中国医科大学2014年7月考试《病理生理学》考查课试题（chinese medical university in july 2014, the exam of pathophysiology examination）

中国医科大学2014年7月考试病理生理学考查课试题（CHINESEMEDICALUNIVERSITYINJULY2014,THEEXAMOFPATHOPHYSIOLOGYEXAMINATION）CHINESEMEDICALUNIVERSITYINJULY2014,THEEXAMOFPATHOPHYSIOLOGYEXAMINATIONTOTALSCORE100TESTTIMESINGLETOPICSELECTIONSHORTANSWERQUESTIONSESSAYQUESTIONSSUBJECTIVEFILLINTHEBLANK20TESTQUESTIONS,20POINTS1THEMECHANISMOFTHEOCCURRENCEOFMULTIPLEURINEINARFPOLYURESISAGLOMERULARFILTRATIONFUNCTIONRECOVERYBNEWBORNRENALTUBULESAREIMMATURECRENALTUBULEOBSTRUCTIONALLEVIATEDDPERMEABLEDIURESISEGFRINCREASEDFULLMARK1ANSWERB2THEADVERSEEFFECTOFSYMPATHETICADRENALMEDULLARYSYSTEMSTIMULATIONONTHEBODYDURINGSTRESSASUPPRESSTHETHYROIDAXISBELEVATEDBLOODGLUCOSECPROMOTEPROTEINGLYCOSIDIOGENESISDSLOWGROWTHEGASTROINTESTINALISCHEMIAFULLMARK1ANSWERE3“WHICHOFTHEFOLLOWINGFACTORSISMOSTCLOSELYASSOCIATEDWITHTHEOCCURRENCEOFOBSTETRICACCIDENTSATHEBLOODISINAHIGHSTATEOFCOAGULATIONBMONONUCLEARPHAGOCYTICCELLSYSTEMFUNCTIONISLOWCMICROCIRCULATIONOFBLOODISSTAGNANTDINCREASEDACTIVITYOFFIBRINOLYTICSYSTEMEINCREASEDCONCENTRATIONSOFCOAGULANTSUBSTANCESINBLOODFULLMARK1ANSWERA,4THEMOSTCHARACTERISTICCHANGEINARTERIALBLOODISTHELACKOFOXYGENINTHERESPIRATORYFUNCTIONAOXYGENCAPACITYDECREASESBTHEPRESSUREOFOXYGENISREDUCEDCDECREASEDOXYGENCONTENTDDECREASEDOXYGENSATURATIONEOXYGENISMOVINGTOTHERIGHTOFTHECURVEFULLMARK1ANSWERBWHICHOFTHEFOLLOWINGISNOTTHECAUSEOFRESPIRATORYACIDOSISARESPIRATORYCENTRALPARALYSISBRESPIRATORYMUSCLEPARALYSISCAIRWAYOBSTRUCTIONDHYPOXEMIAEPNEUMOTHORAXFULLMARK1ANSWERE6THECENTEROFARFISAURINURIAOFRENALTUBULESBTUBULAROBSTRUCTIONCBLOODCLOTTINGINRENALCAPILLARIESDGFRLOWERERENALTUBULAREPITHELIALCELLNECROSISFULLMARK1ANSWERD7THESYMPATHETICADRENALMEDULLARYSYSTEMINHEMORRHAGICSHOCKAALWAYSEXCITEDBEXCITED,THENSUPPRESSED,ANDEVENTUALLYDEPLETEDCSUPPRESSEDDSUPPRESSFIRST,THENEXCITEMENTEGETEXCITED,THENSUPPRESS,ANDTHENGETEXCITEDFULLMARK1ANSWERB8THEFOLLOWINGCLINICALMANIFESTATIONSOFSHOCKAREFALSEAIRRITABILITYORLACKOFEXPRESSIONOREVENCOMABSHORTNESSOFBREATHANDRAPIDPULSECTHEBLOODPRESSUREDROPPEDDPALEORPURPLEELITTLEORNOURINEFULLMARK1ANSWERB9INACUTERESPIRATORYACIDOSIS,THEMAINCOMPENSATORYMODEOFTHEBODYISAEXTRACELLULARBUFFERBCOMPENSATIONREGULATIONOFTHELUNGSCINTRACELLULARBUFFERDBONEBUFFERERENALCOMPENSATORYREGULATIONFULLMARK1ANSWERE10HYPONATREMIAISTHELOWERCONCENTRATIONOFBLOODSODIUMATENDENCYFOR120LBTENDENCYFOR130LCTENDENCYFOR140LDTHETENDENCYFORL150ETENDENCYFOR160LFULLMARK1ANSWERBWHICHOFTHEFOLLOWINGISTHECLINICALMANIFESTATIONOFAHIGHERTEMPERATURERISEACOLDORCOLDBCONSCIOUSHEATCTHELIPSAREMOREDRYDASWEATEDEHYDRATIONFULLMARK1ANSWERC12THENORMALNEUROTRANSMITTERSOFPHENYLETHYLAMINEANDHYDROXYPHENOLAMINEINTHECHEMICALSTRUCTUREARETHENORMALNEUROTRANSMITTERSASEROTONINANDDOPAMINEBNOREPINEPHRINEANDDOPAMINECADRENALINANDNOREPINEPHRINEDACETYLCHOLINEANDPHENYLETHYLAMINEEGLUTAMICACIDANDGLUTAMINEFULLMARK1ANSWERB13MAINRESEARCHONETIOLOGYAGENERALRULESOFDISEASEOCCURRENCEBCAUSESANDCONDITIONSOFDISEASEOCCURRENCECCAUSESOFDISEASEDCONDITIONSOFDISEASEOCCURRENCEEBASICMECHANISMSFORTHEDEVELOPMENTOFDISEASEFULLMARK1ANSWERBTHEFOLLOWINGSUBSTANCESAREENDOGENOUSPYROGENATHISCHOLANOLONEBIL6CEXOTOXINDANTIGENANTIBODYCOMPLEXEENDOTOXINFULLMARK1ANSWERB15THEHYPOXIACAUSEDBYCHRONICEMPHYSEMABELONGSTOABLOODOXYGENDEPRIVATIONBHYPOXIACTOXICOXYGENDEPLETIONINTISSUESDCYCLICHYPOXIAENONEOFTHEABOVEFULLMARK1ANSWERE16WHICHOFTHEFOLLOWINGCAUSESTHEOXYGENTOMOVETOTHERIGHTOFTHECURVEA2,3DPGCONCENTRATIONINCREASEDBBLOODHDECREASEDCDECREASEDBLOODCO2PRESSUREDTHEBLOODTEMPERATUREDECREASEDEHYPOKALEMIAFULLMARK1ANSWERA,WHICHOFTHEFOLLOWINGISALSOKNOWNASHYPERTONICDEHYDRATIONAHIGHCAPACITYHYPONATREMIABLOWVOLUMEHYPERNATREMIACLOWCAPACITYHYPONATREMIADHIGHVOLUMEHYPONATREMIAEHYPERKALAEMIAFULLMARK1ANSWERE18“WHICHOFTHEFOLLOWINGISNOTACLINICALMANIFESTATIONOFTHEINADEQUACYOFCARDIACOUTPUTDURINGHEARTFAILUREASKINCYANOSISBDECREASEDURINEVOLUMECDIFFICULTYBREATHINGDCARDIOGENICSHOCKEFATIGUEFULLMARK1ANSWERC“STRESSRELATEDILLNESSESAREAPRIMARYHYPERTENSIONBSTRESSULCERSCCORONARYHEARTDISEASECHDDALBINOEPTSDFULLMARK1ANSWERD20“WHICHOFTHEFOLLOWINGISANINDICATOROFRESPIRATORYFACTORSAAGBARTERIALCO2PARTIALPRESSURECBUFFERBASEDRESIDUALALKALIESTANDARDBICARBONATEFULLMARK1ANSWERECHINESEMEDICALUNIVERSITYINJULY2014,THEEXAMOFPATHOPHYSIOLOGYEXAMINATIONTOTALSCORE100TESTTIMESINGLETOPICSELECTIONSHORTANSWERQUESTIONSESSAYQUESTIONSSUBJECTIVEFILLINTHEBLANKTHESHORTANSWERATOTALOF5QUESTIONS,20POINTS1ACUTEPHASERESPONSEASOMECHANGESINSERUMCOMPOSITIONCANOCCURINTHESHORTTIMEHOURSTODAYSAFTERTHESTRESS,SUCHASINFECTION,INFLAMMATIONANDTISSUEDAMAGE,ISUSEDINTHEBODYFULLMARKS4POINTS“ISCHEMIAREPERFUSIONINJURYANSWERTHEMAINCAUSEOFFATALDISEASES,SUCHASCORONARYARTERIOSCLEROSISRESULTINGINMYOCARDIALINFARCTION,STROKE,ETCINTHEPROCESSOFRESCUEANDTREATMENTOFISCHEMICDISEASES,DOCTORSGRADUALLYFOUNDTHATTHEMAINFACTORSTHATCAUSEDAMAGETOANORGANIZATION,NOTISCHEMIAITSELF,BUTRATHERTORESTOREBLOODSUPPLY,THEEXCESSFREERADICALSATTACKTHISPARTTOREGAINTHEBLOODSUPPLYOFCELLSWITHINTHEORGANIZATION,THISKINDOFINJURY,ISCALLED“TISSUEISCHEMIAREPERFUSIONINJURY“FULLMARKS4HEATSHOCKPROTEINATHEREISAWIDERANGEOFHOTEMERGENCYPROTEINSFROMBACTERIATOMAMMALSWHENANORGANISMISEXPOSEDTOHIGHTEMPERATURES,ITISTHEHEATTHATTRIGGERSTHESYNTHESISOFSUCHPROTEINSTOPROTECTTHEORGANISMITSELFMANYHEATSHOCKPROTEINSHAVEMOLECULARACTIVITYFULLMARKS4POINTS4RESPIRATORYACIDOSISATHECHARACTERISTICOFRESPIRATORYACIDPOISONINGISTHEDECREASEOFCO2ACCUMULATIONANDPHINTHEBODYTHEMAINREASONISTHEDECREASEOFAIRVENTILATIONFUNCTIONINTHELUNGITCANBESEENINRESPIRATORYOBSTRUCTION,PNEUMONIA,ATELECTASIS,THORACICABDOMINALSURGERY,TRAUMA,ETCTHEBASICMETHODOFTREATMENTISTOREMOVETHEOBSTRUCTIONOFTHERESPIRATORYTRACTANDIMPROVETHEVENTILATIONFUNCTIONFULLMARKS4POINTS5LABORINGBREATHINGDIFFICULTIESAPATIENTSWITHMILDHEARTFAILUREHAVEDIFFICULTYBREATHINGDURINGPHYSICALACTIVITYANDDISAPPEARAFTERRESTFULLMARKS4POINTSCHINESEMEDICALUNIVERSITYINJULY2014,THEEXAMOFPATHOPHYSIOLOGYEXAMINATIONTOTALSCORE100TESTTIMESINGLETOPICSELECTIONSHORTANSWERQUESTIONSESSAYQUESTIONSSUBJECTIVEFILLINTHEBLANK5QUESTIONS,50POINTS1BRIEFLYDESCRIBETHEMECHANISMOFTHESTRESSULCERAAGASTRICMUCOSAISCHEMIATHISISTHEMOSTBASICCONDITIONOFSTRESSULCERFORMATIONDUETOTHEINCREASEOFCATECHOLAMINEINSTRESS,THEBLOODFLOWDECREASEDANDTHEINTESTINALMUCOSAISCHEMIA,ANDTHEDEGREEOFISCHEMIAOFTHEMUCOSAWASPOSITIVELYCORRELATEDWITHTHEDEGREEOFLESIONMUCOSAISCHEMIAMAKEEPITHELIALCELLENERGYISINSUFFICIENT,DOESNOTPRODUCEENOUGHBICARBONATEANDMUCUS,MADEBYTHECLOSECONNECTIONBETWEENMUCOSALEPITHELIALCELLSANDBICARBONATECOVEREDPARTSOFTHEMUCOSALSURFACEMUCOUSLAYERMEDICALEDUCATIONNETCOLLECTIONOFDAMAGEOFGASTRICMUCOSA,GASTRICCAVITYOFHSUITABLECONCENTRATIONDIFFERENCEINTOTHEMUCOUSMEMBRANE,ANDTHEDECREASEOFMUCOSALBLOODFLOWCANTINVADETHEMUCOUSMEMBRANEOFHAWAYINTIME,THEACCUMULATIONOFHINTHEMUCOSACAUSESDAMAGETHEREVERSEDISPERSIONOFHINTHESTOMACHCAVITYISTHENECESSARYCONDITIONFORTHEFORMATIONOFASTRESSULCERTHEHIGHERTHEHCONCENTRATIONINTHESTOMACHCAVITY,THEMOREOFTENTHEMUCOUSMUCOUSLESION,IFTHEPHINTHESTOMACHCAVITYISABOVE35,DOESNOTFORMASTRESSULCERATPRESENT,THEDECREASEOFPHINTHEMUCOSAMAINLYDEPENDSONTHERATIOOFHTOMUCOSALDISPERSIONINTHESTOMACHCAVITYANDTHEBLOODFLOWOFTHEMUCOSAINGASTRICMUCOSALBLOODFLOWPERFUSIONGOODCASES,REVERSEDIFFUSIONTOEXCESSHCANBEINSIDEMUCOSALBLOODFLOWOFHCO3AND/ORBECARRYAWAY,THUSPREVENTINGTHEHDAMAGETOCELLS,ONTHECONTRARY,INTRAUMA,SHOCKANDSTRESSSTATE,GASTRICMUCOSALBLOODFLOWDECREASED,EVENREVERSEDIFFUSIONTOTHEMUCOUSMEMBRANEINTHEAMOUNTOFHINTHEFEW,ALSOWILLMAKETHEMUCOUSMEMBRANEINPHDECREASESSIGNIFICANTLY,LEADINGTOCELLDAMAGECOTHERSECONDARYFACTORSMAYALSOBEINVOLVEDINTHEPATHOGENESISOFSTRESSULCERSINACIDPOISONING,THEBLOODFLOWTOTHEMUCOSALHHASLOWBUFFERABILITY,WHICHCANPROMOTETHEOCCURRENCEOFSTRESSULCERTHEGASTRICMUCOSALISCHEMIAOFTHEBILEREFLUXCANDAMAGETHEBARRIERFUNCTIONOFTHEMUCOSAANDINCREASETHEPERMEABILITYOFTHEMUCOSAIFTHEREISNOBLEEDINGORPERFORATIONOFTHESTRESSULCER,AFTERTHEPRIMARYDISEASEHASBEENCONTROLLED,ITUSUALLYHEALEDCOMPLETELYWITHINAFEWDAYSWITHOUTLEAVINGANYSCARFULLSCORE10POINTS2THEMECHANISMOFRENALANEMIAA“WHENSTARTDAMAGEDRENALFUNCTION,CHRONICKIDNEYDISEASEPATIENTISPRODUCEDBYTHEKIDNEYSECRETIONOFERYTHROPOIETINTOTALAMOUNTWILLNOTBEENOUGHTOMEETTHENEEDSOFTHEBODY,ANDBECOMEONEOFTHEMOSTMAINREASONTOCAUSERENALANEMIAINADDITION,CHRONICRENALINSUFFICIENCYANDUREMIAPATIENTS,PILINGUPINSIDETHEBODYTOMETABOLIZETHETOXINS,REDUCEDSURVIVALTIMEOFREDBLOODCELLSIRONINTAKEREDUCEDANDIRONLOSSINCREASE,REDBLOODCELLSYNTHESISLONGTERMCHRONICKIDNEYDISEASEPATIENTSTOCONTROLTHEINTAKEOFPROTEIN,ANDURINARYPROTEINISFLOWINGFROMTHEPATIENTLOSSCHRONICKIDNEYDISEASEPATIENTSOCCURREDMOREBLEEDINGTENDENCYTHESECONDITIONSARELIKELYTOLEADTOCHRONICKIDNEYDISEASEPATIENTSINRENALANEMIAFULLSCORE10POINTS3DESCRIBETHEBLEEDINGMECHANISMOFDICPATIENTSATHECONSUMPTIONOFCOAGULANTSUBSTANCESINDICDEVELOPMENTPROCESS,AVARIETYOFBLOODCOAGULATIONFACTORSANDPLATELETSMASSCONSUMPTION,ESPECIALLYFIBRINOGEN,PROTHROMBINFACTOR,GENERALLYREDUCEPLATELETTHEREFORE,SOMEPEOPLEHAVEREFERREDTODICASCONSUMPTIVECOAGULOPATHYATTHISTIMETHECLOTTINGPROCESSISHAMPEREDBYALARGEREDUCTIONINCOAGULATION2ACTIVATIONOFFIBRINOLYTICSYSTEMDICISACTIVATEDBYCOAGULATIONSYSTEMANDISOFTENACTIVATEDBYSECONDARYFIBRINOLYTICSYSTEMTHISISMAINLYBECAUSEINTHEPROCESSOFCOAGULATION,THROUGHENZYMATICACTIVATIONPROTEASEEFFECTCAUSEDBYENZYMATICHYDROLYSISFORMEDBYAF,FTHEKALLIKREININTOKALLIKREIN,WHICHMAKETHEFIBRINOLYTICENZYMEINTOAFIBRINOLYTICENZYMESOMEORGANSCONTAININGPLASMINOGENACTIVATORSSUCHASTHEUTERUS,PROSTATE,LUNGS,ETCACTIVATETHEFIBRINOLYTICSYSTEMBYRELEASINGBLOODINTOTHEBLOODWHENTHEBLOODISDEGENERATIVETHEENDOTHELIALCELLSAREDAMAGED,HYPOXIA,STRESS,ETC,ANDTHEYALSOACTIVATETHEFIBRINOLYTICSYSTEM,WHICHLEADSTOTHEINCREASEOFFIBRINOLYSINFIBRINOLYTICENZYMEEXCEPTCANMAKEFIBRINDEGRADATIONORIGINAL,STILLCANHYDROLYSISCLOTTINGFACTORS,ANDTHROMBINORIGINAL,ETC,SOTHEFURTHERREDUCECLOTTINGFACTORS,THATCAUSECLOTTINGDISORDERSANDHEMORRHAGEFULLSCORE10POINTS4ATHISPERIODOFMICROCIRCULATIONBLOODRHEOLOGYHASCERTAINLYCHANGEDTHEBLOODFLOWVELOCITYSLOWEDSIGNIFICANTLY,REDBLOODCELLANDPLATELETAGGREGATION,LEUKOCYTEROLLING,STICKAWALL,EMBEDDEDPLUG,INCREASEDBLOODVISCOSITY,BLOOD“MUD“SLUDGECLOGGED,MICROCIRCULATIONBLOOD,TISSUEPERFUSIONFLOWFURTHERREDUCE,OXYGENISMORESERIOUSTHISISBECAUSEAFTERENTERINGTHIS,DISAPPEARENTRAILSMICROCIRCULATIONBLOODVESSELSINTHEEXERCISESELFDISCIPLINE,MICROARTERIES,THEARTERIESANDCAPILLARIESFIRSTMUSCLECON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