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11 Cards in this Set

  • Front
  • Back
what are some major digestive enzymes released by the pancreas?
Proteolytics:
Trypsin!

also,
chymotrypsin
elastase
-peptidases (amino, carbo, etc)

Amylase

Lipase

Nucleolytics (ribonuclease/deoxyribonuclease)
how does trypsin get activated?
Turned on by enteropeptidase (AKA enterokinase)
what's a big worry for the pancreas, and why is pancreatitis bad? how is this prevented?
all those digestive enzymes can auto-digest, and that's bad.

to stop this,

1. enzymes stored as "pro"

2. compartmentalization into zymogen granules

3. zymogen granules kept at low pH to keep them inactive (pancreas enzymes like neutral-ish pH)

4. trypsin kept off by TIP (trypsin inhibitor protein)
pancreatic secretions over time: how does it compare to saliva?
pancreatic secretions are isotonic, not hypotonic like saliva.

Na++ is high throughout.

Bicarb is high, which makes Cl- low (antiporter system).

Potassium is low, like in plasma generally.
acinar cells in the pancreas: what transporters do they have, and how do they compare to salivary acinars?
they're pretty much identical on the BL side: there's a Na/K pump, of course.

also, the Na/K/2Cl pump.

Also, a random outward channel.

DIfference is on the apical side - there's just a Cl- channel and Na+ paracellular movement.
what transporters are on the duct cell in the pancreas?
all about getting bicarb in: so the apical side has a big HCo3-/Cl- antiporter.

Need Cl- channels letting some into the lumen to drive it - have 2. One is the CFTR.

BL side has to bring in new HCO3-, does it with an Na++ symporer.

Also our typical Na/K and Na/H+ guys.
What are the regulatory proteins that control release of pancreatic secretions? what do they work through?
Secretin and VIP: these work through cAMP.


Gastrin (by GRP), ACH (binding to m3's), and CCK (binding to CCK1 or CCKa, same thing) both turn up the Ca++

all of these cause granules in the acinar cells to fuse to the membrane and get released.
experiments with CCK and VIP, used together and separately - what's found and why?
pancreas, just like the stomach, experiences POTENTIATION.

so, using things that stimulate both cAMP and
the objectives say to know about the cephalic and intestinal phases of pancreatic secretion control. what happens in the cephalic that's important here?
taste/smell/chewing/swallowing all have nervous system stimulation.

so, it makes sense that you'd get ACh release.

Also, remember that the vagovagal response spits out GRP which will up the Gastrin.

So, both ACh and gastrin will use Ca++/cGMP to up pancreatic secretion, just a little (+1)
what about the intestinal phase? this is a bit of a review of the whole thing...
low pH will up the SECRETIN secretion. this is a 3+ effect

fat/protein products: up CCK and ACh a lot.

Bile in the upper intestine is also a big turner-on of pancreatic secretions

note that blood AA levels and glucose have no effect.
what other random two things up secretion in the pancreas really high?
Ca++ in the small intestine, and bile in the intestine.