L19: GI tract motility Flashcards
normal motility helps facilitate what 2 functions of the GI tract
- digestion/absorption
- maintain aboral propagation
what are the 3 stages in swallowing
- voluntary initial stage: movement of bolus to back of oral cavity
- involuntary pharyngeal phase: bolus passes from oral cavity to esophagus
- involuntary esophageal stage: food passes into stomach
what generates peristalsis
the straited muscle portion of the esophagus is innervated by brainstem LMN from the nucleus ambiguus in which a central pattern generator facilitates coordinate contration
what are the steps in the reflex arc
- stretch receptors in the esophageal wall are stimulated by distension
- sensory afferents transmit impulses to dorsal motor nucleus (DMN)
- DMN activates somatic and vagal efferent neurons
- sphincters prevent food and air from entering esophagus
what sphincter in the esophagus acts as a barrier to prevent regurgitaton of stomach content
lower esophageal sphincter
what are the 3 mechanisms involved in the regulation of basal LES tone
- excitatory cholinergic nerves (ACh) favor contraction
- inhibitory nitrergic (NO) pathway favors inhibition
- tonic myogenic property favors contraction
the balance b/w inhibition (NO) and excitation (ACh) is required for normal LES activity
in the excitatory pathway of LES control, neurons from the DMN stimulate _______ neurons which release _______ and _______
cholinergic postganglionic ENS
ACh and substance P
in the inhibitory pathway of LES control, neurons from the DMN stimulate _______ neurons which release _______ and _______
cholinergic postganglionic neurons in the enteric ganglia
release NO, VIP, ATP
what occurs in dysmotility associated w/ or w/out megaesophagus in Mysthenia gravis
antibodies block or destroy Ach receptors at the NMJ, inhibiting contraction of the esophagus; food is unable to be propelled forward
neurodegenerative disease in which degeneration of inhibitory neurons of the myeneteric plexus occurs
Achalasia
explain Achalasia
LES smooth muscle excitation is unopposed (LES remains contracted) due to the loss of inhibitory neurons in the myenteric plexus
ingesta can’t be transported across the LES
what can cause esophageal diverticula
- granulomatous inflammation of mediastinal LNs - inflammed nodes attach to esophagus and pull on it, creating an outpouching
- can also develop as a consequence of a motility abnormality in the esophagus that causes pressure stress on the wall which eventually causes a herniation of esophageal mucosa
what generates baselines motility in the stomach, SI and LI
ICC - the pacemaker cells of the GI tract - cause spontaneously undulating electrical waves of partial depolarization = slow waves
what things can affect the rate of slow waves
- stretch
- pH
- nutrients
- parasympathetic stimulation
- GI hormones
what are factors that can hyperpolarize ICC cells, dimishing or abolishing muscle activity
- inhibitory hormones / neuroeffectors substances
- sympathetic stimulation
- VIP and NO
why does new food trigger increased motility
- food enters GI tract, activating intrinsic endocrine and neural mechanisms that stretch GI tract wall
- ICC activity exceeds threshold potential when cations enter into cell
- Ca+ is released from SR, generating excitation of smooth muscles
what allows for the spread of motility along the GI tract
gap junctions
exist between ICC and longitudinal and circular smooth muscle cells and between smooth muscle cells
they facilitate transmission of electrical activity between smooth muscles and between ICC and smooth muscle cells