pancreas Flashcards
anatomical regions
head neck body tail uncinate - Latin for hooklike
position of pancreas
head in C shape of duodenum
tail in hilum of spleen
perfusion for the panc
branch of superior mesenteric artery and celiac trunk
drainage for panc
hepatic portal vein
exocrine cells
Acini
most of the pancreas
duct cells support this
ducts
columnar epi
have smaller ducts that converge onto it from acinyl cells
islets of Langerhans `
endocrine mainly in tail not connected to duct vascularised - receive hormones hormones straight into the blood stained lighter than acini B cells - most abundant a cells 2nd most abundant delta cells - secrete somatostatin - least abundant
connective tissue
stain lighter than islets
structural support to pancreas
acini arrangement
zymogen secreting - have zymogen granules
zymogen = inactive protease
also active amylase and lipose
go into duct cell - secrete bicarb fluid to dilute enzymes
acini internal
high RER
apical surface - zymogen granules
pancreatic ducts
acinar cells are at the terminal end
secrete viscous low vol fluid into duct
centroacinar cells - between acinar and duct - have cell components of both, function more like duct
duct cell fluid - mobilise enzyme fluid, neutralise acid chime from stomach
embryology of the pancreas
arises at foregut-midgut junction
dorsal and ventral buds
ventral bud is part of the hepatobilary bud
duodenum rotates to form a C shape
ventral bud swings round - lie adjacent to dorsal bud - fuse
ventral becomes main panc duct
journey of panc juice
enters the duodenum via main and accessory panc ducts
blood supply
coeliac artery
superior mesenteric artery
endocrine action of gastrin
produced from stomach, and acts there
Ducts
small ducts converge into large ducts
uncinate process also has duct
combine with bile duct at ampulla of Vater
ampulla of vater drains into duodenum at sphincter of Oddi
common bile duct bifurcates into cystic duct and hepatic ducts
cystic duct drains into gall bladder
hepatic ducts connect to R and L lobe of liver
duct cell production of bicarbonate
CO2 into cell - combine with H2O catalysed by carbonic anhydrase
= carbonic acid
dissociate into proton and bicarb
meanwhile Na paracellularly through tight junction into lumen
water go with Na
= watery secretion
anion gradient created to use anion transporter
high conc of Cl- in cell so CFTR channel activated CL- move out = high quantities in lumen - use conc grad to move bicarb in opp dirn
this is secondary active transport
Bicarbonate secretion
to balance H+ build up
Na moves in cell
use secondary active transport to move Na in and protons out
nbo change in electrality of membrane potential
Na management
needed to maintain conc grad Na-Katpase pump ions against conc grad Na out replenish conc grad K move out through K channels down conc grad
blood around the pancreas
acidic
because protons are pumped out
Zymogens from the pancreas
protease zymogens - procarpoxypeptidase and chymotripsinogen
tripsinogen
procolipase -0 coenzyme for lipid digestion
active enzymes secreted from the pancreas
amylase - break carbs
lipase - lipid enzyme
active enzymes from precursors
trypsinogen - trypsin converted by enterokinase in duodenum
zymogen proteases - proteases by trypsin
procolipase - colipase by trypsin
trypsin also auto catalases - amplify effect of enterokinase
control of trypsin
trypsin inhibitor from zymogen granules in acinar cells
amylase
polysaccharides into disaccharides
dipeptidsases
shorter peptides to AA
amino peptidase, dipeptidase, carboxypeptidase and endopeptidase
lipase and colipase
convert triglycerides to fatty acids and monoglycerides
what happens when there is a lack of trypsin inhibitor eg when gall stone block flow of substances out of the pancreas
build up of enzymes
convert trypsinogen to trypsin w/o enterokinase
= pancreatic autodigestion
= acute pancreatitis
main endocrine secretions of pancreas
insulin- anabolic hormone, glucose uptake, reduce blood glucose, promotes protein synth and lipogenesis
glucagon - increase gluconeogenesis and glycogenolysis - increase blood glucose
somatostatin - suppress other hormones
pancreatic polypeptide
exocrine
secretes pancreatic juice into duodenum via panc duct/common bile duct
digestive func
pancreatic cell differentiation
exocrine - ducts, grape like clusters, acinar cells release proenzymes into duct
endocrine - derived from branching dust system, lose contact with ducts - become islets, diff into a and b
islets
very vascular = all cells close to a site for secretion
pancreatic juice
2 components
low vol, viscous, enzyme rich - acinar cells
high vol, watery, HCO3- rich - duct and centroacinar cells
bicarbonate secretion
duct and centroacinar cells (might have some enzymes)
rich in bicarb
neutralise acid chyme from stomach - prevent damage and, wash enzyme into duodenum make optimum pH for pancreatic enzymes
secretion increase as pH drops
stops at pH 5 - bile and brunners glands also secrete alkaline fluid
mechanism of bicarbonate secretion
bicarbonate formed catalysed by carbonic anhydrase
Na move down conc grad into lumen through TJ paracellularly
water follows
Cl- and bicarb exchannge at lumen (Cl in bicarb out)
Na/H exchange at basolateral membrane at blood stream - Na in
exchange driven by electrochemical gradient
Na gradient into cell maintained by Nak pump - primary AT
K returns to blood via K leak channel
Cl returns to blood via Cl channel
cystic fibrosis
cl channel problem
means there is a lot of mucus
acinar cell enzyme secretion
produced as zympogens protects from autodigestion pancreas contaisn trypsin inibitor enzymes activated in duodenum blockage of pancreatic duct may overload protection and result in autodigestion
altered pancreatic enzyme function
adapt to diet - the enzymes that are produced depends on whether they’re being used
lack of pancreatic enzymes = malnutrition even if diet is ok
orlistat
anti-obesity drug
inhibit pancreatic lipase
don’t absorb fat
= steatorrhoea = increased faecal fat
hormone control of bicarbonate secretion
acid chyme is low pH - activate S cells in lumen wall
s cells secrete secretin - travel to pancreas via liver and heart
bind to receptor on basolateral suyrface of duct cell
increase cAMP
activate Cl- channel
efflux of Cl channels
activate anion exchanger - move bicarbonate out of pancreatic juice
into duodenum through sphincter of Oddi and umplar avvarter
reduces the free acid available by maoing carbonic acid and water and CO2
hormonal control of enzyme secretion
ingestion is stimulus
detected in duodenal wall by I cells
I-cells secrete cholecystokinin
to pancreas
CCK bind to CCK-1 receptors on basolateral surface of acinus
activation of phosphliapse C and IP3
increase cytosolic Ca - amplification signal
trigger exocytosis of zymogen granules, enzyme inhibitors and active enzymes
secreted into terminal ducts
move into pancreatic duct and to duodenum `
central control of enzyme release
vagus nerve secrete ACh
bind to receptors
muscarinic receptors = increase in cytosolic Ca
phases of pancreatic secretion
cephalic phase
gastric phase
intestinal phase
cephalic face
stimulated by sight, smell and taste mediated by VN - release ACh proportion of secretion - 20% for prep and exocytosis of granules activates acinar cells mobilises enzymes - get ready to digest
gastric phase
stimulated by machanoreceptors in distension
mediated by VN - release ACh
proportion of secretion - 10% for prep and exocytosis of granules
activates acinar cells
mobilise enzymes - preparation
intestinal phase
stimulated by acid and nutrients
hormonally mediated
proportion of secretion - 70% food actually in duodenum
activates acinar cells and duct
both enzyme and watery bicarb components are released
-ve feedback loop
hormones to acid and nutrient stimulus = secretion shut off
interaction of signal interaction
CCK alone - no effect on bicarb secretion
secretin alone - increase in bicarb
both - massive amplification of secretin
secretin no effect on CCK mediated enzyme granules
vagus nerve
cholinergic
communicates information from gut to brain
signals go both ways
control over the 2 components of pancreatic secretion
separately controlled
bicarb: secretin - increase cAMP - increase production of bicarb
enzyme secretion: vagal reflex and by a hormone - cholecystokinin bind to acinial cells - increase Ca2+ from intracellular stores and PLC - zymogen granules fuse to membrane and release proenzymes
CCK
cephalic phase end when meal eaten
stop using neuronal signal after cephalic phase
absorption of fat and peptides removes local luminal stimulus for CCK release from mucosa - they don’t activate the enteroendocrine walls
possibly other mechanisms
effect of vagus nerve in comparison to affect of CCK
similar effects
secretin effect on enzyme secretion
no effect
processes during a meal
food mixed and digested in stomach - pH 2
chime squirted into suodenum
H+ ions in duodenum cause secretion of secretin =- pancreatic juice
peptide and fat in duodenum cause rise in CCK and vagal nerves stim enzyme release
peak at 30mins, continue until stomach empty
CCK potentiates effect of secretin on aqueous component
