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Welcome to alexb’s page.
Contributor score: 42

Comments ...

 +0  (nbme23#44)
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I essgu esh' intkga B12 epntleumsp,s hswirteoe eh dulow aevh a mtaotpyicsm nce,iidefyc igh?tr

 +2  (nbme23#14)
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Sinec erthe wree sl"alm tsnomau fo "coiemnmu I thguoht ti ontclu'd be tsieaa.r rnsTu tou ataisre ntsi' sywaal secaenb of unem,l it cna lsao be olabranm rnarwngoi fo unmle, ngwoilal utsj a mlsal mtauon to pssa .r.oth.hug

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 +

 +3  (nbme22#21)
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The owdsr s"omt eefct"iflvye fncoudes em. I tgotuhh to mfeysl "eevn fi it ash hte hsegtih fsipictcyie, s'ti tno very tfecevfie fi sit' tog respu lwo itiiseytsnv -- nscie ti llwi imss a lot of hte uter e's+v (lanfigi to elru in raccen orf teh noes hatt teg )s".meids haTt was a tsyro I oltd ymself taubo ireth ues of hte odsrw tmos" yefltvcfee"i .lol

 +1  (nbme22#46)
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tsrFi Aid 2901 pega 262 iayturtmsol whtrgo cftseef of snertostotee dneulci rde odlbo lecsl. I intkh yeth ectxpe us to owkn h.sti

medstudent  FA 2020 p. 636 +

 +1  (nbme22#8)
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I khnti 'trshee a dUoWlr uensqtio gincdsbrei how tsyicc iirssobf nca aescu fta oubells vaintim cyiiefcend dan how a tiV E fde in thta contxet gtmhi astnfiem liairmsyl to 1B2 .def l(osA in rifts )dai

 +3  (nbme22#1)
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heeTr is a cented UWdorl toiunqse ipgilexnna woh tsih .rwkso nylO aosnre I emmebeerrd ti.

hyperfukus  i had notes from forever ago but i totally forgot lol +
carmustine  UWorld question ID 318 +2

 +6  (nbme22#30)
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It eessm elki a lto of het ecsyismt monituamue iesasesd era traoimcuatl.lfi Is ether a eeanglr uler ofr hs?ti

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)! +1

 +3  (nbme22#1)
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I'st saol jstu hte lnyo poiton atsht' hi"b"ned hte lr.ive

 +0  (nbme22#45)
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sI eht trpa tihw tscatn"no ysngui"td tsju poesspud ot rtspopu ahtt ehs has a pschy eidrodrs altrdee to fnto,creeiimps chhwi si ywh shes' giogn ot resexemt to lnrctoo erh hietg?w

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? +

 +0  (nbme22#25)
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aWth ythe mena by

idlFu pdimrscoe fo awter dan syelre,olctet htiw a veyr lmasl aoumtn fo noptrei nad tehro ersmomoalclu,ce ylmloanr leavse lcleaiprais adn laslm cylpiraltposa eseunvl by a oecrssp leacld r.oifanltti aottrniliF si rampriiyl ivdren yb eht lpliaacry drishctoaty ,puesesrr nda teh oumant etfireld rpe ntui ietm is oiiyndtladla incldfnuee by teh ateyrilmbpie of hte vslees lwla thudmeoile(n and neatbems .n)ameerbm hTe duifl htta iesfltr itno het tseuis wlsof wiithn teh eualcrietnlrl epcas (hte inst)tmiiertu nda smot fo it is aerdrsboeb at het rnuaelv end fo rllpaeciias hwree eht hdtstorcayi eeprsrus is .orwle meoS fo eth ederflti fiuld is eaknt pu by iympactlh svsesel dan enutdrre ot the uril.actinco

 +7  (nbme20#17)
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I usfncoed malepydscioyslt oyenrmds whti ymprria mefssyobliroi cseabue I hthogtu 2-3 fo oehts BCsR eoldko iekl adtpreor tsuJ lkei wneh ehty whos na gmiea fro bolsluu igidhepmop adn e'esrth some rewdi cneosd rip orhught eth lmrebmaaselr/ddu lyaer aimnkg me nktih 'sit ton BP neve hought I o'ndt okwn wath eesl ti dwuol .eb lfm

whoissaad  Made the same mistake +4
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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Hiypoxc mopunlary ncootssvoniaitcr (,)VPH lsao nwnok sa the a-lsrieEednljurLt m,mcinhase si a lyilgoshcpioa neoneopnmh in hcwih llsam ulnapmryo rsereita rosncctti in the resnceep of lraelvao yixahop lwo( xoengy .sele)vl

Wlieh eht enantcaiemn fo iufn/eeorvtitinnloaps itrao nigudr aneogirl cruoitbtnos of rflowia si ieiaef,lbcn HPV nca be tneidartlem udgirn lloabg lvaaolre yhipoxa cihhw uccsro ihwt xeoruesp to gihh d,uletita herew HVP auessc a gifsnticnai iasrncee ni ltoat armnpyoul acarluvs cran,eistes and nulapymor ltariaer u,rrsesep ltpleitayon elgnaid ot mulonapyr yiensotnreph adn yuaopmnlr dm.eae


lovebug  2019 FA, Pg 665. PAH +

Subcomments ...

submitted by sajaqua1(462),
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euBseca hte abyb's rhemto has Type 1 itbaeseD mutlsi,le ti is aspibulle that yteh hda vadetlee dolob loegscu eesvll iudnrg ro orslhyt eebfor rhi.tb nisnuIl sdeo nto orcss het ,netplaca tub lsgecuo ,eosd so ndguri rbthi hte oeennta udowl ahve bnee cmiry.eeyglpch shTi odwul aeld to teh nlaeaotn aanercps ilgersane i,nsnilu rdnvgii uoelscg iton sclle nad nurgtin onwd oecieeuonsgs;lng hist is why het byab is pghcmoicyyel irhgt o.wn

B) dcDereesa lnggoyec teonccin-ntora I 'ontd onkw het gycgeonl ntnonciotarec eoarmdcp to an atuld tnapti,e tub a daseerce in ncygeolg ioaorntnectcn lodwu cienatid ol/gcesnouceyggl elaeer,s ichwh uldwo otn be a omicyhlcpeyg et.sat )C adrsceDee lnoyggce ystnsaeh iayivtt-c eecadsdre egnlyocg synehtsa tyvcitia atedsicni gyeenr baicoams,lt nda uodlw lead ot ghiehr urems ugolesc sele.vl D) acdsDeree meusr slinuin oentcnrctoain- raecdedse suerm niinslu luowd elad ot gihehr esellv fo gsuoelc ni ems.ur E) ceIsnaedr semur ii-ulnkilesn twrhog rtcoa-f FIG eods otn bnid nelayr sa llwe to nlsiniu reteroscp as lsinuni des,o and so owuld aveh ot be in xlmeterye ihhg ocoaeinnsntrct to hvea ihst .tcfefe IFG si siscdoaate itwh tacmios hotgwr nda mesulc vemptenleo.d

yotsubato  His glycogen concentration is high, since he's been hyperglycemic with lots of insulin until birth. +3  
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. +1  

submitted by sajaqua1(462),
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In na edyelrl ittaenp twhi stiaodle elteaedv einlkala ahhsotsapep nalor(m resmu mcuilca adn ph)phstoea eatsPg' deiseas of nboe dusolh eb ta eht otp of teh reiifdan.lfet Tshi eisedsa is deu ot tgdlyesnoarui of lcatoisostec dna lteotobisasc tait;iyvc tirsf an iiatlni esoslttcao eriytcphivtay hs,pea htne scerednia ssolaebtto tytvaiic rfo a x,iuetmr ehnt eoltastsocs onturu""b eilangd ot aireo-ztimrlveoiann nad ecostrcil onbe psaqlu.e In ndoit,ida htsi nca cetare vrriouasoenet stnhus ni hte onseb cwhih aeessedrc narstiecse, deilnga to ghhi tpuotu ccairda eaifurl a( srmliia oembprl anc riase ni nsaevrreiootu uaitflss mfor loodb as.liyds)i On hsygtooli ti wlil aevh a "aoicms" e.ratnpt

A)- ranlesAmuy oenb -ytsc laelrgy a purtdoc of vyyhrtiipetca fo setolsos,act hsit ocrucs eomr ntfeo in eth lsim,b nad whsso a ccysit esacp twhi kailn-looleb .dolatnii B) niroo-Amasgac nsmaaragooic fo het ebno is n tmoals eyprul cytli eo.lisn hTye roucc more eeqtulyrnf in nruoeyg pepelo. C) Nacnii id-cniecfye I acn find onnghti touba namiibtv B3 nicicyeefd vivgionln .nbose B3 deifinetcc srlesut ni alepal,rg htwi eth saciscl eeThr Ds-' eitrmdsiat arh(s ecneclak on 43/CC )aroemdem,t at,eidemn and aiearhd.r )E tamsce-sorOao ondFu tlasom ullvsexceiy ni erngyou p,epeol htis enob rtghwo soucrc ta eth orwhgt e,alpt aitapryluclr ta het aixrmpol ned of eht b,atii dliast den of hte ,muref ro oxlimarp dne fo the ruemshu ni( the onlg beson unaord yuor ekesn or ta uyor ueorlds).hs tI hosws a la,egr dlosi goinrwg smsa atht yma arsie the spterieuom in a rbsnustu pon'etstmd/Canra t.lirngea F) irtstPaco occai-amnr arre ofr nbeig eon f,o if ton eht ylon meactstiat enbo ancecr that si epyrlu sbcaeiolt.tso

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. +1  
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. +2  

submitted by uslme123(44),
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hsiT qutseion akesm on sseen ot m.e eSh sha an rylemxete lwo geinnpo sresrpue ety sha igsns fo cirdnseea inanactrliar Ddi hety mena ot upt 23 cm ????2??H?0??

uslme123  Standard lab values are incorrect, way to go NBME. +2  
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(198),
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tI wsa eth lnyo hrparpleie lugn ccea,nr tsi osal rome ocnmmo in ttiaaessMs uwdol haev nshwo ueillmpt insosel

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  

submitted by welpdedelp(198),
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ctmoHoorihmsse,a aak rnbez"o ibeast."de Ctonna eb doinAds edu ot hte laeiyecprgmyh nda roanml BP

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. +10  
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 +2  

submitted by calcium196(11),
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iqmdd-etiitaUinebu rsiesoylotp is otn eibesrrylv fatfeedc by slniuin. heT osnuqite ksas orf sveberrile wsay tath nsiuinl fsfetac i,t nda niaiutnutoqiib woldu dale to agodteiadnr vai serpas,ote chhiw is nto bsr.ielevre malaccryNulisoc/etp nsginhtu esamk snsee eucbase FOXO si a cittnaisoprnr rt,afoc os it c’tna do tis bjo if ti is ni eth !ocyatlmsp

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. +9  
niboonsh  yes, FOXO is affected downstream of the activation of PI3K. This is a really good video that explains the whole cascade +1  
alexb  According to wikipedia ( 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 ( 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. +