S2M2 physio

  1. proton pump
    • - H/K ATPase in parietal cells
    • - activated by gastrin, ACh and histamine
    • - inhibited by somatostatin and prostaglandins
    • - best target to inhibit acid secretion
  2. pathways of PP activation
    -Gastrin and ACh- increase IC Ca

    -histamine- cAMP p/w **histamine is most potent secretagogue**

    -Somatastatin and prostaglandins- inhibitory via cAMP
  3. alkaline tide
    • - phenomenon seen with acid secretion from parietal cells
    • -CA makes H2CO3 which disassociates into H+ and HCO3-
    • - H is pumped into stomach lumen (H/K ATPase) and HCO3 into the blood (HCO3/Cl coex)
    • - resulting in an increase in pH of th blood
  4. mucous protection in the stomach
    • - ACh and prostaglandins increase mucous secretion, which forms a neutral pH "mucous buffer zone" on the apical surface of gastric cells that prevent autodigestion
    • - mucin gel is viscous and restrict ion diffusion
    • -degraded by pepsin (cheif cell activated secretion) at the mucin core b/c subunits are glycosylated(protected)
  5. tLESR
    • - transient LER relaxation
    • - 20-30 sec relaxation of LES to allow gas venting(burp)
    • - immediately followed by and incresed LES tone then drop down to normal tone
  6. nausea
    - caused by duodenal/ileal contraction
  7. accomodation
    • -vagally mediated relaxation of stomach
    • - this causes no change in pressure in stomach as its volume increases
    • - inhibited by vagotomy
  8. gastric emptying times
    - 30 min-5%, 90 min-50%, 240 min-95%
  9. inhibitors of gastric emptying
    -slowed by secretin and CCK via increased pyloric tone

    - slowed by fat, overdistension, GIP, VIP CCK and NE via decreased peristalsis
  10. enhancers of gastric emptying
    - Gastrin(via CCK-B-r), ACh and NE decrease pyloric tone

    - CHO, distension, gastrin, motilin ACh increase peristalsis
  11. pancreatic secretion
    - primary- enzymes, NaCl and fluid (isotonic)

    -ductal modification- NaHCO3 added
  12. acinar secretion
    CCK( I cell in duodenum) and ACh and GRP (CNS) increase Ca, causing exocytosis

    Secretin (S cells in duodenum) and VIP (CNS) increase cAMP, causing exocytosis
  13. ductular HCO3 secretion
    • - CA in acinar cell makes H2CO3 which disassociates into H and CO3
    • - HCO3 pumped into lumen via HCO3/Cl exchanger
    • - Cl leaks back out via CFTR for continued supply
    • - Na/H exchanger (powered by SAT via NaK ATPase) puts H into interstitial space where EC CA combines it with EC HCO3
    • - Na also leaks between cell bringing H20 with it into lumen
  14. control of CCK release
    -ACh and GRP from CNS=> moniter peptide release from acinar cells=> I cell CCK secretion

    -nutrients => CCK-RP release from epithelium=> I cell CCK secretion

    -trypsin inactivates moniter peptide and CCK-RP
  15. control of secretin release
    -pH<4=> increase S cell secretin release

    -pH>4=> decreased S cell secretin release
  16. SGLT-2
    - Na/ glucose or galactose cotransporter for CHO uptake in enterocyte
  17. GLUT-5
    • - fructose channel in apical and basal membrane of enterocyte
    • - facilitated diffusion only
  18. GLUT-2
    - glucose/galactose and fructose trnsporter on basal surface of enterocyte
  19. PeP T1
    • -di and tripeptide/H coexchanger
    • - dependent of Na/H coexchanger
    • - apical surface of enterocyte
  20. SLC
    • - aa family specific Na/aa cotransporter
    • - single aa
    • - Na dependent
    • - apical surface of enterocyte
  21. polypeptide breakdown
    ingested proteins--low pH and pepsin--> polypeptides and aa-- pancreatic peptidases--> oligopeptides and aa-- brush border peptidases--> di- and tri- peptides and aa
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S2M2 physio
S2M2 physio