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Pancreas
胰腺疾病
DepartmentofSurgeryMaQingyongPancreas
胰腺疾病DepartmentofSu1Anatomy
Thepancreaslieswithintheretroperitoneumintheupperabdomen,lyinginfrontofthesecondlumbervertebraandendinginthesplenichilum.Theglandcanbedividedintofourportions-head,neck,body,andtail.uncinateprocessAnatomyThepancreaslieswith2AnatomyThemainpancreaticduct(theductofWirsung,2~3mmindiameter)coursesalongtheglandfromthetailtotheheadandjoinsthecommonbileductjustbeforeenteringtheduodenumattheampullaofVater(85%).Theaccessorypancreaticduct(theductofSantorini)enterstheduodenum2~2.5cmproximaltotheVater.AnatomyThemainpancreaticduc3theductofWirsungSantoriniampullaofVateruncinateprocess
theductofWirsungSantoriniam4AnatomyBloodsupplyThesuperiorpancreaticoduodenalarteryarisesfromthegastroduedenalartery,runsparalleltotheduodenum,andeventuallymeetstheinferiorpancreaticoduodenalartery,abranchofthesuperiormesentericartery,toformanarcade.Thesplenicarteryprovidestributariesthatsupplythebodyandtailofthepancreas.pancreaticmagnaAAnatomyBloodsupply5superiormesentericarterysplenicarteryarcadesuperiorpancreaticoduodenalarteryinferiorpancreaticoduodenalarterydorsalpancreaticApancreaticmagnaAsuperiormesentericVsuperiormesentericarterysple6〖醫(yī)學〗胰腺疾病課件7Physiology
ExocrineFunctionTheexternalsecretionconsistsofaclear,alkaline(pH7.0~8.3)solutionof750~1000ml/dcontainingdigestiveenzymes.Secretionisstimulatedbythehormonessecretinandcholecystokinin(CCK)andbyparasympatheticvagaldischarge.SecretinandCCKaresynthesized,store,andreleasedfromduodenalmucosalcellsinresponsetospecificstimuli.Acidinthelumenoftheduodenumcausesthereleaseofsecretin,andluminaldigestionproductsoffatandproteincausethereleaseofCCK.PhysiologyExocrineFunction8PhysiologyExocrineFunction
enzymessynthesized,stored(aszymogengranules),andreleasedbytheacinarcellsofthegland,inresponsetoCCKandvagalstinulation.Pancreaticenzymesareproteolytic,lipolytic,andemylolytic.Lipaseandamylasearestoredandsecretedinactiveforms.Theprolyticenzymesaresecretedasinactiveprecursorsandactivatedbytheduodenalenzymeenterokinase.OtherenzymesincluderibonucleasesandphospholipaseA.PhysiologyExocrineFunction9PhysiologyEndocrineFunctionInsulin(51aminoacidresidues,formedinthebetacellsviatheprecursorproinsulin)glucagons(29aminoacids,formedinthecells)pancreaticpolypeptideandsomatostatinareproducedbytheisletsofLangerhans.PhysiologyEndocrineFunction10AcutePancreatitis急性胰腺炎
Acutepancreatitisisoneoffollowingfiveacuteabdomen
Acutepancreatitis,Acuteappendicitis,Intestinalobstruction,PerformedgatroduodenalulcerCholecystitisorcholelithiasis).AcutePancreatitis急性胰腺炎11Etiology
Mostcasesofpancreatitisarecausedbygallstonediseaseoralcoholism;afewresultfromhypercalcemia,trauma,hyperlipidemia,andgeneticpredisposition;andtheremainderareidiopathic.EtiologyMostcasesofpancrea12EtiologyBiliarypancreatitis:About40~60%ofcasesofpancreatitisareassociatedwithgallstonedisease,which,ifuntreated,usuallygivesrisetoadditionalacuteattacks.Bilerefluxpancreaticductactivateenzymes.Obstructionincreasedductpressuredamagepancreaticacinusdistroygland.EtiologyBiliarypancreatitis:13EtiologyAlcoholicPancreatitis:
AlcoholstimulatesgastricacidsecretionwhichincreasesCCK-PZ(cholecystokinandpancreozymin)excretioninduodenumandthenincreasespancreaticsecretion.MakethesphincterspasmandedemaIncreaseductpressure.DirecttoxictopancreasEtiologyAlcoholicPancreatitis14EtiologyInfection:e.g.hepatitisvirus,parotitisvirusandtyphoidbacillus.Traumaandoperation,endoscopy(iatrogenicPancreatitis):followingcommonbileductexploration,especiallyifsphincterotomywasperformed.1).UseofacommonductTtubewithalongarmpassingthroughofsphincterofOddi,2).Dilationofthesphincterto5~7mmduringcommonductexploration.EtiologyInfection:e.g.hepati15EtiologyHypercalcemia:hyperparahtyroidismandotherdisordersaccompaniedbyhypercalcemiaareoccasionallycomplicatedbyacutepancreatitis,itisthoughtthattheincreasedcalciumconcentrationsinpancreaticjuicethatresultfromhypercalcemiamayprematurelyactivateproteases,theymayalsofacilitateprecipitationofcalculiintheduct.EtiologyHypercalcemia:hyperpa16EtiologyHyperlipidemia:
pancreatitisseemstobeadirectconsequenceofthemetabolicabnormality.duringanacuteattackusuallyassociatedwithmormalserumamylaselevels,becausethelipidinterfereswiththechemicaldeterminationforamylase;urinaryoutputofamylasemaystillbehigh.EtiologyHyperlipidemia:17EtiologyDrug-inducedpancreatitis:corticosteroids,estrogen-containingcontraceptives,azathioprine,thiazidediuretics,andtetracyclines.Pancreatitisassociatedwithuseofestrogensisusuallytheresultofdrug-inducedhypertriglyceridemia.EtiologyDrug-inducedpancreati18EtiologyIdiopathicpancreatitisandmiscellaneouscauses:Inabout15%ofpatientsthereisnoidentifiablecauseofthecondition.EtiologyIdiopathicpancreati19PathogenesisEnzymaticdigestion(autodigestion):Trypsinnotonlydestroystissuebutalsoactivatesotherdestructiveenzymessuchaselastaseandlecithinase.Vasoactivesubstancesincludingkinins,kallikrein,andhistamineleadtocardiovasculardysfunctionandcollapse.PathogenesisEnzymaticdigest20PathogenesisIschemia,O-,inflammatorymediatorsMOD(principallyARDS,myocardialdepression,renalinsufficiency,andgastricstressulceration.PathogenesisIschemia,O-,infl21PathologyEdematouspancreatitis:localordiffusededemawithcongestion,enlargement,hard.Microscopically,acinicandinterstitialedema,infiltratedwithinflammatorycellswithsmallfociofhemorrhageandnecrosis.Hemorrhagicandnecroticpancreatitis:hemorrhageandnecrosis,ascites,fatnecrosiswithsaponifyingpatchesinlesserandgreateromenta,mesentery,retroperitonealareas.PathologyEdematouspancreatiti22ComplicationsShock:
Trypsin,tissuenecrosis,infectivetoxinpromotingreleaseofvasoactivesubstancesLossofbodyfluidDICPyogenicinfection:e.g.suppurativeperitonitis,peripancreaticabscess,septicemiaMODS:ARF,ARDS,poisoningencephalopathyPseudocystorchronicpancreatitisComplicationsShock:23ClinicalFindingsSymptomsandsigns:Abdominalpain:Theacuteattachbeginsfollowingalargemealandconsistofsevereepigastricpainthatradiatesthroughtotheback,persistentwithvomitingandretching.WholepancreasbeltbackHeadrightupperabdomenradiatestorightshoulderBodyepigastric(middleupperabdomen)BodyandtailleftupperleftshoulderClinicalFindingsSymptomsand24ClinicalFindingsSymptomsandsigns:
Nauseaandvomiting:withoutrelieftoabdominalpainaftervomitingSignsofperitonealirritation:tenderness,reboundpain,rigidity,guardingDistention:bowelparalysis,decreasedorabsentbowelsounds,silentabdomen,failuretopasseithergasorfeces.ClinicalFindingsSymptomsand25ClinicalFindingsSymptomsandsigns:
HighTwithoutchilling,compressCBDjaundice,decreasedBP,andshock;fulminantpancreatitiscancauseasuddenshockBleeding:Gastrointestinalhematemesisandmelena;bluishdiscolorationintheflank(GreyTurner’ssign)orperiumbilicalarea(Cullen’ssign)ClinicalFindingsSymptomsand26GreyTuner征GreyTuner征27Cullen征Cullen征28ClinicalFindingsLaboratoryfindingsSerumamylaseconcentration:risesfrom3-12h,thepeakis24-48hand2-5dnormalUrinerisesfrom12-24h,slowdecreaseElevatedserumlipaseElevatedhematocritduetodehydrationLowhematocritduetobloodlossClinicalFindingsLaboratoryfi29ClinicalFindingsLaboratoryfindings
ModerateleukocytosisInnecroticpancreatitis:sugar>11.1mmol/L,calcium<2.0mmol/L,PaO2<8.0kPa,increasedBUN,acidosisandevenMODSAbdominalpuncture:bloodyascites,increasedamylaseClinicalFindingsLaboratoryfi30ClinicalFindingsImagingstudyCTandUSshowadiffuseenlargement,necrosis,andascitesX-ray:isolateddilationofasegmentofgut(sentinelloop)consistingofjejunum,transversecolon,orduodenumadjacenttothepancreas.Gasdistendingtherightcolonthatabruptlystopsinthemidorlefttransversecolon(coloncutoffsign)isduetocolonicspasmClinicalFindingsImagingstudy31正常胰腺CT正常胰腺CT32胰腺動態(tài)CT時間胰腺動態(tài)CT時間33膽源性胰腺炎膽源性胰腺炎34〖醫(yī)學〗胰腺疾病課件35
patchofsaponification
patchofsaponification36EssentialsofDiagnosisAbruptonsetofepigastricpain,frequentlywithbackpainNauseaandvomitingElevatedserumorurinaryamylaseCholelithiasisoralcoholism(manypatients)EssentialsofDiagnosisAbrupt37DifferentialDiagnosisAcutecholecystitis:biliarycolic,feverandchills,Murphy’ssignandenlargedgallbladderPepticulcerperforationAcuteabdominalobstructionRenalcolicAcutegastroenteritisCoronarydiseaseDifferentialDiagnosisAcutech38TreatmentMedicaltreatment:thegoalsofmedicaltherapyarereductionofpancreaticsecretorystimuliandcorrectionoffluidandelectrolytederangement.GastricsuctionanddietcontrolOxygenFluidreplacementandnutritionAntibioticsTreatmentMedicaltreatment:th39Treatment(2)Medicaltreatment:CalciumandmagnesiumreplacementAnti-enzymedrugs:
5-FU(250-500mgin5%glucose500ml),octreotide,sandostatin,aprotinin,andH2receptorblockersSpasmolyticandpainkiller–atropine,dolantin,pro-BanthineTCMTreatment(2)Medicaltreatment:40Treatment(3)Surgicaltreatment(necroticPancreatitiswithcomplication,andbiliaryP)Necrosectomy,debridement–removenecrotictissueThoroughdrainage(peritoneallavage)OtherproceduresBiliarypancreatitis–TtubedrainageGastrostomyfordecompressionJejunostomyfornutritionTPN(totalperenteralnutrition)Treatment(3)Surgicaltreatment41ChronicPancreatitis
慢性胰腺炎ChronicPancreatitis
慢性胰腺炎42EssentialsofDiagnosisPersistentorrecurrentabdominalpain.Pancreaticcalcificationonx-rayin50%.Pancreaticinsufficiencyin30%;malabsorptionanddiabetesmellitus.Mostoftenduetoalcoholism.EssentialsofDiagnosisPersist43CarcinomaofthePancreas
胰腺癌
CarcinomaofthePancreas
胰腺癌
44PathologyMostareintheheadofthepancreas(2/3).Ductcellcancerismorethan90%,Therestarefromacinarcells.Metastasisandspreadaremainlyfromlymphaticmetastasisanddirectinvasion.Pathology45ClinicalFindingsSymptomsandsignsUpperabdominalpain(deepseated,andpersistent),distention,discomfortObstructivejaundice:Alimentarysymptoms(poorappetite,anorexia,dyspepsiadiarrheaorconstipation,nauseaandvomitingifinvasiontoduodenumorstomach)Weightloss,faintandcachexiaOthers(fever,mass,ascites)ClinicalFindingsSymptomsand46ClinicalFindingsLaboratorystudyIncreasedamylase,bloodsugar,positivesugartolerancetest,increasedALP,bilirubin,andtransaminaseifthereishepaticmetastasisorCBDobstructionTumormarkers:CEA,CA19-9,PCAA.thelevelsareelevatedinmostpatientswithpancreaticcancerandalsoinothergastrointestinalcancers.ClinicalFindingsLaboratoryst47ClinicalFindingsImagingstudyBUSandCT:CBDandWirsungductdilationwithenlargedgallbladderX-ray:reversed–3signifthetumorlocatedintheheadofthepancreasERCPintheabsenceofamass,anERCPisindicated.itisthemostsensitivetest(95%)fordetectingpancreaticcancerClinicalFindingsImagingstudy48TreatmentPancreaticresectionforpancreaticcancerisappropriateonlyifallgrosstumorcanberemovedwithastandardresection.Forcurablelesionsofthehead,pancreaticoduodenectomy(Whippleoperation)isrequired.Thisinvolvesresectionofthecommonbileduct,thegallbladder,theduodenum,andthepancreastothemidbody.Thereisanincreasingtendencytopreservetheantrumandpylorus.TreatmentPancreaticresection49PancreaticoduodenectomyPancreaticoduodenectomy50TreatmentRadiotherapyshouldbecombinedwithchemotherapy(fluorouracil)forpalliation.Radiotherapyalonehasbeenshowntobenobenefit.TreatmentRadiotherapyshouldb51CarcinomaoftheAmpullaofVaterCarcinomaoftheAmpullaofVa52ClinicalFindingsJaundice:(earlystage)somearefluctuationduetotumornecrosisandexfoliation.EnlargedgallbladderandliverWithinfection–chillsandfeverAbdominalpainOthers(poorappetite,weightloss,diarrhea,nauseaandvomitingetc.)ERCPfordiagnosis.ClinicalFindingsJaundice:(e53TreatmentPancreaticoduodenectomy.TreatmentPancreaticoduodenecto541、病毒性肝炎:由病毒造成的肝炎按照其病毒系列不同分為甲、乙、丙、丁、戊和庚共六種類型病毒性肝炎。能引起肝臟細胞腫脹,是世界上流傳廣泛,危害很大的傳染病之一。1908年,才發(fā)現(xiàn)病毒也是肝炎的致病因素之一。1947年,將原來的傳染性肝炎〔infectioushepatitis〕稱為甲型肝炎〔HepatitisA,HA〕;血清性肝炎〔serumhepatitis〕稱為乙型肝炎〔HepatitisB,HB〕。1965年人類首次檢測到乙型肝炎的外表抗原。我國經濟和科學技術日益開展,學術文化領域百家爭鳴,〔df高血壓958心臟病983u6糖尿病87fr〕特別是思想家的革新精神,為中醫(yī)學理論的創(chuàng)新和突破性進展,提供了有利的文化背景。宋代陳無擇著?三因極一病證方論?一書,〔45傳染病q566丙肝964jo乙肝28jgsx甲肝gh〕提出三因學說;并產生了最具盛名四大學派,劉完素倡導熾熱論;張從正力倡“攻邪論〞;李杲提出“內傷脾胃,百病由生〞的理論;朱震亨創(chuàng)造性地說明了相火的演變規(guī)律。編輯本段明清時期〔df肺25s血液f369血小板t5172紅血球gdf55m白血球fd2〕是中醫(yī)學理論綜合匯編、深化開展,臨床各科辨證體系豐富、提高階段。如明代樓英的?醫(yī)學綱目?和王肯堂的?證治準繩?,清代吳謙等編著的?醫(yī)宗金鑒?和陳夢雷主編的?古今圖書集成·醫(yī)部全錄?等。王清任著?醫(yī)林改錯?,注重實證研究,〔df高血壓958心臟病983u6糖尿病87fr〕糾正了古醫(yī)籍中關于解剖知識的某些錯誤,肯定了“腦主思維〞,開展了瘀血理論。溫病學說的形成和開展,標志著中醫(yī)理論的創(chuàng)新與突破,吳有性著?溫疫論?,葉天士著?溫熱病篇?,吳鞠通著?溫病條辨?等,在藥物學研究方面,〔45傳染病q566丙肝964jo乙肝28jgsx甲肝gh〕李時珍著的?本草綱目?,總結了16世紀以前我國藥物學研究的成就。醫(yī)的診察疾病能參考現(xiàn)代醫(yī)學的微觀分析,將辨證與辨病相結合,實現(xiàn)宏觀與微觀的統(tǒng)一,使中醫(yī)診斷客觀化,即把分析與綜合相結合的方法引入中醫(yī)理、法、方、藥的研究,使二者有機結合,互相借鑒、補充,防止各自的片面性、局限性,這將有利于中西醫(yī)學的優(yōu)勢互補,“和而不同〞,多元開展。近年來,中醫(yī)藥在防治非典、禽流感和艾滋病方面發(fā)揮的獨特作用也證實了二者的有機結合,具有肯定的臨床療效。編輯本段東西方醫(yī)學交融不管是中醫(yī)學還是西醫(yī)學,從二者現(xiàn)有的思維方式的開展趨勢來看,均是走向現(xiàn)代系統(tǒng)論思維,中醫(yī)藥學理論與現(xiàn)代科學體系之間具有系統(tǒng)同型性,屬于本質相同而描述表達方式不同的兩種科學形式??赏诂F(xiàn)代系統(tǒng)論思維上實現(xiàn)交融或統(tǒng)一,成為中西醫(yī)在新的開展水平上實現(xiàn)交融或統(tǒng)一的支撐點,希冀籍此能給中醫(yī)學以至生命科學帶來良好的開展機遇,進而對醫(yī)學理論帶來新的革命。編輯本段現(xiàn)代中醫(yī)史上個世紀末,本世紀初,1996年,清華學界對中醫(yī)氣本質,經絡實質,陰陽,五行,藏象,中醫(yī)哲學觀等都有了新的全面整體創(chuàng)造性的認識和解說。如,鄧宇等發(fā)現(xiàn)的:氣是流動著的‘信息-能量-物質’的混合統(tǒng)一體;分形分維的經絡解剖結構;數(shù)理陰陽;中醫(yī)分形集:分形陰陽集-陰陽集的分形分維數(shù),五行分形集-五行集的分維數(shù);分形藏象五系統(tǒng)-暨心系統(tǒng)、肝系統(tǒng)、脾系統(tǒng)、肺系統(tǒng)、腎系統(tǒng);中醫(yī)三個哲學觀-新提出的第三哲學觀:相似觀-分形論等。還包括近代針灸經絡的開展史,近代中醫(yī)氣的進展簡史,中西醫(yī)結合史,中醫(yī)中藥史等.六種類型的病毒性肝炎遺傳因子不同,除乙型肝炎遺傳因子是DNA外,其余幾型肝炎遺傳因子均為RNA。其中甲型肝炎的傳播途徑是糞口傳播,乙型肝炎的傳播途徑是血液傳播、性傳播和母嬰傳播。疫苗。2、酒精性肝炎:酒精性肝炎早期可無明顯病癥,但肝臟已有病理改變,發(fā)病前往往有短期內大量飲酒史,有明顯體重減輕,食欲不振,惡心,嘔吐,全身倦怠乏力,發(fā)熱,腹痛及腹瀉,上消化道出血及精神病癥。體征有黃疸,肝腫大和壓痛,同時有脾腫大,面色發(fā)灰,腹水浮腫及蜘蛛痣,食管靜脈曲張。從實驗室檢查看,有貧血和中性白細胞增多,紅細胞容積測定〔MCV〕大于95FL,血清膽紅素增高,可達或以上,轉氨酶中度升高,常大于,測定線粒體AST〔mAST〕及其與總AST〔tAST〕的比值,其升高可達12.5+5.2%。并有γ-GT,谷氨酸脫氫酶和堿性磷酸酶活力增高,凝血酶原時間延長。此外,病毒性肝炎還有丙型肝炎、丁型肝炎、戊型肝炎和庚型肝炎。過去被定為己型肝炎病毒的病毒現(xiàn)在被確定為乙型肝炎病毒的一個屬型,因此己型肝炎不存在。在病毒肝炎的疫苗,A型、B型、D型的疫苗已研發(fā)成功;C型、E型、F型的目前無編輯本段宋金元時期精品課件文檔,歡送下載,下載后可以復制編輯。更多精品文檔,歡送瀏覽。1、病毒性肝炎:由病毒造成的肝炎按照其病毒系列不同分為甲、乙55Pancreas
胰腺疾病
DepartmentofSurgeryMaQingyongPancreas
胰腺疾病DepartmentofSu56Anatomy
Thepancreaslieswithintheretroperitoneumintheupperabdomen,lyinginfrontofthesecondlumbervertebraandendinginthesplenichilum.Theglandcanbedividedintofourportions-head,neck,body,andtail.uncinateprocessAnatomyThepancreaslieswith57AnatomyThemainpancreaticduct(theductofWirsung,2~3mmindiameter)coursesalongtheglandfromthetailtotheheadandjoinsthecommonbileductjustbeforeenteringtheduodenumattheampullaofVater(85%).Theaccessorypancreaticduct(theductofSantorini)enterstheduodenum2~2.5cmproximaltotheVater.AnatomyThemainpancreaticduc58theductofWirsungSantoriniampullaofVateruncinateprocess
theductofWirsungSantoriniam59AnatomyBloodsupplyThesuperiorpancreaticoduodenalarteryarisesfromthegastroduedenalartery,runsparalleltotheduodenum,andeventuallymeetstheinferiorpancreaticoduodenalartery,abranchofthesuperiormesentericartery,toformanarcade.Thesplenicarteryprovidestributariesthatsupplythebodyandtailofthepancreas.pancreaticmagnaAAnatomyBloodsupply60superiormesentericarterysplenicarteryarcadesuperiorpancreaticoduodenalarteryinferiorpancreaticoduodenalarterydorsalpancreaticApancreaticmagnaAsuperiormesentericVsuperiormesentericarterysple61〖醫(yī)學〗胰腺疾病課件62Physiology
ExocrineFunctionTheexternalsecretionconsistsofaclear,alkaline(pH7.0~8.3)solutionof750~1000ml/dcontainingdigestiveenzymes.Secretionisstimulatedbythehormonessecretinandcholecystokinin(CCK)andbyparasympatheticvagaldischarge.SecretinandCCKaresynthesized,store,andreleasedfromduodenalmucosalcellsinresponsetospecificstimuli.Acidinthelumenoftheduodenumcausesthereleaseofsecretin,andluminaldigestionproductsoffatandproteincausethereleaseofCCK.PhysiologyExocrineFunction63PhysiologyExocrineFunction
enzymessynthesized,stored(aszymogengranules),andreleasedbytheacinarcellsofthegland,inresponsetoCCKandvagalstinulation.Pancreaticenzymesareproteolytic,lipolytic,andemylolytic.Lipaseandamylasearestoredandsecretedinactiveforms.Theprolyticenzymesaresecretedasinactiveprecursorsandactivatedbytheduodenalenzymeenterokinase.OtherenzymesincluderibonucleasesandphospholipaseA.PhysiologyExocrineFunction64PhysiologyEndocrineFunctionInsulin(51aminoacidresidues,formedinthebetacellsviatheprecursorproinsulin)glucagons(29aminoacids,formedinthecells)pancreaticpolypeptideandsomatostatinareproducedbytheisletsofLangerhans.PhysiologyEndocrineFunction65AcutePancreatitis急性胰腺炎
Acutepancreatitisisoneoffollowingfiveacuteabdomen
Acutepancreatitis,Acuteappendicitis,Intestinalobstruction,PerformedgatroduodenalulcerCholecystitisorcholelithiasis).AcutePancreatitis急性胰腺炎66Etiology
Mostcasesofpancreatitisarecausedbygallstonediseaseoralcoholism;afewresultfromhypercalcemia,trauma,hyperlipidemia,andgeneticpredisposition;andtheremainderareidiopathic.EtiologyMostcasesofpancrea67EtiologyBiliarypancreatitis:About40~60%ofcasesofpancreatitisareassociatedwithgallstonedisease,which,ifuntreated,usuallygivesrisetoadditionalacuteattacks.Bilerefluxpancreaticductactivateenzymes.Obstructionincreasedductpressuredamagepancreaticacinusdistroygland.EtiologyBiliarypancreatitis:68EtiologyAlcoholicPancreatitis:
AlcoholstimulatesgastricacidsecretionwhichincreasesCCK-PZ(cholecystokinandpancreozymin)excretioninduodenumandthenincreasespancreaticsecretion.MakethesphincterspasmandedemaIncreaseductpressure.DirecttoxictopancreasEtiologyAlcoholicPancreatitis69EtiologyInfection:e.g.hepatitisvirus,parotitisvirusandtyphoidbacillus.Traumaandoperation,endoscopy(iatrogenicPancreatitis):followingcommonbileductexploration,especiallyifsphincterotomywasperformed.1).UseofacommonductTtubewithalongarmpassingthroughofsphincterofOddi,2).Dilationofthesphincterto5~7mmduringcommonductexploration.EtiologyInfection:e.g.hepati70EtiologyHypercalcemia:hyperparahtyroidismandotherdisordersaccompaniedbyhypercalcemiaareoccasionallycomplicatedbyacutepancreatitis,itisthoughtthattheincreasedcalciumconcentrationsinpancreaticjuicethatresultfromhypercalcemiamayprematurelyactivateproteases,theymayalsofacilitateprecipitationofcalculiintheduct.EtiologyHypercalcemia:hyperpa71EtiologyHyperlipidemia:
pancreatitisseemstobeadirectconsequenceofthemetabolicabnormality.duringanacuteattackusuallyassociatedwithmormalserumamylaselevels,becausethelipidinterfereswiththechemicaldeterminationforamylase;urinaryoutputofamylasemaystillbehigh.EtiologyHyperlipidemia:72EtiologyDrug-inducedpancreatitis:corticosteroids,estrogen-containingcontraceptives,azathioprine,thiazidediuretics,andtetracyclines.Pancreatitisassociatedwithuseofestrogensisusuallytheresultofdrug-inducedhypertriglyceridemia.EtiologyDrug-inducedpancreati73EtiologyIdiopathicpancreatitisandmiscellaneouscauses:Inabout15%ofpatientsthereisnoidentifiablecauseofthecondition.EtiologyIdiopathicpancreati74PathogenesisEnzymaticdigestion(autodigestion):Trypsinnotonlydestroystissuebutalsoactivatesotherdestructiveenzymessuchaselastaseandlecithinase.Vasoactivesubstancesincludingkinins,kallikrein,andhistamineleadtocardiovasculardysfunctionandcollapse.PathogenesisEnzymaticdigest75PathogenesisIschemia,O-,inflammatorymediatorsMOD(principallyARDS,myocardialdepression,renalinsufficiency,andgastricstressulceration.PathogenesisIschemia,O-,infl76PathologyEdematouspancreatitis:localordiffusededemawithcongestion,enlargement,hard.Microscopically,acinicandinterstitialedema,infiltratedwithinflammatorycellswithsmallfociofhemorrhageandnecrosis.Hemorrhagicandnecroticpancreatitis:hemorrhageandnecrosis,ascites,fatnecrosiswithsaponifyingpatchesinlesserandgreateromenta,mesentery,retroperitonealareas.PathologyEdematouspancreatiti77ComplicationsShock:
Trypsin,tissuenecrosis,infectivetoxinpromotingreleaseofvasoactivesubstancesLossofbodyfluidDICPyogenicinfection:e.g.suppurativeperitonitis,peripancreaticabscess,septicemiaMODS:ARF,ARDS,poisoningencephalopathyPseudocystorchronicpancreatitisComplicationsShock:78ClinicalFindingsSymptomsandsigns:Abdominalpain:Theacuteattachbeginsfollowingalargemealandconsistofsevereepigastricpainthatradiatesthroughtotheback,persistentwithvomitingandretching.WholepancreasbeltbackHeadrightupperabdomenradiatestorightshoulderBodyepigastric(middleupperabdomen)BodyandtailleftupperleftshoulderClinicalFindingsSymptomsand79ClinicalFindingsSymptomsandsigns:
Nauseaandvomiting:withoutrelieftoabdominalpainaftervomitingSignsofperitonealirritation:tenderness,reboundpain,rigidity,guardingDistention:bowelparalysis,decreasedorabsentbowelsounds,silentabdomen,failuretopasseithergasorfeces.ClinicalFindingsSymptomsand80ClinicalFindingsSymptomsandsigns:
HighTwithoutchilling,compressCBDjaundice,decreasedBP,andshock;fulminantpancreatitiscancauseasuddenshockBleeding:Gastrointestinalhematemesisandmelena;bluishdiscolorationintheflank(GreyTurner’ssign)orperiumbilicalarea(Cullen’ssign)ClinicalFindingsSymptomsand81GreyTuner征GreyTuner征82Cullen征Cullen征83ClinicalFindingsLaboratoryfindingsSerumamylaseconcentration:risesfrom3-12h,thepeakis24-48hand2-5dnormalUrinerisesfrom12-24h,slowdecreaseElevatedserumlipaseElevatedhematocritduetodehydrationLowhematocritduetobloodlossClinicalFindingsLaboratoryfi84ClinicalFindingsLaboratoryfindings
ModerateleukocytosisInnecroticpancreatitis:sugar>11.1mmol/L,calcium<2.0mmol/L,PaO2<8.0kPa,increasedBUN,acidosisandevenMODSAbdominalpuncture:bloodyascites,increasedamylaseClinicalFindingsLaboratoryfi85ClinicalFindingsImagingstudyCTandUSshowadiffuseenlargement,necrosis,andascitesX-ray:isolateddilationofasegmentofgut(sentinelloop)consistingofjejunum,transversecolon,orduodenumadjacenttothepancreas.Gasdistendingtherightcolonthatabruptlystopsinthemidorlefttransversecolon(coloncutoffsign)isduetocolonicspasmClinicalFindingsImagingstudy86正常胰腺CT正常胰腺CT87胰腺動態(tài)CT時間胰腺動態(tài)CT時間88膽源性胰腺炎膽源性胰腺炎89〖醫(yī)學〗胰腺疾病課件90
patchofsaponification
patchofsaponification91EssentialsofDiagnosisAbruptonsetofepigastricpain,frequentlywithbackpainNauseaandvomitingElevatedserumorurinaryamylaseCholelithiasisoralcoholism(manypatients)EssentialsofDiagnosisAbrupt92DifferentialDiagnosisAcutecholecystitis:biliarycolic,feverandchills,Murphy’ssignandenlargedgallbladderPepticulcerperforationAcuteabdominalobstructionRenalcolicAcutegastroenteritisCoronarydiseaseDifferentialDiagnosisAcutech93TreatmentMedicaltreatment:thegoalsofmedicaltherapyarereductionofpancreaticsecretorystimuliandcorrectionoffluidandelectrolytederangement.GastricsuctionanddietcontrolOxygenFluidreplacementandnutritionAntibioticsTreatmentMedicaltreatment:th94Treatment(2)Medicaltreatment:CalciumandmagnesiumreplacementAnti-enzymedrugs:
5-FU(250-500mgin5%glucose500ml),octreotide,sandostatin,aprotinin,andH2receptorblockersSpasmolyticandpainkiller–atropine,dolantin,pro-BanthineTCMTreatment(2)Medicaltreatment:95Treatment(3)Surgicaltreatment(necroticPancreatitiswithcomplication,andbiliaryP)Necrosectomy,debridement–removenecrotictissueThoroughdrainage(peritoneallavage)OtherproceduresBiliarypancreatitis–TtubedrainageGastrostomyfordecompressionJejunostomyfornutritionTPN(totalperenteralnutrition)Treatment(3)Surgicaltreatment96ChronicPancreatitis
慢性胰腺炎ChronicPancreatitis
慢性胰腺炎97EssentialsofDiagnosisPersistentorrecurrentabdominalpain.Pancreaticcalcificationonx-rayin50%.Pancreaticinsufficiencyin30%;malabsorptionanddiabetesmellitus.Mostoftenduetoalcoholism.EssentialsofDiagnosisPersist98CarcinomaofthePancreas
胰腺癌
CarcinomaofthePancreas
胰腺癌
99PathologyMostareintheheadofthepancreas(2/3).Ductcellcancerismorethan90%,Therestarefromacinarcells.Metastasisandspreadaremainlyfromlymphaticmetastasisanddirectinvasion.Pathology100ClinicalFindingsSymptomsandsignsUpperabdominalpain(deepseated,andpersistent),distention,discomfortObstructivejaundice:Alimentarysymptoms(poorappetite,anorexia,dyspepsiadiarrheaorconstipation,nauseaandvomitingifinvasiontoduodenumorstomach)Weightloss,faintandcachexiaOthers(fever,mass,ascites)ClinicalFindingsSymptomsand101ClinicalFindingsLaboratorystudyIncreasedamylase,bloodsugar,positivesugartolerancetest,increasedALP,bilirubin,andtransaminaseifthereishepaticmetastasisorCBDobstructionTumormarkers:CEA,CA19-9,PCAA.thelevelsareelevatedinmostpatientswithpancreaticcancerandalsoinothergastrointestinalcancers.C
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