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fizzlo > GIT - acute pancreatisis and cancer > Flashcards

GIT - acute pancreatisis and cancer Flashcards

1
Q

What are the exocrine functions of pancreas?

A

Secrete pancreatic juices and enzymes into duct system

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2
Q

Which cells perform exocrine function of pancreas?

A

Pancreatic Acinar cell - 80% mass

Duct cells!

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3
Q

What are the endocrine functions of the pancreas?

A

Secrete Insulin and glucagon
and satiety hormone too (ghrelin, somarostatin

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4
Q

Why are digestive enzymes stored in secretory granules?

A

To ensure they don’t become prematurely activate. They are stored in inactive form (zymogen)

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5
Q

What is a secretagogue?

A

Molecule that promotes cell to secrete hormone, neurotransmitter

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6
Q

What secretagogue stimulate PAC? What is their effect?

A

Ach for exocytosis of zymogen granules
CCK helps with pancreatic fluid secretion into duct

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7
Q

How do chloride channels act in PAC?

A

Calcium rise activates chloride channel on apical membrane allowing chloride to enter cell

On luminal side chloride aids paracellular transport or water and sodium due to its negative charge so fluid is secreted

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8
Q

What is function of duct cells ?

A

Secrete pancreatic juices and also secrete bicarbonate to control pH and neutralise the juices

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9
Q

Which hormone stimulate duct cell to secrete bicarbonate?

A

Secretin produced from S-cells in duodenum

Able to bind to GPCR receptor and leads to CFTR channel luminal side activation so bicarbonate released into luman

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10
Q

how can a rise in cytosolic calcium be buffered in PACs?

A

the mitochondria which can surround the granules in the cell is able to uptake calcium (temp) via the VDAC and mitch uniporter channel

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11
Q

what does the digestive juice secreted by PAC contain?

A

NaCl
water
digestive enzymes
bicarbonate

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12
Q

how can the PACs influence the duct cells?

A

PACs secrete chloride into lumen allowing HC03- secretion in duct cells

PAC secrete ATP, activating purinergic receptors on duct cell channels = stimulate ductal fluid + HC03- secretion

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13
Q

how can duct cells influence PAC?

A

if the luminal pH (controlled by duct cell) is dysregulated then a prolonged acidic environment would destroy PAC

(Seen in cystic fibrosis)

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14
Q

how do PAC and pancreatic B-cells differ?

A

in function - secrete pancreatic juices or hormones

in cell type - non excitable or excitable

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15
Q

how can insulin production be affected during acute pancreatitis?

A

during AP, PAC can rupture releasing trypsin

trypsin acts on B-cells and blocks insulin production

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16
Q

what are the 3 main causes of AP?

A

alcohol metabolites (POAEE)
bile acids
medicines like aspariganases (childhood Lymphoblastic leukemia)

but others like genetics, having hypercalcaemia

17
Q

despite no cure for AP, how do some people recover?

need evidence for nfkb

A

the pancreas is able to REGENERATE!

also acinar-ductal metaplasia and remodelling of acinar cell genes to look like duct cell

so they don’t produce secretory enzymes and remain protected

18
Q

what is the molecular end result of AP?

A

calcium overload leads to mitch dysfunction and loss of ATP production = necrosis

calcium overload activates digestive enzymes and the secretory granules burst open = autodigestion and inflammation

19
Q

what is the key action of calmodulin?

A

calcium sensitive sensor and becomes activated when calcium binds to its EF hands

able to then downregulate activity of IP3R and RyR

20
Q

why are SOCE channels a preferable target than IP3R in treating AP?

A

they are on cell membrane surface so drug doesn’t need to be permeable to pass the lipid bilayer

21
Q

name 2 ways alcohol can be metabolised?

A

non-oxidative and oxidative routes

22
Q

how can ox. alcohol metabolism lead to AP?

A

acetate is a product and can accumulate in mitch

this means mitch can’t function so no buffer for excess cytosolic calcium

23
Q

how can non ox. alcohol metabolism lead to AP?

A

conversion of alcohol to FA-Ethyl-Esters which can deplete ER stores and affect ATP synthesis too

24
Q

what is particularly dangerous about the alcohol metabolite POAEE?

A

POAEE can activate trypsinogen in granules very quickly

25
Q

how can bile lead to AP?

A

bile can enter cell through various transporters and accumulate and block SERCA activity = Ca2+ excess

bile also activates GPCR on PAC -> deplete ER store

26
Q

what cells make up 2% of pancreatic mass?

A

pancreatic stellate cells and immune cells which are organised very tightly together

both non-excitable cells

27
Q

what are pancreatic stellate cells?

A

quiescent fibroblasts which help maitain structure and store lipid and vit A

in pathology contribute to wound healing, inflammation and eventual fibrosis

28
Q

how are stellate cells implicated in cancer?

A

stellate cells form over 50% of tumoural stroma and support tumour progression

29
Q

why are ACE inhibitors dangerous in patients with or at risk of AP?

A

ACEi lower BP by inhibit BK degrade

during AP, PAC ruptures and release kallikreins which activate bradykinin production (a natural BP lowering peptide) and BK plasma level rise

so v. low BP can lead to pacreatic odema

30
Q

how do stellate cells produce calcium transients?
>what molecule

A

bradykinin binds to type 2 BK receptor on stellate cells and activate calcium signalling and release ECM, cytokine and GF

so stellate cells become active

31
Q

how can stellate cell activation lead to AP?

A

biphasic response where IP3R opens and large Ca+ spike occcurs and then 2nd smaller spike as SOCE occurs

32
Q

how can pancreatic cancer be initiated?
> molecularly

A

activated stellate cells secrete periostin which stimulates cell adhesion and cancer cell growth

33
Q

what molecules do stellate cells secrete when stimulated/activated by Bradykini?

A

nitric oxide and prostaglandins which are pro-i molecules

34
Q

how do PAC and stellate cells communicate with each other?

A

thought that the nitric oxide gas can diffuse to PAC

35
Q
A

fizzlo (13 decks)

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