Pancreas Flashcards

1
Q

Pancreas development
Where does it arise?
What does it start as?
What happens during development?

A

Foregut-Midgut junction
Dorsal+ ventral buds (ventral= part of hepatobiliary bud)
Duodenum rotates to form a C shape, ventral bud swings round to lie adjacent to dorsal bud+ both buds fuse
Ventral bud duct becomes main pancreatic duct

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2
Q

Subdivisions of pancreas

A
Head (main duct comes out to go to duodenum)
Neck
Body
Tail
Uncinate (hook-like part)
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3
Q

Exocrine/ endocrine functions?

A

Both tissues throughout pancreas

More endocrine tissue in tail

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4
Q

How does pancreatic juice reach the duodenum?

A

By main+ accessory pancreatic duct

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5
Q

Anatomy
Where does it lie?
Posterior relations?
Blood supply from?

A

Posterior abdominal wall extending from C-shaped duodenum to hilum side of spleen
Inferior vena cava, abdominal aorta, left kidney
Coeliac+ superior mesenteric arteries

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6
Q

Endocrine secretion

A

Secretion into bloodstream to have effect on distant target organ (Autocrine/Paracrine) (acts as a ductless gland)

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7
Q

Exocrine secretion

A

Secretion into a duct to have a direct local effect

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8
Q

Endocrine secretions of pancreas+ actions
% of gland?
Parts of pancreas with this function?

A

Insulin= anabolic hormone (building up), promotes glucose transport into cells+ storage as glycogen, leads to reduce blood glucose+ promotes protein syntheis+ lipogenesis
Glucagon= Increases gluconeogenesis+ glycogenolysis= increase blood glucose
Somatostatin= Suppresses lots of things
2% of gland
Islets of Langerhans

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9
Q

Exocrine secretions of pancreas
% of gland?
What does it secrete? Via what?

A

98%
Pancreatic juice into duodenum via pancreatic duct/ common bile duct
Digestive function

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10
Q

Pancreatic disease affects?

A

Both exocrine+ endocrine functions

E.g. anyone with type 2 diabetes might also have exocrine problems

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11
Q

Pancreatic cell differentiation:
Exocrine?
Endocrine? Derived from? Which part of pancreas is it more common in?

A

Ducts, Acini (grape-like clusters of secretory units) that have acinar cells that secrete pro-enzymes into ducts

Derived from branching duct system, lose contact with ducts+ become islets, differentiate into α+ β cells secreting into blood
More common in tail than head

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12
Q

Exocrine secretion: Islets composition
Cells?
Secrete?
Property?

A

α cells- secrete glucagon
β cells- secrete insulin
δ cells- secrete somatostatin
Highly vascular= all endocrine cells have close access to a site for secretion

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13
Q

Acinar function

A

Acinar cells- secretory granules containing enzymes ready to be released
Duct cells- line the duct+ don’t have granules (don’t release enzymes)

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14
Q

Pancreatic juice components
Made which cells?
Purpose?

A

Low vol, viscous, enzyme rich fluid- acinar cells

High vol, watery, HCO3- rich alkaline fluid- Duct+ centroacinar cells
Neutralises acid chyme from stomach= prevents damage to duodenal mucosa+ raises pH optimum for pancreatic enzymes+ washes low volume enzyme secretion out of pancreas into duodenum (high vol.)

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15
Q

Effect of duodenal pH on bicarbonate secretion rate

Why does bicarbonate secretion stop when pH= still acidic?

A

As duodenal pH decreases, rate of bicarbonate secretion increases
Bile also contains bicarbonate+ helps neutralise acid chyme too (liver)+ Brunner’s glands secrete alkaline fluid (small intestine)

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16
Q
Mechanism of bicarbonate secretion
Where is this occuring?
Catalysed by?
4 steps
Exchange driven by?
Cystic fibrosis?
A

Duct cells
Carbonic anhydrase
1. Seperation of H+ and HCO3-
2. Na moves down gradient via tight junctions from blood to lumen= H20 follows
3. Cl-/HCO3 exchange at lumen (Cl- in, HCO3- out into lumen)
4. Na+/ H+ exchange at basolateral membrane into bloodstream (H+ out into blood, Na+ into cell)
5. Na gradient into cell from blood maintained by Na/K exchange pump using ATP (primary active transport)
6. K returns to blood via K+ channels
7. Cl returns to lumen via Cl- channels
Exchange driven by electrochemical gradients (Na+ Cl go along gradients)
Cystic fibrosis= Cl- channels dysfunctional= pancreatic cells can’t move Cl- into lumen= viscous enzyme rich secretion in ducts= trypsin activates+ cascade of protease activation= autodigestion of pancreatic cells= inflammation+ pancreatitis

17
Q

H2CO3 in stomach vs pancreas

A

In stomach, H+ goes into gastric juice, HCO3- in blood therefore gastric venous blood= alkaline
In pancreas, HCO3- secreted into juice, H+ into blood therefore pancreatic venous blood is acidic
Therefore by intestine, neutralise each other

18
Q
Enzyme secretion
Cell type?
Pro-enzymes name? Stored?
Protease example?
Pancreas blockage?
A

Acinar cells
Zymogens stored in zymogen granules
Proteases= inactive pro-enzymes= protection from auto-digestion
Trypsin inhibitor to prevent trypsin activation
Auto-digestion= acute pancreatitis in cystic fibrosis

19
Q

Altered pancreatic enzyme function

Lack of enzymes=?

A

Adapt to diet (proteases+ amylases)

Lack= malnutrition

20
Q

Olistat drug function
Side effects?
Used as?

A

Inhibits pancreatic lipases= inhbits intestinal fat absorption
Steatorrhoea- increased faecal fat
Weight loss agent

21
Q

Control of secretion process
Nerve?
3 phases?

A

Vagus nerve- cholinergic via parasympathetic pathways to regulate gut function
Cephalic phase- reflex response to sensory innervation, enzyme rich component only, pancreas ‘mobilised’ more but not much else because food is still a long way. Phase ends when food= eaten

Gastric phase- stimulation of pacreatic secretion from food entering stomach, same mechanism as cephalic

Intestinal phase= most of pacreatic secretion, HORMONALLY mediated when gastric chyme enters duodenum, both components of pancreatic juice stimulated

22
Q

Control of bicarbonate secretion

Occurs in which phase/s?

A
  1. Chyme comes into duodenum (acidic so contains H+)
  2. H+ in contact with S cells= enteroendocrine epithelial cell which secretes secretin when pH= under a certain level.
  3. Secretin travels around blood+ reaches pancreas
  4. Secretin binds to duct cells= increase cAMP= increased bicarbonate
  5. Increase pH= -ve feedback
    Ocurrs in intestinal phase
23
Q

Control of enzyme secretion
Occurs in which phase/s?
How is hormone switched off?

A
  1. Peptides+ fat in duodenum come into contact with C cells (enteroendocrine cells)= release Cholecystokinin (CCK) into blood
  2. CCK travels around circulation+ reaches acinus
  3. Acinus also stimulated by vagus reflex (ACh)
  4. Inctracellular cascade involving release of intracellular Ca2+ and Phospholipase C= granules fuse with membranes+ release contents into duct
  5. Acinus releases pro-enzymes+ trypsin inhibitor

CCK also stimulates bile secretion (liver)
Occurs in all phases
Absorption of fats+ peptides removes local stimulus for CCK release+ unknown mechanisms

24
Q
CCK+ Secretin interaction
CCK effect on bicarbonate?
Vagus effect on bicarbonate?
Secretin effect on enzyme?
Reason?
A

No effect alone but bicarbonate secretion stimulated by secretin increases with CCK
Vagus nerve= no effect alone but bicarbonate secretion stimulated by secretin increases with CCK
Secretin= NO effect on enzyme secretion (CCK does it all)

25
Q

Difference in arrangement of exocrine cells in liver and pancreas?

A
Liver= cells arranged linearly, secrete in canaliculi
Pancreas= cells arranged in curved acini, secrete in ducts