Physio git 5 & 6.


Published on

Physiology gastroenterology 5&6.

  • Be the first to comment

  • Be the first to like this

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Physio git 5 & 6.

  1. 1. Gastrointestinal physiology Transport & mixing of food (Cont). Dr.M.A.M.Shaikhani.
  2. 2. Colonic movements(Ms): • 2 types: • 1.Mixing or segmentation movements(SMs); • Same as in SI . • Large circular constriction contractions scattered along colon. • Caused by the combined contraction of circular muscles (about 2.5 cms) & longitudinal muscle fibers( which are arranged into 3 longitudinal strips called (Tenae coli) cause the colonic wall to bulge outside into baglike sacs causing the appearance of haustrations . • Help in mixing colonic contents & absorbing water & electrolytes from the wall so concentrating it to semifluid, mush, semimush, solid & finally hard food residues called stool. • 2.Propulsive or mass Ms: • · Forward Ms. Help to push stool towards the rectum & initiating the defecation reflex. • More abundant in the transverse & sigmoid colon, stimulated by distention or irritation of colon.
  3. 3. HAUSTRAL CONTRACTIONS Food residue Haustra
  4. 4. MASS MOVEMENTS Food residue Rectum
  5. 5. Defecation reflex: · The rectum is usually empty. · When the stool enters the rectum · The sensation of its presence is transmitted to the myenteric plexus & through parasympathetic pelvic afferent nerves to the spinal cord to initiate colonic contractions through parasympathetic efferent nerves . · External sphincter relaxation occur through skeletal motor nerves starting defecation when the situation is proper as there is higher centers control from conscious cortex over the whole defecation reflex.
  6. 6. Figure 24.25 The Defecation Reflex
  7. 7. Figure 24.25 Stretch receptors Sensory neurone Anal sphincters Parasympathetic neurone Somatic neurone DEFECATION REFLEX Rectum
  8. 8. Reflexes in the colon and rectum Mass movements+ + Food in stomach Food in duodenum Faeces Defaecation reflex Colon rectum anus Ach Spinalcord IAS EAS FAECES + Distention - VIP ATP + - Pudendal nerve
  9. 9. The Defecation Reflex: Summary Removes undigested faeces from the body. Stretch receptors in GIT wall detect distension of rectum. Parasympathetic reflex causes contractions of the sigmoid colon & rectum + relaxation of internal anal sphincter. External anal sphincter (under voluntary control) consciously relaxed if appropriate.
  10. 10. The peristaltic movement of the colon is called: A. Constriction movement. B. Segmentation movement. C. Mass movements. D. Propulsive movements. E. Mixing movements.
  11. 11. Defectaion: A. Is a reflex act. B. Has no conscious control. C. Is completely a reflex act in neoborns. D. Involve autonomic & skeletal nerves. E. Both Internal& external anal sphincters are involved.
  12. 12. Mixing colonic movements: A. Cause colonic segmentation. B. Lead to haustral appearing colon. C. More distally than proximally. D. Involve only longitudinal muscles. E. Similar to those of small intestine.
  13. 13. Neurotransmitters that partcipate in defecation inclde: A. Gastrin. B. Acetylcholine. C. Vasoactive intestinal peptide. D. Adenosine diphosphate. E. CCK.
  14. 14. Secretary functions of GIT: •Of 2 types: •1.Enzymes helping digestion. •2.Mucous for lubrication & protection of GIT mucosal surfaces from excoriation. • Anatomical types of secretary glands: •1.Mucous glands: 2 types: •a.single cell (goblet cells). •b.complex cell mucous glands. •2.Crypts of Liberkhan: deeper & contains specialized secretary cells. •3.Deep tubular glands in stomach & upper duodenum secreting acid & pepsinogen. •4.Complex glands like salivary ,pancreatic & hepatic glands.
  15. 15. 3Mechanisms of stimulation of GIT glands: • 1.Local contact of food with GIT mucosal surfaces activating enteric nervous system through: • A.Chemical irritation. • B. Tactile irritation. • C.Distension. • 2.Autonomic stimulation: • Specially through the parasympathetics (vagi & other cranial parasymp. Nerves) stimulating eso.,stomach,pancreas, Brunner glands in duodenum & glands of distal colon,while secretion in the remainder of SI & 1st 2/3 of large intestine(LI) is stimulated by local myenteric nerves & hormones locally in each segment. • The sympathetics also slightly increase the glandular secretion but through vascular constriction reduces secretion as an overall effect.
  16. 16. Secretion of saliva: • Daily secretion is 1 liter in a rate of 0.5 ml/min. during day & very little during sleep. • It contain 2 major types of secretions: • 1.Serous secretion containing ptyalin ,an alpha- amylase for digesting starch. • 2.Mucous secretion for lubrication.
  17. 17. Secretion of saliva: • Salivary glands consist of acini & ducts ,in the acini there is primary secretion of ptyalin,mucous & extracellular fluid while in the ducts there is K+ & HCO3- secretion & active Na+ reabsorbtion & passive Cl- reabsorbtion,so as a result there is high K+ & HCO3- & low Na+ & Cl- in the saliva.
  18. 18. Secretion of saliva: Functions of saliva: • 1.Digesting starch by ptyalin. • 2.Maintaining oral hygiene /Preventing dental caries, through: • A.Washing away pathogenic bacteria & food particles. • has bactericidal activity through its thiocyanate , proteolytic enzymes as lysozyme & protein antibodies contents. • In sjogren syndrome when there is inflammation of salivary /lacrimal glands there is dry eyes/mouth with premature & severe dental caries.
  19. 19. Nervous regulation of salivary secretion: • Stemulation through parasympathetic NS(PNS) from salivary nuclei located at the brain ponto-medulary junction excited by taste(specially sour) & tactile stimuli(as presence of smooth objects in mouth)& smell. • Inhibited or stimulated by higher centers specially the appetite center located close to PNS center in the anterior hypothalamus which function in response to signals from taste & smell areas of the cerebral cortex or amygdala. • Salivation also occurs in response to reflexes in the stomach& upper intestine by the presence of irritating food or nausea since saliva has diluting & acid neutralizing effect. .
  20. 20. Esophageal secretions: No enzymes , only mucous secreted by simple & complex mucous glands.
  21. 21. CONTROL OF SALIVARY SECRETION cerebral cortex salivary centre in medulla autonomic nerves salivary glands ↑ salivary secretion pressure receptors and chemoreceptors in the mouth other inputs:smell& taste centers conditioned reflex simple reflex
  22. 22. • Gastric secretions: 3 types of secretary glands • 1.Oxyntic(parietal) glands :in the body & fundus of S ,80% of Stomach glands ,secret Hcl,pepsinogen,intrinsic factor & small amount of mucous .It contains 3 types of cells: • a.Mucous neck cells secreting mucous. • b.Peptic or chief cells secreting pepsinogen. • c.Parietal or oxyntic cells secreting Hcl& intrinsic factor essential for vitamin B12 absorption. • 2.Pyeloric glands : in antrum ,secret mainly mucous & very important hormone called Gastrin & small amounts of pepsinogen . • 3.Numerous mucous glands:between the above 2 main glands • Secret large amounts of mucous which covers & protects the S wall by a protective layer from digestion by acid-pepsin.
  23. 23. • Gastric secretions: less important enzymes include gastric lipase,amylase & gelatinase.
  24. 24. HCl Gastrin Histamine Pepsinogen
  25. 25. Activation of pepsinogen to pepsin: • Done by Hcl as it is inactive in an alkaline medium. Regulation of gastric acid secretion: • Stimulated by 3 hormones:ACH(PNS),gastrin & Histamine: • 1.PNS (vagus) stimulation :secreting ACH which can be blocked by anticholinergic drugs pirenzepen used for peptic ulcer(PU) therapy. • 2.Gastrin release from antral glands which can be blocked by proglumide. • 3.Histamine release stimulating H2 receptors which can be blocked by H2 blockers as cimetidin(Tagamet). • The 3 above hormones secret Hcl through activation of the proton pump(H+-K+ ATPase)which is the final common pathway in acid secretion which can be blocked by omperazole ,an effective therapy for peptic ulceration & hyperacidity.
  26. 26. Figure 24.14 The Secretions of Hydrochloric Acid
  27. 27. GASTRIN histamine Parietal cell ECL cell Chief cell D-cell somatostatin - + noradrenaline, CCK, VIP & CGRP Ach H+ - + + Gland lumen + THE CONTROL OF ACID SECRETION
  28. 28. Acid inhibitory therapy H2 receptor antagonists Histamine Parietal cell H2 receptor H+ /K+ ATPase (the proton pump) H+ K+ Proton pump inhibitors Peptic ulcer reflux oesophagitis “heart burn” Tagamet, Zantac, Pepcid AC Omeprazole (Losec/Nexium) Gastrin: Proglumide Vagus: pirenzepine
  29. 29. Inhibition of gastric acid secretion: By: · 1.Acid feed back(FB) inhibition in the presence of excess acid when the S (PH) becomes 3 or less. In patients with (PU) this (FB) inhibition is abnormal so Hcl continue to be secreted in spite of very high acid& low PH in the stomach leading to PU. · 2.Through the enterogastric reflex in the presence of excess acid,fat & protein breakdown products,hyperosmolar fluid ,distention or any irritating factor in the upper SI which cause the release of several inhibitory intestinal hormones as secretin,CCK,Gastrin inhibitory peptide & somatostatin. · 3.Interdigestive period: in this period between meals the S secrets few mls. Of gastric juice containing little enzymes, more mucous & moderate amounts of HCO3 called non-oxyntic type of secretion .This interdigestive type of secretion may change with high enzyme-acid content in patients with PU & those with emotional upsets.
  30. 30. G. Phases of gastric secretion: Consists of 3 phases; 1.cephalic phase : · 1/5 of gastric secretion associated with eating a meal. occurs before or while the food is eaten.It is stimulated centrally. 2.Gastric phase: · 2/3 of total acid secretion associated with eating a mael. · Occurs when the food enters the S stimulated by long vagovagal reflexes,local enteric & gastrin mechanisms. 3.Intestinal phase: · acid secretion in response to presence of food in upper intestine specially the duodenum due to small amounts of gastrin released by duodenal mucosa in response to distention & chemical irritation.
  31. 31. 1. CEPHALIC PHASE Sight, smell or thought of food - Parasympathetic activation of gastric motility & gastric juice secretion Vagus nerve
  32. 32. Food arrival causes muscular reflexes & gastrin secretion by G cells. Gastrin stimulates secretion from both chief & parietal cells. 2. GASTRIC PHASE Gastrin GOGO FOODFOOD
  33. 33. Arrival of food in duodenum triggers release of hormones that inhibit gastric motility & secretions. 3. INTESTINAL PHASE Circulation Secretin & Cholecystokinin (CCK)
  34. 34. 1. Taste sense. 2. Smell sense. 3. Appetite. 4. Gastric irritation. 5. Fear. The following can stimulate saliva:
  35. 35. 1. Parasympathetic stimulation. 2. Sympathetic stimulation. 3. Gastrin. 4. CCK. 5. Somatostatin. The following stimulate gastric acid secretion:
  36. 36. 1. Dental caries. 2. Dry mouth. 3. Impaired overall digestion. 4. Impaired carbohydrate digestion in the mouth. 5. Dysphagia. Impaired salivary secretion can cause:
  37. 37. 1. Histamine receptors. 2. Gastrin receptors. 3. H-K ATPase receptors. 4. Ach receptors. 5. Sympathetic receptors. The final common pathway in gastric acid secretion is:
  38. 38. 1. Gastric phase. 2. Cephalic phase. 3. Intestine phase. 4. Cephalic & intestinal phase. 5. None of the above. Most of the gastric acid secretion occur in: