PATHO UTA TEST 1 EXAM WITH 100%
CORRECT ANSWERS
Atrophy ng- ng ngcorrect nganswer- ngDecrease ngor ngshrinkage ngin ngcell ngsize
ngHypertrophy ng- ng ngcorrect nganswer- ngIncrease ngin ngsize ngof ngcells ngthat ngincrease
ngsize ngof ngaffected ngOrgan
ngHyperplasia ng- ng ngcorrect nganswer- ngIncrease ngnumber ngof ngcells ngin ngan ngorgan
ngor ngtissue ngresulting ngfrom ngan ngincreased ngrate ngof ngcellular ngdivision. ngResults
ngfrom nginjury ngthat ngis ngsevere ngand ngprolonged
ngCompensatory ngHyperplasia ng- ng ngcorrect nganswer- ngAbility ngof ngsome ngorgans ngto
ngregenerate
ngDysplasia ng(atypical nghyperplasia) ng- ng ngcorrect nganswer- ngAbnormal ngchanges ngin
ngsize ngshape ngand ngorganization ngof ngmature ngcells. ngNot nginvolving ngentire
ngthickness ngmay ngbe ngreversed. ngInvolving ngentire ngthickness ngmeans ngcarcinoma
ngin ngsitu ngpre-invasive ngneoplasm
ngMetaplasia ng- ng ngcorrect nganswer- ngReversible ngreplacement ngof ngone ngmature
ngcell ngtype ngby nganother
ngIschemia/hypoxic nginjury ng- ng ngcorrect nganswer- ngLack ngof ngoxygen ngdue ngto
ngdecreased ngoxygen ngin ngthe ngair, ngDecreased ngH/H ngfunction, ngdecreased
ngproduction ngof ngRBC, ngresults ngof ngrespiratory ngor ngcardiac ngdisease, ngpoisoning
ngof ngoxidative ngenzymes ngwithin ngthe ngcells
,ngArteriosclerosis ng- ng ngcorrect nganswer- ngGradual ngarterial ngNarrowing ngand
ngcomplete ngblockage ngby ngblood ngclots ngexample ngand ngMI/stroke
ngPhysiologic ngatrophy ng- ng ngcorrect nganswer- ngShrinkage ngof ngthymus nggland
ngduring ngchildhood
ngPathologic ngatrophy ng- ng ngcorrect nganswer- ngCauses ngdecrease ngin ngworkload,
ngpressure, nguse, ngblood ngsupply, ngnutrition, nghormonal ngStimulation, ngor ngnervous
ngstimulation
ngCauses ngof ngatrophy ng- ng ngcorrect nganswer- ngImbalance ngbetween ngprotein
ngsynthesis ngintegration ngincrease ngin ngcannibalism ngof ngthe ngintracellular
ngorganelles. ngReduction ngof ngstructural ngcomponents ngof ngthe ngcell.
ngAutophagy ng- ng ngcorrect nganswer- ngSelf ngeating ngprocess
ngHypoxic ngcellular nginjury ng- ng ngcorrect nganswer- ngIschemia ngwhich ngprogresses ngto
nghypoxia. ngLack ngof ngoxygen ngdelivered ngto ngthe ngcell ngcauses nga ngdecrease ngin
ngmitochondrial ngfunction. ngCausing nga ngdecrease ngproduction ngof ngATP ngand
ngincreases nganaerobic ngmetabolism
ngReperfusion nginjury ng- ng ngcorrect nganswer- ngMakes ngmassive ngamounts ngof ngfree
ngradicals, ngsuper ngoxide ngand nghydrogen ngperoxide ngfree ngradicals ngcause ngcell
ngdamage ngand ngmitochondrial ngcalcium ngoverload. ngReperfusion ngwill nglead ngto ngPH
ngalterations, ngosmotic ngchanges, nginflammatory ngsignaling ngand ngmitochondrial
ngcalcium ngoverload. ngCauses ngopening ngof ngmitochondrial ngpermeability ngtransition
ngpoor ngwhich ngallows ngfor ngthe ngescape ngof ngATP ngand ngleads ngto ngapoptosis
ngFree ngradicals ng- ng ngcorrect nganswer- ngProduced ngas nga ngresult ngof nga ngnormal
ngcellular ngrespiration, ngproduced ngby ngthe ngabsorption ngof ngextreme ngenergy
ngsources ngsuch ngas ngradiation ngare ngUV nglight, ngproduced ngby ngmetabolism ngof
ngchemicals, ngdrugs ngand ngpesticides, ngproduced ngby ngthe ngtransition ngof ngmetals,
ngproduced ngby ngnitric ngoxide ngacting nglike nga ngchemical ngmediator ngand ngas nga
ngfree ngradical
ngReactive ngoxygen ngspecies ng- ng ngcorrect nganswer- ngGenerated ngduring ngauto
ngoxidation ngin ngthe ngmitochondria ngor ngby ngintracellular ngenzymatic ngpathways.
ngIncreased nglevels ngcan nglead ngto ngcellular ngapoptosis
ngAlcohol ngdeficiencies ng- ng ngcorrect nganswer- ngFolic ngacid, ngmagnesium, ngvitamin
ngB ngsix, ngthiamine ngand ngphosphorus
ngnecrosis ng- ng ngcorrect nganswer- ngCell ngdeath ngoccurring ngin ngthe ngsetting ngof
ngirreversible ngcellular nginjury. ngCharacterized ngby ngrapid ngloss ngof ngplasma
ngmembrane, ngorganelle ngswelling, ngand ngmitochondrial ngdysfunction. ngLeads ngto
, nglocal ngcell ngdeath ngand ngauto nglysis ngwhich ngis ngwhen ngthe ngcell ngcomplete ngauto
ngdigestion.
ngApoptosis ng- ng ngcorrect nganswer- ngprocess ngof ngprogrammed ngcell ngdeath,
ngExpected ngcellular ngprocess ngwhich ngleads ngto ngthe ngcells ngdistraction. ngTriggered
ngby ngsevere ngcell nginjury, ngaccumulation ngof ngmiss ngfolded ngproteins,infections,
ngobstruction ngand ngtissue ngducts ngin ngorgans ngwith ngducts
ngAutophagy ng- ng ngcorrect nganswer- ngAuto ngdigestion ngof ngthe ngcell. ngA ngkey
ngmechanism ngand ngcellular ngproliferation ngin ngdevelopment, ngremodeling, ngaging,
ngcancer, ngheart ngdisease, ngNeurodegenerative ngdisease, ngantigen ngpresentation,
nginflammation nginfection, ngmetabolic ngdiseases.
ngAging ng- ng ngcorrect nganswer- ngProgressive ngloss ngof ngtissues ngand ngorgans ngover
ngtime. ngRisk ngfactors ngfor ngmany ngchronic ngdiseases.
ngSenescence ng- ng ngcorrect nganswer- ngComplete ngand ngpermanent ngcessation ngof
ngcellular ngproliferation. ngCells ngaccumulate ngover ngtime ngand ngcause ngorgan
ngdysfunction. ngCause nga ngloss ngof ngtissue ngrepair ngabilities ngand ngproduces
nginflammatory ngmolecules. ngHelpful ngfor ngwound nghealing ngand ngembryogenesis
ngExtracellular ngchanges ngwith ngaging ng- ng ngcorrect nganswer- ngFinding ngof ngcollagen,
ngincreased ngfree ngradical ngdamage, ngstructural ngchanges ngof ngthe ngfascia, ngtendons,
ngligaments, ngbones ngand ngjoints ngand ngthe ngdevelopment ngof ngarteriosclerosis.
ngAffected ngby ngdecreased ngsynthesis ngand ngincrease ngdegration ngof ngcollagen.
ngResult ngin ngdehydration ngand ngwrinkling ngof ngthe ngskin
ngBody ngchanges ngwith ngaging ng- ng ngcorrect nganswer- ngThymus ngatrophy nglosses ngof
ngova ngand ngwomen, ngdecreased ngspermatogenesis ngand ngmen, ngdecrease
ngresponses ngto nghormones ngfrom ngthe ngbreast ngtissue ngand nginjure ngmetria.
ngGastric ngemptying ngdecreases. ngMuscle ngatrophy ngresult ngfrom ngaging. ngHeight
ngdecreases ngneck ngthighand ngarm ngcircumference ngdecreases ngweight nggain
ngoccurs ngfor ngmen ngand ngfor ngwomen.
ngKetogenesis ng- ng ngcorrect nganswer- ngFormation ngof ngKeytone ngbodies ngand
ngoccurs ngmostly ngin ngthe ngmitochondria ngof ngthe nghepatic ngsites. ngoccurs ngas nga
ngresult ngof ngthe ngunavailability ngof ngglucose. ngDeficient ngamounts ngof ngglucose ngmay
ngoccur ngfrom ngthe ngdepletion ngof ngcarbohydrate ngstores ngor ngmay ngoccur ngbecause
ngthe ngcell ngis ngnot ngable ngto nguse ngglucose.
ngAction ngpotential ng- ng ngcorrect nganswer- ngProcess ngby ngwhich ngexcitable ngcells
ngtransmit nginformation ngto ngone nganother. ngTypically ngoccurs ngin ngnerve ngcells ngand
ngall ngtypes ngof ngmuscle ngcells. ngAlteration ngin ngthis ngmay ngresult ngfrom ngneurologic
ngdisease, ngmuscle ngdisease ngor ngelectrolyte ngin ngbalance ngis.
CORRECT ANSWERS
Atrophy ng- ng ngcorrect nganswer- ngDecrease ngor ngshrinkage ngin ngcell ngsize
ngHypertrophy ng- ng ngcorrect nganswer- ngIncrease ngin ngsize ngof ngcells ngthat ngincrease
ngsize ngof ngaffected ngOrgan
ngHyperplasia ng- ng ngcorrect nganswer- ngIncrease ngnumber ngof ngcells ngin ngan ngorgan
ngor ngtissue ngresulting ngfrom ngan ngincreased ngrate ngof ngcellular ngdivision. ngResults
ngfrom nginjury ngthat ngis ngsevere ngand ngprolonged
ngCompensatory ngHyperplasia ng- ng ngcorrect nganswer- ngAbility ngof ngsome ngorgans ngto
ngregenerate
ngDysplasia ng(atypical nghyperplasia) ng- ng ngcorrect nganswer- ngAbnormal ngchanges ngin
ngsize ngshape ngand ngorganization ngof ngmature ngcells. ngNot nginvolving ngentire
ngthickness ngmay ngbe ngreversed. ngInvolving ngentire ngthickness ngmeans ngcarcinoma
ngin ngsitu ngpre-invasive ngneoplasm
ngMetaplasia ng- ng ngcorrect nganswer- ngReversible ngreplacement ngof ngone ngmature
ngcell ngtype ngby nganother
ngIschemia/hypoxic nginjury ng- ng ngcorrect nganswer- ngLack ngof ngoxygen ngdue ngto
ngdecreased ngoxygen ngin ngthe ngair, ngDecreased ngH/H ngfunction, ngdecreased
ngproduction ngof ngRBC, ngresults ngof ngrespiratory ngor ngcardiac ngdisease, ngpoisoning
ngof ngoxidative ngenzymes ngwithin ngthe ngcells
,ngArteriosclerosis ng- ng ngcorrect nganswer- ngGradual ngarterial ngNarrowing ngand
ngcomplete ngblockage ngby ngblood ngclots ngexample ngand ngMI/stroke
ngPhysiologic ngatrophy ng- ng ngcorrect nganswer- ngShrinkage ngof ngthymus nggland
ngduring ngchildhood
ngPathologic ngatrophy ng- ng ngcorrect nganswer- ngCauses ngdecrease ngin ngworkload,
ngpressure, nguse, ngblood ngsupply, ngnutrition, nghormonal ngStimulation, ngor ngnervous
ngstimulation
ngCauses ngof ngatrophy ng- ng ngcorrect nganswer- ngImbalance ngbetween ngprotein
ngsynthesis ngintegration ngincrease ngin ngcannibalism ngof ngthe ngintracellular
ngorganelles. ngReduction ngof ngstructural ngcomponents ngof ngthe ngcell.
ngAutophagy ng- ng ngcorrect nganswer- ngSelf ngeating ngprocess
ngHypoxic ngcellular nginjury ng- ng ngcorrect nganswer- ngIschemia ngwhich ngprogresses ngto
nghypoxia. ngLack ngof ngoxygen ngdelivered ngto ngthe ngcell ngcauses nga ngdecrease ngin
ngmitochondrial ngfunction. ngCausing nga ngdecrease ngproduction ngof ngATP ngand
ngincreases nganaerobic ngmetabolism
ngReperfusion nginjury ng- ng ngcorrect nganswer- ngMakes ngmassive ngamounts ngof ngfree
ngradicals, ngsuper ngoxide ngand nghydrogen ngperoxide ngfree ngradicals ngcause ngcell
ngdamage ngand ngmitochondrial ngcalcium ngoverload. ngReperfusion ngwill nglead ngto ngPH
ngalterations, ngosmotic ngchanges, nginflammatory ngsignaling ngand ngmitochondrial
ngcalcium ngoverload. ngCauses ngopening ngof ngmitochondrial ngpermeability ngtransition
ngpoor ngwhich ngallows ngfor ngthe ngescape ngof ngATP ngand ngleads ngto ngapoptosis
ngFree ngradicals ng- ng ngcorrect nganswer- ngProduced ngas nga ngresult ngof nga ngnormal
ngcellular ngrespiration, ngproduced ngby ngthe ngabsorption ngof ngextreme ngenergy
ngsources ngsuch ngas ngradiation ngare ngUV nglight, ngproduced ngby ngmetabolism ngof
ngchemicals, ngdrugs ngand ngpesticides, ngproduced ngby ngthe ngtransition ngof ngmetals,
ngproduced ngby ngnitric ngoxide ngacting nglike nga ngchemical ngmediator ngand ngas nga
ngfree ngradical
ngReactive ngoxygen ngspecies ng- ng ngcorrect nganswer- ngGenerated ngduring ngauto
ngoxidation ngin ngthe ngmitochondria ngor ngby ngintracellular ngenzymatic ngpathways.
ngIncreased nglevels ngcan nglead ngto ngcellular ngapoptosis
ngAlcohol ngdeficiencies ng- ng ngcorrect nganswer- ngFolic ngacid, ngmagnesium, ngvitamin
ngB ngsix, ngthiamine ngand ngphosphorus
ngnecrosis ng- ng ngcorrect nganswer- ngCell ngdeath ngoccurring ngin ngthe ngsetting ngof
ngirreversible ngcellular nginjury. ngCharacterized ngby ngrapid ngloss ngof ngplasma
ngmembrane, ngorganelle ngswelling, ngand ngmitochondrial ngdysfunction. ngLeads ngto
, nglocal ngcell ngdeath ngand ngauto nglysis ngwhich ngis ngwhen ngthe ngcell ngcomplete ngauto
ngdigestion.
ngApoptosis ng- ng ngcorrect nganswer- ngprocess ngof ngprogrammed ngcell ngdeath,
ngExpected ngcellular ngprocess ngwhich ngleads ngto ngthe ngcells ngdistraction. ngTriggered
ngby ngsevere ngcell nginjury, ngaccumulation ngof ngmiss ngfolded ngproteins,infections,
ngobstruction ngand ngtissue ngducts ngin ngorgans ngwith ngducts
ngAutophagy ng- ng ngcorrect nganswer- ngAuto ngdigestion ngof ngthe ngcell. ngA ngkey
ngmechanism ngand ngcellular ngproliferation ngin ngdevelopment, ngremodeling, ngaging,
ngcancer, ngheart ngdisease, ngNeurodegenerative ngdisease, ngantigen ngpresentation,
nginflammation nginfection, ngmetabolic ngdiseases.
ngAging ng- ng ngcorrect nganswer- ngProgressive ngloss ngof ngtissues ngand ngorgans ngover
ngtime. ngRisk ngfactors ngfor ngmany ngchronic ngdiseases.
ngSenescence ng- ng ngcorrect nganswer- ngComplete ngand ngpermanent ngcessation ngof
ngcellular ngproliferation. ngCells ngaccumulate ngover ngtime ngand ngcause ngorgan
ngdysfunction. ngCause nga ngloss ngof ngtissue ngrepair ngabilities ngand ngproduces
nginflammatory ngmolecules. ngHelpful ngfor ngwound nghealing ngand ngembryogenesis
ngExtracellular ngchanges ngwith ngaging ng- ng ngcorrect nganswer- ngFinding ngof ngcollagen,
ngincreased ngfree ngradical ngdamage, ngstructural ngchanges ngof ngthe ngfascia, ngtendons,
ngligaments, ngbones ngand ngjoints ngand ngthe ngdevelopment ngof ngarteriosclerosis.
ngAffected ngby ngdecreased ngsynthesis ngand ngincrease ngdegration ngof ngcollagen.
ngResult ngin ngdehydration ngand ngwrinkling ngof ngthe ngskin
ngBody ngchanges ngwith ngaging ng- ng ngcorrect nganswer- ngThymus ngatrophy nglosses ngof
ngova ngand ngwomen, ngdecreased ngspermatogenesis ngand ngmen, ngdecrease
ngresponses ngto nghormones ngfrom ngthe ngbreast ngtissue ngand nginjure ngmetria.
ngGastric ngemptying ngdecreases. ngMuscle ngatrophy ngresult ngfrom ngaging. ngHeight
ngdecreases ngneck ngthighand ngarm ngcircumference ngdecreases ngweight nggain
ngoccurs ngfor ngmen ngand ngfor ngwomen.
ngKetogenesis ng- ng ngcorrect nganswer- ngFormation ngof ngKeytone ngbodies ngand
ngoccurs ngmostly ngin ngthe ngmitochondria ngof ngthe nghepatic ngsites. ngoccurs ngas nga
ngresult ngof ngthe ngunavailability ngof ngglucose. ngDeficient ngamounts ngof ngglucose ngmay
ngoccur ngfrom ngthe ngdepletion ngof ngcarbohydrate ngstores ngor ngmay ngoccur ngbecause
ngthe ngcell ngis ngnot ngable ngto nguse ngglucose.
ngAction ngpotential ng- ng ngcorrect nganswer- ngProcess ngby ngwhich ngexcitable ngcells
ngtransmit nginformation ngto ngone nganother. ngTypically ngoccurs ngin ngnerve ngcells ngand
ngall ngtypes ngof ngmuscle ngcells. ngAlteration ngin ngthis ngmay ngresult ngfrom ngneurologic
ngdisease, ngmuscle ngdisease ngor ngelectrolyte ngin ngbalance ngis.
