Test Bank For Rubin's Pathology: Clinicopathologic Foundations of Medicine 7th Edition by David S. Strayer, Emmanuel Rubin | All Chapters1-34 | Complete Latest Guide A+.
Rubin's Pathology: Clinicopathologic Foundations Of Medicine 7th Edition By David S. Strayer; Emanuel Rubin Md| All Chapters 1-34 Covered| Verified| Rated A+| Latest Edition| Test Bank
TEST BANK for RUBIN'SPATHOLOGY: CLINICOPATHOLOGIC FOUNDATIONSOFMEDICINE 7th Edition by Strayer and Rubin All chapters 1-34 covered
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, Rubin's Pathology: Clinicopathologic Foundations of Medicine
f f f f f
Testbank/Studyguide
f
Chapter 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 f leads 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
3. fhypoxiafcaused 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 f characterized 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 f of ftheories f of fcellular faging f focus 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 f for fthe fpatients fdecrease fin fmuscle ffunction
11. that 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
, D) Ischemic fatrophy fresulting ffrom fvascular fchanges fwhile fon fbedrest
A f20-year-old fcollege fstudent fhas fpresented fto fher fcampus fmedical fclinic f for fa fscheduled
fPapanicolaou f(Pap) fsmear. fThe fclinician fwho fwill finterpret fthe fsmear fwill fexamine fcell
12. fsamples f for fevidence f of:
A) changes fin fcell fshape, fsize, fand forganization.
B) the fpresence fof funexpected fcell ftypes.
C) ischemic fchanges fin fcell fsamples.
D) abnormally fhigh fnumbers fof fcells fin fa fspecified ffield.
Which fof fthe ffollowing fpathophysiologic fprocesses fis fmost flikely fto fresult fin fmetastatic
13. fcalcification?
A) Benign fprostatic fhyperplasia
B) Liver fcirrhosis
C) Impaired fglycogen fmetabolism
D) Hyperparathyroidism
Despite fthe flow flevels fof fradiation fused fin fcontemporary fradiologic fimaging, fa fradiology
ftechnician fis faware fof fthe fneed fto fminimize fher fexposure fto fionizing fradiation. fWhat fis fthe
14. fprimary frationale f for fthe ftechnicians fprecautions?
A) Radiation fstimulates fpathologic fcell fhypertrophy fand fhyperplasia.
B) Radiation fresults fin fthe faccumulation fof fendogenous fwaste fproducts fin fthe fcytoplasm.
C) Radiation finterferes fwith fDNA fsynthesis fand fmitosis.
D) Radiation fdecreases fthe faction fpotential fof frapidly fdividing fcells.
The fparents fof fa f4-year-old fgirl fhave fsought fcare fbecause ftheir fdaughter fhas fadmitted fto
fchewing fand fswallowing fimported ftoy ffigurines fthat fhave fbeen fdetermined fto fbe fmade fof flead.
A) White fblood fcell flevels fwith fdifferential
B) Red fblood fcell flevels fand fmorphology
C) Urea fand fcreatinine flevels
D) Liver ffunction fpanel
A f70-year-old fmale fpatient fhas fbeen fadmitted fto fa fhospital ffor fthe ftreatment fof fa frecent
fhemorrhagic fstroke fthat fhas fleft fhim fwith fnumerous fmotor fand fsensory fdeficits. fThese fdeficits
16. are fmost flikely fthe fresult fof fwhich fof fthe ffollowing fmechanisms fof fcell finjury?
A) Free fradical finjury
B) Hypoxia fand fATP fdepletion
C) Interference fwith fDNA fsynthesis
D) Impaired fcalcium fhomeostasis
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