1. What is the relationship between the anatomy and the pathogenesis of the pancreas?
The pancreas is the second largest digestive gland in the human body and is the organ with the strongest digestive effect. The pancreatic juice secreted by it is the most important digestive fluid in the body. Under normal conditions, pancreatic juice contains inactive, i.e. inactive, pancreatic zymogen in its glandular tissue. The pancreatic juice continuously flows along the pancreatic ducts into the duodenum via the sphincter of Oddi of the common bile duct. Due to the presence of bile in the duodenum and the secretion of an intestinal kinase by the mucosa of the duodenal wall, under the action of both, the pancreatic zymogen begins to transform into a highly active digestive enzyme. If the outflow tract is obstructed, poor excretion can cause pancreatitis.
2, the etiology of pancreatitis?
Pancreatitis is divided into acute pancreatitis (AP) and chronic pancreatitis (CP), which have multiple and complex pathogenic factors, which are summarized below.
Biliary tract diseases Biliary tract diseases are the most common causes of pancreatitis, including cholelithiasis, biliary tract infections and roundworms. In recent years, increasing attention has been paid to the study of common bile duct small stone disease (CBDM), which is believed to directly stimulate the sphincter of Oddi, causing local congestion, edema, spasm, dysfunction and even retrograde contraction, and retrograde cholangiopancreatography (ERCP) combined with bile analysis can confirm the diagnosis early. The above-mentioned etiology causes stenosis of the jugular abdomen or (and) spasm or relaxation of the sphincter of Oddi, resulting in retrograde flow of bile into the pancreatic duct, or return of duodenal fluid into the pancreatic duct, or diffusion of bacteria, toxins, free bile acids, etc. into the pancreas, activating pancreatic enzymes and causing disease.
(1) Binge drinking and overeating: Binge drinking and overeating cause a large amount of chyme to enter the duodenum in a short period of time, stimulating papillary edema, causing spasm of the sphincter of Oddi, and at the same time secreting a large amount of pancreatic juice, causing a rapid increase in pancreatic duct pressure in a short period of time and triggering AP.
(2) Heavy alcohol consumption: ethanol increases pancreatic secretion, and heavy alcohol consumption stimulates spasm of the sphincter of Oddi, edema of the duodenal papilla, obstruction of pancreatic juice discharge, and increase in pancreatic ductal pressure. It has been reported that the risk of AP increases significantly with the intake of alcohol >420g per week.
(3) Endocrine and metabolic disorders: hyperlipidemia increases blood viscosity, serum lipids embolize pancreatic vessels causing pancreatic microcirculation disorders and free fatty acids generated after hydrolysis of triglycerides, causing local microembolism and damage to capillary endothelium and pancreatic cells, and triglycerides are more closely related to the development of pancreatitis than cholesterol, and have a tendency to recur. Hypercalcemia such as hyperparathyroidism, vitamin D excess, multiple myeloma, Ca2+ in the alkaline pancreatic fluid is easy to form stones, calcification of the pancreatic duct, and stimulate pancreatic secretion and activation of pancreatic enzymes. Pregnancy, uremia, diabetic coma is also a rare cause, there are also reports of AP complicated by hypoglycemic ketosis.
(4) Pancreatic duct obstruction: pancreatic duct stones or roundworms, pancreatic duct stenosis, tumors, etc. can cause pancreatic duct obstruction, leading to pancreatitis; in pancreatic schwannoma, most of the pancreatic fluid is drained through the relatively thin parapapillary head causing obstruction and poor drainage, which may also be related to AP.
(5) Surgery and trauma: abdominal trauma such as blunt trauma or penetrating trauma can cause pancreatitis. Post-surgical pancreatitis accounts for about 5-10% of the occurrence of which may be.
① trauma or surgery directly injures pancreatic tissue and ducts, causing edema, pancreatic duct obstruction or impaired blood supply.
② Injury or surgery with hypovolemic shock, inadequate perfusion of blood to the pancreas, or microthrombosis.
③Decrease of pancreatic enzyme inhibitory factor in the pancreatic fluid after surgery.
④High contrast injection pressure during ERCP examination can cause pancreatic injury, temporary hyperamylasemia, or acute pancreatitis.
⑤ Rejection after organ transplantation and the application of immunosuppressive agents can also induce it. Blunt abdominal contusion, after extracorporeal shock wave lithotripsy also predispose to AP.
(6) Sphincter of Oddi dysfunction (SOD): the true etiology is not completely clear, but most of them are still due to biliary tract diseases, and the diagnosis is mainly based on ERCP and sphincter of Oddi fluid pressure measurement (SOM). It was reported that SOD accounted for 31% of the 90 pancreatitis patients studied with unexplained etiology.
(7) Infections: such as acute mumps, viral hepatitis, coxsackievirus, infectious mononucleosis, Echo virus, Chlamydia pneumoniae infection, etc., and Mycobacterium tuberculosis causing pancreatitis have been reported. The viruses or bacteria and their toxins enter the pancreatic tissue through the blood circulation or lymphatic ducts and induce AP. these patients are mostly mild and often disappear on their own with the control of the infection.
(8) Drugs and toxins: many drugs such as thiazide diuretics, glucocorticoids, tetracycline, sulfonamides, warfarin, lamivudine, azathioprine, and vincristine are known to induce AP; zinc is one of the essential elements, the highest content in the body after injection to the pancreas, metallothionein-bound zinc can reduce the toxicity of cadmium, copper, and mercury, but large doses can induce AP.
(9) Pancreatic tumors: tumors can cause infarction and ischemia by compression, or activate pancreatic enzymes by direct infiltration to induce AP. pancreatic cancer has been reported to be closely related to smoking, alcohol consumption, and diabetes.
(10) Duodenal lesions: parapapillary diverticula of duodenum, benign and malignant lesions in the papilla, and posterior duodenal bulb penetrating ulcers cause papillary stenosis and poor drainage of pancreatic juice and induce the disease, among which parapapapillary diverticula has a high rate of misdiagnosis and must be confirmed by ERCP.
(11) Ischemia: When AP occurs in patients with atrial fibrillation, it is often accompanied by transient cerebral ischemia, splenic infarction, lower extremity artery embolism, mesenteric artery embolism, etc. These patients are easily missed or misdiagnosed clinically, which delays the time of treatment and should be especially noted.
(12) Other: other drugs such as hypercalcemia, hyperparathyroidism, certain drugs such as corticosteroids, dihydrocortisone, estrogen, etc., and genetic factors, psychiatric factors, etc. can trigger the disease; autoimmune diseases, genetic factors, post-transplantation of kidney or heart, input collaterals syndrome, etc. In addition, although there are many causes of pancreatitis, but there are still about 8% to 25% of patients with unknown causes, and some reports even 28.9%.
3, the definition and classification of pancreatitis?
Pancreatitis is an inflammatory lesion that occurs in the pancreatic tissue. The pancreas has edema, congestion, or hemorrhage or necrosis. Clinical symptoms such as abdominal pain, abdominal distension, nausea, vomiting, and fever are present. Laboratory tests show elevated levels of amylase in blood and urine, elevated blood creatinine, bilirubin, and blood glucose, and ultrasound and CT suggest swelling, exudation, and or necrosis of the pancreas. The clinical classification of pancreatitis is not based on the amylase level, in other words, the amylase level does not represent the severity of pancreatitis, but the classification of pancreatitis is based on creatinine, bilirubin, elevated blood glucose, ultrasound, CT, etc. Most of the pancreatitis (about 70%) are simple edematous pancreatitis, which can be cured after treatment, and a few are hemorrhagic necrotizing pancreatitis, of which very few are fulminant pancreatitis, although with the in-depth research on the pathogenesis of SAP and the improvement of clinical treatment techniques, the efficacy has improved significantly, but the overall mortality rate is still above 10%, while the mortality rate of fulminant pancreatitis is still more than 50%.
4. Why do patients with cholecystitis and gallstones have pancreatitis?
Gallstones, cholecystitis and other biliary tract diseases are also the main causes of pancreatitis. Gallstones, especially multiple small gallstones, are easily dislodged from the gallbladder into the bile duct when the gallbladder is strongly contracted and stuck in the “common channel”, causing acute pancreatitis. Clinical cases show that 30% of patients with acute pancreatitis are caused by gallstones and cholecystitis.
The gallbladder and the pancreas are homologous in embryogenesis and are naturally very close in anatomical relationship. Although the two ducts “separate” after maturation – draining bile and pancreatic fluid separately – in 80% of normal people the two ducts converge at the end to form a single channel (common channel) that opens at the head of the duodenum. Under normal conditions, although both the pancreatic and bile ducts flow through a single channel into the ten working fingers, bile does not backflow into the pancreatic duct because the pressure in the pancreatic duct is higher than the pressure in the bile duct. Only when the sphincter of Oddi is spastic or the pressure in the bile duct is elevated, such as stone or tumor obstruction, the bile will flow back into the pancreatic duct and enter the pancreatic tissue. At this time, the lecithin contained in the bile is decomposed by the lecithinase A contained in the pancreatic juice into lecithinolytic lecithin, which can have toxic effects on the pancreas. Or in the case of biliary tract infection, bacteria can release kinases that activate pancreatic enzymes, which can also become active substances that can damage and lyse pancreatic tissue. These substances convert the pancreatic zymogen contained in the pancreatic fluid into pancreatic protease, an enzyme with strong digestive activity that penetrates into the pancreatic tissue and causes self-digestion, which can also cause pancreatitis. This type of pancreatitis is clinically known as biliary pancreatitis.
5, hyperlipidemia and pancreatitis?
Hyperlipidemia can promote or trigger pancreatitis. The mechanism of hyperlipidemia complicating pancreatitis is not well understood. It may be that.
(1) increased blood viscosity, resulting in impaired pancreatic circulation and pancreatic hypoxia.
(2) ischemic necrosis of the pancreas due to ischemia of the pancreatic vessels by coagulated fat embolism.
(3) infiltration of the pancreas with fat.
(4) triglycerides are broken down by lipase to form toxic free fatty acids, which damage the walls of small blood vessels and promote the formation of microthrombi, etc.
Currently, it is believed that triglycerides in blood reach 11.25-22.58 mmol/L, which predisposes to acute pancreatitis. There are many factors that cause hyperlipidemia, in addition to genetics and diet, alcohol, pregnancy, oral contraceptives, long-term application of estrogen and vitamin A can cause, should be noted.
6. What is the current status of treatment for acute pancreatitis?
Due to the differences in the level of treatment and the understanding of the treatment plan in each hospital, there is a great difference in the success rate of treatment of severe acute pancreatitis in different treatment units. The “individualized treatment plan” for severe acute pancreatitis has specific contents to deepen its understanding and expand its connotation, and is definitely not synonymous with arbitrary treatment. Severe acute pancreatitis clinical is a dynamic pathological process that is constantly changing, and the treatment plan varies widely from time to time, and the implementation details of the specific course of the disease can not be unified clinically, which makes clinical treatment more difficult.
7, the specific treatment of acute pancreatitis?
The main treatment measures for patients with SAP are
(1) Anti-shock, volume expansion, giving adequate oxygen supply and correcting the disturbance of the internal environment.
(2) Inhibition of pancreatic exocrine function, including fasting, gastrointestinal decompression, acid-control drugs, and application of growth inhibitors.
(3) Combined application of broad-spectrum antibiotics.
(4) Improving pancreatic microcirculation.
(5) Promote the recovery of intestinal function (six grinding drinks: 9 grams each of rhubarb, betel nut, citrus aurantium, mannitol, mucuna pruriens and incense, each flavor may be increased or decreased).
(6) Timely removal of etiology, ERCP treatment for those with biliary obstruction factors, including Oddi sphincterotomy and nasobiliary drainage, or emergency open surgery with cholecystectomy plus common bile duct exploration and drainage, or cholecystostomy.
(7) Surgical intervention, laparoscopic drainage or open pelvic drainage.
8, the status of surgery in the treatment of acute pancreatitis?
Both surgical and non-surgical treatment are important elements of the treatment plan of severe acute pancreatitis, and the distinction between surgical and non-surgical groups of severe acute pancreatitis cannot be made simply, and surgery should be an important measure available in the overall treatment plan. Correctly grasping the timing and indications of surgical interventions in SAP and reasonably selecting surgical interventions are crucial to the prognosis of SAP.
9.Why is pancreatitis mostly “eaten”?
The common causes of acute pancreatitis include improper diet, overeating, especially eating greasy food and drinking alcohol. The pancreatic duct stones, tumors, biliary tract diseases, etc. are also likely to cause acute pancreatitis. Some young people who are confident of their health do not pay attention, eat and drink a lot of high protein and high fat food at once in a short period of time, stimulating the pancreas to secrete a lot of pancreatic fluid rapidly, and if the pancreatic fluid is flooded, it flows backwards into the pancreatic tissue. If combined with the stimulation of wine, it will aggravate the flooding of pancreatic juice and cause acute pancreatitis.
10.Prevention of pancreatitis?
Pancreatitis is all about prevention. Pancreatitis can also be prevented. Both the first acute attack and the acute attack of chronic pancreatitis should be preventable. The main part of prevention is to pay attention to diet. Especially during holidays and various celebratory occasions, we should pay attention.
(1) strictly prohibit alcohol, eat low-fat: drinking alcohol and eating high-fat fatty foods is an important cause of acute attacks or delayed healing of chronic pancreatitis, so be sure to prohibit alcohol and fatty meats. There are necrotizing pancreatitis caused by overeating and death.
(2) rich nutrition, food is not full: chronic pancreatitis is easy to fat diarrhea (slightly eat meat and oil that diarrhea), coupled with long-term difficult to cure, so patients are prone to malnutrition, should eat food rich in nutrients, such as fish, lean meat, protein, tofu, etc., rice, noodles and other carbohydrates and fresh vegetables should be eaten properly, but each meal can not be too full, eat seven or eight minutes full. (If you have diabetes, you should control the intake of carbohydrates). Diet should be less fried, eat more steamed stew, in order to facilitate digestion and absorption. Salt should not be more, more will increase the pancreatic congestion and edema, so light food is better. Vegetables can eat more spinach, broccoli and cauliflower, radish, but must be cooked and eaten to soften the fiber to prevent increased diarrhea. Condiments should not be too acidic, too spicy. Because it can increase the secretion of gastric juices and increase the burden on the pancreas. Fruits can be chosen from peaches, bananas and other fruits that do not have a sour taste. Easy to produce gas to make bloated food should not be eaten such as fried soybeans, fava beans, peas, sweet potatoes, etc.