TESTBANK f
RUBIN'S PATHOLOGY: f
CLINICOPATHOLOGIC
f
FOUNDATIONS OF MEDICINE
f f f
7th Edition By David S. Strayer, Emanuel Rubin
f f f f f f f
TESTBANK f
,Test fBank fRubin's fPathology: fClinicopathologic fFoundations fof fMedicine f7th f Edition
Table fof fContents:
Chapter f1: fCell fAdaptation, fInjury fand fDeath
Chapter f2: fInflammation
Chapter f3: fRepair, fRegeneration fand fFibrosis
Chapter f4: fImmunopathology
Chapter f5: fNeoplasia
Chapter f6: fDevelopmental fand fGenetic fDiseases
Chapter f7: fHemodynamic fDisorders
Chapter f8: fEnvironmental fand fNutritional fPathology
Chapter f9: fInfectious fand fParasitic fDiseases
Section fII: fPathogenesis fof fSystemic fConditions fExpandable fsection
Chapter f10: fAging
Chapter f11: fSystemic fAutoimmune fDiseases
Chapter f12: fSepsis
Chapter f13: fObesity fand fDiabetes fMellitus
Chapter f14: fThe fPathology fof fPregnancy
Chapter f15: fThe fAmyloidoses
Section fIII: fDiseases fof fIndividual fOrgan fSystemsExpandable fsection
Chapter f16: fBlood fVessels
Chapter f17: fThe fHeart
Chapter f18: fThe fRespiratory fSystem
Chapter f19: fThe fGastrointestinal fTract
Chapter f20: fThe fLiver fand fBiliary fSystem
Chapter f21: fThe fPancreas
Chapter f22: fThe fKidney
Chapter f23: fThe fLower fUrinary fTract fand fMale fReproductive fSystem
Chapter f24: fThe fFemale fReproductive fSystem fand fPeritoneum
Chapter f25: fThe fBreast
Chapter f26: fHematopathology
Chapter f27: fThe fEndocrine fSystem
Chapter f28: fThe fSkin
Chapter f29: fThe fHead fand fNeck
Chapter f30: fBones, fJoints fand fSoft fTissue
Chapter f31: fSkeletal fMuscle fand fPeripheral fNervous fSystem
Chapter f32: fThe fCentral fNervous fSystem
Chapter f33: fThe fEye
Chapter f34: fForensic fPathology
,Rubin's fPathology: fClinicopathologic fFoundations fof fMedicine
fChapter f1: fCell fAdaptation, fInjury fand fDeath
Ischemia fand fother ftoxic finjuries fincrease fthe faccumulation fof fintracellular fcalcium fas fa fresult
1. fof:
A) release fof fstored fcalcium ffrom fthe fmitochondria.
B) improved fintracellular fvolume fregulation.
C) decreased finflux facross fthe fcell fmembrane.
D) attraction fof fcalcium fto ffatty finfiltrates.
The fpatient fis ffound fto fhave fliver fdisease, fresulting fin fthe fremoval fof fa flobe fof fhis fliver.
2. fAdaptation fto fthe freduced fsize fof fthe fliver fleads fto f_ of fthe fremaining fliver fcells.
A) metaplasia
B) organ fatrophy
C) compensatory fhyperplasia
D) physiologic fhypertrophy
A fperson feating fpeanuts fstarts fchoking fand fcollapses. fHis fairway fobstruction fis fpartially
fcleared, fbut fhe fremains fhypoxic funtil fhe freaches fthe fhospital. fThe fprolonged fcell fhypoxia
3. fcaused fa fcerebral finfarction fand fresulting _ fin fthe fbrain.
A) caspase factivation
B) coagulation fnecrosis
C) rapid fphagocytosis
D) protein fp53 fdeficiency
Bacteria fand fviruses fcause fcell fdamage fby , fwhich fis funique ffrom fthe fintracellular
4. fdamage fcaused fby fother finjurious fagents.
A) disrupting fthe fsodium/potassium fATPase fpump
B) interrupting foxidative fmetabolism fprocesses
C) replicating fand fproducing fcontinued finjury
D) decreasing fprotein fsynthesis fand ffunction
The fpatient fhas fa fprolonged finterruption fin farterial fblood fflow fto fhis fleft fkidney, fcausing
5. fhypoxic fcell finjury fand fthe frelease fof ffree fradicals. fFree fradicals fdamage fcells fby:
A) destroying fphospholipids fin fthe fcell fmembrane.
B) altering fthe fimmune fresponse fof fthe fcell.
C) disrupting fcalcium fstorage fin fthe fcell.
D) inactivation fof fenzymes fand fmitochondria.
, 6. Injured fcells fhave fimpaired fflow fof fsubstances fthrough fthe fcell fmembrane fas fa fresult fof:
A) increased ffat fload.
B) altered fpermeability.
C) altered fglucose futilization.
D) increased fsurface freceptors.
7. Reversible fadaptive fintracellular fresponses fare finitiated fby:
A) stimulus foverload.
B) genetic fmutations.
C) chemical fmessengers.
D) mitochondrial fDNA.
8. Injured fcells fbecome fvery fswollen fas fa fresult fof:
A) increased fcell fprotein fsynthesis.
B) altered fcell fvolume fregulation.
C) passive fentry fof fpotassium finto fthe fcell.
D) bleb fformation fin fthe fplasma fmembrane.
A fdiabetic fpatient fhas fimpaired fsensation, fcirculation, fand foxygenation fof fhis ffeet. fHe fsteps fon
fa fpiece fof fglass, fthe fwound fdoes fnot fheal, fand fthe farea ftissue fbecomes fnecrotic. fThe fnecrotic
9. fcell fdeath fis fcharacterized fby:
A) rapid fapoptosis.
B) cellular frupture.
C) shrinkage fand fcollapse.
D) chronic finflammation.
A f99-year-old fwoman fhas fexperienced fthe fdecline fof fcell ffunction fassociated fwith fage. fA
10. fgroup fof ftheories fof fcellular faging ffocus fon fprogrammed:
A) changes fwith fgenetic finfluences.
B) elimination fof fcell freceptor fsites.
C) insufficient ftelomerase fenzyme.
D) DNA fmutation for ffaulty frepair.
An f89-year-old ffemale fpatient fhas fexperienced fsignificant fdecreases fin fher fmobility fand
fstamina fduring fa f3-week fhospital fstay ffor fthe ftreatment fof fa ffemoral fhead ffracture. fWhich fof
fthe ffollowing fphenomena fmost flikely faccounts ffor fthe fpatients fdecrease fin fmuscle ffunction
11. fthat funderlies fher freduced fmobility?
A) Impaired fmuscle fcell fmetabolism fresulting ffrom fmetaplasia
B) Dysplasia fas fa fconsequence fof finflammation fduring fbone fremodeling
C) Disuse fatrophy fof fmuscle fcells fduring fa fprolonged fperiod fof fimmobility
RUBIN'S PATHOLOGY: f
CLINICOPATHOLOGIC
f
FOUNDATIONS OF MEDICINE
f f f
7th Edition By David S. Strayer, Emanuel Rubin
f f f f f f f
TESTBANK f
,Test fBank fRubin's fPathology: fClinicopathologic fFoundations fof fMedicine f7th f Edition
Table fof fContents:
Chapter f1: fCell fAdaptation, fInjury fand fDeath
Chapter f2: fInflammation
Chapter f3: fRepair, fRegeneration fand fFibrosis
Chapter f4: fImmunopathology
Chapter f5: fNeoplasia
Chapter f6: fDevelopmental fand fGenetic fDiseases
Chapter f7: fHemodynamic fDisorders
Chapter f8: fEnvironmental fand fNutritional fPathology
Chapter f9: fInfectious fand fParasitic fDiseases
Section fII: fPathogenesis fof fSystemic fConditions fExpandable fsection
Chapter f10: fAging
Chapter f11: fSystemic fAutoimmune fDiseases
Chapter f12: fSepsis
Chapter f13: fObesity fand fDiabetes fMellitus
Chapter f14: fThe fPathology fof fPregnancy
Chapter f15: fThe fAmyloidoses
Section fIII: fDiseases fof fIndividual fOrgan fSystemsExpandable fsection
Chapter f16: fBlood fVessels
Chapter f17: fThe fHeart
Chapter f18: fThe fRespiratory fSystem
Chapter f19: fThe fGastrointestinal fTract
Chapter f20: fThe fLiver fand fBiliary fSystem
Chapter f21: fThe fPancreas
Chapter f22: fThe fKidney
Chapter f23: fThe fLower fUrinary fTract fand fMale fReproductive fSystem
Chapter f24: fThe fFemale fReproductive fSystem fand fPeritoneum
Chapter f25: fThe fBreast
Chapter f26: fHematopathology
Chapter f27: fThe fEndocrine fSystem
Chapter f28: fThe fSkin
Chapter f29: fThe fHead fand fNeck
Chapter f30: fBones, fJoints fand fSoft fTissue
Chapter f31: fSkeletal fMuscle fand fPeripheral fNervous fSystem
Chapter f32: fThe fCentral fNervous fSystem
Chapter f33: fThe fEye
Chapter f34: fForensic fPathology
,Rubin's fPathology: fClinicopathologic fFoundations fof fMedicine
fChapter f1: fCell fAdaptation, fInjury fand fDeath
Ischemia fand fother ftoxic finjuries fincrease fthe faccumulation fof fintracellular fcalcium fas fa fresult
1. fof:
A) release fof fstored fcalcium ffrom fthe fmitochondria.
B) improved fintracellular fvolume fregulation.
C) decreased finflux facross fthe fcell fmembrane.
D) attraction fof fcalcium fto ffatty finfiltrates.
The fpatient fis ffound fto fhave fliver fdisease, fresulting fin fthe fremoval fof fa flobe fof fhis fliver.
2. fAdaptation fto fthe freduced fsize fof fthe fliver fleads fto f_ of fthe fremaining fliver fcells.
A) metaplasia
B) organ fatrophy
C) compensatory fhyperplasia
D) physiologic fhypertrophy
A fperson feating fpeanuts fstarts fchoking fand fcollapses. fHis fairway fobstruction fis fpartially
fcleared, fbut fhe fremains fhypoxic funtil fhe freaches fthe fhospital. fThe fprolonged fcell fhypoxia
3. fcaused fa fcerebral finfarction fand fresulting _ fin fthe fbrain.
A) caspase factivation
B) coagulation fnecrosis
C) rapid fphagocytosis
D) protein fp53 fdeficiency
Bacteria fand fviruses fcause fcell fdamage fby , fwhich fis funique ffrom fthe fintracellular
4. fdamage fcaused fby fother finjurious fagents.
A) disrupting fthe fsodium/potassium fATPase fpump
B) interrupting foxidative fmetabolism fprocesses
C) replicating fand fproducing fcontinued finjury
D) decreasing fprotein fsynthesis fand ffunction
The fpatient fhas fa fprolonged finterruption fin farterial fblood fflow fto fhis fleft fkidney, fcausing
5. fhypoxic fcell finjury fand fthe frelease fof ffree fradicals. fFree fradicals fdamage fcells fby:
A) destroying fphospholipids fin fthe fcell fmembrane.
B) altering fthe fimmune fresponse fof fthe fcell.
C) disrupting fcalcium fstorage fin fthe fcell.
D) inactivation fof fenzymes fand fmitochondria.
, 6. Injured fcells fhave fimpaired fflow fof fsubstances fthrough fthe fcell fmembrane fas fa fresult fof:
A) increased ffat fload.
B) altered fpermeability.
C) altered fglucose futilization.
D) increased fsurface freceptors.
7. Reversible fadaptive fintracellular fresponses fare finitiated fby:
A) stimulus foverload.
B) genetic fmutations.
C) chemical fmessengers.
D) mitochondrial fDNA.
8. Injured fcells fbecome fvery fswollen fas fa fresult fof:
A) increased fcell fprotein fsynthesis.
B) altered fcell fvolume fregulation.
C) passive fentry fof fpotassium finto fthe fcell.
D) bleb fformation fin fthe fplasma fmembrane.
A fdiabetic fpatient fhas fimpaired fsensation, fcirculation, fand foxygenation fof fhis ffeet. fHe fsteps fon
fa fpiece fof fglass, fthe fwound fdoes fnot fheal, fand fthe farea ftissue fbecomes fnecrotic. fThe fnecrotic
9. fcell fdeath fis fcharacterized fby:
A) rapid fapoptosis.
B) cellular frupture.
C) shrinkage fand fcollapse.
D) chronic finflammation.
A f99-year-old fwoman fhas fexperienced fthe fdecline fof fcell ffunction fassociated fwith fage. fA
10. fgroup fof ftheories fof fcellular faging ffocus fon fprogrammed:
A) changes fwith fgenetic finfluences.
B) elimination fof fcell freceptor fsites.
C) insufficient ftelomerase fenzyme.
D) DNA fmutation for ffaulty frepair.
An f89-year-old ffemale fpatient fhas fexperienced fsignificant fdecreases fin fher fmobility fand
fstamina fduring fa f3-week fhospital fstay ffor fthe ftreatment fof fa ffemoral fhead ffracture. fWhich fof
fthe ffollowing fphenomena fmost flikely faccounts ffor fthe fpatients fdecrease fin fmuscle ffunction
11. fthat funderlies fher freduced fmobility?
A) Impaired fmuscle fcell fmetabolism fresulting ffrom fmetaplasia
B) Dysplasia fas fa fconsequence fof finflammation fduring fbone fremodeling
C) Disuse fatrophy fof fmuscle fcells fduring fa fprolonged fperiod fof fimmobility
