Pancreas and Gallbladder Physiology Flashcards
5 different aa cotransporters
neutral, aromatic, imino, positively charged, negatively charged (5 different)
Digestive enzymes are made where in pancreas
acinar cells (as zymogens)
What activates pancreatic zymogens?
enterokinase/enteropeptidase in duodenum
activates trypsin
trypsin activates others
Bicarb comes from where in pancreas?
centroacinar and duct cells
Cephalic/gastric phase pancreatic secretions
30% mostly enzyme
activated by parasympathetic efferents and gastrin
CCK released by
in response to
I-cells in response to fat/aa
Secretin released by
in response to
S-cells in response to H+
CCK intracellular pathway
Ca2+
Hereditary pancreatitis PRSS1 mutation
autosomal dominant
trypsin mutation
Pancreatic insufficiency
90% decrease in enzymes reaching lumen
Lipase is inactive in bile salts. What keeps lipase active in bile salts
colipase
PRSS1 gene
protease, serine 1 trypsinogen mutation premature activation of trypsin autodigestion of pancreas recurrent episodes of pancreatitis
PRSS1 mutations
autosomal dominant
How do pancreatic ductal cells respond to secretin?
mechanistically
CFTR puts Cl- into duct
Cl- is exchanged with HCO3- via Cl-/HCO3- antiporter
bicarb secreted into duct
GLP-1 (glucose-dependent insulinotropic peptide)
origin
action
GLP-1
from K-cells in sm intestine
increase insulin release, decrease H+ release
Leptin and Gherlin
leptin: decreases appetite
Ghrelin: increases appetite, produced by fundus during fasting, lower levels after gastric bypass
Stellate cells
location
function
pathology
liver
store vitamin A
lay down collagen in cirrhosis
How does ZE syndrome cause decreased uptake of lipids, fat soluble vitamins, and bile salts?
pancreatic lipase only active at more basic pH
too much acid = bad
