COPD英文课20120301PPT推荐.ppt

COPD英文课20120301PPT推荐.ppt

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Chronicandunspecificinflammationofbronchiandthesurroundingtissue.Feature:

chronicmucushypersecretionandcough.Morbidity:

3.2%inpopulationover15y，upto15%inelderlyover50y.EtiologyandmechanismEnvironmentFactorsCigarettesmokingOccupationaldustsandchemicalsInfectionsHostFactorsGenesLunggrowthanddefensemechanismChronicBronchitisClinicalmanifestationCharacter:

chroniconset,recurrentattackandlongcourseofdiseaseMainsymptoms:

cough:

chronic,longterm,repeatedlyexpectoration:

mucoidsputum,purulentsputumwheninfectionwheezing:

seeninsomepatientsClinicalmanifestationSign:

1.noobvioussigninearlystage2.sometimesmoistralesandrhonchiExaminationChestx-rayimagingExaminationPulmonaryfunctiontest:

maybenormalinearlystage.Graduallyobstructiveairwayfunctionappeared.Bloodroutine:

elevatedneutrophiloreosinophilSputumexamination:

bacterialcultureguideantibiotictreatmentDiagnosisChroniccoughandsputumproductionfor3consecutivemonthsinatleast2successiveyears（3m/y2y）,excludingotherchroniclungdiseases（TB,Bronchiectasis）DefinitechestimagingorlungfunctionTypingTyping:

1、simple：

cough,sputum2、wheezing：

withwheezing（actuallyChronicbronchitisplusasthma）EmphysemaDefinitionEmphysemaischaracterizedbyenlargementanddestructionofrespiratorybronchiolesand/oralveoliinthelungs.EtiologyEnvironmentFactorsCigarettesmokingOccupationaldustsandchemicalsInfectionsHostFactorsGenes:

Alpha1-antitrypsindeficiencyContributingfactorAirwayobstructionduetochronicinflammationDamagedbronchialcartilageandleadtothelossofsupportingfunctionIncreasedactivityofproteinaseduetochronicairwayinflammationorsmokingAlpha1-antitrypsindeficiencyOthers:

PoornutritionofalveoliorrespiratorybronchioleduetodecreasedbloodsupplybecauseofoppressionofhighairwaypressureCigarettesmokeAlveolarmacrophageNeutrophilPROTEASESAlveolarwalldestruction（Emphysema）Mucushypersecretion（Chronicbronchitis）PROTEASEINHIBITORSNeutrophilchemotacticfactorsCELLULARMECHANISMSOFCOPDNeutrophilelastaseCathepsinsMatrixmetalloproteinasesCytokines（IL-8）Mediators（LTB4）?

CD8+lymphocyte-MCP-11-AntitrypsinTIMPsSLPIElafinNeutrophilelastaseCathepsinsMMP-1,MMP-9,MMP12Granzymes,perforinsOthers.PROTEASE-ANTIPROTEASEIMBALANCEINCOPDPathologyfeatureAlveolarwallsbecomethinnerAlveolarsacsenlargementRuptureofalveoliandformationofblebPathologicalCategoryPanacinar（panlobular）emphysemaGrosssectionoflung.Dilated,saccularairspaces.Incasesofdiseaseduetoa1-antitrypsindeficiency,lowerpartoflungtendstobemoreaffectedMagnifiedsection.DiffuseinvolvementofallportionsofaciniNovartisPanacinar（panlobular）emphysemaGrosssectionoflung.Dilated,saccularairspaces.Incasesofdiseaseduetoa1-antitrypsindeficiency,lowerpartoflungtendstobemoreaffectedMagnifiedsection.DiffuseinvolvementofallportionsofaciniNovartisInpanlobularemphysema,theenlargementanddestructionofairspaceinvolvetheacinusmoreorlessuniformly.Centriacinar（centrilobular）emphysemaMagnifiedsection.Distended,inter-communicating,sac-likespacesincentralareaofaciniMicroscopicsection.DistentionofairspaceswithruptureofalveolarwallsGrossspecimen.InvolvementtendstobemostmarkedinupperpartoflungNovartisCentriacinar（centrilobular）emphysemaMagnifiedsection.Distended,inter-communicating,sac-likespacesincentralareaofaciniMicroscopicsection.DistentionofairspaceswithruptureofalveolarwallsGrossspecimen.InvolvementtendstobemostmarkedinupperpartoflungNovartisIncentrilobularemphysema,respiratorybronchiolesareselectivelyanddominantlyinvolved.COPD-chronicbronchitis-emphysemaCOPDPathophysiologyHypoventialtion-PaO2,PaCO2Airflowobstruction/airwaynarrowingmucuspluggingairwayinflammation,edema,fibrosisairwaycollapseduetoalveolarwalldestructionHyperinflation:

airtrappingGasexchangedefects-PaO2Destructionofalveolarwall/alveolar-capillarymembraneV/Qmismat