Editing Stomach (section)

== '''Physiology''' ==

=== Gastric peptides ===

** Gastrin
*** Produced by G cells in the       antrum
*** Similar in form and       function to CCK
*** Release stimulated by       gastric distension, gastrin-releasing peptide and protein digestion       products. Release inhibited by luminal acid.
*** Primary endocrine regulator       of the secretory phase of a protein meal
**** Stimulates        enterochromaffin-like (ECL) cells to synthesise and release histamine
**** Exerts direct action on        parietal cells to stimulate acid release
**** Trophic effects on        parietal cells and ECL cells
*** Hypergastrinaemia is most       commonly the result of acid-reducing treatment like PPIs
****
** Somatostatin
*** Produced by delta cells -       diffuse neuroendocrine cells located in fundus and antrum
*** Stimulated by antral       acidification and gastrin-releasing peptide, and inhibited by       acetylcholine (from vagal fibres)
*** Acts to inhibit parietal       cell acid secretion directly and also inhibits gastrin release from G       cells and downregulates histamine release from ECL cells
** Histamine
*** Histamine release is       stimulated by gastrin, VIP, ghrelin, achetylcholine, and adrenaline, via       their actions on ECL cells
*** Inhibited by somatostatin
*** Stimulates parietal cells       to release acid
** Ghrelin
*** Produced by enteroendocrine       cells of the oxyntic glands in GIT
*** Levels are highest before       meals during fasting and decrease after meals
*** Decreased levels have been       associated with gastritis, and are seen post-bypass or sleeve       gastrectomy (unknown mechanism)
*** Increases gastric emptying       and motility, and increases gastric acid secretion, in preparation for       digestion

=== Gastric acid secretion ===

** Secreted by parietal cells      via the hydrogen-potassium-ATPase pump
** Three regulators stimulate      release:
*** Acetylcholine - from vagal       nerve
*** Gastrin - hormonal
*** Histamine - paracrine       effects
** Inhibition by somatostatin
** There is always a basal      level of secretion, approximately 10% of total output, which is reduced      by vagotomy and anti-histamine drugs
** Normal total 24 hour output      of gastric fluid is ~1.5L
**

*
* Three phases of gastric acid     secretion
** Cephalic
*** Sight, smell, thought or       taste of food
*** Probably mediated by vagal       nerve
** Gastric
*** Begins when food enters the       gastric lumen
*** Mediated via protein       interactions with antral G cells, and mechanical distension of the       stomach
*** Accounts for most (70%) of       acid secretion
** Intestinal
*** Initiated by entry of chyme       into the duodenum, which stimulates gastric release and suppresses       gastric motility
*** Lasts as long as chyme       remains in the proximal small bowel
* Pharmacological regulation of     acid secretion
** See 'GORD' under medical      management

=== Other secretion products ===

** Intrinsic factor
*** Produced by parietal cells
*** Essential for absorption of       B12 in the TI
*** Secreted in great surplus
*** Not inhibited by PPIs
*** Intrinsic factor deficiency       can develop in patients with pernicious anaemia or those undergoing       total gastrectomy - need B12 supplementation either orally or by       injection
** Pepsin
*** Proteolytic enzyme
*** Secreted by the glands of       the gastroduodenal mucosa
** Mucus and bicarbonate
*** Secreted by surface mucous       cells and mucous neck cells
*** Neutralise gastric acid at       the mucosal surface
*** Production is stimulated by       vagus, cholinergic agonists, prostaglandins, and some bacterial toxins
*** Inhibited by       anticholinergic drugs and NSAIDs
*** Helicobacter pylori breaks       down mucin

=== Gastric motility ===

** Regulation
*** Extrinsic neural control -       PNS and SNS
*** Intrinsic neural control -       enteric nervous system and interstitial cells of Cajal
*** Myogenic control - from the       gastric smooth muscle cells
** Fasting gastric motility -      primarily driven by intrinsic and myogenic control
** Post-prandial gastric      motility
*** Ingestion - decrease in       resting tone of proximal stomach and fundus, primarily mediated by vagal       nerve
*** Repetitive forceful       contractions of the midportion and antral portion to mix food
*** Emptying - mostly       hormonally influenced

=== Gastric barrier function ===

** Blood flow - >50%      reduction in blood flow leads to mucosal injury, and >75% reduction      will see marked mucosal injury

[[Category:Anatomy]]