Lecture 20: GI System Intro + Motility Flashcards
Purpose of GI motility
- Move food/chyme to right place at right time.
- Homogenize/mix food and chyme.
Control mechanisms for GI smooth muscle
- Stretch activation
- Intrinsic neural control
- Extrinsic nerve control
- Hormones
- Pacemaker slow waves
Stretch activation of GI smooth muscle
Food/chyme distension -> alternating circular/longitudinal smooth muscle stretch -> mixing; stretch on its own is usually insufficient for motility due to stimulus dissipation as food digests/homogenizes.
Intrinsic neural control of GI smooth muscle
Myenteric nerve plexus amplifies and coordinates stretch signals. Can act on its own, independent of ANS control.
Extrinsic neural control of GI smooth muscle
Primarily PNS via vagus nerve modulating the myenteric nerve plexus. Includes vagal excitatory/inhibitory fibers stimulating excitatory/inhibitory ME neurons.
Pacemakers of GI smooth muscle
Slow waves fire APs when they reach threshold; basally subthreshold. Slow wave frequency aka Basic Electrical Rhythm -> max contraction frequency. Additional activation e.g. stretch -> RMP depolar. on top of slow waves -> reach threshold.
GI muscularis mucosae function
Prevents food from clogging epithelial mucosal surface
Swallowing reflex chain
- Epiglottis/glottis close off airway as thorax rises
- Swallowing center in brain briefly pauses breathing
- Requires tactile + chemical sensation to initiate (saliva)
Divisions of innervation of esophagus
Upper 1/3rd of esophagus = vagal stimulation of skeletal muscle
Lower 2/3rds of esophagus = ME stimulation of smooth muscle (vagus can stim. ME)
How does gastric motility aid digestion?
Motility mixes food. Additionally, gastric peristalsis + pyloric sphincter contraction creates retrograde propulsion, generating shear forces which help tear food apart.
Peristalsis
Wavelike directional muscle contractions
Gastric receptive relaxation
Stomach compliance increases when a meal is swallowed. Mediated by PNS -> stomach enteric nerve plexi. Coordinated by afferent gastric vagal input, efferent brain swallowing center.
Stomach motility by area
Peristalsis begins in the stomach body too weak to mix, moving food toward the antrum.
The larger antrum wall muscle mixes luminal content and peristaltic waves cause pyloric sphincter muscles to contract.
Enterogastric reflex
Inhibition of gastric emptying by:
- Duodenal distension
- Fat in duodenum**
- High duodenal acidity
- Duodenal lumen hypertonicity
These factors also inhibit acid/pepsin gastric secretion
Primary motility of the small intestine
Segmentation (s. intestine does NOT have peristalsis).
Stationary, rhythmic contract/relax. of intestinal segments that forces chyme back and forth for absorption. Little net movement to large intestine.
Modulation of segmentation
Hormones, ENS, ANS can alter segmentation intensity but NOT frequency. Parasymp./symp. increase/decrease force.
How does chyme move from the small intestine to the colon?
Migrating myoelectrical complex replaces segmentation after absorption. Starts in lower stomach, inhibited by motilin. Repeated waves travel ~2 feet down the intestine, starting further and further.
MMC moves undigested material out and limits time for bacterial growth. Segmentation resumes on feeding.
Large intestine motility
Very slow smooth muscle segmentation occurs and material remains for 18-24 hrs, allowing time for bacterial proliferation.
3-4 times/day mass movement occurs: intense contractile wave over transverse segment to rectum. Parasymp. -> more segmental contract., symp. -> less colonic contract.
Defecation process
Sudden rectal distension initiates the defecation reflex (neural. mediated)
- Mechanoreceptors -> conscious defecation urge
- Sigmoid colon motility increases
- Rectal pressure eventually relaxes the ext. sphincter
Anal sphincters
Internal: involuntary smooth muscle
External: voluntary skeletal muscle
Valsalva manuever
Refers to taking a deep breath before defecating. Causes glottis closure, abdominal/thoracic muscle contraction.
Increases abdominal pressure and intrathoracic pressure, which is transmitted to large intestine.
Neurotransmitters of the GI
Excitatory: ACh
Inhibitory: NO, Vasoactive Intestinal Peptide (VIP), ATP
Small intestine gradient theory
Movement through the small intestine is caused by difference in slow wave BER across s. intestine, with higher frequency BER proximal and lower frequency distal.
Thus net time contracting and net force decreases distally, driving food slowly forward on average.
Haustrations
Colon contractile segments which slice feces to expose new surface area for reabsorption. These are long-lasting contractions, not actual anatomical segments.
