GUT- Gastric Acid Secretion: Regulation Flashcards
describe the contents of gastric acid
Cations: Na+,K+,MG2+, H+
Anions: Cl-, HPO4-, SO4-
pepsins, lipases, mucus, intrinsic factor
What is the pH of the stomach
3.0
what type of cells is the body of the stomach lined with
epithelial cells with tubular glands which are lined with parietal cells
what do the parietal cells secrete
HCl and intrinsic factor
what substance is mainly secreted in the antrum of the stomach
gastrin (HCl still secreted but gastrin secretion increased)
what are the exocrine secretions of the stomach
mucus, acid, pepsinogen
what do enterochromaffin-like cells secrete (ECL cells)
paracrine agents e.g., histamine
which cells secrete HCl
parietal cells
how is gastric acid produced in the stomach lumen
water and carbon dioxide combine in the parietal cell cytoplasm to produce carbonic acid- catalysed by carbonic anhydrase
carbonic acid then disassociates into a hydrogen ion and bicarbonate ion
the hydrogen ion is transported into the stomach lumen via H+-K+ ATPase ion pump
bicarbonate is the transported out of the cell and into the blood in exchange for a Cl- ion
the Cl- ion is then transported into the stomach lumen
this means there are many H+ and Cl- ions in the stomach lumen which (due to their opposite charges_ combine to form HCL
what are the three phases of gastric secretion
Cephalic phase
gastric phase
intestinal phase
what is the purpose of mucus secretion in the stomach
mucus is alkaline, thick and sticky- increases bicarbonate; forms a water insoluble gel on the epithelial cells which protects against HCl
what does rennin do?
curdles milk into caesin clot
what do lipases do
breakdown fatty acids and glycerol
what is the function of intrinsic factor
absorption of vitamin B12
what is the purpose of HCl in the stomach
kills bacteria, aids in denaturation of digested food activates pepsinogen (protein digestion)
what is the cephalic phase
first phase of digestion - seeing food, smelling food, chewing food - promotes the excretion of ACh and Gastrin
how is gastric acid production increased in the stomach
ACh stimulation of parietal cells via release from the vagus nerve - cephalic phase
ACh release via vagus nerve on detection of distension of the stomach - gastric phase
gastrin secretion from G cells in the stomach which are activated by the vagus nerve. Gastrin binds to CCK receptors on the parietal cells which elevates calcium levels causing increases vesicular fusion and increased acid secretion
ECL cells in the stomach secrete histamine which binds to H2 receptors on the parietal cells. this happens as a result of the presence pf gastrin and ACh
what is the gastric phase
distension of stomach, increase in peptide concnetration - promotes the secretion of ACh and Gastrin
what is the intestinal phase
balances the secretory activity of the stomach and the digestive and absorptive capacities of the small intestine
what occurs during the intestinal phase
high acidity of duodenal contents reflexively inhibits acid secretion (to prevent chyme from becoming too acidic)
increase in acidity will inhibit the activity of digestive enzymes, bicarbonate and bile salts
distension of the duodenum, hypertonic solution, amino acids, fatty acids and monosaccharides all inhibit acid secretion
How is gastric acid production decreased
accumulation of acid in an empty stomach between meals - leads to a lower stomach pH which inhibits secretion of gastrin by the production of somatostatin from D cells
enterogastric reflex in the duodenum
presence of chyme in duodenum stimulates entero-endocrine cells to release cholecystokinin and secretin which inhibits gastric acid secretion
other hormones including GIP (glucose dependent insulinotropic peptide) and VIP (Vasoactive intestinal polypeptide) decrease acid production
what are stimulants of HCl secretion
histamine, ACh, gastrin, caffine, alcohol, NSAIDS, nicotine, H.Pylori, genetics, stress
why and how is pepsin secreted
secreted by chief cells in the form of pepsinogen - activated if the concentration of H+ is high
acidity alters the shape which exposes the active site
known as an autocatalytic feedback process
inactivated when food enters the small intestine (bicarbonate and peptides neutralise the H+ ions)
