Slide 1Slide 2Slide 3Slide 4Gastric Phase of DigestionSlide 6Slide 7Slide 8Digestion and Protection Balance in the StomachSlide 10Slide 11Slide 12Slide 13Slide 14Slide 15Intestinal Phase of Gastric SecretionSlide 17Slide 18Slide 19Slide 20Slide 21Slide 22Slide 23Slide 24Slide 25The Digestive System:7. The Three Phases of Digestive Processesdivided into Three Phases:Cephalic PhaseGastric PhaseIntestinal Phase- division is based on where the food processing signal is receivedThe integrated response to the arrival of foodFigure 21.8 modifiedCephalic Phase of the Digestive ProcessesGastric acid (HCl)Intrinsic factorMucusAutonomic neuronsSalivary glandsSecretion and MotilityMasticationDeglutitionBorborygmusGastric Phase of Digestion•Distension of the stomach and the presence of peptides or amino acids in the lumen activate endocrine cells and enteric neurons.•Secretion of:Gastric acid (HCl)Intrinsic FactorMucusPepsinogenGastric lipaseSomatostatinHistamineGastrinFigure 21.8Gastric Phase of the Digestive ProcessesACh: AcetylcholineGRP: gastrin releasing peptideFigure 21.10Digestion and Protection Balance in the StomachModified Figure 21.9bTight junctions Gastric Acid BarrierGastric UlcerSelf-digestion of the stomach results in peptic ulcers.NSAIDs: non-steroidal anti-inflammatory drugs (ibuprofen, aspirin) Gastric Ulceration as an adverse reaction to NSAIDsMucous cells1. Inhibition of mucus secretionProstaglandin(similar in action to somatostatin)2. Inhibition of prostaglandin production and releaseGastric Ulceration by Helicobacter pylori1. H. pylori penetrates the mucus layer of stomach and adheres to the surface of gastric mucosal epithelial cells. 2. Ammonia is produced which neutralizes the gastric acid. 3. H. pylori destroys tight junctions that hold epithelial layer together.4. Gastric ulceration (or Peptic Ulcers) is developed by the destruction of the mucosa, inflammation and mucosal cell death.SulforaphaneGastric UlcerTreatment options for access HCl :1. Ingestion of alkaline ions such as bicarbonate (e.g. Tums, Maalox)2. Proton pump inhibitors block K+/H+ ATPase (e.g. Omeprazole)3. H2 antagonists block action of histamine on parietal cells in stomach (e.g. Ranitidine [Zantac])123Intestinal Phase of Digestion•Intestinal phase of gastric secretion and motilityStimulation Inhibition-> depending on substances recognized in duodenum•Release of Pancreatic Juice and Bile•Stimulation of segmentation in small intestineIntestinal Phase of Gastric SecretionGallbladder Emptying and Release of Pancreatic SecretionsFats(Via circulation)ContractRelaxFigure 21.20DIARRHEA 1. OSMOTIC: Malabsorbed/Maldigested S olutes “Draw-In” Water e.g.: -Lactase Deficiency -Rotavirus -Norovirus 2. SECRETORY: Toxin/Neurotransmitter/ Endocrine Activate Cl- Channel (CFTR) via Second Messenger Pathway e.g., Cholera 3. FAST MOTILITY: Stimulated smooth muscle -> little time for absorption e.g., Inflammatory ResponseWorldwide Distribution of Deaths Caused by Diarrhea in Children Under 5 Years of Age in 2004Global mortality from diarrhea is estimated to be 1.6–2.1 million per year, with most of these deaths occur in children in developing countries under the age of 5 years. (Keusch, G.T., et al. 2006. Diarrheal diseases. In Disease control priorities in developing countries. D.T. Jamison, et al., editors. Oxford University Press. New York, New York, USA. 371–388.)Example: CholeraCholera is an acute intestinal infection caused by ingestion of food or water contaminated with the bacterium Vibrio cholerae. It has a short incubation period, from less than one day to five days, and produces an enterotoxin that causes a copious, painless, watery diarrhoea that can quickly lead to severe dehydration and death if treatment is not promptly given. Vomiting also occurs in most patients.Death rate is 1-3% if treated, but can be 50% if untreated.Figure 21.13Cl- secretion by intestinal and colonic crypt cells and salivary gland cellsSignaling Mechanisms Involved in CholeraCFTRA Better Cholera Treatment: Oral GlucoseH2O+Cl-“Nutrient-coupled“ active Na+ absorption in the small intestine can be stimulated to treat secretory diarrhea (e.g., “rice water”)Treatment of dehydration at sea:“…….Your other option is rectal rehydration. You can take advantage of the fact that the large intestine is designed to absorb fluid from feces before excretion. All you need is a plastic tube, a bag and some rehydration fluid. You can buy an enema bag at a surgical supply house or pharmacy. The technique is not rocket science. Lubricate the business end of the tube with Vaseline or anything similar, and insert it in an inch or two into the rectum.”How does this work?“……..In case of severe dehydration the body will more quickly be hydrated with an enema. It is a method that has saved knowledgeable survivors. You can absorb up to one pint rectally. Be careful not to use salt water (sea water is as dangerous absorbed rectally as it is