GI - Pancreas, Liver Flashcards

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
Q

hepatocytes

A

60% of cell production

responsible for most synthetic/metabolic fxns of liver

26
Q

hepatocyte structure

A

arranged inplates 1 cell thick (increase SA)

polarized: basolateral (sinusoidal) and apical (canalicular) domains

27
Q

stellate (Ito) cells

A

fat-storing cells
contain vitamin A
transformed to myofibroblasts following injury (can secrete collagen into the sinusoids)

28
Q

bile composition

A

excretory: bilirubin, drug metabolites, CHL
secretory: bile, HCO3

29
Q

making bile

A

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
Q

bile fxn

A

emulsify fat droplets
increase SA for digestive enzymes
eliminate excess CHL (solubilize)
facilitate absorption of fat-soluble vitamins

31
Q

how bile works

A

bile particle has a hydrophobic and hydrophilic part
hydrophobic inserts in fat, hydrophilic stays outside
form tiny balls that repel each other

32
Q

gall stones

A

gallbladder stores bile - if CHL isn’t soluble enough it precipitates –> gall stones

33
Q

sphincter of Oddi

A

@ common bile duct/SI jxn

open @ meal time

34
Q

CCK and gallbladder

A

stim gallbladder to contract

relax sphincter of Oddi

35
Q

secretin and gallbladder

A

stimulate secretion of HCO3

36
Q

how does liver know its meal time

A

recovered bile (2/3 of total) return to liver in portal circulation

37
Q

de novo bile salt synthesis

A

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
Q

bile salts – liver feedback

A

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
Q

age changes in liver

A
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
Q

age changes to pancreas

A

pancreatic ductal hyperplasia, fibrosis
down enzyme secretion
down bile salt synthesis (liver)
down potential for fat digestion