GI Motility (wilson)

Question 1

Muscularis layer of GIT is comprised of what 2 muscle layers?

Answer 1

• circular muscle layer (muscle fibers run circumferentially around entire GIT)
• longitudinal muscle layer (muscle fibers run down the length of GIT)

circular compress, longitudinal contract

Question 2

Synctial nature of GIT

Answer 2

GIT smooth muscle cells function as a syncytium via gap junctions (muscle fibers are electronically connected -> low-resistance flow of ions = smooth contraction)

Question 3

Cylic contractions

Answer 3

permit mixing (to aid with digestion) and propel GI contents

Question 4

Tonic contractions

Answer 4

Occur when the tract is quiescent and there is no motility, and stop when enteric innervation is removed.

• Non-propulsive contractile behavior occur continuously.
• upper stomach and sphincters – keeps lumen partially or completely closed to prevent reflux

Question 5

What are “electrical waves” in GI smooth muscle cells?

Answer 5

GI smooth muscle cell is always polarized (more negative than outside the cell) –> differences in AP within GI smooth muscle cell membrane caused by ions moving in/out determine the type of “electrical wave”
- slow waves
- spikes

Question 6

Slow Waves

Answer 6

ARE RHYTMICAL CHANGES! –> do NOT cause muscle contractions, but allow for contractions to be stimulated more easily by RAISING RMP closer to threshold (less neg) (caused by variations in Na+ conductance)
- intensity/frequency vary in different parts of GIT
- unique to GIT smooth muscle!

Question 7

Spike Potentials

Answer 7

TRUE ACTION POTENTIALS (Na+ & Ca2+ channels) that occur when SLOW WAVES REACH THRESHOLD –> cause smooth muscle contraction

• frequency determined by nervous/hormonal stimuli – large amts of Ca2+ enter into cell
• increase in frequency = stronger smooth muscle contractions

Question 8

Slow waves versus Spike Potentials relative to ion influx and contraction conductions

Answer 8

sodium influx changes; calcium influx changes –> only CALCIUM INFLUX leads to contraction!

Question 9

Intrinsic Control // Enteric Nervous System versus Extrinsic Control of the GIT

Answer 9

Intrinsic control // Enteric Nervous System

• Myenteric plexus+++ (controls most of GIT motility!! - in b.w muscle layers)
• Submucosal plexus (controls GI secretion + blood flow – lies in submucosal layer)

Extrinsic control of GIT = Parasympathetic and Sympathetic Nervous Systems
- parasym. NS (stimulates ACh)
- inhibited by symp. NS (NE)

Question 10

Myenteric Plexus

Answer 10

• Intrinsic control of the Enteric Nervous System.
• Located from esophagus to anus b/w the longitudinal and circular smooth muscle layers
• primary stimulatory effects of GI motility; also inhibitory (relax sphincters)

Question 11

Submucosal Plexus function

Answer 11

increases secretion of glands, aids with absoprtion of nutrients, contraction of muscularis mucosa (contracting glands and folds of epithelium of GIT mucosa)

does not greatly contribute to GIT contraction//motility

Question 12

Neurotransmitters of ENS

Answer 12

ACh (increases GI motility)
Norepi/epi (decrease GI motility)

Question 13

Orad portion of GIT is extrinsically controlled primarily by what nerve

Answer 13

Vagus nerve

Cranial division

Question 14

Aborad portion of GIT is extrinsically controlled primarily by what nerve

Answer 14

Pelvic nerves

sacral division

Question 15

Where do preganglionic neurons for sympathetic innervation / extrinsic control of GIT originate

Answer 15

Question 16

Where do postganglionic neurons for sympathetic innervation / extrinsic control of GIT originate

Answer 16

Question 17

Propulsive movements (peristalsis)

Answer 17

cause GIT contents to move forward
- primary stimulus = distension
- other stimuli: chemical or physical irritation; parasymp. nervous system

Question 18

Mixing Movements

Answer 18

non-progressive contractions that are intermittent constrictive rings that can occur for 5-30seconds –> cause chopping or shearing of GI contents

occuring in the BODY of the stomach