L1 Neuro-endocrine Control of Gastro-intestinal Tract PDF

L1: Neuro-endocrine control of Gastro-intestinal tract Learning Outcomes By the end of the lecture, the students will be able to: 1. Outline the general functions of the GIT. 2. Describe the structure of the GIT wall. 3. Recognize the nervous control of the GIT functions. 4. Re...

L1: Neuro-endocrine control of Gastro-intestinal tract Learning Outcomes By the end of the lecture, the students will be able to: 1. Outline the general functions of the GIT. 2. Describe the structure of the GIT wall. 3. Recognize the nervous control of the GIT functions. 4. Recognize the hormonal control of GIT functions. References Guyton & Hall textbook of Medical Physiology. Elsevier, 14th Edition 2021. USMLE STEP I Lecture notes 2017 Physiology. KAPLAN Medical Lo1: The functions of Gastrointestinal tract The function of the alimentary tract is to provide the body with water, electrolytes, vitamins, and nutrients. This requires (1) Movement of food through the alimentary tract. (2) Secretion of digestive juices for digestion of the food. (3) Absorption of water, electrolytes, vitamins, and digestive products. (4) Circulation of blood through the gastrointestinal organs. (5) Control of all these functions by local, nervous, and hormonal systems. Lo2: Structure Of The Gastrointestinal Tract  LO3: Nervous Control of GIT The motor and secretory functions of the GIT are controlled by a local nerve plexus in the gut wall called the Enteric Nerve Plexus. The ENP is called the gut brain. It consists of two plexuses: a. Myenteric plexus (Between the two muscle layers): controls the motility of the GIT. b. Submucosal plexus (in submucosa) controls secretion and blood flow. It receives sensory information from chemoreceptors and mechanoreceptors in the GI tract and uses local reflexes for the control of GIT functions. ENTERIC NERVE PLEXUX a. Parasympathetic system Excitatory on the functions of GIT (increases motility, secretion and blood flow and opens the sphincters) is carried via the vagus and pelvic nerves. (1) The vagus nerve (from medulla of the brain) supplies the esophagus, stomach, pancreas, small intestine and upper large intestine. (2) The pelvic nerve (from sacral segments of spinal cord): supplies lower large intestine, rectum and anal canal. The parasympathetic fibers end on the nerve cells of the myenteric and submucosal plexuses.  b. Sympathetic system: Arises from Thoracic segment & Lumbar segment of spinal cord. It is inhibitory to most functions of GIT (decreases motility, secretion and blood flow and closes the sphincters). The chemical transmitter is adrenaline.  Gastrointestinal Reflexes There are two main types of gastrointestinal reflexes that are essential to gastrointestinal control. 1. Local reflexes that are integrated entirely within the enteric nervous system; mechanical or chemical stimulation of gut receptors increases gut motility and secretion. The center of these reflex is in the enteric plexus. 2. Long reflexes: the center of the reflex is in the spinal cord or brain stem. Such as: (1) Entero-gastric reflex. (2) Gastro-colic reflex (3) defecation reflexes. LO4: Hormonal control GI hormones: These are chemical substances released from endocrine cells in the GI mucosa into the general circulation, and then back to the GIT muscles and glands to modulate secretions and motility. They include gastrin, cholecystokinin (CCK) and secretin and glucose-dependent insulinotropic peptide (GIP).  1. Gastrin Gastrin is secreted from the G cells of the gastric antrum. in response to: (1) Protein in the stomach (chemical stimulation). (2) Distention of the stomach (mechanical stimulation). (3) Vagal stimulation : chemical transmitter is gastrin-releasing peptide (GRP). Atropine does not block vagal stimulation of gastrin secretion. Actions of gastrin (1) Increases H+ secretion by the parietal cells. (2) Increases contraction of the body of the stomach. Inhibition of gastrin secretion H+ in the lumen of the stomach inhibits gastrin release. This negative feedback control ensures that gastrin secretion is inhibited if the stomach contents are sufficiently acidified. Somatostatin inhibits gastrin release. Zollinger–Ellison syndrome (gastrinoma): occurs when gastrin is secreted by non–β-cell tumors of the pancreas. 2. CCK CCK is released from the I cells of the duodenal and jejunal mucosa. Stimulus; presence of proteins and fats in the duodenum and jejunum. Actions: (1) Stimulates contraction of gallbladder and relaxation of the sphincter of Oddi for evacuation of gallbladder. (2) Stimulates pancreatic enzyme secretion. (3) Inhibits gastric emptying: Meals containing fat stimulate the secretion of CCK, which slows gastric emptying to allow more time for intestinal digestion and absorption of fat. 3. Secretin Secretin is released by the S cells of the duodenum. Stimulus: H+ in the lumen of the duodenum. Actions of secretin The main aim of secretin is to reduce the amount of H+ in the lumen of the small intestine. (1) Stimulates pancreatic HCO3– secretion and Pancreatic HCO3– neutralizes H+ in the intestinal lumen. (2) Stimulates HCO3– and H2O secretion by the liver, (3) Inhibits H+ secretion by gastric parietal cells. 4. GIP (glucose-dependent insulinotropic peptide ) Actions of GIP (1) Stimulates insulin release. In the presence of an oral glucose load, GIP causes the release of insulin from the pancreas. Thus, oral glucose is more effective than intravenous glucose in causing insulin release and, therefore, glucose utilization. (2) Inhibits H+ secretion by gastric parietal cells. Stimuli for the release of GIP GIP is secreted by the duodenum and jejunum. GIP is the only GI hormone that is released in response to fat, protein, and carbohydrate.  B. Paracrines are released from endocrine cells in the GI mucosa. diffuse over short distances to act locally on target cells in the GI tract. The GI paracrines are somatostatin and histamine. 1. Somatostatin is secreted by cells throughout the GI tract in response to H+ in the lumen. inhibits the release of all GI hormones. inhibits gastric H+ secretion. 2. Histamine is secreted by enterochromaphin-like cells of the gastric mucosa. increases gastric H+ secretion directly and by potentiating the effects of gastrin and vagal stimulation. C. Neurocrines are synthesized in neurons of the GI tract, moved by axonal transport down the axon, and released by action potentials in the nerves. The GI neurocrines are vasoactive intestinal peptide (VIP), GRP (Gastrin releasing peptide: bombesin), and enkephalins.