5. Pancreas and pancreatitis Flashcards

1
Q

What are the 5 anatomical parts of the pancreas from inferior/right to left?

A
  • Uncinated process
  • Head (fits into the C-shaped duodenum)
  • Neck
  • Body
  • Tail (sits in the hilium of the spleen)
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2
Q

Describe the anatomy of the liver/gall bladder ducts joining with the pancreatic ducts

A
  • Gall bladder secretes into the cystic ducts
  • Liver drains into the right + left hepatic ducts => common hepatic duct
  • Cystic duct + common hepatic duct => common bile duct
  • Common bile duct joins the pancreatic duct at the Ampulla of Vater
  • Pancreatic ducts run along the pancreas, converging into one
  • They drain into the duodenum at the Sphincter of Oddi
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3
Q

Where is the pancreas located?

A

Behind the stomach, between the duodenum and spleen

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4
Q

Describe the vascular anatomy of the pancreas

A
  • Superior mesenteric artery => inferior pancreatic-duodenal artery
  • Coeliac trunk => splenic artery
  • Head of pancreas drains into hepatic portal vein
  • Rest of pancreas drains into splenic vein
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5
Q

Describe the microanatomy of the pancreas (cells/tissue)

A

• 98% are exocrine acini cells and duct cells
• Acini cells
• Duct cells
• Islets of Langerhans (endocrine tissue)
- beta cells (insulin) - most common
- alpha cells (glucagon) - 1/5 of endocrine tissue
- delta cells (somatostatin) - fewest in number
• Connective tissue

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6
Q

Describe the acinar cells

A

• Secretory machinery for enzymes:
- RER
- Ribosomes
- Zymogen granules with pro-enzymes, enzyme inhibitors and active enzymes (lipases and amylase)
• Terminal end of the duct (as they secrete enzyme-rich viscous fluid)
• Duct cells modify it as it moves along

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7
Q

Describe the centroacinar cells

A
  • Separate the acinar cells from the duct cells

* Act like duct cells

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8
Q

Describe the duct cells

A

• Secrete a watery, dilute bicarbonate fluid

  • dilutes and mobilises viscous enzymes
  • helps carry them into pancreatic duct/duodenum
  • neutralises stomach acid in the duodenum (enters via pyloric sphincter)
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9
Q

How is bicarbonate produced in the duct cells?

A

• CO2 diffuses into cell
• CO2 + H2O => H+ + HCO3- [carbonic anhydrase]
• Na+ moves through tight junction from interstitium to duct lumen
- H2O follows
- duct lumen becomes watery
• Chloride is pumped from duct cell to lumen (CFTR - a chloride ion channel)
• Comes back in, exchanging with bicarbonate (Cl/HCO3 exchange pump)
• Bicarbonate can leave the cell into the lumen

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10
Q

Why does duct cell bicarbonate secretion make the pancreatic venous blood acidic?

A

• H+ is also made when HCO3- is made
• Moves out of the cell (basolateral) to prevent build up
- K+ moves out through potassium channels
- K+ swaps back in with Na+ going out (ATPase)
- Na+ swaps back in with H+ going out

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11
Q

What enzymes are found in the zymogen vesicles of acinar cells?

A
• Protease zymogens
- Trypsinogens
• Procolipase - coenzyme for lipid digestion
• Active enzymes
- pancreatic amylase
- lipase
• Trypsin inhibitor
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12
Q

How is trypsinogen activated and what does it do?

A

• Converted into trypsin by enterokinase - in the duodenum brush border
• Trypsin catalyses:
- protease zymogens => proteases
- procolipase => colipase
- trypsinogen => trypsin (autocatalysis)
• Converts long peptides into shorter peptides

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13
Q

Describe the secretion problems with bile?

A
  • Liver secretes bile
  • Collects in gall bladder which contracts to release
  • Common bile duct => Ampulla of Vater => duodenum
  • Gallstone or blockage can cause enzyme accumulation
  • Trypsin inhibitor can’t work efficiently
  • Trypsinogen converts automatically to trypsin [trypsin] without the enterokinase from brush borders
  • Auto-digestion => acute pancreatitis
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14
Q

What are 3 of the protease zymogens?

A
  • Trypsinogen
  • Chymotrypsin
  • Procarboxypeptidase
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15
Q

Summarise the hormonal control of bicarbonate secretion

A
  • Acid chyme in proximal duodenum (from broken down bolus)
  • Low pH stimulates S-cells to release secretin into the blood
  • Secretin travels to the pancreas (via liver and heart)
  • Binds to receptors on the basolateral surface of duct cells
  • Increased cAMP
  • Activation of chloride channels in apical membrane
  • Efflux of chloride
  • More HCO3- leaves the cells
  • forms carbonic acid => water + CO2
  • More alkaline - optimal pH for enzymes
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16
Q

Summarise the hormonal control of acinar cells

A
  • Peptides, amino acids and fats (digested meal) stimulates I-cells
  • I-cells secrete cholecystokinin
  • Travels in blood to pancreas (via liver and heart)
  • Binds to CCK1 receptors on the basolateral surface of acinar cells
  • Increased Phospholipase C
  • Increased cytosolic calcium
  • Granule exocytosis into terminal ducts (containing zymogens, enzyme inhibitors and active enzymes)
17
Q

Describe the central stimulation of acinar cells

A
  • Vagus nerve secretes ACh
  • Binds to muscarinic receptors on basolateral membrane
  • Activation => increase in cytosolic calcium
18
Q

What effect does cholecystokinin and secretin have on duct cell and acinar cell secretions?

A
  • CCK - no affect on secretion rate, but amplifies the effect of secretin on secretion, stimulates acinar cells
  • Secretin - increases rate of bicarbonate secretion, no effect on acinar cells
19
Q

What is acute pancreatitis?

A
  • Acute inflammatory process

* Leads to the necrosis of the pancreatic parenchyma

20
Q

What are the signs and symptoms of acute pancreatitis?

A
  • Severe abdominal pain
  • Nausea
  • Vomiting
  • Diarrhoea
  • Fever
  • Shock
21
Q

What invasive tests can be used to detect acute pancreatitis?

A
  • Endoscopic Retrograde Cholangio-Pancreatograph (ERCP)
  • Endoscope down throat => ampulla
  • Cannula injects dye - X-ray
22
Q

What scoring systems can be used for acute pancreatitis?

A
  • Ranson’s criteria
  • APACHE II
  • SIRS
23
Q

What can cause acute pancreatitis?

A
  • Mechnical e.g. gallstones
  • Toxic e.g. ethanol
  • Metabolic e.g. hypelipidaemia
  • Drugs e.g. steroids
  • Infection e.g. mumps
  • Trauma
  • Congenital
  • Vascular e.g. ischaemia
  • Genetic e.g. CFTR
  • Scorpion bite
  • Autoimmune
24
Q

What are systemic and localised complications of acute pancreatitis?

A
Systemic
• Hypovolaemia
• Hypoxia
• Hypocalcaemia
• Hyperglycaemia
• Multiple organ failure
Localised
• Pancreatic necrosis
• Fluid collections
• Splenic vein thrombosis
• Chronic pancreatitis
25
Q

What is the treatment for acute pancreatitis?

A

• Supportive

  • fluids
  • painkillers
  • nutrition
  • organ support
  • management of complications
26
Q

What is chronic pancreatitis?

A
  • Progressive fibroinflammatory process of the pancreas
  • Permanent structural damage
  • Impairment of exocrine and endocrine function
27
Q

What are the secondary effects of chronic pancreatitis?

A
  • Loss of 90% exocrine function
  • Malabsorption
  • Fat soluble vitamin malabsorption (ADEK)
28
Q

How can you test for chronic pancreatitis?

A
  • X-ray
  • CT scan
  • Faecal elastase
29
Q

How can chronic pancreatitis be managed?

A
  • Stop alcohol and smoking
  • Small meals with low fat
  • Proton pump inhibitors and pancreatic supplements
  • Analgesia