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DIG > Functions and Secretions of the Pancreas > Flashcards

Functions and Secretions of the Pancreas Flashcards

1
Q

Overall functions of the pancreas

A
  • Digestion of nutrients (enzymes)
  • Providing appropriate environment for enzymatic digestion in small bowel
  • Regulating fed + fasted states (eg. insulin)
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2
Q

What is the pancreas arranged into morphologically?

A

Lobules draining into a ductular network that connects the entire gland to the GIT lumen

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3
Q

Types of duct in the pancreatic ductular network

A
  • Intralobular duct
  • Interlobular duct
  • Main pancreatic duct
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4
Q

What does the major pancreatic duct form with the common bile duct in the duodenal wall

A

Ampulla of Vater

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5
Q

Muscular thickening around the ampulla of Vater

A

Sphincter of Oddi

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6
Q

What is the function of the sphincter of Oddi?

A

Regulate and prevent reflux

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7
Q

What do pancreatic secretions empty through and what into?

A
  • Through major duodenal papilla
  • Into descending duodenum
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8
Q

What is each secretory unit of the pancreas comprised of?

A
  • Acinus
  • Small intercalated duct
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9
Q

What is an acinus and what does it do?

A
  • Cluster of acinar cells
  • Synthesise and secrete zymogens, digestive enzymes + isotonic, plasma-like fluid into lumen of epithelial structure
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10
Q

Types of cells in the pancreas and their functions

A
  • Acinar cells
    > Specialised/polarised for production + export of protein
  • Duct cells
    > Specialised for transport of electrolytes
  • Centroacinar cells
    > First cells of intercalated duct located at junction of acinar + duct cells
  • Goblet cells
    > Produce mucous for lubrication, hydration, mechanical protection + immunologic role
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11
Q

What mediate stimulation of acinar cells?

A
  • CCK + muscarinic ACh receptors on basolateral membrane
  • Signal through phospholipase C (PLC/PKC)/Ca2+ pathway
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12
Q

2 routes of activation of acinar cells

A
  • ACh + CCK activate PKC + release of calcium
  • VIP + secretin activate adenylyl cyclase, producing cAMP + activating PKA
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13
Q

Principle function of pancreatic duct cells

A

Secrete an HCO3- rich fluid that alkalinises + hydrates primary secretions of acinar cells

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14
Q

What type of channel is the cystic fibrosis transmembrane conductance regulator (CFTR) and where is it found?

A
  • cAMP-activated Cl- channel
  • Apical membrane of pancreatic duct cells
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15
Q

Mechanism of pancreatic duct cells

A
  • Secretin binding simulates adenylyl cyclase, increasing [cAMP]
  • cAMP stimulates CFTR, causing Cl- efflux into lumen
  • Carbonic anhydrase forms additional HCO3-
  • Cl- in lumen (from CFTR + other) exchanged by Cl-/HCO3- exchanger, to secrete HCO3- into lumen
  • ACh stimulates HCO3- secretion too by muscarinic receptors, increasing [Ca2+] + activating Ca2+-dependent protein kinases
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16
Q

What is secretin secreted by?

A

S cells in the small bowel

17
Q

What happens in cystic fibrosis

A
  • Mutation in CF gene
  • Mutant CFTR prematurely degraded
  • Decreases secretion of HCO3- + water by ducts
  • Results in protein-rich primary secretion thickening in duct lumen
  • Lumen obstruction
18
Q

Consequences of obstructed ductal lumen in cystic fibrosis

A
  • Deficiency of pancreatic enzymes
  • Malnutrition of nutrients –> steatorrhea + diabetes
19
Q

Where is CCK secreted from?

A

Duodenal I cells

20
Q

What stimulates secretion of CCK?

A
  • Response to fatty meal
    > CCKA receptor
    > Parasympathetic NS
  • Luminal CCK-releasing factor - LCRF (endogenously produced proteins secreted into gut lumen)
21
Q

Why do LCRFs not stimulate CCK secretion in the fasting state, but do in the fed state?

A
  • Digestive enzymes break them down in fasting state
  • Digestive enzymes act on chyme in fed state so LCRFs can stimulate I cells
22
Q

Action of somatostatin on pancreatic secretions

A

Inhibits release of CCK + secretin (+ therefore pancreatic secretion)

23
Q

What are used clinically to inhibit pancreatic secretions?

A

Somatostatin analogues

24
Q

3 phases of pancreatic secretion

A
  • Cephalic
  • Gastric
  • Intestinal
25
Q

What percentage of pancreatic secretion is the cephalic phase, and how does it work?

A
  • 25%
  • Sight, taste + smell of food causes nervous activation
  • ACh receptors on acinar cells + duct cells to lesser extent
26
Q

What percentage of pancreatic secretion is the gastric phase, and how does it work?

A
  • 10-20%
  • Release of hormones (mainly gastrin, stimulated by luminal peptides/AAs, from G cells of antrum)
    > Signals through CCK receptors on acinar cells
  • Stimulating neural pathways
    > Gastric distension stimulates pancreatic secretion through vagovagal gastropancreatic reflex
27
Q

What percentage of pancreatic secretion is the intestinal phase, and how does it work?

A
  • 50-80%
  • Chyme enters proximal SI + stimulates secretion by 3 mechanisms:
    > Gastric acid stimulates duodenal S cells to secrete secretin –> HCO3- + fluid from duct cells
    > Lipids stimulates duodenal I cells to release CCK –> digestive enzymes from acinar cells
    > Lipids activate vagovagal enteropancreatic reflex –> acinar cells
28
Q

How does the pancreas prevent autodigestion?

A
  • Digestive proteins stored in secretory granules as inactive precursors
  • Secretory granule membrane impermeable to proteins
  • Enzyme inhibitors (eg. pancreatic trypsin inhibitor SPINK1) co-packaged into secretory granules
  • Condensation of zymogens, low pH + ionic conditions limit enzyme activity
29
Q

How are inactive enzymes from the pancreas activated?

A
  • Coming into contact with small bowel brush-border enzyme enterokinase
  • Converts trypsinogen to trypsin which in turn initiates conversion of all other zymogens
30
Q

Causes of acute pancreatitis

A
  • GET SMASHED:
    > Gallstones
    > Ethanol
    > Trauma (children)
    > Steroids
    > Mumps
    > Autoimmune (SLE, Sjogren’s syndrome)
    > Scorpion sting
    > Hypercalcaemia, hypertriglyceridaemia, hypothermia
    > ERCP
    > Drugs (paracetamol, cisplatin, erhythromycin)
31
Q

What is needed to diagnose acute pancreatitis?

A
  • 2 of following 3:
    > Characteristic abdominal pain (epigastrium radiating to back) - often associated with nausea + vomiting
    > Serum amylase and/or lipase >= 3x upper limit of normal
    > Characteristic findings of acute pancreatitis on CT scan
32
Q

3 phases of pathophysiology of acute pancreatitis

A
  • Phase 1:
    > Premature activation of trypsin within acinar cells (disruption of calcium signalling, cleavage of trypsinogen by lysosomal hydrolase cathepsin-B or decreased activity of the intracellular pancreatic trypsin inhibitor SPINK 1)
    > Activates all other enzymes
  • Phase 2:
    > Intra-pancreatic inflammation (activation of inflammatory + endothelial cells)
  • Phase 3:
    > Extra-pancreatic inflammation including systemic sepsis + multi-organ failure
33
Q

Treatment of acute pancreatitis

A
  • Resting pancreas (IV fluids to combat dehydration)
  • Hourly fluid balance (input + output due to severe hypovolaemia)
  • Pain relief
34
Q

What is chronic pancreatitis?

A

Inflammation of the pancreas that does not heal or improve - gets worse over time + leads to permanent damage

35
Q

Most common and other causes of chronic pancreatitis

A
  • MC = chronic alcohol abuse
  • Other:
    > Hereditary disorders of the pancreas
    > Cystic fibrosis
    > Hypercalcaemia
    > Hyperlipidaemia
36
Q

Treatment of chronic pancreatitis

A
  • Hospitalisation for pain management, IV hydration + nutritional support
  • Supplement resuming of normal diet with synthetic pancreatic enzymes if not enough secreted
  • Nutritious diet low in fat with small, frequent meals
  • ERCP:
    > Enlarge duct openings + drain pseudocysts
    > Stent placement to keep open narrowed pancreatic/bile duct
    > Balloon dilation to dilate/stretch narrowed pancreatic/bile duct

DIG (19 decks)

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