ACUTE PANCREATITIS Xu San rong Department of Gastroenterology Huashan Hospital Fudan university
1 ACUTE PANCREATITIS Xu San rong Department of Gastroenterology Huashan Hospital Fudan university
DEFINITION An acute inflammatory process of the pan creas usually associated with sever pain in the upper abdomen in most instances blood levels of pancrea tic enzymes are increased sever acute pancreatitis: organs failure and/or local complications(necrosis, absc ess, psuedocyst)
2 DEFINITION • An acute inflammatory process of the pancreas usually associated with sever pain in the upper abdomen • in most instances, blood levels of pancreatic enzymes are increased • sever acute pancreatitis: organs failure and/or local complications(necrosis, abscess, psuedocyst)
PATHOLOGY(1) Mild acute pancreatitIs(MAP) characterized by interstitial edema associ- ated with inflammatory cell within parench yma, and microscopic parenchyma necro sis can be detectable
3 PATHOLOGY(1) • Mild acute pancreatitis(MAP) characterized by interstitial edema associated with inflammatory cell within parenchyma, and microscopic parenchyma necrosis can be detectable
PATHOLOGY(2) Sever acute pancreatitis(SAP) Sever necrotizing pancreatitIs(SNP) macroscopic evidence of either focal or diffuse necrosis and hemorrhage of the pancreatic parenchyma
4 PATHOLOGY(2) • Sever acute pancreatitis(SAP) Sever necrotizing pancreatitis(SNP) macroscopic evidence of either focal or diffuse necrosis and hemorrhage of the pancreatic parenchyma
PATHOGENY AND PATHOGENESIS(1) 1 common channel and reflux of duodenal juice Ki nIn stems Sever pain gallstones elastase hemorrhage Bile →( trypsin reflux Trypsin chymotrypsin infection Phospho NipaseA2 Free fat erum Steatolvtic acid calcium enzymes
5 PATHOGENY AND PATHOGENESIS(1) 1 common channel and reflux of duodenal juice gallstones infection Bile juice reflux trypsin Kinin systems elastase Trypsin chymotrypsino PhospholipaseA2 Steatolytic enzymes Sever pain hemorrhage Free fat acid Serum calcium
PATHOGENY AND PATHOGENESIS(2) 2 alcoholic and overeat 3 obstruct of main pancreatic duct 4 diseases round the duodenum/ampullary region 5 postoperative pancreatitis and pancreatic trauma
6 PATHOGENY AND PATHOGENESIS(2) 2 alcoholic and overeat 3 obstruct of main pancreatic duct 4 diseases round the duodenum/ampullary region 5 postoperative pancreatitis and pancreatic trauma
PATHOGENY AND PATHOGENESIS(3) 6 infectious agents 7 medications: corticosteroids, estrogens 8 disorders of endocrinology and metabol ism: hyperparathyroidism, hyperlipidemia 9 others
7 PATHOGENY AND PATHOGENESIS(3) 6 infectious agents 7 medications: corticosteroids, estrogens 8 disorders of endocrinology and metabolism: hyperparathyroidism, hyperlipidemia 9 others:
PATHOGENY AND PATHOGENESIS(4) 6 inflammatory media theory In AP, the leukocytes that appear first in areas of inflammation are neutrophils, then macrophages, monocytes, lymphocytes and other cells. These cells can secrete a lot of inflammatory media (1)platelet activating factor, PAF 2)prostaglandins, PGs
8 PATHOGENY AND PATHOGENESIS(4) 6 inflammatory media theory In AP, the leukocytes that appear first in areas of inflammation are neutrophils, then macrophages, monocytes, lymphocytes, and other cells. These cells can secrete a lot of inflammatory media. (1) platelet activating factor, PAF (2)prostaglandins, PGs
PATHOGENY AND PATHOGENESIS(5) (3)leukotriens, LTS (4) kallikrein kinin systems, KKs (5)tumor necrosis factor-a, TNF-a (6)nitrogen monoxide, NO (7)complements 8)others: nuclear factor KB(NF-KB), toll like receptors(TLRs)
9 PATHOGENY AND PATHOGENESIS(5) (3) leukotriens, LTs (4) kallikrein kinin systems, KKS (5) tumor necrosis factor-, TNF- (6) nitrogen monoxide, NO (7) complements (8) others: nuclear factor B(NF- B), toll like receptors(TLRs)
DIAGNOSIS(1) Clinical characteristics 1 abdominal pain 2 fever 3 nausea and vomiting
10 DIAGNOSIS(1) • Clinical characteristics 1 abdominal pain 2 fever 3 nausea and vomiting
