Chronic pancreatitis: pathogenesis
Last reviewed: 23.04.2024
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In the pathogenesis of chronic pancreatitis, one of the leading mechanisms is the activation of pancreatic enzymes, primarily trypsin, and the "self-digestion" of pancreatic tissue. In experiments on laboratory animals it was shown that the introduction of almost all enzymes of the pancreas into its duct under sufficient pressure causes "self-digestion" of its tissue and inflammatory changes in it; the exception is 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 acts destructively on the elastic "framework" of the walls of the vessels and causes additional vascular Changes that promote hemorrhagic impregnation of pancreatic tissue.
Pathological, premature activation of trypsin from trypsinogen is carried out by enterokinase falling into the pancreatic ducts with dyskinesia of the duodenum. However, recently it has been proved that in pathological conditions, in the presence of an inflammatory process in the pancreas and obstacles to the outflow of pancreatic juice, the activation of trypsin, chymotrypsin and elastase occurs already in the pancreas itself. There is also activation of kallikrein, which contributes to increased vascular permeability, swelling of the gland tissue and increased pain. It is also expected to involve in the exacerbation of the process and other vasoactive substances that enhance capillary permeability, as well as some prostaglandins. It is important, at first - due to edema, and then - and sclerotic changes in acinar tissue, difficulty lymph flow; disturbed microcirculation due to the formation and deposition in the capillaries and venules of fibrin strands and their microthrombin. At the same time, the pancreas thickens due to the proliferation of connective tissue, fibrosis of the gland. In the progression of the process, great importance is attached to autoimmune processes.
With chronic pancreatitis, which occurs without obvious relapses, all these changes gradually or more rapidly progress, in parallel, the functional reserves of the pancreas decrease, and then signs of its functional exo- and endocrine insufficiency show clinical signs. With chronic recurrent pancreatitis due to repeated effects of etiological factors (severe violations of the diet regime, a significant use of alcoholic beverages, especially strong alcoholic beverages, severe infectious diseases, some intoxications, etc.), there are occasional severe exacerbations, morphological and pathophysiological picture resembling acute pancreatitis, remissions. Each aggravation 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 features of its etiology and the presence of concomitant diseases.
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