Alcoholic pancreatitis

The steady growth of incidence of acute pancreatitis, especially its destructive forms, high levels of mortality and a large number of complications, often leading to severe violations of the body until the disability, as well as the existing difficulties of diagnosis and lack of a unified approach to the treatment of this disease forced to pay special attention to the study of this pathology.

We observed 111 patients with acute or acute exacerbation of chronic pancreatitis, of whom 3.6% (4 cases) were patients with pancreatic necrosis, which accounted for 12% of all acute pancreatitis. To date, yet there is no single approach to the etiopathogenetic brand viagra mechanisms of autoliticheskih processes in the pancreas, leading to the development of functional and structural changes in the cells of the body, accompanied by the phenomenon of "evasion of enzymes, as a result of this occurrence giperfementemii. In our observations of hyperamylasemia was 38.7% of the total number of observations (43 cases), including amilazemiya more than 100 g / h / l was 23% (26 cases). Along with the increase of serum amylase was significantly increased level of urine amylase, due in some cases, an increase of glomerular filtration and decreased tubular reabsorption of the enzyme, which in the presence of endotoxemia accompanying phenomenon of pancreatic necrosis, forming chemical bonds with the biologically active protein fractions of average molecular mass, the so-called "middle molecules "serum (Shepilov ZI, Baljakin SO, 1984). The lack of correlation of degree of autolysis of the pancreas and the severity of amylasuria depends on many factors and can not be estimated uniquely, respectively, requires further research in this area.

Considering the mechanisms etiopatogegneza acute pancreatitis, it is necessary to allocate a number of key factors, wherewith are:

Gallstone disease (GSD).

According to our observations, the incidence of acute pancreatitis and exacerbation of chronic pancreatitis in the presence of this pathology was 23.4% (26 cases) of them in one case (0.9%) occurred choledocholithiasis.

Found in the literature, the term "holepankreatit (L. Finger, 2000), which reflects the primary role of biliary pathology in the etiopathogenesis of acute pancreatitis. According to the theory of "common channel" on the background diskeneticheskih phenomena in the gall bladder filled concrements extrahepatic bile ducts and sphincter of Oddi arises bile-pancreatic ductal hypertension, and reflux of bile into the pancreatic duct with intraductal activation of enzymes.

The second place according to our observations extend postoperative pancreatitis occurring in different periods after cholecystectomy (8 cases, which accounted for 7.2% of total cases), 2 cases (1.8%) consisted of patients who had undergone resection of the Billroth-II . A separate group with acute pancreatitis after laparoscopic cholecystectomy and ERCP, were not included in the studies. The high frequency of postoperative pancreatitis is associated with intraoperative injury of pancreatic duct diskineticheskih phenomena in the sphincter of Oddi, resulting from a violation of the neuro-reflex regulation due to surgical intervention. In some cases, the appearance of acute pancreatitis can be regarded as a manifestation of postcholecystectomical syndrome. High frequency of acute pancreatitis that occur after stomach resection due to the presence of duodeno-pancreatic reflux, where the activator of intraductal pancreatic enzymes is enterokinase. Penetration of duodenal contents into the pancreatic duct is possible with dehiscence faterova nipple and increased intraduodenal pressure, which can be observed at duodenostasis often occurs when afferent loop syndrome.

Steadily growing number of alcoholic pancreatitis. According to our observations, the diagnosis of acute alcoholic pancreatitis "exhibited in the two cases. In fact, indications of the systematic use of alcohol in history occur not less than 1 / 3 of patients with acute exacerbation and chronic pancreatitis. For many foreign sources of fact alcohol addiction is the leading mechanism of acute pancreatitis (Ghattas Khoury, 2000). At the cellular level, ethanol contributes to the accumulation of intracellular proteolytic enzymes and their premature activation and release. At ductal some convincing test level, ethanol increases the permeability of the ducts, allowing proteolytic enzymes to penetrate into the tissue of the pancreas, causing autolysis processes. Ethanol increases the content of the protein component of pancreatic juice, reducing the concentration of bicarbonate and trypsin inhibitors. This leads to the formation of protein complexes that prevent the outflow of pancreatic secretion (Emedicine.com).

Addressing issues of etiopathogenesis of acute exacerbation of chronic pancreatitis and to identify allergic factor of this pathology. Currently, more and more attention of scientists began to attract the immunological processes in the pancreas. In our observations noted 2 cases of atopic pancreatitis occurred on the background of sensitization, polyvalent allergy. Patients with this pathology have noted increased pain and aggravation of the severity of the processes of alteration of the pancreas in the background of active treatment with different pharmacological groups, which makes the approach to the treatment of this group of patients is strictly differentiated from the expression of immunological reactions. Often, such a variant of etiopathogenesis of acute pancreatitis combined with neurogenic (T. D. Tsympilova, VM Mavrodi, 1995), when in history there is a stressful situation, leading to an imbalance of the central regulation of pancreatic secretion of feedback.

It must be noted or ischemic angiogenic factor in the pathogenesis of acute pancreatitis (TD Tsympilova, VM Mavrodi, 1995). With a high degree of reliability found that among patients with acute pancreatitis is prevalent in patients aged 40-64 years, when increases the risk of widespread atherosclerosis. Often there are difficulties in the differential diagnosis of destructive pancreatitis flowing with symptoms of pancreatic shock, and myocardial infarction with cardiogenic shock, often have a combination of these two pathologies that are competing in determining the underlying cause of death of patients with pancreatic necrosis. On the background of atherosclerotic vascular lesions of the pancreas arise local thrombosis, which, when there are changes in the hemostatic system leads to irreversible degenerative-necrotic changes in the parenchyma of the organ.

CONCLUSIONS:

For adequate and effective treatment of acute pancreatitis must be considered elements of the pathogenesis of this disease, which in most cases to predict the course and outcome of disease, identify ways of preventing complications, relapse and recurrence, as well as working on a certain link in the pathogenesis of, reduce the degree of destructive changes in the pancreas gland.

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