ENS and motility Flashcards
hirschprungs
aganglinosis of both myenteric ad submocosal plexi–>cannot relax the internal anal sphincter–>dilation of rectum & colon
myenteric fx
between inner adn outre musclse
secretomotor to mucosa
meissnre’s/submucosa
between inner muscle and mucosa
secretory cells endo cells, vessels in mucosa and submucosa
iPANS
primary sensory afferent neurons
respond to chemical and mechanical stimuli –found in both plexuses
loss of icc cells
constipation pyloric stenosis
pseudoobstruction
three major efferents of vomiting center
vagus
phrenic
spinal
intrinsic slow mwave rhythm stimulates motor activtiy
pyloris (not body/fundus)
three phases of fasting state
phase I- period of quiescence
phase II- irregular contractions
phase III- short periods of intense phasic contractions
what happens when feeding happens eat
blocks MMC and begins fed state
1) vagus–>increases fundus relaxation and decrease phasic contraction–> increase stomach volume for food
2) irregular contractions develop in the lower body anf fundus to break up and grind food
3) food emptied into duodenum when small enough
main dx study for gastroparesis
gastric emptying scan
tx of gastroparesis
small frequent meals with low fat and low fiber meds: prokinetics->metoclopromide, etc gastric stimulation surgery (avoid) peg.pej tubes botulinum toxin in pyloris TPN
rome criteria of functional dyspepsia
>1 OF THESE SX post prandial distress syndrome (bothersome fullness after a meal, early satiety, cant finish meal) epigatric pain for > 3 months with no structural dz heartburn excluded
difference between gastroparesis and functional dyspepsia
in FD there’s no correlation between gastric emptying and symptoms
pathophys of FD
psychological factors
ENS dysfunction
discoordiantion- hypersens to gastric distention–>faster upper gastric emptying, but slower lower gastric emptying
hollow visceral myopathy
uncommon
smooth muscle of GI tract wastes away and apersistaliss occurs
