Gastrointestinal Physiology

Gastrointestinal Physiology

Enteric nervous system

* lies in the wall of the gut (esophagus  anus)

* controls GI movement and secretions

* consists of 2 plexuses

o myenteric - peristalsis

o submucosal - secretion and (local) blood flow

* axon endings secrete acetylcholine which excites gastrointestinal activity, and norepinephrine, which inhibits it

Parasympathetic innervation

* cranial

o mouth & pharynx

o VAGUS nerve

 esophagus, stomach, pancreas and (somewhat) the intestines through the first half of the colon

* sacral

o 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

o norepi inhibits the enteric neurons

o 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 stem's 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