Lecture 5: Motility of the GI tract Flashcards
How do the circular and longitudinal muscles of the GI tract differ in function?
Inner circular: contraction decreases diameter of the segment
Outer longitudinal: contraction decreases length of the segment
What are slow waves and how do they relate to AP’s?
- Oscilating depolarization and repolarizations of the membrane potential, but are themselves NOT AP’s!
- AP’s occur when depolarization moves the membrane potential to or above the threshold
What are Phasic contractions; where do they occur in the GI tract?
- Periodic contractions followed by relaxation
- Esophagus, stomach (antrum), SI, and all tissues involved in mixing and propulsion
What are tonic contractions; where do they occur?
- Maintain a basal level of contraction w/o regular period of relaxation
- Stomach (orad), lower esophageal, ileocecal, and internal anal sphincters
How are slow waves related to tonic contractions?
- Even sub-threshold depolarization produces weak, basal contractions
- Even w/o occurence of AP’s, the smooth muscle is not completely relaxed and is exhibiting tonic contractions
How is the number of AP’s on top of a slow wave related to contraction?
Greater # of AP’s on a slow wave, the larger the phasic contractions
What 3 factors cause an increase in the amplitude of slow waves and the number of AP’s?
- Stretch
- ACh
- Parasympathetics
What 2 factors cause a decrease in the amplitude of slow waves and number of AP’s?
- NE
- Sympathetics
What are the main things that the submucosal and myenteric plexus control in the GI?
Submucosal: GI secretions and local blood flow
Myenteric: GI movements
What generates the spontaneous slow wave activity?
Pacemaker regions in the myenteric and submucosal plexuses
What kind of cells are the pacemaker for GI smooth muscle; how do they function?
- Interstitial cells of Cajal (ICC)
- Slow waves occur spontaneously in the ICC and spread rapidly to smooth muscle via gap junctions
- Electric activity in the ICC drives the frequency of contractions
Smooth muscle cells respond to slow wave depolarization by increasing?
Ca2+ channel open probability = more likely to depolarize and generate an AP
Most of the muscles of mastification are innervated by the motor branch of which nerve; what control and causes mastification?
- CN V = Trigeminal N.
- Controlled by nuclei in the brain stem
- Caused by chewing reflex
What are the 3 phases of swallowing; which are voluntary vs. involuntary?
- Oral phase (voluntary) - initiates the swallowing process
- Pharyngeal phase (involuntary)
- Esophageal phase (involuntary)
What are the order of events during the pharyngeal phase of swallowing?
1) Soft palate pulled upward
2) Epiglottis moves
3) UES relaxes
4) Peristaltic wave of contractions is initiated in pharynx
5) Food is propelled through open UES
What controls the esophageal phase of swalloing and what is seen during this phase?
- Controlled by swallowing reflex and the ENS
- 1° Persistaltic wave
- 2° Peristaltic wave - only if necessary!
How is the involuntary swalowing reflex controlled?
Sensory receptors in pharynx sense food –> afferent sensory input via vagus/glossopharyngeal N. –> swallowing center (medulla) –> brain stem nuclei –> efferent input to pharynx
What is a 1° peristaltic wave; controlled by; affect of vagotomy?
- Continuation of pharyngeal peristalsis
- Controlled by medulla
- Cannot occur after vagotomy
What is a 2° peristaltic wave; controlled by; affect of vagotomy?
- Occurs if 1° wave fails to empty the esophagus or if gastric contents reflux into the esophagus
- Medulla and ENS are involved
- Can occur in absence of oral and pharyngeal phases
- Occurs even after a vagotomy
How does swallowing change the intraluminal pressure along the esophagus?
- Immediately after swallowing pressure drops in UES, but then quickly increases so that sphincter closes and food does not come back up.
- This pattern continues segmentally as the food bolus moves through the esophagus and toward the LES/Fundus
Is the pressure high or low in the UES, LES, and Fundus prior to swallowing?
Pressure is high, because these sphincter should be closed
What is the receptive relaxation phenomenon?
The LES and Fundus relax much earlier than would be expected, this is because they are preparing to receive the food bolus
The intrathoracic location of the esophagus poses the challenge of keeping air out of the esophagus at the upper end, and acidic gastric contents out of the lower end. How are these problems solved?
UES and LES are closed, except when food bolus is passing from pharynx to esophagus or from esophagus to stomach
Gastroesophageal reflux occurs when; often seen in what type of patients?
- Intra-abdominal pressure is increased
- Pregnant and morbidly obese
How is the physiology of the esophagus affected by achalasia; what are results of this disease?
- Impaired peristalsis
- Incomplete LES relaxation during swallowing
- Backflow of food (regurgitation), difficulty swallowing both liquids and solid (dysphagia), chest pain
What leads to achalasia?
- Lack of VIP or enteric NS has been knocked out
- Damage to nerves in esophagus, preventing it from squeezing foof into the stomach
What occurs anatomically during GERD; why does it happen; leads to what complications?
- Changes in the barrier between the esophagus and stomach (i.e., LES relaxes abnormally or weakens)
- Motor abnormalities that result in abnormally low pressure in the LES; if intragastric pressure increases, as may occur following a large meal, during heavy lifting, or pregnancy
- Backward wash of acid, peside and bile into esophagus = heartburn and acid regurgitation
- Can lead to complications such as irritation of the lining of the esophagus (esophagitis), scar tissue in esophagus (stricture of esophagus), and Barret’s esophagus