Hormones and Molecules Flashcards
Gastrin
- Release
- Inhibition of release
- Effect
Release: From G cells in the crypts of Liberkuhn (antral mucosa) in response to stretching of the stomach wall and presence of protein food contents (amino acids) in the stomach
Inhibition: Secretin, CCK, GIP, Somatostatin
Effect:
- activates ECL cells to secrete more histamine, thus increasing acid release from parietal cells
- Enhances the activity of the pyloric pump, promoting stomach emptying by increasing gastric motility Increase growth of gastric mucosa
Secretin
- Release
- Effect
- Release: from S cells in the crypts of Lieberkuhn (duodenal mucosa) in response to gastric acid in the duodenum (low pH in the duodenum)
- Effect stimulates the release of:
- water bicarbonate ions from pancreatic and bile epithelium and in the duodenum
- reduces acid secretion from the stomach by inhibiting gastrin release from G cells through somatostatin
- stimulates pepsinogen secretion from parietal cells
- stimulates release of glucagon, insulin, pancreatic polypeptide and somatostatin
CCK - Cholecystokinin
- Release
- Effect
- Release: from i cells in the duodenal and jejunal mucosa in response to fatty substances and protests in chyme
- Effect:
- Inhibit gastric emptying reduce acid secretion from stomach by inhibiting gastrin release from G cells through somatostatin
- stimulates acinar cells of the pancreas to release digestive enzymes
- Increases production of hepatic bile stimulates contraction of gall bladder and
- the relaxation of the sphincter of Oddi resulting in the delivery of bile into the duodenum
Gastric Inhibitory peptide (GIP)
- Release
- Effect
- Release: from K cells in the duodenal and jejunal mucosa in response to fatty substances and glucose in the chyme
- Effect:
- weakly decreases GI motility, thus weakly inhibits stomach emptying weakly
- reduces acid secretion from the stomach by inhibiting gastrin release from G cells through somatostatin stimulates the release of insulin if there is hyperosmolarity of glucose in the duodenum as an incretin hormone
GLP-1
- Release
- Effect
- Release: from L cells in the duodenal and jejunal mucosa in response to fatty substances and glucose in the chyme
- Effect: stimulates release of insulin if there is hyperosmolarity of glucose in the duodenum as an incretin hormone
Somatostatin
- Release
- Inhibition of release
- Effect
- Release: from D cells in the crypts of Liberkuhn (duodenal mucosa) and in the pancreatic islets, in response to excess gastric acid in the stomach and duodenum
- Inhibition of release: vagal stimulation -
- Effect:
- decrease acid secretion by inhibiting G cells, ECL cells and parietal cells
- decrease pepsinogen secretion
- decrease pancreatic and small intestine fluid secretion
- decrease gall bladder contraction, reducing bile delivery to the duodenum decrease the release of insulin and glucagon
Pepsinogen
- Release -
- Effect
- Release: from peptic chief cells in the stomach, due to stimulation of peptic cells by Ach vagal stimulation and also in response to acid in the stomach
- Effect: this is the inactive form of pepsin, Activated into pepsin once it comes into contact with HCl, Pepsin is the active proteolytic enzyme that works in acidic conditions
Pepsin
- Release
- Effect
- Release: result of activation of pepsinogen, activation increased by increased pepsinogen release
- Effect: protein digestion
HCL
- Release
- Inhibition of release
- Effect
- Release: from parietal (oxyntic cells) in the stomach, secretion is increased by histamine (ECL cells) Ach and gastrin
- inhibition of release:
- somatostatin,
- GIP,
- prostaglandin E2 (PGE2)
- secretin -
- Effect: make the conditions in the stomach acidic by lowering the pH, this allows breakdown of food
Intrinsic factor
- Release
- Effect
- Release: from parietal oxyntic cells in the stomach
- Effect: essential for the absorption of B12 in the distal ileum, intrinsic factor binds to vitamin B12 in the stomach and protects it from being digested, the complex reaches terminal ileum and binds to receptors and B12 is absorbed.
Autoimmune destruction of parietal cells leads to deficiency in intrinsic factor which can cause pernicious anaemia
Bicarbonate ions
- Release
- Effect
- Release: from mucosal cells
- stomach
- duodenum
- salivary glands,
- pancreas
- Brunner’s glands (duodenum).
- Secretion is increased by secretin
- Inhibition of release: Substance P
- Effect: Neutralise acid, bicarbonate ions are trapped in the mucus and cover the gastric epithelium
Prostaglandin E2 (PGE2)
- Inhibition of release
- Effect
- Inhibition of release: NSAIDs e.g. Aspirin
- Effect:
- Increases the secretion of bicarbonate ions
- Decreases acid secretion via the opposite intracellular pathway GI pathway to histamine to decrease acid secretion
- This is targeted by NSAIDs e.g. aspirin and so can cause excess and secretion, leading to peptic ulceration
Histamine
- Release -
- Inhibition of release
- Effect
- Release: from ECL cells in response to reduced acid secretion, secretion increased by gastrin and Ach
- Inhibition of release: H2 Receptor antagonists
- Effect: Increases acid secretion via H2 receptors on parietal cells, works via the opposite intracellular pathway (Gs pathway) to PGE2 to increase acid secretion
Trypsinogen -Release - Inhibition of release - Effect
-Release: from acing cells of the pancreas, activated by enterokinase into trypsin - Inhibition of release: Trypsinogen inhibitor - Effect: Inactive form (zymogen) of trypsin, activated by enterokinase, activated autocatalytically by trypsin
Trypsin -Release - Inhibition of release - Effect
-Release: Ad a result of activation of trypsinogen - Inhibition of release: trypsinogen inhibitor - Effect: protein digestion
Enterokinase -Release - Effect
-Release: from the epithelial cells of the intestine - Effect: activates trypsinogen into trypsin
Chymotrypsinogen -Release - Inhibition of release - Effect
-Release: from acinar cells of the pancreas - Inhibition of release: trypsinogen inhibitor - Effect:inactive form (zymogen) of chymotrypsin activated trypsin
Chymotrypsin: -Release - Inhibition of release - Effect
-Release: activation of chymotrypsinogen - Inhibition of release: Trypsinogen inhibitor - Effect: Protein digestion
Procarboxypolypeptidase -Release - Inhibition of release - Effect
-Release: from acinar cells of the pancreas - Inhibition of release: trypsinogen inhibitor - Effect: inactive form (zymogen) of carboxypolypeptidase, activated by trypsin