GI motility Flashcards
describe how movement of stomach smooth muscle is initated? at which cells?
human stomach movement:
- random depolarisation of interstitial cells of cajal is communicated to smooth muscle cells, via gap junctions
- slow waves of electrical activity propagte from dominant pacemake in corpus (see photo)
fill the blanks bestie
the stomach movements are spontaneous, but are modulated by which NS?
= by enteric NS
overall function of the enteric system? (3)
what are two plexi find in enteric nervous system?
what are their locations?
functions?
- *enteric system function:**
- controls GI motility
- controls local blood flow
- controls transmucosal movement of fluids
- *mytenric plexus:
- location: between theinner and outer layers of the muscularis externa**
- function: primary motility controller
- *submucosal plexus:
- location:submucosa**
- function: primarly fluid exchange controller
GI tract dominant nervous control systems:
which (out of CNS, myogenic and ENS) controls:
a) oesphagus?
b) stomach? (3)
c) small intestine
d) colon? (2)
e) anus? (2)
a) oesphagus: CNS contrl (vagus)
b) stomach: myogenic (ICC), ENS & CNS (vagus)
c) small intestine: ENS
d) colon: ENS and myogenic control
e) anus: ENS and CNS (spinal)
what is the migrating motor complex?
where can it originate?
what is its functions? (2)
migrating motor complex: propagating contractions every 90-120 mins. 3 phases
originates:
- *a) stomach -** vagus dependent
- *b) small intestine -** _vagus independent
functions:_
a) clear undigested material
b) prevents bacteria overgrowth
what are the three stages of the migrating motor complex?
- Phase 1 is fairly quiet,
- Phase 2 occurs after an hour or so with small changes in amplitude
- Phase 3 is a great high amplitude contraction - makes u hungry
what two things specifically make u hungry?
- release of hormone ghrelin
- phase three of migrating motor complex
what are 3 stages of digestion?
Cephalic phase: Thought, sight, smell, taste (learned responses). MMCs abolished. Prepares GI tract: saliva, gastric acid, pancreatic secretion, gastrin, ghrelin secretion
Gastric phase: Satiation, early digestion, gastric emptying. This is triggered by mechanical effect. Triggered by mechanical effect.
Intestinal phase: Feedback and satiation. Triggered mainly by chemoreceptor activation within the small bowel.
how does peristalsis occur in oesophagius ? (primary / secondary waves?)
peristalsis:
- bolus enters striated muscle, initiates primary peristaltic wave. pressures changes / waves of contraction push bolus down.
- this stimulates stretch receptors = secondary peristaltic wave of smooth muscle (back up secondary wave) pushes the bolus into the stomach
- *functions of the proximal stomach:**
- what happens when bolus enters stomach? (2 steps)
- what is each step innervated by?
- what method can u do to relieve pressure of stomach? - how does this occur?
functions of the distal stomach? (3)
functions of the proximal stomach:
- *- receptive relaxation:** makes proximal stomach stretch so not immediatly full (vagal-vagal relflex, causes release of CCK)
- *- adaptive relaxation:** ENS releases NO to allow relaxation
- can relieve pressure by _burping (_lets gas out of stomach) via relaxation of LOS
- *functions of the distal stomach:**
- propulsion, retropulsion and further grinding and mixing (propels food agaisnt closed pylorus)
- gastric acid digestion
- only particles of 1-2 mm empty into duodenum
fyi
describe the speed of gastric empty of:
a) liquids?
b) large solid particles
c) viscous chyme?
what is rate of emptyin regulated by?
a) liquids: fast and exponential
b) large solid particles: lag phase - only after sufficient grinding
c) viscous chyme: linear fashion
get slow gastric emptying and promotes satiety
= maintains a constant flow of nutrients into the intestine !!
rate of emptyin regulated by: intestine - neural and hormonal
what are the dudenal and jejunal brakes?
dudenal and jejunal brakes:
- food goes into the duodenum, might be too big - like long chain fatty acids / amino acids. causes the release of CCK
- release of CCK activates vagal efferents
- *3. as a result of vagal efferents:**
- reduces opening of pyloric sphincte
- reductions contractions in corpus
- enhances relaxation of fundus
what is the ileal brake?
- fats reach the ileum (even tho theyre meant to have been absorbed in duodenum)
- causes release of peptide YY & **glucagon-like peptide-1 (GLP-1) by enteroendocrine cells
= slows gastric emptying**
describe how the ENS and peristaltic reflex works:
- how this reflex activated? (2)
- describe the difference between the different motor neurons causing ascending and descending wave of peristalsis:
- what type of NT released?
- what does that cause?
1. Activation of enteric reflexes: can be chemical or mechanical.
- Chemical activation can be through substances from endocrine cells (e.g. 5-HT), nutrients or low Ph
- mechanical via muscle deformation or stretch
motor neurons:
Ascending wave of peristalsis:excitatory neuro-transmission to muscle, mostly by the release of acetylcholine. This causes the contraction and initiate the push.
Descending wave of peristalsis: Inhibitory neurotransmission to muscle, mostly by release of the gas nitric oxide
role of ascending (3), transverse (1) and descending colon? (2)
- *Ascending colon:**
- *-**mixing
- absorption of water / ions / nutrients
- fermentation due to rich no. of living bacteria
- *Transverse colon**:
- Absorption, with relatively rapid transit
- *Descending colon**:
- Storage.
- Partly voluntary transit when defecation needed.
what anatomical features of the colon ensure that peristalsis is modified?
- get bulges of outer circular muscle (haustra), which are held together by three bands of circular muscle: taenia
- taenia can contract in either direction
what are the movements of the ascending colon? (3)
propulsion
retropulsion
segmentation (mixes contenet and increases exposure to mucosa)
how does bolus move along colon? (2)
- constrictive ring occurs (giant migrating concentration) and haustra disappear from a portion of the ascending colon
~20cm of the colon distal to the constrictive ring lose their haustrations and contract as a unit, propelling faecal material into the transverse colon
what happens when bolus goes into rectum?
- Contents continue to enter rectum
- Triggers conscious urge to defecate due to increased pressures
- As contents distend the rectum, the pressure increases passively - active contraction may increase pressure further
- Accompanied by relaxation of internal anal sphincter & contraction of external sphincter
what normally prevents defecation? (2) what changes when u defecate
- *defecation prevented by:**
- Tone of internal anal sphincter & puborectalis
- Mechanical effects of acute anorectal angle. The pubic symphysis and angle act as a mechanical obstruction to defecate moving to the anus.
- *defecate:**
- Puborectalis muscle and external anal spinchter relax
- Intraabdominal pressure increase
- squatting facilaites
