GI - Pancreas, Liver Flashcards
pancreatic secretory structure
digestive enzymes mad ein acinar cells
ductal cells modify filtrate
pancreatic acinar cells secrete
proteases (zymogens): trypsinogen, chymotrypsinogen, procarboxypeptiddase, proelastase
pancreatic amylase
lipases: pancreatic lipase, carboxyl ester lipase, colipase, phospholipase A
pancreatic protection from autodigestion
secrete zymogens that are activated in intestines by membrane bound enterokinase
also secrete trypsin inhibitor
activation of zymogens in SI
enterokinase activates trypsinogen to trypsin
trypsin activates chymotrypsinogen, procarboxypeptidase and trypsinogen
how do active enzymes in SI become inactivated
bacteria
things that stimulate pancreatic acinar cell secretion
CCK*
ACh
secretin
pancreatic potentiation
CCK + ACh = additive
CCK + secretin = potentiation
pancreatic potentiation cause
CCK/ACh use Ca as secondary messenger
secretin use cAMP as secondary messenger
neuronal stim of pancreatic secetions
thought/chew –> vagal and enteric stim acinar/duct (cephalic)
vagovagal/gastropancreatic
distention –> reflexes stim acinar/duct (gastric)
hormonal stim of pancreatic secretions
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
Cystic fibrosis transmembrane conductance regulator (CFTR)
shuttles Cl from duct cell into lumen
makes gradient for HCO3 exchange (HCO3 into lumen)
most powerful regulator of HCO3 secretion
secretin
results of CFTR
liquify protein rich secretion of acinar cells (Cl brings in water)
keep pancreatic proenzymes inactive (alkaline)
importance of CFTR
if don’t dilute protein secretion ducts become blocked
destroy pancreatic tissue, replace with fibrotic tissue
things that cause pancreatitis
alcohol abuse
hepatotoxic drugs
microorganisms
results of pancreatitis
swelling –> compresses panc duct –>. retention of panc secretions –> digestion of panc tissue
liver fxns
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
hepatic portal vein carries
carry venous blood draining the digestive tract
hepatic portal vein fxn
processes/stores newly absorbed nutrients
hepatic portal vein structure
branches repeatedly, forming smaller venules –> sinusoids
hepatic artery carries
arterial blood
hepatic artery fxn
provide liver O2 supply and metabolites for hepatic processing (25%)
hepatic artery structure
branches –> arterioles –> capillaries –> sinusoids
liver lobule structure
hexagonal arrangements of tissue around central vein
3 vessels @ periphery (hepatic artery, portal vein, bile duct)
sinusoids empty into central vein –> hepatic vein
hepatocytes
60% of cell production
responsible for most synthetic/metabolic fxns of liver
hepatocyte structure
arranged inplates 1 cell thick (increase SA)
polarized: basolateral (sinusoidal) and apical (canalicular) domains
stellate (Ito) cells
fat-storing cells
contain vitamin A
transformed to myofibroblasts following injury (can secrete collagen into the sinusoids)
bile composition
excretory: bilirubin, drug metabolites, CHL
secretory: bile, HCO3
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
bile fxn
emulsify fat droplets
increase SA for digestive enzymes
eliminate excess CHL (solubilize)
facilitate absorption of fat-soluble vitamins
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
gall stones
gallbladder stores bile - if CHL isn’t soluble enough it precipitates –> gall stones
sphincter of Oddi
@ common bile duct/SI jxn
open @ meal time
CCK and gallbladder
stim gallbladder to contract
relax sphincter of Oddi
secretin and gallbladder
stimulate secretion of HCO3
how does liver know its meal time
recovered bile (2/3 of total) return to liver in portal circulation
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)
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
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
age changes to pancreas
pancreatic ductal hyperplasia, fibrosis
down enzyme secretion
down bile salt synthesis (liver)
down potential for fat digestion
