Control of GI Function Flashcards
Meissner’s Plexus
The Mucosal nerve plexus that sits between the submucosa and the circular muscle layer
Layers of the Gi Tract (Towards lumen)
Serosa, Longitudinal Muscle, Myenteric Plexus, Circular Muscle, Submucosal Plexus, Submucosa, Muscularis Mucosae, Lamina Propria, Epithelium
Auerbach’s Plexus
Also known as the myenteric plexus, auerbach’s plexus sits between longitudinal and circular muscle layers.
How do hormones of the GI tract reach target cells? How does this differ from paracine/neurocrine mechanisms.
They are secreted into portal circulation, reach the liver, pass into systemic circulation and then eventually arrive at target. The paracrine and neurocrine mechanisms reach the target cells immediately.
Effect of sympathetic nervous system on Gi tract?
Inhibits digestion.
Effect of parasympathetic nervous system on GI tract?
Stimulates digestion via vagus, especially in esophagus and stomach.
Voluntary CNS responses in GI system?
Control of swallowing, contraction of the external anal sphincter.
How does parasympathetic input to GI tract work?
Vagal nerves from the medulla innervate to the distal colic flexure. Then pelvic nerves from the sacral spinal cord innervate the lower colon. First nerve releases ACh to NAChRs. Second nerve releases ACh or peptide to muscarinic receptor on gut.
How does sympathetic innervation of the GI tract work?
Thoracolumbar nerves enter either the chain ganglia (for control of esophagus), or the prevertebral gangia (celiac, superior/inferior mesenteric). First nerve releases ACh, second releases NE.
Where do the following synapses occur? 1) First parasympathetic. 2) Second sympathetic?
Myenteric plexus (Auerbach’s).
Enteric Nervous System
Includes Myenteric (auerbach’s) plexus and the submucosal (meissner’s plexus).
Myenteric Plexus
Also called Auerbach’s, Located between longitudinal and circular layers of muscle. Provide motor innervation to both layers. Provides secretomotor innervation to the mucosa.
Submucosal Plexus
Also called Meissner’s. Contains cell bodies of the enteric nervous system.
Do neurons in the ens contain one NT? Or more?
More than one.
NT responsible for sphincteric relaxation
NO
Enterochromaffin cells
GI hormone secreting cells. Found in islets and between mucosal cells. Can release histamine, dopamine, other regulatory peptides (CCK).
What type of chemical transmitters are most abundant in the GI tract?
Regulatory peptides.
Gastrin: Receptor, producing cell location, stimulation/inhibition, actions.
Binds to CCK receptor B. Made by G cells in the antrum and duodenum. Stimulated by high gastric pH and AAs. Inhibited by gastric acid. PROMOTES GASTRIC ACID SECRETION FROM PARIETAL CELLS. Also a growth factor for enterochromaffin like cells.
Parietal Cell
Makes gastric acid in response to gastrin, histamine, ACh. Has K-ATP hydrogen pump.
Effect of gastrin on parietal and ECL cells?
Agonist. ECL cells produce histimine which stimulate parietal cells.
Cholecystokinin
Binds to CCK-A receptor. Made by I cells in the proximal 2/3 of small intestine in response to fatty acids and AAs. Causes gallbladder contraction, secretion of pancreatic enzymes, slows gastric emptying, induces satiety.
Secretin
Made by S cells in the proximal small intestine. Stimulated by gastric acid and harsh foods/alcohol. Induces secretion of HCO3 from pancreas. Inhibits gastrin release, inhibits intestinal motility.
VIP
Vasoactive Intestinal Peptide. Neuromediator from enteric nervous system. Stimulates epithelial cell secretion, causes smooth muscle relaxation (relaxes LES, Oddi).
Glucagon
Made by pancreatic alpha cells and L cells of the small intestine/colon. Must be processed from proglucagon in pancreas. Regulates glucose homeostasis.
GLP
Glucagon like peptide, cut from proglucagon in small intestine, GLP1 regulates glucose homeostasis and GLP2 maintains GI mucosal mass because of its growth factor activity.
GIP
Glucose-Dependent Insulinotropic Polypeptide. Made by K cells, released in response to hyperglycemia; stimulates beta cells of pancreas to secrete insulin.
Substance P
Neurocrine and paracrine release mechanisms. Proinflammatory, pain sensation. inhibits somatostatin and biliary secretion.
P= Proinflammatory/pain
GRP
Gastrin-releasing peptide. Neurocrine, mediates the vagal release of gastrin. Stimulates GI motility and pancreatic secretion.
Motilin
Made in duodenum, but binds to smooth muscle receptors on gut to cause pro-kinesis.
How does erythromycin effect the gut?
It is a motilin agonist.
Ghrelin
Made in the gastric fundus, increases food intake. Fed state- low levels of gastrin. Upregulated in Prader-Willi syndrome.
PP
Pancreatic polypeptide. Inhibits pancreatic exocrine secretion and gut motility.
PYY
Peptide YY, made in L cells in the distal small intestine (ileum). Stimulated by fatty meals. Is the ileal break, which slows small intestine mobility to increase absorption time. Don’t want to keep sending things to the small intestine if its already busy. Can be compromised in patients with ileal resections, causing diarrhea.
NPY
Neurocrine Homologue of PYY, stimulates appetite and acts as an ileal break.
Somatostatin
Made by D cells in the antrum. Important to know. Live close to G cells and are pH sensors. Acts as a global inhibitor to stop gastric acid secretion, pancreatic secretion, bile flow, slows motiility.