慢性胰腺炎ppt课件

1CHRONIC PANCREATITIS.1CHRONIC PANCREATITIS.2A 49-year-old man was admitted with a nine-month history of intermittent attacks of epigastric pain,jaundice and fever.These attacks usually last up to several days associated with nausea and vomiting.He was well in between attacks and had no loss of weight 2A 49-year-old man was admitte3What is your next step?.3What is your next step?.4Lab ResultsAP=1017GGT=269AST=103ALT=186TB=2(DB=1.1)Alb=3.2Lipase=33(up to 244 during attacks)Amylase=44 Hb=12 WBC=5.7 Plts=223Na=141 K=4.2Ur=15Cr=0.9Ca=8.9FBS:1784Lab ResultsAP=1017Hb=12 5What are arrows?5What are arrows?6Pancreatic calcification.6Pancreatic calcification.7Transabdominal US:No gallstones or mass in head of pancreasCT scan:The extrahepatic bile duct was mildly dilated and generous pancreas was noted but there was no mass.7Transabdominal US:No gallsto8Endoscopic UltrasoundDiffuse hypoechoic enlargement of pancreas.Fine needle aspirate of the pancreas was negative for tumor.8Endoscopic UltrasoundDiffuse9ERCPThere was a long segment of extrahepatic biliary stricture.The pancreatic duct was normal in size but irregular.Brushings,biopsies and bile aspirate were negative for tumor9ERCPThere was a long segment101011The patient underwent Whipples operation Histology of the pancreas showed chronic pancreatitis,no malignancy.11The patient underwent Whipp12Two presentation:Episodes of acute inflammation in a previously injured pancreasChronic damage with persistent pain or malabsorptionEtiology:same as acute pancreatitis“pancreatitis associated with gallstones predaminantly acute or relapsing-acute”More idiopathic types12Two presentation:13Most common cause:In adults:alcohol intakeIn children:cystic fibrosisIdiopathic chronic pancreatitis is the leading cause of nonalcoholic chronic pancreatitis13Most common cause:14PATHOPHYSIOLOGYThe events that initiate an inflamatory process are still not well understoodIn the alcohol-induced:suggested that the primary defect may be the precipitation of protein(inspissated enzyme)In fact,shown that alcohol has direct toxic effect on the pancreas 14PATHOPHYSIOLOGYThe events th15Clinical featuresabdominal pain:may be continuous,intermittent or absentPattern is often atypicalRUQ or LUQ of the backDiffuse throughout upper abdomenMay be referred to the anterior chest or flankTypical form:Persistent,deep-seated,Unresponsive to antacidsWorsened by alcohol intake or a heavy meal(especially fatty foods)Often need narcotics15Clinical featuresabdominal p16Pancreatic insufficiencyWeight lossFat malabsorption:Steatorrhea:15%of patients present with steatorrhea and no painPancreatic diabetes:Like DM1 needs insulin,but risk of hypoglycemia is more than it(because alfa cells is also affectedFat-soluble vitamin deficiency rare16Pancreatic insufficiency17Lab dataAmylase and lipase:usually normalCBC,electrolytes,and liver function tests are typically normalBilrubin and ALP may be increasedImpaired glucose intolerance and elevated fasting blood glucoseSudan staining of feces or quantitative test for steatorrheafecal elastase(Among pancreatic function tests,fecal elastase measurement is the most sensitive and specific,especially in the early phases of pancreatic insufficiency)17Lab dataAmylase and lipase:18Cont,Classic triad“pancreatic calcification,steatorrhea,and diabetes mellitus“usually establishes chronic pancreatitisClassic triad:found in fewer than one-thirdIt is often necessary to perform secretin stimulation test (abnormal when 60%or more of pancreatic exocrine function has been lost)A decreased serum trypsinogen(20ng/ml)or a fecal elastase level of 100ug/mg of stool strongly suggests severe pancreatic insufficiency18Cont,Classic triad“pancrea19Imaging studies Plain films:Pancreatic calcifications:%30most common with alcoholic pancreatitis,but is also seen in the hereditary and tropical forms of the disorder;it is rare in idiopathic pancreatitis.19Imaging studies Plain films 2020212122 CT,MRI,US calcificationsductal dilatationenlargement of the pancreasfluid collections(eg,pseudocysts)22 CT,MRI,US calcification2323242425ERCP Choice when calcifications are not present and there is no evidence of steatorrhea.a normal study should not rule out the diagnosis of chronic pancreatitis 25ERCP Choice when calcificati26ERCPMay provide useful information on the status of the pancreatic ductal system Abnormalities include:1)luminal narowing 2)irregularitis in the ductal system with stenosis,dilation,saculation,and ectasia 3)blockage of the duct by calcium deposits.26ERCPMay provide useful infor272728Endoscopic ultrasonographyThe most predictive endosonographic feature is the presence of stoneOther suggestive features include:visible side branches cystslobularityirregular main pancreatic duct,hyperechoic foci and strands dilation of the main pancreatic duct hyperechoic margins of the main pancreatic duct.28Endoscopic ultrasonographyTh292930Complicationspseudocyst formationbile duct or duodenal obstructionpancreatic ascites or pleural effusion splenic vein thrombosisPseudoaneurysmspancreatic cancer acute attacks of pancreatitis(particularly alcoholics who continue drinking)30Complicationspseudocyst form31DIFFERENTIAL DIAGNOSISPancreatic cancer(most important)older ageabsence of a history of alcohol useweight lossa protracted flare of symptomsonset of significant constitutional symptomspancreatic duct stricture greater than 10 mm in length on ERCP Markers such as CA 19-9 and CEApeptic ulcer diseasegallstonesirritable bowel syndrome Acute pancreatitis31DIFFERENTIAL DIAGNOSISPancre32TREATMENT.32TREATMENT.33PAIN MANAGEMENTstepwise approach:general recommendationspancreatic enzyme supplementation Analgesicsinvasive options33PAIN MANAGEMENTstepwise appr34General recommendationsEstablish a secure diagnosis Cessation of alcohol intakeSmall meals34General recommendationsEstab35Pancreatic enzyme supplementsnot very effectiveresponse may be better in young women with small duct disease.MECHANISM:suppression of feedback loops in the duodenum that regulate the release of cholecystokinin(CCK),the hormone that stimulates digestive enzyme secretion from the exocrine pancreassix tablets of Viokase which contains:16,000 units of lipase30,000 units of protease30,000 units of amylase.35Pancreatic enzyme supplement36Patients should also be treated with acid suppression(either with an H2 receptor blocker or a proton pump inhibitor)to reduce inactivation of the enzymes from gastric acid.36Patients should also be trea37Analgesicsif pancreatic enzyme therapy fails to control pain.short course of narcotics coupled with low dose amitriptyline and a nonsteroidal antiinflammatorySimultaneous short-term hospitalization,with the patient kept NPO to minimize pancreatic stimulation,may also be of benefit in breaking the pain cycle.Chronic narcotic analgesia may be required in patients with persistent significant pain.Long-acting agents such as MS Contin or Fentanyl patches are generally more effective than short acting medications,which last only three or four hours.37Analgesicsif pancreatic enzy38Other medical therapiesoctreotide:cannot be recommended for general use.Antioxidant therapy:vitamin C,E,methionine and selenium 38Other medical therapiesoctre39Specialized approachesCeliac nerve blocksEndoscopic stenting of the pancreatic duct or pancreatic sphincterotomyExtracorporeal shock wave lithotripsySurgery39Specialized approachesCeliac40Maldigestion managementPancreatic enzymes:Steatorrhea could be abolished if 10%of the normal amount of lipase could be delivered to the duodenum at the proper timePoor therapeutic results because of:Lipase is inactivated by gastric acid Food empties from the stomach faster than do the pancreatic enzymesBatches of commercially available pancreatic extracts vary in enzyme activity40Maldigestion managementPancr41Adjuants:H2 blockersSodium bicarbonatePPIs41Adjuants: