Motility of the GI System Flashcards
Tonic vs phasic contractions
Tonic- maintain constant level of contraction without regular periods of relaxation - Stomach, lower esophagus, ileocecal and internal anal sphinctors
Phasic- periodic contractions followed by relaxation- esophagus, stomach, small intestine and tissues involved in mixing and propulsion
Slow waves
They are not APs
Bring membrane potential closer to threshold, number of APs on top of slow wave determine strength of contraction
Increases probability Ca channels will open in smooth muscle
Factors increasing amplitude of slow waves and number of APs
Stretch
Ach
Parasympathetics
Factors decreasing amplitude of slow waves and number of APs
NE
Sympathetics
Submucosal plexus
Controls GI secretions and local blood flow
Generate spontaneous slow wave activity
Myenteric plexus
B/w longitudinal and circular layers
Controls GI movements
Generate spontaneous slow wave activity
Interstitial cells of cajal
Pacemaker cells for GI smooth muscle
Generate and propagate slow waves
Slow waves spread rapidly to smooth muscle via gap junctions
Located in myenteric plexus (and submucosal plexus?)
3 phases of swallowing
Oral phase- voluntary
Pharyngeal phase- involuntary
Esophageal phase- involuntary- control by the swallowing reflex and enteric nervous system
Pharyngeal phase of swallowing
Soft palate is pulled upward–>epiglottis moves–>UES relaxes–>peristaltic wave of Cxs initiated in pharynx–>food propelled through open UES
Esophageal phase of swallowing
Primary/Secondary peristaltic wave
Food in pharynx–>afferent sensory input via vagus/glossopharyngeal nerve–>swallowing center in medulla–>brainstem nuclei–> efferent input to pharynx
Primary peristaltic wave
Continuation of pharyngeal peristalsis
Controlled by the medulla
Cannot occur after vagotomy
Secondary peristaltic phase
Occurs if primary 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 vagotomy
Achalasia- what happens
Difficulty getting food into stomach from esophagus
Impaired peristalsis
Incomplete relaxation of LES during swallowing, food backs up
Elevation of LES resting pressure
What causes those problems to happen in achalasia
Decreased numbers of ganglion cells in myenteric plexus
Degeneration preferentially involves inhibitory neurons involving NO/VIP
Damage to nerve sin the esophagus, preventing it from squeezing food into stomach
GERD - what causes
Changes in the barrier b/w the esophagus and stomach (e.g. LES relaxes abnormally or weakens)
Motor abnormalities that result in abnormally low pressures in LES; if intragastric pressure increases such as following a large meal, during heavy lifting or pregnancy
Receptive relaxation
Decrease pressure and increased volume of the orad region of stomach
Vagovagal reflex
CCK decrease contractions and increased gastric distensibility