Acute Pancreatitis
Premature activation of the pancreas's own digestive enzymes causes it to digest itself, so the pain, the systemic inflammatory response and the organ failure it can trigger are all consequences of autodigestion, not infection.
First principles
Acute pancreatitis is the pancreas digesting itself
The pancreas normally secretes proteolytic and lipolytic enzymes as inactive precursors (zymogens) that are only activated once safely in the duodenum. Acute pancreatitis begins when this safeguard fails and trypsinogen is prematurely activated to trypsin inside the gland itself: triggering a cascade that activates the other digestive enzymes in situ. The result is autodigestion: the pancreas's own enzymes break down pancreatic and peripancreatic tissue, causing oedema, fat necrosis and, in severe cases, haemorrhage. Almost every feature of the disease (the pain, the enzyme rise, the systemic illness) is a direct consequence of this self-digestion, not of an infective or malignant process.
Educational content pending clinical review. Not medical advice.