USMLE题库Cardiology(二)1-10

Cardiology2题库Q1A35-year-oldobeseCaucasianfemalepresentstoyourofficewithprogressivedyspneaanddizzinessonexertion.Shehasnosignificantpastmedicalhistory,butadmitsfollowingseveralstrictweight-reductiondietsandconsumingappetitesuppressantmedicationsinthepast.Herbloodpressureis110/80mmHgandherheartrateis90beatsperminute.Thepatientdiessuddenlysixmonthsaftertheinitialvisit.Whichofthefollowingpathologicfindingswouldyouexpectmostbasedonthepatient'shistory?A.BerryaneurysmsofthecerebralarteriesB.UpperpulmonarylobefibrosisC.RightventricularhypertrophyD.SignificantaorticdilationE.RenalvascularsclerosisF.VascularmedialcalcificationA1Correctanswer:CThekeyclueinthispatient'shistoryisthepastuseofappetitesuppressants.Ingestionoffenfluramine,dexfenfluramine,andphentermineformorethanthreemonths'durationhasbeenassociatedwiththedevelopmentofsecondarypulmonaryhypertension.Patientswithpulmonaryhypertensiongenerallypresentwithexertionaldyspnea(andpossibleexertionalpre-syncope),duetoaninabilityoftherighthearttoadequatelyincreasecardiacoutputagainstincreasedpulmonaryvascularresistanceduringexercise.Forthisreason,systemicbloodpressuremayfallduringexercise.Chronicpulmonaryhypertensionresultsinrightventricularhypertrophyandcorpulmonale.Corpulmonalemayleadtosuddendeathfromalethalcardiacarrhythmia.(ChoiceA)CerebralberryaneurysmsareassociatedwithgeneticdisorderssuchasautosomaldominantpolycystickidneydiseaseandEhlers-Danlossyndrome.Riskfactorsincludehypertensionandsmoking.Thispatient'spastmedicalhistorydoesnotsuggestanyoftheseconditions.(ChoiceB)Bilateralupperlobepulmonaryfibrosismaybecausedbyprogressivemassivefibrosis(asincoalworkerspneumoconiosisandsilicosis),tuberculosis,histoplasmosis,sarcoidosis,allergicbronchopulmonaryaspergillosis,andankylosingspondylitis.Thispatient'spastmedicalhistorydoesnotincludeanyoftheseconditions.Moreover,pulmonaryfibrosisdoesnottypicallypredisposetosuddendeath.(ChoiceD)Aorticdilatationmayoccurasaconsequenceofhypertension,aging,and/oraorticstenosis(post-stenoticdilatation).Aorticaneurysmscanresultfromadvancedatherosclerosis,cysticmedialdegeneration,aortitisduetoinfections(e.g.syphilis)orarteritis(eg.Takayasuarteritis).Thispatient'sage,pastmedicalhistory,andnormalbloodpressurearenotsuggestiveoftheseconditions.(ChoiceE)Renalvascularsclerosismayresultfromatherosclerosis,fibromusculardysplasia,orsystemicvasculitis(e.g.polyarteritisnodosa).Thispatient'spastmedicalhistorydoesnotsuggesttheseconditions.(ChoiceF)Medialcalcinosisisaconditionmarkedbycalcificdepositsinmusculararteriesinpersonsolderthanage50.Thefemoraltibial,radial,andulnararteries,aswellasthearterialsupplytothegenitaltract,aremostcommonlyaffected.Thesecalcificationsarevisibleradiographically,andoftenpalpableonphysicalexam.However,theydonotnarrowthevessellumen,andthereforegenerallyremainasymptomaticanddonotpredisposetosuddendeath.Q2A60-year-oldmandevelopsacutesubsternalchestpain，sweating，andnausea.ECGshowsacuteST-elevationsinleadsII,III,andaVF.Reperfusiontherapyisnotgivenduetounderlyingcirrhosisandhistoryofvaricealbleeding.Heisdiagnosedwithamyocardialinfarction,andiseventuallydischargedfromthehospitalwithconservativemanagement.Twelvedaysafterhismyocardialinfarction,heisfounddeadonthefloorofhisapartment.Lightmicroscopywouldmostlikelyrevealwhichofthefollowingchangesintheaffectedmyocardium?A.EdemaandpunctatehemorrhagesB.HypereosinophilicmyocytesC.DenseinterstitialneutrophilinfiltrateD.ExtensivemacrophagephagocytosisofdeadcellsE.FibrovasculargranulationtissuewithneovascularizationF.DensecollagenscarG.NormalmyocardiumCorrectanswer:ESevendaysfollowingacutemyocardialinfarction,granulationtissuebeginstoreplacethezoneofdeadcardiacmuscle.Thisgranulationtissuealongwithneovascularizationismostprominentonlightmicroscopyatdays10-14post-infarction.MajorhistologicchangesdetectablevialightmicroscopydevelopinthefollowingtemporalsequenceTimeaftermyocardialinfarctionPredominantlightmicroscopicchanges0-4hrsminimalchange4-12hrsearlycoagulationnecrosis,edema,hemorrhage,wavyfibers12-24hrscoagulationnecrosisandmarginalcontractionbandnecrosis1to5dayscoagulationnecrosisandneutrophilicinfiltrate5to10daysmacrophagephagocytosisofdeadcells10to14daysgranulationtissueandneovascularization2weeksto2monthscollagendeposition/scarformationChoiceA)Edemaandpunctatehemorrhagesmaybedetectedininfarctedmyocardiumbylightmicroscopyfromapproximately4hoursto12hoursfollowingmyocardialinfarction.(ChoiceB)Cytoplasmichypereosinophiliaisoneoftheearliestlightmicroscopicsignsofcoagulativenecrosisofcardiacmyocytes.Itbeginsapproximately4hoursaftertheonsetoflethalischemia.Bypost-infarctionday12,however,mostofthedeadmyocyteshavebeenphagocytosedbymacrophages.(ChoiceC)Approximately24hoursfollowingacutemyocardialinfarction,neutrophilicinfiltrationofthezoneofdeadmyocardiumbegins.Thisacuteinflammatoryinfiltratethenbecomesincreasinglyprominentbeforerecedingaroundday5to7.(ChoiceD)Macrophagephagocytosisofinfarctedmyocardiumbeginsataround5dayspost-infarctionandisusuallycompletebyday10,whentheaccumulatedmacrophagesbegintober