“…4 The pathophysiology of acute pancreatitis includes activation of trypsinogen into trypsin within the acinar cells upon increased ductal pressures and adenosine triphosphate depletion resulting in increased intra-acinar calcium concentration which activates zymogens. 5,6 This leads to the destruction of pancreatic parenchyma and the release of Damage Associated Molecular Patterns (DAMPs) that activate neutrophils and trigger the inflammatory cascade responsible for the systemic manifestation of acute pancreatitis. As a result, increased capillary permeability and damage of the endothelium results along with microvascular thrombosis that leads to multiorgan dysfunction syndrome (MODS).…”