acute + chronic pancreatitis Flashcards
what actually is acute pancreatitis and what causes it.
autodigestion of the pancreas by pancreatitic enzymes. triggering an inflammatory reaction.
if treated early can be reversable.
stellate cells in pancreas activated by products of breakdown of alcohol. Gall stones can block the acini duct, the two most common causes
I GET SMASHED
Idiopathic
Gall stones
Ethanol
Trauma
Steroids
Mumps + malignancy
Autoimmune
Scorpion sting
Hypertriglycerides or Hypercalcaemia or Hypothermia
ERCP
Drugs (Azathioprine, Sodium Valporate, Statins)
differential diagnosis for acute pancreatitis + clinical signs and symptoms
MI, Gall bladder disease, gastric ulcer, AAA, Duodenal ulcer.
Severe epigastric P radiating to the back
vom
epigastric tenderness
ileus- in the duodenum espesh.
low grade fever.
cullens sign (periumbilical discolouration)
grey-turners sign- (flank discolouration) - both due to bleeding.
systemically unwell signs- hypotensive, hypoxic, inc RR, multi organ failure, calcifications.
investigations for acute pancreatitis.
FBC + LFT–> raised amylase in 75% of patients, (not very prognostic but quite cheap, up and down fast) if more than 2.5x baseline can diagnose AP.
Serum lipase more sensitive + specific but more expensive.
CT- gold standard but only used if clinically unsure. (48hr test usually)
USS to check for gall stones. + done early can dictate management (stone vs alcohol)
how would you know who might need ICU treatment in acute pancreatitis.
Modified Glasgow score is most commonly used => mnemonic is PANCREAS
o P => PaO2 < 8Kpa
o A => age => at risk if they are above 55 years old
o N => neutrophilia, WBC >15
o C => hypocalcaemia <2 => a sign of severe pancreatitis, you get a release of lipase, this causes lipolysis, the free fatty acids bind to Ca2+ creating Ca2+ soap deposits in the abdomen, reducing serum Ca2+
o R => renal, so urea >16
o E => enzymes, LDH > 600 and AST/ALT > 200 => LDH is raised in response to damaged tissues and also in response to hypoxia (lactate dehydrogenase), and a high AST/ ALT suggests that a gallstone is impacted in the distal end of the common bile duct, causing the pancreatitis.
§ Therefore, high AST suggests gall-stone pancreatitis
o A => Albumin <32, decreased in severe inflammation (due to IL-6)
o S => sugars, glucose would be high in severe pancreatitis (as insulin cells are being damaged), glucose >10
Note that the cytokines released from the inflammation can cause ARDS, reduce surfactant and therefore cause PaO2 to drop
management and complications of acute pancreatitis
Wide cannula/ central line–> fluids
monitor fluid in and out, monitor for AKI
?abx
if obstructed biliary system- ERCP
if gallstones- cholecystectomy
if fails to settle- with additional necrosis and worsening organ function –> fine needle aspiration surgical necrosectomy, radiological drainage.
Complications: pancreatic pseudo-cyst –> more than 6cm, + 3/12 + symptoms- needs Rx - needle into stomach.
duodenal ileus.
what is chronic pancreatitis- aetiology
inflammatory condition- affecting exocrine and endocrine functions.
80% alcohol excess
20% idiopathic
genetic elements- Cystic fibrosis, haemochromatosis
clinical signs and symptoms of Chronic pancreatitis
pain- worsening 15-30 mins after a meal.
5-25 years after symptoms begin you get pancreatic insufficiency- steatorrhea, DM - in the maj- 20 years after symptoms.
investigations of chronic pancreatitis
abdo x-ray –> pancreatic calcification (lipase being released breaks down fatty acids– these bind to calcium)
Gold standard is CT (for calcification)
can use functional tests- faecal elastase- if imaging inconclusive
management of chronic pancreatitis
enzymatic suppliments- Creon
analgesia
antioxidants ? not that useful.
annual Hba1c as high risk of DM.
