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

中国医科大学2014年7月考试病理生理学考查课试题（CHINAMEDICALUNIVERSITYJULY2014EXAMPATHOPHYSIOLOGYEXAMINATIONQUESTIONS）CHINAMEDICALUNIVERSITYJULY2014EXAM“PATHOPHYSIOLOGY“EXAMINATIONQUESTIONSTOTALSCORE100TESTTIMERADIOEXAMINATIONSHORTANSWERQUESTIONSEXPOSITIONSUBJECTIVECLOZETESTRADIOEXAMINATIONQUESTIONS20QUESTIONS,20POINTSINTHE1ARFPOLYURIASTAGE,THEMECHANISMOFPOLYURIAISAGLOMERULARFILTRATIONFUNCTIONRECOVERYBRENALTUBULARIMMATUREFUNCTIONCRENALTUBULEOBSTRUCTIONISALLEVIATEDDOSMOTICDIURESISEGFRADDEDFULLMARKS1ANSWERB2,WHENSTRESSOCCURS,THESYMPATHETICADRENALSYSTEMHASANADVERSEEFFECTONTHEORGANISMASUPPRESSESTHYROIDAXISBRAISESBLOODSUGARCPROMOTESPROTEINGLUCONEOGENESISDGROWSSLOWLYEGASTROINTESTINALISCHEMIAFULLMARKS1ANSWERE3WHICHOFTHEFOLLOWINGFACTORSISMOSTLIKELYTOBETHEMOSTCLOSELYRELATEDTODICINOBSTETRICACCIDENTSATHEBLOODISINHYPERCOAGULABLESTATEBMONONUCLEARPHAGOCYTESYSTEMISLOWFUNCTIONINGCMICROCIRCULATIONANDBLOODSTASISDFIBRINOLYTICSYSTEMINCREASEDACTIVITYEINCREASEDLEVELSOFPROCOAGULANTSUBSTANCESINBLOODFULLMARKS1ANSWERA4THEMOSTCHARACTERISTICCHANGESINARTERIALBLOODAREHYPOXIA,WHICHOCCURSWHENRESPIRATORYINSUFFICIENCYOCCURSAOXYGENCAPACITYDECREASEDBOXYGENPARTIALPRESSUREDECREASECOXYGENCONTENTDECREASEDDOXYGENDESATURATIONEOXYGENSHIFTCURVERIGHTSHIFTFULLMARKS1ANSWERB5WHICHOFTHEFOLLOWINGISNOTTHECAUSEOFRESPIRATORYACIDOSISARESPIRATORYPARALYSISBRESPIRATORYMUSCLEPARALYSISCAIRWAYOBSTRUCTIONDHYPOXEMIAEPNEUMOTHORAXFULLMARKS1ANSWERETHECENTRALLINKOFTHE6ARFISARENALTUBULEREGURGITATIONBRENALTUBULEOBSTRUCTIONCCAPILLARYCOAGULATIONINTHEKIDNEYDGFRDOWNENECROSISOFRENALTUBULAREPITHELIALCELLSFULLMARKS1ANSWERD7WHENHEMORRHAGICSHOCKOCCURS,THESYMPATHETICADRENALMEDULLASYSTEMISINPLACEAHASBEENVERYEXCITEDBGETSEXCITEDFIRST,THENSUPPRESSES,ANDFINALLYFAILSCHASBEENINHIBITINGDINHIBITSFIRSTANDTHENGETSEXCITEDEGETSEXCITEDFIRST,THENSUPPRESSES,ANDTHENGETSEXCITEDFULLMARKS1ANSWERB8WHICHOFTHEFOLLOWINGCLINICALMANIFESTATIONSOFSHOCKISWRONGAIRRITABILITYORINDIFFERENCEOREVENCOMABHASSHORTNESSOFBREATHANDRAPIDPULSECBLOODPRESSUREDROPSDPALEORCYANOTICEOLIGURIAORABSENCEFULLMARKS1ANSWERB9WHENACUTERESPIRATORYACIDOSISOCCURS,THEMAINMODEOFCOMPENSATIONISAEXTRACELLULARBUFFERINGCOMPENSATORYREGULATIONOFBLUNGCINTRACELLULARBUFFERINGDSKELETALBUFFERCOMPENSATORYREGULATIONOFEKIDNEYFULLMARKS1ANSWERE10HYPONATREMIAMEANSLOWERBLOODSODIUMCONCENTRATIONA120MMOL/LB130MMOL/LC140MMOL/LD150MMOL/LE160MMOL/LFULLMARKS1ANSWERB11WHICHOFTHEFOLLOWINGISTHECLINICALMANIFESTATIONOFTHERISEINBODYTEMPERATUREACOLDORCOLDBCONSCIOUSLYHOTCLIPSAREDRYDKHANEDEHYDRATIONFULLMARKS1ANSWERC“12ISASTRUCTURALLYSIMILARNEUROTRANSMITTERTHATISSIMILARINCHEMISTRYTOTHATOFTHEPSEUDONEUROTRANSMITTER,PHENETHYLANDETHANOLAMINE“A,5,SEROTONIN,ANDDOPAMINEBNOREPINEPHRINEANDDOPAMINECEPINEPHRINEANDNOREPINEPHRINEDACETYLCHOLINEANDETHYLAMINEEGLUTAMICACIDANDGLUTAMINEFULLMARKS1ANSWERB13ETIOLOGYSTUDYTHEGENERALRULEOFADISEASECAUSESANDCONDITIONSOFBDISEASETHECAUSEOFCDISEASEDCONDITIONSFORDISEASEOCCURRENCETHEBASICMECHANISMOFEDISEASEDEVELOPMENTFULLMARKS1ANSWERB14WHICHOFTHEFOLLOWINGSUBSTANCESBELONGSTOENDOGENOUSPYROGENAAETIOCHOLANOLONEBIL6EXOTOXINCDANTIGENANTIBODYCOMPLEXEENDOTOXINFULLMARKS1ANSWERB15CHRONICEMPHYSEMACAUSEDBYHYPOXIABELONGSTOABLOODHYPOXIABHYPOTONICHYPOXIACTISSUETOXICHYPOXIADCYCLICHYPOXIANOMORETHANEFULLMARKS1ANSWERE16WHICHOFTHEFOLLOWINGCANMAKEOXYGENMOVEAWAYFROMTHECURVEA2,ELEVATED3DPGCONCENTRATIONBBLOODHDECREASEDCDECREASEDTHECO2PARTIALPRESSUREOFBLOODDDECREASEDBLOODTEMPERATUREEHYPOKALEMIAFULLMARKS1ANSWERA17WHICHOFTHEFOLLOWINGISCALLEDHYPERTONICDEHYDRATIONAHIGHVOLUMEHYPONATREMIABHYPONATREMIAOFLOWVOLUMECHYPONATREMIAOFLOWVOLUMEDHIGHVOLUMEHYPERNATREMIAEHYPERKALEMIAFULLMARKS1ANSWERE18WHICHOFTHEFOLLOWINGISNOTACLINICALMANIFESTATIONOFINSUFFICIENTCARDIACOUTPUTINHEARTFAILUREASKINCYANOSISBDECREASEDURINEOUTPUTCHASDIFFICULTYBREATHINGDCARDIOGENICSHOCKEISTIREDANDWEAKFULLMARKS1ANSWERC19STRESSINDEPENDENTDISEASESAREAPRIMARYHYPERTENSIONBSTRESSULCERCCORONARYARTERYDISEASEDALBINISMEPTSDFULLMARKS1ANSWERD20WHICHOFTHEFOLLOWINGISANINDICATOROFRESPIRATORYFACTORSAAGCO2PARTIALPRESSUREOFARTERIALBLOODBCBUFFERBASEDBASERESIDUEESTANDARDBICARBONATEFULLMARKS1ANSWERECHINAMEDICALUNIVERSITYJULY2014EXAM“PATHOPHYSIOLOGY“EXAMINATIONQUESTIONSTOTALSCORE100TESTTIMERADIOEXAMINATIONSHORTANSWERQUESTIONSEXPOSITIONSUBJECTIVECLOZETESTSIMPLEANSWER5QUESTIONS,20POINTS1ACUTEPHASEREACTIONANSWERCERTAINCHANGESINSERUMCOMPONENTSMAYOCCURWITHINASHORTPERIODHOURSTODAYSAFTERINFECTION,INFLAMMATION,TISSUEDAMAGEANDOTHERSTRESSORSAREACTINGONTHEBODYFULLMARKS42“ISCHEMIAREPERFUSIONINJURYANSWERISTHEMAINCAUSEOFFATALDISEASES,SUCHASCORONARYATHEROSCLEROSISCAUSEDBYMYOCARDIALINFARCTION,STROKEMODERATEINISCHEMICDISEASERESCUEANDTREATMENTPROCESS,MEDICALSCIENTISTSGRADUALLYFOUNDTHEMAINFACTORSCAUSINGDAMAGETOTHEORGANIZATION,NOTTHEISCHEMIAITSELF,BUTTORESTORETHEBLOODSUPPLY,EXCESSIVEFREERADICALSATTACKTHEREGAINBLOODSUPPLYWITHINTHETISSUECELLSCAUSEDBYTHISKINDOFINJURY,CALLEDISCHEMIAREPERFUSIONINJURY“FULLMARKS43HEATSHOCKPROTEINANSWERTHEREISACLASSOFHEATRESPONSIVEPROTEINSWIDELYFOUNDINBACTERIAANDMAMMALSWHENORGANISMSAREEXPOSEDTOHEAT,THEYARESTIMULATEDBYHEATTOSYNTHESIZETHEPROTEINTOPROTECTTHEORGANISMITSELFMANYHEATSHOCKPROTEINSHAVEMOLECULARCHAPERONEACTIVITYFULLMARKS44RESPIRATORYACIDOSISANSWERRESPIRATORYACIDOSISISCHARACTERIZEDBYACCUMULATIONOFCO2INTHEBODYANDDECREASEDPHTHEMAINREASONISTHATTHEPULMONARYVENTILATIONFUNCTIONISREDUCEDITISFOUNDINRESPIRATORYTRACTOBSTRUCTION,PNEUMONIA,ATELECTASIS,CHESTANDABDOMINALSURGERY,TRAUMA,ETCTHEBASICMETHODOFTREATMENTISTORELIEVERESPIRATORYTRACTOBSTRUCTIONANDIMPROVEPULMONARYVENTILATIONFUNCTIONFULLMARKS45EXERTIONALDYSPNEAANSWERMILDHEARTFAILUREOCCURSONLYDURINGPHYSICALEXERTION,BREATHINGDIFFICULTY,ANDDISAPPEARSAFTERRESTFULLMARKS4CHINAMEDICALUNIVERSITYJULY2014EXAM“PATHOPHYSIOLOGY“EXAMINATIONQUESTIONSTOTALSCORE100TESTTIMERADIOEXAMINATIONSHORTANSWERQUESTIONSEXPOSITIONSUBJECTIVECLOZETESTDISCUSSIONQUESTIONS5QUESTIONS,50POINTS1DESCRIBETHEPATHOGENESISOFSTRESSULCERANSWERAGASTRICMUCOSALISCHEMIATHISISTHEMOSTBASICCONDITIONFORTHEFORMATIONOFSTRESSULCERBECAUSEOFTHEINCREASEOFCATECHOLAMINEINTHESTRESS,THESPLANCHNICBLOODFLOWISREDUCEDANDTHEGASTROINTESTINALMUCOSAISISCHEMIC,ANDTHEDEGREEOFMUCOSALISCHEMIAISPOSITIVELYCORRELATEDWITHTHEDEGREEOFLESIONTHEEPITHELIALCELLSOFMUCOSAISCHEMIAENERGYSHORTAGE,CANNOTPRODUCEENOUGHBICARBONATEANDMUCUS,WHICHBYEPITHELIALCELLTIGHTJUNCTIONSBETWEENANDCOVEREDONTHEMUCOSALSURFACEOFTHEBICARBONATEMUCUSLAYEROFMEDICALEDUCATIONCOLLECTEDGASTRICMUCOSALBARRIERCONSISTINGOFTHEDESTRUCTIONOFTHESTOMACHCAVITYWITHINTHEHCONCENTRATIONDIFFERENCEINTOTHEMUCOSAANDMUCOSALBLOODTHEREDUCTIONINTHEFLOWANDWILLNOTINVADETHEMUCOSAHPROMPTLYREMOVED,CAUSEHTOACCUMULATEINMUCOUSMEMBRANEANDCAUSEDAMAGEBREVERSEDISPERSIONOFHINTOTHEMUCOSAOFTHESTOMACHTHISISANECESSARYCONDITIONFORTHEFORMATIONOFSTRESSULCERSTHEHIGHERTHECONCENTRATIONOFHINTHESTOMACHCAVITY,THEMORESERIOUSTHEMUCOSALLESIONS,ANDIFTHEPHINTHESTOMACHISMAINTAINEDABOVE35,ITCANNOTFORMSTRESSULCERITISTHOUGHTTHATTHEDECREASEOFPHINMUCOSAMAINLYDEPENDSONTHERATIOOFTHEREVERSEDISPERSIONOFHINTHESTOMACHCAVITYTOTHEMUCOSALBLOODFLOWINGASTRICMUCOSALPERFUSIONUNDERGOODCONDITIONS,EXCESSIVEHREVERSEDIFFUSIONINTOTHEMUCOSAINTHEBLOODSTREAMCANBEHCO3AND/ORCARRYAWAY,THUSPREVENTINGHDAMAGEOFCELLS,WHEREASINTRAUMAANDSHOCKSTRESS,REDUCINGGASTRICMUCOSALBLOODFLOW,EVENREVERSEDIFFUSIONTOTHEMUCOSAHISNOTMUCH,WILLALSOMAKECHANGESINPHDECREASEDSIGNIFICANTLY,RESULTINGINCELLDAMAGECOTHERTHEREARESOMESECONDARYFACTORSMAYALSOBEINVOLVEDINTHEONSETOFSTRESSULCER,WHENTHEACIDOSIS,THEBLOODFLOWTOTHEMUCOSALHBUFFERCAPACITYISLOW,CANPROMOTETHEOCCURRENCEOFSTRESSULCERINTHECASEOFBILEREFLUXGASTRICMUCOSALISCHEMIA,MUCOSALBARRIERFUNCTIONCANBEIMPAIRED,MUCOSALPERMEABILITYINCREASED,ANDHREVERSEREFLUXMUCOSAINCREASEDSTRESSULCER,IFTHEREISNOBLEEDINGORPERFORATIONANDOTHERCOMPLICATIONS,AFTERTHEPRIMARYDISEASEHASBEENCONTROLLED,USUALLYWITHINAFEWDAYSCOMPLETEHEALING,WITHOUTSCARRINGFULLMARKS102DESCRIBETHEMECHANISMOFRENALANEMIAANSWER“WHENTHERENALFUNCTIONWASDAMAGED,INPATIENTSWITHCHRONICKIDNEYDISEASEBYRENALSECRETIONOFERYTHROPOIETINAMOUNTWILLNOTBEENOUGHTOMEETTHENEEDSOFTHEBODY,ANDTHUSBECOMEONEOFTHEMAJORCAUSESOFRENALANEMIAINADDITION,CHRONICRENALFAILUREANDUREMIAPATIENTS,INTHEACCUMULATIONOFALARGENUMBEROFMETABOLICTOXINS,REDUCEREDBLOODCELLSURVIVALTIMEIRONINTAKEREDUCINGANDIRONLOSSINCREASED,INSUFFICIENTSYNTHESISOFREDBLOODCELLSINPATIENTSWITHCHRONICKIDNEYDISEASELONGTERMCONTROLOFPROTEININTAKE,ANDURINARYPROTEINSOURCEDRAINFROMTHEPATIENTSPATIENTSWITHCHRONICNEPHROPATHYTHEBLEEDINGTENDENCYTHESEARELIKELYTOLEADTORENALANEMIAINPATIENTSWITHCHRONICNEPHROPATHYFULLMARKS103DESCRIBETHEBLEEDINGMECHANISMINDICPATIENTSANSWER1THECONSUMPTIONOFCOAGULATIONSUBSTANCESDURINGTHEDEVELOPMENTOFDIC,ALLKINDSOFCOAGULATIONFACTORSANDPLATELETCONSUMPTION,ESPECIALLYFIBRINOGEN,PROTHROMBIN,FACTORV,VIII,X,VIIIGENERALLYREDUCEDPLATELETTHEREFORE,DICHASBEENCALLEDCOAGULOPATHYCONSRMPTIVERIGHTNOWTHECOAGULATIONPROCESSISHAMPEREDBYALARGEREDUCTIONINCOAGULATIONSUBSTANCESTWOACTIVATIONOFFIBRINOLYSISSYSTEMTHEACTIVATIONOFSECONDARYFIBRINOLYSISSYSTEMOCCURSAFTERACTIVATIONOFTHECOAGULATIONSYSTEMATDICTHISISMAINLYBECAUSEINTHEPROCESSOFBLOODCOAGULATION,ACTIVATEDBYENZYMEPROTEASEENZYMEHYDROLYSISEFFECTCAUSEDBYTHEFORMATIONOFAFXIIXII,XIIFPREKALLIKREININTOKALLIKREIN,WHICHPLASMINOGENINTOPLASMINSOMEPLASMINOGENACTIVATORORGANSSUCHASTHEUTERUS,PROSTATE,LUNGS,ETCUNDERGODEGENERATIONANDNECROSISDUETOINTRAVASCULARCOAGULATIONWHENACTIVATED,THEACTIVATORSRELEASELARGEAMOUNTSOFBLOODINTOTHEBLOODANDACTIVATETHEFIBRINOLYTICSYSTEMENDOTHELIALCELLDAMAGE,HYPOXIA,STRESSCANALSOACTIVATEFIBRINOLYTICSYSTEM,RESULTINGININCREASEDPLASMININADDITIONTOPLASMINOGENTOFIBRINOGENDEGRADATION,HYDROLYSIS,BUTALSOCOAGULATIONFACTORVIIIANDPROTHROMBIN,THECOAGULATIONFACTORISFURTHERREDUCED,RESULTINGINDYSFUNCTIONOFBLOODCOAGULATIONANDBLEEDINGFULLMARKS10THEMECHANISMOF4STAGNANTANOXIAPHASEOFSHOCKMICROCIRCULATIONSTASISANSWERTHEMICROCIRCULATIONANDHEMORHEOLOGYCHANGEDOBVIOUSLYBLOODFLOWRATEWASSLOWEDDOWN,THEREDBLOODCELLANDPLATELETAGGREGATION,LEUKOCYTEROLLING,ADHESION,IMPACTION,BLOODVISCOSITYINCREASED,THEBLOOD“MUD“SLUDGEMICROCIRCULATIONSTASIS,CONGESTION,ANDFURTHERREDUCETHETISSUEPERFUSION,HYPOXIAISMORESERIOUSTHISISBECAUSEINTHISPERIOD,THEVISCERALMICROCIRCULATIONVASOMOTIONDISAPPEARED,ARTERIOLE,AFTERARTERIOLESANDPRECAPILLARYSPHINCTERCONTRACTIONWEAKENEDOREVENEXPANSION,ALARGENUMBEROFBLOODPOUREDINTOTRUECAPILLARYNETWORKVENULESAREDILATED,TOO,BUTBECAUSEOFSLOWBLOODFLOW,CELLIMPACTION,MICROCIRCULATIONINCREASEDRESISTANCETOOUTFLOW,THERESISTANCEISGREATERTHANTHECAPILLARYRESISTANCEBEFOREAFTERFULLMARKS105BRIEFLYDESCRIBETHEMECHANISMOFHYPOXIAINDUCEDBYCARBONMONOXIDEPOISONINGANSWERCARBONDIOXIDETHROUGHTHERESPIRATORYINHALATIONLUNG,THROUGHBLOODANDHEMOGLOBINDIFFUSEALVEOLARWALLHBCOMBINATIONOFCARBOXYHEMOGLOBINCOHBCOANDHBBYWIDEOXYGENAFFINITYTHAN240TIMES