Pancreas Flashcards

Pancreas anatomy; Pancreas function; Pancreatic regulation; Pancreatitis

1
Q

What is the embryological origin of the pancreas?

A

Develops around day 35-39 from two sites:
-Ventral pancreatic bud
-larger dorsal pancreatic bud
day 40-55 duodenum twist to move ventral pancreas towards dorsal pancreas
Endocrine pancreas arises from stem cells at duct branch points
Exocrine pancreas arises from endoderm tubules
Day 56 dorsal and ventral pancreas fuse together, dorsal pancreatic duct fuses with common bile duct and ventral pancreatic duct becomes Ampulla of Vater

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2
Q

Where is the pancreas found?

A

Head sits in C shaped part of duodenum

Tail sits in hilum of spleen

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3
Q

What are the 5 divisions of the pancreas?

A

Head, neck, body and tail

Uncinate process

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4
Q

How is the pancreas perfused?

A

Branches of superior mesenteric artery and coeliac trunk

Drains into hepatic portal vein

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5
Q

What are key features of pancreatic tissue?

A

Columnar epithelium lining pancreatic ducts
Islets of Langerhans
Acini (pancratic acinus)

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6
Q

What cells are found in the Islets of Langerhans?

A

α cells that secrete glucagon
β cells that secrete insulin 70%
δ cells that secrete somatostatin

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7
Q

What is the structure of a pancreatic acinus?

A

circular arrangement of acinar cells connecting to duct cells via centroacinar cells

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8
Q

What is the role of an acinar cell?

A

Secrete enzyme rich fluid
Low volume very viscous
Lots of RER
Lots of vesicles

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9
Q

What is the role of duct cells?

A
Modifies the acinar secretions
High volume
Secrete watery dilute bicarbonate rich fluid to:
Neutralise chyme
Decrease viscosity
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10
Q

How do pancreatic secretions drain into the duodenum?

A

pancreatic ducts converge to form larger pancreatic duct
combines with bile duct to form the ampulla of Vater
Drains into major duodenal papilla at the sphincter of Oddi

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11
Q

How is HCO3- produced and secreted from duct cells and how is the concentration of sodium managed?

A

CO2 diffuses into cell and combines with H2O to form H+ and HCO3- catalysed by carbonic anhydrase
Some Na+ moves down its concentration gradient via the paracellular pathway and some H2O passes by osmosis due to osmotic gradient - produces watery secretion
Cl- moves out of CFTR activated channels and this allows
HCO3- exchange for lumen Cl- via anion exchanger
H+ must be managed in order to prevent it damaging cell actions
H+ pumped out and Na+ pumped in at basolateral membrane
Na+/K+ ATPase used to pump Na+ back out and as K+ concenration inside cell increases, they leave via a K+ channel

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12
Q

How is HCO3- secretion controlled?

A

Drop in duodenal pH activates S cells spread amongst enterocytes
S cells secrete secretin
Secretin travels in blood all the way round back to pancreas
Secretin then binds to G protein coupled receptors on duct cells
This increases cAMP messenger concentration
Causes activation of Cl- channels in apical membrane and Cl- moves out
This provides concentration gradient for 2 active transport so increased activity of anion exchanger and therefore efflux of HCO3-

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13
Q

How is enzyme secretion controlled?

A

Fats and peptides are detected by I cells
Causes a Cholecystokinin release from I cells
CCK travels in blood round to pancreas and binds to CCK1 receptors on acinar cells
This activates PLC/IP3 2nd messenger (also activated by ACh released from vagus nerve binding to mucosine receptors)
Causes an increase in cytosolic Ca2+
Causes exocytosis of vesicles containing zymogen, inhibitor and enzyme granules
enzymes activated by enterokinase in duodenum

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14
Q

What are the phases of secretion, their key mediators and target cells?

A

Cephalic - Vagus nerve, acinar cells
Gastric - vagus nerve, acinar cells
Intestinal - hormones, acinar and duct cells

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15
Q

What stimulates the cephalic phase secretions?

A

Sight, smell, taste of food

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16
Q

What stimulates the gastric phase secretions?

A

Stomach distension

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17
Q

What stimulates the intestinal phase secretions?

A

Acid and nutrient detection in duodenum

18
Q

What hormones effect HCO3- secretion?

A

Secretin increases HCO3- secretion but no effect on enzyme secretion
CCK has not much effect on secretion
CCK amplifies the effect of secretin on bicarbonate secretion

19
Q

What does the pancreas secrete?

A
Zymogens:
-Protease zymogens
-Typsinogen
-Procolipase
Active enzymes:
-Lipase
-Amylase
Trypsin inhibitor
20
Q

What does the liver secrete?

A

Bile

21
Q

What does the duodenum secrete?

A

Enterokinase

22
Q

What stimulates the conversion of trypsinogen to trypsin?

A

Enterokinase

Trypsin

23
Q

What stimultes the conversion of protease zymogens to proteases?

A

Trypsin

Enterokinase

24
Q

What stimulates the conversion of procolipase to colipase?

A

Trypsin

25
Q

What does bile do?

A

Emulsifies fats into triglycerides

26
Q

What do colipase and lipase do?

A

Break down triglycerides into fatty acids and monoglycerides

27
Q

What do trypsin and proteases do?

A

Break down large peptides into shorter ones

28
Q

What does amylase do?

A

Break polysaccharides down into disaccharides

29
Q

What inhibits the conversion of trypsinogen into trypsin and why?

A

Trypsin inhibitor in the pancreas

Trypsin activation amplifies all other enzyme activations in the small intestine so it must be controlled

30
Q

How does pancreatitis occur?

A

Pancreatic duct obstruction impedes flow of pancreatic juice
causes accumulation of enzymes that cant be controlled by trypsin inhibitor
once inhibitor overwhelmed trypsinogen turns to trypsin without enterokinase
this leads to pancreatic autodigestion
= ACUTE PANCREATITIS

31
Q

What is acute pancreatitis?

A

Acute inflammatory process that leads to necrosis of pancreatic parenchyma

32
Q

What are signs and symptoms of pancreatitis?

A
Severe abdominal pain
 nausea
vomiting
diarrhoea
 fever
shock
33
Q

What are the main causes of pancreatitis?

A

Gallstones
Ethanol
Trauma

Steroids
Mumps
Autoimmune
Scorpion bite
Hyperlipiaemia/hypercalcaemia/hypothermia
ERCP
Drugs
34
Q

What are systemic complications of pancreatitis?

A
Hypovolaemia
Hypoxia
Hypocalcaemia
Hyperhlycaemia
DIC
Multiple organ failure
35
Q

What are localised complications associated with pancreatitis?

A

Pancreatic necrosis
Fluid collections - mature into pseudocysts
Splenic vein thrombosis/pseudoaneurysm
Chronic pancreatitis

36
Q

What is the available treatment options for acute pancreatitis?

A
Supportive treatments
fluids
painkillers
nutrition
organ support
management of complications
37
Q

What is chronic pancreatitis?

A

Progressive fibroinflammatory process of the pancreas that results in permanent structural damage which leads to impairment of exocrine and endocrine function

38
Q

How can chronic pancreatitis be managed?

A

Stop alcohol and smoking
Small meals, low fat
Proton pump inhibitors and pancreatic supplements
Analgesia

39
Q

How is acute pancreatitis investigated?

A

Chest and abdominal X ray
Ultrasound
CT scan
MRCP- magnetic resonance cholangiopancreatography
ERCP-Endoscopic retrograde cholangiopancreatography

40
Q

How is chronic pancreatitis investigated?

A

Plain X ray
CT scan
Faecal elastase