Study Guide Flashcards
(90 cards)
explain the neural mechanisms controlling GI functions - local, short, long
- local: myenteric -> muscle (peristalsis)
- short: afferent to ganglion outside CNS (DRG) -> muscle (anatomical sphincter stuff)
- long: afferent vagus -> solitary tract -> DMVN -> efferent vagal to muscle (peristalsis)
explain the neural mechanisms controlling GI functions - peristalsis, rhythmic segmentation, tonic contractions
- peristalsis: local reflex
- rhythmic segmentation: local and long reflex to mix shit
- tonic contractions: local reflex to move things aborally
understand how intrinsic neural connections can generate intrinsic reflexes
local reflexes, so stretch receptor stimulates inhibitory motor neuron and excitatory motor neuron
- inhibitory: VIP, NO relaxation aborally
- excitatory: ACh contraction towards mouth
describe mechanisms involved in swallowing
RRGSP: raise soft palate, resp stopped, glottis closed, sphincters relaxed (UES, LES), peristalsis of bolus to epiglottis, over epiglottis and into esophagus
what is the swallowing reflex?
pressure sensors in pharynx sense food -> medulla swallowing center coordinates relaxation of UES and LES
what is voluntary about swallowing?
raising soft palate
what controls the LES?
local reflexes, VIP and NO
what are some of the problems with esophageal function?
- achalasia: LES has too much tension, lower esophagus gets super dilated
- GERD: LES not closed, gastric reflux into esophagus
what is receptive relaxation and where does it occur?
bolus in the esophagus (long reflex) stimulates relaxation of proximal stomach to make room for incoming food
what neural mechanisms control receptive relaxation?
long reflexes
explain neural control of gastric emptying
distention of duodenum (long reflex) inhibits gastric emptying
what are other non-neural controls that regulate gastric emptying?
- excitatory (from gastric): gastrin, distention
- inhibitory (from intestine): acidic duodenal pH, hypertonic chyme, fat digestion
how is the pattern of gastric contractions immediately after eating different from that seen after fasting for several hours?
-interdigestive phase: MMC (migrating motility complex) controlled by motilin/deals w/ circular muscle
how does this influence GI functions: gastrin
- increases parietal secretions
- increases chief cell secretions
how does this influence GI functions: glucagon
- increases lipolysis
- increases gluconeogenesis
- inhibits glycogenesis
how does this influence GI functions: secretin
(from duodenum)
- inhibits gastric emptying
- inhibits gastrin
- decreased parietal cell secretion
- increases chief cell secretion
- increase HCO3- secretion from pancreas
how does this influence GI functions: CCK
(from duodenum… response to fat)
- relaxes sphincter of Oddi
- contracts gallbladder
- slows gastric emptying
- stimulates pancreatic lipase
- stimulates HCO3-
how does this influence GI functions: GIP
- stimulates somatostatin
- inhibits gastric emptying
- decreases gastrin (via somatostatin)
how does this influence GI functions: motilin
-regulates MMC
how does this influence GI functions: VIP
-SM relaxation
how does this influence GI functions: somatostatin
- slows gastric emptying
- down-regulates gastrin
- inhibits chief and parietal statin
how does this influence GI functions: GRP (from vagus)
-stimulates endocrine cells to release gastrin
describe the function of slow waves. what cells and membrane events are responsible for generating slow waves?
BER (basal electrical rhythm) - interstitial cells of Cajal and pacemaker type cells in proximal stomach -> spreads to longitudinal muscle -> spreads to myenteric plexus -> circular muscle -> travels along these fibers via gap junctions, which changes membrane potential
what contractile behaviors are seen in the small intestine and what neural mechanisms control these contractions?
- interdigestive: MMC (motilin)
- digestive: MMC stops
- peristalsis, rhythmic segmentation, tonic contraction