Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI Midterm > Motility of GI Tract > Flashcards

Motility of GI Tract Flashcards

1
Q

Major activity in GI tract

A

Motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is motility?

A
  • contraction and relaxation of walls and sphincters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the four functional layers of the GI tract?

A

Mucosal layer
Submucosa
Muscularis externa
Serosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is part of the mucosal layer?

A
  • epithelium
  • lamina propria
  • muscularis mucosae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the muscularis mucosae?

function?

A

SMOOTH MUSCLE

- its contraction will change the shape and surface area of epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is function of the muscle layers ( muscularis propria)?

A

SMOOTH MUSCLE

  • inner circular muscle
  • outer longitudinal muscle

provide motility to GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is function of circular muscle?

A

contraction will decrease DIAMETER of segment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is function of longitudinal muscle?

A

contraction will decrease LENGTH of segment

- shortening the length of bowel contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Are slow waves the same as Action potential?

A

NO!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are slow waves?

A

depolarization and repolarization of the membrane potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What modulates AP and strength of contraction?

A

neural activity and hormonal activty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens after slow waves?

A

slow waves are followed by contraction (tension) of muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Phasic contractions

- examples

A

periodic contactions followed by relaxation

- esophagus, stomach (antrum) , small intestine, tissues for mixing and propulsion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Tonic Contractions

- examples

A
  • maintains CONSTANT level of contraction without regular periods of relaxation
  • stomach (orad), lower esophageal, ileocecal, and internal anal sphincters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Relationship between slow waves, APs, contractions in smooth muscle

A

The greater the # of APs on top of the slow, the larger the contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What will increase the amplitude of slow waves? effects?

A

1) stretch
2) Acetylcholine
3) Parasympathetics

increase contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What will decrease the amplitude of slow waves? effects?

A

1) Norepinephrine
2) Sympathetics

decrease contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What mainly controls GI movements?

A

MYENTERIC PLEXUS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is part of the enteric nervous system/

A

1) Submucosal plexus

2) Myenteric plexus (Auerbach’s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe submucosal plexus

  • location
  • function
A

in the submucosa

- mainly controls GI secretion and local blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe Myenteric plexus

  • location
  • function
A

aka Auerbach’s
- btw longitudinal and circular layers

  • mainly control GI movements
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Role of Pacemaker region in plexuses

A

Pacemaker regions in myenteric and submucosal plexuses generate spontaneous slow wave activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What cells are the pacemaker of GI smooth muscle?

A

Interstitial Cells of Cajal (ICC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe Interstitial Cells of Cajal (ICC)

  • function
  • cell type
A
  • generate and propagate slow waves
  • slow waves occur SPONTANEOUSLY in ICC and spread rapidly to smooth muscle via GAP JUNCTIONS
  • drives frequency of contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe Mastication

  • innervation
  • controlled by what
  • function
A
  • innervated by motor ranch of fifth cranial nerve
  • both voluntary and involuntary
  • controlled by nuclei in brain stem
  • chewing reflex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Phases of Swallowing (3)

  • describe in detail
  • involuntary/ voluntary
A

1) Oral Phase ( voluntary)
- initiate swallowing process
2) Pharyngeal phase (involuntary)
soft palate is pulled forward-> epiglottis moves -> UES relaxes-> peristaltic wave of contractions is initiated in pharynx-> food is propelled through open UES
3) Esophageal phase (involuntary)
- control by the swallowing reflex and ENS
-Primary peristaltic wave
- Secondary peristaltic wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the involuntary swallowing reflex controlled by?

- pathway

A

Medulla

Food in pharynx-> afferent sensory input via vagus/glossopharyngeal N.-> swallowing center (medulla)-> brainstem nuclei-> efferent input to pharynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Two Types of peristaltic waves

A

1) Primary peristaltic wave

2) Secondary peristaltic wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Primary peristaltic wave

A
  • continuation of pharyngeal peristalsis
  • controlled by the medulla
  • can NOT occur after vagotomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Secondary peristaltic wave

A
  • occurs if primary wave fails to empty the esophagus or if gastric contents reflux into esophagus
  • Medulla & ENS are involved
  • can occur in absences of oral & pharyngeal phass
  • occurs EVEN after vagotomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How does pressure change during swallowing as food bolus passes?

A

as food goes down, pressure increases in the region where the food bolus is down the esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Problems with intrathoracic location of esophagus (2)

- how are these problems solved

A

1) keeping air out of esophagus at upper end
2) keeping acidic gastric contents out of the lower end

Solution
- UES and LES are closed, except when food bolus is passing from pharynx to esophagus or from esophagus to stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Achalasia

  • description (3)
  • causes (2)
  • symptoms
A
  • impaired peristalsis
  • incomplete LES relaxation during swallowing
  • elevation of LES resting pressure

Causes

  • lack of VIP or ENS
  • damage to nerves in esophagus, prevent it from squeezing food into stomach
  • backflow of food in throat (regurgitation), difficulty in swallowing to both liquids and solids (dysphagia), chest pain
34
Q

GERD

  • causes
  • symptoms
A
  • changes in barrier between esophagus and stomach
  • motor abnormalities that result in low pressures in LES
  • persistent reflux and inflammation
  • backwash of acid, pepsin, bile into esphagus
  • heartburn and acid regurgitation
  • irritation/scar of esophageal lining
  • Barrett’s esophagus
35
Q

Anatomical division of stomach

A

Fundus
body
Antrum

36
Q

Regions of stomach

A

1) Orad Region
- Fundus
- Upper half of body

2) Caudad Region
- lower half of body
- antrum

37
Q

3 muscle layers of stomach

A

circular
longitudinal
oblique

38
Q

Extrinsic innervation of stomach

A

parasympathetics and sympathetics

39
Q

Intrinsic innervation of stomach

A

myenteric and submucosal plexus ( ENS)

40
Q

Receptive Relaxation

  • location
  • describe
  • reflex
  • hormone
A

Orad region

  • decrease pressure and increase volume
  • vagovagal reflex
  • minimal contractile activity
  • little mixing or ingested food occurs there

CCK decrease contractions and increase gastric distensibility

41
Q

Mixing and Digestion

  • location
  • describe
A
  • peristaltic contraction (mid stomach-> pylorus)
  • contractions increase in force and velocity as they approach the pylorus
  • frequency is 3-5 waves/min

Retropulsion: contents propelled back into stomach for further mixing and REDUCTION of particle size

42
Q

Sequence of gastric motility

A

1) food comes in stomach-> initial peristaltic wave
2) Pylorus is opened
3) Mixing in lower stomach
4) Retropulsion
5) Propulsion into duodenum

  • takes a few hours
43
Q

Regulation of gastric contraction

- what will increase/ decrease contractions

A

Increase contraction (increase AP):

1) Parasympathetic stimulation
2) Gastrin
3) Motilin

Decrease contraction (decrease AP):

1) sympathetic stimulation
2) secretin
3) GIP

44
Q

How can you increase gastric emptying? (4)

A

1) decrease distensibility of orad
- distensibility= ability to become stretched, dilated, enlarged
2) increase force of peristaltic contractions of caudad stomach
3) decrease tone of pylorus
4) increase diameter and inhibition of segmenting contractions of proximal duodenum

45
Q

What inhibits gastric emptying? (4)

A

1) Relaxation of Orad (increase in distensibility)
2) decrease force of peristaltic contractions
3) increase tone of pyloric sphincter
4) segmentation contractions in intestine

46
Q

Entero-gastric reflex

- how?

A

negative feedback from duodenum that will slow down rate of gastric emptying

acid in duodenum-> stimulate secretin release-> inhibit stomach motility via gastrin inhibition

fats in duodenum-> stimulate CCK and GIP-> inhibit stomach motility

hypertonicity in duodenum-> unknown hormone-> inhibit gastric emptying

47
Q

Disorders of gastric motility

  • symptoms
  • causes
  • treatment
A

Symptoms: fullness, loss of appetite, nausea, vomit

Causes: gastric ulcer (scar tissue), cancer (physical obstruction), eating disorders, vagotomy

Treatment: pyloroplasty, balloon dilation

48
Q

Gastroparesis

A
  • slow emptying of stomach/paralysis in absence of mechanical obstruction
  • DM most common
  • injury to vagus nerve

symptoms: nausea, vomit, fullness when eating, weight loss

49
Q

Migrating Myoelectric Complex

A
  • periodic, bursting peristaltic contractions
  • occur at 90 mins intervals, during fasting
  • Motilin play role
  • inhibited during feeing
  • large particle of undigested residue
50
Q

Small Intestine motility

A
  • mix chyme and digestive enzyme and pancreatic secretion
  • expose nutrients to intestinal mucosa for absorption
  • propel unabsorbed chyme along the small intestine to large intestine
51
Q

Segmentation Contractions

A
  • generates back and forth movement

- produce no forward, propulsive movement along the small intestine

52
Q

Peristaltic contractions

A
  • circular and longitudinal muscles works in opposition to complement each other’s actions
  • reciprocally innervated
53
Q

Electrical activity in small intestine

A

slow wave frequency

  • Duodenum: 12 cycles/ min
  • Jejunum: 10 cycles/ min
  • Ileum- 8 cycles/ min
54
Q

Serotonin in peristaltic reflex

A

released by enterochromaffin cells and bind to receptos in IPANS

55
Q

Myenteric plexus regulation in SI

A

relaxation and contraction of intestinal wall

56
Q

Submucosal (meissner) plexus regulation in SI

A

senses lumen environment

57
Q

Neural input in SI contractions

A
  • peristaltic reflex mediated by ENS

- PNS stimulates and SNS inhibits contractions

58
Q

Hormonal control in SI contraction

A

— Serotonin stimulates contractions
— Certain prostaglandins can stimulate contractions
— E, released from adrenal glands, inhibits contractions
- gastrin, CCK, motilin, and insulin tend to stimulate contractions
- secretin and glucagon tend to inhibit contractions

59
Q

Vomiting Reflex

  • controlled by
  • nerves
  • pathway
A
  • coordinated by medulla
  • nerve impulses are transmitted by vagus and sympathetic afferents to multiple brain stem nuclei
  • reverse peristalsis in SI-> stomach and pylorus relaxation-> forced inspiration to increase abdominal pressure-> movement of larynx -> LES relaxation-> glottis closes-> forceful expulsion of gastric contents
60
Q

Ileocecal Junction

A

sphincter that control contents coming from SI into LI

  • distention of ileum-> relaxation of sphincter
  • distention of colon -> contraction of sphincter
61
Q

Anatomical features of LI

  • muscle layers
  • sphincters
  • haustra
A

Muscle layer

  • longitudinal
    • taeniae coli: 3 flat bands of longitudinal fibers that run from cecum to rectum
  • Circular
    • continuous from the cecum to anal canal

Sphincter:

  • internal anal sphincter (smooth muscle)
  • external anal sphincter (striated muscle)

Haustra: small pouches that give LI a segmented appearance
- no fixed

62
Q

Innervations of LI

  • ENS
  • PNS
  • SNS
  • Somatic pudendal nerves
A
  • ENS
    • concentrated beneath teneae
    • innervate muscle layers
  • PNS
    • vagus nerve: cecum, ascneding and transverse colon
    • pelvic nerves: sacral portion of spinal cord (S2-S4), descending and sigmoid colon, rectum
  • SNS
    • superior mesenteric ganglion: proximal regions
    • inferior mesenteric ganglion: distal regions
    • hypogastric plexus: distal rectum & anal canal
  • Somatic pudendal nerves; external anal sphincter
63
Q

Motility in LI

A 
• Occur in the colon, 
over large distances 
• 1 - 3 times/day 
• Stimulate defecation 
reflex 
• A final mass movement 
propels the fecal 
content into the rectum
64
Q

Poor Motility in LI

- effects

A

greater absorption

- hard feces in transverse colon -> constipation

65
Q

Excess Motility in LI

- effects

A

less absorption

  • diarrhea
  • loose feces
66
Q

Motility of rectum and anal canal

A 
• Rectum fills intermittently 
- Mass movements 
- Segmentation contractions 
• As it fills with feces, SM 
wall of the rectum 
contracts & INTERNAL anal 
sphincter RELAXES 
(rectosphincteric reflex) 
• The EXTERNAL anal 
sphincter is tonically CLOSED (under voluntary control)
67
Q

Rectosphincteric reflex & defecation

  • under what control
  • mediated by
A

• Under neural control
— Controlled partially by ENS
— Reflex is reinforced by
cortex activity of neurons within the spinal cord

-Sensation of rectal 
distention & voluntary 
control of the external anal 
sphincter are mediated by 
pathways within the spinal 
cord that lead to the 
cerebral cortex
  • destruction will cause loss of voluntary control od defecation
68
Q

Hirschsprung Disease

  • cause
  • result
  • symptoms
  • treatment
A

cause: ganglion cells absent from colon segment

Result:

  • VIP level low
  • SM constriction
  • loss of coordinated movement
  • colon contents accumulate
  • difficulty of passing stool

Symptoms: poor feeding, jaundice, vomiting, constipation, swollen belly, malnutrition

Treatment: surgical resection of colon segment lacking ganglia

69
Q

Vago-vagal reflex

A

long reflex
- generally stimulatory (increase motility, secretomotor, vasodilatory activities)
afferent (75)
efferent (25)

70
Q

Intestino-intestinal reflex

A

depends on extrinsic
connections; inhibitory

if an area of the bowel
distended, contractile activity in the rest of the
inhibited

71
Q

Enterogastric Reflex

A

Negative feedback from d

will slow down the rate of gastric emptying

72
Q

Gastroileal reflec (gastroenteric)

A

gastric distentionsrelaxes ileocecal sphincter

73
Q

Gastro- & duodeno-colic reflexes

A

distention of
stomach/duodenum initiates mass movements
- Transmitted by way of the ANS

74
Q

Defecation reflex (rectosphincteric)

A

rectal distention initiates defecation

75
Q

Gastrin

A

secreted G cells of antrum & duodenum

stimulates motility

76
Q

CCK

A

secreted from I cells of duodenum and jejenum

stimulates motility

77
Q

Insulin

A

secreted from pancreatic beta cells

stimulates motility

78
Q

Motilin

A

secreted from duodenum & jejunum

stimulates motility

79
Q

Serotonin

A

neurotransmitter

stimulates motility

80
Q

Secretin

A

secreted by S cells of duodenum

inhibits motility

81
Q

Glucagon

A

secreted from pancreatic alpha cells

inhibits motility

GI Midterm (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions