GI Secretions Flashcards
(31 cards)
CFTR
on luminal side
activated by cAMP, moves Cl into the lumen
Na/Cl/K transporter
On blood side
Moves Na, 2Cl, and K into the epithelial cell to start secretion process of water
Na/K atpase
moves Na out of cell against gradient
maintains the gradients for all of this to work
What ultimately causes water to enter the lumen
Cl in the lumen, Na follows, and then Water will follow
Calcium gated Cl Channel
on the luminal side. Ca stimulates Cl influx into the lumen
Control of water into the lumen - CFTR
mechanism of control is production of cAMP
PGE2 will bind the E2 receptor, Gs protein, which increases cAMP
MAJOR WAY of controlling secretions.
Get Cl out, Na and H2O will follow.
Control of water into lumen - Ca-Cl channel
controlled using NT GALANIN, released from enteric nervous system.
activates Ca Cl channel via Gq protein, increase IP3 and DAG, increase Ca from intracellular stores, channel opens.
Major control of salivation
Parasympathetic
Serous salivary secretion
alpha amylase
K+ and HCO3- higher than plasma. added by duct cells
Mucous secreted saliva
hypotonic, low Na and Cl, high K and HCO3-
esophageal secretions
mucuous for lubrication and protection
Cardiac gland secretion
Mucus
Oxyntic Gland secretion
mucus
HCL, IF
pepsinogen
Pyloric Glands
mucous
gastrin
pepsinogen
Parietal Cells
Acid secretion
Creation of HCl
CO2+H2O with carbonic anhydrase to H2CO3 to H+ and HCO3
want to get the H+ to the lumen
Cl- moves into cell via HCO3/Cl antiport, then moves from cell to lumen
H+ is actiely pumped out of cell H/K atpase
Increasing Gastric Acid Secretion
Ach and Gastrin bind to parietal cells and causes a small increase
a larger increase happens when they bind to ECFL cells, at M3 receptors and CCKb receptors respectively. Causing the ECFL to produce histamine. which binds to H2 receptor on parietal cell, causing a large increase in HCL secretion
How does histamine work to increase HCl secretion
Gs coupled receptro increases cAMP
ramps up the H/K atpase
Inhibition of gastric acid secretion
D cells produce somatostatin= inhibitory
gastrin binds D cells to decrease gastric acid secretion
CCK inhibits gastric acid secretion
PGE2 decreases acid secretion binds Gs, decreases camp, HK never turned on
What stimulates pepsinogen secretion
secretin
gastrin
Ach
H+
Gastric Mucus Barrier
mucus secretion triggered by PGE2
forms gel barrier in stomach
asprinin blocks PGE2 (blocking PGE2 affects both the mucosa and the HCl secretion) double whammy
Phases of Gastric secretion
Cephalic (increase secretionh, sight, smell thought) Gastric phase (increase secretion, food in stomach) Intestinal phase (increase in enzymes, distention of intestine, decrease gastric acid secretion)
Pancreatic enzyme secretion
(from acinar cells)
Proteolytic (trypsinogen, chymotrypsinogen, procarboxypeptidase)
amylase
lipase (lipase, cholesterol esterase, phospholipase)
enterokinase activates trypsin, trypsin activates the others and self
pancreas also secretes a trypsin inhibitor to prevent autolysis
Pancreatic bicarb secretion
(made by centroacinar cells in the duct)
these duct cells also secrete water
CO2+H20 in the presence of carbonic anhydrase goes to H2CO3 to HCO3 and H+
HCO3 goes into the lumen via HCO3/Cl exchanger.
goal is to neutralize gastric acids and make an environment that pancreatic and intestinal enzymes can work in
