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GI Relationships > Motility Of GI > Flashcards

Motility Of GI Flashcards

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1
Q

Slow waves

A
  • Not APs
  • Depolarization (membrane potential becomes less -)/repolarization (MP becomes more -) of membrane potential
  • Frequency of slow waves determines frequency of AP, therefore frequency of contractions
  • Originate in interstitial cells of Cajal
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2
Q

Phasic Contractions

A

Periodic contractions followed by relaxation
Seen in esophagus, antrum of stomach, SI
**Mixing and propulsing

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3
Q

Tonic contractions

A

Maintain a constant level of contraction without regular relaxation periods
Found in orad of stomach, lower esophageal, IC, int. Anal sphincters

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4
Q

ACh effect on Slow waves

A

ACh increases amplitude of slow waves and # of APs
Other stimulators of slow waves: stretch/parasympathetics
*Increase membrane potential

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5
Q

NE effect of slow waves

A

NE decreases amplitude of slow waves
Sympathetics w/ same effect
Creates hyperpolarization

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6
Q

Submucosal Plexus of Meissner

A
  • Found between submucosa and circular muscle layer

- Controls GI secretions and local blood flow

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7
Q

Myenteric plexus of Auerbach

A
  • Found between longitudinal and circular muscle layers

- Controls GI movements

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8
Q

Oral Phase

A

Voluntary and initiates swallowing process

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9
Q

Pharyngeal phase

A

Involuntary
- Soft palate pulled upward, epiglottis moves, UES relaxes, peristaltic wave of contractions initiated in pharynx and food is propelled through open UES

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10
Q

Esophageal Phase

A

Involuntary

Control by the swallowing reflex and ENS

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11
Q

Neural control of digestion

A

Mastication: 5th CN
Swallowing: 9th/10th CN

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12
Q

Primary Peristaltic Wave

A

Continuation of pharyngeal peristalsis

*Medulla controlled (cannot occur with vagotomy)

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13
Q

Secondary Peristaltic Wave

A

Occurs if primary wave fails to empty esophagus or if reflux occurs
*Medulla and ENS control (can occur post-vagotomy)

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14
Q

Issues w/ intrathoracic location of eso

A
  1. Keep air out at upper end

2. Keep acid gastric contents out of lower end

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15
Q

Achalasia

A
  • Impaired peristalsis
  • Incomplete LES relaxation during swallowing (food backs up)
  • LES resting P increases
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16
Q

Causes of Achalasia

A

Lack of VIP/ENS knocked out

Damage to esophageal nerves, preventing it from squeezing food into stomach

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17
Q

Effects of Achalasia

A

Backflow of food in throat
Difficulties swallowing
Chest pain

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18
Q

GERD

A
  • Changes in barrier b/w esophagus and stomach
  • LES relaxes abnormally/weakens
  • Persistent GERD can lead to irritation of esophagus, strictures and Barrett’s esophagus
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19
Q

Causes of GERD

A
  • Motor abnormalities resulting in abnormally low pressures in LES
  • When intragastric pressure increases (large meal, pregnancy, heavy lifting)
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20
Q

Receptive Relaxation

A
  • In orad region of stomach
  • Decreases pressure and increases volume in orad region
  • Vagovagal reflex
  • Orad has minimal contractile activity
  • CCK decreases contractions and increases gastric distensibility
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21
Q

Caudad region of stomach

A
  • Primary contractile event occurs midstomach-pylorus
  • Contractions increase with force and velocity approaching pylorus
  • 3-5 waves/minute = maximum
  • Retropulsion*
22
Q

Increased AP and force of contraction

A

Parasympathetic stimulation
Gastrin
Motility

23
Q

Decreased AP and force of contractions

A

Sympathetic Stimulation
Secretion
GIP (increased insulin)

24
Q

Gastric emptying

A

Via coordinated contractile activity of stomach, pylorus, and proximal small intestine

25
Q

Rate of gastric emptying increases with

A
  • Decreased orad distensibility
  • Increased force of peristaltic contractions in caudad stomach
  • Decreased tone of pylorus
  • Increased diameter and inhibition of segmenting contractions in prox. Duodenum

= 3hrs

26
Q

Factors that inhibit gastric emptying:

A
  • Relaxation of orad (increased distensibility)
  • Decreased force of peristaltic contractions
  • Increased tone of pyloric sphincter
  • Segmentation contractions in intestine
27
Q

Enterogastric reflex

A
  • Negative feedback from duodenum slows down rate of gastric emptying
  • Acid in duodenum stimulates secretin release and inhibits stomach motility via gastrin inhibition
  • Fats in duodenum stimulates CCK and GIP which inhibits stomach motility
  • Hypertonicity in duodenum inhibits gastric emptying
28
Q

Slow gastric emptying

A
  • Associated with disorders of gastric motility

- Causes: gastric ulcer, cancer, eating disorders, vagotomy

29
Q

Gastroparesis

A
  • Slow emptying of stomach w/o mechanical obstruction
  • DM common cause
  • Vagal injury
    Sx: N/V, feeling of fullness, weight loss, abdominal discomfort
30
Q

Migrating Myoelectric complex

A
  • Periodic, bursting peristaltic contractions
  • 90 min intervals
  • Motilin mediates complex
31
Q

Segmental Contractions

A

Back and forth movements

No forward/propulsive movements along SI

32
Q

Peristaltic contractions

A

Circular and longitudinal muscles work in opposition to each other and complement actions

33
Q

ICC and Smooth muscle in SI

A
  • Slow waves always present
  • Slow waves do NOT initiate contractions in SI
  • Spike potentials (aka AP) needed for muscle contractions
  • Slow wave frequency sets max. Frequency of contractions
34
Q

Stimulate Contractions

A
  • PNS
  • Serotonin
  • Prostaglandins
  • Gastrin
  • CCK
  • Motilin
  • Insulin
35
Q

Inhibit Contractions

A
  • Epinephrine
  • Secretin
  • Glucagon
36
Q

Vomiting Reflex

A

Medulla coordinates

  1. Reverse peristalsis
  2. Stomach and pylorus relax
  3. Forced inspiration to increase abdominal pressure
  4. Mvmt of larynx
  5. LES relaxation
  6. Glottis closes
  7. Forceful expulsion of gastric contents
37
Q

Flow from SI to LI

A

Ileum distention causes relaxation of sphincter
Colonic distention causes contraction of sphincter

**Via Ileocecal Valve

38
Q

Muscle layers of LI

A
  • Longitudinal w/ teniae coli
  • Circular run from cecum to anal canal
  • Internal anal sphincter (smooth m)
  • External anal sphincter (skeletal m)
39
Q

Haustras

A

Small pouches that give LI segmented appearance (not fixed)

40
Q

Parasympathetic Innervation of LI

A
  • Vagus n.: cecum, ascending and transverse colon

- Pelvic nn.: sacral portion of spinal cord (S2-S4): descending and sigmoid colon and rectum

41
Q

Sympathetic Innervation of LI

A
  • T10-L2
  • Superior mesenteric ganglion: proximal regions
  • Inferior mesenteric ganglion: distal regions
  • Hypogastric plexus: distal rectum and anal canal
42
Q

Somatic pudendal nn.

A

External anal sphincter

43
Q

Key function of LI motility

A

Water absorption/vitamin absorption

Conversion of digested food into feces

44
Q

Motility of rectum/anal canal

A
  • Rectum fills intermittently (mass movements and segmental contractions)
  • As it fills with feces, SM wall of rectum contracts and Int. Anal Sphincter relaxes (rectosphincteric reflex)
  • Ext. Anal sphincter voluntarily relaxes
45
Q

Rectosphincteric reflex and defecation

A
  • Neural Control (partially by ENS and reinforced with spinal cord neurons)
  • Sensation and voluntary control of EAS by pathways leading to cerebral cortex
  • Destruction of these pathways causes loss of voluntary control of defecation
46
Q

Hirschsprung’s Disease

A

VIP levels low - SM constriction/loss of coordinated mvmt. - colon contents accumulate

47
Q

Vago-vagal reflex

A

Long reflex
Generally stimulatory (increases motility, secretomotor, vasodilatory activities)
75% afferent
25% efferent

48
Q

Intestino-intestinal reflex

A

Inhibitory if bowel is distended

Contractile if rest of bowel is inhibited

49
Q

Enterogastric reflex

A

Negative feedback from duodenum will slow down rate of gastric emptying

50
Q

Gastroileal reflex (gastroenteric)

A

Gastric distention relaxes ileocecal sphincter

51
Q

Gastro and duodeno-colic reflexes

A

Distention of stomach and duodenum initiates mass mvmts.

Via ANS

52
Q

Defecation reflex (rectospincteric)

A

Rectal Distention initiates defecation

GI Relationships (7 decks)

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