Acute pancreatitis is characterised by:
- inflammation
- proteolysis - from release of proteases
- fat necrosis - from release of lipase and phospholipase
- haemorrhage - from release of elastase
The activation of trypsin is thought to play a key role by:
- activating other pro-enzymes in the acinar cells
- activating the kinin system and initiating the clotting and complement systems
Three mechanisms are postulated:
- acinar cell injury - causing release of intracellular pro-enzymes which are then activated. This may be the mechanism in acute pancreatitis associated with alcohol binging, viruses, drugs, ischaemia and trauma.
- duct obstruction - a gallstone may impact at the ampulla and obstruct the pancreatic duct causing increased intraductal pressure and hence intercellular leakage of enzymes from small ducts into the interstitium. Alternatively, damage to the sphincter of Oddi allows reflux of duodenal contents into the pancreas. Lecithin in the refluxed material is converted by phospholipase A to lysolecithin which is highly toxic to acinar cells. In chronic alcoholism, acute attacks of pancreatitis may result from the precipitation of proteinaceous plugs in the pancreatic ducts which cause fibrosis and atrophy of the pancreas.
- derangement in the intracellular transport of pancreatic enzymes - enzymes activated within the lysosomes by hydrolases.
Toxaemia results from the systemic absorption of enzymes and toxins. The sequestration of calcium into the areas of fat necrosis produces hypocalcaemia while the escape of large volumes of fluid into the peritoneal cavity results in hypovolaemic shock.