Digestive System-Physiology.ppt

15,850 views

Published on

2 Comments
12 Likes
Statistics
Notes
No Downloads
Views
Total views
15,850
On SlideShare
0
From Embeds
0
Number of Embeds
38
Actions
Shares
0
Downloads
727
Comments
2
Likes
12
Embeds 0
No embeds

No notes for slide

Digestive System-Physiology.ppt

  1. 1. Dr. Shamanthakamani Narendran MD (Pead), Ph.D. (Yoga Science)
  2. 2. SALIVA  A clear, tasteless, odorless, slightly acid (pH 6.8) viscid fluid, consisting of the secretion from the parotid, sublingual, and submandibular salivary glands and the mucous glands of the oral cavity.  Its function is to keep the mucous membrane of the mouth moist, to lubricate the food during mastication, and, in a measure, to convert starch into maltose, the latter action being effected by a diastatic enzyme, ptyalin.
  3. 3. Composition of saliva  Total amount = 1000 to 1500 mL/day.  More after meals and relatively less during sleep. Under resting condition % of Total Output Submandibular gland  70 . Parotid gland  25 . Sublingual gland  5 .  The volume depends on the ability of salivary glands to secrete water.  Specific gravity 1.002 to 1.012  pH slightly acidic 6.0 to 7.4
  4. 4. CONSTITUENTS OF SALIVA Water 99.5% Solids 0.5%Gases CO2, O2, N2 Cellular constituents  Yeast cells  Bacteria  Protozoa  Polymorphonuclear leucocytes  Desquamated epithelial cells Organic 0.3% Inorganic 0.2%  NaCl  KCl  CaCO3  Calcium Phosphate  Potassium thiocyanate  Acidic & Alkaline sodium phosphate
  5. 5.  It is the continuous secretion of saliva even when there are no stimulating factors.  This helps to keep the mucous membranes of mouth and pharynx moist.  This is possibly because of small amounts of Acetylcholine being secreted continuously in the glands. Spontaneous secretion
  6. 6.  Conditioned or Acquired Reflex, Cephalic phase – Stimulation of some special sense organ other than taste, eg, smell, sight or hearing or thinking about food.  Unconditioned or Inherent reflex – in this, food should be actually given or taken. (1) Reflex from the mouth; chief place for the normal unconditioned stimulus. (2) Esophogo-salivary reflex; sensory stimulus arise from esophagus. Secretion due to stimulus
  7. 7.  Gastrointestinal Phase – It occurs when food has been swallowed and reflexes originate in the stomach & upper intestine especially when irritating food is swallowed. It is also seen in many irritating conditions of stomach for instance, gastritis, gastric cancer, etc. Increased salivation before vomiting is a typical example.
  8. 8. NOTE  It is possible that stimulus for salivation may arise in other viscera also. For instance, in pregnancy increased salivation occurs. It is believed that the sensory stimulus arises from distended uterus.  As the food is chewed, the contraction of the muscles of mastication help to push out the saliva accumulated in the ducts and acini of the glands. Mastication acts not as a real stimulus but through its mechanical effect.  Nausea & disagreeable substance also cause salivary secretion.  There is no hormonal regulation.
  9. 9. Preparation of food for swallowing  Mucin acts as a good lubricant for swallowing.  Mucin softens the mass of food.  Saliva moistens the mouth and facilitates chewing & mixing of food and thus in bolus formation & deglutition. Solvent actions  Taste is a chemical sensation.  Unless the substance be in solution the taste buds cannot be stimulated.  Saliva acts as a solvent. Function of saliva
  10. 10. Antibacterial or cleansing action  Constant flow of saliva removes bacteria from any area where bacteria can grow.  Saliva contains several factors that can destroy bacteria like several proteolytic enzymes like lysozyme, thiocyanate ions.  Saliva often contains significant amount of protein antibodies that can destroy oral bacteria including those that cause dental caries. Speech  Moistening of lips and mucous membranes by saliva aids in speech.  Decrease in salivary secretion cause impairment of speech.
  11. 11. Digestive function Boiled starch Amylase and M altase Breakdown of beta-1, 4 glucosidic linkages Maltotriose and some glucose
  12. 12. Excretory function  Many substances both organic and inorganic are secreted to saliva.  In diabetes mellitus, glucose is secreted.  In Nephritis, urea is secreted  Viruses of rabies and poliomyelitis  Alkaloids like morphine and antibiotics  Alcohol content of saliva has been used for medicolegal purpose (alcohol test)  Smoker’s saliva contain thiocyanates.
  13. 13. Regulation of water balance  When liquid is lost from the body salivary glands are subjected to dehydration effect. This arouses a sense of thirst. Helps in heat loss  Frothing found in animals (dog, sheep, etc.) Removes irritating factor  Saliva helps to remove the irritating factor by diluting or neutralising it. It thus prevents injury to mucous membranes. Applied  Decrease or absence of salivary secretion  Xerostomia  Excessive salivary secretion  Sialorrhea (seen in patients with cancer of esophagus)
  14. 14. GASTRIC SECRETION, GASTRIC ANALYSIS  Gastric analysis measurement of pH and acid output of stomach contents;  Basal acid output can be determined by collecting the overnight gastric secretion or by a 1-hr collection;  Maximal acid output is determined following injection of histamine;  Output is measured by titration with a strong base.
  15. 15. Composition of gastric secretion  Volume = 1500 to 2000 mL/day (depending upon diet)  pH 0.5 to 1.5  Gastric juice is Isotonic to blood
  16. 16. CONSTITUENTS OF GASTRIC JUICE Water 99.45% Solids 0.55% Organic 0.40%  Pepsinogen (Pepsin I, II, III)  Mucin  Gelatinase, Urease, Carbonic anhydrase  Cathepsin, Gastricsin  Gastric Renin  Intrinsic factor  Lysozyme Inorganic 0.15%  HCL  NACL  KCL  CACL2  Calcium Phosphate  Magnesium Phosphate  Bicarbonates
  17. 17. Function (in short)  The enzyme pepsin, with HCL digests protein upon the stage of peptone  Renin coagulates caseinogen of milk  Gastric lipase digests fat to some degree  HCL acts as antiseptic and causes some hydrolysis of all the foodstuffs  Excretion  toxin, heavy metal, certain alkaloids, etc. Regulation of gastric secretion  It is a coordinated neurohormonal control.
  18. 18. Cephalic phase  There is reflex activity: Afferent formed by sensory pathways arising from retina (sight), tongue (taste), ear, etc. Efferent through vagus.  Since food is actually present in mouth, the gastric juice released in this phase is called Psychic or Appetite juice.  It reaches its peak within 1 hour & may persist for 3 hours.  The juice is highly acidic & rich in pepsin  Appetite juice is abolished by Atropinization or sectioning of vagi.
  19. 19. Gastric phase  In this presence of food in the stomach causes gastric secretion.  It is brought about by (1) Nervous stimulation (2) GI Hormones (Gastrin)  The gastric juice is released after a latent period of 30-60 minutes, the response lasts for 2 hours.
  20. 20. Gastric glands Nervous stimulation Long reflex or vagovagal reflex Presence of food in stomach Mucous membrane of stomach is stimulated Afferents go via the vagus Medullary centre Efferents come via vagus Synapse in the intrinsic plexuses Release of gastric juice (Gastrin) G-cells in pyloric glands
  21. 21. Gastric glands Nervous stimulation Short reflex or Intramural reflex Distension of stomach by food Mucous membrane of stomach is stimulated Afferents go to internal plexus Efferents from internal plexus Release of gastric juice Gastrin cells in pyloric glands
  22. 22. Gastrin  Produced by G-cells in the walls of the glands  G-cells are flask shaped with a broad base containing many gastric granules and a narrow apex that reaches the surface. Microvilli project from the apical end into the lumen. Molecular forms of gastrin are 1. G17 or little gastrin containing 17 amino acid residues 2. G37 or big gastrin containing 37 amino acid residues  G17 is more abundant but both are important.
  23. 23. All gastrins occur as  Sulphated form (gastrin I)  Non-sulphated form (gastrin II)  Gastrin is inactivated in kidneys & small intestine.
  24. 24. Action of gastrin  Stimulation of gastric acid secretion rich in HCL and pepsin.  Stimulation of growth of gastric mucosa  Insulin & Glucagon secretion only after a protein meal.  Increase GI Motility  Contraction of gastroesophageal junction  Increase release of (a) Succus Entericus, (b) Bicarbonates, enzymes in bile and pancreatic juice.
  25. 25. Factors affecting gastrin secretion Stimuli that increase secretion Stimuli that decrease secretion Luminal: Protein digestion product Distension of Lumen Luminal: Acid Blood Borne: Calcium, Epinephrine Blood Borne: Secretin, GIP, VIP, Glucagon, Calcitonin Neural: Vagovagal reflexes, Intramural reflexes
  26. 26. Regulation of gastrin secretion More gastrin secretion More acid released in antrum Acid feeds back to inhibit gastric secretion (-ve Feedback)
  27. 27. Intestinal Phase  Presence of gastric chyme in the upper part of small intestine cause release of gastric juice  Latent period in 2 to 3 hours. Lasts for 8 hours. Accounts for less than 20% of total acid secreted in the stomach.  An intestinal hormone, Entro-oxyntin is responsible for this phase. Inter-Digestive Phase  Even after prolonged fast, HCL is found in gastric juice of man which occurs in an intermittent fashion & cause is unknown.
  28. 28. Other factors  Which increase secretion (a) Hypoglycemia, (b) Alcohol & caffeine.  Which decrease secretion (a) Emotions, fear, grief, panic. (b) High level of [H+] in the pyloric antrum or proximal duodenum. (c) Presence of fat in duodenum (d) Presence of hyperosmolar concentration in duodenum. (e) Hormones from intestine namely GIP, Enteroglucagon, VIP, Secretin, Enterogastrone,
  29. 29. Clinical assessment of Gastric Secretion [Gastric Analysis or Fractional Test Meal] Procedure  The subject is asked to take light diet previous night & is called fasting next morning.  Ryles tube is introduced upon the second mark.  Fasting juice is collected, so as to completely empty the stomach. Juice collected is placed in a separate flask for analysis.  Any one test meal is given. There are certain standard test meals (a) 7% 50mL alcohol, (b) 300mL oat meal gruel, (c) Dry toast with a cup of tea.
  30. 30.  After giving a test meal, gastric samples are collected every 15 minutes for 3 hours. Each time about 10mL of the contents are aspirated. Each sample is placed in a separate flask for analysis.
  31. 31. Each sample is analysed as follow:  Free acid: It is titrated with standard alkali (0.1 N NaOH) till pH 3.5 is obtained. Acidity is expressed in clinical units in terms of number of milliliters of standard alkali required to titrate 100 mL of gastric sample to pH 3.5.  Total acid: Sample is further titrated with the alkali till pH 8.5 is obtained. It is expressed in clinical units as a amount of standard alkali required to titrate 100mL of gastric sample to pH 8.5.
  32. 32.  Combined acid: It includes chloride of HCL Combined HCL Combined HCL inorganic chloride etc.  Strach & Sugar: Presence indicates that stomach is not yet emptied.  Bile: It regurgitates from duodenum. Presence indicates that pyloric sphincter is open & the stomach has started emptying.  Blood: Presence in first one or two samples may be due to injury caused during the passage of Ryles tube, otherwise blood is not the normal constituent. It’s presence in all the samples indicates that there is hemorrhage which may be due to gastric ulcer or gastric cancer.
  33. 33.  Lactic acid: It is product of fermentation & therefore it is high when acid secretion is less  Mucus: Normally, some amount is present. Excess indicates that there is irritation of stomach mucosa.  Pepsin: Its presence indicates that peptic cells are functional  Tubeless gastric analysis: Cation exchange resin is given by mouth. This is dissociated in stomach by HCL. The liberated cations are absorbed & are excreted in urine. The amount of cations excreted in urine indicates the amount of acid secreted.
  34. 34.  Insulin test: Instead of standard test meal, 7 units of insulin is injected subcutaneously. This produces hypoglycemia, which stimulates Vagus nerve & causes secretion of gastric juice.  Secretion depends on integrity of Vagus nerve. Therefore the test is done after vagotomy operation which is done for treating peptic ulcer, to judge whether all vagal fibers to the stomach are cut or not.
  35. 35. PANCREATIC SECRETION  An elongated lobulated retroperitoneal gland, devoid of capsule, extending from the concavity of the duodenum to the spleen;  It consists of a flattened head (caput) within the duodenal concavity, an elongated three-sided body extending transversely across the abdomen, and a tail in contact with the spleen.  The gland secretes from its exocrine part pancreatic juice that is discharged into the intestine and from the its endocrine part the internal secretions, insulin and glucagon.
  36. 36. Composition & function of pancreatic juice  Daily output is about 2.5 liters.  pH is alkaline 7.5 to 8.5  Inorganic components are Na+, HCO3-, Cl-, etc  Organic components are the various digestive enzymes 1. Proteolytic enzymes: (a) Trypsinogen (b) Chymotrypsinogen (c) Procarboxypeptidase (d) Proelastase.
  37. 37. 2. Amylolytic enzyme (a) Pancreatic amylase 3. Lipolytic enzyme (a) Pancreatic lipase (b) Cholesterol esterase (c) Phospholipase A & B (d) Colipase 4. Nucleic acid splitting enzyme (a) Ribonuclease (b) Deoxyribonuclease.
  38. 38.  Trypsin Inhibitor: It is secreted by acinar cells & prevents the activation of Trypsinogen to Trypsin & thus prevents autodigestion of pancreas.  The enzymes are secreted into the second part of duodenum in their inactive forms.  When gastric chyme enters the duodenum, it causes secretion of Enterokinase by duodenal cells which converts trypsinogen to trypsin.
  39. 39. Blood Vessel Ductal Cell Lumen Na+ Na+ Na+ K+ K+ Active Transport K+ HCO3 - Cl- Cl- Active - (CA – Carbonic Anhydrase) H2O+CO2 CA H+ +HCO3- HCO3 - ATPase Na+ -K+ ATPase Na+ -K+ Pump
  40. 40. HCO3 - Cause  Alkaline pH by neutralising the acidity of gastric chyme thus activates pancreatic enzymes.  Stops the action of gastric pepsin. Regulation : 1. Cephalic phase : Thought, slight or smell of food  Centers in the medulla via associated pathways in the brain  Pancreas to release juice rich in enzymes  Efferent via vagus.
  41. 41. 2. Gastric phase Food in stomach  Distension of stomach  Vagovagal reflex  Pancreatic secretion rich in enzymes. 3. Intestinal phase When food reaches the Intestine, (a) The acidity of chyme cause secretion of Secretin. (b) Fatty acids & protein digestion products cause secretion of Cholecystokinin (CCK-Pz) These two hormones are absorbed & carried to liver by portal circulation.
  42. 42. Applied physiology  Acute pancreatitis Block in one of pancreatic duct Accumulation of enzymes in pancreas Trypsin inhibitor efficacy lost Accumulation of pancreatic enzyme in pancreas Conversion of enzyme into active forms in pancreas Autodigestion of pancreas.
  43. 43. Applied physiology  Cystic fibrosis Acini become fibrosed No secretion of enzyme Pancreatic insufficiency
  44. 44. Pancreatic sufficiency test  Small fraction of Pancreatic enzymes enter the blood either via lymphatics or directly.  When there is a block in the pancreatic duct, the enzymes in the acini are reabsorbed & their blood concentration becomes higher.  Serum Amylase Activity: 60 to 180 Somogyi units.
  45. 45.  In Acute Pancreatitis, this value becomes 500 Somogyi units.  Normal urine contains small traces of amylase which rise in Acute Pancreatitis.  Fecal fat content: In Pancreatic insufficiency. Pancreatic lipase is absent. Triglycerides are not broken down & therefore heavy amount of fat in stool, ie, Steatorrhea.  Normal action of CCK-Pz and Secretin is lost in Pancreatitis.
  46. 46. BILE The yellowish brown or green fluid secreted by the liver and discharged into the duodenum where it aids in the emulsification of fats, increases peristalsis, and retards putrefaction; contains sodium glycocholate and sodium taurocholate, cholesterol, biliverdin and bilirubin, mucus, fat, lecithin, and cells and cellular debris.
  47. 47.  Bile from hepatocytes  hepatic ducts  Liver Bile  Bile evacuated from gallbladder and delivered into the duodenum via common bile duct is called Gall Bladder Bile.  Daily output of bile is 0.5 to 1 litre.  Osmolarity of bile is 300 millosmole/liter, ie, same as of plasma & isotonic with blood.
  48. 48. Liver Bile Gallbladder Bile 1. Specific gravity 1.010 to 1.011 1.026 to 1.040 2. pH definitely alkaline 8.0 to 8.6 slightly alkaline or slightly acidic 6.8 to 7.6 3. Water 98% 89% 4. Organic constituents in gm% a. Bile salts b. Bilirubin c. Cholesterol d. Lecithin e. Fatty acids 1.1 0.04 0.1 0.04 0.12 0.6 0.3 0.3 to 0.9 0.3 0.3 to 1.2
  49. 49. Liver Bile Gallbladder Bile 5. Inorganic constituents in mEq/lit a. Na+ b. K+ c. HCO3 - d. Cl- e. Ca++ 145 5 28 100 5 130 12 10 25 23
  50. 50. Bile acids via blood stimulate parenchymal secretion Vagal stimulation causes weak contraction of gallbladder Cholecystokinin via blood stream causes 1. Gallbladder contraction 2. Relaxation of sphincter of Oddi Bile stored and concentrated up to 15 times in gallbladder Secretin via blood stream stimulates liver ductal secretion
  51. 51. Most of the bile synthesized in hepatocytes are recycled by means of Enterohepatic Circulation. Bile enters the second part of duodenum through common bile duct and proceeds downwards For the upper small intestine  Bile is absorbed by diffusion From ileum & upper colon  Bile is absorbed by active transport. Into portal venous  to liver sinusoids  picked up by hepatocytes  into bile canaliculi  Bilary tree Again to duodenum
  52. 52.  80-90% of bile salts are absorbed from the small intestine.  10-20% enter the colon & are converted to salts of lithocholic acid & deoxycholic acid which are excreted in stool.  The total bile acid pool [3.5g] recycles via Enterohepatic Circulation & the entire pool recycles twice/meal and 6-8 times/day.
  53. 53. Bile acids  Synthesized by the hepatocytes from cholesterol.  2 types (a)Primary Bile acids  Cholic acid & Chenodeoxycholic acid; (b)Secondary Bile acids  Deoxycholic acid & Lithocholic acid  Primary bile acids are converted bile acids by the action of bacteria in ileum & colon by removal of the hydroxyl group.  Secondary bile acid reenters the portal circulation and the liver & are again excreted via Enterohepatic Circulation by liver as secondary bile acid only.
  54. 54. Bile salts:  Bile acids are conjugated with either taurine or glycine and in our body these acids are present either as sodium taurocholate or as sodium glycocholate which are therefore known as bile salts. Micellar formation:  When bile acid concentration reaches 2-5 millmoles/lit, bile salts tend to form Micelles  The concentration of bile salts at which they form micelles is called Critical Micellar Concentration.
  55. 55.  Micelles are Amphipathic, ie, they have both hydrophilic & hydrophobic parts.  In a micelle, the bile salts are present like spades of a bicycle while phospholipids interdigitate.  The hydrophilic polar side of the bile salts & phospholipid are in the peripheral side while the hydrophobic nonpolar ends are present in central region.  Such a micelle can carry cholesterol & triglycerides which go to occupy central region.
  56. 56.  Cholesterol & triglycerides are water insoluble but when they are within the micelle they are water soluble because micelle is water soluble. Cholesterol Bile salts Phospholipid Triglyceride
  57. 57. Bile Lipid : Bile acid + cholesterol  Bile pigments: Bilirubin [Major] & Biliverdin  Bilirubin formed from the hem portion of hemoglobin.  In the liver, bilirubin is conjugated with glucuronic acid to form Bilirubin Glucuronide & is secreted in the bile.
  58. 58. Control of bile secretion  Bile acid dependent flow (BADF) Bile formed in liver  Bile stored in gallbladder  Gallbladder contracts  Bile enters duodenum  80-90% bile salts reabsorbed from small intestine  Carried to liver through blood stream  Bile salts stimulates liver  More bile formed  Bile enters duodenum.  Bile acid independent flow (BAIF) Some flow of bile occurs from liver without the effect of bile acid.
  59. 59.  Ductular secretion: Ductules of biliary tree secrete H2O & HCO3 - Amount of bile from common bile duct = BADF + BAIF + Ductular secretion  Influence of foodstuff: Fats & proteins stimulate bile secretion. Carbohydrate have no such effect.  Secretin: Increases bile flow, so it is suggested that Hepatocrinin may be a specific liver hormone present in intestine released by the action of food.  It has been noted that bile secretion increases about 1 hour after meal, remains high for about 2- 5 hours and then declines.
  60. 60. Function of bile Bile is essential for life  Digestion: Bile is essential for the complete digestion of fats and to some extent of proteins and carbohydrates. This action is due to the presence of bile salts, which act in the following ways. (a) By reducing surface tension, (b) Activating action, & (c) Solvent action  Absorption: bile helps in the absorption of various substances. This is also due to presence of bile salts. (a) Fats – (1) Hydrotropic action, (2) Bile salts reduce the surface tension of the absorbing epithelium; (b) Iron, calcium, & (c) Vitamin A, D, E, & K
  61. 61.  Excretion. Certain substances are excreted through bile, for instance (a) Some metals like copper, zinc, mercury, etc., (b) Toxins, bacteria, etc., (c) Bile pigments, (d) cholesterol and lecithin are probably chief excretory products.  Laxative action. Bile salts stimulate peristalsis. When introduced directly into the colon it stimulates peristalsis of these parts.  Cholagogue action. Bile acts as its own stimulant.  Bile helps to maintain a suitable pH of the duodenal contents and thus helps the action of all enzymes.
  62. 62.  Lecithin and cholesterol, present in bile, also help in some ways.  Mucin of bile acts as a buffer and a lubricant.  Regurgitation of bile in the stomach helps to neutralize gastric acidity and thus prevents the injurious effect of acids on gastric mucosa.  From the above functions it is evident that bile is important not only as digestive juice but also for various other purposes.
  63. 63. GASTROINTESTINAL HORMONES  They are hormonally active polypeptides that play a role in regulation of gastrointestinal secretion & motility.  Few of these hormones act as neurotransmitters in the intrinsic plexus of nerves of GIT.  They are also found in the brain where they act as neurotransmitters, hence they are called Gut Brain Peptides.
  64. 64. Sources:  The GI hormones are secreted by the APUD cells.  APUD cells (amine precursor uptake & decarboxylation) mainly take up amine precursor & decarboxylation them to give GI hormones.  APUD cells are of neural crest origin.  Also found in hypothalamus, islets of langerhans, lung, etc.
  65. 65. The GI hormones are:  Gastrin  Gastric Releasing Peptide  Glicentin  Serotonin  Somatostatin  Bombesin  Neurotensin  Vasoactive Intestinal Peptide (VIP)  Gastric Inhibitory Peptide (GIP)  Glucagon  Secretin  Substance P  Cholecystokinin- Pancreozymin (CCK-Pz)  Motilin  Opiod Peptides
  66. 66. Classification:  Gastrin family  Primary members are Gastrin & CCK-Pz.  Secretin family  Primary members are Secretin, Glucagon, Glicentin, VIP, GIP 1. Gastrin  Chemistry: Macroheterogenic forms 34 Amino acids (G-24) 17 Amino acids (G-17) 14 Amino acids (G-14) Microheterogenic forms C-terminal tetrapeptide N- terminal tetrapeptide Sulphated & nonsulphated forms Amidated & nonamidated forms G17 is the principal form
  67. 67. 2. Cholecystokinin – Pancreozymin (CCK-Pz or CCK) Macroheterogenic forms CCK-58 (58 amino acids) CCK-39 CCK-33 CCK-12 CCK-8 C-terminal tetrapeptide Microheterogenic forms Sulphated form (7th amino acid residue is sulphated) Amidated form (C-terminal amidated)
  68. 68. Factors  Luminal factors  Positive feedback effect of bile and pancreatic juice  Secretin
  69. 69. DEGLUTITION  Deglutition or swallowing is a complicated mechanism, principally because most of the time the pharynx subserves several other functions besides swallowing & is converted only for a few seconds at a time into a tract from propulsion of food.
  70. 70.  Deglutition or swallowing: To pass anything through the fauces, pharynx, and esophagus into the stomach; to perform deglutition.
  71. 71. About 2400 swallows/day  It is divided into 3 stages Oral  Voluntary  It initiates swallowing Pharyngeal  Involuntary  It involves passage of food from pharynx to esophagus Esophageal  Involuntary  It promotes passage of food from the esophagus to stomach
  72. 72. Nervous control of pharyngeal stage Afferent Ring of nerve plexus of pharyngeal opening with greatest sensitivity in the tonsillar pillar via Trigeminal, Glossopharyngeal, Vagus Nucleus  Tractus Solitarius  Nucleus ambiguous Efferent To pharyngeal musculature & tongue via 5the, 9th , 10th , 12th cranial nerves & even a few of superior cervical nerves.
  73. 73.  The areas in the medulla & lower pons that control swallowing or deglutition are collectively called swallowing or deglutition centers.  Deglutition apnea is the inhibition of respiration during act of deglutition in the pharyngeal stage lasting for 1 or 2 seconds. The centers of respiration & deglutition are situated close by in the medulla. The swallowing enter specifically inhibits the respiratory center of medulla during this time, halting respiration at any point in its cycle to allow swallowing to proceed.
  74. 74. Receptive relaxation of stomach:  As the food in the esophagus reaches the lower end of esophagus due to the esophageal peristaltic wave passing towards the stomach, a wave of relaxation transmitted through myenteric Inhibitory neurons precedes the constriction.  Furthermore, the entire stomach and to lesser extent, even the duodenum becomes relaxed as the wave of relaxation reaches the lower end of esophagus and thus are prepared ahead of time to receive the food propelled down the esophagus during swallowing act.
  75. 75. Nervous control:  Peristaltic waves are initiated by vagal reflexes that are a part of the overall swallowing mechanism.  Lower Esophageal Sphincter (LOS):  The lower end of esophagus, extending from about 2 to 5 cm above its junction with the stomach is thickened & functions as a LOS or Gastroesophageal Sphincter.  Physiologically, it remains tonically contracted in contrast to the middle and upper part of esophagus which normally remains completely relaxed.
  76. 76.  When a peristaltic swallowing wave passes down the esophagus, Receptive relaxation relaxes the LOS ahead of peristaltic wave & allows easy propulsion of swallowed food into stomach.  The stomach contents are highly acidic & contain many proteolytic enzymes.  The esophageal mucosa, except in the lower 1/8th of the esophagus is not capable of resisting for long the digestive action or gastric secretion. Fortunately, the tonic constriction of the LOS helps to prevent significant reflux of stomach contents into the esophagus except in abnormal conditions.
  77. 77. Applied  Achalasia cardia: Failure of LOS to relax or dysphagia.  Heartburn: Reflex of gastric contents into the esophagus giving rise to burning sensation at the lower end of esophagus.  Belching: The voiding of gas or of a small quantity of acid fluid from the stomach through the mouth.  Paralysis of muscle of Palate: Failure to seal off the nasopharynx from the buccal cavity.
  78. 78. Methods of study  Barium swallow [Rat-tail appearance of Achalasia cardia].  Intraluminal pressure measurement by balloons.  Open tipped tubes  transducers.  Esophagoscopy.
  79. 79. MOVEMENTS OF SMALL INTESTINE The types of movements of small intestine are  Mixing contraction or Segmentation contraction  Propulsive or peristaltic contraction  Pendulous contraction  Movements of villi.
  80. 80. Mixing contraction  When a portion of the small intestine becomes distended with chyme, the stretch of the intestinal wall elicits localized concentric or ring-like contractions spaced at intervals along the intestine  The segments between these contraction may be 1 cm in length  Contracted part relaxes & the ballooned up relaxed part forms a concentric contracted ring.  Each time a new set of contraction develops at a different point.  Development & rate (frequency) of these contractions is based on basic electric rhythm or electrical changes in the intestinal muscles.
  81. 81. Mixing contraction - Functions  It helps in digestion due to proper mixing of food with enzymes of digestive juices  In absorption due to constantly changing the layer of fluid in contact with mucosa and pressure  In improvement of intestinal circulation It is slightly propulsive in nature also and are reflex response related to local myenteric plexus.
  82. 82. Peristaltic contraction  Peristalsis is described to be a composite wave, consisting of a wave of relaxation followed by a wave of constriction. It is a translatory movement and travels down the gut in an aboral direction.  Bayliss & Starling or Law of Intestine or Myentric Reflex.  Peristaltic & rhythmic segmenting are present simultaneously.  Rush Wave or Peristaltic Rush.  Gradient of rhythirsicity.
  83. 83. Peristaltic contraction - Causes  Stimulation of vagus increases and that of sympathetic inhibits peristalsis  Vagotomy on the other hand decreases the peristaltic activity only to a minor extent.  The local nerve plexus (Auerbach’s plexus) helps in coordination of peristaltic movement.  Distention of the intestine, normally caused by presence of food, movements due to a stretch reflex – Myentric reflex  Reflex inhibition of whole of the small intestine may take place due to stretching of lower part of small intestine.
  84. 84.  These inhibitions may be removed by stimulation of splanchnic nerves.  Presence of local nerve plexus are required for this & the afferent receptors of which are present in the mucous membrane of intestine.  Liberation of 5-Hydroxytryptamine (Serotonin) from the enterochromaffin cells is possible mediator in this reflex action.  Role of a basic polypeptide substance P as a mediator has also been suggested.  Role of endocrines: Pituitrin excites the movements.  Gastroileal reflex.
  85. 85. Peristaltic contraction - Functions  Chief function is propagation of the food.  Other functions are same as of segmentation movement.
  86. 86. Pendular contraction  2 important movement of intestine are mixing and propulsions.  End segment of intestine show side-to-side movement called pendular movement  They facilitate progress of chyme & also help in mixing digestive juices with food and increasing blood flow to intestine which enables maximum absorption.
  87. 87. Movements of Villi  Side-to-side movement – Help admixture & absorption.  Pumping movement – Help in increase flow of blood and lymph  Protecting action due to the contraction of muscularis mucosa.
  88. 88. THE SMALL INTESTINE – Evoked Movement & Evoked Digestive Process Duodenum  Evoked Movement: Non-propulsive peristalsis (contraction with no preliminary relaxation) and rhythmic segmenting movements involve the circular muscle and are regulated by the myenteric plexus. Pendular (swaying) movements alternate with the above, and involve the longitudinal muscle. These movements thoroughly mix the chyme with intestinal, pancreatic & hepatic secretions.
  89. 89. Duodenum  Evoked Digestive Process: Secretion and Breakdown. Food contacts mucous membranes lining intestine, activating release of secretin + cholesystokinin. These, along with vagal activation, trigger release into duodenum of 1) pancreatic enzymes via pancreatic duct; 2) bile from gall bladder via hepatic duct. Breakdown of protein, fat and carbohydrates into amino acids, monosaccharides and fatty acids is carried out.
  90. 90. Jejunum  Evoked Movement: Propulsive peristalsis (contraction preceded by relaxation) is regulated by the myenteric plexus acting on both circular and longitudinal muscle. This moves the contents toward ileum.  Evoked Digestive Process: Absorption. Breakdown products are actively transported from intestinal lumen to blood and lymph vessels by epithelial cells in the luminal brush border.
  91. 91. Ileum  Evoked Movement: Propulsive peristalsis same as above Reflex relaxation of the ileocecal valve, contents pushed into cecum of large intestine.  Evoked Digestive Process: Absorption. Similar, but less as chyme moves toward cecum. Remember: Ilium has fewer/lower plicae circularis, and more/shorter vasa recta than does jejunum.
  92. 92. GI WALL CROSS SECTION
  93. 93. Ileocecal valve & ileocecal sphincter  Principal function of ileocecal valve is to prevent back flow of fecal contents from the colon into small intestine.  The lips of the ileocecal valve protrude into the lumen of the cecum and therefore are forcefully closed when excess pressure builds up in cecum & tries to push the cecal contents backward against the lips.  The valve usually can resist reverse pressure 50-60 cm of water.
  94. 94.  The wall of the ileum from several centimeters immediately preceding the ileocecal valve has a thickened muscular coat called the ileocecal sphincter.  This sphincter normally remains mildly constricted and slows the emptying of ileal contents into cecum except immediately after a meal, when a gastroileal reflex intensifies the peristalsis in the ileum.  The resistance of emptying at the ileocecal valve prolongs the stay of chyme in the ileum and thereby facilitates absorption. Only about 1500 mm of chyme empty into the cecum each day.
  95. 95. Feedback control of the ileocecal sphincter:  Whenever cecum is distended, the contraction of the ileocecal sphincter is intensified and heal peristalsis inhibited which greatly delays emptying of additional chyme from the ileum.  Any irritant in the cecum delays emptying for instance, an inflamed appendix can cause such intense spasm of the ileocecal sphincter and paralysis of the ileum that they block emptying of the ileum.  These reflexes are mediated both by the way of the myenteric plexus in the gut wall itself and through extrinsic nerves especially reflexes by way of the prevertebral sympathetic ganglia.
  96. 96. GASTRIC EMPTYING  Food entering stomach is a mixture of solids & liquids but as it passes through pylorus, it is liquid chyme.  Gastric emptying depends on (a) Balance between force & frequency of gastric peristalsis. (b) Pyloric resistance.
  97. 97. Factors influencing gastric emptying  Distension of stomach  Effects of composition of chyme  Osmolarity of chyme  Effect of fat  Effect of acid  Products of protein digestion  Effect vagal stimulation  Hormones
  98. 98. MASTICATION  The process of chewing food in preparation for deglutition and digestion; the act of grinding or comminuting with the teeth.  It is the rhythmic movement of the Jaws, tongue, & lips when the food is in the mouth.  It takes place at temperomandibular joint  It is the first mechanical process to which the food subjected to in its progress though the GIT.  Incisors for cutting, Molars for grinding
  99. 99. Chewing reflex  The presence of bolus of food in mouth causes reflex inhibition of muscles of mastication & the lower jaw drops down.  The initiates the stretch reflex of the jaw muscles that leads to rebound contraction.  This automatically leads to closure of teeth, but it alos compresses the bolus of food against the lining of mouth, which inhibits the jaw muscles once again, allowing the jaw to drop & to rebound.
  100. 100. Saliva: It assists in mastication as follows:  By dissolving some of readily soluble food components.  By partly digesting starch in the food by action of enzyme alpha-amylase (Ptyalin)  It softens the mass of food  By converting the bolus with mucus to make it move about easily.
  101. 101. Muscles of mastication :  Masseter, temporalis, medial & lateral Pterygoids supplied by mandibular nerve.  Buccinator supplied by facial nerve. Centres of mastication :  Areas of reticular formation  Hypothalamus & Amygdaloid  Lower part of postcentral gyrus.
  102. 102. Importance of mastication :  It adds to the pleasure of eating tasty food and gives a sense of contentment and satisfaction.  Prolonged stimulation of taste sensation may increase the secretion of digestive juices.  Chewing of fruits & vegetables is important as the cellulose covering around the nutrient part must be broken before swallowing.
  103. 103.  Digestive enzyme act only on the surface area & the rate of digestion highly depends on the total surface area of food particles exposed to the digestive secretion.  The smaller size of food particles increase the ease with which food is emptied from stomach into the intestine.
  104. 104. FUNCTIONS OF LARGE INTESTINE  Absorption of water & electrolytes and important nutrient substances except fatty acid.  Acts as a temporary storage space for waste products of digestion.  Acts as an incubator for various bacteria which synthesize certain vitamins like Vit K & Vit B complex & contribute to overall nutritional status of individual.
  105. 105.  During its prolonged stay in colon, water is absorbed from chyme so that 1000-1200 mL of chyme which enters the cecum per day is transformed to semisolid mass called feces which is 150-200 mL/day  Movements of large intestine are comparatively slower and may be due to the poor development of myenteric plexus and it is scanty extrinsic innervation by vagus.
  106. 106.  Mucus in large intestine has – prevents excoriation, provides adherent qualities for holding fecal matter together, protects intestinal wall from great amount of bacterial activity occurring in feces, alkalinity of mucus secretion provides a barrier to prevent acids formed deep in feces from attacking intestinal wall.  Secretion of water & electrolytes in response to irritation.  Absorption of sodium
  107. 107. THE LARGE INTESTINE – Evoked Movement & Function Cecum  Evoked Movement: Pulls valve edges together, closing it.  Function: Contents prevented from reflux into ileum.
  108. 108. Ascending, transverse, and descending colon  Evoked Movement: Rhythmic, segmenting movements (under control of myenteric plexus and circular muscle) are weak due to low intrinsic and extrinsic (vagal & pelvic splanhnic) innervation. Peristaltic movements are strong, under control of myenteric plexus; the longitudinal muscle (=teniae coli), shortens and widens the colon; and the circular muscle pushes the colonic contents caudally.  Function: Contents exposed to mucosal surface, and water is reabsorbed, leaving the waste products of digestion. Empty the contents of one section into the next.
  109. 109. Rectum  Evoked Movement: Involuntary reflex. Stretching causes opening (i.e. inhibition) of the internal anal sphincter (circular smooth muscle). Autonomic innervation (via parasympathetic preganglionics of the sacral cord, and postganglionics of the myenteric plexus) aids inhibition. Voluntary control. Somatic motor neurons in the sacral cord inhibit contraction of the external anal sphincter (striated muscle) via the pudendal nerves.
  110. 110.  Function: Fecal contents accumulate, gradually raising pressure on the external anal sphincter. Fecal contents expelled.
  111. 111. DEFECATION
  112. 112. BASAL METABOLIC RATE  Oxygen utilization of an individual during minimal physiologic activity while awake; an obsolete test determined by measuring oxygen consumption of a fasting subject at complete bodily and mental rest and a room temperature of 20°C.  Energy, in terms of heat, produced as a by- product of total cellular metabolism is essential for the maintenance of life of the organism.
  113. 113.  The amount of energy, required for any individual varies directly with the degree of activity and environmental condition, but the rate of energy production in an individual by it’s overall cellular metabolism is more or less constant under some standard condition known as Basal Metabolism.  The rate of its energy production at basal condition per hour & per sq. meter of body surface area is known as Basal Metabolic Rate.
  114. 114. The basal conditions  The person should be awake but at complete rest, both physical & mental.  The person should remain in normal condition of environment, ie, at normal temp, pressure, humidity.  The person should be without food at least for 12-18 hours, ie, in the postabsorptive state.  The person should be without food at least for 12-18 hours, ie, in the postabsorptive state.
  115. 115.  The BMR may be defined as the amount of heat given out by a subject who, though awake, is lying in a state of maximum physical & mental rest under comfortable physical & mental rest under comfortable conditions of temperature, pressure, & humidity, 12-18 hours (postabsorptive) after meal.  BMR is expressed as the heat production per sq metre of body surface per hour.  In adult male – normal BMR = 40 calories/m2 /hr.  In adult female – normal BMR = 37 calories/m2 /hr.
  116. 116. BMR Determination  Direct calorimetry.  Indirect calorimetry.  Benedict-Roth Spirometer (only BMR)  Douglas Bag (BMR & Metabolic Rate)
  117. 117. Measurement  Measure the oxygen consumption of the subject using Benedict-Roth apparatus.  O2 consumption per hour is determined & it is then multiplied with 4.825 cal to obtain the heat production per hour. Obtained value is then divided by the surface area – of the person, to get the final result.  BMR  Total heat production / hour Body surface area (m2 )
  118. 118.  Comparing the BMR of the subject with that of normal person is expressed as % Difference = Difference in BMR x 100 / Normal BMR Reads formula: Bedside method  BMR = 0.75 [PR + 0.74 x 99] –72  PR = Pulse Rate, PP = Pulse Pressure
  119. 119. Factor affecting BMR  Surface area & BMR are inversely related.  Age: BMR is low in newborn; but it is higher in small children and is maximum at 5-6 yrs. It then gradually decreases with age advancement  Sex:BMR of males is higher than females of same built & age.  Season: BMR decreases in summer months, but increases in winter.  Racial variations of BMR are also observed.  Sleep: BMR decreases by 10-15% in sleep.  Drugs: Caffeine, benzedrine, etc. increase the BMR. The reverse in observed by anesthetics.
  120. 120.  Hormones: Thyroid hormone, growth hormone. Epinephrine etc. increase BMR of many tissues of our body.  Habit: Trained athletes and manual workers have a slightly higher BMR than persons leading a sedentary life.  Diet: Prolonged undernutrition lowers the metabolic rate.  Pregnancy: BMR of pregnant woman is the sumtotal of her own metabolism as in her non- pregnant state & combined with that of the fetus.  Body temperature: BMR increases by about 12% with the rise of 10 C [such as fever]
  121. 121. Conditions increasing BMR  Hyperthyroidism  Fever  Cardiorenal disease with dyspnea [25-50%]  Leukemia [21-80%]  Polycythemia [10-40%], etc.
  122. 122. Conditions decreasing BMR  Starvation & undernutrition  Hypothyroidism  Addition’s disease  Lipid nephrosis, etc. Importance of nothing BMR  For prescribing a diet of adequate caloric value.  For the diagnosis of various pathological conditions specially in hypothyroidism & hyperthyroidism.  To note the effect of different types of food & drug on BMR.
  123. 123. BALANCED DIET  A diet is the kinds of food on which a person or group lives.  A balanced diet is defined as one which contains variety of foods in such quantities and proportions that the need for energy, amino acids, vitamins, minerals, fats, carbohydrates, and other nutrients is adequately met for maintaining health, vitality and general well being and also makes a small provision for extra nutrients to withstand short duration of leanness.
  124. 124.  The dietary pattern varies widely in different parts of the world.  It is generally developed around the kinds of good produced depending upon the climatic conditions of the region, economic capacity, religion, customs, taboos, tastes and habits of the people.
  125. 125. Nutrients Main functions Carbohydrates Energy Fats Energy Proteins Energy Protection against infection Growth and repair Minerals & Water Growth repair Regulation of tissue infection Vitamins Protection against infection Regulation of tissue function
  126. 126. Dietary goals recommended by WHO are as below  Dietary fat should be limited to approximately 20- 30% of total daily intake.  Saturated fats should contribute no more than 10% of the total energy intake. Unsaturated vegetable oils should be substituted for remaining fat requirement.  Protein should constitute approximately 15-20% of the daily intake.  Carbohydrates rich in natural fibre should constitute the remaining food energy. Excessive consumption of refined carbohydrates should be avoided.
  127. 127.  Sources rich in energy such as fats and alcohol should be restricted.  Salt intake should be reduced to an average of not more than 5 g per day.  Junk foods such as colas, ketchups and other foods that supply empty calories should be reduced.  The diet should be adapted to special needs of growth, pregnancy, lactation, physical activity, medical disorders (eg. Diabetes)
  128. 128. The dietary sources of energy are  Proteins  4 kcal/g  Fats  9 kcal/g  Carbohydrates  4 kcal/g Broadly the total energy requirement of an individual is made up of 3 components  Energy required for Basal Metabolism  Energy required for daily activities – walking, sitting, standing, dressing. Etc.  Energy expenditure for occupational work – light work, moderate work, heavy work.
  129. 129. Nutritional problems in public health  Low birth weight  Protein energy malnutrition. Clinical forms – Kwashiorkor and Marasmus  Vitamin deficiencies – Xerophthalmia (dry eye) refers to all the ocular manifestations of vitamin A deficiency  Nutritional anemia  Iodine deficiency disorders  Endemic fluorosis seen in many parts of world where drinking water contains excessive amounts of fluorine (3-5 mg/l)
  130. 130. Nutritional factors important in selected diseases  Cardiovascular disease  Diabetes  Obesity  Cancer Conclusion  A balanced Diet has become an accepted means to safeguard a population from nutritional deficiencies.

×