Rubin's Pathology 7th Edition
TEST BANK Rubin's Pathology
Clinocopathologic Foundations of Medicine
Pathology textbook Strayer and Rubin
Rubin's Pathology study guide
Rubin's Pathology test bank
Clinical pathology test questions
Rubin's Pathology exam prep
7th Edition Rubin's Pathology
Pat...
A) releaseHofHstoredHcalciumHfromHtheHmitochondria.
B) improvedHintracellularHvolumeHregulation.
C) decreasedHinfluxHacrossHtheHcellHmembrane.
D) attractionHofHcalciumHtoHfattyHinfiltrates.
TheHpatientHisHfoundHtoHhaveHliverHdisease,HresultingHinHtheHremovalHofHaHlobeHofHhisHliver.
2. AdaptationHtoHtheHreducedHsizeHofHtheHliverHleadsHtoH_ ofHtheHremainingHliverHcells.
A) metaplasia
B) organHatrophy
C) compensatoryHhyperplasia
D) physiologicHhypertrophy
AHpersonHeatingHpeanutsHstartsHchokingHandHcollapses.HHisHairwayHobstructionHisHpartiallyH cl
eared,HbutHheHremainsHhypoxicHuntilHheHreachesHtheHhospital.HTheHprolongedHcellHhypoxia
3. causedHaHcerebralHinfarctionHandHresulting _HinHtheHbrain.
A) caspaseHactivation
B) coagulationHnecrosis
C) rapidHphagocytosis
D) proteinHp53Hdeficiency
BacteriaHandHvirusesHcauseHcellHdamageHby ,HwhichHisHuniqueHfromHtheHintracellular
4. damageHcausedHbyHotherHinjuriousHagents.
A) disruptingHtheHsodium/potassiumHATPaseHpump
B) interruptingHoxidativeHmetabolismHprocesses
C) replicatingHandHproducingHcontinuedHinjury
D) decreasingHproteinHsynthesisHandHfunction
TheHpatientHhasHaHprolongedHinterruptionHinHarterialHbloodHflowHtoHhisHleftHkidney,Hcausing
5. hypoxicHcellHinjuryHandHtheHreleaseHofHfreeHradicals.HFreeHradicalsHdamageHcellsHby:
A) destroyingHphospholipidsHinHtheHcellHmembrane.
B) alteringHtheHimmuneHresponseHofHtheHcell.
C) disruptingHcalciumHstorageHinHtheHcell.
D) inactivationHofHenzymesHandHmitochondria.
, 6. InjuredHcellsHhaveHimpairedHflowHofHsubstancesHthroughHtheHcellHmembraneHasHaHresultHof:
A) increasedHfatHload.
B) alteredHpermeability.
C) alteredHglucoseHutilization.
D) increasedHsurfaceHreceptors.
7. ReversibleHadaptiveHintracellularHresponsesHareHinitiatedHby:
A) stimulusHoverload.
B) geneticHmutations.
C) chemicalHmessengers.
D) mitochondrialHDNA.
8. InjuredHcellsHbecomeHveryHswollenHasHaHresultHof:
A) increasedHcellHproteinHsynthesis.
B) alteredHcellHvolumeHregulation.
C) passiveHentryHofHpotassiumHintoHtheHcell.
D) blebHformationHinHtheHplasmaHmembrane.
AHdiabeticHpatientHhasHimpairedHsensation,Hcirculation,HandHoxygenationHofHhisHfeet.HHeHstep
sHonH aHpieceHofHglass,HtheHwoundHdoesHnotHheal,HandHtheHareaHtissueHbecomesHnecrotic.HTh
eHnecrotic
9. cellHdeathHisHcharacterizedHby:
A) rapidHapoptosis.
B) cellularHrupture.
C) shrinkageHandHcollapse.
D) chronicHinflammation.
AH99-year-oldHwomanHhasHexperiencedHtheHdeclineHofHcellHfunctionHassociatedHwithHage.HA
10 groupHofHtheoriesHofHcellularHagingHfocusHonHprogrammed:
.
A) changesHwithHgeneticHinfluences.
B) eliminationHofHcellHreceptorHsites.
C) insufficientHtelomeraseHenzyme.
D) DNAHmutationHorHfaultyHrepair.
AnH89-year-
oldHfemaleHpatientHhasHexperiencedHsignificantHdecreasesHinHherHmobilityHandH staminaHduri
ngHaH3-
weekHhospitalHstayHforHtheHtreatmentHofHaHfemoralHheadHfracture.HWhichHofH theHfollowingHp
henomenaHmostHlikelyHaccountsHforHtheHpatientsHdecreaseHinHmuscleHfunction
11 thatHunderliesHherHreducedHmobility?
.
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