Sem 4 molecules and mechanisms Flashcards
Gastrin
Released from G cells in crypts of Liberkuhn (antral mucosa) response to stretching of stomach wall and presence of protein in stomach. Inhibited by secretin, CCK, GIP and somatostatin.
Function: activates ECL cells to secrete histamine, inc acid release from parietal cells. enhances activity of pyloric pump, promoting stomach emptying by inc gastric motility. Inc growth of gastric mucosa.
secretin
released from S cells in crypts of liberkuhn (duodenal mucosa) in response to gastric acid in duodenum - low PH. Stimulates release of watery bicarbonate ions from pancreatic and bile epithelium + in duodenum. reduces acid secretion from stomach by inhibiting gastrin release from g cells through somatostatin. stimulates pepsinogen from parietal cells. stim release glucagon insulin oancreatic polypeptide and somatostatin.
cholecystokinin CCK
released from I cells in duodenum and jejunal mucosa in response fatty substances and proteoses in chyme. Inhibits gastric emptying, reduces acid decretion from stomach by inhibiting gastrin release from G cells through somatostatin. stimulatess acinar cells of pancreas to release digestive enzymes, inc production of bile, contraction of gall bladder and relac sphincter of Oddi so bile delivered duodenum.
Gastric inhibitory peptide
releasaed from K cells in duo and jejunal mucosa in response to fatty substances and glucose in chyme. Weakly dec GI motility so weakly inhibits stomach emptying. Weakly reduces acid secretion from stomach by inhibiting gastrin release from G cells through somatostatin. stimulates insulin if hyperosmolarity of glucose in duodenum as incretin hormone.
GLP-1
released from L cells in duo and jejunal mucosa in respnce fatty substances and glucose in chyme. stimulate release of insulin if hyperosmolarity of glucose in duodenum as an incretin hormone.
somatostatin
released from D cells in crypts of Lieberkuhn (duo mucosa) and in pancreatic islets in response excess gastric acid in stomach and duodenum. inhibited by vagal stimulation. dec acid secretion by inhibiting G cells, ECL cells and parietal cells. dec pepsinogen sec. dec pancreatic and SI fluid secretion, dec gall bladder contraction thus reducing bile delivery to duodenum. Dec release of insulin and glucagon.
pepsinogen
released from peptic/chief cells in stomach, from stimulation of cells by Ach (vagal) and responce to acid. Inactive form of pepsin, activated into by HCL, pepsin is proteolytic enzyme that works in acidic conditions.
pepsin
activated from pepsinogen, activation inc by inc pepsinogen release. used in protein digestion
HCL
released from parietal/oxyntic cells in stomach, inc by histamine-ECL cells, Ach and gastrin. Inhibited by somatostatin, GIP, prostaglandinE2, Secretin. Makes the conditions in the stomach acidic. Allows breakdown of food.
intrinsic factor
released from parietal/oxyntic cells in stomach. Essential for absorption of vit B12 in distal ileum. It binds to vit b12 to protect from being digested in stomach, complex reaches terminal ileum where IF binds to receptor and vit b12 is absorbed. Autoimmune destruction of parietal cells leads to deficiency in intrinsic factor which can cause pericious anaemia.
bicarbonate ions
released from mucosal cells and brunners glands in duodenum. secretion inc by secretin. Inhibited by substance P. it neutralises acid and transported in mucus that covers gastric epithelium
mucus
released from mucous surface cells in stomach in responce to contact with food or iritation.
prostaglandin E2 PGE2
inhibited by NSAIDS like aspirin. Inc secretion of bicarbonate ions, dec acid secretion. Gi pathway. this is why can cause peptic ulcers as excess acid secretion.
histamine
released from ECL cells in responce to reduced acid secretion, secretion inc by gastrin and Ach. Inhibited by H2 receptor antagonists. increases acid secretion via H2 receptors on parietal cells. works via opposite intracellular pathway-Gs to PGE2 to inc acid.
trypsinogen
From acinar cells of pancreas, activated by enterokinase into trypsin. Inhibited by trypsinogen inhibitor. its the zygomen of trypsin, activated by enterokinase, activated autocatalytically by trypsin.
trypsin
result from activation of trypsinogen. stoped by trypsinogen inhibitor. Involved in protein digestion.
enterokinase
from the epithelial cells of intestine. activates trypsinogen into trypsin
chymotrypsinogen
released from acinar cells in pancreas. inhibited by trypsinogen inhibitor. inactive form of chymotrypsin, activated by trypsin.
chymotrypsin
result of activation of chymotrypsinogen. inhibited by trypsinogen inhibitor. protein digestion.