Gastrointestinal physiology


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Gastrointestinal physiology

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  • Insert Process Fig. 24.12 with verbiage. Insert Animation: Hydrochloric Acid Production by Parietal Cells in the Gastric.exe
  • Insert Process Fig. 24.13 A. Insert Animation: Three Phases of Gastric Secretion.exe
  • Insert Process Fig. 24.13 B with verbiage. Insert Animation: Three Phases of Gastric Secretion.exe
  • Insert Process Fig. 24.13 C with verbiage. Insert Animation: Three Phases of Gastric Secretion.exe
  • The tongue is the only muscle in the body attached at one end
    Tongue Held Down Tight
    Have you ever wondered what keeps you from swallowing your tongue? Look in the mirror at what's under your tongue and you'll see your frenulum (say: fren-yuh-lum). This is a membrane (a thin layer of tissue) that connects your tongue to the bottom of your mouth. In fact, the whole base of your tongue is firmly anchored to the bottom of your mouth, so you could never swallow your tongue even if you tried!
    Thou mayest preserve discretion and that thy lips may keep knowledge Proverbs 5:2
  • Why you need saliva to taste foods. In order for food to have taste, chemicals from the food must first dissolve in saliva. Once dissolved, the chemicals can be detected by receptors on taste buds.
    Saliva also breaks down food caught in the teeth, protecting them from bacteria that cause decay. Furthermore, saliva lubricates and protects the teeth, the tongue, and the tender tissues inside the mouth.
    Excessive saliva can be caused by either an increase in your body's production of saliva or a decrease in your ability to swallow or keep saliva in your mouth.
    Causes of increased saliva production
    Dentures that are new or don't fit well
    Infection in your mouth
    Medications, such as clozapine, isoproterenol, pilocarpine and reserpine
    Stomatitis (an inflammation of mucous membranes in your mouth)
    Rarer causes of increased saliva production include the following conditions:
    Arsenic poisoning
    Bell's palsy (a condition that causes facial muscle weakness or paralysis)
    Esophageal atresia (a disorder present at birth in which the esophagus doesn't develop properly)
    Mercury poisoning
    Rabies (a deadly virus spread to people from the saliva of infected animals)
    Syphilis (a bacterial infection usually spread by sexual contact)
    Tuberculosis (an infectious disease that affects your lungs)
    Causes of a decreased ability to swallow or to retain saliva in your mouth
    Acute sinusitis
    Enlarged adenoids
    Tumors that affect your tongue or lip movement
    Conditions that affect your muscle coordination or the function of your oral cavity also may decrease your ability to swallow or to retain saliva in your mouth. These conditions include:
    Cerebral palsy (a disorder that affects your ability to coordinate body movements)
    Down syndrome
    Multiple sclerosis (a disease in which your body's immune system attacks the sheath that covers your nerves)
    Parkinson's disease
  • “Food going down the wrong hole” Trachea( respiratory syst.)
    You have 2 tubes connected to your mouth. One is your oesophagus, the normal route for food, the other is your trachea which is involved in respiration.There are several safety mechanisms present to prevent food/drink going down the wrong way. The first is a skin flap at the back of your throat called the epiglottis. This covers your trachea when you swallow food. On top of your trachea is your larynx, which contains your vocal cords. These cords will close and go into spasm if food/water gets to them. Finally if the food/water gets into your trachea, you have a cough reflex which should expel it.
  • Sensory Nerves
    Nerve signals originating in the mouth bring information to the brain about the food we are chewing. For instance they "tell" the brain about the size, temperature and texture of food. This information directs the efforts of the muscles of chewing which work together to generate a food bolus that is suitable for swallowing. As the swallowing reflex advances through its different phases, these nerves trigger the reflexive closing of the larynx and the epiglottis, which prevent food and liquid particles from entering the lungs.
     swallowing is one of the most complicated tasks performed by the nervous system. It occurs in three sequential phases that require the carefully coordinated function of muscles in the mouth, pharynx, larynx and esophagus -- all of which are under the control of cranial nerves.
     sensory nerves involved in swallowing:
    Trigeminal (cranial nerve V)
    Facial (cranial nerve VII)
    Glossopharyngeal (cranial nerve IX)
    Vagus (cranial nerve X)
    Cranial Nerve Nuclei
    The muscles of swallowing are controlled by several cranial nerve nuclei. These are:The nucleus ambiguous (of the vagus and glossopharyngeal nerves)
    The dorsal motor nucleus (of the vagus nerve)
    The hypoglossal nucleus (of the hypoglossal nerve)
  • The nasopharynx (epi)(nasal part of the pharynx) is the uppermost part of the pharynx. It extends from the base of the skull to the upper surface of the soft palate;[1] it differs from the oral and laryngeal parts of the pharynx in that its cavity always remains patent (open).
    The Oropharynx(meso) (oral part of the pharynx) reaches from the Uvula to the level of the hyoid boneThe Laryngopharynx (hypo)the portion of the pharynx below the upper edge of the epiglottis, opening into the larynx and esophagus
  • The esophagus is 25cm long.
    From the mouth, the bolus is passed through the pharynx into the esophagus.
    The esophagus conducts food to the stomach by peristalsis.
    Skeletal muscles surround the esophagus just below the pharynx and form the upper esophageal sphincter.
    Smooth muscles in the last portion of the esophagus form the lower esophageal sphincter.
  • Achalasia-decreased mobility of the lower 2/3 of the esophagus along with constriction of the LES
  • 2)Heartburn can occur after a large meal, which can raise the pressure in the stomach enough to force acid into the esophagus.
    Gastro-esophageal reflux can also cause coughing and irritation of the larynx in the absence of any esophageal symptoms.
    5) The acid in the esophagus triggers a secondary peristaltic wave and also stimulates increased salivary secretion.
    This helps to neutralize the acid and clear it from the esophagus.
  • The enzymes secreted by the pancreas digest respectively:
    Nucleic acids to fatty acids
    Amino acids
  • Zymogen secretion protects pancreatic cells from autodigestion
  • Note pancreatic secretion increases during a meal, mainly as result of stimulations by hormones secretin a primary stimulant of bicarbonate secretion. Secretin major stimulus is the acidity of the deodenum
    The afferent nerve ending of the intestinal wall is acted upon by luminal and fatty acids which initiates reflexes that acts on the pancreas thus increasing both enzyme and bicarbonate secretion.
    Note cephalic and gastric stimuli also play a role in the pancreatic exocrine secretion. This is possible by way of the parasypathetic nerves to the pancreas. Therefore the taste of foods or the distension of the stomach by food will lead to increased pancreatic seceretion.
  • (*)It is for this effect insulin is best known. Failure of glucose transport is the main characteristic of and the acute risk associated with diabetes
    Where amino acid concentration increases in the blood after ingestion of a protein containing meal. Therefore increasing plasma glucose which stimulates the uptake of these amino acids by the muscle an other cells thereby lowering their concentration.
    In the case of hormonal control an example would be GIP (glucose-dependent insulinotropic peptide) which is secreted by endocrine cells in the GI tract in response to eating stimulates insulin secretion. With this mechanism insulin is secreted earlier and therefore not dependent on blood glucose level only thus avoiding peaks in the blood glucose concentration (for example just after meal time)
  • Its major physiological effects are in the liver and opposes those of insulin
    The end result of these chain of events would be increased plasma concentration of glucose and ketones which are important for the postabsorptive period and to prevent hypoglycemia.
  • Note bile contains six major ingredients these are:
    Bile salts
    Lecithin (a phospholipid)
    Cholesterol (The liver also secrets cholesterol from the blood into bile)
    Bile pigment and small amounts of other metabolic end products
    Trace metals
    Bicarbonate ions and other salts
  • A small cross section of the liver showing the location of the bile canaliculi and ducts with respect to blood and liver cells. The bile (green) is formed by uptake by liver cells (hepatocyte) of bile salts and secreted into bile canaliculi
  • The cyclic pathway of bile salts is known as enterohepatic circulation
    Note a small amount of bile salts escapes during is cycle and is lost in feces. This however, does not hamper bile’s most important component as the liver synthesizes cholesterol to replace them.
  • The predominate bile pigment is bilirubin which is yellow in colour thus urine gains it colour from bilirubin. Note while passing through the intestinal tract some bile pigments are absorbed into the blood, others undergo bacterial enzyme modification gaining a brown colour characteristic to that of feces where as, the remainder is excreted via urine.
  • The sphincter of oddi relaxes shortly after the start of a fatty meal while, the gallbladder contracts discharging concentrated bile into the duodenum.
    The hormone CCK (cholecystokinin) is responsible for signaling gallbladder contraction and sphincter relaxation
    Age group Amount of calcium to consume daily, Age group in milligrams (mg)
    0–6 months 210 mg
    7–12 months 270 mg
    1–3 years 500 mg
    4–8 years 800 mg
    9–18 years 1,300 mg
    19–50 years 1,000 mg
    51–70+ years 1,200 mg
  • Gas - Flatus
  • Congenital/ secondary or developmental intolerance
    Congenital – gene mutation that prevents production of lactase. Happens soon after birth.
    Secondary – desiese that destroys the lining of the small intestine along with lactase. (Celiac sprue.)
    Aisan’s 100% by age 5. Blacks 70% by age 10.
    not the same as lactose deficiency.
    Developmental – adult-type hypolactasia. Spoken about above.
  • DISTENSION – The state of being distended, enlarged, swollen from internal pressure.
  • IBD- derived form Crohn’s and Ulcerative Colitus
    Crohn’s and ulcerative colitus – result form a genetic predisposition to having an inappropiate immune response to infection
  • Constipation – result of decreased colonic motility. Symptoms produced by over distension of rectum, and not by the absorption of toxic bacterial products
    Definition -  having a bowel movement fewer than three times per week. ( National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK))
    It is a symptom not a disease
    For more info:
  • Can be caused by decreased fluid absorption, increased fluid secretion or both.
    Def’n - loose, watery stools. Having diarrhea means passing loose stools three or more times a day. Acute diarrhea is a common problem that usually lasts 1 or 2 days and goes away on its own.
    For more info :
  • Gastrointestinal physiology

    1. 1. The Digestive System
    2. 2. Digestive Process Figure 23.2
    3. 3. GI Tract External environment for the digestive process Regulation of digestion involves: Mechanical and chemical stimuli – stretch receptors, osmolarity, and presence of substrate in the lumen Extrinsic control by CNS centers Intrinsic control by local centers
    4. 4. Receptors of the GI Tract Mechano- and chemoreceptors respond to: Stretch, osmolarity, and pH Presence of substrate, and end products of digestion They initiate reflexes that: Activate or inhibit digestive glands Mix lumen contents and move them along
    5. 5. Nervous Control of the GI Tract Intrinsic controls Nerve plexuses near the GI tract initiate short reflexes Short reflexes are mediated by local enteric plexuses (gut brain) Extrinsic controls Long reflexes arising within or outside the GI tract Involve CNS centers and extrinsic autonomic nerves
    6. 6. Nervous Control of the GI Tract Figure 23.4
    7. 7. Secretions of the Stomach Chyme: ingested food plus stomach secretions Mucus: surface and neck mucous cells Viscous and alkaline Protects from acidic chyme and enzyme pepsin Irritation of stomach mucosa causes greater mucus Intrinsic factor: parietal cells. Binds with vitamin B12 and helps it to be absorbed. B12 necessary for DNA synthesis HCl: parietal cells Kills bacteria Stops carbohydrate digestion by inactivating salivary amylase Denatures proteins Helps convert pepsinogen to pepsin Pepsinogen: chief cells. Packaged in zymogen granules released by exocytosis. Pepsin catalyzes breaking of covalent bonds in proteins. G-cells: secrete the hormone gastrin which stimulates HCl secretion from parietal cells
    8. 8. Hydrochloric Acid Production 1. CO2 and Cl- diffuse from the blood into the stomach cell. 2. CO2 combines with H2O to form H2CO3. 3. H2CO3 dissociates into bicarbonate (HCO3- ) and H+ . 4. H+ combines with Cl- in duct of gastric gland to form HCl- . 5. An ATP pump is necessary to pump the HCl- into the duct since the concentration of HCl- is about a million times more concentrated in the duct than in the cytosol of the cell.
    9. 9. Regulation of Gastric Secretion Neural and hormonal mechanisms regulate the release of gastric juice Stimulatory and inhibitory events occur in three phases Cephalic (reflex) phase: prior to food entry Gastric phase: once food enters the stomach Intestinal phase: as partially digested food enters the duodenum
    10. 10. Release of Gastric Juice Figure 23.16
    11. 11. Cephalic Phase The taste or smell of food, tactile sensations of food in the mouth, or even thoughts of food stimulate the medulla oblongata. Parasympathetic action potentials are carried by the vagus nerves to the stomach. Preganglionic parasympathetic vagus nerve fibers stimulate postganglionic neurons in the enteric plexus of the stomach. Postganglionic neurons stimulate secretion by parietal and chief cells (HCl and pepsin) and stimulate the secretion of the hormone gastrin. Gastrin is carried through the circulation back to the stomach where it stimulates further secretion of HCl and pepsin.
    12. 12. Gastric Phase Distention of the stomach activates a parasympathetic reflex. Action potentials are carried by the vagus nerves to the medulla oblongata. Medulla oblongata stimulates further secretions of the stomach. Distention also stimulates local reflexes that amplify stomach secretions.
    13. 13. Intestinal Phase  Chyme in the duodenum with a pH less than 2 or containing lipids inhibits gastric secretions by three mechanisms 1. Sensory input to the medulla from the duodenum inhibits the motor input from the medulla to the stomach. Stops secretion of pepsin and HCl. 2. Local reflexes inhibit gastric secretion 3. Secretin, gastric inhibitory polypeptide, and cholecystokinin produced by the duodenum inhibit gastric secretions in the stomach.
    14. 14. Regulation of Gastric Emptying Gastric emptying is regulated by: The neural enterogastric reflex Hormonal (enterogastrone) mechanisms These mechanisms inhibit gastric secretion and duodenal filling Carbohydrate-rich chyme quickly moves through the duodenum Fat-laden chyme is digested more slowly causing food to remain in the stomach longer
    15. 15. Regulation of Gastric Emptying Figure 23.19
    16. 16. Microscopic Anatomy of the Liver Figure 23.24c, d
    17. 17. Histology of the Liver  Connective tissue septa branch from the porta into the interior  Divides liver into lobules  Nerves, vessels and ducts follow the septa  Lobules: portal triad at each corner  Three vessels: hepatic portal vein, hepatic artery, bile duct (hepatic duct in diagram)  Central vein in center of lobule  Central veins unite to form hepatic veins that exit liver and empty into inferior vena cava Hepatic cords: radiate out from central vein. Composed of hepatocytes Hepatic sinusoids: between cords, lined with endothelial cells and hepatic phagocytic (Kupffer) cells Bile canaliculus: between cells within cords
    18. 18. Functions of the Liver Bile production: 600-1000 mL/day. Bile salts (bilirubin), cholesterol, fats, fat-soluble hormones, lecithin Neutralizes and dilutes stomach acid Bile salts emulsify fats. Most are reabsorbed in the ileum. Secretin (from the duodenum) stimulates bile secretions, increasing water and bicarbonate ion content of the bile Storage Glycogen, fat, vitamins, copper and iron. Hepatic portal blood comes to liver from small intestine. Nutrient interconversion Amino acids to energy producing compounds Hydroxylation of vitamin D. Vitamin D then travels to kidney where it is hydroxylated again into its active form Detoxification Hepatocytes remove ammonia and convert to urea Phagocytosis Kupffer cells phagocytize worn-out and dying red and white blood cells, some bacteria Synthesis Albumins, fibrinogen, globulins, heparin, clotting factors
    19. 19. Composition of Bile A yellow-green, alkaline solution containing bile salts, bile pigments, cholesterol, neutral fats, phospholipids, and electrolytes Bile salts are cholesterol derivatives that: Emulsify fat Facilitate fat and cholesterol absorption Help solubilize cholesterol Enterohepatic circulation recycles bile salts The chief bile pigment is bilirubin, a waste product of heme
    20. 20. Regulation of Bile Release Figure 23.25
    21. 21. Blood and Bile Flow Through the Liver
    22. 22. Pancreas  Pancreas both endocrine and exocrine  Head, body and tail  Endocrine: pancreatic islets. Produce insulin, glucose, and somatostatin  Exocrine: groups acini (grape-like cluster) form lobules separated by septa.  Intercalated ducts lead to intralobular ducts lead to interlobular ducts lead to the pancreatic duct.  Pancreatic duct joins common bile duct and enters duodenum at the hepatopancreatic ampulla controlled by the hepatopancreatic ampullar sphincter
    23. 23. Pancreatic Secretions: Pancreatic Juice Aqueous. Produced by columnar epithelium lining smaller ducts. Na+ , K+ , HCO3 - , water. Bicarbonate lowers pH inhibiting pepsin and providing proper pH for enzymes Enzymatic portion: Trypsinogen Chymotrypsinogen Procarboxypeptidase Pancreatic amylase Pancreatic lipases Deoxyribonucleases and ribonucleases Interaction of duodenal and pancreatic enzymes. Enterokinase from the duodenal mucosa and attached to the brush border activates trypsinogen to trypsin. Trypsin activates chymotrypsinogen to chymotrypsin Trypsin activates procarboxypeptidase to carboxypeptidase. Trypsin, chymotrypsin and carboxypeptidase digest proteins: proteolytic. Pancreatic amylase continues digestion of starch Pancreatic lipase digests lipids Deoxyribonucleases and ribonucleases digest DNA and ribonucleic acid, respectively
    24. 24. Bicarbonate Ion Production in Pancreas
    25. 25. Regulation of Pancreatic Secretion Figure 23.28
    26. 26. Secretions of Large Intestine Mucus provides protection Parasympathetic stimulation increases rate of goblet cell secretion Pumps: bacteria produce acid and the following remove acid from the epithelial cells that line the large intestine Exchange of bicarbonate ions for chloride ions Exchange of sodium ions for hydrogen ions Bacterial actions produce gases (flatus) from particular kinds of carbohydrates found in legumes and in artificial sugars like sorbitol Bacteria produce vitamin K which is then absorbed Feces consists of water, undigested food (cellulose), microorganisms, sloughed-off epithelial cells
    27. 27. Digestion, Absorption, Transport Digestion Breakdown of food molecules for absorption into circulation  Mechanical: breaks large food particles to small  Chemical: breaking of covalent bonds by digestive enzymes Absorption and transport Molecules are moved out of digestive tract and into circulation for distribution throughout body
    28. 28. Carbohydrates: Hydrolyzed into Monosaccharides Glucose is transported to cells requiring energy; insulin influences rate of transport
    29. 29. Lipids  Include triglycerides, phospholipids, steroids, fat-soluble vitamins  Bile salts surround fatty acid and glycerol to form micelles  Chylomicrons are 90% triglyceride, 5% cholesterol, 4% phospholipid, 1% protein.  Chylomicrons enter blood stream and travel to adipose tissue. In blood, triglycerides converted back into fatty acids and glycerol where they are transported into the adipose cells, then converted back into triglycerides.
    30. 30. Transport of Lipids Across Intestinal Epithelium
    31. 31. Fatty Acid Absorption Figure 23.36
    32. 32. Lipoproteins  All lipids carried in the blood are done so in combination with protein to make them soluble in plasma.  Cholesterol: 15% ingested; 85% manufactured in liver and intestinal mucosa  Lipids are lower density than water; proteins are higher density than water  Chylomicrons: 99% lipid and 1% protein (extremely low density); enter lymph  VLDL: 92% lipid, 8% protein  Form in which lipids leave the liver  Triglycerides removed from VLDL and stored in adipose cells. VLDL has been converted to LDL.  LDL: 75% lipid, 25% protein  Transports cholesterol to cells  Cells have LDL receptors  # of LDL receptors become less once cell’s lipid/cholesterol needs are met.  HDL: 55% lipid, 45% protein  Transports excess cholesterol from cells to liver
    33. 33. Transport of LDL into Cells
    34. 34. Proteins Pepsin breaks proteins into smaller polypeptide chains Proteolytic enzymes produce small peptide chains Dipeptides, tripeptides, amino acids After absorption, amino acids are are carried through the hepatic portal vein to the liver.
    35. 35. Amino Acid Transport
    36. 36. Chemical Digestion: Nucleic Acids Absorption: active transport via membrane carriers Absorbed in villi and transported to liver via hepatic portal vein Enzymes used: pancreatic ribonucleases and deoxyribonuclease in the small intestines
    37. 37. Electrolyte Absorption Most ions are actively absorbed along the length of small intestine Na+ is coupled with absorption of glucose and amino acids Ionic iron is transported into mucosal cells where it binds to ferritin Anions passively follow the electrical potential established by Na+ K+ diffuses across the intestinal mucosa in response to osmotic gradients Ca2+ absorption: Is related to blood levels of ionic calcium Is regulated by vitamin D and parathyroid hormone (PTH)
    38. 38. Water Absorption 95% of water is absorbed in the small intestines by osmosis Water moves in both directions across intestinal mucosa Net osmosis occurs whenever a concentration gradient is established by active transport of solutes into the mucosal cells Water uptake is coupled with solute uptake, and as water moves into mucosal cells, substances follow along their concentration gradients
    39. 39. Water and Ions Water: can move in either direction across wall of small intestine depending on osmotic gradients Ions: sodium, potassium, calcium, magnesium, phosphate are actively transported
    40. 40. Introduction toIntroduction to GastrointestinalGastrointestinal PhysiologyPhysiology
    41. 41. Gastrointestinal System(GIS)Gastrointestinal System(GIS) The main function of the GIS is to process ingested food into molecular forms that are transferred, with salts and water to the body’s internal environment where the circulatory system can distribute them to cells. This system includes the Gastrointestinal Tract (GI) which is made up of; mouth, pharynx, oesophagus, stomach, small intestine, large intestine and accessory organs. The accessory organs include; salivary glands, liver, gall bladder and pancreas
    42. 42. Organ Exocrine secretions Digestion Absorption Bulk transport/ Function Mouth and Pharynx Salivary glands Salt and water Mucus Amylase Chewing breaks down food particles Amylase partially digests polysaccharides No Moistens and lubricates food particles Oesophagus Mucus No No Moves food to stomach by peristaltic waves Provides lubrication Stomach HCl Pepsins Mucus Solubilises food particles, kills microbes, activates pepsinogens to pepsin Pepsins break down protein No Store food particles Regulate rate at which contents are emptied into the small intestine Pancreas Enzymes Bicarbonate Carbohydrates Fats Proteins and Nucleic acids No Neutralize HCl entering the small intestine
    43. 43. Organ Exocrine secretions Digestion Absorption Bulk transport/ Function Liver Bile Salts Bicarbonate Organic waste products and trace metals Solubilizes water insoluble fats No Neutralizes HCl entering the small intestine Elimination of feces Gall Bladder No No No Stores and concentrates bile between meals Small Intestine Enzymes Salt and water Mucus Hydrolytic enzymes break down carbohydrates, fats and proteins into monosaccharides , fatty acids, amino acids Monosaccharides, fatty acids, amino acids, vitamins, minerals, water Maintain fluidity of luminal contents Lubrication Large Intestine Mucus No Salt, water Storage and concentration of undigested matter Mixing and propulsion of contents Defecation
    44. 44. Structure of the GI Tract WallStructure of the GI Tract Wall The wall of the gastrointestinal tract has the same general structure from mid-oesophagus to the anus. The wall comprises: - mucosa, -submucosa, -muscularis externa - serosa.
    45. 45. Walls of the GI Tract In the small intestine finger like projections called villi which extend from the luminal surface. The centre of each villus is occupied both by lacteal (single blind- ended lymphatic vessel) and a capillary network. The surface of each villus is covered with a layer of epithelial cells whose surface membrane form projections called microvilli
    46. 46. Epithelial Function The increased surface area of the wall in the small intestine by villi and microvill allow for mass absorption. The invaginatons in the wall form exocrine glands and allow passage of substances. They also have a paracrine function which refers to the ability of the endocrine cells within the epithelial layer to release hormones and bind to the receptors of nearby cells to affect their function.
    47. 47. Epithelia Lifetime 17 Billion epithelial cells are replaced each day. The entire epithelium of the small intestine is replaced approximately every five days. The rapid cell turnover makes the lining of the intestinal tract suseptible to damage by agents that inhibit cell division (e.g. anticancer drugs)
    48. 48. Digestion & Absorption ObjectivesDigestion & Absorption Objectives Describe the process involved in the breakdown and absorption of ingested carbohydrates. Describe fat absorption, resynthesis of triglycerides and phospholipids, the formation of chylomicrons and the absorption into the lacteals. Describe the absorptive mechanisms involved in protein absorption.  Describe the absorption mechanisms for the different water- and fat soluble vitamins, noting the special role of intrinsic factor in the absorption of vitamin B 12. Describe the epithelial processes involved in the active absorption
    49. 49. Digestion and AbsorptionDigestion and Absorption Overview of the four basic digestive processes: Digestion: dissolving and breaking down process of food into small molecules. Absorption: the process whereby molecules produced from digestion moves from the GI tract across a layer of epithelial cells and enters the blood. Secretion: The release of substances that aid in digestion. ( HCL acid, bile and digestive enzymes) Motility: Contraction of the GI tract .
    50. 50. Digestion and AbsorptionDigestion and Absorption Carbohydrates:
    51. 51. Digestion and AbsorptionDigestion and Absorption Carbohydrates
    52. 52. Digestion and AbsorptionDigestion and Absorption Glucose & Galactose enter epithelial cells via sodium-linked secondary active transport across the epithelial membrane. Fructose enters by facilitated diffusion.  These monosaccharides exit via the Basolateral Membrane by facilitated diffusion transporters and then diffuse into the capillaries.
    53. 53. Digestion and AbsorptionDigestion and Absorption Proteins  Proteins need to be broken down into smaller molecules (amino acids, dipeptides & tripeptides) before they can be absorbed by the small intestine.  Proteases involved in this process are : -Pepsin: secreted as pepsinogen into the stomach -Trypsin: secreted as trypsinogen into small intestine. -Chymotrypsin: secreted as chymotrypsinogen, into small intestine. -Carboxypeptidase: secreted as procarboxypeptidase into small intestine. -Aminopeptidase (brush border enzyme) is also used.
    54. 54. Digestion and AbsorptionDigestion and Absorption
    55. 55. Digestion and AbsorptionDigestion and Absorption
    56. 56. Digestion and AbsorptionDigestion and Absorption Free Amino acids enter absorptive epithelial cells via sodium-linked secondary active transport across the apical membrane. Others are transported via facilitated diffusion into cells. Dipeptides and Tripeptides are actively transported across the apical membrane and then broken down to amino acids within the cell. Amino acids from the cell enter the capillaries via facilitated diffusion across the basolateral
    57. 57. Digestion and AbsorptionDigestion and Absorption Fats  Fats are ingested in the form of Triglycerides. Fat digestion occurs almost entirely in the small intestine whereby lipase splits bonds linking fatty acids to the first and third carbon atoms of glycerol. Two fatty acids and a monoglyceride are produced. Ingested fats aggregate into large lipid droplets in the upper portion of the stomach. (insolubility in water). Emulsification: breakdown of large lipid droplets into smaller droplets resulting in an increased rate of digestion.
    58. 58. Digestion and AbsorptionDigestion and Absorption Fats
    59. 59. Digestion and AbsorptionDigestion and Absorption  ‘Mechanical disruption of fat globlets’ (contractions of stomach and small intestine) & ‘ An emulsifying agent’ (Phospholipids in food and secreted bile salts) is needed for the emulsification of fat.  Non polar regions on phospholipids and bile salts associate with the non polar interior of the lipid droplets.  Repulsion of other lipid droplets occurs preventing reaggregation.  Although accessibility to lipase is impaired, colipase (secreted from pancreas) binds lipase onto the surface of the lipid droplet.
    60. 60. Digestion and AbsorptionDigestion and Absorption Micelles: similar in structure to emulsion droplets & comprise clusters of bile salts, fatty acids, monoglycerides & phospholipids. (Polar ends oriented toward micelle surface; nonpolar portions form micelle’s core). Micelles continuously breakdown & reform which increases absorption. Broken-down micelles release its contents (fatty acids and monoglycerides) which diffuse into epithelial cells. Fatty acids and monoglycerides enter the intestinal lumen and triglycerides are released into the interstitial fluid. Re-synthesis of triglycerides occurs on
    61. 61. Digestion and AbsorptionDigestion and Absorption  Chylomicrons: extracellular fat droplets containing triglycerides and other lipids (phospholipids, cholesterol & fat-soluble vitamins) which have been absorbed in the absorption process. Chylomicrons released from epithelial cells enter lacteals and then into the lymph. A basement membrane(extracellular glycoprotein layer) prevents entry of chylomicrons into the capillaries.
    62. 62. Digestion and AbsorptionDigestion and Absorption
    63. 63. Digestion and AbsorptionDigestion and Absorption Water & Minerals: Small amounts of water are absorbed in the stomach in spite of the absence of solute absorbing mechanisms. Significant absorption takes places in the epithelial membranes of the small intestine. A water concentration difference is required for net water diffusion and this is established via active absorption of solutes.( active transport of sodium across epithelium) Water moves by osmosis across the epithelium. Iron absorption Increased iron deposition leads to hemochromatosis.
    64. 64. Mouth  Food enters the digestive tract through the mouth.  As food enters the mouth, breakdown begins:  Mechanical breakdown by chewing (teeth) and actions of the tongue.  Chemical breakdown of starch by production of salivary amylase from the salivary glands.
    65. 65. SalivaSaliva  Salivary amylase hydrolyzes internal α1-4 bonds within starch.  A second digestive enzyme, lingual lipase, is produced by lingual serous glands on the tongue and in the back of the mouth.  This enzyme hydrolyzes dietary triacylglycerols (triglycerides) in the stomach.  Mucus secretions found in saliva contain glycoproteins.  Mucus lubricates food and coats and protects the oral mucosa.
    66. 66.  The secretion of saliva is controlled by both sympathetic and parasympathetic neurons.  There is no hormonal regulation of salivary secretion.  In the absence of ingested material, a low rate of salivary secretion keeps the mouth moist.  In the presence of food, salivary secretion increases markedly.  This reflex response is initiated by chemoreceptors (acidic fruit juices are a particularly strong stimulus) and pressure receptors in the walls of the mouth and on the tongue.  Increased secretion of saliva is accomplished by a large increase in blood flow to the salivary glands, which is mediated by both neural activity and paracrine/autocrine agents released by the active cells in the salivary gland.  The volume of saliva secreted per gram of tissue is the largest secretion of any of the body’s exocrine glands.
    67. 67. SwallowingSwallowing  Swallowing is a complex reflex initiated when pressure receptors in the walls of the pharynx are stimulated by food or drink forced into the rear of the mouth by the tongue.  These receptors send afferent impulses to the swallowing center in the brainstem medulla oblongata.  This center then elicits swallowing via efferent fibers to the muscles in the pharynx and esophagus as well as to the respiratory muscles.
    68. 68.  Swallowing is an example of a reflex in which multiple responses occur in a temporal sequence determined by the pattern of synaptic connections between neurons in a brain coordinating center.  Since both skeletal and smooth muscles are involved, the swallowing center must direct efferent activity in both somatic nerves (to skeletal muscle) and autonomic nerves (to smooth muscle).  Simultaneously, afferent fibers from receptors in the esophageal wall send information to the swallowing center that can alter the efferent activity.
    69. 69. PharynxPharynx  Swallowing moves ingested material (bolus) from the mouth into the pharynx.  The pharynx is 14-16cm long.  As the ingested material (bolus) moves into the pharynx, the soft palate elevates and lodges against the back wall of the pharynx.  This prevents food from entering the nasal cavity.  Impulses from the swallowing center inhibit respiration, raise the larynx, and close the glottis (the area around the vocal cords and the space between them).  This keeps food from moving into the trachea.  As the tongue forces the food farther back into the pharynx, the food tilts a flap of tissue, the epiglottis, backward to cover the closed glottis, thereby preventing food from entering the trachea.
    70. 70. PharynxPharynx  The pharynx is divided into three sections:  the nasopharynx  the oropharynx  the laryngopharynx
    71. 71. How the Esophagus Works….How the Esophagus Works….  As a person swallows, food moves from the mouth to the throat, also called the pharynx (1).  The upper esophageal sphincter opens (2) so that food can enter the esophagus,  where waves of muscular contractions, called peristalsis, propel the food downward (3).  The food then passes through the lower esophageal sphincter (4)  and moves into the stomach (5).
    72. 72. “Food goin’ down d wrong hole”
    73. 73.  Once in the esophagus, the food is moved toward the stomach by a progressive wave of muscle contractions that proceeds along the esophagus, compressing the lumen and forcing the food ahead of it.  Such waves of contraction in the muscle layers surrounding a tube are known as peristaltic waves.  One esophageal peristaltic wave takes about 9 s to reach the stomach.
    74. 74. Upper Esophageal Sphincter Lower Esophageal Sphincter  The esophageal phase of swallowing begins with relaxation of the upper esophageal sphincter.  Immediately after the food has passed, the sphincter closes, the glottis opens, and breathing resumes.  The lower esophageal sphincter opens and remains relaxed throughout the period of swallowing, allowing the arriving food to enter the stomach.  After the food has passed, the sphincter closes, resealing the junction between the esophagus and the stomach.
    75. 75.  The ability of the lower esophageal sphincter to maintain a barrier between the stomach and the esophagus when swallowing is not taking place is aided by the fact that the last portion of the esophagus lies below the diaphragm, and is subject to the same abdominal pressures as is the stomach.  This prevents the formation of a pressure gradient between the stomach and esophagus that could force the stomach’s contents into the esophagus.
    76. 76. Heartburn Some people have less efficient lower esophageal sphincters, resulting in repeated episodes of refluxed gastric contents into the esophagus (gastro-esophageal reflux), heartburn, and in extreme cases, ulceration, scarring, obstruction, or perforation of the lower esophagus. The lower esophageal sphincter not only undergoes brief periods of relaxation during a swallow but also in the absence of a swallow. During these periods of relaxation, small amounts of the acid contents from the stomach are normally refluxed into the esophagus.
    77. 77.  Multiple mechanisms, including neural and hormonal, regulate gastroesophageal sphincter pressure.  The musculature of the gastroesophageal sphincter has a tonic pressure.  It is normally higher than the intragastric pressure (the pressure within the stomach).  This high tonic pressure at the gastroesophageal sphincter keeps the sphincter closed.  Keeping this sphincter closed is important.  It prevents gastroesophageal reflux: the movement of substances from the stomach back into the esophagus.
    78. 78. The StomachThe Stomach The stomach is a typically J shaped enlargement of the GI tract. It connects the oesophagus to the duodenum (the first part of the small intestine).
    79. 79. Anatomy of the StomachAnatomy of the Stomach The stomach has four (4) main regions: The cardia The fundus The body The pyloric region The pyloric antrum The pyloric canal The phyloricsphinter
    80. 80. Histology of the StomachHistology of the Stomach The stomach wall is composed of the same four(4) basic layers as the rest of the GI tract, with certain modifications. The surface of the mucosa is a layer of simple columnar epithelial cells called mucous surface cells. The epithelial cells extend down into the lamina propia, where they form columns of secretory cells called gastric glands that line many narrow channels called gastric pits. Secretions from the gastric glands flow into each gastric pit and into the lumen of the stomach.
    81. 81. Gastric pits contain four (4) major secretory cells: Chief cells  Pepsinogen  Activation of pepsinogen by low pH to form pepsin  Once pepsin is formed, it can act on pepsinogen to produce more pepsin  Pepsin is a protease for protein digestion Parietal cells  HCl  Kills microbes in food  Denatures protains  Converts pepsinogen to pepsin  Intrincis factors  Needed for absorption of vitamin B12 G-cells (enteroendocrine cell)  Secretes gastrin hormone  Gastrin activates gastric juice secretion and gastric smooth muscle “churning”  Gastrin activates gastroileal reflex which moves chyme from ileum to colon Mucus cells  Protective role of mucus against acid and digestive enzymes
    82. 82. The submucosa layer of the stomach is composed of areolar connective tissue. The muscularis has three (3) (rather than two) layers of smooth muscle: An outer longitudinal layer A middle circular layer An inner oblique layer (limited to the body of the stomach). The serosa (simple squamous mesothelium and areolar connective tissue) covering the stomach is part of the viseral peritoneum.
    83. 83. Functions of the StomachFunctions of the Stomach Storage  Because of its accordionlike folds (called rugae), the wall of the stomach can expand to store two to four liters of material. Temporary storage is important because you eat considerably faster than you can digest food and absorb its nutrients. Mixing  The stomach mixes the food with water and gastric juice to produce a creamy medium called chyme. Controlled release  Movement of chyme into the small intestine is regulated by a sphincter at the end of the stomach, the pyloric sphincter.
    84. 84. Physical breakdown  Three layers of smooth muscles (rather than the usual two) in the muscularis externa churn the contents of the stomach, physically breaking food down into smaller particles. In addition, HCl denatures (or unfolds) proteins and loosens the cementing substances between cells (of the food). The HCl also kills most bacteria that may accompany the food. Chemical breakdown  Proteins are chemically broken down by the enzyme pepsin. Chief cells, as well as other stomach cells, are protected from self-digestion because chief cells produce and secrete an inactive form of pepsin, pepsinogen. Pepsinogen is converted to pepsin by the HCl produced by the parietal cells. Only after pepsinogen is secreted into the stomach cavity can protein digestion begin. Once protein digestion begins, the stomach is protected by the layer of mucus secreted by the mucous cells.
    85. 85. Hydrochloric Acid Production
    86. 86. HCl is produced in the parietal cells through a complex series of reactions. Carbon dioxide diffuses into the parietal cell and the enzyme carbonic anhydrase catalyzes a reaction between the carbon dioxde and water to form carbonic acid. Carbonic acid dissociates into bicarbonate ion and hydrogen ion and the bicarbonate ion is transported back into the bloodstream. An ion exchange molecule in the plasma membrane exchange bicarbonate going out for chloride coming in.
    87. 87. Proton pumps powered by H+/K+ ATPases is used to transport the potassium and hydrogen ions. The hydrogen ions are actively transported into the duct of the gastric gland and the negatively charged chloride ions diffuse with the positively charged hydrogen ions. Potassium ions are counter transported into the parietal cells in exchange for hydrogen ions. The potassiun ions leak back into the lumen via potassium channels. The net result is production of HCl in the parietal cells and its secretion into the duct of the gastric gland.
    88. 88. Four (4) chemical messengers regulate acid secretion:  GastrinGastrin  released from G-cell  stimulates acid secretion  Acetylcholine (Ach)Acetylcholine (Ach)  released from the plexus neurons  stimulates acid secretion  HistamineHistamine  released from ECL cells  stimulates acid secretion  potentiates the response to gastrin and Ach.  SomatostatinSomatostatin –  released from endocrine cells in the gastric wall  Acts on parietal cells to inhibit acid secretion  Inhibits release of gastrin and histamine  Parietal cell membranes contain receptors for all 4 of these molecules. Not only do these chemical messengers act directly on the parietal cells, they also influence each other’s secretion.  Pepsinogen secretion parallels acid secretion, i.e. most of the factors stimulate or inhibit acid secretion exert the same effect on pepsinogen secretion.
    89. 89. Three Phases of Gastric SecretionThree Phases of Gastric Secretion Regulation of stomach secretion is divided into three (3) phases: • Cephalic • Gastric • Intestinal
    90. 90. Cephalic phase:Cephalic phase:  Taste, sight, tactile sensation of or thought of food in the mouth sends nervous impulse to the medulla oblongata.  These impulses cause parasympathetic neurons via the vagus nerves to stimulate secretion of HCl, pepsinogen and mucus in the stomach.  The parasympathetic stimulation also results in secretion of gastrin from the lower part of the stomach.  Gastrin travels through the bloodstream and further stimulated HCl and pepsinogen secretion in the upper and middle part of the stomach.
    91. 91.  Gastric Phase:Gastric Phase:  Food has entered and distended the stomach. The pH of the stomach is also altered because protein has entered the stomach and buffered some of the stomach acid causing a low pH.  This distention activated a parasympathetic reflex via the medulla oblongate, and also has a direct stimulatory effect on the gastric glands. The result is the continued secretion of HCl and pepsinogen.  Negative feedback control of acid secretion is done by somatostatin. As the contents of the gastric lumen become more acidic, the stimuli that promote acid secretion decrease.
    92. 92.  Intestinal phaseIntestinal phase  Chyme has entered the duodenum so gastric secretion is no longer needed.  When the chyme contains lipids from the digestion of fats or contains enough HCl to bring its pH to below 2, gastric secretion is inhibited.  The lipid and hydrogen ions inhibit gastric secretion by three simultaneous actions.  They cause impulses to go to the medulla oblongata to decrease parasympathetic stimulation of gastric glands  They set up local reflexes, via neurons in the wall of the gut, that decrease gastric secretion.  They cause the release of three local hormones collectively called enterogastrones (secretin, CCK inhibitory peptides) which travel via the circulation to the gastric glands and inhibit their secretion.
    93. 93. Gastric MotilityGastric Motility
    94. 94. After food enters the stomach, gentle, rippling, peristaltic movements called mixing waves pass over the stomach every 15-25 seconds. These waves macerate food, mix it with gastric juice and reduce it to a soupy liquid called chyme. As digestion proceeds, more vigorous mixing waves begin at the body of the stomach and intensify as they reach the pylorus. As food reaches the pylorus, each mixing wave forces several milliliters of chyme into the duodenum through the pyloric sphincter. Most chyme is forced back into the body of the stomach where mixing continues.
    95. 95. The next wave pushes the chyme forward again and forces a little more into the duodenum. These forward and backward movement of gastric contents are responsible for most mixing in the stomach. The rhythm of gastric waves are generated by pacemaker cells in the longitudinal smooth muscle layer. These smooth muscle cells undergo spontaneous depolarization- repolarization cycles (slow waves) known as basic electrical rhythm of the stomach. These slow waves are conducted through gap junctions along the stomach’s longitudinal muscle layer and also induce similar slow waves in overlying circular muscle layer.
    96. 96. Slow wave oscillations in the membrane potential of gastric smooth muscle fibers trigger bursts of action potentials when threshold potential is reached at the wave peak. Membrane depolariztion bring the slow wave closer to threshold. Increasing the action potential frequency and thus the force of smooth muscle contraction.
    97. 97. Regulation of Gastric EmptyingRegulation of Gastric Emptying Stimulation of gastric emptying:  Gastric emptying, the periodic release of chyme from the stomach into the duodenum, is regulated by both neural and hormonal reflexes, as follows: 1. Stimuli (distention of the stomach, presence of partially digested proteins, alcohol and caffeine) initiate gastric emptying. 2. These stimuli increase the secretion of gastrin and generate parasympathetic impulses in the vagus (X) nerves. 3. Gastrin and nerve impulses stimulate contraction of the lower oesophagus sphincter, increase motility of the stomach and relax the pyloric sphincter. 4. The net effect of these actions is gastric emptying.
    98. 98. Inhibition of Gastric emptying Inhibition of Gastric emptying is controlled by the enterogastric reflex and CCK. 1. Stimuli (distention of the duodenum and the presence of fatty acids, partially digested proteins and glucose) in the duodenal chyme initiate gastric emptying. 2. These stimuli the enterogastric reflex: Nerve impulses propagate from the duodenum to the medulla oblongata, where they inhibit parasympathetic stimulation and stimulate sympathetic activity in the stomach. The same stimuli also increase secretion of CCK. 3. Increased sympathetic impulses and CCK both decrease gastric motility. 4. The net effect if these actions is inhibition of gastric emptying.
    100. 100.  The proteolytic enzymes are secreted in inactive forms (zymogens) and then activated in the duodenum by other enzymes. Activation is acquired in steps and is catalyzed by enterokinase. This is embedded in the luminal plasma membrane of the intestinal epithelial cells. Proteolytic enzymes splits off a peptide from pancreatic trypsinogen thus forming the active enzyme trypsin
    101. 101. When activated trypsin which is also a proteolytic enzyem similarly splits off peptide fragments and in so doing activates the other pancreatic zymogens (this is in addition to its role in protein digestion). Note bicarbonates function is to neutralize acid entering the deodenum from the stomach. Also CCK responsible for the secretion of enzymes, (inclusive of those for fat, and protein digestion). CCK’s release is dependent on the levels/presence of fatty acids and amino acids in the duodenum
    102. 102. Glucagon, Insulin and Blood Glucose Regulation The islets of Langerhans (clusters of emdocrine cells) secrets these two peptide hormones. Insulin  Secreted by beta cells of islets of Langerhans within the pancreas when blood glucose level. Stimulates the uptake of glucose from the blood stream and does this by increasing the transport of glucose from the blood to muscle cells and adipocytes. Also a net uptake of glucose by the liver.
    103. 103. Insulin secretion and subsequently signaling leads to the movement of a glucose transport protein GLUT 4 from the intracellular vesicles to the cell membrane. (*) Once in the cell membrane the GLUT4 protein allows more glucose to enter the cell thus lowering the blood glucose level. Note insulin secretion is not only dependent on blood glucose levels. Secretion is also dependent on: Elevated amino acid concentration Hormonal controls The autonomic neurons to the islets of Langerhans
    104. 104.  Glucagon Secreted by the alpha cells of Langerhans within the pancreas at low blood glucose levels also by neural and hormonal inputs to these islets. Stimulates the release of glucose to the blood stream. It binds to specific receptors to set off a chain of events which makes glucose available i.e. Increased glycogenolysis (glycogen break down Increased gluconeogenesis Increases in the synthesis of ketones
    105. 105. BILE SECRETION AND LIVER FUCTION Bile is secreted by liver cells into a number of small ducts (the bile canaliculi which converge to form the common hepatic duct. Note bile salts and lecithin are synthesized in the liver and helps to solubilize fat in the small intestine Where as cholesterol, bile pigments and trace metals are extracted from the blood by the liver and excreted via the bile. Bicarbonate ions neutralize acid in the duodenum
    106. 106. When fatty meals are being digested most of the bile salts entering the intestinal tract via bile are absorbed by specific sodium-coupled transporters in the ileum. Absorbed bile salts are returned via the portal vein to the liver where they are secreted once again. Bile salts uptake from portal blood into hepatocytes is driven by secondary active transport coupled to sodium Cholesterol homeostasis in the blood and the process by which cholesterol –lowering drugs work is maintained by the secretion of bile followed by the excretion of cholesterol in feces.
    107. 107. Bile pigments are substances formed from the heme portion of hemoglobin when digestion of old or damaged erythrocytes occurs in the spleen and liver. Bile components are secreted by two different cells, they are:  Hepatocytes which secrets bile salts and pigments, lecithin.  Epithelial cells which secrets most of the bicarbonate rich salt solutions Secretion of the salt solution by the bile ducts is stimulated by secretin in response in response to acidity in the duodenum. Note the secretion of bile salts is controlled by the concentration of bile salts within the blood
    108. 108. The liver is always secreting bile however, greater secretion occurs at meal times (during and just after). The sphincter of oddi is a ring of smooth muscles surrounding the common bile duct at the point at which it enters the duodenum. When closed the diluted bile secreted by the liver is shunted into the gallbladder. It is at this point the organic components of bile (water and sodium chloride) are absorbed into the blood
    109. 109. The Small Intestine
    110. 110. Secretion Intestinal epithelium secretes mineral ions such as, sodium, chloride and bicarbonate ions into the lumen and water follows by osmosis. Chloride is the primary ion that determines the magnitude of fluid secretion. Various hormonal ,paracine signals as well as toxins and bacterial toxins can increase the frequency of these channels and fluid secretion. Water movement into the lumen occurs when the stomach is hypertonic, this then causes osmotic movement of water.
    111. 111. Absorption All fluid secreted by the small intestine is absorbed back into the blood. Large volumes of fluid which includes, salivary, gastric, hepatic, pancreatic secretions and ingested water is simultaneously absorbed from lumen into the blood. There is a large net absorption of water from small intestine. Absorption is achieved by transport of ions mostly sodium from lumen into the blood with water followed by osmosis.
    112. 112. Motility Stationary concentration and relaxation of intestinal segments occurs during the digestion of a meal. Each contracting segment is a few cm long and the digestion last for a few seconds. Chyme in the lumen is forced up and down the intestine. Segmentation- the rhythmical contraction and relaxation of the intestine. Mixes the chyme in lumen and bringing it into contact with intestinal wall.
    113. 113. Segmentation movement -initiated by electrical activity by pacemaker cells with circular smooth muscle layer. -intestinal basic electrical rhythm produces oscillations in the smooth muscle membrane potential. If threshold is reached action potentials are triggered that increase muscle contraction. -the frequency of segmentation is set by the frequency of the intestinal basic rhythm -unlike the stomach that has a single rhythm 3 mins/sec intestinal rhythm varies along the length of the intestine. -each successive region have a slightly lower frequency than the
    114. 114. Motility Produces a slow migration of the intestinal contents toward the large intestine. Segmentation intensity can be altered by hormones: Enteric nervous system and autonomic nerves. Parasympathetic activity increases the force of contraction. Sympathetic stimulation decreases it.
    115. 115. Migrating myoelectric complex Begins in the lower portion of stomach. Repeated waves of peristaltic activity. Moves any undigested material remaining in the small intestine into the large intestine that is long enough to grow and multiply excessively. Rise in plasma concentration of intestinal hormone MOTILIN initiates MMC. Motilin stimulates MMCs via both the enteric and autonomic nervous system.
    116. 116. Motility Contractile activity in certain regions of the small intestine can be altered by reflexes. Eg, segmentation intensity in the ileum increases during periods of gastric emptiness (gastroileal reflex) Intestino intestinal reflex lead to complte cessastion of motility.
    117. 117. Large Intestine 6.5CM in diameter, 1.5m long First portion Cecum Cecum forms a blind ended pounch that extends to appendix COLON: 3 SEGMENTS Ascending Transverse Descending (forms sigmoid colon) Function –is to store and concentrate faecal material before defecation.
    118. 118. Large intestine Chyme enters the cecum through the ilocecal sphincter. Sphincter relaxes each time the terminal portion of the ileum contracts. Chyme enters the large intestine. The primary absorptive process in the intestine is active transport of Na+ from lumen to blood. Also osmotic absorption of water. There is a net movement of K+ from blood into the large intestine lumen. Stimulated by cAMP
    119. 119. Motility &Defecation Contraction of circular smooth muscle produce segmentation motion. Slower than small intestine Following a meal a wave contraction known as mass movement spreads over transverse segment of intestine to rectum Unlike a peristaltic wave in the small intestine, the smooth muscle in the intestine remains contracted for some time after mass mov’t Parasympathetic input increases segmental contractions whereas sympathetic input decreases colonic contractions
    120. 120. PATHOPHYSIOLOGY OF THE GASTROINTESTINAL TRACT Peptic Ulcer Disease, Vomiting and Gallstones, Lactose Intolerance, IBD, Constipation and Diarrhoea
    121. 121. DEFINITION Peptic Ulcer Disease (PUD)= These are areas of tissue degradation that can be caused by increased acid and pepsin or impaired mucosal defenses such as decreased bicarbonate secretions. Ulcers are normally found in the stomach (gastric), duodenum (duodenal) and oesophagus (oesophagal).
    122. 122. Common Risk Factors for Gastric Mucosal Disruption Associated with Helicobacter pylori. Alcohol NSAID- Induced gastritis or ulcers are frequently “silent”. Corticosteroids Tobacco Coffee/ Caffeine
    123. 123. Clinical Manifestation Pain (epigastic burning) Nausea, vomiting or bloating Weight Loss Upper Gastrointestinal haemorrhaging or blood in the stomach
    124. 124. Diagnostic Methods Abdominal X-ray Blood Count Endoscopy and biopsy of ulcer H pylori testing
    125. 125. Therapy In mild disease, treat with bismuth or misoprostal For H pylori give antibiotics
    126. 126. Vomiting Vomiting is the forceful expulsion of the contents of the stomach and upper intestinal tract through the mouth. It is a complex co-ordination by a region in the brainstem, the medulla oblongata.
    127. 127. Causes of Vomiting Gastric contents get into the respiratory tract Food poisoning Overeating Concussion Vomiting can be induced by stimulation of the chemoreceptor zone, vestibular apparatus and the GI tract
    128. 128. Consequences Intestinal Blockage Aspiration Pneumonia Disturbances in acid-base balance Dehydration Electrolyte Depletion
    129. 129. Diagnosis Blood Tests- to check electrolytes and blood cell count Urinalysis- to check for dehydration and infection CT Scan- to check for head injuries X-ray
    130. 130. Treatment Most of the time, vomiting go away on their own and could be managed at home. If vomiting occurs, fluids are given by the mouth or through a vein into the bloodstream.
    131. 131. Gallstones Gallstones are solid particles that form from the bile in the gallbladder. There are two types of them: 1. Cholesterol Stones and 2. Pigment Stones. Gallstones can be any size, from as tiny as a grain of sand to large as a golf ball.
    132. 132. Problems of Gallstones Gallstones within the gallbladder often cause no problems. If they are too large or too many, they cause extreme pain. They may also cause problems if they move out of the gallbladder. If there movements lead to blockage of any of the ducts connecting the gallbladder, liver or pancreas with the intestine, serious complications may occur. Blockage of a duct can cause bile or digestive enzymes to be trapped in the duct. If these conditions go untreated, they can even cause death.
    133. 133. Gallstone Causes The stones form when the amount of cholesterol or bilirubin in the bile is high. Pigment stones form most often in people with liver disease or blood disease, who have high levels of bilirubin. Poor muscle tone may keep the gallbladder from emptying completely. The presence of residual bile may promote the formation of gall stones.
    134. 134. Risk Factors for the Formation of Gallstones Female Gender Being Overweight Losing a lot of weight quickly on a starvation diet Taking of certain medications such as birth control pills or cholesterol lowering drugs.
    135. 135. Treatment Intake of only clear liquids to give the gallbladder a rest. Avoid fatty or greasy meals. Use of painkillers. Use of drugs made with bile acids. Gallstone surgery called Cholecystectomy.
    136. 136. LACTOSE INTOLERANCE LACTOSE -milk carbohydrate -digested by LACTASE, into its components absorbed by glucose & galactose active transport
    137. 137. Lactase Enzyme Embedded in luminal plasma membranes of intestinal epithelial cells Present at birth Production decreases after 2 yrs Lactose intolerance- inability to digest lactase.
    138. 138. Increases concentration in small intestine Decreases osmotic gradient, therefore, water retained in lumen. Lactose-containing fluid moves to large intestine bacteria digests lactose metabolizes monosaccharides produces gas & short chain fatty acids
    139. 139. Gas distends colon and produces pain Short chain fatty acids draws water into intestinal lumen which leads to diarrhea Lactose intolerance causes mild discomfort to severe dehydrating diarrhea Solution: lactose free products/lactase tablets
    140. 140. INFLAMMATORY BOWEL DESEASE (IBD) Crohn’s Disease & Ulcerative Colitis Chronic inflammation of the bowel
    141. 141. Crohn’s Disease Occurs anywhere along GI tract (mouth–anus) Most common at the end of the ileum Inflammation and thickening of bowel wall causes narrowing or blockage of lumen and hence, pain 1st symptoms – pain in lower right abdomen & diarrhea (sometimes fever) Often mistaken for acute appendicitis Relief: defecation (temporary)
    142. 142. Colitis Confined to colon Caused by disruption of normal mucosa with bleeding, edema & ulcerations In an extreme case bowel wall thins and tissue lost, so holes break bowel wall Symptoms: diarrhoea , rectal bleeding, abdominal cramps
    143. 143. IBD con’t Most common in caucasians (late teens to early 20’s and > 60) Caused by environmental and genetic factors As a result of weak immune system and poor tissue repair Responses to normal microorganisms in intestinal lumen
    144. 144. Treatment Initially – 5-aminosalicylate drugs e.g. sulfasalazine antibacterial & anti-inflammatory effect In severe case – glucocorticoids or removal of diseased bowel New drug therapy – immunosuppressive medicines Diet changes aid in healing (NB: overuse of glucocorticoids may cause bone loss)
    145. 145. CONSTIPATION AND DIARRHEA Common Belief: Unless you have a bowel movement everyday, ‘toxic’ substances from fecal matter (in large colon) will poison you! WHAT DO YOU THINK???
    146. 146. Toxic agents after a prolonged period of time – still to be discovered HOWEVER, fecal retention for days or weeks may lead to:- Headache Loss of appitite Nausea Abdominal distention These are all symptoms of CONSTIPATION
    147. 147. The longer the fecal matter remains in large intestine, the more water absorbed, feces become drier and defecation becomes difficult and painful Common in the elderly, or anyone with damage to the enteric nervous system (decreased motility of large intestine) or emotional stress Cure –distension from dietary fibre or laxatives
    148. 148. Dietary fibre – cellulose & other complex polysaccharides - not digested in small intestine, produces distension in large intestine, leads to motility - Bran, Fruits, Veggies Laxatives – increase frequency/ease of defecation - fiber is a laxative - mineral oils (lubricate feces) - Mg & Al salts (epsom salts) (water retention) - Caster oil (stimulates intestinal tract) - causes dependence
    149. 149. Diarrhea Large, frequent, watery, stools Causes:  fluid absorption, fluid secretion Increased motility caused by distension (not the other way around!) Secretory diarrhoea – bacterial, protozoan & viral diseases (E. coli) - Cholera and Traveller's diarrhoea
    150. 150. CHOLERA - Caused by bacteria Releases toxin that stimulates cyclic AMP Opens chloride channels Increase in chloride ions Increase water content in lumen Massive life threatening diarrhoea (dehydration, decreased blood vol.)
    151. 151. TRAVELLER’S DIARRHEA - Produced by several species of bacteria, parasites, viruses - Produces secretary diarrhoea (same process at cholera) Other consequences of severe diarrhoea are potassium depletion, metabolic acidosis
    152. 152. Treatment Dehydrating effect can be balanced by drinking salt- glucose solution to replace fluids (by active transport). Until diarrhoea subsides, a change is diet can help. Avoid caffeine, greasy foods, high fibre foods and lactose rich foods