b. Responses/Reflexes Food bulk stretches the fundus of stomach, activating mechanoreceptors GI peptides activate chemoreceptor s o o o
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1 QUIZ/TEST REVIEW NOTES SECTION 2 GASTRIC PHASE OF DIGESTION DIGESTIVE SYSTEM CHAPTER 21 I. ENTERIC NERVOUS SYSTEM a. Defined and Crrelatin with Shrt Reflexes Fund in walls f LUMEN Invlved in shrt reflexes Reflexes that riginate within the enteric nervus system (ENS) and are integrated withut utside input It can als crdinate functins with autnmic neurns bringing signals frm CNS Learning Objectives: Differentiate lng and shrt reflexes f digestin Identify surce and functin f secretary prducts f stmach mucsal glands Explain mlecular basis f gastric acid prductin, regulatin f acid prductin, and treatment ptins fr acid reductin, including prtn-pump inhibitrs Describe prcess f digestin, absrptin, mtility and secretin in stmach Describe neurendcrine cntrls f gastric hase Describe digestive prcesses f carbhydrates, fats, and prteins in stmach Cntrl Mtility, Secretin, Grwth ENS netwrk integrates sensry infrmatin then initiates respnses thrugh submucasal neurns that cntrl secretin by GI epithelia cells and myenteric neurns that influence mtility At this stage it is n lnger a Feedfrward/cephalic reflex mechanism because fd is present b. Respnses/Reflexes Fd bulk stretches the fundus f stmach, activating mechanreceptrs GI peptides activate chemreceptr s GI Peptides excite r inhibit mtility and secretin GI Peptides secreted may act as hrmnes r Paracrine signals GI Peptides are secreted int the bld and may act n GI tract, accessry rgans (pancreas), distant rgans (brain)
2 II. Gastric secretins influenced by bth Lng and Shrt Reflexes GASTRIC PHASE: GASTRIC SECRETIONS a. Beginning Digestive activity in stmach begins with lng vagal reflex f cephalic phase even befre fd arrives When fd arrives in stmach, stimuli in gastric lumen initiate series f shrt reflexes that cnstitute gastric phase f digestin Distensin/Expansin f stmach and peptide/amin acid presence in lumen activates: endcrine cells and enteric neurns Hrmnes, Neurcrine secretins, and Paracrine mlecules influence mtility and secretin b. Mucus Secretins Mucus surface cells secrete mucus and Bicarbnate (HCO - 3 ) Mucus frms a physical barrier and bicarbnate creates chemical buffer Bicarbnate is a chemical barrier that neutralizes acid n the mucus layer Drps the ph level dwn by 1 X 10^5; frm a ph f 2 t a ph f 7 (acidic neutral) c. Gastric Acid Secretin 1. G Cells Secrete Gastrin Stimulated by ACh, peptides, amin acids Functin: Stimulate gastric acid secretin 2. Enterchrmaffin-like Cells (ECL) Secrete Histamine Stimulated by ACh, gastrin (frm G Cells) Functin: Stimulates gastric acid secretin 3. Parietal Cells Secrete Gastric Acid (HCL) and Intrinsic Factr Stimulated by ACh, gastrin, histamine Functin: HCL = Activates pepsin and kills bacteria Intrinsic Factr = Cmplexes with Vitamin B 12 t permit absrptin Acid secretin is linked t bicarbnate absrptin
3 G-Cells Gastrin ECL- Cells Histamine Parietal- Cells Gastric Acid (HCL) d. Gastric Enzyme Secretin 1. Chief Cells Secrete pepsin (frm pepsingen/gen)and gastric lipase Stimulated by ACh Acid, Secretin Functins: Pepsin: Digest prteins Gastric Lipase: Digest fats Gastric Lipase Acid Chief Pepsin e. Hrmne Secretin 1. D Cells Secreted smatstatin Stimulated by Acid in the stmach Functin: Inhibits gastric acid secretin
4 OVERVIEW GASTRIC SECRETION Cephalic reflex, parasympathetic neurns fr Vagus nerve stimulate G cells t release gastrin int the bld (1). The presence f amin acids r peptides in the lumen triggers a shrt reflex fr gastrin release Gastrin in turn prmtes acid release, bth directly and indirectly by stimulating histamine release (2) Histamine is released frm ECL cells in respnse t gastrin and ACh frm the enteric nervus system (1). Histamine diffuses t its target, the parietal cells, and stimulates acid secretin by cmbining with H 2 receptrs n parietal cells Acid in the stmach lumen stimulates pepsingen release frm chief cells thrugh a shrt reflex (3). In the lumen, acid cnverts pepsingen int pepsin, and prtein digestin begins Acid als triggers smatstatin release frm D cells (4). Smatstatin acts via negative feedback t inhibit secretin f gastric acid, gastrin, and pepsingen
5 III. GASTRIC MOTILITY a. Stimulated by 1. Distensin 2. Lng And Shrt Reflexes - Influenced by hrmnes, Paracrine signals and autnmic nervus system Parasympathetic: Rest and digest/enhance GI functins Sympathetic: Fight r flight/inhibit GI functins - Shrt Reflexes f ENS effect myenteric neurns that influence mtility b. Mixing 1. Autrhythmic slw waves f peristalsis - Spntaneus cycles f deplarizatin and replarizatin - Des nt reach threshld with each cycle - Graded accrding t the amunt f Ca 2+ that enters the fiber - The lnger the duratin f the slw wave the mre actins ptentials that fire, and the great the cntractin frce in the muscle - Can be mdified by neurtransmitters, hrmnes, r Paracrine mlecules c. Gastric Emptying 1. Peristalsis prpels chime thrugh pylric sphincter - Peristaltic cntractins create frward mvement - Prgressive waves f cntractin that ccur behind the blus 2. Rate f emptying slwed by intestinal phase factrs
6 IV. GASTRITIS AND PEPTIC ULCER DISEASE a. Cmprmise f the mucus-bicarbnate barrier Definitin: Is a inflamed area in the stmach r dudenum that extends frm a break in the surface epithelium pas the muscularis mucsae; G.E.R.D = Gastr Esphageal Reflux Disease 1. Peptic (Gastric) ulcers 10% Stmach Mst caused by bacterium H. Pylri, rest caused by high levels f acid frm enhanced enzyme prductin 2. Frequency f Dudenal ulcers 90% Dudenal Mst caused by bacterium H. Pylri, rest caused by high levels f acid frm enhanced enzyme prductin Can be fund in dudenum frm gastric acid and stmach enzymes chime may carrier, r which is present in the E.C.F. when the stmach passes int the dudenum b. Causes c. Treatment H 2 Blckers Pepcid AC Tagamet Axid Zantac 1. Helicbacter Pylri Bacterium that thrives in high ph envirnment f stmach and Dudenum H. Pylri explit the large amunts f urea released by the stmach in prtein/amin acid digestin H. Pylri used urea t prtect themselves frm the acidic envirnment 2. Hypersecretin f acid (Dyspepsia) (a) Excessive gastrin prductin by pancreatic tumrs (b) Hyperactive Vagus stimulatin Increased amunt f parasympathetic stimulatin 3. Aggravating factrs (a) Alchl (b) NSAIDs Mst cmmn causes f ulcers Nnsteridal Anti-Inflammatry Drugs (Aspirin/Tylenl) (c) Caffeine and spices 1. Eliminatin f Helicbacter Pylri 2. Acid cntrl (a) Vagtmy (b) Acid Suppressin 1) Antacids 2) H 2 -Receptr Blcker Prtn Pump Inhibitrs Prilsec Nexium Histamine receptr antagnists Bind cmpetitively t histamine H 2 receptrs n parietal cells Histamine is a Paracrine that stimulates acid secretin by the stmach; s by inhibiting it yu inhibit acid sectin 3) Prtn Pump Inhibitrs By inhibiting the efflux f prtns frm the parietal cells Cl - has nthing t bind with; can n lnger bind with H + t frm HCL Blck H + -K + -ATPase Pump
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