Gi--Pancreatic And Bile Secretion

Front 1

What granules and what organelle are seen in volume in the pancreas?

Back 1

Zymogen granules and lots of ER

Front 2

What is the most important hormone governing pancreatic ENZYME secretions? What does it bind? What is the second most important?

Back 2

CCK
It binds CCK-A
2nd most important is ACh

Front 3

What other receptors are present on the pancreas besides the CCK-A receptor?

Back 3

Secretin and VIP receptors--not as important as CCK and ACh

Front 4

What are some active enzymes found within the pancreas? How does it work?

Back 4

LIPASE--needs colipase to work and colipase is cleaved to be active only by trypsin

Front 5

True/False: If you change your diet, then the pancreas will change what enzymes it secretes.

Back 5

TRUE--it will adjust to produce either more lipase or more amylase

Front 6

What percent of bicarb is secreted by the duodenum itself?

Back 6

40% from crypts and surface cells

Front 7

True/False: The pancreatic primary secretion is analogous to salivary primary secretion

Back 7

FALSE--most of the pancreatic secretion is made by the ducts

Front 8

What happens in the pancreatic secretions at high flow rate?

Back 8

DRAMATIC increase in bicarb

Front 9

How are ions secreted from the acinar cells?

Back 9

Na+/K+ pump builds Na+ outside the cell in the interstitial space
Na/K/Cl cotransporter pulls in all three and is driven by the Na+ gradient
K+ escapes back to interstitium through its channel
Cl- is then secreted into the acinus through an apical Cl- channel
This Cl- buildup in the acinus creates a gradient that flows back down into the cell through a BICARB/Cl- EXCHANGER

Front 10

What transporter is critical in pancreatic secretions in Cl- transport?

Back 10

CFTR

Front 11

Are pancreatic ducts permeable to water?

Back 11

YES

Front 12

What is the tonicity of the bicarb solution in the acinus?

Back 12

Isotonic

Front 13

How does gastrin come into play in the pancreas?

Back 13

It binds the CCK-A receptor that is similar to its normal CCK-B receptor and stimulates secretion

Front 14

What occurs to stimulate the pancreas during the duodenal/intestinal phase?

Back 14

Fat and protein stimulates I cells to make CCK
Protons from stomach stimulate S cells to release secretin which pushes water out into the ducts?

Front 15

Which is more important to stimulate pancreatic activity--food or acid?

Back 15

FOOD--acidity never really gets low enough

Front 16

What are the most important systemic regulators of pancreatic secretions?

Back 16

pH<4.5 and FA's cause release of secretin from S cells in the duodenum; fat, peptides, and amino acids cause CCK release from I cells of the duodenum

Front 17

Bile makeup.

Back 17

Gallbladder bile is much more concentrated than hepatic bile in all respects

Front 18

Bile acids that have a 7' Hydroxyl group will be?

Back 18

More hydrophilic.

Front 19

What is a secondary bile acid and how is it made?

Back 19

in the gut--OH group is stripped off and so the bile acid is more hydrophobic

Front 20

Where do primary and secondary bile acids get conjugated?

Back 20

In the liver--taurine and glycine is added

Front 21

Why are bile salts conjugated to amino acids?

Back 21

It makes them more soluble--easier to make micelles and fat digestion is more efficient

Front 22

How are bile salts transported into the hepatocyte? Out?

Back 22

By sodium dependent co-transport
Primary active transport

Front 23

TRUE/FALSE: CFTR is not important in bile ducts.

Back 23

FALSE

Front 24

Secretin, glucagon, and VIP receptors in bile duct transporters cause what?

Back 24

Increase in cAMP that causes CFTR channels to transport more Cl-

Front 25

What is enterohepatic circulation?

Back 25

Bile salts are reabsorbed in the terminal ileum--bacteria have stripped off 7'OH group and stripped off AA conjugation

Front 26

Why do we need a gallbladder?

Back 26

Bile salts are excellent detergents that solubilize fat--if they are stored in the gallbladder then we can minimize losses and prevent exposure

Front 27

How is bile concentrated?

Back 27

Na/Cl exchanger and H+/Bicarb exchanger--salt is moved across cell to BL membrane and into the interstitium and draws water with it
Tight junctions = high resistance epthelium

Front 28

Is the tight junction really tight?

Back 28

NO--we are talking about electrical resistance and this is a leaky junction that allows water through and therefore only a small amount of salt is needed to be moved across to draw a lot of water

Front 29

True/False: Vagal stimulation has an effect on bile production

Back 29

TRUE--it stimulates gallbladder contraction

Front 30

Gall stones occur why?

Back 30

When there is an imbalance in the levels of cholesterol vs. bile salt.

Front 31

How is bilirubin metabolized?

Back 31

It is a breakdown product of hemoglobin
It is conjugated to plasma albumin to be carried in the blood to the liver
It is taken up in the liver and binds GLUCURONIC ACID to become more soluble
It is secreted into bile and ends up in the gut
It is deconjugated by bacteria in the gut into bilirubin
Bilirubin is converted to urobilinogen
Some urobilinogen is reabsorbed to portal circulation(THE IMPORTANT PART OF THIS PROCESS) and this goes to the kdineys to be excreted in the urine

Front 32

Why is urobilinogen important?

Back 32

It is eliminated partially in the kidneys

Front 33

What are the three types of jaundice?

Back 33

Pre-hepatic i.e. increased hemolysis; Sickle cell anemia, thalassemia and hemolytic disease of the newborn

Intra-hepatic i.e. decreased conjugation or decreased uptake of bilirubin; hepatitis, cirrhosis, liver cancer; neonatal jaundice

Post-hepatic i.e. obstruction of bile flow; cholelithiasis, structural disorders of the bile duct, obstruction due to tumors

Front 34

What eventually happens to urobilinogen?

Back 34

It is oxidised to urobilin and stercobilin