NBME 7 Explanations

Block 1
4. E.Primordialgermcellmigration:thetumorshowsahaphazardarrangementofsomatictissues
representingderivativesofecto...,meso..andendoderm.....itisacharacteristicofgermcells.Teratomais
derivativeofprimitivestreakwhichinvolvesprocessofgermcellmigration.Fornumber4...Thisisacase
ofSacrococcygealteratoma..)....Sacrococcygealteratomaisoneoftheextragonadalgermcelltumors...
Thesetumorscanbefoundanywhereonthemidline,particularlytheretroperitoneum,theanterior
mediastinum,thesacrococcyx,andthepinealgland.Otherlesscommonsitesincludetheorbit,suprasellar
area,palate,thyroid,submandibularregion,anteriorabdominalwall,stomach,liver,vagina,andprostate.
Theclassictheorysuggeststhatgermcelltumors(GCTs)intheseareasarederivedfromlocal
transformationofprimordialgermcellsmisplacedduringembryogenesis...whichmeansdefectin
primordialgermcellmigrationhttp://emedicine.medscape.com/article/278174overview.....MyanswerIs
EEF...isforsacralagenesisSomitedevelopmentD..isforspinabifidaneuraltubeclosureC..is
forneurocristopathies,whichincludeconditionssuchasfrontonasaldysplasia,WaardenburgShah
syndrome,andDiGeorgesyndrome,......etcneuralcrestformationB..isclearHematopoiesisA...isfor
cranialabnormalities.....headmesenchymeproliferation
6.B.ClassIIMHCmoleculepeptideloadingProfessionalAPCsareveryefficientatinternalizingantigen,
eitherbyphagocytosis.Theacidiccompartmentsofmacrophagesarealsoresponsibleforthedegradation
ofingestedmicroorganisms)orbyreceptormediatedendocytosis,andthendisplayingafragmentofthe
antigen,boundtoaclassIIMHCmolecule,ontheirmembrane.TheTcellrecognizesandinteractswith
theantigenclassIIMHCmoleculecomplexonthemembraneoftheantigenpresentingcell.
7. D.Pyruvatecarboxylasetheproblemisthatsheishypoglycemiaandthenwithaninfusionw/glucose,
ithelps.Sotheproblem,ismakingglucosehence,youneedpyruvatecarboxylaseenzymefor
gluconeogenesis.Adeficiencyofpyruvatecarboxylasecancauselacticacidosisasaresultoflactatebuild
up.Normally,excesspyruvateisshuntedintogluconeogenesisviaconversionofpyruvateinto
oxaloacetate,butbecauseoftheenzymedeficiency,excesspyruvateisconvertedintolactateinstead.Asa
keyroleofgluconeogenesisisinthemaintenanceofbloodsugar,deficiencyofpyruvatecarboxylasecan
alsoleadtohypoglycemiaPyruvatecarboxylaseisamitochondriaenzymerequiringbiotin.Itisactivated
byacetylCoA(frombetaoxidation.Theproductoxaloacetate(OAA),acitricacidcycleintermediate,
cannotleavethemitochondriabutisreducedtomalatethatcanleaveviaaMalateshuffle.Inthecytoplasm
malateisreducedto(OAA).Pyruvatecarboxylasedeficiencyisaninheriteddisorderthatcauseslacticacid
andotherpotentiallytoxiccompoundstoaccumulateintheblood.Highlevelsofthesesubstancescan
damagethebody'sorgansandtissues,particularlyinthenervoussystem.Pyruvatecarboxylasedeficiency
isararecondition,withanestimatedincidenceof1in250,000birthsworldwide.Thisdisorderappearsto
bemuchmorecommoninsomeAlgonkianIndiantribesineasternCanada.
8.A.GolgicomplexIcelldiseaseisanautosomalrecessivedisordercausedbyadeficiencyofGlcNAc
phosphotransferase,whichphosphorylatesmannoseresiduestomannose6phosphateonNlinked
glycoproteinsintheGolgiapparatuswithinthecell.Withoutmannose6phosphatetotargetthemtothe
lysosomes,theenzymesaretransportedfromtheGolgitotheextracellularspace,resultinginlarge
intracellularinclusionsofmoleculesrequiringlysosomaldegradationinpatientswiththedisease.The
Golgiapparatusisunabletotargetthelysosomalprotein(whichisnormal)tothelysosome.Withoutproper
functioningofNacetylglucosamine1phosphotransferase,abuildupofsubstancesoccurswhenenzymes
areunabletotravelinsideofthelysosomeICellDisease:(Inclusioncelldisease).Inheritedlysosomal
storagedisorder;failureofadditiontomannose6phosphatetolysosomeproteins(enzymearesecreted
outsidethecellinsteadofbeingtargetedtothelysosme.Resultincoarsefacialfuture,cloudedcorneas,
restrictedjoinmovement,andhighplamalevelsoflysosomes.Oftenfatalchildhood.
19. B.GM2gangliosideTaysachdisease:AR,Progresiveneurodegeneration,developmentaldelay,
cherryredspotonmacula,lysosomalwithonionskin,NOHEPATOMEGALY.Def.enzime:
HexosaminidaseA;Accumulatedsubstrate:G2ganglioside.(FApage111).
25. D.Rest(systolic<diastolic)vs.Moderateexercise(systolic<diastolic)thecardiaccyclewhereby
coronaryarteriesdeliveroxygentothemyocardiumisduringdiastole........whetheritissystolicor
diastolic.....thisismyassumption.nomatterifthepersonisatrestordoingexercise,thecoronaryblood

flowisalwaysmoreduringdiastole.althoughthedurationofflowisgreatestduringrestasopposeto
exercisewhentheheartrateisfasterandthusdiastoleisoflessduration.Coronarybloodflowoccurs
mostlyduringdiastole,becauseduringsystolethebloodvesselswithinthemyocardiumarecompressed.
Increasedheartrates,whichreducethetimefordiastolefilling,canreducethemyocardialbloodsupply
andcauseischemia.Dynamicexerciseincreasescoronarybloodflowinproportiontotheheartrate,with
peakvaluesduringmaximalexercisetypicallythreetofivetimestherestinglevel.
32. C.ThyroidstimulatinghormoneTSH:Thyroidstimulatinghormone(alsoknownasTSHor
thyrotropin)isapeptidehormonesynthesizedandsecretedbythyrotropecellsintheanteriorpituitary
gland,whichregulatestheendocrinefunctionofthethyroidgland.TSHisthe1ststepinevaluationof
thyroidfunction.
33. B.AdenocarcinomaoftheendometriumAdenocarcinomaoftheendometrium:Carcinoma
endometrialistheMostcommongynecologicmalignancy.peakoccurrenceat5565yearofage.Clinically
presentswithvaginalbleeding.Typicallyproceededbyendometrialhyperplasia.Riskfactorsinclude
prolongeduseofestrogenwithoutprogestins,obesity,diabetes,hypertension,nulliparityandlate
menopause.Increasemyometrialinvasion,decreaseprognosis.(FApage487)
34. C.GlobuspallidusParkinsondiseaseSurgeryanddeepbrainstimulationPlacementofanelectrode
intothebrain.Theheadisstabilizedinaframeforstereotacticsurgery.Treatingmotorsymptomswith
surgerywasonceacommonpractice,butsincethediscoveryoflevodopa,thenumberofoperations
declined.Studiesinthepastfewdecadeshaveledtogreatimprovementsinsurgicaltechniques,sothat
surgeryisagainbeingusedinpeoplewithadvancedPDforwhomdrugtherapyisnolongersufficient.[35]
SurgeryforPDcanbedividedintwomaingroups:lesionalanddeepbrainstimulation(DBS).Targetareas
forDBSorlesionsincludethethalamus,theglobuspallidusorthesubthalamicnucleus.[35]Deepbrain
stimulation(DBS)isthemostcommonlyusedsurgicaltreatment.Itinvolvestheimplantationofamedical
devicecalledabrainpacemaker,whichsendselectricalimpulsestospecificpartsofthebrain.DBSis
recommendedforpeoplewhohavePDwhosufferfrommotorfluctuationsandtremorinadequately
controlledbymedication,ortothosewhoareintoleranttomedication,aslongastheydonothavesevere
neuropsychiatricproblems.[29]Other,lesscommon,surgicaltherapiesinvolvetheformationoflesionsin
specificsubcorticalareas(atechniqueknownaspallidotomyinthecaseofthelesionbeingproducedinthe
globuspallidus)
37. C.IleumCrohnDisease:Alsoknownasregionalenteritis,isaninflammatorydiseaseoftheintestines
thatmayaffectanypartofthegastrointestinaltractfrommouthtoanus,causingawidevarietyof
symptoms.Itprimarilycausesabdominalpain,diarrhea(whichmaybebloodyifinflammationisatits
worst),vomiting,orweightloss,[1][2][3]butmayalsocausecomplicationsoutsidethegastrointestinal
tractsuchasskinrashes,arthritis,inflammationoftheeye,tiredness,andlackofconcentration.[1]Crohn's
diseaseisthoughttobeanautoimmunedisease,inwhichthebody'simmunesystemattacksthe
gastrointestinaltract,causinginflammation;itisclassifiedasatypeofinflammatoryboweldisease.There
isevidenceofageneticlinktoCrohn'sdisease,puttingindividualswithsiblingsafflictedwiththedisease
athigherrisk.[4]Itisthoughttohavealargeenvironmentalcomponentasevidencedbyahigherincidence
inwesternindustrializednationscomparedtootherpartsoftheworld.Malesandfemalesareequally
affected.SmokersaretwotimesmorelikelytodevelopCrohn'sdiseasethan.Grossmorphology:
transmuralinflamation,Cobblestonemucosa,creepingfat,bowellwallthickning,(stringsignonbarium
swallowxray)linear,ulcers,fissures,fistulas.Microscopicmorphology:Noncaseatinggranulomasand
lymphoid
39. C.MembranousnephropathyMembranousGlomerulonephritis:LMdiffusecapillaryandGBM
thickening.EM"spikeanddome"appearancewithsubepithelialdeposits.IFgranular.Causedbydrugs
(penicillamine,Gold,NSAID).Mostcommoncauseofadultnephroticsyndrome.Thecloselyrelated
termsmembranousnephropathy[1]andmembranousglomerulopathy[2]bothrefertoasimilar
constellationbutwithouttheassumptionofinflammation.Somepatientsmaypresentasnephrotic
syndromewithproteinuria,edemawithorwithoutrenalfailure.Othersmaybeasymptomaticandmaybe
pickeduponscreeningorurinalysisashavingproteinuria.Adefinitivediagnosisofmembranous
nephropathyrequiresakidneybiopsy.
41. F.Tronchantericbursa,Trochantericbursitisischaracterizedbypainfulinflammationofthebursa
locatedjustsuperficialtothegreatertrochanterofthefemur.Patientstypicallycomplainoflateralhippain,

althoughthehipjointitselfisnotinvolved.Thepainmayradiatedownthelateralaspectofthethigh.The
termgreatertrochantericpainsyndrome(GTPS)isnowbeingcommonlysubstitutedfortrochanteric
bursitis,becausetheinflammatoryetiologyofthepainisbeingrefutedbycurrentresearch,using
ultrasonographic,magneticresonanceimaging(MRI)based,andhistologicevidence.Flexionor
anteversion(140):iliopsoas(withpsoasmajorfromvertebralcolumn);tensorfascialatae,pectineus,
adductorlongus,adductorbrevis,andgracilis.Thighmusclesactingashipflexors:rectusfemorisand
sartorius.
43.C.MedialcollateralligamentMedialcollateralligament"knownasthetibialcollateralligament
too.MCLstrainsandtearsarefairlycommoninAmericanfootball.Mostlythecenterandtheguardsare
oneswhogetthisinjury,duetothegriptrendontheircleats.AnMCLinjurycanbeverypainfulandis
causedbyavalgusstresstoaslightlybentknee,oftenwhenlanding,bendingoronhighimpact.
Dependingonthegradeoftheinjury,thelowestgrade(grade1)cantakebetween2and10weeksforthe
injurytofullyheal.Recoverytimesforgrades2and3aredifficulttopredictbecauseoftheamountof
damagedonecantakeweekstoseveralmonths.Itisdifficulttoapplypressureontheinjuredlegforat
leastafewdays.
44. A.TheyattributedthedifferenceinsuccessratestochancealoneInorderforittobestagistical
significance,youneedthePvaluetobe0.05aka95%ButsincethePvaluehereis0.3aka70%..itisonly
duetochance.ThePvalueforastudyshouldbelessthan0.05.Thisvaluemeansthatwhenweperforma
study,the95%ofthetimetheobservationsarerite&5%ofthetimetheobservationareduetochance
alone.InthisquestionthevalueofPis0.3whichmeansthattheprobabilitythattheseobservationsaredue
tochancealoneis30%,whichisnotastatisticallyacceptablenumber.
48. .B.AcidificationcausingincreasedammoniumionexcretionAmmoniumisbasic,hence,toexcreteit,
youneedtoacidifiyit.Lactuloseinhibitsbacterialammoniaproductionbyacidifyingthecontentofthe
bowel.Itpromotesgrowthofcolonicflora.Thegrowingbiomassusesammoniaandnitrogenfromamino
acidstosynthesisebacterialprotein,whichinturninhibitsproteindegradationtoNH3.Lactuloseleadsto
lessammoniabyinhibitingbacterialureadegradationandreducescolonictransittime,thusreducingthe
timeavailableforammoniaproductionandexpeditingammoniaelimination.
49. D.MetaplasiaoftheesophagealepitheliumThisisacaseofGERD...withesophagitisforthelast8
months...Gastroesophagealrefluxdisease(GERD)occurswhentheamountofgastricjuicethatrefluxes
intotheesophagusexceedsthenormallimit,causingsymptomswithorwithoutassociatedesophageal
mucosalinjury(ie,esophagitis).PathogenesisofGERD...TransientrelaxationofLESandIneffective
esophagealclearanceofrefluxmaterial(bileacidandgastricjuice)...hencetheamountofacidthatis
secretedbythestomachdoesnthaveanysignificanteffect...alsowhetherthereisHpyloriornothasno
significance...aswellaswhetherthestomachisatrophicornot...HenceIgoformetaplasiaofthe
esophagealepithelium(giventhe8monthhistory)Barrett'sesophagusisaconditioninwhichthenormal
squamousepitheliumoftheesophagushasbeenreplacedbyanabnormalredcolumnarepitheliumcalled
specializedintestinalmetaplasia.Specializedintestinalmetaplasiaisred,likenormalstomachtissue,but
doesnotlooklikestomachtissueunderthemicroscope.
Block2
7. E.IncreasedplasmingenerationIncreaseplasmintoincreasefibrinolysis(todegradefibrin=bleeding)
normalcoagulationisdisruptedandabnormalbleedingoccursfromtheskin(e.g.fromsiteswhereblood
samplesweretaken),thegastrointestinaltract,therespiratorytractandsurgicalwounds.Thesmallclots
alsodisruptnormalbloodflowtoorgans(suchasthekidneys),whichmaymalfunctionasaresult.The
activationofthecoagulationcascadeyieldsthrombinthatconvertsfibrinogentofibrin;thestablefibrin
clotbeingthefinalproductofhemostasis.Thefibrinolyticsystemthenfunctionstobreakdownfibrinogen
andfibrin.Activationofthefibrinolyticsystemgeneratesplasmin(inthepresenceofthrombin),whichis
responsibleforthelysisoffibrinclots.Thebreakdownoffibrinogenandfibrinresultsinpolypeptides
calledfibrindegradationproducts(FDPs)orfibrinsplitproducts(FSPs).Inastateofhomeostasis,the
presenceofplasminiscritical,asitisthecentralproteolyticenzymeofcoagulationandisalsonecessary
forthebreakdownofclots,orfibrinolysis.
10.E.OsteoclastsOsteopetrosis,,alsoknownasmarblebonediseaseisanextremelyrareinheriteddisorder
wherebythebonesharden,becomingdenser,Normalbonegrowthisachievedbyabalancebetweenbone

formationbyosteoblastsandboneresorption(breakdownofbonematrix)byosteoclasts.Inosteopetrosis,
thenumberofosteoclastsmaybereduced,normal,orincreased.Mostimportantly,osteoclastdysfunction
mediatesthepathogenesisofthisdisease.deficiencyofcarbonicanhydraseinosteoclastsisnoted.The
absenceofthisenzymecausesdefectivehydrogenionpumpingbyosteoclastsandthisinturncauses
defectiveboneresorptionbyosteoclasts,asanacidicenvironmentisneededfordissociationofcalcium
hydroxyapatitefrombonematrix.Hence,boneresorptionfailswhileitsformationpersists.Excessivebone
isformed.Osteopetrosis:Calcium....unaffectedPhosphate...unaffectedAlkalinphosphatase....elevated
ParathyroidHormone....unaffectedSymptoms:PainFrequentfractures,especiallyofthelongbones,which
oftendonothealNervecompression,leadingtoheadache,blindness,deafnessHematologicaldifficulties,
includinganemicthrombocytopenia,leukopeniaEnlargedspleenOsteomyelitisFrontalbossingoftheskull
Unusualdentition,includingmalformedandunerruptedteeth,InfectionBleedingStrokeTheprobable
diagnosisisosteopetrosis...frontalbossingisnotthemajorfactortodiagnosisrickets.h/ofrequentfractures
morecommoninosteopetrosis.andlongbonesalwayshavebroadenedmetaphysis.alsohaveincreasedbone
densityandthickbonecortex.wecantfindincreasebonedensityandbroadenedmetaphysisndiaphysisof
longbonesinrickets.so...decreasedosteoclasticfunctionisthebestans..
15. A.GainofstabilizinghydrophobicinteractionsinthedeoxygenatedformofhemoglobinS1
Hemoglobinisanassemblyoffourglobularproteinsubunits(polypeptidechains)....2Eachsubunitis
composedofaproteinchaintightlyassociatedwithanonproteinhemegroup.3Eachproteinchain
arrangesintoasetofalphahelixstructuralsegmentsconnectedtogetherinaglobinfoldarrangement,
4.Adulthemoglobinismadeof2alphaand2betachains5Thesefourpolypeptidechainsareboundto
eachotherandstabilizedbyasaltbridges...whichisanoncovalentbonding...duetointeractionbetween
anioniccarboxylate(RCOO)andcationicammonium(RNH3+)intheaminoacidsbhydrogenbonds,c
hydrophobicinteractions....oilandwaterdonotcombinebecauseofhydrophobicinteraction...and
hydrophobicinteractionisapropertyofnonpolarmoleculesandthisinteractionisalsousedinthecaseof
proteinfoldingwherebymostfoldedproteinshaveahydrophobiccoreinwhichsidechainpacking
stabilizesthefoldedstate,andchargedorpolarsidechainsonthesolventexposedsurfacewherethey
interactwithsurroundingwatermolecules.6thehydrophobiceffectisimportanttounderstandthe
structureofproteinsthathavehydrophobicaminoacids,suchasalanine,valine,leucine,isoleucine,
phenylalanine,andmethioninegroupedtogetherwiththeprotein...andhydrophobicinteractionisbetween
individualaminoacids7Ordinarily,thehemoglobinmoleculesexistassingle,isolatedunitsintheredcell,
whethertheyhaveoxygenboundornot...8Sicklehemoglobinexistsasisolatedunitsintheredcellswhen
theyhaveoxygenbound.9Whensicklehemoglobinreleasesoxygenintheperipheraltissues,however,the
moleculestendtosticktogetherandformlongchainsorpolymersLetusseewhathappensinsicklecell
anemia...glutamicacid(hydrophillic)isreplacedbyhydrophobicvaline(whichincreasesthenumberof
hydrophobicaminoacids...whichinturnincreaseshydrophobicinteractions)..andthesehydrophobic
interactionsstabilizethepolymerizedsicklehemoglobin....
17.E.SchizoidSchizoidpersonalitydisorder(SPD)isapersonalitydisordercharacterizedbyalackof
interestinsocialrelationships,sometimessexuallyapathetic,atendencytowardsasolitarylifestyle,
secretiveness,andemotionalcoldness.SPDisnotthesameasschizophrenia,althoughtheysharesome
similarcharacteristicssuchasdetachmentorbluntedaffectandthereisincreasedprevalenceofthedisorder
infamilieswithschizophrenia.
22. B.Gastrointestinal....thepatientisexposedtohighlevelsofradiationandthiscausesacuteradiation
syndromeStagesofAcuteradiationSyndrome1)prodrome...nausea,vomiting,anorexia,fatigue,diarrhea,
abdominalcramping,anddehydrationwhichareGITSymptom2)clinicallatency,3)manifestillness,and
4)recoveryordeathmyanswerisGIT
28. E.GermlineinactivationoftheBRCA1geneBRCA1isahumantumorsuppressorgenethatproduces
aproteincalledbreastcancertype1susceptibilityprotein.BRCA1isexpressedinthecellsofbreastand
othertissue,whereithelpsrepairdamagedDNA,ordestroycellsifDNAcannotberepaired.IfBRCA1
itselfisdamaged,damagedDNAisnotrepairedproperlyandthisincreasesrisksforcancers.Certain
variationsoftheBRCA1geneleadtoanincreasedriskforbreastcancer.Womenwithanabnormal
BRCA1orBRCA2genehaveuptoan60%riskofdevelopingbreastcancerbyage90;increasedriskof
developingovariancancerisabout55%forwomenwithBRCA1mutationsandabout25%forwomen
withBRCA2mutations.

30. .C.RapidemptyingofhyperosmolarchimeintothesmallbowelThedumpingsyndromeisMost
peopleareunabletotoleratecertainfoodsaftergastricbypass,especiallyfoodswithhighsugarorfat
content.Eatingthesefoodscancausethedumpingsyndrome,whichmaycausenauseaandvomiting,
diarrhea,abloatedfeeling,dizzinessandsweating.
32. D.ReleaseofacetylcholineintotheprimarysynapticcleftBotulinumtoxinisaproteinproducedbythe
bacteriumClostridiumbotulinum,andisextremelyneurotoxicTheheavychainofthetoxinisparticularly
importantfortargetingthetoxintospecifictypesofaxonterminals.Thetoxinmustgetinsidetheaxon
terminalsinordertocauseparalysis.Followingtheattachmentofthetoxinheavychaintoproteinsonthe
surfaceofaxonterminals,thetoxincanbetakenintoneuronsbyendocytosis.Thelightchainisableto
cleaveendocytoticvesiclesandreachthecytoplasm.Thelightchainofthetoxinhasproteaseactivity.The
typeAtoxinproteolyticallydegradestheSNAP25protein,atypeofSNAREprotein.TheSNAP25
proteinisrequiredforvesiclefusionthatreleasesneurotransmittersfromtheaxonendings(inparticular
Acetylcholine).[58]BotulinumtoxinspecificallycleavestheseSNAREs,andsopreventsneurosecretory
vesiclesfromdocking/fusingwiththenervesynapseplasmamembraneandreleasingtheir
neurotransmitters.
33. EThespinothalamictractisasensorypathwayoriginatinginthespinalcord.Ittransmitsinformation
tothethalamusaboutpain,temperature,itchandcrudetouch.Thepathwaydecussatesatthelevelofthe
spinalcord,ratherthaninthebrainstemliketheposteriorcolumnmediallemniscuspathwayand
corticospinaltract.Thecellbodiesofneuronsthatmakeupthespinothalamictractarelocatedinthespinal
ganglia.Theseneuronsreceiveinputfromsensoryfibersthatinnervatetheskinandinternalorgans.A.Left
Dorsalcolumns(pressure,vibration,touchandproprioception)C.LeftLateralCorticospinaltract
(voluntarymotor)E.LeftSpinothalamictract:pain&temperature
47. DAnesophagealmotilitystudy(EMS)oresophagealmanometryisatesttoassessmotorfunctionof
theUpperEsophagealSphincter(UES),EsophagealbodyandLowerEsophagealSphincter(LES).
Indications:AnEMSistypicallydonetoevaluatesuspecteddisordersofmotilityorperistalsisofthe
esophagus.Theseincludeachalasia,diffuseesophagealspasm,nutcrackeresophagusandhypertensive
loweresophagealsphincter.Thesedisorderstypicallypresentwithdysphagia,ordifficultyswallowing,
usuallytobothsolidsandliquidseveninitially.Otherpatientswithspasmdisordersmayhavethetestdone
todiagnosechestpainthoughtnottobeofcardiaccause.Thetestisnotusefulforanatomicaldisordersof
theesophagus(thatis,disordersthatdistorttheanatomyoftheesophagus),suchaspepticstricturesand
esophagealcancer.
49.CIdeasofreference
Block3
4. E.ProductionofextendedspectrumBlactamseTheantimicrobialresistancetoallmentionedantibiotics
....Betalactamantibiotics(Penicillinanditsgeneration)iscausedbyproductionofextendedspectrumbeta
lactamase
10.CTheUrachusisthepartoftheallantoidsductbetweenthebladderandtheumbilicus.Themedian
umbilicalligamentisastructureinhumananatomy.Itisashriveledpieceoftissuethatrepresentsthe
remnantoftheembryonicurachus.Itextendsfromtheapexofthebladdertotheumbilicus,onthedeep
surfaceoftheanteriorabdominalwall.Itisunpaired.ItiscoveredbythemedianumbilicalfoldLateralto
thisstructurearethemedialumbilicalligament(whichisadifferentstructure,nottobeconfused)andthe
lateralumbilicalligament.
11. A.AutoimmuneAddisonDisease:Chronicadrenalinsufficiencyduetoadrenalatrophyordestruction
bydisease(Autoimmmune,TB,metastasis).1deficiencyofaldosteroneandcortisolcausinghypotension,
andskinhyperpigmentation.(FApage291)Becauseprimaryhypocortisolismismanifestedasadeficiency
inglucocorticoidreleasefromtheadrenalcortex,increasedACTHwillbereleasedbythepituitaryinorder
totriggerreleaseoftheabsentglucocorticoid;itisbecauseofthisoverstimulationofACTHthatbronzing
oftheskinoccurs.Insecondaryortertiaryhypocortisolism,thereisadeficiencyofeitherCRHorACTH
releasebythehypothalamusorpituitarygland,respectively.TheformerwillmanifestasnoACTHrelease
whilethelatterwillmanifestasphysiologic(normal)ACTHrelease;neitherwillcauseanoverproduction
ofACTH.Onexamination,thefollowingmaybenoticed:[2]Lowbloodpressurethatfallsfurtherwhen
standing(orthostatichypotension)InlongstandingAddison'sDisease,thepinnaoftheearmaybecome

calcifiedMostpeoplewithprimaryAddison'shavedarkening(hyperpigmentation)oftheskin,including
areasnotexposedtothesun;characteristicsitesareskincreases(e.g.ofthehands),nipple,andtheinside
ofthecheek(buccalmucosa),alsooldscarsmaydarken.Thisoccursbecausemelanocytestimulating
hormone(MSH)andadrenocorticotropichormone(ACTH)sharethesameprecursormolecule,Pro
opiomelanocortin(POMC).Afterproductioninanteriorpituitarygland,POMCgetscleavedintoGamma
MSH,ACTHandBetalipotropin.ThesubunitACTHundergoesfurthercleavagetoproduceAlphaMSH,
themostimportantMSHforskinpigmentation.InsecondaryandtertiaryformsofAddison's,skin
darkeningdoesnotoccur.MedicalconditionssuchastypeIdiabetes,autoimmunethyroiddisease
(Hashimoto'sthyroiditisandgoiter)andvitiligooftenoccurtogetherwithAddison's(ofteninthesettingof
Autoimmunepolyendocrinesyndrome).Hence,symptomsandsignsofanyoftheformerconditionsmay
alsobepresentintheindividualwithAddison's.
12. C.MembraneEthanol(ethylalcohol)andisopropanol(isopropylalcohol)arealcoholsthatkill
bacteria.Alcoholskillbacteriabyfirstmakingthelipidsthatarepartoftheouterprotectivecellmembrane
ofeachbacteriumcellmoresolubleinwatersothatthecellmembranebeginstoloseitsstructuralintegrity
andfallapart.Asthecellmembranedisintegrates,alcoholcanthenenterthecellanddenatureproteins
withineachbacterium.
16. A.AnticholinesterasedrugonlyAnacetylcholinesteraseinhibitor(oftenabbreviatedAChEI)oranti
cholinesteraseisachemicalthatinhibitsthecholinesteraseenzymefrombreakingdownacetylcholine,
increasingboththelevelanddurationofactionoftheneurotransmitteracetylcholine.Somemajoreffects
ofcholinesteraseinhibitors:Actionsontheautonomicnervoussystem,thatisparasympatheticnervous
systemwillcausebradycardia,hypotension,hypersecretion,bronchoconstriction,GItracthypermotility,
anddecreaseintraocularpressure.SLUDGEsyndrome.Actionsontheneuromuscularjunctionwillresult
inprolongedmusclecontraction
19. B.NecrosisofepithelialcellsinproximalconvolutedtubulesATN,Itmaybeclassifiedaseithertoxic
orischemic.ToxicATNoccurswhenthetubularcellsareexposedtoatoxicsubstance(nephrotoxicATN).
IschemicATNoccurswhenthetubularcellsdonotgetenoughoxygen,aconditionthattheyarehighly
sensitiveandsusceptibleto,duetotheirveryhighmetabolism.Acutetubularnecrosisisclassifiedasa
"renal"(i.e.notprerenalorpostrenal)causeofAcuterenalfailure.DiagnosisismadebyaFeNA
(fractionalexcretionofsodium)>3%andpresenceofmuddycastsinurinalysis.Onhistopathology,there
isusuallytubulorrhexis,thatis,localizednecrosisoftheepitheliallininginrenaltubules,withfocalrupture
orlossofbasementmembrane.Proximaltubulecellscanshedwithvariableviabilityandnotbepurely
"necrotic".
22. B.LeftsubthalamicnucleusHemiballismusisusuallycharacterizedbyinvoluntaryflingingmotionsof
theextremities.Themovementsareoftenviolentandhavewideamplitudesofmotion.Theyarecontinuous
andrandomandcaninvolveproximaland/ordistalmusclesononesideofthebody.Somecaseseven
includethefacialmuscles.Itiscommonforarmsandlegstomovetogether.Themoreapatientisactive,
themorethemovementsincrease.Withrelaxationcomesadecreaseinmovements.Thesubthalamic
nucleusessentiallyprovidestheexcitementneededtodrivetheglobuspallidus.Injurytothisareaorits
efferentorafferentconnectionscaninducethisdisorder.Thestructureitselfisaregulatorofmotor
functionandisalsoinvolvedinassociativeandlimbicfunctions.Itwastraditionallythoughtthatthe
disorderwasonlycausedbyinjurytothesubthalamicnucleus,butnewstudiesareshowingthatdamageto
otherareasofthebraincanalsoberesponsibleforcausingthisdisorder.Hemiballismuscausedbylesions
inthesubthalamicnucleusismoreseverethanotherformsofthedisorder.
29. C.NeurolepticmalignantsyndromeNeurolepticmalignantsyndrome(NMS)isalifethreatening
neurologicaldisordermostoftencausedbyanadversereactiontoneurolepticorantipsychoticdrugs.It
generallypresentswithmusclerigidity,fever,autonomicinstabilityandcognitivechangessuchas
delirium,andisassociatedwithelevatedcreatinephosphokinase(CPK).Incidenceofthediseasehas
declinedsinceitsdiscovery(duetochangesinprescriptionhabits),butitisstillapotentialdangerto
patientsbeingtreatedwithantipsychotics.Becauseofitsunpredictability,thereisnoonesetcourseof
actiontotreatthesyndrome,butgenerally,removaloftheantipsychoticdrugtreatment,alongwith
supportivemedicalmanagement,leadtoapositiveoutcome.
35. D.PyelonephritisPyelonephritisisanascendingurinarytractinfectionthathasreachedthepyelum
(pelvis)ofthekidney.Iftheinfectionissevere,theterm"urosepsis"isusedinterchangeably(sepsisbeinga

systemicinflammatoryresponsesyndromeduetoinfection).Itrequiresantibioticsastherapy,and
treatmentofanyunderlyingcausestopreventrecurrence.Itisaformofnephritis.Itcanalsobecalled
pyelitis.Severecasesofpyelonephritisleadtosepsis,asystemicresponsetoinfectioncharacterizedby
fever,araisedheartrate,rapidbreathinganddecreasedbloodpressure(occasionallyleadingtoseptic
shock).Whenpyelonephritisorotherurinarytractinfectionsleadtosepsis,itistermedurosepsis.Most
casesof"communityacquired"pyelonephritisareduetobowelorganismsthatentertheurinarytract.
CommonorganismsareE.coli(7080%)andEnterococcusfaecalis.Hospitalacquiredinfectionsmaybe
duetocoliformsandenterococci,aswellasotherorganismsuncommoninthecommunity(e.g.Klebsiella
spp.,Pseudomonasaeruginosa).Mostcasesofpyelonephritisstartoffaslowerurinarytractinfections,
mainlycystitisandprostatitis.Acutepyelonephritisisapotentiallyorganand/orlifethreateninginfection
thatcharacteristicallycausessomescarringofthekidneywitheachinfectionandmayleadtosignificant
damagetothekidney(anygivenepisode),kidneyfailure,abscessformation(eg,nephric,perinephric),
sepsis,orsepsissyndrome/shock/multiorgansystemfailure.Mostcasesof"communityacquired"
pyelonephritisareduetobowelorganismsthatentertheurinarytract.CommonorganismsareE.coli(70
80%)andEnterococcusfaecalis.Antibioticsarethemainstayoftreatment.Mildcasesmaybetreatedwith
oraltherapy,butgenerallyintravenousantibioticsarerequiredfortheinitialstagesoftreatment.Thetype
ofantibioticdependsonlocalpractice,andmayincludefluoroquinolones(e.g.ciprofloxacin),betalactam
antibiotics(e.g.amoxicillinoracephalosporin),trimethoprim(aloneorincombinationwith
sulfamethoxazole).Aminoglycosidesaregenerallyavoidedduetotheirtoxicity,butmaybeaddedfora
shortduration.
36. D.PosteriorinferiorcerebellarTheposteriorinferiorcerebellarartery(PICA),thelargestbranchofthe
vertebralartery,isoneofthethreemainarterialbloodsuppliesforthecerebellum.Itwindsbackward
aroundtheupperpartofthemedullaoblongata,passingbetweentheoriginsofthevagusandaccessory
nerves,overtheinferiorcerebellarpeduncletotheundersurfaceofthecerebellum,whereitdividesinto
twobranches.Themedialbranchcontinuesbackwardtothenotchbetweenthetwohemispheresofthe
cerebellum;whilethelateralsuppliestheundersurfaceofthecerebellum,asfarasitslateralborder,where
itanastomoseswiththeanteriorinferiorcerebellarandthesuperiorcerebellarbranchesofthebasilarartery.
Branchesfromthisarterysupplythechoroidplexusofthefourthventricle.DiseasesInfarctionofthis
arteryduetothrombosisorastrokeleadstolateralmedullarysyndrome,alsoknownasPICAsyndromeor
Wallenbergsyndrome.SevereocclusionofthisorvertebralarteriescouldleadtoHorner'sSyndromeas
well.
37. A.BotuliniumLambertEatonmyasthenicsyndrome(LEMS)maincausalcancersmallcelllung
cancerInLEMS,antibodiesagainstVGCC,particularlytheP/QtypeVGCC,decreasetheamountof
calciumthatcanenterthenerveending,hencelessacetylcholinecanbemobilizedtotheneuromuscular
junction.Apartfromskeletalmuscle,theautonomicnervoussystemalsorequiresacetylcholine
neurotransmission;thisexplainstheoccurrenceofautonomicsymptomsinLEMS.P/Qvoltagegated
calciumchannelsarealsofoundinthecerebellum,explainingwhysomeexperienceproblemswith
coordination.AntibodiesmayalsobindotherVGCCs.ManypeoplewithLEMS,bothwithandwithout
VGCCantibodies,havedetectableantibodiesagainsttheM1subtypeoftheacetylcholinereceptor;itis
thoughtthattheirpresenceparticipatesinalackofcompensationfortheslowcalciuminflux.
38. C.Glucose6phophataseGlycogenstoragediseasetypeI(GSDI)orvonGierke'sdisease,isthemost
commonoftheglycogenstoragediseases.Thisgeneticdiseaseresultsfromdeficiencyoftheenzyme
glucose6phosphatase.Thisdeficiencyimpairstheabilityofthelivertoproducefreeglucosefrom
glycogenandfromgluconeogenesis.Sincethesearethetwoprincipalmetabolicmechanismsbywhichthe
liversuppliesglucosetotherestofthebodyduringperiodsoffasting,itcausesseverehypoglycemia.
Reducedglycogenbreakdownresultsinincreasedglycogenstorageinliverandkidneys,causing
enlargementofboth.Bothorgansfunctionnormallyinchildhoodbutaresusceptibletoavarietyof
problemsintheadultyears.Othermetabolicderangementsincludelacticacidosisandhyperlipidemia.
Frequentorcontinuousfeedingsofcornstarchorothercarbohydratesaretheprincipaltreatment.Other
therapeuticmeasuresmaybeneededforassociatedproblems.
43. E.Uncompensatedrespiratoryacidosis.CompensatedRespiratoryacidosis.........lowPH,high
Bicarbonate,andhighPco2whileUncompensatedRespiratoryacidosis.....lowPH,lowBicarbonateand
highPco2hereishowtoIDAcidBase:3rulestofollow1.lookatthepH:Acid,basicrespective2.lookat

CO2andHCO3>whichoneoftheseistheonethatchangesthemostfromtheirnormalvalue3.Findout
ifAcidBaseiscompensateorNotbylookingatthelowerof#2>thatisdoesitincreaseslightlyor
decreaseslightly?So,ifHCO3andCO2goesthesamedirectioneitherbothhighorbothlowno
compensationoccurnowcallmeifyouunderstandorneedmoreinfo1.phis6.8soitisacid2.PCO2is
theonethatchangesmost3.pCO2ofthispatientis804.normalpCO2is3345mmHG355.HC03ofthis
patientis12normalHC03is2228adifferenceof106.PCO2changesthemostfromtheirnormalvalue
respiratoryrespiratory(#2)acidosis(#1).Metabolicacidosis,PC02predicted=(1.5)(HC03)+8,PC02
Measured(givenintheequation)>PC02predictedCoExistingmetabolicacidosis&respiratoryacidosis
PC02Measured(givenintheequation)<PC02predictedCoExistingmetabolicacidosis&respiratory
alkalosis.MetabolicalkalosisoPC02predicted=(40)+[(0.7)(HC03givenintheequation24)oPC02
Measured(+/5givenintheequation)>PC02predictedCoExistingmetabolicalkalosis&respiratory
acidosisoPC02Measured(+/5givenintheequation)<PC02predictedCoExistingmetabolicalkalosis
&respiratoryalkalosisRespiratoryacidosisoAcuteproblem:LooktoseeifHC03iscompensatedor
notNormalPCO2is40;normalHC03is241.(increase1mEq/LforHC03)/(increase10mmHg
PCO2)thenitiscompensated2.IfPC02iscompensated,but,HC03is>24CoExistingrespiratory
acidosis&metabolicalkalosis3.IfPC02iscompensated,but,HC03is<24CoExistingrespiratory
acidosis&metabolicacidosisRespiratoryalkalosisoAcuteproblemLooktoseeifPC02is
compensatedornotNormalPC02is40;normalHC03is241.(Decrease2mEq/LforHC03)/
(decrease10mmHgPCO2)thenitiscompensated2.IfPC02iscompensated,but,HC03is>24
CoExistingrespiratoryalkalosis&metabolicalkalosis3.IfPC02iscompensated,but,HC03is<24
CoExistingrespiratoryalkalosis&metabolicacidosi
44. A.AirwaycompressionInnormalpatients,afterasmallamountofgashasbeenexhaled,theflowis
limitedbyairwaycompressionanddeterminedbytheelasticrecoilofthelungandresistanceupstreamof
thatpoint.Inrestrictivediseases,themaximumflowrateisreduced,asisthetotalvolumeexpired.The
flowisabnormallyhighinthelatterpartofexpirationbecauseofincreasedrecoil.Inobstructivediseases,
theflowrateisverylowinrelationtolungvolume,andascoopedoutappearanceisoftenseenfollowing
thepointofmaximalflow.
45.B.DistentionofairspacesdistaltoterminalbronchiEmpysema...permanentenlargementofallpartof
therespiratoryunit...respiratorybronchioles,alveolar,alveoliCauses:cigarettesmokingalpha1antitrypsin
deficiencyThereare2types....1.Centriacinar...ischaracterizedbytrappingofairintherespiratory
bronchiole...elasticfibersofthedistalTBaredestroyed,causingobstructiontoairflow...thiscausesthe
trappedairtodistendtheRBs,whoseelastictissuesupportisdestroyed.2.panacinar...ischaracterizedby
trappingofairintheentirerespiratoryunitebehindthecollapsedTB
46.D.SeverecombinedimmunodeficiencySeverecombinedimmunodeficiency(SCID),(alsoknownas
"Alymphocytosis,""GlanzmannRinikersyndrome,""Severemixedimmunodeficiencysyndrome,"and
"Thymicalymphoplasia")isageneticdisorderinwhichboth"arms"(BcellsandTcells)oftheadaptive
immunesystemareimpairedduetoadefectinoneofseveralpossiblegenes.SCIDisasevereformof
heritableimmunodeficiency.Itisalsoknownasthe"bubbleboy"diseasebecauseitsvictimsareextremely
vulnerabletoinfectiousdiseasesandsomeofthem,suchasDavidVetter,becomefamousforlivingina
sterileenvironment.SCIDistheeffectofahighlycompromised,somuchitisalmostconsideredabsent,
immunesystem.ThegenemutationsthatcauseSCIDarenotjustforthedisorder.ThebuildupofdATP,
whichinducesthecelltomakecytochromec,destroysandsignalsforapoptosisinallrapidlyproliferating
cells.ThisincludescellsintheGItract,immunesystemlymphocytes,andspermcells.Chronicdiarrhea,
earinfections,recurrentPneumocystisjiroveciipneumonia,andprofuseoralcandidiasiscommonlyoccur.
Thesebabies,ifuntreated,usuallydiewithin1yearduetosevere,recurrentinfectionsunlesstheyhave
undergonesuccessfulHematopoieticstemcelltransplantation.
48.D.Periodprevalence...ThestudydesignisCaseControlandincasecontrolstudiesucanonly
determinetheprevalenceofthedisease...Inthiscasethedurationisoneyearanditisperiodprevalence
ratherthanpointprevalence
Block4

2. A.Capsularpolysaccharidethepatienthadacryptococcalinfection,thisfungusisheavilyencapsulated
yest,foundinsoil,pingeondroppings.CultureonSubouraudagar.SainwithIndiaInkandwiththelatex
agglutinationtestdetectspolysaccharidecapsularantigen.
10. C.Decreaseddiffusingcapacityforcarbonmonoxide(DLco)pulmonaryedemaincreasesthethickness
ofthealveolocapillaryspace,increasingthedistancetheoxygenmustdiffusetoreachblood.Thisimpairs
gasexchangeleadingtohypoxia,increasestheworkofbreathing,andeventuallyinducesFIBROSISOF
THEAIRSPACE.AfterapatientistreatedforARDS,themembranewillbethickened=hyaline
membrane,hence,theCOcantbediffused.Sowegetadecreaseddiffusingcapacityforcarbonmonoxide
(DLco)
17.C.lipopolysaccharidestimulatingproductionoftumornecrosisfactor.Lipopolysaccharides(LPS),also
knownaslipoglycans,arelargemoleculesconsistingofalipidandapolysaccharidejoinedbyacovalent
bond;theyarefoundintheoutermembraneofGramnegativebacteria,actasendotoxinsandelicitstrong
immuneresponsesinanimals.Mostcasesofsepticshock(approximately70%)arecausedbyendotoxin
producingGramnegativebacilli.Endotoxinsarebacterialwalllipopolysaccharides(LPS)consistingofa
toxicfattyacid(lipidA)corecommontoallGramnegativebacteria,andacomplexpolysaccharidecoat
(includingOantigen)uniqueforeachspecies.AnalogousmoleculesinthewallsofGrampositivebacteria
andfungicanalsoelicitsepticshock.FreeLPSattachestoacirculatingLPSbindingprotein,andthe
complexthenbindstoaspecificreceptor(CD14)onmonocytes,macrophages,andneutrophils.
EngagementofCD14(evenatdosesasminuteas10pg/mL)resultsinintracellularsignalingviaan
associated"Tolllikereceptor"protein4(TLR4),resultinginprofoundactivationofmononuclearcellsand
productionofpotenteffectorcytokinessuchasIL1andTNF.ImmuneresponseLPSfunctionhasbeen
underexperimentalresearchforseveralyearsduetoitsroleinactivatingmanytranscriptionfactors.LPS
challengealsoproducesmanytypesofmediatorsinvolvedinsepticshock.Humansaremuchmore
sensitivetoLPSthanotheranimals(e.g.,mice).Adoseof1g/kginducesshockinhumans,butmicewill
tolerateadoseuptoathousandtimeshigher.[13]Thismayrelatetodifferencesinthelevelofcirculating
naturalantibodiesbetweenthetwospecies.[14][15]Saidetal.showedthatLPScausesanIL10
dependentinhibitionofCD4TcellexpansionandfunctionbyupregulatingPD1levelsonmonocytes
whichleadstoIL10productionbymonocytesafterbindingofPD1byPDL.
20..A.DislocationGlutealfoldissignofCHD(congenitalhipdysplasia).Ifpatientwasintheirteens(13
16)thenitwouldbeaslippedepiphysealdiscAdislocatedhipisaconditionthatcanbecongenitalor
acquired.Congenitalhipdislocationsaremuchmorecommoningirlsthaninboys.Thepelvisandfemur
arethetwomainbonesthatformthehipjoint.Thereisanarticulationoftheheadofthefemurandthe
acetabulumofthepelvis.Together,theymakethehipjointanenarthrodialjoint.Therearetwopelvic
bones(rightandleft),eachconsistingoftheIlium,ischium,andthepubis.Theyconnecttoformthe
symphysispubisontheanteriorside,whiletheposteriorsideconnectswiththesacrumandcoccyxtoform
sacroiliacjoints.[2]Thesebonesarejoinedwithhelpofstrongligaments,makingthemslightly,movable
joints.Therearefivestronganddenseligamentsthathelptoreinforcethehipjoint.Theyincludethe
iliofemoralligament,theteresligament,thepubofemoralligament,theischiofemoralligament,andthe
zonaorbicularisligament.Theiliofemoralligamenthelpstopreventhiphyperextension,asitisoneofthe
strongestligamentsinthebody.Theteresligamentslightlylimitshipadduction,whilethepubofemoral
ligamentlimitsexcessiveextensionandabduction.Theischiofemoralligamentlimitsinternalrotationof
thehip,whilethezonaorbicularisligamenthelpsmaintaincontactinthejoint.Congenitalhipdislocation
mustbedetectedearlywhenitcanbeeasilytreatedbyafewweeksoftraction.Ifitisnotdetected,the
child'shipmaydevelopincorrectlyseenwhenthechildbeginstowalk.Ifonehipisaffectedthechildwill
havealimpandlurchandwithbilateraldislocationtherewillbeawaddlinggait.Onphysicalexam,with
thebabyinthesupineposition,theexaminerflexesthehipsandkneesbothto90degrees,and,holdingthe
knees,pushesgentlydownward,whichmayinduceaposteriordislocationorsubluxation.Keepingthe
babyinthis90degreeflexedposition,theexaminerthenexternallyrotatesthethighs.Anormalinfantwill
demonstratenoevidenceofdislocation.ItcanalsobedetectedwiththeGaleazzitest.Congenitalhip
dislocationismuchmorecommoningirlsthanboys.Acquiredhipdislocationsareextremelypainfuland
commonlyoccurduringcaraccidents.Theymaybetreatedbysurgicalrealignmentandtraction.
21. E.Urinarytractinfection.BPHCommoninmen>50y/o.Hyperplasia(Nohypertrophy)ofthe
prostategland.Maybeduetoanagerelatedinestradiolwithpossiblesensitizationoftheprostateto

growthpromotingeffectsofDHT.Characterizedbyanodularenlargementoftheperiurethral(lateraland
middle)lobes,whichcompresstheurethraintoaverticalslit.Oftenpresentwithfrequencyofurination,
nocturia,difficultystartingandstoppingthestreamofurine,anddysuria.Mayleadtodistentionand
hypertrophyofthebladder,hydronephrosis,andUTIs.Notconsideredapremalignantlesion.PSA.Tx:
1antagonists,(Terazosin,Tamsulosin),whichcauserelaxation
25.A.Osteoblastactivityatthefracture=increasedosteoblasticactivityinresponsetothestressfracture.
28.B.FilgrastimFilgrastimisagranulocytecolonystimulatingfactor(GCSF)analogusedtostimulate
theproliferationanddifferentiationofgranulocytes.[1]ItisproducedbyrecombinantDNAtechnology.
Thegeneforhumangranulocytecolonystimulatingfactorisinsertedintothegeneticmaterialof
Escherichiacoli.TheGCSFthenproducedbyE.coliisonlyslightlydifferentfromGCSFnaturallymade
inhumans.TherapeuticusesFilgrastimisusedtotreatneutropenia[2](alownumberofneutrophils),
stimulatingthebonemarrowtoincreaseproductionofneutrophils.Causesofneutropeniainclude
chemotherapyandbonemarrowtransplantation.Filgrastimisalsousedtoincreasethenumberof
hematopoieticstemcellsinthebloodbeforecollectionbyleukapheresisforuseinhematopoieticstemcell
transplantation.Itisproducedbymanycompaniesworldwide.
33.C.DirectbranchfromtheaortaGonadalvesselscomefromtheabdominalaortaBloodsupplytothe
testisprimarilyoriginatesfromthetesticularartery,whicharisesfromtheaorta.Othersourcesofblood
supplyincludethedeferentialartery,whichsuppliestheepididymisandthevasdeferensandthe
cremastericarterysuppliestheperitesticulartissues.Thetesticularartery(themalegonadalartery,also
calledtheinternalspermaticarteriesinoldertexts)isabranchoftheabdominalaortathatsuppliesblood
tothetestis.Itisapairedartery,withoneforeachofthetestes.Itisthemaleequivalentoftheovarian
artery
C.IncubationunderstrictanaerobicconditionsClostridiumperfringensisaGrampositive,rodshaped,
anaerobic,sporeformingbacteriumofthegenusClostridium.C.perfringensiseverpresentinnatureand
canbefoundasanormalcomponentofdecayingvegetation,marinesediment,theintestinaltractof
humansandothervertebrates,insects,andsoil.Clostridiumperfringensisthemostcommonbacterialagent
forgasgangrene,whichisnecrosis,putrefactionoftissues,andgasproduction.Itiscausedprimarilyby
Clostridiumperfringensalphatoxin.Thegasesformbubblesinmuscle(crepitus)andthecharacteristic
smellindecomposingtissueIntheUnitedKingdomandUnitedStates,C.perfringensbacteriaarethe
thirdmostcommoncauseoffoodborneillness,withpoorlypreparedmeatandpoultrythemainculpritsin
harboringthebacterium.Theclostridiumperfringensenterotoxin(CPE)mediatingthediseaseisheatlabile
(inactivatedat74C)andcanbedetectedincontaminatedfood,ifnotheatedproperly,andfeces.
38.D.IncreaseK+excretionPatienthadCHF,"LVF",alwaysifpulmonaryedemaLHFthemainsymptom
theSOBCan'tgetbloodoutoftheheartb/ctheLVfails,increasedtheEDVbecauseallthebloodcannot
getout,thenthepressureandvolumewillgobacktotheleftatrium,backintothepulmonaryvessels,
increasedthehydrostaticpressureandthenPULMONARYEDEMAWhathappenintheCHF?:Decreased
thecardiaoutputregulatedbyRAASystemliketheBloodpressure,therenalperfusionisdecreasedthen
thereninincreasesreninconvertangiotensinogenintoangiotensinI.ACEfoundmainlyinendotelial
cellsofpulmonaryvessels,convertsangiotensinIintoangiotensinII.AngiotensinIIhasapotenteffectsto
stimulatesecretionofaldosteroneandtocausearteriolarvasoconstriction.stimulatesreabsorptionofNa+
andALSOCauseincreasedrenalexcretionofpotassiumaffectingtheplasmaK_concentration
39.D.Inhibitionofprostacyclin(PGI2)formationwithoutinhibitionofthromboxaneA2inplatelets
42.B.LingualthyroidLingualthyroidisaRAREcondition,withanincidenceof1:100,000.This
infrequentcongenitalanomalyisoftenasymptomaticuntilapathologicstresssuchassystemicdiseaseor
physiologicstresssuchaspubertycausesenlargementoftheectopictissue,leadingtodysphagia,
dysphonia,anddyspnea.Theworkupshouldincluderoutinebloodworkincludingthyroidfunctiontests
thyrotropin,thyroxine,andthyroidhormonebindingratio;iodinethyroidscintigraphy;andcomputerized
tomographyormagneticresonanceimaging.Themajorityofpatientsrequiresurgicalexcisionofthe
symptomaticmassand,incaseofabsenceoforthotopicthyroidtissue,longtermthyroidhormone
replacement.
44.B.DNAsynthesisFolatedefficiency:megaloblasticanemia(PMNnucleusmorethat5lobesasisseen
inthefig)THFisformedfromthevitaminFolatethrough2reductionscatalyzedbyDHFreductase.It
picksup1carbonunitfromavarietyofdonorsandenterstheactive1carbonpool.Importantpathways

requiringformsofTHFfromthispoolincludethesynthesisofallpurinesandthymidine,whichinturnare
usedforDNAandRNAsynthesisduringcellgrowthanddivision.(KaplanBioch.bookpage268).