南非、肯尼亚11日行程(EK)Title

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SelfDirectedLearningModuleGastroenterology–Crohn’sDiseaseAbbyWatkins酒店设计’sDiseaseAimofthismoduleToincreasetheunderstandingofCrohn’sdiseasebylookingattheunderlyingpathologyandcausesandthenmovingontousethisinformationtounderstandthedifferentclinicalpresentationsandsubsequenttreatmentoptions.LearningoutcomesBytheendofthismodule,youshouldunderstand:ThepathologicalfeaturesofCrohn’sdiseaseTheepidemiologyandnaturalhistoryofthediseaseThecomplexaetiologyofthediseaseThevaryingclinicalpresentationsofthediseaseaswellashowtomakeadiagnosisTheprinciplesofmanagingthediseasebothmedicallyandsurgically.HowtousethismoduleThismoduleisdesignedbyastudentforstudents.Thedataisup-to-dateandthereferencesandreadinglistareattheend.Themoduleisdividedintosectionstoallowforthecontenttobetackledinbite-sizedchunks.Attheendofeachsectionisasetofquestionssuchastrue/false,multiplechoiceandfillintheblanks.Pleasehavepaperandapenhandytowritedownyouranswers.Thisisdesignedtoseehowwellyouhaveunderstoodthesectiontoallowyoutogaugethedepthofyourlearning.Attheendofthemoduleisaseriesofclinicalcasestudiesandextendedmatchingquestionsforyoutoputtheinformationyouhavelearntintopractiseandseehowyoudo.Ihopeyouenjoyit!Epidemiology&PathologyofCrohn’sDisease•Crohn’sdisease(CD)isachronicrelapsinginflammatoryconditionusuallywithflare-upsalternatingwithperiodsofremission,andanincreasingdiseaseseverityandincidenceofcomplicationsastimegoeson.•Itcanaffectanypartofthegastrointestinaltractfromthemouthtotheanus.Fortypicalsites&proportionofpatientsaffectedseebelow:Ileocaecal–45%Colononly–25%TerminalIleumonly–20%ExtensiveSmallBowel–5%Other:anorectal,gastroduodenual,oralonly–5%EpidemiologyEpidemiologyIncidence:7/100000pop/yrPrevalence:100/100000pop/yrWorldwidedistributionbutmorecommonintheWest.Jewsaremoreaffectedthannon-JewsFemalesareaffectedmorethanmales1.2:1Bimodalagedistribution:20-40yrs/60-80yrsTheincidenceislowerinnon-whiteraces.TheincidenceisrisingEpidemiologyPathologyItischaracterisedbypatchytransmuralinflammation.Thechronicinflammatoryprocessleadsofthickeningofthebowelwallandcancauseanarrowedlumen.InearlyCDthereareprominentlymphoidfolliclesfollowedbyaphthoidulceration.Laterthisprogressestolargerdeepfissuringulcersseparatedbynormallookingmucosa(cobble-stoning),fibrosis,stricturingandfistulation.Thesechangesareoftensegmentallydistributed(skiplesions).CLICKONTHEPICTURESFORALARGERVIEW&DESCRIPTIONPathologySomeofthecomplicationsofCDareoutlinedbelow:Fistulaformation–abnormalchannelsofcommunicationcanforminCDbetweenloopsofbowel,bladderandskin.IftheCDisinthecolon,fistulaecanformbetweenthecolonandvaginaorbetweenthecolonandperineum.Thediagramontherightshowsthebeginningofafistulaformationwithafissureextendingthoughmucosatowardsthemuscularwall.BelowisacartoonrepresentationofafistulastartingfromanareaofulcerationObstruction-typicallyoccursfromstricturesoradhesionswhichnarrowthelumen,blockingthepassageoftheintestinalcontents.Thiscanbeseeninthebariumfollow-throughtotheright.Questions:EpidemiologyandPathologyQuestions:EpidemiologyTrueorfalse.A).Crohn’sdiseaseeffectsonlythesmallbowel.B).Crohn’sdiseasehasabimodalagedistribution.C).Theincidenceisdecreasing.ANSWERSQuestions:PathologyFillintheblank.1).Crohn’sdiseaseischaracterisedbyt_______inflammation.2).Thediscontinuousnatureofthediseaseisseeass___l______.3).Deepfissuringulcersseparatedbynormallookingmucosaisknownasc_______s________.ANSWERSAetiologyandPathogenesisofCrohn’sDiseaseAetiology&PathogenesisTheaetiologyofCrohn’sdiseaseisunknown.Therearemanyproposedpathogenicmechanisms,someofwhicharerepresentedinthisdiagram.Asthereisnoonecause,itislikelythatCrohn’sdiseaseisanoutcomeofinteractionsbetweengeneticpredisposition,environmentalfactorsandthesubsequentreactionofthehostimmunesystem.GeneticsusceptibilityEnvironmentalfactorsHostImmuneResponseCrohn’sDiseaseGeneticFactorsThereare3mutationsontheCARD15geneonChromosome16thatareassociatedwithsomeformsofCD.TheriskofdevelopingCDinincreasedforty-foldifhomozygousforallthreemutations.Themutationsappeartoaltermonocyterecognitionoftheconstituentfloraofthegut.ItispossiblethatfunctionaldefectsinCARD15preventinnateimmunityfrombalancingresistancetothemicrobesinthegutinCDpatients,leadingtouncontrolledinflammationandmucosaldamage.HowevertheCARD15mutationsonlyaccountfor20-30%ofcasesofCDandCDisnotfoundinorientalpopulationswhohavethemutations.ThereforethisgeneisnotnecessaryforCD.Itislikelythatthereareothersusceptibilitygenesthatinfluencehowtheimmunesysteminteractswiththegutflorawhichmaybediscoveredinthefuture.Putativelocihavebeenmappedtochromosome12(IBD2),6(IBD3)and14(IBD4).GeneticsusceptibilityEnvironmentalFactorsAwiderangeofenvironmentalfactorshavebeenfoundtoplayarole:Smoking–PatientswithCDaremorelikelytohavebeensmokersandsmokingmayworsenCDandincreasetheriskofrelapse/surgicalintervention.Diet–ActiveCDmayimprovewhenanormaldietischangedtoaliquidformuladiet.Bacterialinfection–ThereissomeevidenceimplicatingE.coli,M.paratuberculosis,themeaslesvirusandL.monocytogenesinthepathogenes

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