Pancreatitis: drug treatment and its role in recovery

Pancreatitis: drug treatment and its role in recovery

I. Determination of pancreatitis and its classification

Pancreatitis is an inflammatory disease of the pancreas, characterized by damage to its parenchyma and impaired its exocrine (production of digestive enzymes) and endocrine (the production of hormones, such as insulin) functions. Inflammation occurs when digestive enzymes, usually activated in the intestine, are activated inside the pancreas, starting to digest its own tissues. This self -transmission leads to inflammation, swelling, hemorrhages and, in severe cases, necrosis (wipes of tissues) of the pancreas.

Pancreatitis is classified into two main forms: acute and chronic.

Acute pancreatitis (op): characterized by a sudden onset of pancreatic inflammation. The severity of acute pancreatitis varies from a mild, self -limiting shape to a severe, threatening form of shape, accompanied by organ dysfunctions and complications such as necrosis, pseudo -vodokists and infection. Acute pancreatitis usually has a clear trigger that can be identified, for example, stones in the gall bladder or alcohol abuse.
Chronic pancreatitis (HP): It is a progressive inflammatory disease of the pancreas, characterized by irreversible morphological changes and functional failure. Chronic inflammation leads to fibrosis (the formation of scar tissue), atrophy (reduction of size) and calcification (calcium deposit) of the pancreas. This leads to digestion (exocrine deficiency) and the development of diabetes (endocrine deficiency). Chronic pancreatitis is often caused by prolonged alcohol abuse, genetic predisposition, autoimmune diseases or recurrent acute pancreatitis.

II. Etiology and pathogenesis of pancreatitis

Understanding the causes and mechanisms of the development of pancreatitis is necessary for effective treatment and prevention.

A. Etiology of acute pancreatitis:

The most common causes of acute pancreatitis are:

Gallstone disease: Stones in the gall bladder can block the general bile duct or pancreatic duct (or both), which leads to an increase in the pressure in the pancreas and the activation of enzymes inside the gland. This is a “general screaming theory” – the migration of small stones through the veils of the papilla, causing obstruction and reflux bilia into a pancreatic duct.
Alcohol abuse: Chronic alcohol consumption is a significant risk factor for both acute and chronic pancreatitis. Alcohol has a direct toxic effect on the cells of the pancreas (acynar cells), increases the secretion of pancreatic juice, causes sphincter of Oddi and increases the viscosity of pancreatic juice, contributing to the formation of protein plugs.

Less common causes of acute pancreatitis include:

Hyperyglyceridemia: Very high levels of triglycerides in the blood can cause damage to the pancreas.
Hypercalcemia: An increased level of calcium in the blood can stimulate premature activation of pancreatic enzymes.
Medicines: Some drugs, such as Azatioprine, 6-Merkaptopurin, Didanosine, Valproic acid and estrogen, are associated with the development of acute pancreatitis.
Trauma: The stupid abdominal injury or surgical interventions in the pancreatic can cause pancreatitis.
Infections: Viral infections, such as pig, cytomegalovirus (CMV) and Koksaki virus, can cause pancreatitis.
Autoimmune diseases: Rarely, autoimmune diseases, such as systemic lupus erythematosus (SLE), can be associated with pancreatitis.
Hereditary factors: Genetic mutations affecting the function of the pancreas can predispose to pancreatitis. The most common genetic causes include mutations in PRSS1 (tripsinogen gene), spinK1 (tripsin inhibitor) and CFTR (transmembrane conductor regulator for cystic fiber).
Idiopathic pancreatitis: In approximately 10-20% of cases, the cause of acute pancreatitis cannot be established, and it is classified as idiopathic.

B. Pathogenesis of acute pancreatitis:

The pathogenesis of acute pancreatitis is a complex cascade of events that begins with the premature activation of pancreatic enzymes inside the pancreas. The key stages include:

Premature activation of enzymes: Instead of activating in the small intestine, tripsinogen, the inactive form of trypsin, it is activated inside the pancreatic acynar cells. This can be caused by various factors, such as an increase in intracellular calcium, damage to acinar cells and violation of tripsin inhibiting mechanisms.
Self -digestion: Activated Tripsin triggers the activation of other pancreatic enzymes, such as elastasis, phospholipase A2 and chipripsin. These enzymes begin to digest pancreatic tissue, causing inflammation and damage.
Inflammatory answer: Damaged pancreatic cells release pro-inflammatory cytokines, such as factor of tumor necrosis-alpha (TNF-α), Interleukin-1 (IL-1) and Interleukin-6 (IL-6). These cytokines attract immune cells (neutrophils, macrophages) in the pancreas, increasing the inflammatory response.
System effects: Inflammatory mediators and pancreatic enzymes enter the bloodstream, causing systemic effects, such as systemic inflammatory response syndrome (SSVO), acute respiratory failure (ARDS), renal failure and shock.
Necrosis and complications: In severe cases of acute pancreatitis, inflammation can lead to necrosis (death of tissues) of the pancreas. Necrosis can be sterile (non -infected) or infected. Infected necrosis is associated with high mortality. Other complications include the formation of a pseudo -Kistyst (fluid accumulations surrounded by a wall of granulation tissue), abscesses and thrombosis of the sphere vein.

B. Etiology of chronic pancreatitis:

The most common causes of chronic pancreatitis:

Alcohol abuse: Chronic abuse of alcohol is the main cause of chronic pancreatitis in developed countries. The mechanisms with which alcohol causes chronic pancreatitis, include a direct toxic effect on acinar cells, an increase in the secretion of pancreatic juice, the formation of protein plugs and the activation of stelled pancreatic cells that contribute to fibrosis.
Hereditary pancreatitis: Genetic mutations that affect the function of the pancreas can cause chronic pancreatitis, often with the early beginning. The most common genes associated with hereditary pancreatitis include PRSS1, Spink1 and CFTR.
Autoimmune pancreatitis (AIP): This is a form of chronic pancreatitis caused by an autoimmune reaction when the immune system attacks the pancreas. There are two types of AIP: type 1 associated with IgG4-Associated disease, and type 2 associated with inflammatory intestinal diseases.
Idiopathic pancreatitis: In many cases, the cause of chronic pancreatitis cannot be established, and it is classified as idiopathic. Some cases of idiopathic pancreatitis can be associated with undeveloped genetic factors or the influence of environmental factors.
Other reasons: Less common causes of chronic pancreatitis include obstruction of the pancreatic duct (for example, tumor, stricture or cyst), cystic fibrosis and tropical pancreatitis (pancreatitis, found in tropical regions and associated with malnutrition and environmental factors).

G. Pathogenesis of chronic pancreatitis:

The pathogenesis of chronic pancreatitis is characterized by progressive inflammation, fibrosis and pancreatic atrophy. Key mechanisms include:

Repeating episodes of acute inflammation: In patients with chronic pancreatitis, repeated episodes of acute inflammation are often observed, which lead to cumulative damage to the pancreas.
Activation of stellar pancreatic cells: The stellar cells of the pancreas are the main cells responsible for the synthesis of collagen and other components of the extracellular matrix. In response to inflammation and damage, stelled cells are activated and begin to excessively produce collagen, which leads to fibrosis.
Oxidative stress: An increased level of oxidative stress plays a role in the pathogenesis of chronic pancreatitis. Free radicals damage the pancreatic cells and contribute to inflammation and fibrosis.
Violation of microcirculation: Chronic inflammation can disrupt microcirculation in the pancreas, which leads to ischemia (insufficient blood supply) and further damage to tissues.
Neuropathy: Chronic pancreatitis is often accompanied by neuropathy, damage to the nerves in the pancreas. Neuropathy contributes to the development of chronic pain, which is a common and exhausting symptom of chronic pancreatitis.
Epithelial-mechanical transition (EMP): EMP is a process by which epithelial cells lose their cell compounds and acquire mesenchymal properties. EMP can play a role in pancreatic fibrosis in chronic pancreatitis.

III. Diagnosis of pancreatitis

Accurate and timely diagnosis of pancreatitis is crucial for the start of appropriate treatment and prevention of complications.

A. Diagnostics of acute pancreatitis:

The diagnosis of acute pancreatitis is usually based on a combination of clinical signs, laboratory research and visualization.

Clinical signs: Typical symptoms of acute pancreatitis include:
- Strong pain in the upper abdomen, which can radiate to the back.
- Nausea and vomiting.
- Soreness on palpation of the abdomen.
- Fever.
- Tachycardia (rapid heartbeat).
Laboratory research:
- Amylase and serum lipase: An increase in the level of amylase and serum lipase is three times higher than the upper boundary of the norm is a key diagnostic criterion of acute pancreatitis. Lipase is more specific for the pancreas than amylase and remains increased longer.
- General blood test (UAC): The UAC can detect leukocytosis (an increased amount of leukocytes), which indicates inflammation.
- Biochemical blood test: Biochemical blood test can detect deviations such as an increased level of glucose, bilirubin, alkaline phosphatase and alanineine -spraise (ALT).
- Lipid profile: Measurement of the level of triglycerides is necessary to exclude hypertriglyceridemia as the causes of pancreatitis.
Preview:
- Computed tomography (CT) with contrast: CT is the most common visualization method for the diagnosis and assessment of the severity of acute pancreatitis. CT can identify pancreatic edema, necrosis, pseudocysts and other complications.
- Ultrasound examination of the abdominal cavity: Ultrasound can be used to detect bile stones that can cause pancreatitis. However, ultrasound is less sensitive than CT for assessing the pancreas.
- Magnetic resonance cholangiopancreatography (MRHPG): MRHPG is a non -invasive visualization method that can be used to assess the pancreatic and bile ducts. MRHPG can be useful for identifying the causes of the obstruction of the ducts, such as stones or tumors.

B. Diagnostics of chronic pancreatitis:

Diagnosis of chronic pancreatitis can be more complicated than the diagnosis of acute pancreatitis, since symptoms can be non -specific and intermittent.

Clinical signs: Typical symptoms of chronic pancreatitis include:
- Chronic abdominal pain, which can be constant or periodic.
- Stiatorae (fat stool) due to malabsorption of fat.
- Loss of weight.
- Diabetes.
Laboratory research:
- Amylase and serum lipase: Emplage levels and serum lipases can be normal or slightly increased in patients with chronic pancreatitis.
- Calprotek’s: Calprotetin Kala is a marker of inflammation in the intestines. Increased levels of caloprotectin feces can indicate chronic pancreatitis.
- Test for fecal elastasis-1: Fecal elastasis-1 is an enzyme produced by the pancreas, which breaks down proteins in the intestines. Low levels of fecal elastasis-1 indicate exocrine pancreatic failure.
- Gluczotolerant test (GTT): GTT is used to diagnose diabetes.
Preview:
- Computed tomography (CT): CT can identify calcifiers in the pancreas, the expansion of the pancreatic duct and other signs of chronic pancreatitis.
- Magnetic resonance cholangiopancreatography (MRHPG): MRHPG is the most sensitive method of visualization for the diagnosis of chronic pancreatitis. MRHPG can identify changes in the pancreatic duct, such as strictures, dilatation and stones.
- Endoscopic ultrasound examination (Eusta): Eusta is an invasive visualization method, which includes the introduction of an endoscope with an ultrasonic sensor in the stomach and duodenum. Eusta can provide a detailed image of the pancreas and surrounding tissues. Eusta also allows you to get a biopsy of pancreatic tissue for histological examination.
- Stimulating secret test: Stimulating secrets is a method for evaluating the exocrine function of the pancreas. During the secrets test, the hormone, which stimulates the secretion of pancreatic juice, is administered intravenously. Then pancreatic juice is collected and its volume and content of bicarbonates are measured. A decrease in the volume and content of bicarbonates indicates the exocrine deficiency of the pancreas.

IV. Medical treatment of acute pancreatitis

Medication treatment of acute pancreatitis is aimed at facilitating pain, reducing inflammation, maintaining hydration and preventing complications. In most cases, acute pancreatitis requires hospitalization.

Anesthesia:
- Opioid analgesics: Opioids, such as morphine, fentanil and hydromorphone, are usually used to stop severe pain in acute pancreatitis. Opioids are effective for relief of pain, but can cause side effects, such as nausea, vomiting, constipation and oppression of breathing.
- Nonsteroidal anti -inflammatory drugs (NSAIDs): NSAIDs, such as ketorolax, can be used as an addition to opioids to relieve pain. NSAIDs are less effective than opioids for relief of severe pain, but have less side effects.
- Local anesthesia: In some cases, local anesthesia can be used, such as an epidural blockade, to relieve pain.
Infusion Therapy:
- Intravenous fluid administration: Acute pancreatitis is often accompanied by dehydration due to vomiting, reducing fluid intake and fluid leakage in third spaces (for example, into the abdominal cavity). Intravenous administration of a fluid (usually a physiological solution or a solution of lactate ringer) is necessary to maintain hydration and perfusion of organs.
- Correction of electrolyte violations: Acute pancreatitis can lead to electrolyte disorders such as hypocalcemia (low blood calcium), hypokalemia (low blood potassium) and hypomagnesia (low blood magnesium). Correction of these electrolyte disorders is important to maintain the normal function of organs.
Power support:
- Nothing through the mouth (NPO): In the past, patients with acute pancreatitis were recommended to stay on NPO (nothing through the mouth) for several days to give the pancreas to “rest”. However, modern studies show that early enteric diet (nutrition through the gastrointestinal tract) is safe and useful for patients with acute pancreatitis.
- Entereal nutrition: Entereal nutrition is preferable to parenteral nutrition (intravenously nutrition), since it helps to maintain the intestinal function and reduces the risk of infections. Enteral food can be carried out through a nasogastric probe (a probe inserted through the nose into the stomach) or the nasoeunal probe (a probe inserted through the nose into the small intestine).
- Parenteral nutrition: Parenteral nutrition is shown to patients who do not tolerate enteric nutrition or who have contraindications to enteric nutrition.
Proton pump inhibitors (IPP):
- Omeprazole, pantoprazole, эzomeprazole: IPP is drugs that reduce the production of gastric acid. IPP can be used to reduce the stimulation of the pancreas with gastric acid and reduce pain.
Antibiotics:
- Imipenem, meropenem, ciprofloxacin: Antibiotics are shown only to patients with infected pancreatic necrosis. Antibiotics should not use routine in patients with acute pancreatitis, since they do not improve the outcome and can contribute to the development of antibiotic resistance.
Other drugs:
- Octreotide: Octreotide is an analogue of somatostatin, which reduces the secretion of pancreatic enzymes. Octreotide is not recommended to use rutino in patients with acute pancreatitis, since it does not improve the outcome.
- Protease inhibitors: Protease inhibitors, such as testinin, can theoretically be useful in acute pancreatitis, blocking the activation of pancreatic enzymes. However, clinical studies have not shown that protease inhibitors are effective in acute pancreatitis.

V. Drug treatment of chronic pancreatitis

Medication treatment of chronic pancreatitis is aimed at facilitating pain, improving digestion and treatment of complications.

Anesthesia:
- Analgesics: Anesthesia is an important part of the treatment of chronic pancreatitis. Various analgesics can be used, including:
  - Nonsteroidal anti -inflammatory drugs (NSAIDs): NSAIDs can be used to relieve mild and moderate pain.
  - Tramadol: Tramadol is an opioid analgesic that can be used to relieve moderate and severe pain.
  - Opioid analgesics: Opioids, such as morphine, oxicone and hydraulic fabric, can be used to stop severe pain. Opioids should be used with caution due to the risk of dependence and side effects.
  - Adjuvant analgesics: Adjuvant analgesics, such as antidepressants (for example, amitriptyin, dulcesetine) and anticonvulsant drugs (for example, gabapentin, pregabalin), can be used to treat neuropathic pain, which is often found in chronic pancreatitis.
- Fires of the pancreas: Fires of the pancreatic can help reduce pain, improving digestion and reducing pancreatic stimulation.
- Blockade of the womb: The blockade of the celiac plexus is a procedure in which an anesthetic is introduced into the celiac plexus, a network of nerves located in the abdominal cavity. The blockade of the celiac plexus can relieve pain in some patients with chronic pancreatitis.
- Surgical intervention: Surgical intervention can be considered to relieve pain in patients with chronic pancreatitis who do not respond to other treatment methods.
Fires of the pancreas:
- Lipase, amylase, protease: Fires of the pancreas contain lipase, amylase and protease, enzymes that help digest fats, carbohydrates and proteins. Fires of the pancreas are used to treat exocrine pancreatic insufficiency, which is often found in chronic pancreatitis. The enzyme pancreatic drugs are taken during meals to help digest food. The dosage of the enzymes of the pancreas varies depending on the severity of exocrine pancreatic insufficiency.
Vitamins:
- Fatable vitamins (A, D, E, K): Chronic pancreatitis can lead to a deficiency of fat -soluble vitamins, since fats are not digested properly. Patients with chronic pancreatitis may need to take additives with fat -soluble vitamins.
- Vitamin B12: Chronic pancreatitis can lead to a deficiency of vitamin B12, since the pancreas produces a castle factor that is necessary for the absorption of vitamin B12. Patients with chronic pancreatitis may need to receive vitamin B12 injections.
Treatment of diabetes sugar:
- Insulin: In patients with chronic pancreatitis, diabetes often develops. Patients with diabetes may need insulin treatment or other drugs to reduce blood sugar.
Treatment of other complications:
- Pseudo -vsists: Pseudocysts are clusters of fluid that can form in the pancreas or around it. Pseudocysts can cause pain, infection or obstruction of the ducts. Pseudocysts can be drained surgically or endoscopic.
- Obstation of the gall duct: Chronic pancreatitis can cause obstruction of the bile duct, which leads to jaundice (yellowing of the skin and eye proteins). Outstation of the bile duct can be eliminated surgically or endoscopic.
- Slezer -free thrombosis: Chronic pancreatitis can cause thrombosis (thrombus formation) in the spleen Vienna. The thrombosis of the spleen vein can lead to splenomegaly (an increase in the spleen) and bleeding from varicose veins of the esophagus. The thrombosis of the sphere vein can be treated with anticoagulants (drugs that thin blood) or splenectomy (spleen removal).

VI. The role of changing lifestyle in the treatment of pancreatitis

A change in lifestyle is an important part of the treatment of both acute and chronic pancreatitis.

Refusal of alcohol: Refusal of alcohol is one of the most important changes in lifestyle that patients with pancreatitis can do. Alcohol is the main cause of both acute and chronic pancreatitis. The continuation of alcohol consumption can lead to further damage to the pancreas and worsen the symptoms.
Termination of smoking: Smoking is also a risk factor for the development of pancreatitis. The cessation of smoking can help reduce the risk of pancreatitis and improve the general health.
Diet:
- Low fat diet: Patients with pancreatitis should follow a low fat diet, since fats are difficult to digest when the pancreas does not function properly. It is recommended to avoid fatty, fried and treated food.
- Frequent meals in small portions: Patients with pancreatitis should often eat meals in small portions, and not three large meals per day. This helps to reduce the load on the pancreas and improve digestion.
- Adequate protein consumption: Protein is important for restoration of tissues and maintaining health. Patients with pancreatitis should consume a sufficient amount of protein from low -fat sources, such as chicken, fish, tofu and legumes.
- Sufficient fluid consumption: Patients with pancreatitis should drink a sufficient amount of fluid to prevent dehydration.
- Limiting simple carbohydrates: Limiting the consumption of simple carbohydrates, such as sugar, white flour and products containing corn syrup with a high fructose content, helps maintain a stable blood sugar level, which is especially important for patients with diabetes caused by pancreatitis.
Exercise: Regular exercises can help improve the general health status and reduce the risk of pancreatitis complications.

VII. Future directions in the treatment of pancreatitis

Studies in the field of pancreatitis continue, and new treatment methods appear.

Target therapy: New drugs are being developed that affect specific molecules involved in the pathogenesis of pancreatitis. For example, drugs are being developed that block the activation of pancreatic enzymes or reduce inflammation.
Cell therapy: Cell therapy is a new approach to the treatment of pancreatitis, which includes a transplant of healthy pancreatic cells to restore the function of the pancreas.
Gene therapy: Gene therapy is a new approach to the treatment of pancreatitis, which includes the introduction of genes into the pancreas to restore its function.
Immunotherapy: Immunotherapy is a new approach to the treatment of autoimmune pancreatitis, which includes the use of drugs for the modulation of the immune system.
Microbia: The role of microbioma (communities of microorganisms living in the intestine) in the development and progression of pancreatitis is studied. Perhaps in the future it will be possible to use probiotics or other methods for the modulation of a microbioma to treat pancreatitis.
Artificial pancreas: For patients with diabetes caused by pancreatitis, artificial pancreas systems are developed, which automatically control the level of glucose in the blood and administer insulin as necessary.
Predictive markers: New biomarkers are identified that can help predict the severity of acute pancreatitis and the risk of complications. These biomarkers can help doctors make more reasonable treatment decisions.
Development of new visualization methods: New visualization methods are being developed, which can provide a more detailed image of the pancreas and surrounding tissues. This can help doctors diagnose pancreatitis at an early stage and evaluate the severity of the disease.

VIII. Complications of pancreatitis and their drug treatment

Pancreatitis, both acute and chronic, can lead to various complications that require specific drug treatment.

A. Complications of acute pancreatitis:

Infected necrosis: Treatment includes a wide spectrum of action (for example, carbapenems, fluoroquinolones) aimed at gram -negative and anaerobic bacteria. In severe cases, surgical intervention or minimum invasive methods for removing infected necrotic material may be required.
Pseudo -vsists: Unfinished pseudocysts that do not cause symptoms usually do not require treatment. Symptomatic pseudocysts can be drained endoscopically or surgically. Infected pseudocists require drainage and antibiotic therapy.
Systemic inflammatory response syndrome (SSVO) and sepsis: Treatment includes intravenous fluid administration, wide spectrum antibiotics and vasopressors to maintain blood pressure.
Acute respiratory failure (ARDS): Treatment includes artificial lung ventilation and other supporting measures.
Renal failure: Treatment includes intravenous fluid administration and, in severe cases, dialysis.
Slezer -free thrombosis: Anticoagulant therapy may be required.

B. Complications of chronic pancreatitis:

Diabetes sugar: Treatment includes insulin or other drugs to reduce blood sugar.
Exocrine pancreatic failure: Treatment includes enzyme pancreatic enzyme preparations.
Pancretical duct strictures: May require endoscopic stenting or surgical intervention.
Pain syndrome: Treatment includes analgesics, enzymes of the pancreas, the blockade of the wander -up plexus and, in severe cases, surgical intervention.
Nutrient deficiency: Treatment includes dietary changes and additives of vitamins.
Pancreatic cancer: Patients with chronic pancreatitis are at increased risk of developing pancreatic cancer.

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