8.2 Pancreatic Disease Flashcards

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1
Q

Describe two ways by which pancreatic ductal obstruction can lead to premature pancreatic protease activation

A
  1. Acinar cell injury causes premature activation of proteases
  2. Inflammatory mediators cause intracellular calcium buildup, leading to premature trypsinogen activation
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2
Q

How can early inflammation lead to pancreatic ductal obstruction? What can this cause?

A

Can cause
- Oedema/swelling
- Fibrosis/scarring
- Sludge debris formation (like gallstones)

This can lead to acinar cell injury and calcium buildup, causing pancreatitis

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3
Q

What are the consequences (symptoms/signs) of exocrine pancreas insufficiency?

A
  • Malabsorption (less enzymatic breakdown)
  • Steatorrhoea (less TAG absorption)
  • Abdo pain (/duodenal damage, pancreatic inflammation)
  • Unexplained weight loss (2° to malabsorption)
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4
Q

Is acute pancreatitis a medical emergency? What are the complications/natural history?

A

Yes, it is a medical emergency. Can lead to:

  • Multiorgan failure (due to systemic inflammation)
  • Necrosis and infection of the pancreas can then occur, which can cause sepsis
  • Pancreatic haemorrhage
  • Hypovolaemia (2° to haemorrhage or oedematous necrosis)
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5
Q

List some symptoms/signs of acute pancreatitis, and explain their mechs

A
  • Pain (inflammation/autodigestion)
  • Nausea/vomiting (irritating surrounding structures, no fat emulsification, gastroparesis)
  • Jaundice (inflammation causes compression of common bile duct)
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6
Q

List four biochemical disturbances that can occur in pancreatitis, and explain how they occur

A
  1. Hyperglycaemia (loss of insulin control)
  2. Hypocalcaemia (calcium salt formation in pancreas)
  3. Hyperbilirubinaemia (2° to common bile duct obstruction; therefore conjugated)
  4. Elevated pancreatic enzymes (instead of GI, dying cells leak into bloodstream)
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7
Q

Provide a proper mech for how hypercholesterolaemia predisposes to gallstone formation

A
  • Ordinarily, cholesterol can be used to make bile salts
  • In hypercholesterolaemia, we have excess cholesterol, meaning there is too much to all be converted into bile salts
  • So, some of the cholesterol precipitates out of solution, forming cholesterol gallstones
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8
Q

What biomarkers might we use to assess pancreas function/pathology?

A
  • Ca 19-9 (screen for possible cancer)
  • Lipase/amylase (elevated in pancreatitis)
  • INR or Platelets may be decreased if comborbid w/ liver dysfunction
  • Serum bicarbonate (low in exocrine dysfunction of the pancreas)
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9
Q

How do we treat pancreatic cancer?

A
  • Surgery
  • Radiotherapy
  • Chemotherapy
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10
Q

How do we treat pancreatitis?

A
  • Fasting (lower need for digestive enzymes)
  • IV fluids (esp. if oedema/haemorrhage)
  • Antibiotics (prevent necrosis -> infection)
  • Pain relief
  • Other organ support (in the setting of multiorgan failure)
  • Surgery/endoscopic drainage (in the setting of necrosis)
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11
Q

List four triggers that can cause premature activation of trypsinogen, leading to autodigestion and pancreatitis

A
  • Gallstone blockage (pressure buildup if pancreatic duct is blocked)
  • Alcoholism (can damage acinar cells)
  • High triglycerides (high levels of resultant fatty acids can cause enzyme activation)
  • Infection (initial inflammation causes enzyme activation, leading to more inflammation)
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