S2M2 physio

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S2M2 physio
2012-03-13 15:57:51
S2M2 physio

S2M2 physio
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  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
  22. surface lipolysis
    • - lipolysis of TAGs on surface of micelle
    • - lipase performs lipolysis
    • - colipase brings TAG and lipase together
    • - liberated FA and MAG taken up into micelle
  23. multivalent cation absorption
    • - Ca and Fe
    • - absorbed in proximal duodenum
  24. control of H2O secretion in intestines
    • - submucosal neuronal ACh and VIP release stimulate secretion
    • - absorption NOT regulated
    • -PNS input through ENS promotes net secretion of electrolytes and water
  25. oral rehydration therapy
    • - mixture of water, Na and glucose given
    • - action of SGLT1 will increase glucose and Na uptake and water will then follow
  26. MMC
    • -migrating motor complex
    • - strong waves of contraction from stomach to terminal ileum acting as a sweeper(during fasting)
    • - at peak of MMC motilin is releases
    • - after feeding its action is mixing and propulsive
  27. interstitial cells of Cajal (ICC)
    • - pacemaker of gut membrane potentials
    • - in close contact with neurons of the myenteric plexus
  28. Liver detoxification
    • Phase 1- P-450 mediated modification
    • Phase 2- conjugation
    • Excretion
    • -a drug can enter phase 1 or 2, or go thru both or go straight to excretion
  29. glucuronyl transferase
    -bilirubin + glucuronic acid-> bilirubin diglucuronide
  30. cholangiocyte
    • - HCO3 secretion from bile duct
    • - increased by secretin, glucagon and VIP

    -NBC- Na/HCO3 cotranporter on basolateral surface
  31. final pH of urine
    - dictated by IC cells of the CD
  32. final [Na] and [K] in urine
    • - dictated by principal cells in the CD
    • - Aldo and ADH sensitive ENaC is the gate
  33. Aldosterone
    • - Na reabsorption (via ENaC channel implantation)
    • - K (apical K channels) and H secretion
    • - BL Na/K ATPases