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1、Acute PancreatitisXUE Huiping,Acute Pancreatitis,Pancreatitis is an inflammatory process in which pancreatic enzymes autodigest the gland.,Pancreatitis is an inflammator,The gland can sometimes heal without any impairment of function or any morphologic changes. This process is known as acute pancrea
2、titis. It can recur intermittently, contributing to the functional and morphologic loss of the gland, the pathological change referred to as chronic pancreatitis.,The gland can sometimes heal,Acute pancreatitis refers to an attack involving a previously normal pancrease.Chronic pancreatis is applied
3、 to an attack involving a previously, permanently damaged pancrease.,Acute pancreatitis refers to,Acute pancreatitis is an acute inflammatory process of the pancreas, with variable involvement of other regional tissue or remote organ systems. Although pancreatic function and structure usually return
4、 to normal, the risk of recurrent attacks is 20 to 50% unless the precipitating cause is removed. The disease includes a broad spectrum of pancreatic disease, which varies from mild parenchymal edema to severe hemorrhagic pancreatitis associated with subsequent gangrene and necrosis. 急性胰腺炎（acute pan
5、creatitis）是指胰酶在胰腺内激活后引起胰腺组织自身消化的急性化学性炎症。,Acute pancreatitis is an acut,A sensible classification system separates pancreatitis into mild and severe disease based on physiologic findings, laboratory values, and radiologic imaging.,A sensible classification syst,Mild pancreatitis is not associated wit
6、h organ dysfunction or complications, and recovery is uneventful. Severe pancreatitis is associated with decreased function of the pancreas, local and systemic complications, and a complicated recovery.,Mild pancreatitis is not assoc,Both cysts are indicated by the large white arrows.renal colic6.el
7、evations persist for a longer period than serum amylaseNasogastric Suction reduce vomiting and abdominal distension reduce pancreatic exocrine secretion by reducing secretion releaseSurrounding areas of fat necrosis are also prominent.These are chalky白垩的 areas of dead adipose tissue that are found w
8、ithin the peripancreatic tissue and throughout the abdomen.PATHOGENESISperitoneal lavage: remove toxins and various metabolites2.HemorrhagicUltrasound examination showing two large pancreatic pseudocysts.valproic acid丙戊酸;, 轻型急性胰腺炎是指仅有很轻微的脏器功能紊乱，没有明显腹膜炎体征及严重代谢紊乱等临床表现，临床恢复顺利者。该型病理上绝大多数为水肿型胰腺炎，少数也可有胰腺实
9、质坏死。,Both cysts are indicated by th,Severe pancreatitis is defined as a local complication and/or organ failure.,Severe pancreatitis is defined,重症急性胰腺炎是指急性胰腺炎伴有脏器功能障碍，或出现坏死、脓肿或假性囊肿等局部并发症，或两者兼有。该型病理上绝大多数为坏死型胰腺炎，但少数情况下水肿型胰腺炎也可表现为重症胰腺炎。,重症急性胰腺炎是指急性胰腺炎伴有脏器功能障碍，或出现坏死、,Local complications are defined as (
10、1) acute fluid collections;(2) pancreatic necrosis;(3) pancreatic abscess;(4) pancreatic pseudosyst,Local complications are define, The clinical presentation of acute pancreatitis is variable, from episodes of mild abdominal discomfort alone to a severe illness associated with hypotension, metabolic
11、 derangements, sepsis, fluid sequenstration, multiple organ failure or even death. It is always accompanied by an increased concentrations of pancreatic enzymes in blood and in urine., The clinical presentation of,急性胰腺炎(acute(共107张)课件,Choledocholithiasis(胆总管石病) and ethanol abuse account for 70 to 80
12、% of all cases.,Choledocholithiasis(胆总管石病) an, Gallstones may cause pancreatitis by impacting in the ampulla of Vater. The incidence of gallstone-associated pancreatitis parallels that of cholelithiasis(胆石症): it peaks at ages 50 to 70, and women outnumber men by 2 to 1., Gallstones may cause pancrea
13、,Causes of Acute PancreatitisObstruction:Biliary tract disease: cholelithiasis, tumor, ascarid, stenosis pancreatic duct obstruction: neoplasms, cysts,pancreas divisum annular pancreas ampullary stenosis, duodenal diverticulum Duodenal obstructionAlcoholHyperlipidemiaHypercalcemiaHereditaryTrauma:ex
14、ternal, operative,ERCPIschemia:hypotension,cardiopulmonary bypass, atheroembolism,vasculitisInfectious causes: parastic bacterial viral fungalDrugs:steroids,azathioprine 6-mercaptopurine, Idiopathic,Causes of A,Obstructive Causes,Choledocholithiasis胆总管石病Ampullary obstruction by tumor or sphincter of
15、 Oddi hypertensionCholedochocele胆总管囊肿Periampullary duodenal diverticulum(憩室)Pancreas divisum : annular(环状的) pancreasPrimary or metastatic pancreatic tumorParasites in pancreatic duct: Clonorchis(支睾吸虫), Ascaris,Obstructive CausesCholedocholi,Drugs,azathioprine硫唑嘌呤/6-mercaptopurine6-巯基嘌呤; valproic aci
16、d丙戊酸; estrogens雌激素; metronidazole灭滴灵，甲硝唑; loop diuretics, including thiazides 噻嗪类, furosemide速尿; pentamidine; sulfonamides, including sulfasalazine; methyldopa: L-asparaginase; tetracyclines, etc.,Drugsazathioprine硫唑嘌呤/6-merca,Pathogenesis1.A complicated pathophysiologic process2.Enzyme autoactivati
17、on and self-digestion (key point)3. Many agents participating in the process4. Complete mechanism remaining unknown,Pathogenesis1.A,Pancreatic self-protective mechanism1.mucopolysaccharide on pancreatic duct epithelia2.proenzyme3.pancreatin inhibitor4.acinus metabolism activity5. Anti-reflux mechani
18、sm: oddis sphincter pancreatic duct sphincter,Pancreatic self-protective mec,Initiation factor in Earlier period,Initiation factor in Earlier p,1. Pancreatic Enzyme Abnormally ActivatedBile refluxBile common channel pancreatic duct 1.hypertension in pancreatic duct 2.premature activation of pancreat
19、ic enzymes 3.injury to the lining of the pancreatic ducts pancreatic edema or necrosis MODS,1. Pancreatic Enzyme Abnormal, Duodenal Refulxduodenal enterokinase pancreatic ducttrypsinogen trypsinelastasnogen elastasephospholipasogen phospholipase lecithin lysolecthin, Duodenal Refulxduodenal ent,2.Al
20、cohol Toxicitystimulate the pancreas to secrete pancreatic hypertention tiny pancreatic duct and acinus rupture pancreatic juice spillage spasm of the sphinctor of oddidirect injury to pancreas,2.Alcohol Toxicitystimulate,3.Pancreatic Microcirculation Disordersystemic hypotensionhyperlipidemia: trig
21、lycerides lipase free acid fatty acids injure pancreatic microcirculationartheroembolismvasculitis,3.Pancreatic Microcirculation,Aggravatiing factors in later periodInfection: pancreatic abscessIntestinal bacteria translocationCytokine and systemic inflammation reaction syndromeTNF IL-1 IL-6 PAF MSO
22、FFree radicals,Aggravatiing factors in later,PATHOGENESIS,Premature activation of zymogens(酶原) and the escape of activated enzymes from acinar cells and pancreatic ducts set the stage for the autodigestive process that represents acute pancreatitis.,PATHOGENESISPremature activa,PATHOGENESIS,Protease
23、s(蛋白酶) released into the blood are inactivated by circulating inhibitors, including 2-macroglobulin(巨球蛋白). 1-antitrypsin(抗胰蛋白酶), and the C1-esterase(酯酶) inhibitor.,PATHOGENESISProteases(蛋白酶) re,tetracyclines, etc.This process is known as acute pancreatitis.Large arrow indicates inflamed pancreas.bil
24、iary procedure: endoscopic sphincterotomy cholecystectomy remove the CBD stoneThe pancreas is diffusely involved, and its margins are difficult to define because of the massive peripancreatic inflammation, which is reflected in the streaking seen in this scan.重症胰腺炎是一多因素、累及多环节的疾病。Choledochocele胆总管囊肿P
25、eriampullary duodenal diverticulum(憩室)Causes of Acute PancreatitisObstruction:Biliary tract disease: cholelithiasis, tumor, ascarid, stenosis pancreatic duct obstruction: neoplasms, cysts,pancreas divisum annular pancreas ampullary stenosis, duodenal diverticulum Duodenal obstructionAlcoholHyperlipi
26、demiaHypercalcemiaHereditaryTrauma:external, operative,ERCPIschemia:hypotension,cardiopulmonary bypass, atheroembolism,vasculitisInfectious causes: parastic bacterial viral fungalDrugs:steroids,azathioprine 6-mercaptopurine, IdiopathicThe ionized calcium concentration remains normal, and symptoms of
27、 tetany(手足抽搐) are extremely rare.increased pancreatic duct permeabilityOverview of the pancreatic glandSurrounding areas of fat necrosis are also prominent.,In addition, trypsin(胰蛋白酶) activates kallikrein(激肽释放酶), a peptidase(肽酶), which then cleaves several peptides, including bradykinin(缓激肽) and kal
28、lidin(胰激肽), from their inactive precursors in blood plasma.,PATHOGENESIS,tetracyclines, etc.In addition,PATHOGENESIS,These peptides, termed kinins(激肽), have various deleterious effects including vasodilatation, increased vascular permeability, pain, and neutrophil(嗜中性粒细胞) accumulation.,PATHOGENESIST
29、hese peptides, te,Two mechanisms may trigger pancreatic autodigestion,zymogen activation within the pancreatic acinar cell.increased pancreatic duct permeability,Two mechanisms may trigger pan,PATHOGENESIS,After the acinar cell is triggered, it provokes an intense inflammatory response in the pancre
30、as. Weeping of pancreatic juice into the peripancreatic space or microperforations of the pancreatic ductal system can lead to pseudocyst formation.,PATHOGENESISAfter the acinar c,PATHOGENESIS,Subsequent hypoperfusion to the gland can convert mild edematous/interstitial pancreatitis to necrotizing p
31、ancreatitis. At this point, release of toxic factors into the systemic circulation, such as trypsin, elastase, phospholipase A2, and platelet activating factor or other cytokines, can lead to cardiovascular and pulmonary collapse. The necrotic pancreas can become secondarily infected from hematogeno
32、us or transperitoneal sources.,PATHOGENESISSubsequent hypoper,急性胰腺炎(acute(共107张)课件,重症胰腺炎是一多因素、累及多环节的疾病。首先是几种致病因素引发胰腺腺泡的损伤，释放多种受激活的胰酶及炎症细胞因子，有多种细胞的过度激活和相互作用，产生氧自由基和炎症介质引起胰腺、腹膜和一些主要器官(肺、脑)的血管通透性增加，最后导致了重症胰腺炎及其并发症的发生。,重症胰腺炎是一多因素、累及多环节的疾病。首先是几种致病因素引,Pathology1.Edematous pancreatitis:*interstitial edema*
33、inflammatory cell infiltration of the gland parenchyma2.Hemorrhagic or necrotizing pancreatitis*extensive pancreatic and peripancreatic fat necrosis *parenchymal necrosis,Pathology1,Overview of the pancreatic gland,The pancreatic gland contains three major types of cells. The duct cells make up abou
34、t 10% of the pancreas and secrete solutions rich in bicarbonate. The acinar cells comprise over 80% of the pancreas and they synthesize and secrete pancreatic enzymes.,Overview of the pancreatic gla,Overview of the pancreatic gland,The islet cells make up about 10% of the pancreas and form the endoc
35、rine portion of the pancreas. The four major types of islet cells secrete the hormones insulin, glucagon, somatostatin, and pancreatic polypeptide.,Overview of the pancreatic gla,急性胰腺炎(acute(共107张)课件,Interstitial,The gross architecture of the gland is preserved, but it is edematous. Hemorrhage is ab
36、sent. Interstitial edema and inflammatory cells within the parenchyma are prominent. Disruption of the normal acinar cell architecture is common and may contribute to characteristically reduced enzyme secretion.,InterstitialThe gross architec,Interstitial edema and inflammatory cells within the pare
37、nchyma,Interstitial edema and inflamm,Hemorrhagic,Macroscopically, marked tissue necrosis and hemorrhage are apparent. Surrounding areas of fat necrosis are also prominent. These are chalky白垩的 areas of dead adipose tissue that are found within the peripancreatic tissue and throughout the abdomen. La
38、rge hematomas血肿often are located in the retroperitoneal腹膜后的space.,HemorrhagicMacroscopically, ma,Hemorrhagic,The microscopic appearance of the pancreas parallels the gross changes, with marked fat and pancreatic necrosis.Vascular inflammation and thrombosis are common.,HemorrhagicThe microscopic app
39、,急性胰腺炎(acute(共107张)课件,急性胰腺炎(acute(共107张)课件,Fat necrosis,Fat necrosis seen at surgery is associated with peripancreatic release of lipase, with hydrolysis of triacylglycerols (triglycerides) to toxic fatty acids.,Fat necrosisFat necrosis seen,Clinical Presentation,Steady, dull, or boring midepigastri
40、c pain associated with nausea and vomiting is the classic presentation of acute pancreatitis.,Clinical PresentationSteady, d,Abdominal pain,predominant clinical featuremidepigastrium, in the right or left upper quadrantsThe pain reaches peak intensity within 15 minutes to 1 hour from onset, in contr
41、ast to the more abrupt onset of pain with a perforated viscus. a penetrating pain, radiating to the back (It radiates straight to the midline of the lower thoracic vertebral region in about 50% of patients and is usually worse in the supine position.),Abdominal pain predominant cl,Abdominal pain,rar
42、e patients without abdominal pain but with a severe systemic illness ( hypotension, hypoperfusion and depression of mental status) - Painless acute pancreatitis is very rare but carries a grave prognosis because the patients frequently present in shock.,Abdominal painrare patients wi,Clinical Presen
43、tation,Nausea and vomitingAbdominal Distentionresulting from a paralytic ileus arising from retroperitoneal irritation or ascites or a retroperitoneal phlegmonJaundice distal common bile duct obstruction by gallstones compression of the distal CBD by pancreatic head edema or by other uncommon findin
44、gs,Clinical PresentationNausea an,Abdominal Distention,Paralytic ileus(麻痹性肠梗阻) with abdominal distention may develop during the first few days, signifying extension of the inflammatory process into the small intestinal and colonic(结肠的) mesentery(肠系膜).,Abdominal DistentionParalytic,Clinical Presentat
45、ion of Sever Pancreatitis,Circulatory Derangements: hypotention, hypovolemia, hypoeffusion circulating myocardial depressant factor decreased preload to the heartreduced systemic vascular resistancesepsis-like syndromehyperdynamic stateelevated cardiac outputlowered systemic vascular resistancelower
46、ed arteriovenous oxgen difference,Clinical Presentation of Sever,Clinical Presentation of Sever Pancreatitis,left pleural effusionpulmonary failure tachypnea, dyspnea and cyanosiscerebral abnormalities belligerence, confusion, psychosis and comaTurner sign and Cullen sign a bluish color in the flank
47、s or around the umbilicus, (representing blood dissecting to those areas from the retroperitoneum near the pancreas along fascial planes),Clinical Presentation of Sever,One to 2 weeks after the onset, large ecchymoses(瘀斑) may appear in the flanks侧腹 (Grey Turners sign) or the umbilical area (Cullens
48、sign);,One to 2 weeks after the onset,One to 2 weeks after the onset, large ecchymoses(瘀斑) may appear in the flanks侧腹 (Grey Turners sign) or the umbilical area (Cullens sign);,One to 2 weeks after the onset,One to 2 weeks after the onset, large ecchymoses(瘀斑) may appear in the flanks侧腹 (Grey Turners
49、 sign) or the umbilical area (Cullens sign);,One to 2 weeks after the onset,Physical Examination,Initial physical examination reveals mild fever and tachycardia(心动过速); Hypotension is present in 30 to 40% of patients.,Physical ExaminationInitial p,Physical Examination,epigastria tenderness, rigidity
50、and rebound tenderness (There is marked tenderness to deep palpation of the upper abdomen, but signs of peritoneal irritation are frequently absent.)bowel sounds decreased or absent palpable massswollen pancreasPseudocystabscess,Physical Examinationepigastria,Laboratory Test,Laboratory Test,Serum Am
