急性胰腺炎acute(共107張)課件

1、Acute PancreatitisXUE HuipingAcute PancreatitisPancreatitis is an inflammatory process in which pancreatic enzymes autodigest the gland.Pancreatitis is an inflammatorThe gland can sometimes heal without any impairment of function or any morphologic changes. This process is known as acute pancreatiti

2、s. 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 to a

3、n 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 to no

4、rmal, 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 pancreati

5、tis）是指胰酶在胰腺內(nèi)激活后引起胰腺組織自身消化的急性化學(xué)性炎癥。 Acute pancreatitis is an acutA sensible classification system separates pancreatitis into mild and severe disease based on physiologic findings, laboratory values, and radiologic imaging.A sensible classification systMild pancreatitis is not associated with organ d

6、ysfunction 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 assocBoth cysts are indicated by the large white arrows.renal colic6.elevations p

7、ersist 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白堊的 areas of dead adipose tissue that are found within the

8、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; 輕型急性胰腺炎是指僅有很輕微的臟器功能紊亂，沒有明顯腹膜炎體征及嚴(yán)重代謝紊亂等臨床表現(xiàn)，臨床恢復(fù)順利者。該型病理上絕大多數(shù)為水腫型胰腺炎，少數(shù)也可有胰腺實(shí)質(zhì)壞死。 Both c

9、ysts are indicated by thSevere pancreatitis is defined as a local complication and/or organ failure.Severe pancreatitis is defined重癥急性胰腺炎是指急性胰腺炎伴有臟器功能障礙，或出現(xiàn)壞死、膿腫或假性囊腫等局部并發(fā)癥，或兩者兼有。該型病理上絕大多數(shù)為壞死型胰腺炎，但少數(shù)情況下水腫型胰腺炎也可表現(xiàn)為重癥胰腺炎。 重癥急性胰腺炎是指急性胰腺炎伴有臟器功能障礙，或出現(xiàn)壞死、Local complications are defined as (1) acute fluid

10、collections;(2) pancreatic necrosis;(3) pancreatic abscess;(4) pancreatic pseudosystLocal 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 derangements, se

11、psis, 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張)課件Choledocholithiasis(膽總管石病) and ethanol abuse account for 70 to 80% of all cases.Chole

12、docholithiasis(膽總管石病) an Gallstones may cause pancreatitis by impacting in the ampulla of Vater. The incidence of gallstone-associated pancreatitis parallels that of cholelithiasis(膽石癥): it peaks at ages 50 to 70, and women outnumber men by 2 to 1. Gallstones may cause pancrea Causes of Acute Pancre

13、atitisObstruction:Biliary tract disease: cholelithiasis, tumor, ascarid, stenosis pancreatic duct obstruction: neoplasms, cysts,pancreas divisum annular pancreas ampullary stenosis, duodenal diverticulum Duodenal obstructionAlcoholHyperlipidemiaHypercalcemiaHereditaryTrauma:external, operative,ERCPI

14、schemia:hypotension,cardiopulmonary bypass, atheroembolism,vasculitisInfectious causes: parastic bacterial viral fungalDrugs:steroids,azathioprine 6-mercaptopurine, Idiopathic Causes of AObstructive CausesCholedocholithiasis膽總管石病Ampullary obstruction by tumor or sphincter of Oddi hypertensionCholedo

15、chocele膽總管囊腫Periampullary duodenal diverticulum(憩室)Pancreas divisum : annular(環(huán)狀的) pancreasPrimary or metastatic pancreatic tumorParasites in pancreatic duct: Clonorchis(支睪吸蟲), AscarisObstructive CausesCholedocholiDrugsazathioprine硫唑嘌呤/6-mercaptopurine6-巰基嘌呤; valproic acid丙戊酸; estrogens雌激素; metronid

16、azole滅滴靈，甲硝唑; loop diuretics, including thiazides 噻嗪類, 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 autoactivation and self-digestion (key po

17、int)3. Many agents participating in the process4. Complete mechanism remaining unknown Pathogenesis1.A Pancreatic self-protective mechanism1.mucopolysaccharide on pancreatic duct enzyme3.pancreatin inhibitor4.acinus metabolism activity5. Anti-reflux mechanism: oddis sphincter pancreati

18、c duct sphincterPancreatic self-protective mecInitiation factor in Earlier periodInitiation factor in Earlier p1. Pancreatic Enzyme Abnormally ActivatedBile refluxBile common channel pancreatic duct 1.hypertension in pancreatic duct 2.premature activation of pancreatic enzymes 3.injury to the lining

19、 of the pancreatic ducts pancreatic edema or necrosis MODS1. Pancreatic Enzyme Abnormal Duodenal Refulxduodenal enterokinase pancreatic ducttrypsinogen trypsinelastasnogen elastasephospholipasogen phospholipase lecithin lysolecthin Duodenal Refulxduodenal ent2.Alcohol Toxicitystimulate the pancreas

20、to secrete pancreatic hypertention tiny pancreatic duct and acinus rupture pancreatic juice spillage spasm of the sphinctor of oddidirect injury to pancreas2.Alcohol Toxicitystimulate 3.Pancreatic Microcirculation Disordersystemic hypotensionhyperlipidemia: triglycerides lipase free acid fatty acids

21、 injure pancreatic microcirculationartheroembolismvasculitis3.Pancreatic Microcirculation Aggravatiing factors in later periodInfection: pancreatic abscessIntestinal bacteria translocationCytokine and systemic inflammation reaction syndromeTNF IL-1 IL-6 PAF MSOFFree radicalsAggravatiing factors in l

22、ater PATHOGENESISPremature 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 activaPATHOGENESISProteases(蛋白酶) released into the blood are inactivat

23、ed 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) retetracyclines, etc.This process is known as acute pancreatitis.Large arrow indicates inflamed pancreas.biliary procedure: endoscopic sphincterotomy chol

24、ecystectomy 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.重癥胰腺炎是一多因素、累及多環(huán)節(jié)的疾病。Choledochocele膽總管囊腫Periampullary duodenal diverticulum(憩室)Causes o

25、f Acute PancreatitisObstruction:Biliary tract disease: cholelithiasis, tumor, ascarid, stenosis pancreatic duct obstruction: neoplasms, cysts,pancreas divisum annular pancreas ampullary stenosis, duodenal diverticulum Duodenal obstructionAlcoholHyperlipidemiaHypercalcemiaHereditaryTrauma:external, o

26、perative,ERCPIschemia:hypotension,cardiopulmonary bypass, atheroembolism,vasculitisInfectious causes: parastic bacterial viral fungalDrugs:steroids,azathioprine 6-mercaptopurine, IdiopathicThe ionized calcium concentration remains normal, and symptoms of tetany(手足抽搐) are extremely rare.increased pan

27、creatic duct permeabilityOverview of the pancreatic glandSurrounding areas of fat necrosis are also prominent.In addition, trypsin(胰蛋白酶) activates kallikrein(激肽釋放酶), a peptidase(肽酶), which then cleaves several peptides, including bradykinin(緩激肽) and kallidin(胰激肽), from their inactive precursors in b

28、lood plasma.PATHOGENESIStetracyclines, etc.In additionPATHOGENESISThese peptides, termed kinins(激肽), have various deleterious effects including vasodilatation, increased vascular permeability, pain, and neutrophil(嗜中性粒細(xì)胞) accumulation.PATHOGENESISThese peptides, teTwo mechanisms may trigger pancreat

29、ic autodigestionzymogen activation within the pancreatic acinar cell.increased pancreatic duct permeabilityTwo mechanisms may trigger panPATHOGENESISAfter the acinar cell is triggered, it provokes an intense inflammatory response in the pancreas. Weeping of pancreatic juice into the peripancreatic s

30、pace or microperforations of the pancreatic ductal system can lead to pseudocyst formation.PATHOGENESISAfter the acinar cPATHOGENESISSubsequent hypoperfusion to the gland can convert mild edematous/interstitial pancreatitis to necrotizing pancreatitis. At this point, release of toxic factors into th

31、e 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 hematogenous or transperitoneal sources.PATHOGENESISSubsequent hypoper

32、急性胰腺炎(acute(共107張)課件重癥胰腺炎是一多因素、累及多環(huán)節(jié)的疾病。首先是幾種致病因素引發(fā)胰腺腺泡的損傷，釋放多種受激活的胰酶及炎癥細(xì)胞因子，有多種細(xì)胞的過度激活和相互作用，產(chǎn)生氧自由基和炎癥介質(zhì)引起胰腺、腹膜和一些主要器官(肺、腦)的血管通透性增加，最后導(dǎo)致了重癥胰腺炎及其并發(fā)癥的發(fā)生。重癥胰腺炎是一多因素、累及多環(huán)節(jié)的疾病。首先是幾種致病因素引 Pathology1.Edematous pancreatitis:*interstitial edema*inflammatory cell infiltration of the gland parenchyma2.Hemorrha

33、gic or necrotizing pancreatitis*extensive pancreatic and peripancreatic fat necrosis *parenchymal necrosis Pathology1Overview of the pancreatic glandThe pancreatic gland contains three major types of cells. The duct cells make up about 10% of the pancreas and secrete solutions rich in bicarbonate. T

34、he acinar cells comprise over 80% of the pancreas and they synthesize and secrete pancreatic enzymes.Overview of the pancreatic glaOverview of the pancreatic glandThe islet cells make up about 10% of the pancreas and form the endocrine portion of the pancreas. The four major types of islet cells sec

35、rete the hormones insulin, glucagon, somatostatin, and pancreatic polypeptide.Overview of the pancreatic gla急性胰腺炎(acute(共107張)課件InterstitialThe gross architecture of the gland is preserved, but it is edematous. Hemorrhage is absent. Interstitial edema and inflammatory cells within the parenchyma are

36、 prominent. Disruption of the normal acinar cell architecture is common and may contribute to characteristically reduced enzyme secretion.InterstitialThe gross architecInterstitial edema and inflammatory cells within the parenchymaInterstitial edema and inflammHemorrhagicMacroscopically, marked tiss

37、ue necrosis and hemorrhage are apparent. Surrounding areas of fat necrosis are also prominent. These are chalky白堊的 areas of dead adipose tissue that are found within the peripancreatic tissue and throughout the abdomen. Large hematomas血腫often are located in the retroperitoneal腹膜后的space.HemorrhagicMa

38、croscopically, maHemorrhagicThe microscopic appearance of the pancreas parallels the gross changes, with marked fat and pancreatic necrosis.Vascular inflammation and thrombosis are common.HemorrhagicThe microscopic app急性胰腺炎(acute(共107張)課件急性胰腺炎(acute(共107張)課件Fat necrosisFat necrosis seen at surgery i

39、s associated with peripancreatic release of lipase, with hydrolysis of triacylglycerols (triglycerides) to toxic fatty acids.Fat necrosisFat necrosis seen Clinical PresentationSteady, dull, or boring midepigastric pain associated with nausea and vomiting is the classic presentation of acute pancreat

40、itis.Clinical PresentationSteady, dAbdominal pain predominant clinical featuremidepigastrium, in the right or left upper quadrantsThe pain reaches peak intensity within 15 minutes to 1 hour from onset, in contrast to the more abrupt onset of pain with a perforated viscus. a penetrating pain, radiati

41、ng 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 clAbdominal painrare patients without abdominal pain but with a severe systemic illness ( hypotension, hypoperfu

42、sion 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 wiClinical PresentationNausea and vomitingAbdominal Distentionresulting from a paralytic ileus arising from retr

43、operitoneal 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 findingsClinical PresentationNausea anAbdominal DistentionParalytic ileus(麻痹性腸梗阻) with abdominal diste

44、ntion may develop during the first few days, signifying extension of the inflammatory process into the small intestinal and colonic(結(jié)腸的) mesentery(腸系膜).Abdominal DistentionParalyticClinical Presentation of Sever PancreatitisCirculatory Derangements: hypotention, hypovolemia, hypoeffusion circulating

45、 myocardial depressant factor decreased preload to the heartreduced systemic vascular resistancesepsis-like syndromehyperdynamic stateelevated cardiac outputlowered systemic vascular resistancelowered arteriovenous oxgen differenceClinical Presentation of SeverClinical Presentation of Sever Pancreat

46、itisleft pleural effusionpulmonary failure tachypnea, dyspnea and cyanosiscerebral abnormalities belligerence, confusion, psychosis and comaTurner sign and Cullen sign a bluish color in the flanks or around the umbilicus, (representing blood dissecting to those areas from the retroperitoneum near th

47、e pancreas along fascial planes)Clinical Presentation of SeverOne to 2 weeks after the onset, large ecchymoses(瘀斑) may appear in the flanks側(cè)腹 (Grey Turners sign) or the umbilical area (Cullens sign);One to 2 weeks after the onsetOne to 2 weeks after the onset, large ecchymoses(瘀斑) may appear in the

48、flanks側(cè)腹 (Grey Turners sign) or the umbilical area (Cullens sign);One to 2 weeks after the onsetOne to 2 weeks after the onset, large ecchymoses(瘀斑) may appear in the flanks側(cè)腹 (Grey Turners sign) or the umbilical area (Cullens sign);One to 2 weeks after the onsetPhysical ExaminationInitial physical

49、examination reveals mild fever and tachycardia(心動過速); Hypotension is present in 30 to 40% of patients.Physical ExaminationInitial pPhysical Examinationepigastria tenderness, rigidity and rebound tenderness (There is marked tenderness to deep palpation of the upper abdomen, but signs of peritoneal ir

50、ritation are frequently absent.)bowel sounds decreased or absent palpable massswollen pancreasPseudocystabscessPhysical ExaminationepigastriaLaboratory TestLaboratory TestSerum AmylaseTotal serum amylase activity is the test most frequently used to diagnose acute pancreatitis.The level rises 6 to 12

51、 hours after onset of symptoms and remains elevated for 3 to 5 days in most cases. (hyperamylasemia is observed within 24-48 hrs; gradually return to normal values during the subsequent 2-5days)Serum AmylaseTotal serum amylaSerum AmylaseValues more than 3 times the upper limit of normal are highly s

52、pecific for acute pancreatitis but are found in only 80 to 90% of cases.The magnitude of the rise in serum amylase does not correlate with the severity of the attack, nor does prolonged hyperamylasemia indicate developing complications.the absence of hyperamylasemia cant exclude the diagnosis of acu

53、te pancreatitis (extensive pancreatic necrosis)Serum AmylaseValues more than Disorders Associated with hyperamylasemiaIntra-Abdominal Extra-AbdominalPancreatic disorders Salivary gland disordersacute pancreatitis mumpschronic pancreatitis parotitistrauma traumacarcinoma calculipseudocyst irradiation

54、 sialoadenitispancreatic ascites impaired amylase excretionabscess renal failureNonpancreatic disorders mecroamylasemiabiliary tract disease Miscellaneusintestinal obstruction pneumoniamesenteric infarction pancreatic pleural effusionperforated peptic ulcer mediastinal pseudocystperitonitis cerebral

55、 traumaafferen loop syndrome severe burnsacute appendicitis diabetic reto acidosiseuptured ectopic pregnancy pregnancysalpingitis drugsruptured aortic aneurysm bisal buminemia Disorders Associated with hypeUrinary Amylasea sensitive index of the pancreatitiselevations persist for a longer period tha

56、n serum amylase some other diseases also manifest hyperamylasuriaa normal urinary amylase cant preclude the pancreatitisUrinary Amylasea sensitive indSeparation of total serum amylase into its pancreatic (P) and salivary (S) isoenzymes and measurements of urinary amylase output add little to the dia

57、gnostic information.Separation of total serum amylThe amylase-creatinine clearance ratio (ACR) (the ratio of amylase concentration in urine over plasma, divided by the corresponding values for creatinine) is useful in diagnosing asymptomatic macroamylasemia, in which aggregates of circulating amylas

58、e escape glomerular filtration and the ACR is abnormally low.The amylase-creatinine clearan淀粉酶 這一古老的檢查方法雖已應(yīng)用了半個(gè)多世紀(jì)，但對胰腺炎的診斷仍不失為良好而簡便可行的手段。由于胰酶在胰管內(nèi)逆流入血或滲出液重吸收入血，則在急性胰腺炎時(shí)血、尿的淀粉酶有所升高。血淀粉酶正常值，溫氏單位256單位，蘇氏單位500單位。急性胰腺炎（輕型）發(fā)作后612小時(shí)即升高，4872小時(shí)逐漸恢復(fù)正常，尿淀粉酶約在發(fā)病后1224小時(shí)升高，要持續(xù)35天。但急性重型胰腺炎升高的時(shí)間要提前。臨床上對淀粉酶值的變化要作全面的

59、分析，再結(jié)合臨床其他癥狀才能做出正確的判斷。淀粉酶 這一古老的檢查方法雖已應(yīng)用了半個(gè)多世紀(jì)，但對淀粉酶血淀粉酶值正常：有兩種情況，其一表明病已痊愈，血淀粉酶值恢復(fù)正常，同時(shí)全身情況良好，無腹部體征。其二在重癥急性胰腺炎的初檢或治療中，淀粉酶也可不升高，說明病情會進(jìn)行性加重惡化。因?yàn)橐认傧倥荽罅繅乃?、崩潰，已不能分泌淀粉酶，即所謂的“枯竭”現(xiàn)象。這一現(xiàn)象在急性重癥胰腺炎中時(shí)有發(fā)生，應(yīng)予以高度重視。淀粉酶血淀粉酶值正常：有兩種情況，其一表明病已痊愈，血淀粉酶淀粉酶 血淀粉酶升高：有時(shí)病人出現(xiàn)腹痛，并伴血淀粉酶升高，但臨床的癥狀、體征并不支持胰腺炎，這時(shí)就應(yīng)考慮到血清淀粉酶檢測往往是非特異性的。臨床

60、常見的一些急腹癥也可伴有血淀粉酶升高，如膽囊炎、膽石癥、膽道梗阻、腸梗阻、消化性潰瘍病穿孔、腸系膜血栓形成以及使用嗎啡后。膽石癥時(shí)可能是由于排石對Oddi括約肌的刺激，使之痙攣，血淀粉酶一過性升高。消化性潰瘍穿孔（特別是十二指腸球部穿孔）時(shí)，含有大量胰液的腸內(nèi)容物進(jìn)入腹腔后，淀粉酶被腹膜吸收則血淀粉酶值升高。腸梗阻后，腸腔內(nèi)腸液淤積，淀粉酶通過受損的腸壁滲入腹腔而被吸收。因此，對血淀粉酶的升高必須結(jié)合臨床進(jìn)行判斷，決不可因單純血淀粉酶升高而診斷為胰腺炎。淀粉酶 血淀粉酶升高：有時(shí)病人出現(xiàn)腹痛，并伴血淀粉酶升淀粉酶 巨淀粉酶血癥：是一罕見病癥，其原因不明，可能是由于病人血中的淀粉酶與大分子物質(zhì)形