Diabetes

The main pathogenesis of acute pancreatitis

Pancreatitis is diagnosed when the pancreas becomes inflamed for a variety of reasons. When the organ swells, the outflow of enzymes becomes difficult, which is why the body's tissues begin to digest themselves.

Despite the use of modern and effective methods of treatment, the mortality from pancreatitis is quite high. In normal types of the disease, the patient dies in 7-15% of cases, with destructive types - up to 70%.

Since the risk of developing complications of pancreatic diseases is very high, it is important to know about the etiological features and pathogenesis of pancreatitis. Detailed information about the disease can be found in the presentation below.

Causes of pancreatitis

In 80% of cases, the appearance of the disease factors lie in alcohol abuse, pathologies of the gallbladder and ducts. In 45% of cases, it is noted that choledocholithiasis, cholelithiasis, contraction of canals with cysts and tumors, intestinal pathologies contribute to the formation of pancreatic inflammation.

Each concomitant disease has its own reasons for development. However, they all lead to the emergence of acute pancreatitis.

The leading factors in the pathogenesis of pancreatitis are: obstruction of the release of pancreatic enzyme through the ducts. Therefore, the treatment of the underlying disease begins with the treatment of all associated pathologies.

The etiology of acute pancreatitis is mainly associated with chronic alcoholism. In this case, the pattern of development of the disease lies in the dysfunction of the liver and gland canals.

Alcohol products increase secretion, making the discharge more viscous. This increases the pressure in the channel, which leads to pancreatic intoxication, disrupts enzyme synthesis in it, and upsets the metabolic processes in the liver.

Another common cause of pancreatitis is the nutritional factor. In this case, inflammation develops when a person abuses meat, fatty and fried foods.

Less commonly, the pathophysiology of pancreatitis triggers for a number of other reasons:

  1. viral infections (mumps, Coxsackie virus, hepatitis);
  2. genetic predisposition (cystic fibrosis);
  3. bacteria (mycoplasma, campylobacter);
  4. ulcers of the digestive tract;
  5. pancreas injury;
  6. congenital pathologies of organ development;
  7. medication (estrogen, corticosteroids, diuretics, azathioprine);
  8. disorder of metabolic processes caused by the presence of a number of diseases (vasculitis, diabetes, AIDS).

Also, pancreatitis develops as a result of surgical intervention carried out in case of pancreatic and biliary duct pathologies. Trauma to the organ can occur during dilatation of strictures, endoscopy, prosthetics, papillotomy and other types of operations.

Postoperative pancreatitis is a complication of surgical treatment. It occurs when damage to the ducts of the gland and their hypertension.

Rare causes of pancreatic inflammation include worm infestation (infection with ascaris), hyperparathyroidism (parathyroid pathology) and organophosphate poisoning.

Other infrequent factors of the onset of the disease include the scorpion sting and ischemia of the mesenteric basin, which occurs during the formation of a mesenteric artery thrombus.

Pathogenesis of acute pancreatitis

The acute phase of pancreatic inflammation is a toxic enzymopathy. The main element in the development of the disease is the isolation of specific enzymes from the body of acinar cells (inactive profences).

The process starts due to the active stimulation of the exocrine function of the organ, an increase in pressure or reflux of bile in the Wirsung duct, and the obstruction of the ampulla of the duodenal papilla.

Due to intraductal hypertension, the walls of the terminal ducts become more permeable, which activates the enzymes. The pathogenesis of acute pancreatitis leads to the launch of self-digestion processes, in which lipolytic enzymes (lipase, phospholipase A) are involved.

It is noteworthy that lipase does not affect only healthy cells. Phospholipase A damages cell membranes where lipase easily penetrates. The release of the latter contributes to enhanced lipid breakdown and triggers destructive processes. Of all the enzymes concentrated in the zone of inflammation, granulocyte elastase is the most damaging for the pancreas - this is the main link in the pathogenesis of acute pancreatitis.

The result of the action of enzymes is foci of lipid pancreatic necrobiosis. Near these areas, as a consequence of inflammation, a demarcation shaft is formed, delimiting the affected areas with healthy tissues.

When the pathobiochemical process ends at this stage, fatty pancreatonecrosis develops. If the pH changes (from 3.5 to 4.5) due to the accumulation of fatty acids in the pancreatic cells affected by lipase, then the trypsinogen inside the cells is converted to trypsin. It triggers proteinases and lysosomal enzymes, which leads to proteolytic irreversible changes in pancreatocytes.

Elastase dissolves vascular walls and interlobular connective tissue jumpers. This leads to instantaneous spread throughout the pancreas and nearby organs of self-digesting enzymes.

The final condition for the pathogenesis of acute inflammation of the parenchymatous organ is early activation of pancreatic enzymes. Under the influence of trypsin, a number of processes are launched that end with a pathobiochemical disorder:

  • enzyme pancreatic zymogens are activated;
  • blood clotting increases;
  • fibrinolysis changes;
  • stimulates kallikrein-wedge system.

In addition to local disruptions caused by pathological disorders in the parenchymal organ, there is a general poisoning of the body.

Extensive intoxication contributes to the damage of other organs - the heart, kidneys, liver and lungs.

Mechanisms of development of other types of pancreatitis

Classification of pancreatitis includes different types of the disease. Their pathogenesis may differ slightly. Thus, a rare calculous type of inflammation of the gland occurs when concrements are formed in the affected excretory duct (carbonic acid and phosphoric acid).

They look like small stones or gray-white sand. And pathological changes in the pancreas, where calculus accumulates, are due to inflammation and expansion of the excretory duct.

The pathogenesis of the alcoholic form of pancreatitis is that alcohol increases the tone of the sphincter of Oddi. This prevents the exocrine secretion from flowing out and creates hypertension in small ducts. Alcohol has a number of other negative actions:

  1. Enhances enzymes in the gland, which stimulates proteolytic enzymes and triggers autolysis of organ cells.
  2. It increases the secretion of gastric juice and hydrochloric acid, which increases the production of secretin, which provokes exocrine hypersecretion in the organ.

The pathogenesis of biliary pancreatitis is associated with the ingress of bile and pancreatic juice. Such processes are triggered when pressure rises in the duodenum and biliary ducts. Based on this, the definition of the disease was formed as a chronic inflammatory process caused by damage to the liver and biliary tract.

Biliary pancreatitis can be caused by morphological changes occurring in the sphincter of Oddi or duodenal papilla. Trypsin activity contributes to the lysis of the parenchyma and its self-digestion.

In the case of biliary disease, all the affected areas of the gland are overgrown with fibrous tissue. In the absence of timely treatment, the organ ceases to function.

A genetic variety of pathogenesis develops when a gene is mutated, which is inherited. Failure occurs when replacing the amino acid leucine to valine.

Hereditary pancreatitis is also accompanied by trypsin dysfunction in the cells. As a result, the pancreas begins to digest its own tissues.

Allergic form of pancreatic inflammation occurs mainly in patients suffering from seasonal rhinitis, urticaria or bronchial asthma. The mechanism of development of this type of disease is based on the occurrence of an allergic reaction occurring in three stages:

  • body sensitization;
  • the formation of antibodies to the pathogen;
  • damage to the tissues of the parenchymal gland.

The development of autoimmune processes contributes to many factors and changes. Therefore, allergic pancreatitis has a complex mechanism of pathogenesis.

Symptoms and treatment of pancreatitis

Identifying pancreatitis is easiest when it occurs in the acute phase. In this case, the clinical picture of the disease is most pronounced.

The leading symptoms of pancreatic inflammation are severe persistent epigastric pain, often radiating to the left hypochondrium, due to which the patient may even lose consciousness. Discomfort increases when the patient lies down or consumes food.

In addition to pain, pancreatitis is accompanied by vomiting, febrile temperature, nausea and yellowing of the skin. A number of patients have hemorrhages in the navel area. Still patients complain of heartburn and flatulence.

The lack of treatment for acute pancreatic inflammation will lead to the development of a number of dangerous complications - diabetes, abdominal syphilis, cystic fibrosis, and thrombosis of blood vessels. Therefore, treatment should be carried out in a hospital under the supervision of doctors.

The main goals of therapy:

  1. the elimination of painful symptoms;
  2. removal of pancreatic enzymes from the blood stream;
  3. appointment of a special diet.

Modern man often neglects the rules of a healthy and balanced diet, which leads to problems with digestion. Therefore, an important component of the treatment of pancreatitis is to provide calm to the diseased organ through fasting and diet. On the first day of hospitalization, the patient cannot eat anything, then he is given a drip with glucose and only then he goes on a light diet.

Since acute inflammation is accompanied by pain, a strong analgesic drug is often prescribed. Also, special solutions (Contrycal, Trasilol) are injected intravenously into the patient to eliminate the intoxication of the body with pancreatic enzymes. If necessary, antibiotics and calcium preparations are prescribed.

If there is no improvement after a week of drug treatment, laparotomy is performed. During the operation, the surgeon removes dead areas of the parenchymal organ. In emergency cases, with the formation of pseudocysts (accumulation of dead tissues, enzymes) in the pancreas, drainage is done.

Information about acute pancreatitis is provided in the video in this article.

Watch the video: Management of Acute Pancreatitis - Stephen Kim, MD. UCLA Digestive Diseases (September 2019).