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Comments ...

 +0  (nbme23#44)
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I sugse 'hes agktni B12 umptlpne,ses sioertwhe eh would have a motmpytsiac id,iyecefcn hirt?g


 +2  (nbme23#14)
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Since ehter wree as"llm tsounma fo inuemomc" I guohtht it n'ctoldu be sa.reati urnTs otu asirate s'nit ysaawl sbancee fo uml,en ti nac sloa be alnrbaom irnwargno of mnule, nlaogwli sjut a mslal mouatn ot pssa uh.rg..tho

adong  I don't think that's true, atresia literally means closure/absence of the lumen. I also got tripped up by the meconium but that could be just GI epithelium that was shed while in utero etc. I wouldn't change your definition of atresia. +2
srdgreen123  one thing i would say is that in the case its due to failure of recanalization and not due to failure of formation like other types of atresia, so its possible that when it was de-canalized, it was not 100% closed allowing for some meconium to pass +

 +5  (nbme22#21)
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heT odswr o"mts iyffclt"evee ouedfnsc m.e I hotgthu to lmfyes enve" fi it sha eth ihtesgh sfipii,tycec is't not vrey eicvefeft fi s'ti ogt srepu olw ivtiyitesns -- nscie it wlli mssi a olt fo eht uret +'sev (giilanf to uerl in cnarec fro teh neos taht etg .)sdei"ms ahtT wsa a royst I ldto ylsefm abtou thier esu fo eht sdrow mt"os vf"lyteieecf ol.l


 +1  (nbme22#46)
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isFtr dAi 9012 gape 622 uotaitsmlyr ghorwt esefftc fo esronteotets dlenuic dre olobd s.ecll I kntih thye cxetpe us ot wnok sti.h

medstudent  FA 2020 p. 636 +

 +1  (nbme22#8)
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I nithk ethsre' a dorlUW tniueosq isredingbc who ticsyc bfisoirs cna eucas fta olsbeul mntivai cidcnefeiy nad who a Vti E fde ni taht otcextn mhtig nasmtief sriilyalm ot 1B2 def. oAs(l ni ifrst )adi


 +4  (nbme22#1)
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eehrT si a decnet UrWold toisnqeu pinaelxngi hwo tsih wrsko. ylOn ornesa I mdeerrebem i.t

hyperfukus  i had notes from forever ago but i totally forgot lol +
carmustine  UWorld question ID 318 +3

 +6  (nbme22#30)
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tI essem klei a olt of het eistymsc nuiemmauot esdsaesi rea riol.lficttuama Is herte a reelgan reul rfo shit?

ls3076  Really good observation +2
acidfastboi  Never forget what our lord and savior Dr. Sattar says - environmental trigger in a genetically predisposed individual (aka multifactorial)! +3

 +3  (nbme22#1)
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st'I lsoa tjus eth ylno optoin that's ebhni"d" the ilrv.e


 +0  (nbme22#45)
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Is eht ptra thiw ttsnonac" sng"ytidu tusj podspsue ot srotupp tath ehs sah a pcyhs esroddri tldraee ot ompcrisenfie,t ichhw si ywh 'shse nggoi to stxremee to rcontol her ehitgw?

rrasha2  No, the constant studying is to trick you into thinking shes abusing amphetamines.Amphetamines decrease appetite so a lot of people abuse them for weight loss. That combined with increased concentration to study all day errrday.. #onehellofadrug +
rrasha2  forgot to mention, another side effect of amphetamines would be increased BP due to the increased catecholamines..don't forget to keep an eye out for that +1
dentist  would amphetamines influence electrolytes at all? +1

 +0  (nbme22#25)
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aWht htey eman by l.ntt.aroi.fi

ldFiu resopidmc of etrwa adn tysorlet,elec thiw a yerv lasml tuaomn fo porinte dna oreht cosrlumcalemeo, lnylrmao seavel psliaelacir adn mlals potpsilaayrlc nvseule by a pressco leldca rla.ftionti tnlFtiraio is amrpliiyr rvined yb eht parclialy coidtsarhyt see,purrs nda eht natoum defrtlie per tiun mtie si ydnalidtaoli dnfeluicne by teh baieeiprmytl fo the esvesl llaw hemueln(tiod nda mtebnsae )nremb.aem ehT idful htta sfliter onti hte euists wslfo inithw hte ilrelarnlucet eacsp (hte urimisitet)tn dna tmso of ti is obbreseard at teh elnravu dne of alirlsceipa rhwee teh syrihotdatc rpsuseer si wl.roe oSem fo the idlrtefe udlif is natke up yb hlapctiym esvesls dan runtrdee to het iloria.ntcuc


 +8  (nbme20#17)
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I uedfcson pdsmesiclytyaol syerdomn htwi ymrirpa meliiorfyobss usbeaec I ttughoh 2-3 of thsoe CBsR doeokl leki erpdorat scle.l Jsut eilk nweh teyh ohws an mgaie ofr sbullou gdoiimhpep nda e'ethsr mose edirw ndeosc rpi tourghh het dmlme/lberadrsua rleay inmgka me htkin tsi' otn BP neev uhhogt I ontd' wokn waht lees ti ldouw b.e mfl

whoissaad  Made the same mistake +9
targetusmle  i thought exactly the same!! 2 cells looked like tear drop cells :/ +2
ilovemypuppies2295  I thought there were tear drop cells too. Seemed like it should be a metaplasia then. Oh well +
lynn  I did the same, but looking at FA19 pg 423 it says "ineffective hematopoiesis --> defects in cell maturation of nonlymphoid lineage." You can get bilobed neutrophils, or if it progressed to AML you'd see auer rods. Nothing about tear drop cells. Then on pg 406 tear drop cells would be seen in myelofibrosis, and possibly thalassemias +
waterloo  I thought the same, but I think that would be myelofibrosis, not myelodysplastic. Hb is really high here too. Pretty tricky for them to put that there, easy knee jerk. +1
jawnmeechell  Interestingly enough, agnogenic myeloid metaplasia is the old name for myelofibrosis, with "agnogenic" being synonymous with "idiopathic." (or did everyone already know this) +

 +8  (nbme21#13)
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ixHopyc lupyormna vosrctiosnnictao H(V,)P lsoa wnokn as the tdirjlnerEL-ealus ai,cmhemns si a lygapiicsohlo enonnepmoh in iwhch lslam ypmnauorl asreetri ocnristtc ni hte nerepesc fo avllerao oyahixp wlo( xeyong s.v)eell

helWi teh neaatemcnni of nnoeloaptsin/ivuefrit taori gndiur grilenao iortsotcnub fo iorfalw is cienafbeil, PHV anc be aerdeltnmti rgduni olablg laavlreo ixoayhp whchi csucro twih uepeosxr ot ihgh dt,taleui weerh HVP csaesu a iiiastngcnf nesaecir in tlota mlraoupyn aarvucsl sacsreeit,n nad ryampluon eaalirrt spersre,u yliltetoapn egaldin to umyplnaor osnnrhyepiet and nmrluaoyp dmaee.

phi/kvwonow/:tn._tocis/xpouiircrnaiostocHsy_rtpi.dyglmeki/iaapen

lovebug  2019 FA, Pg 665. PAH +




Subcomments ...

submitted by sajaqua1(535),
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seeacuB eht syb'ba oermth sha pTey 1 tbDiease ltmsle,ui ti si alepubisl ahtt htye adh avtldeee loobd oeuscgl elselv durgin ro ltyshor erefob bt.rih nniulIs edos ont ssroc eth ctan,epla btu ogclsue d,ose so ugrind btirh het tnonaee luodw ehav eenb lryycepegmh.ci Tshi odwlu ldae ot hte laaneotn nrcseaap erinaslge ,iunsinl iidrgnv euclsgo oint eclls nda irnntgu down ongeuloeessin;cg isth is why hte bbya si hypmcycgielo tgihr onw.

B) saceDdree cgegoynl -oteanoicrtncn I 'dnot nkow the yncelggo catnonticnreo dcrmpoae ot na uadlt np,ieatt btu a edcaeser in ngclgoye crtoncniaeont dwluo niicedta ugsglyencoloc/ge se,eerla cihwh wuodl tno eb a pyhcoliegmcy s.tate C) Desrdceea eyngoglc tensashy vycttii-a deaerscde ognglecy aehnsyts ytctivai tsancdiei egeryn aotalscmi,b adn olduw aeld to rihhge sumer lceuogs es.lelv )D eedraecsD uemrs isninlu cnoer-otticnna ecareddes userm insnilu owudl eadl ot ehgirh leelsv fo oseclug in er.usm )E sanIeecrd umers lnie-kslniui gowthr a-rctof IFG esdo ton bnid aleynr sa well ot nslnuii cerrestpo as siuninl e,dso dna os oldwu vahe ot eb ni exryemtle ihhg eciotnnasnoctr ot eavh stih ftecfe. IFG is ostscadaie with iasomct orhgtw dan lescmu dven.lopemet

yotsubato  His glycogen concentration is high, since he's been hyperglycemic with lots of insulin until birth. +4  
alexb  Also explains why he's 12 pounds. +3  
krewfoo99  Also, think of it like this: Insulin causes hypoglycemia, thus this baby must have increased insulin. It is also an anaobolic hormone which is clear by the babys weight. Insulin increases glycogen synthase activity, and causes an increase in concentrations of glycogen. Decrease in insulin would do exactly the opposite +1  
tyrionwill  fetus of a mom with DM will develop pancreatic beta cell hyperplasia, which leads to insulinemia trying to reduce the blood glucose. after birth, the excessive blood glucose will be automatically withdrawn while the insulin at that moment is still high, which leads to hypoglycemia. +2  


submitted by sajaqua1(535),
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nI na drlylee anitpet htwi oedtlsai alteveed analkile etpspaaoshh o(rlnma esurm acilumc dna eh)tosppha t'aPegs sadeise fo nbeo loudhs be at the pto of het refl.naetfidi siTh seidase si ued ot dorniagueystl of alsoteictsoc and aossteoicblt tytaiivc; rftis an tlinaii ssetctoaol yrthiceptiayv ,ahspe neht reacsneid toaoebstsl ytictaiv rfo a ,teirmxu etnh osclaeostts bounu"rt" ediangl to oloizmrinnreaa-vtei nda reiscltco nboe paeq.sul nI doi,itnad tshi cna arcete uaoorveenrsit snthsu in eht snbeo which ereeasscd tesscinare, dganlei ot hhig tptuou draaicc aefirlu (a mlsiiar erompbl nca rsiae in tovaroruenise saftusil omrf doblo asyi)dl.si nO yhoiglost it lilw eavh a ico"sma" .enptrat

-)A luemsAnyar noeb s-ytc lerlgya a cdruotp of rhyivtticpyea of stsctso,eola htsi usrcco mero tfeno ni eht lmbs,i adn wssoh a sytcci pecsa with laobil-olnek lnoatii.d B) noomas-Argaic gomsirnaaaco of eht bneo si n salmto uyrlep itylc nles.io eyhT cocur rmeo ulrfeyneqt ni goureyn olee.pp C) Nnciai eie-ndiyfcc I anc fdni htoning oabtu aimtibvn 3B efinycdeic gnvoilivn n.sebo 3B ceinitefcd uesltrs in egl,rapal hiwt het icalscs erTeh -D's siaitdmter (sahr acekecln no C/C43 e)tdoe,marm in,aeemtd and ad.aierrh E) cassamto-eoOr uoFdn mltaso xuvyelsleci ni neguyro oepelp, htis beno thrgow uoccsr at eht tgrohw ,atlep yurriactlpla ta hte xlmriaop den fo teh iat,ib sltdai nde fo the efurm, ro roipalmx den fo teh usrheum ni( the gonl seonb ranodu uory eksne ro ta oyru olhd.sus)re tI ssowh a e,rlag dslio rgogwin amss taht mya seira teh petermisou in a rnusutbs /atntompCdre'nas ieg.nlrta )F satiPorct icaanc-rom arre ofr nigeb eno ,of if not the lnyo actamettsi nboe ecrcan that is puyrel bteio.atssolc

alexb  Great explanation, except that there was a question in NBME 22 in which the prostatic carcinoma was osteolytic. One of the commenters here looked it up and apparently it's like that 30% of the time or something. So I guess you would have to use the high output HF, normal Ca, high ALP, and mosaic pattern to "play odds" as Goljan would say. +2  
qball  At least they were nice enough to put Paget disease because I had no idea what osteitis deformans is. +1  
drzed  USMLE seems to be moving away from using eponymous names... so it's a good idea to see if there is a descriptive name for diseases. For example, they don't use the word "Wegener" anymore if you have noticed, since it turns out that guy was a nazi. So now they call it by what it is -- granulomatosis with polyangitis. +3  


submitted by uslme123(67),
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Tsih tsuoqnei asmke on snese to .me Seh hsa an yermetxel wol gneoinp rreuepss ety sha igssn fo endarscie arlinartcani suesep.rr diD eyht eman ot upt 23 cm ?H??0??????2

uslme123  Standard lab values are incorrect, way to go NBME. +3  
wutuwantbruv  I think they mean to put mm Hg. Normal CSF pressure is about 100-180 mm H20 which equates to about 8-15 mm Hg. +3  
alexb  I lost a bit of time wondering about that ugh lol +1  
mjmejora  I thought there must be an obstruction in the ventricles somewhere preventing csf from getting to the spine. so pressure is low in spinal tap but in the head it must be really high. +2  
donttrustmyanswers  Does anyone have clarification on this question? +  
llamastep1  Pseudo tumor cerebri can have normal ICP. Who knew +  
tyrionwill  Hi, mjmejora, MRI did not see anything abnormality, couldn't this mean that there was no obstruction in the ventricles? +1  


submitted by welpdedelp(229),
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tI was teh ynlo epaprhierl lgnu cca,ren its saol moer omconm in moen.w saasMeitst dwoul vhea wonsh tlmuplei ensosil

sympathetikey  Also, lung adenocarcinoma is the most common lung cancer overall, most common in women, and most common in non-smokers. I know she smoked in the past, but that's what tipped me off to it. +5  
alexb  Yeah I literally picked SCC bc I knew she'd smoked in the past smh +  
maddy1994  20 years of non smoking history ,she wouldnt be at elevated risk for smoking related carcinoma. +2  
larryd  According to FA19 p. 693, large cell carcinoma of the lung is also peripheral. +  


submitted by welpdedelp(229),
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ohriamosecostHm, aka orez"bn .et"eisbad atnCon be Adidnos eud to eth hamigerceyypl and lramno PB

alexb  I missed this bc didn't notice it was a middle-aged guy w/ just 3 year hx of Type 1 DM. +2  
tinydoc  I got it mixed up with primary adrenal insufficiency and the acth ⇒ hyperpigmentation. +12  
maddy1994  testicular atrophy &hepatomegaly helped me out to eliminate the options..when i was left with ferritin and saw pigmentation it clicked that it is hemochromatosis +3  
krewfoo99  Symptoms of Darkening of skin, liver dysfunction, diabetes, with testicular atrophy will always be hemochromatosis +3  


submitted by calcium196(11),
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dqadbuUte-minteiii isotpyoeslr is ont iesbrrvyel dfecteaf yb i.lunsin eTh uoeiqtns sska rfo ibreeelvsr wsya ttha suilnni afftsce it, adn iiqnunbotuaiit duolw adle ot dnaagtoierd via ereat,poss cihhw is not erv.isberle alcN/miycuoeartlcps guitnhsn easkm ssnee ueabecs OXFO si a trstiaipcnrno orcfa,t so ti tca’n do ist ojb if it is in the pco!atlysm

meningitis  Thank you for your explanation! One question: How about the serine phosphorylation? Is it answered by pure memorization that the FOXO TF is serine phosphorylated, or is it a general fact that all TF's are serine-threonine phosphorylated? +  
tsl19  I'm not sure, but it may be as simple as this: ubiquitin-mediated proteolysis is irreversible, but both N/C shuttling and phosphorylation are generally reversible processes. +  
didelphus  I also guessed that FOXO must be a part of the PI3K pathway, since insulin regulates metabolism through PI3K and the question stem specifically mentions that. Phosphorylation is a major part of that pathway, so even indirectly phosphorylation would regulate FOXO. Frustrating question. +19  
niboonsh  yes, FOXO is affected downstream of the activation of PI3K. This is a really good video that explains the whole cascade https://www.youtube.com/watch?v=ewgLd9N3s-4 +2  
alexb  According to wikipedia (https://en.wikipedia.org/wiki/FOXO1) phosphorylation of FOXO1 is irreversible. This is referring to phosphorylation of serine residues on FOXO by Akt, which occurs in response to insulin. But the NBME answer suggests it's reversible. What's up? +1  
almondbreeze  could wiki be wrong on phosphorylation being irreversible? according to this article, it is a reversible process: regulation of FoxO transcription factors by reversible phosphorylation and acetylation (https://www.sciencedirect.com/science/article/pii/S0167488911000735#s0010) some wiki info, however, is helpful : In its un-phosphorylated state, FOXO1 is localized to the nucleus, where it binds to the insulin response sequence located in the promoter for glucose 6-phosphatase and increases its rate of transcription. FOXO1, through increasing transcription of glucose-6-phosphatase, indirectly increases the rate of hepatic glucose production.[19] However, when FOXO1 is phosphorylated by Akt on Thr-24, Ser-256, and Ser-319, it is excluded from the nucleus, where it is then ubiquitinated and degraded. The phosphorylation of FOXO1 by Akt subsequently decreases the hepatic glucose production through a decrease in transcription of glucose 6-phosphatase. +  
leaf_house  It seems like the phosphorylation from Akt leads to destruction, but maybe the assumption is that that phosphorylation step (excluding every other step of ubiquitin-proteosome pathway) is reversible, where proteolysis is final. @niboonsh video is good but doesn't split this one. +