BMS_260_Week12_Notes.pdf BMS 260
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This 5 page Class Notes was uploaded by Mikaela Maldonado on Friday April 15, 2016. The Class Notes belongs to BMS 260 at Colorado State University taught by Dr. Russell Anthony in Spring 2016. Since its upload, it has received 19 views. For similar materials see Biomedical Sciences in Biomedical Sciences at Colorado State University.
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Date Created: 04/15/16
Accessory Digestive Organs Pancreas Underneath the liver Endo/exocrine gland Tubular epithelial Endocrine – insulin and glucagon Majority is exocrine Main pancreatic duct – Duct of Wirsung Accessory duct – duct of Santorini Alveoli – cells (pyramid shaped acinar) Exocrine cells secrete enzymes Duct cells secrete bicarbonate Liver 2 lobes right is large left is smaller sits underneath the diaphragm common hepatic duct –central join of many hepatocyte = liver cell gall bladder – stores bile until it is needed secretory organ - bile processes and stores nutrients – glucose in the form of glycogen fat in liver filter and function in the removal of old red blood cells which leader to hemoglobin processing and generation of bilirubin (pigment in bile) synthesis of plasma proteins (albumin, clotting protein, angiotensin) common bile duct empties into the duodenum bile salts will also recycle back to the liver through the hepatic portal vein (75% of the blood to the liver hepatic portal system delivers absorbed nutrients to liver for processing before them enter the general systemic circulation hepatic lobule central vein in the center empty into hepatic vein coalesce into the hepatic portal vein portal triad on the edge hepatic artery 25% of blood and most oxygen portal vein 75% deoxygenated blood branch of bile duct Kuppfer cells Anchored macrophages within liver Sinusoids Bile ducts run through sinusoids Canniculi travel out of liver primarily Salivary glands Acinus region – produce material Glanular portion Serous cells – zymogen portion Mucus cells – lubrication Concentration of Na, K, Cl, HCO3, H20 is very similar to that of blood Amylase Starch splitting enzyme Amylose – simple no branching Amylopectin – branching Cleaves alpha 1.4 linkages Does not cleave alpha 1.6 linkages (gives branch) Does not cleave beta 1.4 linkages – found in cellulose Does not cleave at terminal alpha 1.4 Does not cleave at alpha 1.4 linkages next to a branch point Will end up with Maltose – 2 glucose molecules Maltotriose – 3 glucose molecules Oligosaccharides Stomach Gastric glands Chief cells – pepsinogen Parietal cells -> HCL and intrinsic factor Endocrine cells G cells release gastrin which increase release of HCl D cells release somatostatin – decrease release of HCl Pepsinogen Reacts with HCl to produce pepsin Pepsin Is a protease – cleaves proteins at aromatic amino acids Parietal cells – release HCl – pH of 0.8 – helps to kill bacteria Mucus protects the stomach HCl Activates pepsinogen to pepsin Helps with hydroloysis of protein Fe digestion/absorption Fe 3+ (ferric iron) Needs to be Fe 2+ (ferrous) to be absorbed in the small intestine Protons are actively pumped out through ATPase pump into the lumen Pump inhibitors are Prilosec and pepeid HCO3 goes towards blood Can measure a slight rise in blood pH right after eating Alkaline tide Intrinsic factor Acts as a carrier for vitamin B12 Helps its absorption in ileum HCl production decreases with ages as well as intrinsic factor that leads to a B 12 deficiency Regulation Volume/composition rather than nutritional state of the body Absorb all the nutrients taken in Basic principles of control ENS Submucosal plexus only resides in small/large intestine Myenteric plexus CNS System through regulation of SNS and PNS Gastrointestinal Tract Wall Mucosa Epithelium Lamina propria Muscularis mucosa Submucosa Major blood and lymphatic vessels Submuscosal plexus Muscularis externa Circular muscle Myenteric plexus Longitudinal muscle Serosa Cephalic phase Stimuli – brain – increase enteric neural activity – gastrin secretion – histamine – HCl (increase gastrin)– somastatin – inhibits more HCl Gastric phase stimuli Luminal distension Amino acid and peptides Vagal nerve release of ectylcholine ENS Gastrin releasing peptide (GRP) stimulate to release gastrin Ach inhibits D cells Chemoreceptors – stimulate chief cells (release pepsinogen – protein digestion) Mechanoreceptors – stimulate G cells, parietal cells As the pH drops – stimulate D cells to secrete somatostatin Chyme – products of gastric digestion Intestinal phase Decrease pH, increase fat, a.a., hyper tonicity – neural receptors (ENS) increase secretion of enterogastrones (hormones) Short reflexes decrease emptying Long reflexes increase sympathetic efferents and decrease parasympathetic Enterocytes – epithelial lining of intestine and specialized ones produce cholecystokinin (CCK) CCK paired with secretin inhibit stomach activity Pancreatic secretions Trypsinogen, chymotrypsinogen Endoproteases – creates small peptides (also true for pepsin) Carboxypeptidase – exoprotease, cleave off a. a. Enterokinase – cleaves trypsinogen into trypsin Trypsin – activates chymotrypsinogen and procarboxypeptidase Control Increase fatty acids and a.a,, CCK, and enzyme secretion Liver – bile secretion Involved in fate digestion Bile salts – derivative of cholesterol Cholesterol Bilirubin Lecithin (phospholipid) Secretin will stimulate bile production Carbohydrates, proteins, lipids, Calcium, iron and folate – absorbed in duodenum Bile acids, B12 – ileum absorbs Proteins Pepsin creates peptide fragments stomach trypsin and chymotrypsin in small amounts Enterocyte absotption of amino acids Apical membrane – Na coupled transport individual a.a. Fragments are digested to a. a. by carboxypeptidase form pancreas and aminopeptidase on luminal side of small intestine Proton cotransport of small peptids (2-3 a. a.) PepT1 is a proton cotransporter
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