pancreas Flashcards

(54 cards)

1
Q

anatomical regions

A
head
neck 
body 
tail 
uncinate - Latin for hooklike
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2
Q

position of pancreas

A

head in C shape of duodenum

tail in hilum of spleen

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3
Q

perfusion for the panc

A

branch of superior mesenteric artery and celiac trunk

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4
Q

drainage for panc

A

hepatic portal vein

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5
Q

exocrine cells

A

Acini
most of the pancreas
duct cells support this

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6
Q

ducts

A

columnar epi

have smaller ducts that converge onto it from acinyl cells

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7
Q

islets of Langerhans `

A
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
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8
Q

connective tissue

A

stain lighter than islets

structural support to pancreas

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9
Q

acini arrangement

A

zymogen secreting - have zymogen granules
zymogen = inactive protease
also active amylase and lipose
go into duct cell - secrete bicarb fluid to dilute enzymes

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10
Q

acini internal

A

high RER

apical surface - zymogen granules

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11
Q

pancreatic ducts

A

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

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12
Q

embryology of the pancreas

A

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

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13
Q

journey of panc juice

A

enters the duodenum via main and accessory panc ducts

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14
Q

blood supply

A

coeliac artery

superior mesenteric artery

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15
Q

endocrine action of gastrin

A

produced from stomach, and acts there

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16
Q

Ducts

A

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

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17
Q

duct cell production of bicarbonate

A

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

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18
Q

Bicarbonate secretion

A

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

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19
Q

Na management

A
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
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20
Q

blood around the pancreas

A

acidic

because protons are pumped out

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21
Q

Zymogens from the pancreas

A

protease zymogens - procarpoxypeptidase and chymotripsinogen
tripsinogen
procolipase -0 coenzyme for lipid digestion

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22
Q

active enzymes secreted from the pancreas

A

amylase - break carbs

lipase - lipid enzyme

23
Q

active enzymes from precursors

A

trypsinogen - trypsin converted by enterokinase in duodenum
zymogen proteases - proteases by trypsin
procolipase - colipase by trypsin
trypsin also auto catalases - amplify effect of enterokinase

24
Q

control of trypsin

A

trypsin inhibitor from zymogen granules in acinar cells

25
amylase
polysaccharides into disaccharides
26
dipeptidsases
shorter peptides to AA | amino peptidase, dipeptidase, carboxypeptidase and endopeptidase
27
lipase and colipase
convert triglycerides to fatty acids and monoglycerides
28
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
29
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
30
exocrine
secretes pancreatic juice into duodenum via panc duct/common bile duct digestive func
31
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
32
islets
very vascular = all cells close to a site for secretion
33
pancreatic juice
2 components low vol, viscous, enzyme rich - acinar cells high vol, watery, HCO3- rich - duct and centroacinar cells
34
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
35
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
36
cystic fibrosis
cl channel problem | means there is a lot of mucus
37
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 ```
38
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
39
orlistat
anti-obesity drug inhibit pancreatic lipase don't absorb fat = steatorrhoea = increased faecal fat
40
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
41
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 `
42
central control of enzyme release
vagus nerve secrete ACh bind to receptors muscarinic receptors = increase in cytosolic Ca
43
phases of pancreatic secretion
cephalic phase gastric phase intestinal phase
44
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 ```
45
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
46
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
47
-ve feedback loop
hormones to acid and nutrient stimulus = secretion shut off
48
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
49
vagus nerve
cholinergic communicates information from gut to brain signals go both ways
50
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
51
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
52
effect of vagus nerve in comparison to affect of CCK
similar effects
53
secretin effect on enzyme secretion
no effect
54
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