Acute & Chronic Pancreatitis Flashcards

1
Q

Describe the anatomy of the pancreas

A
  • retroperitoneal
  • lies between aorta and stomach
  • 5 parts: head, neck, body, tail, uncinate process
  • head lies in ‘C’ shape of duodenum
  • superior mesenteric artery sits posterior to pancreas
  • superior mesenteric artery + v pass between head and uncinate process of pancreas + give off branches that enter small bowel mesentery
  • tail is in contact w/ the spleen
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2
Q

What is the exocrine function of the pancreas?

A
  • acinar cells -> produce digestive enzymes and bicarbonate
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3
Q

What is the endocrine function of the pancreas?

A

Islets of Langerhans contain 4 main cell types:

  • alpha cells - glucagon
  • beta cells - insulin
  • delta cells - somatostatin
  • PP cells - pancreatic polypeptide
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4
Q

What is the difference between acute and chronic pancreatitis?

A
  • acute pancreatitis: process that occurs on the back-ground of a previously normal pancreas and can return to normal after resolution of the episode
  • chronic pancreatitis: continuing inflammation with irreversible structural changes
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5
Q

What are the causes of acute pancreatitis?

A

I GET SMASHED

  • Idiopathic
  • Gallstones (most common)
  • Ethanol (most common)
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion venom
  • Hypothermia, hypercalcaemia, hypertriglyceridaemia
  • ERCP
  • Drugs (SAND: steroids + sulphonamides, azothioprine, NSAIDs, diuretics (loop/thiazide))
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6
Q

What is the pathogenesis of acute pancreatitis?

A
  • inflammation is secondary to premature + exaggerated activation of digestive enzymes within pancreas
  • acute rise in intracellular calcium initiates
  • leading to early activation of typsinogen -> trypsin
  • impairment of trypsin degradation by chymotrypsin C
  • these activated enzymes -> cellular necrosis + autolysis
  • gallstones: occlude pancreatic drainage at level of ampulla -> pancreatic ductular hypertension -> inc cytosolic free ionised Ca2+
  • alcohol interferes w/ Ca2+ homeostasis in pancreatic acinar cells
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7
Q

What are the symptoms of acute pancreatitis?

A
  • nausea
  • vomiting
  • anorexia
  • epigastric pain (+ back pain)
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8
Q

What are the possible clinical signs of pancreatitis?

A
  • tachycardia, hypotension, oliguric
  • Grey-Turner’s sign - bilateral flank bruising
  • Cullen’s sign - peri-umbilical bruising
  • Fox’s sign - ecchymosis over inguinal area
  • upper abdominal tenderness
  • ileus
  • low-grade fever
  • if gallstone aetiology: jaundice or cholangitis
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9
Q

What are differentials for epigastric pain?

A
  • gastric ulcer
  • acute cholecystitis
  • acute pancreatitis
  • chronic pancreatitis
  • abdominal aortic aneurysm
  • achalasia
  • oesophageal rupture
  • inferior MI
  • intestinal obstruction
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10
Q

What are the necessary investigations for acute pancreatitis?

A
  • serum lipase -> x3 increased
  • serum amylase -> x3 increased
  • AST/ALT -> gallstone disease if inc
  • FBC -> leukocytosis
  • CRP -> increased
  • arterial blood gas -> hypoxaemia + disturbances
  • AXR -> sentinel loop
  • CXR -> atelectasis + pleural effusion (left)
  • transabdominal USS
  • CT scan 48-72 hrs after dx
  • MRCP
  • ERCP
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11
Q

How do you assess severity of acute pancreatitis?

A
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12
Q

What is the management of acute pancreatitis?

A
  • ABC
  • 4 principles:
    • fluid resuscitation (IVF, catheter, strict FB monitoring)
    • analgesia
    • pancreatic rest (+/- nutritional support - NJ/TPN)
    • determining underlying cause
  • 95% settle w/ conservative management
  • if severe pancreatitis -> HDU
  • antibiotics controversial -> commence if necrotic/infected necrosis (Imipenem), but not routinely
  • surgery only v rarely required
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13
Q

What is the pathogenesis of chronic pancreatitis?

A
  • increase in activated trypsin within pancreas
  • result of inc/premature activation of trypsinogen
  • or by impaired inactivation of activated enzyme from pancreas
  • leads to precipitation of proteins within duct umen in form of plugs
  • these then form a nidus for calcification
  • also cause of ductal obstruction -> ductal hypertension + panc damage
  • alcohol impairs calcium regulation -> promote trypsinogen activation
  • alcohol only factor interacting w/ env +/- genetic influences
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14
Q

What are the clinical features of chronic pancreatitis?

A
  • chronic upper abdominal pain (type B)
  • steatorrhoea (fat malabsorption)
  • anorexia
  • diabetes
  • malabsorption (-> weight loss)
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15
Q

What are common causes of chronic pancreatitis?

A
  • alcohol abuse
  • chronic steroid/NSAID use
  • no cause found in 25%
  • cystic fibrosis (most common in cause in children)
  • gallstones rarely cause chronic pancreatitis
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16
Q

How do you diagnose chronic pancreatitis?

A
  • typical triad: chronic upper abdo pain, malabsorption (weight loss/steatorrhoea) and calcification of pancreas (on AXR/CT)
  • blood glucose -> elevated
  • serum amylase + lipase -> elevated
  • faecal elastase -> low
  • CT scan -> calcifications, enlargement, ductal dilation
  • Abdo USS -> cavities, duct irregularity, contour, calcification
  • AXR -> calcifications
  • EUS/ERCP/MRCP
17
Q

What is the management of chronic pancreatitis?

A

mainstay of management is conservative + medical

  • analgesia
  • treatment of secondary diabetes
    • diet, oral hypoglycaemics, insulin
  • treatment of malabsorption
    • nutritional support, pancreatic enzyme supp (CREON)

surgical intervention is extremely rare (pancreatic transplants)