Test bank for rubin s pathology

TEST BANK FOR RUBIN’S PATHOLOGY
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OF MEDICINE 7TH EDITION 2023 HIGH G
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1. Ischemiavandvothervtoxicvinjuriesvincreasevthevaccumulationvofvintracellularvcalciumvasvavresultvo
f:
A) releasevofvstoredvcalciumvfromvthevmitochondria.

B) improvedvintracellularvvolumevregulation.
C) decreasedvinfluxvacrossvthevcellvmembrane.
D) attractionvofvcalciumvtovfattyvinfiltrates.
2. Thevpatientvisvfoundvtovhavevlivervdisease,vresultingvinvthevremovalvofvavlobevofvhisvliver.vAdaptat
ionvtovthevreducedvsizevofvthevlivervleadsvtov_ ofvthevremainingvlivervcells.
A) metaplasia
B) organvatrophy
C) compensatoryvhyperplasia
D) physiologicvhypertrophy
Avpersonveatingvpeanutsvstartsvchokingvandvcollapses.vHisvairwayvobstructionvisvpartiallyvcl
eared,vbutvhevremainsvhypoxicvuntilvhevreachesvthevhospital.vThevprolongedvcellvhypoxiavca
3. usedvavcerebralvinfarctionvandvresulting _vinvthevbrain.
A) caspasevactivation
B) coagulationvnecrosis
C) rapidvphagocytosis
D) proteinvp53vdeficiency
4. Bacteriav andv virusesv causev cellv damagev byv ,v whichv isv uniquev fromv thev intracellularv damagevcau
edvbyvothervinjuriousvagents.

, A) disruptingvthevsodium/potassiumvATPasevpump
B) interruptingvoxidativevmetabolismvprocesses
Chapterv1:vCellvAdaptation,vInjuryvandvDeath
C) replicatingvandvproducingvcontinuedvinjury



TEST BANK FOR RUBIN’S PATHOLOGY: CL
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MEDICINE 7TH EDITION ( WITH ANSWER K
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EY)
5. Thevpatientvhasvavprolongedvinterruptionvinvarterialvbloodvflowvtovhisvleftvkidney,vcausingvh
ypoxicvcellvinjuryvandvthevreleasevofvfreevradicals.vFreevradicalsvdamagevcellsvby:
A) destroyingvphospholipidsvinvthevcellvmembrane.
B) alteringvthevimmunevresponsevofvthevcell.
C) disruptingvcalciumvstoragevinvthevcell.

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D) decreasingvproteinvsynthesisvandvfunction
D) inactivationvofvenzymesvandvmitochondria.

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GUIDE 2023 v

,TEST BANK FOR RUBIN’S PATHOLOGY:
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OF
MEDICINE 7TH EDITION ( WITH ANSWER
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KEY)


6. Injuredvcellsvhavevimpairedvflowvofvsubstancesvthroughvthevcellvmembranevasvavresultvof:
A) increasedvfatvload.
B) alteredvpermeability.
C) alteredvglucosevutilization.
D) increasedvsurfacevreceptors.
7. Reversiblevadaptivevintracellularvresponsesvarevinitiatedvby:
A) stimulusvoverload.
B) geneticvmutations.
C) chemicalvmessengers.
D) mitochondrialvDNA.
8. Injuredvcellsvbecomevveryvswollenvasvavresultvof:
A) increasedvcellvproteinvsynthesis.
B) alteredvcellvvolumevregulation.
C) passiveventryvofvpotassiumvintovthevcell.
D) blebvformationvinvthevplasmavmembrane.
Avdiabeticvpatientvhasvimpairedvsensation,vcirculation,vandvoxygenationvofvhisvfeet.vHevstepsvonva
vpiecevofvglass,vthevwoundvdoesvnotvheal,vandvthevareavtissuevbecomesvnecrotic.vThevnecroticvcellv

9. deathvisvcharacterizedvby:
A) rapidvapoptosis.
B) cellularvrupture.
C) shrinkagevandvcollapse.
D) chronicvinflammation.
10. Av99-year-
oldvwomanvhasvexperiencedvthevdeclinevofvcellvfunctionvassociatedvwithvage.vAvgroupvofvthe
oriesvofvcellularvagingvfocusvonvprogrammed:

, A) changesvwithvgeneticvinfluences.
B) eliminationvofvcellvreceptorvsites.
C) insufficientvtelomerasevenzyme.

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