GI - Pancreas, Liver Flashcards

(40 cards)

1
Q

pancreatic secretory structure

A

digestive enzymes mad ein acinar cells

ductal cells modify filtrate

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2
Q

pancreatic acinar cells secrete

A

proteases (zymogens): trypsinogen, chymotrypsinogen, procarboxypeptiddase, proelastase
pancreatic amylase
lipases: pancreatic lipase, carboxyl ester lipase, colipase, phospholipase A

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3
Q

pancreatic protection from autodigestion

A

secrete zymogens that are activated in intestines by membrane bound enterokinase
also secrete trypsin inhibitor

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4
Q

activation of zymogens in SI

A

enterokinase activates trypsinogen to trypsin

trypsin activates chymotrypsinogen, procarboxypeptidase and trypsinogen

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5
Q

how do active enzymes in SI become inactivated

A

bacteria

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6
Q

things that stimulate pancreatic acinar cell secretion

A

CCK*
ACh
secretin

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7
Q

pancreatic potentiation

A

CCK + ACh = additive

CCK + secretin = potentiation

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8
Q

pancreatic potentiation cause

A

CCK/ACh use Ca as secondary messenger

secretin use cAMP as secondary messenger

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9
Q

neuronal stim of pancreatic secetions

A

thought/chew –> vagal and enteric stim acinar/duct (cephalic)
vagovagal/gastropancreatic
distention –> reflexes stim acinar/duct (gastric)

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10
Q

hormonal stim of pancreatic secretions

A

acid in SI –> secretin stim duct cells
AA/FA in SI –> CCK stim vagovagal reflexes to acinar/duct
distention/hypertonicity –> enteropancreatic reflexes stim acinar/duct

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11
Q

Cystic fibrosis transmembrane conductance regulator (CFTR)

A

shuttles Cl from duct cell into lumen

makes gradient for HCO3 exchange (HCO3 into lumen)

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12
Q

most powerful regulator of HCO3 secretion

A

secretin

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13
Q

results of CFTR

A

liquify protein rich secretion of acinar cells (Cl brings in water)
keep pancreatic proenzymes inactive (alkaline)

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14
Q

importance of CFTR

A

if don’t dilute protein secretion ducts become blocked

destroy pancreatic tissue, replace with fibrotic tissue

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15
Q

things that cause pancreatitis

A

alcohol abuse
hepatotoxic drugs
microorganisms

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16
Q

results of pancreatitis

A

swelling –> compresses panc duct –>. retention of panc secretions –> digestion of panc tissue

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17
Q

liver fxns

A

intermediary metabolism (for other organs)
metabolize drugs
synthesize plasma proteins
store glycogen, fat, Fe, Cu, vit A, D, B12
activation of vit D
excretion of CHL/bilirubin
fat digestion

18
Q

hepatic portal vein carries

A

carry venous blood draining the digestive tract

19
Q

hepatic portal vein fxn

A

processes/stores newly absorbed nutrients

20
Q

hepatic portal vein structure

A

branches repeatedly, forming smaller venules –> sinusoids

21
Q

hepatic artery carries

A

arterial blood

22
Q

hepatic artery fxn

A

provide liver O2 supply and metabolites for hepatic processing (25%)

23
Q

hepatic artery structure

A

branches –> arterioles –> capillaries –> sinusoids

24
Q

liver lobule structure

A

hexagonal arrangements of tissue around central vein
3 vessels @ periphery (hepatic artery, portal vein, bile duct)
sinusoids empty into central vein –> hepatic vein

25
hepatocytes
60% of cell production | responsible for most synthetic/metabolic fxns of liver
26
hepatocyte structure
arranged inplates 1 cell thick (increase SA) | polarized: basolateral (sinusoidal) and apical (canalicular) domains
27
stellate (Ito) cells
fat-storing cells contain vitamin A transformed to myofibroblasts following injury (can secrete collagen into the sinusoids)
28
bile composition
excretory: bilirubin, drug metabolites, CHL secretory: bile, HCO3
29
making bile
primary bile acids (synthesized from CHL) conjugated w/ glycine/taurine, secreted as a Na salt --> more soluble secondary bile acid made by bacteria in SI by dehydroxylation
30
bile fxn
emulsify fat droplets increase SA for digestive enzymes eliminate excess CHL (solubilize) facilitate absorption of fat-soluble vitamins
31
how bile works
bile particle has a hydrophobic and hydrophilic part hydrophobic inserts in fat, hydrophilic stays outside form tiny balls that repel each other
32
gall stones
gallbladder stores bile - if CHL isn't soluble enough it precipitates --> gall stones
33
sphincter of Oddi
@ common bile duct/SI jxn | open @ meal time
34
CCK and gallbladder
stim gallbladder to contract | relax sphincter of Oddi
35
secretin and gallbladder
stimulate secretion of HCO3
36
how does liver know its meal time
recovered bile (2/3 of total) return to liver in portal circulation
37
de novo bile salt synthesis
when bile is returned, liver knows its meal time (@ meal time use only recycled bile salts) when no bile returned, liver knows its no longer meal time (then use all de novo)
38
bile salts -- liver feedback
positive feedback: bile salts in portal blood stimulates rate of secretion by liver negative feedback: bile salts in portal blood inhibits the synthesis of new bile acids by liver
39
age changes in liver
``` repair of damaged cells is slower ability to withstand stress goes down down blood flow down drug metabolism (up half life, side effects) down production/flow of bile ```
40
age changes to pancreas
pancreatic ductal hyperplasia, fibrosis down enzyme secretion down bile salt synthesis (liver) down potential for fat digestion