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Flashcards in Motility Deck (20):

Migrating Myoelectric Complex

– housekeeping function during fasting state sweeps undigested material and bacteria out of the upper GI tract and into the colon
o Prevents unwanted gases & protects the intestinal mucosa of upper GI tract from bacteria growth
o Occurs from mid-stomach through the terminal ileum (beginning of large intestine)
o Independent of vagal stimulation
o Begins 3-4 hours after eating and lasts 75-120 minutes
o 3-4 phases; only stage 3 has strong contractions(lasts 10 minutes); dependent on hormone motilin secreted into lood from M cells of small intestine


Slow Waves

= resting membrane potential – basic electral rhythm (BER)
o NOT action potentials; always present regardless of the membrane potential
o Reflects changes in the resting membrane potential probably caused by variations in the activity of the Na/K ATPase pump in the interstitial cells of Cajal throughout the GI tract
o Always present but frequency changes down the tract (3 per minute in stomach; 12 per minute in intestines)
o Slow waves can cause some contractions in the stomach, contractions in rest of tract are caused by action potentials generated on the peaks of slow waves


Slow Waves that Depolarize

o Depolarization above -40mV stimualtes action potentials; greater the depolarization (more above -40mV), the more action potentials, and the greater the contractions
o # of action potentials generated on a slow wave are directly related to force of contractions
o Sets the maximal possible rate of contraction/propulsion through the GI tract


Action Potentials

– generated by calcium entry via voltage-gated channels that cause depolarization
o Plateau – result of slow movement of calcium and sodium
o Repolarization – slow due to delayed increase in potassium leaving the cell



– mastication and deglutition (swallowing = opening of upper esophageal sphincter)



o 2 types of propulsion (primary and secondary esophageal peristalsis)
 Primary – used most often and controlled by Swallowing Center in medulla; some vagal
 Secondary – larger than usual bolus gets stuck in esophagus; esophageal distention sensed by mechanoreceptors; salvation and submucosal secretions increased to lubricate the bolus; myenteric plexus of the enteric nervous system contracts the smooth muscle near the bolus to increase propulsion towards the stomach
o Lower esophageal sphincter relaxes when bolus arrives



– smooth muscle disorder preventing relaxation of sphincter; causes dilation of esophagus; fix by cutting the sphincter open but risk of stomach acid refluxing up



o Receptive relaxation - mechanoreceptors sense food and increase volume of stomach to allow more in
 Mediated by vagus nerve by releasing vasoactive intestinal peptide (VIP)
o Absorption and release of different substances takes different amounts of time (saline first, acidic/carbohydrates/protein, fatty lipids last)
o G-cells release gastrin into bloodstream to stimulate hydrochloric acid production in stomach
o Gastric contractions include an oblique muscular layer in addition to the standard longitudinal and circular layers in rest of GI tract


Treatments Changing Receptive Relaxation

-Gastric bypass – loss of receptive relaxation making you feel “full” very fast; reduced the ability of stomach to accommodate food
- Vagotomy – cut vagus nerve and patients feel full sooner


Small Intestine

(duodenum, jejunum, ileum)
o Receptive relaxation
o Peristalsis and Segmentation
o ***REMEMBER BER and MMC continue through the small intestine***



o Under vagal/extrinsic control NOT enteric nervous system
 coordinated stimulation of both excitatory and inhibitory neurons allows contraction behind the bolus and relaxation in front
o Propulsion typically travels towards the anus but REVERSE (retrograde) peristalsis occurs during vomiting and in rectum when defecation reflex is voluntarily stopped



– purpose of mixing and propulsion
o Under intrinsic (enteric NS) control
o Contraction occurs in front and behind the bolus to cause Bidirectional propulsion
o Contractions occur similar rate to peristalsis
o May be propagated over longer areas of intestine than peristalsis


Gall Bladder

o Contraction of gall bladder releases bile
o Cholesycstokinin (CCK) hormone opens sphincter of Oddi and causes contraction of gall bladder to eject stored bile into the duodenum


Large Intestine

– BER is slow here except when mass movement are stimulated for rapid/fast movement
o Contains 3 bands of longitudinal smooth muscle called Taneia Coli that contract to create haustrae (pockets) via segmental propulsion (DIFFERENT from segmentation
o Slow movement and storage (segmental propulsion) followed by fast movement for expulsion (mass movement/peristalsis); transit time is variable and can depend on fiber and other factors
o Segmental Propulsion from formation of haustra and mass movements which are peristaltic
 Facilitates the last absorption of sodium and water (“colonic salvage”) since colon doesn’t have any villi


Mass Movement

– occur 3-4 times per day and are associated with eating (gastrocolic reflex)
 Controlled by vagus nerve and hormones (mainly gastrin)
 Stimulated in response to chyme in upper GI
 Haustra will smooth out into a tube and mass movement contraction forces the feces into the descending colon and rectum stimulating defecation reflex; clears out the lower GI tract for new food that will soon be there


Defecation/Rectosphincteric Reflex

– under conscious control
o Mechanoreceptors stretch the enteric nerves and cause relaxation of the internal anal sphincter
o External anal sphincter – voluntary control
 We can induce a vulsalva movement that increases abdominal pressure and triggers reflex to expel food (POOP)


Hirshsprung's Disease

= MEGA colon
o Smooth muscle disorder involving loss of enteric nerves in the distal portion of the colon
o Internal anal sphincter never relaxes so waste builds up in the colon


Fever & Diarrhea

o Anything that increases metabolism will increase the activity of the Na/K ATPase pump and thus increase motility in the gut
o Fever – increases metabolism  increases Na/K Pump activity  increase number of slow waves increases chance for more action potentials  increases movement of chyme  less chance/time for absorption  increase chances of diarrhea


Things that stimulate depolarization

-parasympathetics/Ach, stretch, gastrin, serotonin, tachykinin


things that stimulate hyperpolarization

-sympathetics/NE, VIP(vasoactive intestinal peptide), NO