1、Acute PancreatitisXUE HuipingA c u t e P a n c r e a t i t i sPancreatitis is an inflammatory process in which pancreatic enzymes autodigest the gland.P a n c r e a t i t i s i s a n i n f l a m m a t o rThe gland can sometimes heal without any impairment of function or any morphologic changes.This
2、process is known as acute pancreatitis.It can recur intermittently,contributing to the functional and morphologic loss of the gland,the pathological change referred to as chronic pancreatitis.T h e g l a n d c a n s o m e t i m e s h e a l Acute pancreatitis refers to an attack involving a previousl
3、y normal pancrease.Chronic pancreatis is applied to an attack involving a previously,permanently damaged pancrease.A c u t e p a n c r e a t i t i s r e f e r s t o Acute pancreatitis is an acute inflammatory process of the pancreas,with variable involvement of other regional tissue or remote organ
4、systems.Although pancreatic function and structure usually return 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 asso
5、ciated with subsequent gangrene and necrosis.急性胰腺炎（急性胰腺炎（acute pancreatitis）是指胰酶在胰腺内激活后引起）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。胰腺组织自身消化的急性化学性炎症。A c u t e p a n c r e a t i t i s i s a n a c u tA sensible classification system separates pancreatitis into mild and severe disease based on physiologic findings
6、,laboratory values,and radiologic imaging.A s e n s i b l e c l a s s i f i c a t i o n s y s tMild pancreatitis is not associated with organ dysfunction or complications,and recovery is uneventful.Severe pancreatitis is associated with decreased function of the pancreas,local and systemic complicat
7、ions,and a complicated recovery.Mi l d p a n c r e a t i t i s i s n o t a s s o cBoth cysts are indicated by the large white arrows.renal colic6.elevations persist for a longer period than serum amylaseNasogastric Suction reduce vomiting and abdominal distension reduce pancreatic exocrine secretion
8、 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 within the peripancreatic tissue and throughout the abdomen.PATHOGENESISperitoneal lavage:remove toxins and various metabolites2.HemorrhagicUltrasound ex
9、amination showing two large pancreatic pseudocysts.valproic acid丙戊酸;轻型轻型急性胰腺炎是指仅有很轻微的脏器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型病理上绝大多数为水肿型水肿型胰腺炎，少数胰腺炎，少数也可有胰腺实质坏死。也可有胰腺实质坏死。B o t h c y s t s a r e i n d i c a t e d b y t hSevere pancreatitis i
10、s defined as a local complication and/or organ failure.S e v e r e p a n c r e a t i t i s i s d e f i n e d重症重症急性胰腺炎是指急性胰腺炎急性胰腺炎是指急性胰腺炎伴有伴有脏器功能障碍，或出现坏死、脏器功能障碍，或出现坏死、脓肿或假性囊肿等局部并发症，或脓肿或假性囊肿等局部并发症，或两者兼有两者兼有。该型病理上绝大多数为。该型病理上绝大多数为坏死型坏死型胰腺炎，但少数情况下水肿型胰腺炎，但少数情况下水肿型胰腺炎也可表现为重症胰腺炎。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
11、伴有脏器功能障碍，或出现坏死、Local complications are defined as(1)acute fluid collections;(2)pancreatic necrosis;(3)pancreatic abscess;(4)pancreatic pseudosystL o c a l c o m p l i c a t i o n s a r e d e f i n e The clinical presentation of acute pancreatitis is variable,from episodes of mild abdominal discomfor
12、t alone to a severe illness associated with hypotension,metabolic 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.T h e c l i n i c a l p r e s e n t a t i o n o f急性胰腺炎(a
13、 c u t e(共1 0 7 张)课件Choledocholithiasis(胆总管石胆总管石病病)and ethanol abuse account for 70 to 80%of all cases.C h o l e d o c h o l i t h i a s i s(胆总管石病)a n Gallstones may cause pancreatitis by impacting in the ampulla of Vater.The incidence of gallstone-associated pancreatitis parallels that of cholelith
14、iasis(胆石症胆石症):it peaks at ages 50 to 70,and women outnumber men by 2 to 1.G a l l s t o n e s m a y c a u s e p a n c r e a C a u s e s o f AObstructive CausesCholedocholithiasis胆总管石病胆总管石病Ampullary obstruction by tumor or sphincter of Oddi hypertensionCholedochocele胆总管囊肿胆总管囊肿Periampullary duodenal d
15、iverticulum(憩室憩室)Pancreas divisum:annular(环状的环状的)pancreasPrimary or metastatic pancreatic tumorParasites in pancreatic duct:Clonorchis(支睾吸虫支睾吸虫),AscarisO b s t r u c t i v e C a u s e s C h o l e d o c h o l iDrugs azathioprine硫唑嘌呤硫唑嘌呤/6-mercaptopurine6-巯基嘌呤巯基嘌呤;valproic acid丙戊酸丙戊酸;estrogens雌激素雌激素;m
16、etronidazole灭滴灵，甲硝唑灭滴灵，甲硝唑;loop diuretics,including thiazides 噻嗪类噻嗪类,furosemide速尿速尿;pentamidine;sulfonamides,including sulfasalazine;methyldopa:L-asparaginase;tetracyclines,etc.D r u g sa z a t h i o p r i n e 硫唑嘌呤/6-m e r c a P a t h o g e n e s i s1.A P a n c r e a t i c s e l f-p r o t e c t i v
17、e m e cI n i t i a t i o n f a c t o r i n E a r l i e r p1.P a n c r e a t i c E n z y m e A b n o r m a l D u o d e n a l R e f u l xd u o d e n a l e n t2.A l c o h o l T o x i c i t ys t i m u l a t e 3.P a n c r e a t i c Mi c r o c i r c u l a t i o n A g g r a v a t i i n g f a c t o r s i n
18、l a t e r PATHOGENESIS Premature activation of zymogens(酶原酶原)and the escape of activated enzymes from acinar cells and pancreatic ducts set the stage for the autodigestive process that represents acute pancreatitis.P A T H O G E N E S I SP r e m a t u r e a c t i v aPATHOGENESIS Proteases(蛋白酶蛋白酶)rel
19、eased into the blood are inactivated by circulating inhibitors,including 2-macroglobulin(巨球蛋白巨球蛋白).1-antitrypsin(抗胰蛋白酶抗胰蛋白酶),and the C1-esterase(酯酶酯酶)inhibitor.P A T H O G E N E S I SP r o t e a s e s(蛋白酶)r etetracyclines,etc.This process is known as acute pancreatitis.Large arrow indicates inflamed
20、 pancreas.biliary 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。Choledocho
21、cele胆总管囊肿Periampullary 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 obstructionAlcoholHyperl
22、ipidemiaHypercalcemiaHereditaryTrauma: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 t
23、etany(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(胰蛋白酶胰蛋白酶)activates kallikrein(激肽释放酶激肽释放酶),a peptidase(肽酶肽酶),which then cleaves several peptides,including bradykinin(缓激肽缓激肽)and
24、 kallidin(胰激胰激肽肽),from their inactive precursors in blood plasma.PATHOGENESISt e t r a c y c l i n e s,e t c.I n a d d i t i o nPATHOGENESIS These peptides,termed kinins(激肽激肽),have various deleterious effects including vasodilatation,increased vascular permeability,pain,and neutrophil(嗜中性粒细嗜中性粒细胞胞)a
25、ccumulation.P A T H O G E N E S I S T h e s e p e p t i d e s,t eTwo mechanisms may trigger pancreatic autodigestionzymogen activation within the pancreatic acinar cell.increased pancreatic duct permeabilityT w o m e c h a n i s m s m a y t r i g g e r p a nPATHOGENESIS After the acinar cell is trig
26、gered,it provokes an intense inflammatory response in the pancreas.Weeping of pancreatic juice into the peripancreatic space or microperforations of the pancreatic ductal system can lead to pseudocyst formation.P A T H O G E N E S I S A f t e r t h e a c i n a r cPATHOGENESIS Subsequent hypoperfusio
27、n to the gland can convert mild edematous/interstitial pancreatitis to necrotizing pancreatitis.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 co
28、llapse.The necrotic pancreas can become secondarily infected from hematogenous or transperitoneal sources.P A T H O G E N E S I S S u b s e q u e n t h y p o p e r急性胰腺炎(a c u t e(共1 0 7 张)课件重症胰腺炎是一多因素、累及多环节的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泡的损伤，释放多种受激活的胰酶及炎症细胞因子，有多
29、种细胞的过度激活和症细胞因子，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起胰腺、腹膜和一些主要器官(肺、脑肺、脑)的血管通透性增加，最后导致了重症胰的血管通透性增加，最后导致了重症胰腺炎及其并发症的发生。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 P a t h o l o g y1Overview of the pancreatic gland The pancreatic gland contains three major types of cells.The duct ce
30、lls make up about 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.O v e r v i e w o f t h e p a n c r e a t i c g l aOverview of the pancreatic gland The islet cells make up about 10%of
31、the pancreas and form the endocrine portion of the pancreas.The four major types of islet cells secrete the hormones insulin,glucagon,somatostatin,and pancreatic polypeptide.O v e r v i e w o f t h e p a n c r e a t i c g l a急性胰腺炎(a c u t e(共1 0 7 张)课件Interstitial The gross architecture of the gland
32、 is preserved,but it is edematous.Hemorrhage is absent.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.I n t e r s t i t i a l T h e g r o s s a
33、 r c h i t e c Interstitial edema and inflammatory cells within the parenchymaI n t e r s t i t i a l e d e m a a n d i n f l a m mHemorrhagic Macroscopically,marked tissue necrosis and hemorrhage are apparent.Surrounding areas of fat necrosis are also prominent.These are chalky白垩的白垩的 areas of dead
34、adipose tissue that are found within the peripancreatic tissue and throughout the abdomen.Large hematomas血肿血肿often are located in the retroperitoneal腹膜后的腹膜后的space.H e m o r r h a g i c Ma c r o s c o p i c a l l y,m aHemorrhagic The microscopic appearance of the pancreas parallels the gross changes,
35、with marked fat and pancreatic necrosis.Vascular inflammation and thrombosis are common.H e m o r r h a g i c T h e m i c r o s c o p i c a p p急性胰腺炎(a c u t e(共1 0 7 张)课件急性胰腺炎(a c u t e(共1 0 7 张)课件Fat necrosis Fat necrosis seen at surgery is associated with peripancreatic release of lipase,with hydr
36、olysis of triacylglycerols(triglycerides)to toxic fatty acids.F a t n e c r o s i s F a t n e c r o s i s s e e n Steady,dull,or boring midepigastric pain associated with nausea and vomiting is the classic presentation of acute pancreatitis.C l i n i c a l P r e s e n t a t i o n S t e a d y,d It ra
37、diates straight to the midline of the lower thoracic vertebral region in about 50%of patients and is usually worse in the supine position.)A b d o m i n a l p a i n p r e d o m i n a n t c lPainless acute pancreatitis is very rare but carries a grave prognosis because the patients frequently present
38、 in shock.A b d o m i n a l p a i n r a r e p a t i e n t s w iC l i n i c a l P r e s e n t a t i o n N a u s e a a n Paralytic ileus(麻痹性肠梗阻麻痹性肠梗阻)with abdominal distention may develop during the first few days,signifying extension of the inflammatory process into the small intestinal and colonic(结
39、肠结肠的的)mesentery(肠系膜肠系膜).A b d o m i n a l D i s t e n t i o n P a r a l y t i cC l i n i c a l P r e s e n t a t i o n o f S e v e rC l i n i c a l P r e s e n t a t i o n o f S e v e r One to 2 weeks after the onset,large ecchymoses(瘀斑瘀斑)may appear in the flanks侧腹侧腹(Grey Turners sign)or the umbilic
40、al area(Cullens sign);O n e t o 2 w e e k s a f t e r t h e o n s e t One to 2 weeks after the onset,large ecchymoses(瘀斑瘀斑)may appear in the flanks侧腹侧腹(Grey Turners sign)or the umbilical area(Cullens sign);O n e t o 2 w e e k s a f t e r t h e o n s e t One to 2 weeks after the onset,large ecchymose
41、s(瘀斑瘀斑)may appear in the flanks侧腹侧腹(Grey Turners sign)or the umbilical area(Cullens sign);O n e t o 2 w e e k s a f t e r t h e o n s e t Initial physical examination reveals mild fever and tachycardia(心动过心动过速速);Hypotension is present in 30 to 40%of patients.P h y s i c a l E x a m i n a t i o nI n
42、i t i a l pP h y s i c a l E x a m i n a t i o n e p i g a s t r i aL a b o r a t o r y T e s t Total serum amylase activity is the test most frequently used to diagnose acute pancreatitis.The level rises 6 to 12 hours after onset of symptoms and remains elevated for 3 to 5 days in most cases.()S e
43、r u m A m y l a s e T o t a l s e r u m a m y l a Values more than 3 times the upper limit of normal are highly specific 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 hyp
44、eramylasemia indicate developing complications.the absence of hyperamylasemia cant exclude the diagnosis of acute pancreatitis(extensive pancreatic necrosis)S e r u m A m y l a s e V a l u e s m o r e t h a n D i s o r d e r s A s s o c i a t e d w i t h h y p eU r i n a r y A m y l a s e a s e n s
45、i t i v e i n d Separation of total serum amylase into its pancreatic(P)and salivary(S)isoenzymes and measurements of urinary amylase output add little to the diagnostic information.S e p a r a t i o n o f t o t a l s e r u m a m y l The amylase-creatinine clearance ratio(ACR)(the ratio of amylase c
46、oncentration in urine over plasma,divided by the corresponding values for creatinine)is useful in diagnosing asymptomatic macroamylasemia,in which aggregates of circulating amylase escape glomerular filtration and the ACR is abnormally low.T h e a m y l a s e-c r e a t i n i n e c l e a r a n淀粉酶淀粉酶
47、这一古老的检查方法虽已应用了半个多世纪，但对胰腺这一古老的检查方法虽已应用了半个多世纪，但对胰腺炎的诊断仍不失为良好而简便可行的手段。由于胰酶在炎的诊断仍不失为良好而简便可行的手段。由于胰酶在胰管内逆流入血或渗出液重吸收入血，则在急性胰腺炎胰管内逆流入血或渗出液重吸收入血，则在急性胰腺炎时血、尿的淀粉酶有所升高。血淀粉酶正常值，温氏单时血、尿的淀粉酶有所升高。血淀粉酶正常值，温氏单位位256单位，苏氏单位单位，苏氏单位500单位。急性胰腺炎（轻型）单位。急性胰腺炎（轻型）发作后发作后612小时即升高，小时即升高，4872小时逐渐恢复正常，尿小时逐渐恢复正常，尿淀粉酶约在发病后淀粉酶约在发病后1
48、224小时升高，要持续小时升高，要持续35天。但天。但急性重型胰腺炎升高的时间要提前。临床上对淀粉酶值急性重型胰腺炎升高的时间要提前。临床上对淀粉酶值的变化要作全面的分析，再结合临床其他症状才能做出的变化要作全面的分析，再结合临床其他症状才能做出正确的判断。正确的判断。淀粉酶 这一古老的检查方法虽已应用了半个多世纪，但对淀粉酶淀粉酶 血淀粉酶值正常：有两种情况，其一表血淀粉酶值正常：有两种情况，其一表明病已痊愈，血淀粉酶值恢复正常，同明病已痊愈，血淀粉酶值恢复正常，同时全身情况良好，无腹部体征。其二在时全身情况良好，无腹部体征。其二在重症急性胰腺炎的初检或治疗中，淀粉重症急性胰腺炎的初检或治疗
49、中，淀粉酶也可不升高，说明病情会进行性加重酶也可不升高，说明病情会进行性加重恶化。因为胰腺腺泡大量坏死、崩溃，恶化。因为胰腺腺泡大量坏死、崩溃，已不能分泌淀粉酶，即所谓的已不能分泌淀粉酶，即所谓的“枯竭枯竭”现象。这一现象在急性重症胰腺炎中时现象。这一现象在急性重症胰腺炎中时有发生，应予以高度重视。有发生，应予以高度重视。淀粉酶血淀粉酶值正常：有两种情况，其一表明病已痊愈，血淀粉酶淀粉酶淀粉酶 血淀粉酶升高：有时病人出现腹痛，并伴血淀粉酶升高，但血淀粉酶升高：有时病人出现腹痛，并伴血淀粉酶升高，但临床的症状、体征并不支持胰腺炎，这时就应考虑到血清临床的症状、体征并不支持胰腺炎，这时就应考虑到血
50、清淀粉酶检测往往是非特异性的。临床常见的一些急腹症也淀粉酶检测往往是非特异性的。临床常见的一些急腹症也可伴有血淀粉酶升高，如胆囊炎、胆石症、胆道梗阻、肠可伴有血淀粉酶升高，如胆囊炎、胆石症、胆道梗阻、肠梗阻、消化性溃疡病穿孔、肠系膜血栓形成以及使用吗啡梗阻、消化性溃疡病穿孔、肠系膜血栓形成以及使用吗啡后。胆石症时可能是由于排石对后。胆石症时可能是由于排石对Oddi括约肌的刺激，使之括约肌的刺激，使之痉挛，血淀粉酶一过性升高。消化性溃疡穿孔（特别是十痉挛，血淀粉酶一过性升高。消化性溃疡穿孔（特别是十二指肠球部穿孔）时，含有大量胰液的肠内容物进入腹腔二指肠球部穿孔）时，含有大量胰液的肠内容物进入腹
