The pathophysiology of pancreatitis is generally considered in three phases:
Phase 1
Obstruction of bile or pancreatic ducts, or direct toxicity, leads to premature activation of trypsin within pancreatic acinar cells which activates a variety of injurious pancreatic digestive enzymes.
Phase 2
Intrapancreatic inflammation which can lead to necrosis, haemorrhage, infection or the collection of fluid and formation of a pseudocyst.
Phase 3
Extrapancreatic inflammation.
Phases 2 and 3 can, in approximately 10-20% of cases, lead to shock and SIRS.
Aetiology and pathogenesis of acute pancreatitis [4]
Pathogenesis of acute pancreatitis | Aetiology |
Ductal obstruction | Gallstones Alcohol* Post endoscopic retrograde cholangiopancreatogpraphy (ERCP) Malignancy Mucinous tumours Pancreas divisum Sphincter of Oddi dysfunction |
Acinar cell injury | Alcohol* Trauma Ischaemia Drugs (e.g. Corticosteroids, azathioprine, and thiazides) |
Defective intracellular transport | Alcohol* Hereditary Hypercalcaemia Hypertriglyceridaemia Autoimmune |
*Alcohol triggers acute pancreatitis via multiple mechanisms.