Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Final Physiology
OSU-CHS endocrine and GI hormones
| Question | Answer |
|---|---|
| Gastrin Releasing peptide | Released from the enteric nervous system in the stomach. It acts on G-cells to increase release of gastrin in pyloric stomach. |
| Gastrin | stimulates the release of HCl from parietal cells in the fundic stomach. It also stimulates the growth of gastric mucosa. Gastrin release is inhibited by too much HCl, or by somatostatin from S cells. |
| Enkephalins/opiods | contract sphincter; ↓ int secretion |
| VIP | (mucosal neurons)↑ GI water and electrolyte secretion; ↑ smooth muscle relaxation; ↑ pancreatic bicarb secretion; ↑ int vasodilatation |
| Substance P | (released from upper small intestine, colon, CNS)—stimulate salivary flow, GI motility, and transmits pain |
| Neuropeptide Y | released from mucosal neurons to produce smooth muscle relaxation, ↓ intestinal secretion |
| The enteric nervous system | is made up of more than 100 million neurons. More than the entire spinal cord. It consists of the myenteric and submucousal plexuses and either acts on secretion of substances or motility. Can be altered by the autonomic nervous system. |
| Meissner's plexus | also called submucousal plexus. Innermost layer of nerves. -Sm and lg int only -Controls secretions -Only in small and large intestine |
| Myenteric Plexus | “Auerbach’s Plexus” Between circular and longitudinal muscle From esophagus to rectum Controls movement of the contents not the secretions. |
| Zollinger Ellison Disease | Gastrin turned on in places other than the stomach. Can be good sized tumor or a lot of little ones. Goes to the stomach and stimulates over production of HCl form the parietal cells. Can need stomach removal. not regulated by feedback |
| CCK | released from duodenum I cells; stimulates Gallbladder contractions, pancreatic enzyme release, secretion of HCO3- from pancreas, growth of exocrine pancreas and Gallbladder, & slows stomach emptying |
| Secretin | released from duodenum S cells; stimulates pancreatic bicarb release and decreased stomach H+ secretion by acting on both parietal and inhibiting gastrin. augments the effects of CCK |
| GIP or Glucose Dependent Insulinotropic Peptide | released by small intestine K cells to increase insulin release. Its job is to cause the pancreas’s islets of Langerhaun’s to secrete insulin. |
| Somatostatin | released from pancreatic islets’ delta cells; inhibits other GI hormones. Also released from hypothalamus and the stomach. This is a hormone don’t forget that they are released into the blood. Inhibits the release of gastrin in the stomach. |
| Pancreatic polypeptide | released from pancreatic islets’ F cells; inhibits bicarb & enzyme release and increases gallbladder relaxation |
| Achalasia | Lower esophageal sphincter LES doesn’t relax properly; causes food to be stuck in the esophagus |
| Smooth muscle contraction | Calcium enters the cell and binds calmodulin - Ca-Cal bind to Myosin Light chain kinase – phosphorylates myosin light chain so that it can bind to actin. |
| Slow waves | oscillating depolarization and repolarization of membrane potential; NOT APs;Originate in myenteric plexus (the outer plexus) they have pace makers interstital cells of Kahall;Rate is 3-12/min, faster in sm int, slower in colon |
| Remember that slow waves | make it easier to have an action potential; if they have an action potential during a slow wave then they will have muscle contraction coinciding that the slow wave of depolarization. |
| To speed stomach emptying | decrease distensability of the orad stomach, increase the contractions of the caudad stomach, relax pylorus, and stop duodenal contractions. |
| To slow gastric emptying | ↑ distensibility of the orad stomach;↓ force of contraction of the caudad stomach;Contractions of the pylorus;Stimulation of duodenal segmenting contractions Fat in duodenum via CCK H+ ions in duodenum (via ENS) |
| Small intestine motility with 5HT stimulation (serotonin) | Is created by Acetylcholine and substance P causing contraction in some areas, while NO, VIP, PACAP, and ATP are causing relaxation in others. Must work this way for mass movement. |
| Intestino-intestinal reflex | Overdistension leads to relaxation of large part of small intestine |
| Gastroileal reflex | When motor functions of stomach are elevated, ileal motility increases |
| Gastrocolic reflex | Distention of the stomach by food increases the motility of the colon and freq of mass mvts |
| Erythromycin has been used with constipation or a sluggish gut. However, it is not used long term. | True; it mimics motilin which stimulates gut movement. |
| The colon | reabsorbs water just like the distal collecting duct of the kidney. It is also acted on by Vasopressin (ADH) to increase the reabsorption of water and insert aquaporins. |
| chief cells releases... | pepsinogen and are located in the body of the stomach. |
| Parietal cells | release intrinsic factor for B12 reabsorption and HCl secretion. |
| HCl increase | histamine, ATP, and Gastrin |
| HCl decrease | atropine, cimetidine, somatostatin, prostoglandin |
Created by:
vpack87
Popular Physiology sets