Gastrointestinal Physiology
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Gastrointestinal Physiology
Enteric nervous system
lies in the wall of the gut (esophagus anus)
controls GI movement and secretions
consists of 2 plexuses
myenteric – peristalsis
submucosal – secretion and (local) blood flow
axon endings secrete acetylcholine which excites gastrointestinal activity, and norepinephrine, which inhibits it
Parasympathetic innervation
cranial
mouth & pharynx
VAGUS nerve
esophagus, stomach, pancreas and (somewhat) the intestines through the first half of the colon
sacral
via the pelvic nerves, innervate the lower half of the intestines
postganglionic neurons in the plexuses cause activity of the enteric nervous system
Sympathetic innervation
originate between T-5 and L-2
(most) preganglionic spinal neurons join the sympathetic chains and travel through peripheral ganglia, where their signals are dispersed to numerous neurons that spread throughout the gut
sympathetic innervation is spread fairly evenly throughout the GI system, unlike the parasympathetic neurons
stimulation inhibits GI activity
norepi inhibits the enteric neurons
norepi slightly inhibits the smooth muscle directly
Some afferent nerve fibers have their cell bodies in the enteric nervous system. Irritation of gut mucosa, excessive distention of the gut, or specific chemicals in the gut can stimulate these fibers to excite or inhibit. One of these has its cell bodies in the enteric nervous system and sends its axons through autonomic nerves to the prevertebral sympathetic ganglia.
Cholecystokinin (CCK) induces contraction of the gallbladder and inhibits stomach motility. CCK is secreted by the I cells of the duodenum and jejunum in response to breakdown products of fat, fatty acids, and monoglycerides. CCK is a competitive inhibitor of gastrin.
Gastrin increases HCl production and stomach motility. Gastrin is secreted by the G cells in the pyloric glands found in the stomach antrum. Gastrin is released in response to vagal and enteric nervous stimulation.
Secretin has (mild) inhibitory effects on (most of) the GI tract. Secretin is secreted by S cells of the mucosa in the duodenum in response to acidity of the chyme.
Gastric Inhibitory Peptide (GIP) decreases motor activity of the stomach. GIP is secreted by the mucosa in the upper small intestine in response to fatty acids, amino acids, and carbohydrates.
Peristalsis, waves of contraction of the smooth muscle surrounding the gastrointestinal tract that cause movement of the bolus, is usually initiated by the distention of (any point in) the gut. Gastrin, insulin, CCK, and serotonin all enhance intestinal motility, whereas secretin and glucagon inhibit it.
Parasympathetic stimulation increases blood flow to the GI tract as well as increasing its secretions, while sympathetic stimulation significantly decreases blood flow to the entire GI tract.
Distention of the duodenum causes inhibition of stomach emptying by 1) direct stimulation of the enteric nervous system, 2) stimulation of extrinsic nerves that stimulate inhibitory (sympathetic) nerves to the stomach, and 3) stimulating the vagus nerve, inhibiting the brain stems normal excitatory signals. Breakdown products of protein digestion, hypertonic/hypotonic solutions, and pH in the duodenum also inhibit stomach emptying.
Gastric mucus is secreted by the pyloric glands and surface mucus cells. It protects the stomach lining from the acidic, proteolytic environment of the stomach lumen.
Secretion
Parasympathetic stimulation rate of glandular secretion.
Sympathetic stimulation (somewhat) the rate of secretion, but blood flow to the area.
Acetylcholine, gastrin, and histamine stimulate secretion of