What are the pathogenic mechanisms of acute pancreatitis?

Acute pancreatitis is generally a disease characterized by acute inflammatory reaction of pancreatic tissue. Its pathogenesis is mainly associated with premature activation of pancreatic self-digestion, release of inflammatory mediators, increased pressure in the pancreatic duct, intestinal bacterial translocation, and microcirculatory disturbances. The details are as follows:

1. Premature activation of pancreatic self-digestion: Under normal conditions, digestive enzymes secreted by the pancreas exist in an inactive proenzyme form. When affected by factors such as alcohol or biliary diseases, these proenzymes are prematurely activated into active digestive enzymes. These activated enzymes attack the pancreas's own tissues, leading to pancreatic cell necrosis and triggering an inflammatory response.

2. Release of inflammatory mediators: After pancreatic injury, inflammatory cells in the body—such as neutrophils and macrophages—are activated. These cells release large amounts of inflammatory mediators, including tumor necrosis factor (TNF) and interleukins. These mediators exacerbate local pancreatic inflammation and may spread to other organs.

3. Increased pancreatic duct pressure: Factors such as pancreatic duct stones or tumors in the pancreatic head can cause obstruction of the pancreatic duct, resulting in elevated intraductal pressure. Excessively high pressure damages the epithelial cells lining the pancreatic duct, causing leakage of pancreatic juice into the pancreatic interstitium. This leakage activates digestive enzymes, thereby triggering pancreatic inflammation.

4. Intestinal bacterial translocation: During acute pancreatitis, the intestinal barrier function is impaired, allowing gut bacteria and toxins to cross the intestinal barrier and enter the bloodstream. These pathogens and toxins can reach the pancreas and other organs via circulation, worsening pancreatic inflammation and potentially causing systemic infection.

5. Microcirculatory disturbance: The pancreas relies on a rich microcirculatory network for blood supply. In conditions such as shock or vascular spasm, microcirculatory dysfunction occurs, leading to ischemia and hypoxia in pancreatic tissue. Ischemia and hypoxia further damage pancreatic cells and intensify the inflammatory response, creating a vicious cycle.

In daily life, individuals should avoid excessive alcohol consumption and overeating, and actively treat biliary diseases to reduce the risk of developing acute pancreatitis. Once the disease occurs, prompt medical attention is necessary. Treatments such as fasting, fluid resuscitation, and inhibition of pancreatic enzyme secretion help reduce pancreatic damage and promote recovery.