Introduction Flashcards
To understand how the GI system is regulated by the parasympathetic, sympathetic, and enteric branches of the autonomic nervous system.
ENS allows GIT to function independently form the rest of the body. Some information is relayed to the CNS
Parasympathetic and sympathetic can regulate GIT directly and indirectly – modulating at the endocrine level or directly at level of smooth muscle. Difference also to note: sympathetics have postganglionic fibers that interact with ENS neurons where parasympathetics have pre-ganglionic fibers (indirect) that interact with ENS neurons and postganglionic fibers for direct.
To understand how key excitatory (acetylcholine, serotonin) and inhibitory (norepinephrine, dopamine, nitric oxide, vasoactive intestinal peptide) neurotransmitters regulate GI function.
Think of this in terms of fight or flight (sympathetic) vs. rest and digest (parasympathetic). SNS and PNS mainly use NE and Ach, respectively. ENS uses Ach, Serotonin, Dopamine, NO, and VIP.
Ach = excitatory
NE, Epi, Dopa = inhibitory.
5-HT = excitatory (interneurons)
Dopa specifically inhibits ENS neuronal firing via D2 receptors.
NO and VIP = inhibitory (induce smooth muscle relaxation)
To understand how acetylcholine, CO2, vasoactive intestinal peptide, and norepinephrine regulate blood flow to the gastrointestinal tissues.
factors that increase blood flow = PNS, VIP, low O2 (high CO2), hyperosmolarity
Factors that decrease blood flow = SNS via NE and alpha adrenergic receptors
vasodialtors = Ach, CO2, hyperosmolarity, and VIP
vasoconstrictors = NE
postprandial hyperemia = 8fold increase in blood flow following a meal
To understand the basic mechanism of gastrointestinal smooth muscle contraction (i.e. membrane potential of GI smooth muscle, regulators that change the membrane potential of GI smooth muscle, resting slow wave, spike potential, migrating motor complex).
no constant RMP, instead a continuous depolarization and repolarization = “resting slow wave”
potential for spike potential during depolarization if stimuli such as stretch or Ach. (could also be suppressed by NE)
segmental = mixing
peristaltic = moving
reverse peristaltic = storing and keeping empty
MMC migrating motor complex = GI contractions during fasting to contents moving toward anus. Motilin regulates and initiates. ENS and vagus help too.
To understand the role of sphincters in antegrade movement and the key regulators of sphincter opening.
striated muscle = upper esophageal sphincter, upper 1/3 esophaguus and external anal sphincters
6 total sphincters upper esophagus lower esophagus pyloric sphincter ileocecal sphincter internal anal external anal
To understand how key hormones (cholecystokinin, gastrin, motilin, peptide YY, secretin, and somatostatin) regulate GI function.
- Page 9 of handout
CCK = increase enzyme secretion, increase contraction, decrease emptying, increase relaxation
Gastrin = promote gastric acid secretion
Motilin = increase smooth muscle contraction
Peptide YY= decrease enzyme and fluid secretion
Secretin = increase HCO3- secretion, decrease acid secretion, delay gastric emptying
Somatostatin = decrease acid secretion, increase fluid absorption, decrease smooth muscle contraction, decrease secretions, decrease bile flow
To understand how key paracrine regulators (prostaglandins, histamine, somatostatin) regulate GI function.
- pg. 10 of handout
The paracrine regulators target stomach and intestine.
PG = increase blood flow, decrease acid secretion, increase mucus/bicarb, increase motility, increase fluid secretion
Hist = increase acid secretion, increase fluid secretion
Somatostatin = decrease acid secretion, increase fluid absorption, decrease smooth muscle contraction
