7. Motility of the GI Tract Flashcards
In the mucosal layer, the muscularis mucosae consists of smooth muscle and changes the shape and surface area of the epithelium. What consists of the muscularis (externa) layer? (3)
Circular muscle
Myenteric plexus
Longitudinal muscle
What are the two different functions of the circular and longitudinal muscles of the muscularis layer?
Circular: decreases the size of the diameter of the segment
Longitudinal: decreases the length of the segment
Along with the myenteric plexus of auerbach in between the circular and longitudinal muscles in the musclaris, what is the other important plexus ?
Meissner plexus of the submucosa
Slow waves are a unique feature of GI smooth muscle. Slow waves are depolarization and repolarization of the membrane potentional but is not what?
An Action potential
When do action potentials occur in the GI smooth muscle?
when the depolarization moves the membrane potential above the threshold to positive potentials
mechanical response (tension/contraction) follows the electrical response. What is in charge of the frequency of contraction and what is in charge of the actual contraction?
Frequency is controlled by slow waves while the strength of contraction is controlled by how many action potentials/spike potentials are on each wave
Phasic and tonic are contraction of smooth muscle that are key for motility along the GI tract. What are phasic contractions and where do they occur? (4)
phasic is periodic contractions WITH relaxation
occurs in esophagus, stomach (antrum), SI and ALL tissues involved in mixing
What are tonic contractions and where do they occur? (4)
Tonic maintain a constant level of contraction without relaxation
Eg: Stomach (orad), Lower esophageal sphincter, ileocecal valve, internal anal sphincter
When the slow wave barely reaches threshold, what does this mean for the spike/action potentials?
What about when there is a large slow wave?
When the slow wave barely passes, there will be less action potentials and less contraction
When there are large slow waves, there will be more APs and more, stronger contraction
What nervous system and hormone increases the amplitude of slow waves due to stretch?
Parasympathetics via acetylcholine, which increases slow waves= inc. in AP = inc. motility
What nervous system and hormone decreases the amplitude of slow waves, causing hyperpolarization?
Sympathetic nervous system via norepinephrine, decreasing APs and motility/digestion
The submucosal plexus controls GI gland secretions and blood flow while the myenteric plexus of auerbach controls what?
Control movement of the GI
What cells are the pacemaker for GI smooth muscle, generate/propagate the frequency of the slow waves?
interstitial cells of Cajal (ICC), works parallel with the myenteric plexus
Electrical activity in the ICC drives the frequency of slow waves, thus the frequency of contractions. How do the slow waves of the ICC spread rabidly to smooth muscle?
Gap/tight junctions
Mastication, or chewing, is controlled by muscles that are innervated by the?
motor branch of the fifth cranial nerve (trigeminal nerve)
Mastication is caused by a chewing reflex which is controlled by?
the nuclei in the brain stem
note: the chewing reflex is both voluntary and involuntary
Swallowing is initially voluntary in the oral phase and then becomes involuntary in the pharyngeal phase. What are the steps in this phase? (5)
Soft palate pulled up epiglottis moves UES relaxes Peristatic wave of contractions in pharynx food is propelled through open UES
The pharynx and the first 1/3 of the esophagus is comprised of what type of muscle? How about the later 2/3 of the esophagus?
skeletal and then smooth muscle
After the oral and pharyn phase, the last phase is the esphageal phase, which is involuntary. What is this phase controlled by? (2)
swallowing reflex and the ENS
consists of primary/secondary peristaltic wave
The involuntary swallowing reflex is controlled by the medulla. What are the steps in the reflex? Starting with food in the pharynx and ending with efferent input to pharynx? (3)
- Food
- afferent sensory input via vagus/glossopharyngeal N.
- Signal to swallowing center in medulla
- Brainstem Nuclei
During the esophagus phase there are 2 peristaltic waves. The primary wave is controlled by the medulla as a continuation of pharyngeal peristalsis and does not work after vagotomy (damage to vagus), what about the secondary wave?
Occurs if primary fails to empty esophagus or if there is gastric reflux into stomach. Medulla and ENS regulate. Pharyngeal peristalsis does not need to occur, still occurs after vagal damage
During swallowing there are changes in pressure along the esophagus as the food bolus passes through it. What is the main difference between throacic pressure and sphincter pressure?
Thoracic pressure is subatmospheric and when food passes cause an increase in pressure
UES, LES, and Fundus have high are above atmospheric pressure and decrease as the bolus comes through (relax sphincter so less pressure)
Two problems with the location of the intrathoracic esophagus: 1. keeping air out of the upper end of the esophagus. 2. keeping acid out of the lower end. How are these problems solved?
UES/LES are closed except when food is passing through :)
Achalasia occurs when the LES stays closed during swallowing, impariing peristalsis. Causing increase in food build up and increase in pressure in the LES. How does this occur ? (2)
Vasoactive intestinal peptide is lacking (dilator)
ENS has been knocked out/damage of nerves
