Pathogenesis of pancreatitis
The pathogenesis of pancreatitis has been studied for many years, and, nevertheless, not all the processes leading to its development have been studied. Studies have been conducted so far, since they can help in the treatment and prevention of this disease. Even with the use of modern diagnostic methods to identify the cause of pancreatitis is not possible. In 20% of patients, the association between the onset of the disease and the etiologic factor can not be traced.
Reasons for
Pancreatitis can develop under the influence of many factors. All causes of the disease can be divided into: congenital and acquired.
Congenital or hereditary factors include cystic fibrosis, aminoaciduria, etc.
Here are the most common of the acquired factors :
- Alcohol intoxication. This is the leading cause of pancreatitis. It is 80% of all other factors that cause the disease.
- Diseases of the gallbladder, liver, biliary tract.
- Peptic ulcer of the stomach and duodenum.
- Acute renal failure.
- Autoimmune diseases.
- Endocrine pathology: Itenko-Cushing's disease, hyperparathyroidism.
- Injuries to the abdomen.
- Exposure to household, food and industrial toxins, drug overdose.
- Vascular diseases: nonspecific aortoarteriitis.
Pathogenesis of acute pancreatitis
In the development of pancreatitis, hypersecretion of pancreatic juice plays an important role, increasing pressure in the excretory system and premature activation of enzymes. The pathogenesis of the disease is associated with hypersecretion of pancreatic juice, which can be provoked by excessive consumption of food containing a large amount of fat. Such a diet stimulates an abundant secretion of juice, because of which the intra-flow pressure increases.
The enzyme theory is based on a violation of the physiological excretion of enzymes from the pancreas. Enzymes that become active, even in the parenchyma of the body cause its destruction. The most dangerous enzyme is trypsin. It affects the kallikrein-kinin system, thereby increasing vascular permeability, causing edema and other microcirculatory disturbances. In acute pancreatitis, such changes occur in a short time, causing severe intoxication and shock.
The pathogenesis of pancreatitis is associated with the action of the lipase enzyme, which destroys the cell membranes and triglycerides. As a result of their breakdown, free fatty acids are formed, the pH shifts towards acidosis. Acidic medium activates trypsin and the destruction of pancreatic structures begins. Since the body cells also contain enzymes, a cascade of destructive processes is triggered. Cellular hydrolytic enzymes destroy the walls of blood vessels and other tissues, which causes hemorrhages in the parenchyma of the pancreas.
Given the mechanisms of pancreatitis development, it can be concluded that the initial stages are the processes of fatty pancreatitis, and then they flow into the hemorrhagic pancreatic necrosis.
Has the basis of the infectious theory of pancreatitis. Its pathogenesis is based on the development of the disease due to the penetration of microorganisms into the organ glands. Infectious agents can penetrate the parenchyma of the pancreas through the duct system, lymph or blood. It is not rare to develop purulent complications in the tissue of the organ.
The neural-reflex theory is not devoid of anatomical and functional principles. Due to the violation of nervous regulation, in particular, with an increase in the tone of the vagus nerve, the activity of the secretory apparatus of the pancreas and its sensitivity to hormonal and nutritional irritants increase.
Pancreatitis has an effect on systemic hemodynamics. The pathogenesis of vascular disorders is based on increasing the permeability of the vessel walls and the transition of the liquid part of the blood to the interstitial space, the development of hypovolemic shock. Vascular insufficiency rapidly increases without appropriate medical measures and rarely leads to death.
pathogenesis of biliary pancreatitis
This type of pancreatitis develops in the pathology of the biliary system. The pathogenesis of biliary pancreatitis is associated with casting pancreatic juice and bile. These processes occur when the pressure in the bile duct or duodenum increases.
The reason may be a morphological change in the sphincter of Oddi or the large duodenal papilla. In the pancreas, activated trypsin leads to lysis of the parenchyma and self-digestion. Further, the destroyed areas of the body are replaced by fibrous tissue. All pathological processes in biliary pancreatitis lead to loss of gland function.
Alcoholic pancreatitis
Alcohol intake is a signal for the allocation of a large amount of pancreatic juice. It is characterized by a richness of proteins and a low content of bicarbonates. Such a secret has a thick consistency and leads to blockage of the outflow ducts and formation of calcifications. The pathogenesis of this process is completed by the development of autolysis and the formation of retention cysts, pseudocysts.
additional mechanism contributing to the formation of stones in the ducts, is the lack of litostatina - a protein that stabilizes the calcium. It performs an important function, since the pancreatic juice is saturated with calcium salts. It is known that alcohol causes a spasm of the sphincter of Oddi, renders the overall metabolic effects( hypermetabolism), stimulate exocrine and endocrine and enhances gastric acid-producing function.
Pathogenesis of hereditary pancreatitis
In the family form of pancreatitis, a gene mutation occurs. The pathogenesis of the hereditary form is based on the replacement of the amino acid leucine with valine.
This mutation results in a disruption of the deactivation of trypsinogen within the cell. As a result, trypsinogen is converted to trypsin, which leads to the autolysis process.
Allergic pancreatitis
Allergic pancreatitis occurs more frequently in patients with asthma, urticaria, allergic rhinitis. In this type of disease, the organ allergic reaction plays a role. It is divided into three stages:
- On the ground, the sensitivity of the organism
- Stage 2 takes place with the formation of antibodies to the allergen
- Last stage - the pancreatic tissue damage
What can cause autoimmune process? These are the products of protein breakdown, microbial toxins, tissue elements of the patient in violation of immune tolerance. When examining blood, antipancreatic antibodies and circulating immune complexes can be detected.
The disadvantage of the above-mentioned theories is that they single out one cause of the development of the disease. According to modern studies, the etiological factor triggers a cascade of immunological, vascular and metabolic processes.
Therefore, it can be concluded that the disease is multifactorial, complex mechanisms of pathogenesis and influenced by all the physiological and pathological processes in the human body.
