrin inhibition.

35
Q

What happens when there is fat in the duodenum?

A

Stimulates CCK and GIP which inhibit stomach motility.

36
Q

What happens when there is hypertonicity in the duodenum?

A

An unknown hormone inhibits gastric emptying.

37
Q

Gastroparesis

A

Slow emptying of stomach/paralysis of stomach in the absence of mechanical obstruction.

38
Q

Most common cause of gastroparesis:

What else can cause it?

A

DM

Damage to vagus n.

39
Q

Migrating myoelectric complex (MMC)

A

Empties large undigested particles in the stomach.

40
Q

MMCs (4)

A

Periodic, bursting peristaltic contractions.
Occur at 90 min invervals during fasting.
Motilin plays a significant role in mediating it.
Inhibited during feeding.

41
Q

Segmental contractions

A

Back-and-forth movements that do not produce a forward movement along SI.

42
Q

When is there slow wave activity?

A

ALWAYS

43
Q

What sets the max. freq. of contractions?

A

Slow waves

44
Q

Slow wave freq. in the:
Duodenum:
Jejunum:
Ileum:

A

D - 12 cycles/min
J - 10 cycles/min
I - 8 cycles/min

45
Q

How does serotonin affect the peristaltic reflex?

A

It is release by enterochromaffin cells and binds to IPAN receptors, initiating the peristaltic reflex.

46
Q
Hormonal control of contractions
Serotonin
Prostaglandins
Epi
Gastrin, CCK, Motilin, insulin
secretin, glucagon
A
Serotonin : +
Prostaglandins : +
Epi : -
Gastrin, CCK, Motilin, insulin : +
Secretin, glucagon : -
47
Q

Vomiting reflex is controlled by:

A

Medulla

48
Q

Events of vomiting (7)

A
Reverse peristalsis.
Stomach and pyloric relaxation.
Increased abdominal pressure.
Movement of larynx.
LES relaxes.
Glottis closes.
Gastric contents thrown up.
49
Q

What does distention of the ileum do the sphincter?

Distention of the colon?

A

Relaxes it to allow the flow from ileum to colon.

Constricts sphincter, preventing backflow into the SI.

50
Q

Taeniae coli

A

3 flat bands of longitudinal fibers that run from cecum to rectum in the longitudinal muscle.

51
Q

Internal anal sphincter is:

External anal sphincter is:

A

Involuntary (SM)

Voluntary (skeletal muscle)

52
Q

Haustras

A

Small pouches that give the LI its segmented appearance.

They are NOT fixed.

53
Q

ENS innervation of the LI

A

Concentrated beneath teneae coli.

Innervate muscle layers.

54
Q

PSNS innervation of LI
Vagus n.
Pelvic ns.

A

Vagus n.: cecum, ascending and transverse colon.

Pelvic ns.: sacral portion of spinal cord, descending and sigmoid colon, rectum.

55
Q

SNS innervation of LI (T10-L2)
Superior mesenteric ganglion:
Inferior mesenteric ganglion:
Hypogastric plexus:

A

Superior mesenteric ganglion: proximal regions
Inferior mesenteric ganglion: distal regions
Hypogastric plexus: distal rectum and anal canal

56
Q

Somatic pudendal ns. innervate:

A

External anal sphincter

57
Q

Mass movements

A

Occur over long distances.
1-3x day
Stimulate defecation reflex.
Propels fecal content into rectum.

58
Q

What happens to the wall of the rectum and the internal anal sphincter when the rectum fills with feces?

A

SM wall of rectum contracts and the internal anal sphincter relaxes.

59
Q

Vagovagal reflex

A

Stimulatory reflex

60
Q

Intestino-intestinal reflex

A

Inhibitory reflex

61
Q

Gastroileal (gastroenteric) reflex

A

Negative feedback from duodenum will slow rate of gastric emptying.

62
Q

Gastro and duodeno-colic reflexes

A

Distention of stomach/duodenum initiates mass movements

63
Q

Rectosphincteric (defecation) reflex

A

Rectal distention initiates defecation