GI Motility & Regulation Flashcards
Describe the two major types of motility in the GI tract, their function in digestion and the differences between them.
- Mixing- segmentation
2. Propulsive Movement- peristalsis
Explain how the sympathetic and parasympathetic systems communicate with intestinal smooth muscle
The vagus nerve carries preganglionic parasympathetics which stimulate postganglionic parasympathetics in the enteric plexus of the stomach wall.
Describe the characteristics of the basic electrical rhythm (BER) of the small intestine and its relation to smooth muscle contractile activity.
The BER (also called “slow waves”) refers to the spontaneous, rhythmic waves of depolarization that occur at a rate of 12 per minute in the duodenum/small intestine (contrast to 3 per minute in the stomach). The BER is like a pacemaker in the GI tract.
- Spontaneous depolarizations
- Muscle-derived (myogenic)
- When you add ACh, action potentials can fire at every peak (not just some peaks) and this happens at a frequency set by the BER, resulting in a wave-like contraction of peristalisis
List the stimulus that initiates the swallowing sequence and the events that follow. Identify the point at which the swallowing sequence switches from voluntary to involuntary.
- Voluntary Phase: You chew, tell your tongue to push food backward toward pharynx. This pushes the soft palate upward and the upper constrictor muscle contracts. Together, these two actions close off the nasopharynx.
From this point on swallowing becomes a reflex.
- Pharyngeal Phase: Direct food into the esophagus and keep it out of the trachea. For 1-2 seconds respiration is inhibited centrally, the larynx raises and the glottis closes to prevent the bolus from entering the trachea.
- Esophageal Phase: The upper esophageal sphincter relaxes, and the coordinated contraction (or peristaltic wave) of the middle and lower constrictor muscles propels the bolus into the esophagus.
Explain the mechanism of esophageal motility and peristalsis, and the role of the upper and lower esophageal sphincters in this process.
The Esophagus transports and adjusts food temperature
Muscular walls transition from skeletal to smooth muscle
Thick muscular walls produce strong peristatic waves
The lower esophageal sphincter is the gatekeeper between esophagus and the stomach. Failure to relax due to damage/loss of enteric nevers of the LES is called achalasia and can make swallowing difficult. Inappropriate LES relaxation can cause acid reflux
Describe the storage, digestion, and motility roles of the stomach.
Storage: In fundus and body, which is comprised of a thin muscular layer. Volume can stretch up to 4 liters!
Digestion: Mechanical digestion via mixing waves which creates chyme. Chemical digestion via salivary amylase, lingual lipase and HCL production
Motility: Paristaltic waves push bolus toward the antrum at the frequency of BER. Contractions become stronger and faster. Because the pyloric sphincter is so teeny tiny, a lot of the chyme is pushed backward in retropulsion, which actually helps mix the food more!
List the phases of the migrating motility complex (MMC)].
Between meals MMC sweep down the gastric antrum and along the small intestines.
Wave of peristalsis begins in the stomach, travels to the ileocecal sphincter and then repeats. At any one time 40cm of intestine is involved.
Each wave is receded by a rise in the plasma concentration of hormone motilin released by small intestine
Eating terminates MMC
Compare and contrast the colonic motor activity during a “mass movement” with that during haustral shuttling and the consequence of each type of colonic motility.
Mass movement:
•Forward propulsion that occurs 1-3 times/day (usually after meal). Hhaustration stops during mass movements
•Intense wave of contraction that moves content over larger distances – “strips” an area of large intestine clear of contents. The colon remains contracted for a while
• Overall movement is slow (maximum rate of 5-10 cm/hour)
Haustrations:
•Similar to segmentation, but more forceful. Mix & dry the chyme such that only 100-200 mL of fluid lost daily in the feces
•Occur in anatomicaly pre-defined locations of the circular muscle layer
•Governed by BER from interstitial cells (~6/min): usually no AP generated
•Stronger contractions (e.g. ACh) by prolonging BER
Describe the sequence of events occurring during defecation, differentiating those that are under voluntary control from those under involuntary control.
Filling of the rectum via mass movement causes relaxation of the internal anal sphincter via release of VIP and NO from intrinsic nerves in the rectoanal inhibitory reflex. This is largely a spinal reflex mediated by the pelvic nerves.
This reflex relaxation (intrinsic control) is followed immediately by voluntary constriction of the external anal sphincter (comprised of skeletal muscle). For defecation to occur, there must be voluntary relaxation of the external sphincter.
Evacuation is enhanced by simultaneous contraction of the rectus abdominus, diaphram and other levator ani muscles, which increases abdominal pressure. Similarly, the valsalva maneuver (attempted expiration against a closed mouth and nasal passage) can assist evacuation.
*Describe the various parts of chemical digestion
Digestion by salivary amylase continues until inactivated by acidic gastric juice (unless already bound to a substrate)
Acidic gastric juice activates lingual lipase, which digest triglycerides into fatty acids and diglycerides
Parietal cells secrete H+ and Cl- separately but net effect is HCl production which kills many microbes, denatures proteins
*Gastrin
Secreted by G cells in the gastric antrum. It is secreted in response to the presence of food in the stomach. It increases peristaltic contraction and decreases plyloric tone to increase the rate of gastic emptying
*Cholycystokinin (CCK)
secreted by enteric endocrine cells in response to the arrival of fats in the duodenum. CCK decreases gastric motility, providing a further method by which the duodenum decreases the rate of gastric emptying to ensure intestinal absorptive capacity is not overwhelmed
*Hydrochloric acid
secreted by parietal cells in the stomach, and there are factors which promote and inhibit secretion.
*What promotes gastric secretion?
- ACh: acts on M3 receptors in the basolateral membrane of the parietal cell directly, on ECL cells to activate histamine release, and on D cells to suppress the release of somatostatin.
- Gastrin: Binds to CCK2 receptors on the ECL cell (main function) to activate histamine release, and to CCK2 receptors on the parietal cell (lesser function) to stimulate acid secretion.
- Histamine: released by ECL cells, binds to H2 receptors on parietal cell basolateral membrane. Increases parietal cell acid secretion.
*What suppresses gastric secretion?
• Prostaglandins: Act through inhibitory G proteins to reduce levels of cAMP required in the histamine acid secretion pathway.
• Somatostatin, released by gastric D cells, inhibits Gastrin release → decreases acid secretion from parietal cells. It also inhibits ECL cells AND cAMP in parietal cells, thus reducing Histamine and, of course, acid secretion.
o NOTE: ACh turns D cells off → reduce somatostatin levels → favor Gastrin production + acid secretion
• GIP and Peptide YY inhibit parietal cell function.
