Téma: 

Pathophysiology of acute pancreatitis

Petr Dítě, Ivo Novotný

Etiologically acute pancreatitis is a heterogeneous disease. However, the common denominator of pathophysiological changes of the gland is activation of pancreatic enzymes with liberation of proinflammatory mediators, cytokines including. Heterogeneity of the disease might be summarized as follows: a. activation of pancreatic proenzymes into active enzymes – development of trypsine plays the fundamental role. So called phenomenon of co-localization is currently reported, where zymogennous granules and lysozomes combine and vacuole develops. This process leads to activation of proenzyme trypsinogen into trypsine which results in autodigestion of the gland. b. Active trypsine activates other systems, as bradycinine, calicreine-cinine system and leads to coagulation changes because free enzymes damages vascular endothelium that results in morphological picture of vasculitis. Vasoconstruction development causes changes in perfusion of gland parenchyme and development of tissue ischemia and induction of free oxygen radicals affecting as the function of cell membranes so cell organelles, mitochondria including. c. the role of calcium in cellular death or hyperstimulation of pancreatic acinose cells function is crucial. It is proved that abnormal increasing of intracellular calcium causes activation of trypsine and damage of pancreatic acines. d. Regardless of etiology of acute pancreatitis mechanisms of intracellular changes are universal. This is related to effect of liberalization of cytokines and mediators of inflammatory processes. Sequestration of neutrophils into the region of inflammation is a very important phenomenon . Their depletion is related to the load and course of acute pancreatitis. Despite progress of our knowledge of etiopathogenesis of the disease there are many factors that have not been explained.

Ročník 2008  Témy časopisu Gastroenterology for practice 4 / 2008

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