Pancreas and Gallbladder Physiology Flashcards

1
Q

5 different aa cotransporters

A

neutral, aromatic, imino, positively charged, negatively charged (5 different)

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2
Q

Digestive enzymes are made where in pancreas

A

acinar cells (as zymogens)

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3
Q

What activates pancreatic zymogens?

A

enterokinase/enteropeptidase in duodenum
activates trypsin
trypsin activates others

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4
Q

Bicarb comes from where in pancreas?

A

centroacinar and duct cells

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5
Q

Cephalic/gastric phase pancreatic secretions

A

30% mostly enzyme

activated by parasympathetic efferents and gastrin

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6
Q

CCK released by

in response to

A

I-cells in response to fat/aa

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7
Q

Secretin released by

in response to

A

S-cells in response to H+

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8
Q

CCK intracellular pathway

A

Ca2+

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9
Q

Hereditary pancreatitis PRSS1 mutation

A

autosomal dominant

trypsin mutation

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10
Q

Pancreatic insufficiency

A

90% decrease in enzymes reaching lumen

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11
Q

Lipase is inactive in bile salts. What keeps lipase active in bile salts

A

colipase

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12
Q

PRSS1 gene

A
protease, serine 1
trypsinogen mutation
premature activation of trypsin
autodigestion of pancreas
recurrent episodes of pancreatitis
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13
Q

PRSS1 mutations

A

autosomal dominant

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14
Q

How do pancreatic ductal cells respond to secretin?

mechanistically

A

CFTR puts Cl- into duct
Cl- is exchanged with HCO3- via Cl-/HCO3- antiporter
bicarb secreted into duct

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15
Q

GLP-1 (glucose-dependent insulinotropic peptide)
origin
action

A

GLP-1
from K-cells in sm intestine
increase insulin release, decrease H+ release

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16
Q

Leptin and Gherlin

A

leptin: decreases appetite
Ghrelin: increases appetite, produced by fundus during fasting, lower levels after gastric bypass

17
Q

Stellate cells
location
function
pathology

A

liver
store vitamin A
lay down collagen in cirrhosis

18
Q

How does ZE syndrome cause decreased uptake of lipids, fat soluble vitamins, and bile salts?

A

pancreatic lipase only active at more basic pH

too much acid = bad