Chronic pancreatitis - Pathogenesis

In the pathogenesis of chronic pancreatitis, one of the leading mechanisms is the activation of pancreatic enzymes, primarily trypsin, and "self-digestion" of pancreatic tissue. Experiments on laboratory animals have shown that the introduction of almost all pancreatic enzymes into its duct under sufficient pressure causes "self-digestion" of its tissue and inflammatory changes in it; the exceptions are amylase and carboxypeptidase. Of particular importance in the development of pancreatitis is trypsin, which causes coagulation necrosis of acinar tissue with leukocyte infiltration, as well as A- and B-phospholipases, which destroy the phospholipid layer of membranes and cells, and elastase, which has a destructive effect on the elastic "framework" of vascular walls and additionally causes vascular changes that contribute to hemorrhagic impregnation of pancreatic tissue.

Pathological, premature activation of trypsin from trypsinogen is carried out by enterokinase, which enters the pancreatic ducts during dyskinesia of the duodenum. However, it has recently been proven that under pathological conditions, in the presence of an inflammatory process in the pancreas and obstacles to the outflow of pancreatic juice, activation of trypsin, chymotrypsin and elastase occurs in the pancreas itself. Activation of kallikrein also occurs, which contributes to an increase in vascular permeability, edema of the gland tissue and increased pain. Participation in the exacerbation of the process of other vasoactive substances, increasing capillary permeability, as well as some prostaglandins is also assumed. It is important, initially - due to edema, and then - sclerotic changes in the acinar tissue, obstruction of lymph outflow; microcirculation is disrupted due to the formation and deposition of fibrin threads in capillaries and venules and their microthrombosis. At the same time, the pancreas becomes compacted due to the proliferation of connective tissue and fibrosis of the gland. Autoimmune processes play a major role in the progression of the process.

In chronic pancreatitis, occurring without obvious relapses, all these changes gradually or more rapidly progress, in parallel with this, the functional reserves of the pancreas decrease, and then signs of its functional exo- and endocrine insufficiency clinically manifest. In chronic recurrent pancreatitis, as a result of repeated effects of etiologic factors (sharp violations of the dietary regimen, significant consumption of alcoholic beverages, especially strong ones, severe infectious diseases, some intoxications, etc.), severe exacerbations periodically occur, resembling acute pancreatitis in their morphological and pathophysiological picture, which are then replaced by remissions. Each exacerbation is the cause of a sharp progression of the disease.

This general pattern of development and progression of chronic pancreatitis is undoubtedly influenced by the characteristics of its etiology and the presence of concomitant diseases.

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