Innervation of the GI system Flashcards
Describe endocrine control of the gut
All hormones produced by the gut=peptides, eg gastrin.
Antral distention + bolus stimulates the ENS, Ach and vagus nerve. This stimulates secretion of gastrin releasing peptide. GRP will bind to G cells in the antrum, allowing gastrin release
Gastrin and Ach act on parietal cells to secrete HCl. It can also act on ECL cells/histamine secreting cells. Secreted histamine binds to its H2 receptor on parietal cells, causing acid secretion.
Are other hormones involved in modulating gut transit time?
Other hormones are involved in modulating gut transit time
Oestradiol and progesterone have this effect in women
What happens if there is too much acid in the stomach?
Ach and gastrin can produce high acid volumes which may cause ulcers.
Prostaglandins inhibit the activity of the parietal cells and also promote bicarbonate and mucus secretion.
Somatostatin stops gastrin mediated HCl secretions
Describe Paracrine Control of the Gut in controlling acid
Paracrine agents go to their nearby target cells via interstitial fluid.
Somatostatin is a gastric paracrine hormone. It stops gastrin mediated HCl secretions:
-G cells release gastrin which secretes HCl from parietal cells
-when hay acid hypersecretion, D cells detect H+ ions
-This stimulates them to release somatostatin which inhibits G cells which inhibit HCl production
How does the fundus relax?
The fundus relaxes via 3 main mechanisms:
Receptive, adaptive and feedback relaxation
Describe receptive relaxation
Bolus stimulates Pharyngeal mechanoreceptors which send impulses to the vagal centre in the medulla.
This processes them and sends efferent impulses back to the fundus via the vagus nerve
NO/VIP is released, relaxing the fundus.
Describe adaptive relaxation
Gastric mechanoreceptors detect the presence of a bolus, which causes distension
This stimulates afferent fibres, which send impulses to the vagal centre in the medulla
An inhibitory vagal fibre is then stimulated, releasing VIP/NO at the fundus.
Describe feedback relaxation
Fatty, acidic and hyperosmolar conditions are detected by the duodenum.
These conditions stimulate inhibitory impulses from the vagal centre to the fundus, causing relaxation
This prevents gastric emptying until acidic chyme is neutralised or fats have been broken down
Describe the 2 nerve plexuses that control motor and secretory function in the gut
Myenteric plexus controls motor function. It is in the muscularis.
Cholinergic stimulation increases gastric motility + secretion. Adrenergic stimulation decreases gastric motility + secretion
This is v important to move food aborally (to anus)
The submucosal (Meissner’s) plexus controls secretory function.
How fast is metabolic control of the gut?
Rate depends on the material’s absorption ability:
Carbs are emptied quickly into duodenum.
Proteins are slow emptying, fatty foods even slower
Fatty acids in the duodenum decrease gastric emptying as they stimulate the duodenal mucosa to secrete CCK. This increases contractility of the pyloric sphincter
Describe peristalsis
Peristalsis is a propulsive contractile wave. Internal circular muscles relax, external longitudinal muscles contract
A bolus causes distension of the gut wall which initiates contraction
Vagal inhibitory fibres secret VIP/NO, and vagal excitatory fibres secrete ACh + Substance P. These control motility:
ACh contracts the smooth muscle behind the bolus. VIP/NO relax the muscle ahead of the bolus. This propels the bolus aborally in a rhythmic, wave-like pattern
Rate of contraction is slowest in the colon
How does motilin and glucagon affect gastric movement?
Motilin increases fundic contraction rate
Glucagon decreases motility
