Ecay Secretions 2

Front 1

acinar cells make up

Back 1

80% of the gland , ductal 4%, and islet 2%

Front 2

paras stimulate

Back 2

and symps inhibt

Front 3

Pancreatic juices neutralize stomach acid and secrete 1L a day.

Back 3

Is always isotonic w/ plasma but has varying compositions

Front 4

As secretion rate increases

Back 4

HCO3 increases and Cl- decreases. At very low rates, more CL- than HCO3

Front 5

duct aqueus component of neutralization

Back 5

The aqueous component is secreted by the duct and centroacinar cells. It contains
HCO3
- that can be up to several times its concentration in plasma.

Front 6

A basolateral Na/H transporter uses Na inward gradient to pump H+ out and

Back 6

alkalinizes the cytoplasm and favors production of HCO3
- in the cytoplasm by carbonic
anhydrase. HCO3 accumulates in cytoplasm. There is also a Na/HCO3 mechanism

Front 7

Co2 is also used to make HCO3 in cell

Back 7

Excreted H+ combines with HCO3
- in plasma
to generate more CO2. CO2 diffuses into cells easily. Oh- for CA rexn come from the dissociation of water.

Front 8

HCO3 exits the lumen through a

Back 8

Cl-/HCO3 antitransport mechanism mechanism (cl in) however can recycle back into the lumen (cl-) through the cystic fibrosis Cl- channel

Front 9

Na and K+ are also in the lumen

Back 9

lumen negative pulls Na+ in

Front 10

Secretin acts to cause secretion by

Back 10

activating the CFTC via phosphorylation via cAMP mechanism and PKA, and also activates the basolateral Na/HCO3 mech

Front 11

Ach stimulates HC03 secretion by

Back 11

activating Gq, which in turn stimulates PLC to release DAG which stimulates PLC and IP3 which release Ca2+ from internal stores.

Front 12

Enzymes of the Pancreas aid in digestion and

Back 12

All enzymes
are synthesized and secreted by the acinar cells. Lipase and lipase amylase are active upon
secretion. Pancreatic proteases are secreted in an inactive form (proenzymes).

Front 13

How is pancreatic acinar cell stimulated

Back 13

CCK and
acetylcholine stimulate a rise in cytosolic
calcium and activation of protein kinase C
(PKC). These intracellular second
messengers are the main regulators of acinar
enzyme secretion. Secretin and VIP activate
cyclic AMP production, which provides an
additional but minor stimulus for protein
secretion.

Front 14

So the pancreatic products both aqueus and zymogen are released by

Back 14

Acid entering the duodenum stimulates secretion of the aqueous component.
2) Fatty acids and protein in the duodenum stimulate secretion of the enzymatic
component.

Front 15

Cephalic phase (Low volume high enzyme secretion.)

Back 15

not a vagovagal response from food that causes acetycholin to stimulate acinar cells for release

Front 16

Another phase of the vagovagal reflex is the release of Gastrin from g cells inthe stomach via GRP peptide releasing hormones

Back 16

that activate CCK release in the pancreatic acini. Peptides, food in stomach, and sight smell taste of food do this.

Front 17

Fat and protein in the intestinal phase

Back 17

cause ach to produce aciini secretion

Front 18

H + acs on S cells for secretin, and proteins act on I cells to release CCK which

Back 18

stimulate receptors on duct cells for Hco3- release and to act on receptors of accini cells for enzyme release respectively (intestinal phase)

Front 19

Gastric phase (Low volume high enzyme secretion.)

Back 19

Distention of proximal or distal stomach stimulates pancreatic secretion through a
vagovagal reflex. Since this is mediated by acetylcholine it is mainly a low volume, high
enzyme secretion. Again gastrin has no effect. The gastric phase is small, only 5-10%
of the total pancreatic response to a meal.

Front 20

Intestinal phase (High volume, high enzyme)

Back 20

70-80% of maximal response.
Acid in the duodenum releases secretin from duodenal S-cells. Secretin is the principal
stimulator of aqueous secretion (HCO3
-).

Front 21

Intestinal Phase

Back 21

Fat and protein stimulate release of CCK from duodenal I-cells. CCK is primary stimulant
of enzyme secretion. In addition, chemoreceptors in duodenum for acid, fat, peptides
amino acids initiate vagovagal reflexes, and the release of ACH.

Front 22

Potentiation of Intestinal phase

Back 22

Alone, CCK and ACH have little effect on duct cells, but greatly potentiate effects of
secretin on the aqueous component.

Front 23

Somatostatin,
pancreatic
polypeptide

Back 23

Inhibits release or action
of CCK, secretin, and
acetylcholine

Front 24

Secretin release is dependent on pH

Back 24

Secretin release begins at a pH of
4.5 and increases linearly to pH 3.0.
After 3.0, an increase in secretin
release depends on acidification of
additional duodenal area.

Front 25

CCK release is dependent on fats and amino acids

Back 25

CCK release is stimulated by l-amino
acids and fatty acids of 8 carbons or
more. Phenylalanine, tryptophan and
methionine are the most effective
amino acids.

Front 26

Where do you find secretin and CCK secreting cells

Back 26

Secretin- and CCK-secreting entero
chromaffin (ECL) cells are present
throughout the duodenum and
jejunum.

Front 27

neutralization of a meal gastric acids

Back 27

Most pH neutralization in the duodenum is due to pancreatic HCO3
-. However, the liver
and duodenal mucosa can also secrete HCO3
-. Enzyme secretion increases rapidly after
chyme enters duodenum and peaks 30 min later at 70-80% of maximum.

Front 28

Second messengers:
1. Secretin - cAMP
2. Acetylcholine - Ca2+ via IP3
3. CCK - Ca2+ via IP3

Back 28

Secretin + ACh = potentiation Secretin + CCK = potentiation ACh + CCK = additive

Front 29

VERY IMPORTANT BUT NOT CLINICALLY

Back 29

Secretin does NOT potentiate CCK or ACh stimulation of acinar cell enzyme
secretion.

Front 30

How much pancreatic enzyme is needed

Back 30

Pancreatic enzymes must be reduced to 20% or less for fatty acids to show up in stool.
(steatorrhea). Thus, pancreatic enzymes are secreted in great excess.

Front 31

Pancreatic secretions

Back 31

Enzymes are produced by acinar cells. HCO3 is produced by the ductal cells.

Front 32

The major stimuli for enzyme secretion is CCK and acetylcholine (from vagus and
enteric nerves).

Back 32

yep

Front 33

The major stimulus for HCO3 secretion is secretin.

Back 33

yeper

Front 34

CCK and acetylcholine potentiate the effect of secretin on ductal cells.

HOWEVER

Back 34

Secretin does
not potentiate the effects of CCK and acetylcholine on acinar cells.

Front 35

At high rates
of secretion, HCO3 is high and Cl is low.

Back 35

This is due to the action of a Cl/HCO3
exchanger on the lumenal membrane of ductal cells.

Front 36

Cephalic phase - (low volume, high enzyme) Stimuli similar to cephalic phase of gastric
secretion.

Back 36

Mediated by vagus release of acetylcholine and its affect on acinar secretion.

Front 37

Gastric phase

Back 37

(low volume, high enzyme) Vagovagal reflex response to gastric
distention.

Front 38

Intestinal phase - (high volume, high enzyme) 70-80% of maximal response.

Back 38

Mediated
by GI peptide hormones secretin and CCK, which are released from S-cell and I-cell
enterochromafin (EC) cells in the duodenum, and acetylcholine released from vagus and
enteric nerves.

Front 39

do review questions

Back 39

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