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Lecture 14

deepa.chrisilda. PHPY 303 3 Englisch 49 Karten

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  1. 1Structures of Digestive Tract-3 salivary glands in the oral cavity. Important for secreting saliva.
    -site where food is first stored and the digestion of protein and fats is in the stomach.
    -gastric chyme enters the small intestine (duodenum, jejunum, ileum).
    -small intestine is the major site of digestion and absorption.**
  2. 2Structures and Functions of the Digestive SystemAccessory Organs: parotid salivary gland, sublingual salivary, submandibular salivary gland, liver, gallbladder, pancreas.
    Secretes their secretions directly into the target organ.
  3. 3Pancreas Secretions-meets with liver secretions and gall bladder secretions and contents are dumped into duodenal region.
  4. 4Impact of GI Health on All Systems-Gut microflora and probiotics can impact stress and behaviour.
    -Water keeps blood volume and electrolytes, nutrients for optimal muscle and nerve activity.
    -need water absorption to maintain blood volume in the circ. system.
    -salt are important for muscular system to function well.
  5. 5External Gastrointestinal Tract-continuous with the external environment (ingest air or eat a dirty apple).
    -enzymes that are anti-microbial in the GI tract. Not all bacteria are sanitized in the oral cavity.
  6. 6PicPic
  7. 7Overall Function of the Digestive SystemOverall Function of the Digestive System
  8. 8Host Defense: Mucosal Immune System and Commensal BacteriaCommensal Bacteria--contribute to the digestion of food (fermentation of dietary fiber), provide essential nutrients (secondary and deconjugated bile acids), prevent pathogenic microorganisms from colonizing the intestine (c. difficle, v. cholera in the lumen, and salmonella and listeria(invasive). Can cause massive dehydration, lots of fluid loss through diarrhea.
  9. 9Human intestinal Microbiota-10^13 –10^14 microorganisms
    -72 bacterial phylotypes
    -1mL in large intestine*
    -1000 species
    -1 trillion organisms.
    -does not cause infections because it is kept under control.
    -very important in preventing colonization of super bugs.
  10. 10Bile Acids-important for digestion and eventual absorption of lipid byproducts.
    -secondary bile acids can be reabsorbed and taken back into the liver.
  11. 11Poo Capsules-contain frozen feces that can cure clostridum difficule infection.
    -cultured intestinal bacteria from healthy individuals.
    -nasogastric tube and enema.
  12. 12Commensal Bacteria (ON EXAM)-good bacteria.
    -friendly and reside in the lumen of the gut.
    -host intestine must stay hyporesponsive to the commensal bacteria but have to be able to defend against invasive pathogenic bacteria. *
    -BALANCE BETWEEN INFLAMMATORY RESPONSES AGAINST INVASIVE PATHOGENS AND SUPPRESSIVE MECHANISMS AGAINST COMMENSAL BACTERIA. *
    -probiotics increase the growth of commensal bacteria "friend" and reduces the bad pathogenic bacteria "foe".
    *
  13. 13Cell-Cell Communication in the GI tract1) Chemoreceptors - stimulated by elevated levels of H+, protein, fat and carbs.
    2) Osmoreceptors - stimulated by elevated osmolality.
    3) Mechanoreceptors - stimulated by distention of the gut wall or stretching.
    The GI tract is further regulated by:
    -Neural Reflexes (ANS) - short and long term reflexes. Long term involves the autonomic system [sym and parasym.]
    -Extensive enteric nervous system found in the wall of the digestive tract-intrinsic nerves of the gut located on the inside of the gut wall and muscle. "Little brain. Independent and controls gut function.
    -Hormones and paracrine factors - paracrine cells.
  14. 14Overview of Neural Control of GI System-higher centers can control the enteric nervous system.
    -vagovagal reflex afferent signals integrate in CNS autonomic centers and relay back to GI organs vis PSNS efferents.
    -vagovagal relfex is an example of how gut functions can be controlled by longer neural reflexes.
    -X=ENS can function independently of extrinsic inputs.
    -cutting the vagus nerve, you can still get normal response because ENS is independent of extrinsic inputs.
  15. 15Release of ACh-causes contractility or release of NT in the mucosa which increases secretion.
  16. 16Vagovagal Reflex-The parasympathetic vagus nerve composed of both afferents and efferents carries signals from stretch receptors, osmoreceptors, and chemoreceptors to dorsal vagal complex* where the signal may be further transmitted to autonomic centers in the medulla.
    -Efferent fibers of the vagus then carry signals to the gastrointestinal tract up to 2/3 of the Transverse Colon.
    -vagovagal reflex controls contraction of the gastrointestinal muscle layers in response to distension of the tract by food. -This reflex also allows for the accommodation of large amounts of food in the gastrointestinal tracts.
  17. 17Extrinsic Branches of the Autonomic System-parasympathethic=excitatory
    -sympathetic=inhibitory
    -***both sympathetic and parasympathetic cause increase in secretion.**ONLY different when there is parasym. excitation and sym. inhibition.
    -there is parasym. innervation through the vagus and pelvic nerves.
    A. Preganglionic parasympathetic innervation by the vagus (cranial nerve 10) and pelvic nerves of the sacral spinal cord. Dashed line --input for striated muscle
    •B: Postganglionic sympathetic innervation from the coeliac ganglion (CG), superior mesenteric ganglion (SMG) and inferior mesenteric ganglion (IMG
  18. 18ANS and ENS-inputs from ANS regulate the ENS
    -Parasym. inputs= come from vagus and cranial nerves.
    -Sym. inputs = comes from 3 main ganglia. coelic, superior mesenteric, and inferior mesenteric.
    -the MYENTERIC PLEXUS has nerve ganglia between the longitudinal and circular muscle that receives input from parasym. inputs.
  19. 19Functional Layers of the ENS and Relationship to Layers of Small Intestine-intestine has functional layers:
    1) Duodenum
    2) Jejunum
    3) Ileum
    -they have interstitial cells of Cajal (CC) = pacemaker cells used for nerve to muscle communication and nerve to epithelial communication. They drive the membrane potential to more depolarized levels which transfer to the smooth muscle cells.
    -inside the intestine, there is an inner lining called mucosa (millions of cells that cover fingerlike projections)
    -submucosal plexus= connective tissue that has nerve that regulates secretion.
  20. 20Submucosal Plexus-has nerve ganglia which regulates secretion.
  21. 21Myenteric Plexus-has nerve ganglia.
  22. 22Deep Muscular Plexus-NO GANGLIA.
  23. 23ICC Functions in the Gut-generation of slow wave activity.
    -coordination of active propagation of slow waves.
    -transduction of motor neural inputs from ENS to muscle.
    -mechanosensation of the stretch of GI muscles.
    -destruction of the ICC's in diabetes=leads to impaired gastric motility. = gastroparesis*
    -iCC is close to the nerve ganglia in the myenteric plexus, it can transfer a lot of NT (Ach) to be detected in the smooth muscle.
  24. 24ICC Functions in the Gut Cont'd-driving smooth muscle contractility is the Minor network of ICC in the deep muscular plexus, DOES NOT HAVE NERVE GANGLIA BUT HAS NERVE VARICOSITIES WHICH ARE NERVE ENDINGS THAT ARE FILLED WITH NT. *(one third down from the sub mucosalayer). These have minor ICC networks that can actually take over pace making function if the ICC in the myenteric plexus is gone. **
  25. 25TEST QUES. WHERE ARE THE NERVE GANGLIA LOCATED?**MYENTERIC PLEXUS
    AND SUB-MUCOSAL PLEXUS.*
  26. 26ICC'S need functional c-kit receptors (C-kit= a receptor type tyrosine kinase binds to ligand stem cell factor)-important for the development of nerve ganglia and ICC in myenteric plexus.
    -if there is no k-cit receptor, the ICC don't migrate to its destination site which the myenteric plexus.
    -c-kit mutations lead to abnormal development of nerve ganglia and ICC in myenteric plexus.
    -c-kit knockouts= non-functional.
  27. 27Regulation of Gastrointestinal Tract by Peptides/Non-peptide Mediators-GI tract is modulated by hormones (endocrines), paracrines, neurocrines or
    immune/juxtacrine factors.
    -mediators are peptides, derivatives of amino acids or non-peptides from various sources.
    -ALL GI HORMONES ARE PEPTIDES BUT NOT ALL PEPTIDES IN THE GI TRACT ARE HORMONES. Some are NT or immune factors.
    -5 GI hormones that are peptides.
  28. 28Cell to Cell Communication in the Gut: Four Regulatory Pathways-Endocrine Mediators= released in response to neural activity and chemical and mechanical signal triggered by foodstuff, act @ a DISTANT SITE*.
    -Paracrine/Immune/Neurocrine substances act at IMMEDIATE AREA OF RELEASE.
    -like NT, paracrine mediators are readily metabolized or reabsorbed to limit duration of activity.
  29. 29Blood Supply to the Digestive Organ-splanchnic circulation is critical for delivery of GI hormones (gastrin, GIP, motilin, secretin, CCK).
    -blood flows from the intestine to the liver first via portal vein.
    -the target could be the pancreas or the stomach to induce acid secretion.
  30. 30Criteria that defines a gastrointestinal hormone (4 of them)1. Physiologic event in one segment alters the activity of another (distant site).
    2. Effect persists after neural connections have been severed.
    3. A substance isolated from the site of stimulation must mimic effect of physiologic stimulus when given intravenously.
    4. Hormone identified chemically and structure confirmed by synthesis.
  31. 31Gastrin released from the antrumGastrin G cells are found in the stomach and intestine. **
    -other hormones are mostly found in the small intestine.
  32. 32Sources of 5 GI Hormones (KNOW FOR EXAM)**Sources of 5 GI Hormones (KNOW FOR EXAM)**
  33. 33Sources of GI Hormones Cont'd-Distribution of GI peptides with full status as hormones.
    -Shaded regions indicate major release sites under normal conditions
    -*Trophic factor = promotes growth of mucosa and pancreas (seen in gastrinoma
  34. 34Pure GI Hormones and ActionsPure GI Hormones and Actions
  35. 35Gastrin-comes from G cells in the antrum of the stomach and some in the duodenum.
  36. 36CCK-comes from I cells in the duodenum, jejunum, neurons in ileum and colon. Stimulates bicarbonate secretion from the liver.
  37. 37Secretin-comes from S cells in the small intestine.
    -secretes bicarbonate.
  38. 38GIP-comes from K cells in the duodenum and jejunem.
    -secreted in response to glucose and fats in the duodenum and causes insulin release from pancreas.
  39. 39Motilin-endocrine cells in upper GI tract, released from the duodenum in low glucose levels.
  40. 40Endocrine Cells in the Gut1. Open cells- endocrine cells contact the lumen. Apical membrane is open and contacts the lumen so it senses the luminal contents. ALL 5 HORMONES ARE OPEN CELL TYPES.
    ex) G-cells.
    2. Closed Endocrine cells- ECF like cells , responsible for histamine and they have no connection to the luminal surface.
  41. 41Paracrines-responsible for secreting factors for nearby sites.
    -released from ECL cells that secrete histamine which diffuses to nearby parietal cells which is responsible for acid secretion which are stimulated to undergo stimulation and release of acid.
    -diffuse through the extracellular space to their target tissues.
    -interact with receptors close to the site of release, and biological effects are limited by a short distance for diffusion (like neurocrines).
    -often there is big effects due to scattered and abundant distributions of paracrine cells found on small intestine and antrum so large effect. Scattered throughout the mucosa.
  42. 42Two Important Paracrine Agents 1. Histamine** 2. Somatostatin**Know for final.
  43. 43Histamine-derivative of histidine.
    -NOT A PEPTIDE
    -regulator acting as a paracrine.
    -produced by ECL cells and mast cells.
    -released by gastrin
    -stimulates acid secretion in the stomach
    -potentiates actions of ACh and gastrin on acid secretion. SYNERGISTIC EFFECT.
    -antacid meds, cimetidine, ranitidine, block H2 receptors* which reduces the amount of acid in the stomach.
    -also has to do with intestinal Cl secretion, mast cells in the lamina regulate the Cl- secretion into the lumen and followed by water secretion into the lumen.
  44. 44Somatostatin-GI peptide
    -functions as a paracrine.
    -comes from D cells
    -inhibits gastrin release when antral mucosa is acidified (pH is low) and directly inhibits gastric acid secretion from parietal cells.
    –Distributed in gastric and duodenal mucosa and the pancreas.
    –Inhibits release of all gut hormones**
  45. 45Juxtacrine (Immune) Communication-mast cells in the lamina propria release histamine will affect intestinal smooth muscle cells and epithelial cells.
    -can affect the secretion of Cl in the mucosa.
  46. 46Neurocrines-released near target tissue (like paracrines)
    -peptides (VIP from enteric nerves relaxes GI smooth muscle), non-peptide (ACh), or gases (NO).
    -need to diffuse across a narrow gap (synapse)
    -may stimulate or inhibit release of endocrines or paracrines.
    -GRP (gastrin releasing peptide) is vagal stimulated release, mediates vagal release of gastrin.
    -ACh (not a peptide) stimulates acid secretion from parietal cells.
  47. 47NO IS THE MAJOR INHIBITORY NT IN THE GUT***-promotes gut relaxation.
  48. 48Notes Cont'd-the gut is innervated by the enteric nervous system and the autonomic nervous system (sym and parasym).
    -cut the innervation from autonomic nervous system and it can still function due to the "little brain" being the enteric nervous system being present.
    -This is rich in peptides. The brain is another major source of peptides.
    -The enteric nervous system can equal the amount in the brain and there are different NT which are peptides, non-peptides or gases.
  49. 49NeurocrinesNeurocrines

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3 PHPY 303 Karteikarten am Lecture 14, erstellt von deepa.chrisilda. am 24/04/2016.
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