病理生理学重点名词解释与简答题

病理生理学重点名词解释与简答题First,thenounexplanationThebasicpathologicalprocess:mainlyreferstoavarietyofdiseasesmayoccur,common,completesetsoffunctions,metabolismandstructuralchanges.Health:healthmeansnotonlysicknessorillness,butalsoacomplete,physical,mental,andsocialstateofbeing.Disease:diseaseisundercertainconditionscausedbythecauseofdamage,duetothebodysselfregulatorydisorderandtheoccurrenceofabnormallifeprocess.Etiology:acauseofdiseasethatischaracteristicofthediseaseandisknownasthecauseofthedisease.Incentives:factorsthatcontributetothedevelopmentofdiseasearecalledtriggers.Braindeath(braindeath):thepermanentcessationofthefunctionoftheorganismasawholeisapermanentlossofthefunctionofthebrain.Atpresent,thestandardofbraindeathabovetheforamenmagnumisgenerallyused.Hypotonicdehydration:alsocalledhyponatremiaoflowvolume,characterizedbylosingNa+morethandehydration,serumNa+concentration130mmol/L,plasmaosmoticpressure150mmol/L,plasmaosmolality,310mmol/L,extracellularfluidvolumeandextracellularfluidvolumearereduced.Waterintoxication:highsolubilityhyponatremia,characterizedbydecreasedserumsodium,serumNa+concentration,130mmol/L,plasmaosmoticpressure280mmol/L,butthetotalbodysodiumisnormalorincreased,thepatienthaswaterretention,sothatthevolumeoffluidincreasessignificantly.Dehydrationfever:becauseofthedecreaseofwaterfromtheskin,theheatisaffected,leadingtoelevatedbodytemperature,calleddehydrationfever.Edema:excessivefluidthatiscallededemaintheinterstitialspaceorinsidethebodycavity.Hyperkalemia:serumpotassiumlevelsarehigherthan5.5mmol/LHypokalemia:serumpotassiumlevelsbelow3.5mmol/L.Disturbanceofacid-basebalance:theexcessiveacidbaseoverload,seriousdeficiencyorregulatorydisturbancecausedbypathologicalconditionsleadtothePHabnormalconditioncausedbythedestructionofacid-basehomeostasisintheenvironment.Metabolicacidosis:atypeofacid-basedisturbancecharacterizedbyanincreaseinextracellularfluidH+oraprimarydecreaseinHC03-andadecreaseinPH.Respiratoryacidosis:aC02disorderorexcessiveintakecausesadisturbanceofacid-basebalancecharacterizedbyaprimaryincreaseinplasmaH2CO3andadecreaseinPH.Metabolicacidosis:extracellularliquidincreaseorlossofH+,HCO3-inplasmaincreasedandPHincreasedprimaryacid-basedisorderscharacterizedbytype.Respiratoryalkalosis:atypeofacid-basedisturbancecharacterizedbyhyperventilationofthelungsandprimarydecreaseinplasmaH2CO3andelevatedPH.Mixedacid-basedisturbance:therearetwoorthreesimpletypesofacid-basedisturbancesinthesamepatient.Hypoxia(hypoxia):pathologicalchangesincellularmetabolism,function,andmorphologicalstructureresultingfromreducedoxygensupplyorimpairedoxygenuse.Cyanosis(cyanosis):whentheuniformconcentrationofdeoxygenatedhemoglobininthebloodcapillaryofmorethan5g/dl,theskinandmucousmembraneswerepurple.Typefour:hypoxiaandhypoxichypoxia,bloodtype,hypoxiacirculatoryhypoxia,hypoxia.Enterogenouscyanosis:methemoglobinemiaduetoeatingleadstoalargenumberofhemoglobinoxidationcausedby.Shock:thiswordbyShock,andEnglishshock,variousstrongriskfactorsactingonthebody,thecirculationdecreaseddramatically,tissueandorganperfusionofmicrocirculationisseriouslyinsufficient,andsystemiccriticalpathologicalprocessofvitalorgansfunction,metabolicdisorderserious.MODS(multipleorgandysfunctionsyndrome):referstotheseveretrauma,infection,shock,theoriginalorgandysfunctionofpatientsatthesametimeorwithinashortperiodoftimehaveappearedmorethantwoorgansystemdysfunctionthathomoiostasismustrelyonclinicalinterventiontomaintainsyndrome.Systemicinflammatoryresponse(SIRS):duetoinfectionornoninfectioncauseseffectsonthebodycausedbyuncontrolledselfsustainedamplificationandsystemicinflammatoryresponsesyndromeselfdestruction.Compensatoryanti-inflammatoryresponsesyndrome(CARS):referstoinfectionortraumacancausethebodytoproduceimmunefunctiondecreasingandincreasingendogenousanti-inflammatoryreactionistoostrongonsusceptibilitytoinfection.DIC(disseminatedintravascularbleeding):aroleinthepathogenicfactor,thecoagulationsystemwasactivatedandinducedbymicrothrombosis,orsecondaryfibrinolysis,resultinginbleeding,shock,organdysfunctionandmicroangiopathichemolyticanemiainapathologicalprocess.FDPfibrindegradationproducts:allkindsoffragmentsproducedbyFbnandFbgenzymehydrolysis.Schistocyte:redcelldeformationofaspecialshape,calledschistocyte,shape,star,moonshapedhelmet,referredtoastheredcelldebris.Thedebrisisfragile,pronetohemolysis.Heartfailure:variouscausesofheartpumpdysfunction,cardiacoutputortoreducerelatively,apathologicalprocesscannotmeetthemetabolicneedsoftheorganization.Myocardialstrain(muscle)sourceexpansion:Thesourceofexpansion:reducethemyocardialtensionduetostrokevolume,theventricularenddiastolicvolumeincreased,preloadledtotheincreaseoftheinitiallengthofthemusclefibersincreased,thenenhancemyocardialcontractility,metabolismincreasesstrokevolume,heartcavityenhancedmyocardialcontractilitywiththisexpansioncalledheartsourceexpansion.Myogenicexpansion:long-termvolumeoverloadandheartfailurecausedbydilatedcardiomyopathy,mainlycausedbyexcessivesarcomerestretch,theheartcavityenlargement,heartcavitywiththeexcessivestretchanddecreasedmyocardialcontractilitywithexpansioncalledmyogenicexpansion.Respiratoryfailure:duetorespiratorydysfunction,thearterialoxygenpressureislowerthanthenormalrange,thepathologicalprocesswithorwithoutcarbondioxidepartialpressure.Restrictivehypoventilation:duringtheexpansionofthealveolibyalveolarventilationcausedbythelackofrestrictions.Obstructivehypoventilationduetoairwayobstructioncausedbyairwaystenosisorobstruction.Functionalshunt:partofalveolarventilationlesionssignificantlyreducedbloodflowandweight,notless,evenbecauseofinflammatoryhyperemiatoincreasebloodflow(suchaslobarpneumoniaearly),Theratioofalveolarminuteventilationandpulmonarybloodflowperminutewassignificantlyreduced,sothatthevenousbloodflowsthroughthealveolarpartwithoutadequatearterialandincorporationofarterialblood,thesimilararteriovenousshortcircuit,calledfunctionalshunt,alsoknownasblooddoping.Deadspaceventilation:somecauseeffect,canmakesomealveolarreducedbloodflow,VA/Qsignificantlyincreased,bloodflowandlessaffectedpartofalveolarventilationandalveolarventilationcannotbefullyutilized,adeadspacelikeventilation.Pulmonaryencephalopathyduetorespiratoryfailurecausedbybraindysfunction,patientscanbeexpressedasaseriesofneuropsychiatricsymptomssuchasorientation,memoryimpairment,mentaldisorder,headache,drowsiness,coma,etc.ARDS(acuterespiratorydistresssyndrome):respiratorydysfunctioncausedbyalveolarcapillarymembraneinjurycausedbyvariousreasonsandtheoccurrenceofacuterespiratoryfailuresyndromeclinicalcharacteristics,ischaracterizedbyprogressivedyspneaandhypoxemia.Hepaticencephalopathy:referstoneuropsychiatricsyndromesecondarytosevereliverdiseases.Falseneurotransmitter:phenylethanolamineandoctopamineinchemicalstructureandnormalneurotransmitternorepinephrineanddopaminearesimilar,butcannotcompletetheauthenticityofneurotransmitterfunction,knownasfalseneurotransmitter.Hepatorenalsyndrome:referstoacuterenaltubularnecrosisincirrhoticpatientswithdecompensationoccurredinfunctionalrenalfailureandseverehepatitis.AcuterenalfailureduetoGFRdecreasedrapidly,orrenaltubulardegenerationandnecrosisinapathologicalprocesscausedbyacutesevere,oftenoliguria,azotemia,hyperkalemia,metabolicacidosisandwaterintoxicationsyndrome.Chronicrenalfailure:Anydiseaseofrenalunitdestruction,inthemonthsandyearsorlongeraftertheremainingnephroncannotfullyremovemetabolicwasteandenvironment,thustomaintaintheconstantinthegradualemergenceofmetabolicwasteretentionandwaterelectrolyteandacid-basebalancedisordersandrenalendocrinedysfunction.Azotemia:bloodcreatinine,uremia,uricacidandothernonproteinnitrogen(NPN)contentincreasedsignificantly,calledazotemia(azotemia).NormalhumanbloodNPNis2535mg%,theureanitrogenis10-15mg%.Renalhypertension:hypertensioncausedbyrenalparenchymaldiseasecalledrenalhypertension.Uremia:referstoacuteorchronicrenalfailuretoseverestage,metabolitesandtoxinsaccumulateinthebody,water,electrolyteandacid-basebalancedisordersandsomeendocrinedisorderscausedbyaseriesofsystemicfunctionandmetabolicdisordersyndrome.Two,shortanswerquestionsThe1.diagnosticcriteriaforbraindeathAccordingtothedeterminationofbraindeathistheirreversiblecomaandbrainresponse:second,stopbreathingfor15minutes,artificialrespirationstillnospontaneousbreathing:thecranialnervereflex:thepupilorfixed:thebrainwavesdisappeared:thecompletecessationofcerebralbloodcirculation(cerebralangiography).2.whattypeofdehydrationcausedbythelossoffluidshock?Why?Hypovolemichyponatremia(lowpermeabilityglue)iseasytocausethelossoffluidshock.(1)theextracellularfluidBianthroughthepressuredrop,nothirst,Waterreducing.(2)theextracellularfluidBianthroughpressurereduction,ADHreflexsecretiondecreased,nosignificantdecreaseinurinevolume.(3)extracellulartointracellularfluidtransfer,furtherreducetheextracellularfluid.Theeffectonthebodyof3.waterintoxication.Theextracellularfluidbecauseoftoomuchwateranddiluted,theserumsodiumconcentrationdecreased,theosmoticpressuredrop.Inadditiontothekidneycannotbetoomuchwatertobedischarged,thewaterisrelativelyhighosmoticpressureinsidethecelltransfercausedbycelledema,thevolumeofintracellularfluidandextracellularfluidwereincreasedandtheosmoticpressuredecreased.Becausethecellliquidcapacitygreaterthantheextracellularfluidretentioncapacity,somostofthemoistureaccumulationinthecells,thereforeinmildwaterintoxication,interstitialwaterretentiondegreeisstillnotenoughtocauserecessiveedemaoftheconcave.Acutewaterintoxication,thenervecellsinthebrainedemaandintracranialpressure,thecerebralsymptomsappearedearliestandprominent,canoccurinvariousneuropsychiatricsymptoms,suchasgaze,aphasia,confusion,lethargy,irritabilityandotherdirectionalarrhythmia,andpapilloedema,severecasescanoccurduetocerebralherniacausedbyrespiratoryandcardiacarrestpatientswithmild,chronicorwaterpoisoningisslow,symptomsareoftennotobvious,manycoveredbythesymptomsandsignsofprimarydisease,canhavedrowsiness,headache,nausea,vomiting,musclespasmsandpainsymptomssuchasweakandfeeble.4. theendovascularliquidexchangeimbalancesedemamechanism.Drivingforceofliquidfilteroutwardintravascularhydrostaticpressureistheaverageeffective,promptingliquidflowsbacktothecapillaryforceiseffectivecolloidosmoticpressure,undernormalcircumstances,thetissuefluidisslightlylargerthanthereturngenerated.Lymphatictissuefluid,theremainingpartofthelymphaticsystemsubjecttorefluxrefluxintothebloodcirculation,normaladultsinaquietstateabout120mlhoursenzymeliquidthroughthelymphaticsystemintothebloodcirculation.Interstitialhydrostaticpressure,acceleratetheformationrateoflymphnode.Inadditionthelymphaticwallpermeabilityhighprotein,easytopass.Therefore,notonlycanbelymphatictissuefluidgeneratedslightlymorebacktothebodycirculation,andcanreducecapillaryleakageofproteinmacromolecules,cellmetabolismwillbeabsorbedintothesystemiccirculation.Theoneormorefactorssimultaneouslyorsuccessivelydisorders,maybecomeanimportantreasonfortheoccurreneeofedema.5. hypokalemiaandhyperkalemiacancausemuscleparalysisanditsmechanism?Hypokalemiaismainlyduetohyperpolarizationarrest.TheratioofK+/K+etheincreaseofhypokalemia,andmusclecellnegativerestingpotential,therestingpotentialandthresholdpotentialintervalincreases,cellexcitabilityanddecreased,evennotseriouswhenexcited,i.e.cellsinthehyperpolarizedstateblock.Hyperkalemiaduetotherestingpotentialofskeletalmuscleistoosmall,sothefastsodiumchannelinactivation,extracellularpolarizationtoblockandcannotbeexcited.6. severevomitingcausedbythedisturbaneeofacid-basebalanee?Theanalysisofitsmechanism.Severevomitingcanleadtometabolicalkalosismechanism:H+lostthegastricjuice,thedigestivetractofHCO3-H+isnotneutralizedandabsorbedintotheblood;thelossofClingastricjuice,cancausehypochloremicalkalisis:K+lostthegastricjuice,cancausehypokalemicalkalosis:thelosscausedbyalargeamountofgastricjuice,effectivecirculatingbloodvolumereduction,Secondaryaldosteronismcausedbymetabolicalkalosis.7. oliguriaofacuterenalfailurecanoccurandwhattypeofacid-basedisorders?Why?Theindexofacid-basebalaneewillbechanged?Canoccurbecauseofmetabolicacidosis,renalfunctionandacidalkali,insevererenalfailure,cannotbefixedinacidbyurinaryexcretion,especiallysulfuricacidandphosphoricacidaccumulationinthebody,resultingintheincreaseofH+concentrationHCO3-concentrationdecreased,duetoreducedHCO3-,soAB,SBandBBsignificantlydecreased.NegativeBEincreased,PHdecreasedbyPaco2secondaryrespiratorycompensation,downABvSB.8. hemorrhagicshockcausedbyhypoxiawhichtype.Hemorrhagicshock,duetoalargenumberofbloodlossandtissuecausedbylackofblood,tissueoxygendeficiency,cancausecirculatoryhypoxia.9. pulmonaryedemacancausehypoxiawhatkindof?Themechanismofhypoxia?Cancausehypoxichypoxia,duetopulmonaryedema,ventilationfunctionoffertilizerlimitedcausedbyalveolarP02decreased,pulmonaryventilationdysfunctionbyalveolardiffuseintothebloodoxygenreduction,Pa02andlackofoxygen,causedbyhypoxichypoxia.Mechanismanalysisof10.chronichypoxiaerythrocytosis.WhenthenumberofredbloodcellsinchronichypoxiaismainlyduetotheincreaseinrenalproductionandreleaseoferythropoietinEPO;hypoxiacanincreasetheactivityofHIF-1incytoplasm,HIF-1geneandEPO3enhancerbinding,enhancedtheexpressionofEPOgene,theEPOincreased,themolecularweightofEPOwas34000oftheeggwhitesugar,canpromotestemcelltheoriginalredbloodcelldifferentiation,andpromotethedifferentiation,proliferationandmaturation,acceleratethesynthesisofhemoglobin,thebonemarrowreticulocyteandredbloodcellsreleasedintotheblood.Themechanismofthe11.earlyontheplateauofthepeopleoftheshortnessofbreath.Highaltitudethinair,lowoxygencontent,atthebeginningoftheplateau,duetohypoxia,causedbyPA02islowerthan60mmHgandstimulationofthecarotidandaorticbodiesofperipheralchemoreceptorafferentmedullaaftersinusimpulse,andvagusnervereflexinducedbydyspnea.Signlevel12.arterialbloodpressurecanbeusedtojudgetheshock?Why?No,becausetheshockearlysympathoadrenomedullaryexcitement,heartrate,contractilityincreased,bloodtransfusionandinfusionthroughtheirown,aswellasincreasedrenalreabsorptionofsodiumandwater,increasetheturnoutput,sothattheincreasedcardiacoutput,plustheperipheralresistanceincreased,sothebloodpressurewasnotobvious.13.makethenarrationofmicrocirculationchangesofearlyshockcharacteristicsandsignificanceofcompensation.Istheearlystageofshockshockcompensatory,thesympatheticnervousexcitement,increasedcatecholamine,someorgansofsmallvascularcontractionorspasm,especiallymicroartery,afterarteriolesandprecapillarysphinctercontraction,theprecapillaryresistanceincreased,capillaryclosure,truecapillarynetworkreducedbloodflow,bloodflowslowsdown;betaadrenergicreceptorthestimulatedarteriovenousanastomosesareopen,bloodthroughthedirectpathwayandopenthearteriovenousanastomosisreflux,microcirculationofnonnutritivebloodflowincrease,reducenutrientflow,severehypoxicischemictissue.Ontheonehand,changesinthemicrocirculationofskincausedbyabdominalvisceralandkidneyischemiaorhypoxia,ontheotherhand,ithasacertainsignificancetotheoverallcompensation.Themainperformanceis:bloodredistribution,autologousbloodtransfusion,thetransfusion.Mechanismofchangesofmicrocirculationduringshock14.II.Themechanismofchangeanddevelopmentofshockmicrocirculationduringlongtimemicrovascularcontractionandischemia,hypoxia,acidosisandvarioushumoralfactors.Theacidpoisoning:tissueoxygenpartialpressuredropcausedbyhypoxia,C02andaccumulationoflacticacidandacidpoisoning.Acidpoisoningcausesvascularsmoothmusclereactivitytocatecholaminesdecreasedmicrovasculardiastolic.Thelocalvasodilatormetabolitesincreased:long-termischemiaandhypoxia,acidosisstimulatesthereleaseofhistaminefrommastcellsincreased,ATPdecompositionproductsofadenosineaccumulation,kininsgenerationincreases,cancausevascularsmoothmusclerelaxationandtelangiectasia.Thechangesofbloodrheology:shockprogressionbloodflowdecreasedobviously,microslowbloodflowinerythrocyteaggregationandeasy:theeffectofhistamineoncapillarypermeability,plasmaextravasation,bloodviscosityincreased;perfusionpressuredecreased,resultinginleukocyterolling,adhesionandadhesiontoendothelialcells,bloodblockedpostcapillaryresistanceincreased.Theeffectofendotoxincausedbyvascularsmoothmusclerelaxation,leadingtopersistenthypotension.Whatisthe15.mostcommonmultipleorgandysfunctionintheetiologyofMODS?Itspathogenesis?80%oftheMODSpatientsintothehospitalhaveobviousshock.Infectiouscauses,suchassepsisandsevereinfection,about70%MODScanbecausedbyinfection,especiallyseriousinfectioncausedbysepsis.Noninfectiousetiologysuchassurgeryandtrauma,surgeryandtrauma,noinfectioncanoccurinpureMODS.Thepathogenesisofuncontrolledsystemicinflammatoryresponse.Theproinflammatoryandanti-inflammatorymediumbalancedisorders.Theotherfactorsleadtoorgandysfunction:organmicrocirculationperfusion,highmetabolism,ischemiareperfusioninjury.Whatisthemechanismof16.DIG.Tissuefactor,coagulation,activatedcoagulationsystem;vascularendothelialcellinjury,anticoagulationcontroldisorders:thedestructionofalargenumberofbloodcellsbyactivatedplateletprocoagulantsubstancesintotheblood.Whatisthemechanismof17.DIGcausedashock?Becauseofthenumerousmicrovascularthrombus,obstructionofmicrocirculation,sothatbloodvolumedecreasedsignificantly.Theextensivehemorrhagebloodvolumecanbereduced.Theinvolvementofmyocardialinjury,decreaseincardiacoutput.TheactivationofthecoagulationfactorXII,canhaveactivationofthekininsystem,complementsystemandfibrinolyticsystem,producesomevasoactivesubstances,suchasbradykinin,complementcomponent.Complementthebasophilsandmastcellstoreleasehistamine,bradykinin,histaminecaninducevascularsmoothmusclerelaxation,increasedpermeability,theperipheralresistaneedecreased,thereductionofthereturnedbloodvolume.SomecomponentsoftheFDPcanenhancetheeffectofhistamine,bradykinin,promotemicrovascularexpansion.18. testthecompensatoryresponsetoheartheartfailure.Theheartrate,cardiacstressofexpansionandenhancescardiaccontractilityandventricularremodelingcardiacinsufficiencyafterthetypeofcompensatorycardiachypertrophyanditsmechanism,sarcomerereplication.Cardiachypertrophycanbecausedbyavarietyofreasons.Whenpartofmyocardialcellloss,Theresidualmyocardialhypertrophyreactioncanoccur:Iong-termoverloadcancauseoverloadmyocardialhypertrophy,overloadandcardiacresponseinaccordaneewithdifferentformscanbedividedintooverloadcardiachypertrophy:concentrichypertrophy,cardiacfunctioninIong-termexcessiveloadpressure,systolicwalltensionincreasemyocardialsarcomereaparalleltypehyperplasia,thickeningofmyocardialcells.Eccentrichypertrophy,heartintheIong-termexcessiveloadcapacity,diastolicwalltensionincreasemyocardialsarcomerewasserieshyperplasia,myocardialcellgrowth,ventricularvolumeincreases:whiletheheartenlargementandsystolicwallstressincreases,andthusstimulatetheproliferationofsarcomereparallel.19. brieflydescribethemechanismandsignificaneeofheartratereductionduringheartfailure.Themechanismofheartrateis:duetodecreasedcardiacoutput,heartratecausedbytheintracardiacresidualbloodvolumeisincreased;reducetheheartpumpblood,ventricularenddiastolicvolumeandpressure,canstimulatetherightatriumandvenacavavolumereceptor,viavagalafferentfibersinthevagusnervetopivot,inhibition,sympatheticstimulation.Ifthecombinedhypoxiacanstimulatetheaorticbodyandcarotidbodychemoreceptor,reflexexcitabilitycausesheartratetoaccelerate.Significanee:cardiacoutputistheproductofstrokevolumeandheartrate,inacertainrange,canimprovetheheartrate,cardiacoutput,andcanimprovethediastolicbloodpressure,bloodperfusiontothecoronaryartery,tomaintainarterialbloodpressure,whichisofpositivesignificancetothebloodsupplytovitalorgans.20. whatisthemechanismofdyspneacausedbyheartfailure?Whattypesofdyspneadoyouhave?Mechanism:lungcongestionandpulmonaryedemaleadtolowerlungcompliance.Tobreathethesameamountofair,itisnecessarytoincreasetheworkdonebytherespiratorymuscleandconsumemoreenergy,sothepatientfee