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ailmentary > pancreas > Flashcards

pancreas Flashcards

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
Q

amylase

A

polysaccharides into disaccharides

26
Q

dipeptidsases

A

shorter peptides to AA

amino peptidase, dipeptidase, carboxypeptidase and endopeptidase

27
Q

lipase and colipase

A

convert triglycerides to fatty acids and monoglycerides

28
Q

what happens when there is a lack of trypsin inhibitor eg when gall stone block flow of substances out of the pancreas

A

build up of enzymes
convert trypsinogen to trypsin w/o enterokinase
= pancreatic autodigestion
= acute pancreatitis

29
Q

main endocrine secretions of pancreas

A

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
Q

exocrine

A

secretes pancreatic juice into duodenum via panc duct/common bile duct
digestive func

31
Q

pancreatic cell differentiation

A

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
Q

islets

A

very vascular = all cells close to a site for secretion

33
Q

pancreatic juice

A

2 components
low vol, viscous, enzyme rich - acinar cells
high vol, watery, HCO3- rich - duct and centroacinar cells

34
Q

bicarbonate secretion

A

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
Q

mechanism of bicarbonate secretion

A

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
Q

cystic fibrosis

A

cl channel problem

means there is a lot of mucus

37
Q

acinar cell enzyme secretion

A 
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
Q

altered pancreatic enzyme function

A

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
Q

orlistat

A

anti-obesity drug
inhibit pancreatic lipase
don’t absorb fat
= steatorrhoea = increased faecal fat

40
Q

hormone control of bicarbonate secretion

A

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
Q

hormonal control of enzyme secretion

A

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
Q

central control of enzyme release

A

vagus nerve secrete ACh
bind to receptors
muscarinic receptors = increase in cytosolic Ca

43
Q

phases of pancreatic secretion

A

cephalic phase
gastric phase
intestinal phase

44
Q

cephalic face

A 
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
Q

gastric phase

A

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
Q

intestinal phase

A

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
Q

-ve feedback loop

A

hormones to acid and nutrient stimulus = secretion shut off

48
Q

interaction of signal interaction

A

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
Q

vagus nerve

A

cholinergic
communicates information from gut to brain
signals go both ways

50
Q

control over the 2 components of pancreatic secretion

A

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
Q

CCK

A

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
Q

effect of vagus nerve in comparison to affect of CCK

A

similar effects

53
Q

secretin effect on enzyme secretion

A

no effect

54
Q

processes during a meal

A

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

ailmentary (15 decks)

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