UB PGY 451LEC - Gastrointestinal Physiology

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Gastrointestinal Physiology (Hudson)Saliva- INCREASED by BOTH sympathetic and parasympathetic stimulationo Most dependent on parasympathetic- Solute concentration higher than plasma- Bicarbonate concentration lower than plasma- Secretion with decrease if you cut vagal input to salivary gland- Modification by saliva ductal cell involves secretion of K+ & bicarbonate- Secretion caused by NE and Ach- Slightly acidicDIGESTION OF MACROMOLECULESProteins- Absorbed in jejunum- Tri- and di-peptides, some free AAs- Trypsin digests proteins into peptides (active in stomach bc pH)o Tryspsinogen cleaved to trypsin in duodenum (from pancreas)Fats- Mostly triglycerides (cholesterol and phospholipids)o Digested to monoglycerides and free fatty acids- Products of fat digestion absorbed by lymphatic vesselsCarbohydrates- Starch, glycogen, cellulose most common- Monosaccharides- Lactose  glucose and galactose- Maltose  2 glucose- Sucrose  glucose and fructose- Osmotic diarrhea if not broken down (lactose intolerance)Transport across lumen- Galactose and glucose use SGLT1 (coupled with Na+)o Secondary active transport- Fructose uses facilitated diffusion (GLUT5)- All use GLUT2 facilitated diffusion out of cellParietal cells- Secrete HCl+- Depend on enzyme carbonic anhydrase- Stimulated by histamine, Ach, and gastrin- Blocked by H2 receptor blockers- Require ATP- Depends Na+/H+ exchange at basolateral membraneChief cells- In gastric mucosa- Secrete pepsinogen- Stimulated by AchG-cells- Secrete gastrin in response to acid secretion- Secreted in the stomach- GRP causes release of gastrinM-cells- Secrete motilin- Targets smooth muscle of duodenumECL cells- Releases histamine in response to acid secretion, Ach stimulation- Gastrin binds to CCKB receptorD-cells- Located in the antrum of the stomach- Secrete somatostatin in response to increase in H+ concentration of gastric contento Feedback inhibition of gastrin secretionVasoactive Intestinal Peptide (VIP)- Inhibits intestinal motility (so does NO)- Released from neurons in enteric nervous systemSubstance P- Excites intestinal motility (so does Ach)Cephalic phase- Increased flow of APs along vagus nerve to stomach- Stimulation of salivaResectioning of distal ileum- Can’t absorb fat or Vitamin B12- Can’t absorb fat b/c can’t absorb bile Chylomicrons- Fats are transported from intestinal cells to vascular space in thisform- Absorbed fats combine with cholesterol and proteins in the intestinal cells to form chylomicrons; released into lymphatic systemPancreas- Endocrine: insulin and glucagon- Exocrineo I-cells  CCK: secretes digestive enzymes (acinar cells) Stimulated by AA, fatty acids, and peptides Causes contraction of gallbladder (bile release) Inhibits gastric emptyingo Secretin: aq secretion of Na+ and HCO3- HCl is the stimulus for its release (acid in duodenum) Secreted by duct cells and apical Cl-/HCO3- antiporto Activated in the duodenumLiver- Synthesized blood proteins, hormones- Detoxifies certain substances- Produces urea- Gluconeogenesis- DOES NOT secrete digestive enzymesSlow waves in small intestinal smooth muscle cells - Oscillating release of membrane potentials - Doesn’t have to create a contraction- Spontaneous cycles of depolarization and repolarization- Interstitial cells of Cajalo Pacemakers for slow wave activity- Phasic contractions: last only seconds, in stomach and small intestine- Tonic contractions: last minutes and occur in stomachReception relaxation keeps intra-gastric pressure low following deglutition.The GI tract does NOT continuously regulate absorption.Accessory organs of digestive system:- Pancreas, salivary gland, liver, gallbladderMedulla oblongata- Swallowing center in the brain- Coordinates muscular reflexesCystic fibrosis- Defects in CFTR- Inability to transport chlorideDiarrhea- Accompanies intestinal infectionso Bacterial toxins enhance the secretion of KCl from the cells,which pulls fluid into the intestine- Secretory diarrhea: overactivation of secretion of Cl-o Imbalance between absorption & secretion- Osmotic diarrhea: unabsorbable component soaks up water and carries it out of the body in feces because no osmotic gradient- Motility related diarrhea: food irritates gut & chyme moves too fast- Inflammatory diarrhea: damage to mucosa, attempt to repair itHelicobacter pylori- Stimulates an inflammatory response - Bacteria living in mucosa; generates products to protect itself from acid- Causes gastric ulcers; best treatment is proton pump inhibitors


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UB PGY 451LEC - Gastrointestinal Physiology

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