NBME PATHOLOGY FINAL EXAM NEWEST 2024
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ACTUAL EXAM 2 VERSIONS (VERSION A AND B)
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COMPLETE 400 QUESTIONS AND CORRECT
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DETAILED ANSWERS (VERIFIED ANSWERS)
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|ALREADY GRADED A+||BRAND NEW VERSION!
g g g g
VERSIONgA
Typicalgvignettegforgsarcoidosisg-
gANSWERnonspecificgsymptomsglikegcough,gangina,gdyspnea,gfatigue,gfever,gweightglos
s,gskinglesions
Histologicalgfindingsgforgsarcoidosisg-gANSWERnon-
caseatingggranulomas,gmultinucleatedgepithelioidgcells,ggiantgcells,glymphocytes.
- well-formed,gepithelioid,gnon-
necrotizingggranulomasgdistributedgalonggtheglymphaticsgneargbronchigandgbloodgvess
elsg(lymphangiticgpattern)
- bilateralghilargadenopathygongCXR
Sarcoidosisgisgonegpotentialgcausegofg-gANSWERrestrictiveglunggdisease
Whatglabsgmightgbegelevatedgingpatientsgwithgsarcoidosis?g-gANSWER-
gelevatedgserumgACEglevels
- elevatedgESR
- elevatedgC-reactivegprotein
- hypercalcemia
- hypercalciuria
EpsteingBarrgVirusgroutegofgtransmissiong-gANSWER-grespiratorygsecretions,gsaliva
- "kissinggdiseases"
Epstein-BarrgVirusgtypicalgpresentationg-gANSWER-gteengorgyounggadult
- fatigue,gfever,gsoregthroat,genlargedglymphgnodes
- swollen,gerythematousgtonsils
EPVglabgfindingsg-gANSWER-gelevatedgALTgandgAST
- positivegmonospotgtestg-gheterophilegantibodygtest
- lymphocytosis
,Wheregdogkidneygstonesgform?g-
gANSWERMaygoccurganywheregalonggthegurinarygtract:grenalgtubules,grenalgpelvis,guret
ers,gbladder,gand/orgurethra.
1. ureteropelvicgjunction:gwheregrenalgpelvisgtransitionsgintogthegureter
2. ureterovesicalgjunction:gwhereguretergmeetsgurinarygbladder
3. mid-ureter
4. distalgureter
Whatgaregthegdifferentgnephrolithiasisgconditionsg(3)?g-gANSWER-
gstaghorngcalculus:gmixturegofgmagnesiumgammoniumgphosphategandgcalciumgphospha
te.gArisegingagsettinggofgchronicgurinaryginfectiongwithgureasegsplittinggbacteriaglikegProte
usgmirabilis
- calciumgoxalategstones:gmostgcommon,goccursgwhengcalciumgbindsgwithgoxalategduegt
ogexcessgoxalate.gTreatedgwithgdietgchanges,gincreasedgfluidgintake,gsometimesgthiazid
es.
- uricgacidgstones:gexcessgpurines.gtreatedgbygincreasinggurinegpH,gdietgchange,gflui
dgintake.
PathogenesisgofgPSGNg-gANSWER-
gTypegIIIghypersensitivitygreactiong(immunegcomplexgmediated);gcirculatinggorgplantedga
ntigen
PSGNglightgmicroscopyg-
gANSWERdiffusegendocapillarygproliferation;gleukocyticginfiltration
PSGNgDIFg-gANSWERgranulargIgGgandgC3gingGBMgandgmesangium
PSGN:gElectrongMicroscopyg-
gANSWERSubepithelialghumps,gsubendothelialgdepositsgingearlygdiseasegstages
PSGNgclinicalgpresentationg-gANSWER-grecentghistorygofggroupgAgstrep
- cangrangegfromgasymptomaticgmicroscopicghematuriagtogfull-blowngnephriticgsyndrome
Rapidlygprogessivegglomerulonephritisg(RPGN)gclinicalgpresentationg-gANSWER-
gnephriticgsyndrome,grapidgprogression
PSGNghistologicgfindingsg-gANSWER-gglomeruligareghypercellulargandgenlarged
- globalgandgdiffuse
- interstitialgedemagandginflammation
- presencegofgWBCsgingglomerulargcapillarygloops,gdamagegtogglomeruli,gRBCsgandgRB
CgcastsgingthegtubulesgallgleadgtogWBCs,gRBCs,gandgRBCgcastsgingthegurine.
PSGNglabgfindingsg-gANSWER-
gRBCs,gRBCgcasts,gdysmorphicgRBCs,gWBCs,gandgproteingingurine
- elevatedgASOgtiters
- decreasedgC3gandgnormalgC4gserumgcomplementglevels
- Throatgandgskingculturesgoftengnegative
DescribegGoodpasturegSyndromeg-gANSWER-gduegtoganti-GBMgAbs
,- causesgglomerulonephritisgandgpulmonaryghemorrhage
WhatgisgthegmostgcharacteristicgfindinggofgRPGN?g-gANSWER-
gglomerulargcrescentsgconsistinggofgproliferatinggparietalgcells,gmonocytes,gmacrophage
s,gTglymphocytes,gplasmagproteins,gchemokines,gcytokines,gandgoftengfibringstrands.
RPGNglightgmicroscopyg-gANSWER-gextracapillarygproliferationgwithgcrescents;gnecrosis
WhatgaregthreegpotentialgcausesgofgRPGN?g-gANSWER1.gGoodpasturegSyndrome
2. Granulomatosisgwithgpolyangiitis
3. Systemicglupusgerythematosus
DescribegthegIFgstaininggpatternsgofgRPGNgwithgrespectgtogthegthreegpotentialgcauses.
g-gANSWER-gGoodpasturegSyndrome:glineargstaininggofgGBMgwithgIgG
- Granulomatosisgwithgpolyangiitis:gnogdeposits
- SLE:ggranulargdeposits
RPGNgelectrongmicroscopyg-gANSWER-
gwrinklinggofgthegGBMgwithgfocalgdisruptionsgisgpresentgingallgtypesgofgthegdisease
WhatgkindgofghypersensitivitygreactiongisgGoodpasturegsyndrome?g-
gANSWERTypegIIg(antibodygmediated)
TreatmentgforgGoodpasturegsyndromeg-gANSWER-gintensivegplasmapheresis
- corticosteroids
- cytotoxicgagents
DescribegminimalgchangegdiseasegMOAg-gANSWER-
gunknowngetiologygbutgthoughtgtogbegimmune-mediated
- damagegtogpodocytegfootgprocessesgallowsgleakagegofgalbumingintogthegurinarygspac
eg(nephrotic)
MCDghistologicgfindingsg-gANSWER-gmostgglomeruligaregnormal
- cellsgingPCTgmayghavegfoamygorggranulargcytoplasmgduegtoglipidgandgproteingresorptio
n
MCDgDIFgfindingsg-gANSWER-gnegative
MCD,gelectrongmicroscopyg-gANSWER-geffacementgofgfootgprocesses,gnogdeposits
HowgdoesgexcessivegproteinuriagingMCDgcausegedema?g-gANSWER-
glossgofgproteingthroughgurinegcausesghypoproteinemia,gwhichgresultsgingdecreasedgintra
vasculargcolloidgosmoticgpressure.
- fluidgescapesgintoginterstitium,gdecreasesgplasmagvolumegandgGFR
- ActivationgofgRAASgandgreleasegofgnatriureticgpeptidesgwhichgcausesgwatergretention
, HowgdoesgMCDgcauseghypercholesterolemia?g-
gANSWERSignificantghypoproteinemiagleadsgtogcompensatorygproteingsynthesisgbygtheg
liver,gincludingglipoproteins.
WhatgisgthegtreatmentgforgMCD?g-gANSWERcorticosteroids
MembranousgNephropathygpathogenesisg-gANSWER-
gIgG4gAbsgaregdirectedgagainstgagpodocytegmembranegantigenglikegPLA2R.gThesegAbsg
cangactivategthegMACgandgdamagegpodocytes.
HowgisgMNgtreatmentgdifferentgfromgMCD?g-
gANSWERMNgdoesgnotgrespondgwellgtogcorticosteroids
MNgclinicalgmanifestationsg-gANSWER-gedemagandgascitesgfromghypoalbuminemia
- hypercoagulablegstategwithgrenalgveingorgDVTgfromglossgofgantithrombing3,gorgproteinsg
CgorgSgingurine
- hypercholesterolemia
- hypogammaglobulinemiagfromgurinaryglossg(nonselectivegproteinuria)
MNghistologicgfindingsg-gANSWER-genlargedgglomeruligbutgnormalgcellularity
- peripheralgcapillarygwallsgdiffuselygthickened
- spikegandgdomegappearance
- segmentalgorgglobalgsclerosis
- interstitialgmononuclearginflammationgandgfoamygproximalgtubulargepithelialgcells
MNglightgmicroscopyg-gANSWERdiffusegcapillarygwallgthickening
MNgDIFg-gANSWER-ggranulargIgGgandgC3galonggGBM;gdiffuse
MNgelectrongmicroscopyg-
gANSWERsubepithelialgdepositsgfootgprocessgeffacement
WhatgaregsomegcommongcausesgofgsecondarygMN?g-gANSWER-gmalignancies
- infections
- drugs
- toxins
- autoimmunegdiseases
- SLE
CausegofgIgAgnephropathyg-
gANSWERIgAgimmunegdepositiongingthegglomerulargmesangium
IgAgnephropathygpathogenesisg-
gANSWERabnormallygglycosylatedgIgA1gmoleculesgfromgmucosagexposeghiddengisotop
es,gleadinggtogimmunegcomplexgformationgingthegcirculation.gThesegcomplexesgdepositgi
ngthegmesangium.
ClinicalgpresentationgofgIgAgnephropathyg-gANSWERrecurrentghematuriagorgproteinuria
g g g g g g
ACTUAL EXAM 2 VERSIONS (VERSION A AND B)
g g g g g g g g
COMPLETE 400 QUESTIONS AND CORRECT
g g g g
DETAILED ANSWERS (VERIFIED ANSWERS)
g g g
|ALREADY GRADED A+||BRAND NEW VERSION!
g g g g
VERSIONgA
Typicalgvignettegforgsarcoidosisg-
gANSWERnonspecificgsymptomsglikegcough,gangina,gdyspnea,gfatigue,gfever,gweightglos
s,gskinglesions
Histologicalgfindingsgforgsarcoidosisg-gANSWERnon-
caseatingggranulomas,gmultinucleatedgepithelioidgcells,ggiantgcells,glymphocytes.
- well-formed,gepithelioid,gnon-
necrotizingggranulomasgdistributedgalonggtheglymphaticsgneargbronchigandgbloodgvess
elsg(lymphangiticgpattern)
- bilateralghilargadenopathygongCXR
Sarcoidosisgisgonegpotentialgcausegofg-gANSWERrestrictiveglunggdisease
Whatglabsgmightgbegelevatedgingpatientsgwithgsarcoidosis?g-gANSWER-
gelevatedgserumgACEglevels
- elevatedgESR
- elevatedgC-reactivegprotein
- hypercalcemia
- hypercalciuria
EpsteingBarrgVirusgroutegofgtransmissiong-gANSWER-grespiratorygsecretions,gsaliva
- "kissinggdiseases"
Epstein-BarrgVirusgtypicalgpresentationg-gANSWER-gteengorgyounggadult
- fatigue,gfever,gsoregthroat,genlargedglymphgnodes
- swollen,gerythematousgtonsils
EPVglabgfindingsg-gANSWER-gelevatedgALTgandgAST
- positivegmonospotgtestg-gheterophilegantibodygtest
- lymphocytosis
,Wheregdogkidneygstonesgform?g-
gANSWERMaygoccurganywheregalonggthegurinarygtract:grenalgtubules,grenalgpelvis,guret
ers,gbladder,gand/orgurethra.
1. ureteropelvicgjunction:gwheregrenalgpelvisgtransitionsgintogthegureter
2. ureterovesicalgjunction:gwhereguretergmeetsgurinarygbladder
3. mid-ureter
4. distalgureter
Whatgaregthegdifferentgnephrolithiasisgconditionsg(3)?g-gANSWER-
gstaghorngcalculus:gmixturegofgmagnesiumgammoniumgphosphategandgcalciumgphospha
te.gArisegingagsettinggofgchronicgurinaryginfectiongwithgureasegsplittinggbacteriaglikegProte
usgmirabilis
- calciumgoxalategstones:gmostgcommon,goccursgwhengcalciumgbindsgwithgoxalategduegt
ogexcessgoxalate.gTreatedgwithgdietgchanges,gincreasedgfluidgintake,gsometimesgthiazid
es.
- uricgacidgstones:gexcessgpurines.gtreatedgbygincreasinggurinegpH,gdietgchange,gflui
dgintake.
PathogenesisgofgPSGNg-gANSWER-
gTypegIIIghypersensitivitygreactiong(immunegcomplexgmediated);gcirculatinggorgplantedga
ntigen
PSGNglightgmicroscopyg-
gANSWERdiffusegendocapillarygproliferation;gleukocyticginfiltration
PSGNgDIFg-gANSWERgranulargIgGgandgC3gingGBMgandgmesangium
PSGN:gElectrongMicroscopyg-
gANSWERSubepithelialghumps,gsubendothelialgdepositsgingearlygdiseasegstages
PSGNgclinicalgpresentationg-gANSWER-grecentghistorygofggroupgAgstrep
- cangrangegfromgasymptomaticgmicroscopicghematuriagtogfull-blowngnephriticgsyndrome
Rapidlygprogessivegglomerulonephritisg(RPGN)gclinicalgpresentationg-gANSWER-
gnephriticgsyndrome,grapidgprogression
PSGNghistologicgfindingsg-gANSWER-gglomeruligareghypercellulargandgenlarged
- globalgandgdiffuse
- interstitialgedemagandginflammation
- presencegofgWBCsgingglomerulargcapillarygloops,gdamagegtogglomeruli,gRBCsgandgRB
CgcastsgingthegtubulesgallgleadgtogWBCs,gRBCs,gandgRBCgcastsgingthegurine.
PSGNglabgfindingsg-gANSWER-
gRBCs,gRBCgcasts,gdysmorphicgRBCs,gWBCs,gandgproteingingurine
- elevatedgASOgtiters
- decreasedgC3gandgnormalgC4gserumgcomplementglevels
- Throatgandgskingculturesgoftengnegative
DescribegGoodpasturegSyndromeg-gANSWER-gduegtoganti-GBMgAbs
,- causesgglomerulonephritisgandgpulmonaryghemorrhage
WhatgisgthegmostgcharacteristicgfindinggofgRPGN?g-gANSWER-
gglomerulargcrescentsgconsistinggofgproliferatinggparietalgcells,gmonocytes,gmacrophage
s,gTglymphocytes,gplasmagproteins,gchemokines,gcytokines,gandgoftengfibringstrands.
RPGNglightgmicroscopyg-gANSWER-gextracapillarygproliferationgwithgcrescents;gnecrosis
WhatgaregthreegpotentialgcausesgofgRPGN?g-gANSWER1.gGoodpasturegSyndrome
2. Granulomatosisgwithgpolyangiitis
3. Systemicglupusgerythematosus
DescribegthegIFgstaininggpatternsgofgRPGNgwithgrespectgtogthegthreegpotentialgcauses.
g-gANSWER-gGoodpasturegSyndrome:glineargstaininggofgGBMgwithgIgG
- Granulomatosisgwithgpolyangiitis:gnogdeposits
- SLE:ggranulargdeposits
RPGNgelectrongmicroscopyg-gANSWER-
gwrinklinggofgthegGBMgwithgfocalgdisruptionsgisgpresentgingallgtypesgofgthegdisease
WhatgkindgofghypersensitivitygreactiongisgGoodpasturegsyndrome?g-
gANSWERTypegIIg(antibodygmediated)
TreatmentgforgGoodpasturegsyndromeg-gANSWER-gintensivegplasmapheresis
- corticosteroids
- cytotoxicgagents
DescribegminimalgchangegdiseasegMOAg-gANSWER-
gunknowngetiologygbutgthoughtgtogbegimmune-mediated
- damagegtogpodocytegfootgprocessesgallowsgleakagegofgalbumingintogthegurinarygspac
eg(nephrotic)
MCDghistologicgfindingsg-gANSWER-gmostgglomeruligaregnormal
- cellsgingPCTgmayghavegfoamygorggranulargcytoplasmgduegtoglipidgandgproteingresorptio
n
MCDgDIFgfindingsg-gANSWER-gnegative
MCD,gelectrongmicroscopyg-gANSWER-geffacementgofgfootgprocesses,gnogdeposits
HowgdoesgexcessivegproteinuriagingMCDgcausegedema?g-gANSWER-
glossgofgproteingthroughgurinegcausesghypoproteinemia,gwhichgresultsgingdecreasedgintra
vasculargcolloidgosmoticgpressure.
- fluidgescapesgintoginterstitium,gdecreasesgplasmagvolumegandgGFR
- ActivationgofgRAASgandgreleasegofgnatriureticgpeptidesgwhichgcausesgwatergretention
, HowgdoesgMCDgcauseghypercholesterolemia?g-
gANSWERSignificantghypoproteinemiagleadsgtogcompensatorygproteingsynthesisgbygtheg
liver,gincludingglipoproteins.
WhatgisgthegtreatmentgforgMCD?g-gANSWERcorticosteroids
MembranousgNephropathygpathogenesisg-gANSWER-
gIgG4gAbsgaregdirectedgagainstgagpodocytegmembranegantigenglikegPLA2R.gThesegAbsg
cangactivategthegMACgandgdamagegpodocytes.
HowgisgMNgtreatmentgdifferentgfromgMCD?g-
gANSWERMNgdoesgnotgrespondgwellgtogcorticosteroids
MNgclinicalgmanifestationsg-gANSWER-gedemagandgascitesgfromghypoalbuminemia
- hypercoagulablegstategwithgrenalgveingorgDVTgfromglossgofgantithrombing3,gorgproteinsg
CgorgSgingurine
- hypercholesterolemia
- hypogammaglobulinemiagfromgurinaryglossg(nonselectivegproteinuria)
MNghistologicgfindingsg-gANSWER-genlargedgglomeruligbutgnormalgcellularity
- peripheralgcapillarygwallsgdiffuselygthickened
- spikegandgdomegappearance
- segmentalgorgglobalgsclerosis
- interstitialgmononuclearginflammationgandgfoamygproximalgtubulargepithelialgcells
MNglightgmicroscopyg-gANSWERdiffusegcapillarygwallgthickening
MNgDIFg-gANSWER-ggranulargIgGgandgC3galonggGBM;gdiffuse
MNgelectrongmicroscopyg-
gANSWERsubepithelialgdepositsgfootgprocessgeffacement
WhatgaregsomegcommongcausesgofgsecondarygMN?g-gANSWER-gmalignancies
- infections
- drugs
- toxins
- autoimmunegdiseases
- SLE
CausegofgIgAgnephropathyg-
gANSWERIgAgimmunegdepositiongingthegglomerulargmesangium
IgAgnephropathygpathogenesisg-
gANSWERabnormallygglycosylatedgIgA1gmoleculesgfromgmucosagexposeghiddengisotop
es,gleadinggtogimmunegcomplexgformationgingthegcirculation.gThesegcomplexesgdepositgi
ngthegmesangium.
ClinicalgpresentationgofgIgAgnephropathyg-gANSWERrecurrentghematuriagorgproteinuria
