RUBIN'S PATHOLOGY: CLIN
k k
ICOPATHOLOGIC FOUNDATI k
ONS OF MEDICINEk k
7th Edition By David S. Strayer, Emanuel Rubin
k k k k k k k
TEST BANK k
,TestkBankkRubin'skPathology:kClinicopathologickFoundationskofkMedicinek7thk Edition
TablekofkContents:
Chapterk1:kCellkAdaptation,kInjurykandkDeath
Chapterk2:kInflammation
Chapterk3:kRepair,kRegenerationkandkFibrosis
Chapterk4:kImmunopathology
Chapterk5:kNeoplasia
Chapterk6:kDevelopmentalkandkGenetickDiseases
Chapterk7:kHemodynamickDisorders
Chapterk8:kEnvironmentalkandkNutritionalkPathology
Chapterk9:kInfectiouskandkParasitickDiseases
SectionkII:kPathogenesiskofkSystemickConditionskExpandableksection
Chapterk10:kAging
Chapterk11:kSystemickAutoimmunekDiseases
Chapterk12:kSepsis
Chapterk13:kObesitykandkDiabeteskMellitus
Chapterk14:kThekPathologykofkPregnancy
Chapterk15:kThekAmyloidoses
SectionkIII:kDiseaseskofkIndividualkOrgankSystemsExpandableksection
Chapterk16:kBloodkVessels
Chapterk17:kThekHeart
Chapterk18:kThekRespiratorykSystem
Chapterk19:kThekGastrointestinalkTract
Chapterk20:kThekLiverkandkBiliarykSystem
Chapterk21:kThekPancreas
Chapterk22:kThekKidney
Chapterk23:kThekLowerkUrinarykTractkandkMalekReproductivekSystem
Chapterk24:kThekFemalekReproductivekSystemkandkPeritoneum
Chapterk25:kThekBreast
Chapterk26:kHematopathology
Chapterk27:kThekEndocrinekSystem
Chapterk28:kThekSkin
Chapterk29:kThekHeadkandkNeck
Chapterk30:kBones,kJointskandkSoftkTissue
Chapterk31:kSkeletalkMusclekandkPeripheralkNervouskSystem
Chapterk32:kThekCentralkNervouskSystem
Chapterk33:kThekEye
Chapterk34:kForensickPathology
,Rubin'skPathology:kClinicopathologickFoundationskofkMedicinek
Chapterk1:kCellkAdaptation,kInjurykandkDeath
Ischemiakandkotherktoxickinjurieskincreasekthekaccumulationkofkintracellularkcalciumkaskakresultko
1. f:
A) releasekofkstoredkcalciumkfromkthekmitochondria.
B) improvedkintracellularkvolumekregulation.
C) decreasedkinfluxkacrosskthekcellkmembrane.
D) attractionkofkcalciumktokfattykinfiltrates.
Thekpatientkiskfoundktokhavekliverkdisease,kresultingkinkthekremovalkofkaklobekofkhiskliver.kAdapt
2. ationktokthekreducedksizekofkthekliverkleadsktok_ ofkthekremainingkliverkcells.
A) metaplasia
B) organkatrophy
C) compensatorykhyperplasia
D) physiologickhypertrophy
Akpersonkeatingkpeanutskstartskchokingkandkcollapses.kHiskairwaykobstructionkiskpartiallykcl
eared,kbutkhekremainskhypoxickuntilkhekreacheskthekhospital.kThekprolongedkcellkhypoxiakca
3. usedkakcerebralkinfarctionkandkresulting _kinkthekbrain.
A) caspasekactivation
B) coagulationknecrosis
C) rapidkphagocytosis
D) proteinkp53kdeficiency
Bacteriakandkviruseskcausekcellkdamagekby
4. ,kwhichkiskuniquekfromkthekintracellulark
damagekcausedkbykotherkinjuriouskagents.
A) disruptingktheksodium/potassiumkATPasekpump
B) interruptingkoxidativekmetabolismkprocesses
C) replicatingkandkproducingkcontinuedkinjury
D) decreasingkproteinksynthesiskandkfunction
Thekpatientkhaskakprolongedkinterruptionkinkarterialkbloodkflowktokhiskleftkkidney,kcausingkh
5. ypoxickcellkinjurykandkthekreleasekofkfreekradicals.kFreekradicalskdamagekcellskby:
A) destroyingkphospholipidskinkthekcellkmembrane.
B) alteringkthekimmunekresponsekofkthekcell.
C) disruptingkcalciumkstoragekinkthekcell.
D) inactivationkofkenzymeskandkmitochondria.
, 6. Injuredkcellskhavekimpairedkflowkofksubstanceskthroughkthekcellkmembranekaskakresultkof:
A) increasedkfatkload.
B) alteredkpermeability.
C) alteredkglucosekutilization.
D) increasedksurfacekreceptors.
7. Reversiblekadaptivekintracellularkresponseskarekinitiatedkby:
A) stimuluskoverload.
B) genetickmutations.
C) chemicalkmessengers.
D) mitochondrialkDNA.
8. Injuredkcellskbecomekverykswollenkaskakresultkof:
A) increasedkcellkproteinksynthesis.
B) alteredkcellkvolumekregulation.
C) passivekentrykofkpotassiumkintokthekcell.
D) blebkformationkinkthekplasmakmembrane.
Akdiabetickpatientkhaskimpairedksensation,kcirculation,kandkoxygenationkofkhiskfeet.kHekstepskonkak
piecekofkglass,kthekwoundkdoesknotkheal,kandkthekareaktissuekbecomesknecrotic.kTheknecrotickcellk
9. deathkiskcharacterizedkby:
A) rapidkapoptosis.
B) cellularkrupture.
C) shrinkagekandkcollapse.
D) chronickinflammation.
Ak99-year-
10. oldkwomankhaskexperiencedkthekdeclinekofkcellkfunctionkassociatedkwithkage.kAkgroupkofkthe
orieskofkcellularkagingkfocuskonkprogrammed:
A) changeskwithkgenetickinfluences.
B) eliminationkofkcellkreceptorksites.
C) insufficientktelomerasekenzyme.
D) DNAkmutationkorkfaultykrepair.
Ank89-year-
oldkfemalekpatientkhaskexperiencedksignificantkdecreaseskinkherkmobilitykandkstaminakduringkak
3-
11. weekkhospitalkstaykforkthektreatmentkofkakfemoralkheadkfracture.kWhichkofkthekfollowingkpheno
menakmostklikelykaccountskforkthekpatientskdecreasekinkmusclekfunctionkthatkunderlieskherkredu
cedkmobility?
A) Impairedkmusclekcellkmetabolismkresultingkfromkmetaplasia
B) Dysplasiakaskakconsequencekofkinflammationkduringkbonekremodeling
C) Disusekatrophykofkmusclek cellskduringkakprolongedkperiodkofkimmobility