S2M2 physio

• - H/K ATPase in parietal cells
• - activated by gastrin, ACh and histamine
• - inhibited by somatostatin and prostaglandins
• - best target to inhibit acid secretion

-Gastrin and ACh- increase IC Ca

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

-Somatastatin and prostaglandins- inhibitory via cAMP

• - 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

• - 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)

• - 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

- caused by duodenal/ileal contraction

• -vagally mediated relaxation of stomach
• - this causes no change in pressure in stomach as its volume increases
• - inhibited by vagotomy

- 30 min-5%, 90 min-50%, 240 min-95%

-slowed by secretin and CCK via increased pyloric tone

- slowed by fat, overdistension, GIP, VIP CCK and NE via decreased peristalsis

- Gastrin(via CCK-B-r), ACh and NE decrease pyloric tone

- CHO, distension, gastrin, motilin ACh increase peristalsis

- primary- enzymes, NaCl and fluid (isotonic)

-ductal modification- NaHCO3 added

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

• - 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

-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

-pH<4=> increase S cell secretin release

-pH>4=> decreased S cell secretin release

- Na/ glucose or galactose cotransporter for CHO uptake in enterocyte

• - fructose channel in apical and basal membrane of enterocyte
• - facilitated diffusion only

- glucose/galactose and fructose trnsporter on basal surface of enterocyte

• -di and tripeptide/H coexchanger
• - dependent of Na/H coexchanger
• - apical surface of enterocyte

• - aa family specific Na/aa cotransporter
• - single aa
• - Na dependent
• - apical surface of enterocyte

ingested proteins--low pH and pepsin--> polypeptides and aa-- pancreatic peptidases--> oligopeptides and aa-- brush border peptidases--> di- and tri- peptides and aa