Gastric Digestion 2x PDF

GASTRIC DIGESTION Gastric Phase of the Response to a Meal Oct. 31, 2024 Story of Alexis St. Martin’s gastric fistula & American Physiologist Dr. William Beaumont (1822-1833) 1838  The thoughtful bo...

GASTRIC DIGESTION Gastric Phase of the Response to a Meal Oct. 31, 2024 Story of Alexis St. Martin’s gastric fistula & American Physiologist Dr. William Beaumont (1822-1833) 1838  The thoughtful bowel The ugly gut is more intellectual than the heart, and has a greater capacity for “feeling” more nerve cells in the bowel than in the spinal cord has all the classes of neurotransmitters Neural control Short-loop reflex ? Long-loop reflex ?  Regions of the stomach lower oesophageal sphincter Pyloric Fundus sphincter “Pacemaker Duodenum zone” - peristaltic contractions Corpus “acid-secreting” Antrum “muscular pump”  Enteroendocrine cells THIRD EDITION HUMAN PHYSIOLOGY AN INTEGRATED APPROACH Dee Unglaub Silverthorn, Ph.D. PowerPoint® Lecture Slide Presentation by Dr. Howard D. Booth, Professor of Biology, Eastern Michigan University Furness, J. B. et al. (2013) The gut as a sensory organ Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2013.180 Stomach as an endocrine organ 1. Gastrin 2. Histamine 3. Serotonin 4. Somatostatin 5. Melatonin 6. Ghrelin 7. Obestatin 8. Peptide YY 9. ANP 10. Leptin 11. Neuropeptide W 12. Nesfatin-1 13. Estrogen The Stomach Storage Digestion HCl – parietal C. Lipase – chief C. Pepsin – chief C. Protect walls HCO3- Mucus Stomach motility (1) Gastric filling (2) Gastric storage (3) Gastric mixing (4) Gastric emptying Gastric filling— receptive relaxation of the fundus and body of the stomach Where do we usually vagal fibers -- vasoactive intestinal see receptive relaxation? polypeptide (VIP) and NO Gastric storage— the fundic area -a pocket of gas very little mixing movements in the body and fundus food stored in the relatively quiet body, not mixed Gastric mixing for the mixing of food with gastric secretions to produce chyme each antral peristaltic wave propels chyme forward toward the pyloric sphincter tonic contractions of the pyloric sphincter normally keeps it almost, but not completely, closed  Gastric emptying— antral peristaltic contractions driving force for gastric emptying amount of chyme that escapes into the duodenum with each peristaltic wave before the pyloric sphincter closes tightly depends upon the strength of peristalsis  Gastric emptying— antral peristaltic contractions driving force for gastric emptying amount of chyme that escapes into the duodenum with each peristaltic wave before the pyloric sphincter closes tightly depends upon the strength of peristalsis Regulation of gastric emptying both neural and hormonal mechanisms fat, acid, hypertonicity, peptides and distension duodenal and jejunal mucosa have receptors intrinsic nerve plexuses (short reflex) and autonomic nerves (long reflex) “enterogastric reflex” hormones released from the duodenal mucosa “enterogastrones” (CCK, gastrin etc.)  Which one of the statements below is right about secrterin acid in the duodenum production? Scretein in produced in respose to low ph levels in stomach. Increases rated of gadteric emptying to cambat higher ph Secreterin stulates contraction of pylroic digestion in the duodenum –pH? sphincter and increases duodenal motility acid in the duodenum secretin diminishes the rate of gastric emptying by inhibiting antral contractions by stimulating contraction of the pyloric sphincter while duodenal motility increases fat digestion products in the duodenum and jejunum decreases the rate of gastric emptying cholecystokinin (CCK) and gastric inhibitory peptide from the duodenum fat may be still in the stomach after 6 hours a protein and carbohydrate meal may empty in 3 hours osmotic pressure of duodenal contents hyperosmotic solutions in the duodenum and jejunum slow the rate of gastric emptying-an unidentified hormone  Which one of the sentances below is peptides and amino acids in the duodenum right about the gastrins ability to diminish rate of gastric emptying release gastrin from G cells – antrum and duodenum gastrin increases the strength of antral contractions increases constriction of the pyloric sphincter net effect  diminishes the rate of gastric emptying Distension too much chyme in the duodenum inhibits the emptying of even more gastric contents Storage function PYLORUS not to exceed the small intestine’s capacity In summary, Central nervous system Sympathetic _ Parasympathetic activity + activity Intramural intrinsic Decreased gastric emptying plexuses Unidentified Secretin CCK, GIP hormone ACID FATS Hypertonicity : Duodenal chemoreceptors Emotions through the autonomic nerves influence gastric smooth muscle excitability sadness and fear -decrease motility anger and aggression -increase it intense pain -inhibits motility, throughout the GI by increased sympathetic activity Gastric secretions- mucosal gland cells in gastric pits 2 liters/day gastric juice (1) the oxyntic mucosa (2) the pyloric gland area  Exocrine cells: Endocrine cells: secrete into the lumen secrete into circulation or locally mucus cells G-cells chief (zymogen) cells D-cells parietal cells enterochromaffin -like (ECL) cells  Cells of the gastric (corpus) gland Gland lumen Surface epithelial cells - protective role Proliferating cells Parietal cells - H+ secrete acid to lumen Enterochromaffin-like cell (ECL) - secrete histamine Chief cells - secrete pepsinogen to lumen  THE GASTRIC MUCOSA Major cell types Functions surface epithelial - mucus, HCO3- chief (zymogen) - pepsinogen CORPUS parietal - HCl, intrinsic factor enterochromaffin-like - histamine (ECL) D-cells - somatostatin surface epithelial - mucus, HCO3- chief (zymogen) - pepsinogen ANTRUM G-cells - gastrin D-cells - somatostatin Mucus a protective barrier against several forms of potential injury to the gastric mucosa: *lubricating–protects against mechanical injury *protects stomach wall from self-digestion *protects against acid injury by neutralizing HCl -alkaline Hydrochloric acid Luminal pH - falls as low as 2 H+  actively transported against a tremendous concentration gradient: [H+] in the lumen, 3 to 4 million times >in blood Cl-  actively pumped – much smaller gradient - only 1 ½ times Parietal cells - abundance of mitochondria  Parietal cell ultrastructure A resting parietal cell An acid-secreting activated parietal cell. Tubulovesicles fused with the membranes of the intracellular canaliculus, open to the lumen of the gland and lined with abundant long microvilli. Gastric acid secretion  Gastrin secretion Endocrine G cells -pyloric gland area  gastrin into blood carried back to body & fundus gastrin stimulates parietal and chief cells  secretion of a highly acidic gastric juice Gastrin - also trophic for mucosa of the stomach and small intestine What kind of control mechanism? Histamine is the strongest agonist of H+ secretion, gastrin and ACh are much weaker agonists Paracrine Endocrine Neurocrine Parietal cell Neurocrine works in both a direct and indirect way. Phases of gastric secretion and their regulation Long and short reflexes in the stomach Cephalic phase Conditioned reflexes: Smell, taste, chewing, swallowing, hypoglycemia Vagus Nucleus Vagus nerve 1 ACh 2 G cell ACh Parietal cell GRP GASTRIN in blood  Cephalic phase Vagus  -stimulates parietal cells directly (ACh) -stimulates the release of gastrin (bombesin or Gastrin Releasing Peptide) accounts for 30 % of the response to a meal can be blocked by vagotomy sham feeding (chew and spit) Atropine blocks the direct effects on the parietal cell, but not gastrin-mediated effect Gastric phase Vagus nerve Distension Amino acids, peptides G cell ACh Parietal cell GRP GASTRIN  Gastric phase Gastric phase distension vagovagal and short reflexes stimulate both gastrin release and acid secretion protein, partially digested to peptides and aminoacids both neural and chemical mechanisms accounts for 60% of the acid response to a meal Alcohol, caffeine, decaffeinated coffee Intestinal phase protein digestion products in the duodenum stimulate acid secretion: intestinal gastrin enterooxyntin circulating amino acids accounts for 10 % of the total response to a meal Intestinal phase gastrin release is inhibited at antral pHs below 3 gastrin release is inhibited when antral pH3)  Control of G-cell function Protein/peptides/ Stomach amino acids H+ (antrum) lumen + + G-cell D-cell Gastrin somatostatin releasing + - peptide Stomach body (corpus): (GRP) GASTRIN ECL cell/ circulation parietal cell  Somatostatin-paracrine effect Protein/peptides/ Stomach amino acids H+ (antrum) lumen + + G-cell D-cell Gastrin releasing + - somatostatin peptide (GRP) GASTRIN ACh + - ACh VAGUS NERVE  Control of acid secretion HCl - not essential for gastrointestinal function it does perform several functions: 1. pepsinogen  active pepsin -acid medium - 2. breakdown of connective tissue and muscle fibers- 3. kills most of the microorganisms ingested - Intrinsic factor IF, a glycoprotein secreted by parietal cells vitamin B12 + IF –endocytosis- in the terminal ileum Vit. B12- essential for normal formation of RBC gastric mucosal atrophy - an autoimmune attack against parietal cellspernicious anemia most determinant result- the loss of intrinsic factor regular injections of vitamin B12 Pepsinogen secretion synthesized, packaged and stored in the chief cells zymogen granules release pepsinogen upon appropriate stimulation “autocatalysis” Stimulation of Chief Cells in Response to a Meal Most of the agents that stimulate parietal cells to secrete/inhibit acid also control release of pepsinogen other enzymes Lipase attaches to the surface of lipid droplets in the emulsion generates FFA & monoglyceride from dietary triglyceride (10%) not essential for normal digestion and absorption of dietary lipids gelatinase The mucus-bicarbonate barrier of the gastric mucosa The stomach lining is protected from gastric secretions by the gastric mucosal barrier luminal membranes of gastric mucosal cells - almost impermeable to H+ lateral edges of these cells - tight junctions acid cannot diffuse mucus provides a protective coating When the mucosa is damaged… acid and pepsin diffuse into the mucosa: acid  release of histamine  stimulates secretion of more acid  further histamine “a vicious cycle” “gastric mucosal barrier” entire stomach lining is replaced every 3 days (rapid mucosal turnover) When gastric mucosal barrier is broken gastric wall is injured by its acidic and enzymatic contents an erosion or peptic ulcer of the stomach wall H. pylori has some advantages to live in the acidic environment where other bacteria cannot survive: motile, equipped with 4-6 flagella  tunnel through and live under thick mucus layer settles in the antrum (no-acid producing parietal cells) produces urease breaks down urea into ammonia (NH3) and CO2 NH3  buffers acid locally secretes toxins that cause inflammation- weakens the gastric mucosal barrier  Acid inhibitory therapy Proton pump inhibitors H+ K+ H+/K+ ATPase (the proton pump) reflux oesophagitis “heart burn” Parietal cell H2 receptor H2 receptor Peptic ulcer Histamine antagonists The stomach absorbs no food No food or water is absorbed into the blood Stomach is impermeable to H2O Carbohydrate and protein digestion have not been completed No special transport mechanisms to facilitate absorption ethyl alcohol and aspirin are absorbed directly Except aspirin, most drugs are not absorbed until they reach the small intestine Alcohol can be absorbed even more rapidly by the small intestinal mucosa greater surface area can be absorbed more slowly if gastric emptying is delayed Vomiting or emesis “the forceful expulsion of gastric contents through the mouth” not by reverse peristalsis the stomach does not actively participate stomach, esophagus, gastroesophageal sphincter, and pyloric sphincter are all relaxed major force of expulsion  contraction of respiratory muscles (diaphragm) and abdominal muscles Vomiting a deep inspiration closure of the glottis contracting diaphragm descends downward on the stomach abdominal muscles compress the abdominal cavity the stomach is squeezed the gastric contents are forced into the esophagus glottis is closed-vomited material does not enter the airways uvula is elevated-close off the nasal cavity Vomiting often when the vomitus first enters the esophagus pharyngoesophageal sphincter remains closed  no gastric content enters the mouth distension of the esophagus  secondary peristaltic waves  force the gastric contents back into the stomach cycle repeats itself - contents are squeezed up into the esophagus again “retching or heaves” Vomiting when the pressure becomes great enough person thrusts out the jaw  pulling pharyngoesophageal sphincter to open gastric contents forced through the esophagus out through the mouth duodenum contracts strongly intestinal contents back into stomach “yellowish bile” Cycle repeated - until the stomach is emptied Vomiting salivation, sweating, rapid heart rate, sensation of nausea generalized discharge of the autonomic nervous system nausea, vomiting and retching can be initiated by - from receptors throughout the body afferent input to the vomiting center (in the medulla) causes of vomiting chemical agents, drugs (emetics) or noxious (harmful) substances act either on the upper portions of GIT stimulate chemoreceptors in the chemoreceptor trigger zone adjacent to vomiting center  psychogenic vomiting induced by emotional factors (sight, smell, anxiety, stressful situations) causes of vomiting touch stimuli on the back of the throat irritation and distension of the stomach and duodenum elevated intracranial pressure rotation and acceleration of the head (motion sickness) intense pain from a variety of organs With excessive vomiting Large losses of secreted fluids and acids reduction in plasma volume dehydration circulatory problems loss of acids from the stomach can lead to metabolic alkalosis Beneficial effect of vomiting vomiting due to irritation of the digestive tract – useful in removing noxious material from the stomach – not allowing to be absorbed emetics are given in the case of accidental ingestion of a poison In summary Guyton & Hall,14th Ed. Chapters 65-67.  Thank you for your attention Socrative Student Login http://b.socrative.com Room: H2QS5PWGR