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Human Phys
Gastric secretion
| Question | Answer |
|---|---|
| Stomach anatomy | Top: esophagus, lower esophageal sphincter, fundus Inside: oxyntic glandular mucosa Lower: pyloric glandular mucosa, antrum, pylorus Duodenum onwards |
| What are the functions of the stomach? | Serves as a large reservoir for large volume of food that may be ingested in a single meal Motility fragments food into smaller particles Provides sterile acid environment Breakdown proteins into peptides |
| What is the structure of the gastric mucosa? | Mucosa is lined with gastric glands and surface epithelial cells Parietal cells secrete HCl and intrinsic factor Chief cells secrete pepsinogens Parietal cells predominate in fundus Mucous secreting cells predominate in pyloric region |
| Gastric tissue renewal | - corpus gland lined with isthmus stem cells and troy chief cells - isthmus stem cells: fast, constant renewal - troy chief cells: intermittent, slow renewal |
| How are gastric acids secreted? | Gastric juice = salts + water + HCl + pepsins + intrinsic factor + mucous Concentrations of ions in gastric juice as a function of the rate secretion |
| At low rates of flow | gastric juice is hypertonic to plasma |
| At high flow rates | gastric juice approaches isotonicity and is mainly HCl |
| How is gastric acid secreted following a meal? | - usually low secretion of HCI - gastric ulcer patients secrete less - duodenal ulcer patients secrete more |
| Parietal cell role: resting state | - cytoplasm full of tubulovesicles & internalised intracellular canaliculus (channels) |
| Parietal cell role: active state | - tubulovesicles have fused with the membrane of the intracellular cannaliculus which is now open to the lumen of the gland and lined with microvilli |
| Secretion of protective barrier | Mucous contains mucin glycoproteins, secreted by mucous neck cells (exocytosis) Fluid high in K+ and HCO3- secreted by epithelial cells, mucus layer is alkaline Secretion of mucous is stimulated by stimuli enhancing acid and pepsinogen secretion |
| Control gastric acid secretion | - in parietal cells: gastrin, histamine, ACh and somatostatin are secondary messangers into cell lead to H+ acid secretion |
| Phases of gastric secretion | Cephalic phase is elicited before food reaches the stomach e.g. sight, taste and smell of food Gastric phase is elicited by the presence of food in the stomach Intestinal phase is elicited by mechanisms that originate in the duodenum and upper jejunum |
| Cephalic phase | - stimulatory food info - cerebral cortex/hypothalamus/medulla oblangata - vagus nerve - stimulates stomach secretory behaviour |
| Gastric phase | - stretch receptors activated - medulla - vagus nerve - food chemicals/rising pH activate chemoreceptors - g cells secrete gastrin in blood - stimulates stomach secretory activity |
| Intestinal phase | - stomach empties (low pH, duodenum food) - intestinal gastrin release into blood - stimulates stomach secretory activity |
| Protective and aggressive mechanisms | 1) Mucous secretion, HCO3- secretion 2) Acid environment, Pepsin activity |
| What are stomach ulcers? | - theories: (i) High acidity of gastric juice kills bacteria and (ii) too much acid secretion causes ulcers Ulcer formation occurs when the mechanisms protecting the epithelial lining of the stomach are outweighed by the onslaught of acid-pepsin attack |
| Inhibitors of acid secretion | - Ranitidine (H2 receptor) - Omeprazole The actions of these drugs reduce the amount of acid secretion, which promotes the repair of gastric lesions |
| Helicobacter pylori | - High correlation between infection with Hp and incidence of ulcers - more prevalent in developing countries |
| HP and DU associations | Treatment of DUs with the antibacterial bismuth produces longer remissions than treatment with H2 antagonists Erradication of Hp drastically reduces recurrence of DUs |
| Triple therapy | - treated with Bismuth, Antibiotics, PPIs Triple therapy = PPI + tetracycline + metronidazole |