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sweetlu
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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
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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
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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
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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)
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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
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nausea
- caused by duodenal/ileal contraction
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accomodation
- -vagally mediated relaxation of stomach
- - this causes no change in pressure in stomach as its volume increases
- - inhibited by vagotomy
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gastric emptying times
- 30 min-5%, 90 min-50%, 240 min-95%
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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
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enhancers of gastric emptying
- Gastrin(via CCK-B-r), ACh and NE decrease pyloric tone
- CHO, distension, gastrin, motilin ACh increase peristalsis
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pancreatic secretion
- primary- enzymes, NaCl and fluid (isotonic)
-ductal modification- NaHCO3 added
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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
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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
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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
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control of secretin release
-pH<4=> increase S cell secretin release
-pH>4=> decreased S cell secretin release
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SGLT-2
- Na/ glucose or galactose cotransporter for CHO uptake in enterocyte
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GLUT-5
- - fructose channel in apical and basal membrane of enterocyte
- - facilitated diffusion only
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GLUT-2
- glucose/galactose and fructose trnsporter on basal surface of enterocyte
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PeP T1
- -di and tripeptide/H coexchanger
- - dependent of Na/H coexchanger
- - apical surface of enterocyte
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SLC
- - aa family specific Na/aa cotransporter
- - single aa
- - Na dependent
- - apical surface of enterocyte
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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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