acute pancreatitis Flashcards

1
Q

what is acute pancreatitis?

A

inflammation of the pancreas

can be distinguished from chronic pancreatitis by its limited damage to secretory function of the gland

repeated episodes of acute pancreatitis can lead to chronic pancreatitis

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2
Q

what are the causes of acute pancreatitis?

A

usually secondary to gallstone disease or excess alcohol consumption

also

GET SMASHED

Gallstones
Ethanol
Trauma

Scorpion bite
Mumps
Autoimmune disease e.g SLE
Steroids
Hypercalcaemia
ERCP
Drugs e.g azathioprine and NSAIDs or diuretics
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3
Q

what is the pathogenesis of acute pancreatitis?

A
  • cause will trigger a premature and exaggerated activation of digestive enzymes in the pancreas
  • resultant pancreatic inflammatory response causes increase in vascular permeability and subsequent fluid shift
  • enzymes released from pancreas into systemic circulation causing auto digestion of fats = fat necrosis = free fatty acids = react with serum ca = hypocalcaemia

end stage pancreatitis = complete necrosis of the pancreas

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4
Q

what are the clinical features of acute pancreatitis?

A
  • sudden onset severe epigastric pain which can radiate through the back
  • Nausea and vomitting
  • epigastric tenderness, with/without guarding
  • cullens sign (bruising around umbilicus)
  • grey turners (bruising in the flanks)
  • tetany from hypocalcaemia (secondary to fat necrosis)
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5
Q

what are the DD for abdominal pain that radiates to the back?

A
  • AAA
  • renal calculi
  • chronic pancreatitis
  • aortic dissection
  • peptic ulcer disease
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6
Q

what investigations are done?

A
  • Serum amylase (3x normal limit to consider pancreatitis, can also be raised in bowel perforation, ectopic pregnancies or DKA)
  • LFTs asses for cholestatic involvement
  • serum lipase is more accurate as it remains elevated longer than amylase, but its not as avaliable
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7
Q

what is used to asses the severity of acute pancreatitis within the first 48 hours of admission?

A

The modified Glasgow criteria

patient scoring 3 or more should be considered to have severe pancreatitis

mnemonic for score is PANCREAS

P = pO2
A = age
N = neutrophils 
C = calcium
R = renal function (urea)
E = enzymes (LDH + AST)
A = albumin
S = sugar (blood glucose)
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8
Q

what imaging can be done?

A
  • abdominal US if underlying cause unknown. Used to identify gallstones and for evidence of duct dilation.
  • not routine for acute pancreatitis but AXR can show sentinel loop sign, a dilated proximal bowel adjacent to pancreas which occurs secondary to localised inflammation.
  • contrast enhanced CT scan if initial assessment inconclusive (6-10 days after admission)
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9
Q

how is acute pancreatitis managed?

A

supportive measures, no curative measure.

  • IV fluid resuscitation and o2 therapy as required (use a crystalloid)
  • NG tube if vomitting
  • catheter to monitor urine output and start a fluid balance chart. Aim for urine output of >0.5ml/kg/hr
  • opiod analgesia
  • broad spectrum antibiotic eg imipenem for prophylaxis in cases of confirmed pancreatic necrosis
  • caused by gallstones = early laparoscopic cholecystectomy
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10
Q

what are the systemic complications of acute pancreatitis?

A
  • Disseminated intravascular coagulation
  • acute respiratory distress syndrome
  • hypocalcaemia
  • hyperglycaemia secondary to destruction of islets of langerhans and subsequent disturbance to insulin metabolism
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11
Q

Pancreatic necrosis is a local complication of acute pancreatitis. what is it?

A
  • ongoing inflammation = ischaemic infarction of pancreas = persistent systemic inflammation
  • confirm pancreatic necrosis by CT imaging , treatment will often warrant pancreatic necrosectomy
  • pancreatic necrosis = prone to infection, and should be suspected in clinical detonation of the patient and raised infection markers.
  • definitive diagnosis of infected pancreas necrosis is confirmed by fine needle aspiration of the necrosis.
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12
Q

a pancreatic pseudocyst is a local complication of pancreatitis. what is it?

A
  • a collection of fluid containing pancreatic enzymes, blood and necrotic tissue, and can occur anywhere within or adjacent to the pancreas.
  • usually in the lesser sac, obstructing gastro epiploic foramen by inflammatory adhesions.
  • usually formed weeks after initial pancreatitis episode.
  • Lack an epithelial lining so are a pseudocyst. Have a vascular and fibrotic wall surrounding collection.
  • can be found incidentally on imaging or present with symptoms of mass effect.g biliary obstruction/gastric outlet obstruction.
  • prone to haemorrhage and rupture and can become infected.
  • conservative management is preferred as half will spontaneously resolve. Present for 6 weeks +, unlikely to resolve and can treat endoscopically with drainage or surgical debridement.
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13
Q

true or false,

Amylase and lipase levels are typically lower in chronic pancreatitis than in acute pancreatitis

A

TRUE

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