内科学教学课件：Poisoning

PoisoningDefinitionthetoxicchemicalmaterialenteringhumanbodyandaccumulatingtopoisonousquantity,bringoutthewholebodydiseasewhichiscalledpoisoning.Thechemicalmaterialwhichcancausepoisoningiscalledpoison.Poisoningcanbeclassifiedacuteorchronicaccordingtothecontactingtime,doseandtoxicityClinicalManifestationAcutepoisoningSkin（burn、cyanopathy、icterus）eye（pupilenlarged、myosis,opticneuritis）Nervalsystem（coma,phrenitis、musclefiberflickering、convulsion、paralysis、anoia）Pulmonarysystem（breathingsmell、breathquickly、breathslower、lungedema）ClinicalManifestationCardiovascularsystem（arrhythmia、cardiacarrest、shock）urinarysystem（putrescenceofkidneytubule、shortofkidneyblood、jamofkidneytubule）Bloodsystemsymptoms:（anemia、bleeding、obstructionofbloodconcreting）FeverChronicpoisoningDiagnosiscontractinghistoryclinicmanifestationbodyliquidandpoisonexamTreatmentPrinciple:leavethetoxicplaceatonceurgentresuscitationandsuittheremedytothecase

eliminatethetoxinnotbeabsorbedchoosethemostusefuldetoxifyingmedicinePreventcomplicationeliminatethetoxinnotbeabsorbeda:hastenemesisb:gastriclavagec:laxationd:enemae:diuresibloodpurification:hemodialysis,hemoperfusion,plasmapheresisTreatmentOrganophosphorousInsecticidesPoisoningInhibitacetylcholineesterase,leadtoAchaccumulating,cholinergicnervecontinuedactuation,excitefirstandfaillatterly,bringonaseriesofMuscarinic,Nicotinic,CNSsymptom.Definition病因

1.Productcourse3.dailylife2.working毒物的吸收和代谢

迅速分布全身各脏器以肝浓度最高其次为肾、肺、脾肌肉和脑最少主要在肝内代谢进行生物转化主要经胃肠道、呼吸道、皮肤和黏膜吸收氧化后毒性反而增强吸收后6～12小时血中浓度达高峰通过肾由尿排泄

48小时后完全排出体外Kid-neyLiverKid-ney乙酰胆碱酯酶磷酰化胆碱酯酶有机磷杀虫药有机磷农药和胆碱酯酶结合示意图中毒机制乙酰胆碱蓄积，胆碱能受体受到持续冲动抑制乙酰胆碱酯酶的活性毒蕈碱样、烟碱样和中枢神经系统症状因昏迷和呼吸衰竭而死亡胆碱能受体各亚型在体内的分布受体名称受体亚型分布 毒蕈碱(M）型受体

M1 腺体，胃黏膜

M2心脏、中枢和外周神经元突触前膜

M3 腺体、平滑肌、脑

烟碱（N）型受体

N1（神经元型）神经节后神经元胞体上、中枢神经

N2（肌肉型）运动终板（神经肌肉接头）突触后膜1.Acutepoisoning

1)Muscarinicsymptom

2)Nicotinicsymptom

3)CNSsymptom

2.Delayedpolyneuropathy:

3.Intermediatesyndrome:suddendeathafterillomen

4.Localallergicdermatitis,conjunctivacongestion,myosisManifestationLabexamDegree

Mild:50%<Che<70%MsymptomModerate:30%<Che<50%M&NsymptomSevere:Che<30%M&NsymptomandCNSsymptomDiagnoseHistory,physicalexamandlabexamallcanproveit,especiallythechereduceDifferenttocarbamateinsecticides

TreatmentTreatmentEliminatethetoxicantquicklyDetoxifyingmedicine:1)Principleearly,ample,combined,repeated.2)Reactivatecholinesterase:relieveNsymptom.PAM-CI,PAM3)Atropine:atropinizationrelieveMandCNSsymptom,notrelieveNsymptom胆碱酯酶复能药的作用原理Treatment3.suittheremedytothecaseMaintainheatandlungfunctionPulmonaryedemashockCerebraledemaArrhythmiaAtropinedopamineDehydratingagent,glucocorticalhormoneAnti-arrhythmic2)plasmaexchange3)Graduallyreducedetoxificationdoseandstopuntilthesymptomsdisappear4)Observeatleastfor3-7daysTreatment停药及出院标准中毒症状基本消失和全血ChE活力恢复至60%以上（含60%）,可停药观察停药12～24小时,如ChE活力仍保持在60%以上,可考虑出院AcuteCarbonMonoxidePoisoningInhalantcoaccumulatetocertainconcentrateandcausehypoxia.DefinitionMechanismCOconjunctHbtoproducecarboxyhemoglobinwhichcannotcarryoxygenordegrade,andshiftO2curvetoleft.DegreeofhypoxiaisproportiontothepercentofcarboxyhemoglobininHbBrainandheartarefrailPathologyDiein24hours:bloodcolorassumecherryred,congestion,edemaandbleedingspotexistintheorgansDieinafewdays:thebraincongest,edema,necrosisanddegenerateMyocardialischemiaeveninfarction

Manifestation1.Acutepoisoning1)mild:10%<COHb<20%,obviousnervesymptom,relievequickly2)moderate:30%<COHb<40%,coma,reflexweaken,restorecompletely,withoutcomplication3)severe:40%<COHb<60%deepcoma,reflexdisappear,seriouscomplicationsoccur,highmortality,sequelaetoextentManifestation2.Latentencephalopathy:after2-60daysoffalserecovering1)symptomofnervedamage:aphrenia,delirium,decorticatingstatus2)Parkinson`ssyndrome:3)Hemiparalysis,pathologicalreflex,incontinence4)Blind,aphasia,secondaryepilepsy5)CerebralandperipheralnervedamageLabexamCOHbinbloodtestElectroencephalogramCTTreatmentLeaveaccidentplace,re