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Welcome to haliburton’s page.
Contributor score: 208

Comments ...

 +0  (nbme24#4)
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AF 1207 astest that aeausclrarxvt ilemhsoys hsa ecudainj werhe OAB iytciliotpambin dwoul on.t

 +6  (nbme24#18)
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alxibfImni is a hapFNlT-a nti.hrobii ormf pbuedm αNFT- sha nebe tamtdsdneore ot aevh a ltrneac lore ni hte stoh espensro gtsaian ieutlcosub,sr dgilnunic roanmgaul nfmarooit dan eht tnatcnenmio fo siedsae 5141.(,) lyabNo,t eitdisnboa angisat FNαT- eucddni otiiaaernvtc of tiubeosurcls

bigjimbo  TB can spread to psoas L1-2 often, which then goes to the actual L1-L2 vertebrae itself (Potts or osteomyelitis) +4
cbreland  I get why the TNF inhibitor would cause Tb and it literally said osteomyelitis, but the question says "gram stain is negative". Does that mean it doesn't gram stain?? I read it as it having a negative gram stain and crossed out Tb osteomyelitis as a result +
jsanmiguel415  Mycobacterium doesn't gram stain due to mycolic acid in it's membrane. It'll take the carbol-fuschin stain (acid fast) or grow on a lowenstein-jensen culture but not gram +1

 +4  (nbme23#46)
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lmbldeteus sah a neci enmipocun rof hte ldielk saeinvcc:

Rtse nI cePae a:lsywA

nnfaIlz ue
oloPi lka)S(
tiastH eip A

paulkarr  Also, the nice little puppet show from sketchy for those visual learners like me. +1
makinallkindzofgainz  just remembered that MMR is a live attenuated vaccine +
faus305  how could i forget that puppet show?! +

 +2  (nbme22#40)
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Pdaerr iiWll = tarPelan elnteiod aar(tlip or .fll)u oeNtd fro gnp.tmnriii nuCosi ot nAengmnla o(tepopsi tidlo.een)

FA 2:170 52% of esasc ued ot lameatrn aeitnaulrnp msdyoi ot(w neatylrlma edpnmirit negse era icerde;ev on teanparl egne .dire)evec

drjungly  Physeo video explain this very clearly, +

 +4  (nbme22#5)
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nirdgccoa ot ebdltuseml ilkn ns ss NRA muts arcry NAR epdtdnene NAR rympeeolsa s(o htta si u)t.o

sla,o drgoacicn ot embdluslte eehrt rea ervy wfe sd RAN ,risvseu os m"ost l"kliye illw eb ss. sl,oA NtdeRAdnpne-e ADN arsoeymlpe = eRveres ai.nrpTctsaser enSic HVI si a ss ps ANR risvu thwi R,T yhv'ete rescibdde na VHI .cinsuo otn eurs dyenbo itsh.

nc1992  negative stranded can't be read by a translator so it needs to be transcribed into + first. Only then can it be used for protein. + is basically mRNA already. There's only one double stranded RNA family as far as I know- Reovirus so no encephalitis +9

 +12  (nbme22#14)
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siht gemai hwsos hyccltipoym iy.ttoixc

itsh mieag wssoh htat eth biuldpu fo TAPd ntbiihsi RRN odibuce(noiletr )adtu,srcee chiwh iinhstib eht rste TPdN hsisnesty.

sbnou egmia oshsw NRR is eth ttgrae fo yoyauhre.rdx

leaf_house  That second image is solid gold. +3

 +4  (nbme22#29)
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pg:tenoha yotorcuccscp

metreTnta n:opiots mpoAh B: nbsid ltoseoergr &-;gt rspoe in guanfl amernemb g&;t- kales nctn se.ot nca add ict:elsnyuFo oeecvrtnd ot F5U- to ithinib iunccle cadi nhsseitsy

m1ust:o4odtpop.cl0btieeri/l/ieoy6tosc/mlghbe.ms1lyf1cs/t1un/ i1tuthieemoo8m/blpocclnp0sgehisoiemtbdat:rb1/p5os1.-/rm/t4/cly.

passplease  How did you know it was cryptoccocus and not something else like candidiasis? +1
jsanmiguel415  Was stuck between cryptococcus and candida as well. I think the tip might be that Candida is in mold form at higher (body) temp. But amphotericin b can be used for both and given that it's a serious infection you would probably just go straight for that instead of fluconazole. +
schep  Patients with T cell dysfunction (HIV) are more susceptible to cutaneous candida infections (esophagitis, etc). Patients with neutropenia (chemotherapy, post-transplant) are more susceptible to invasive candida infections (bloodstream infection, meningitis) +

 +8  (nbme22#37)
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rrsfouiacmulb apislyads ni the felt lrnae .a uecssa olw lwfo rueinstgl ni wlo R.FG crnCohi wlo RFG ceassu lauburt ap.royth ecrte(px nad nerceefer blew.o)

aTlburu hratpoy is a rnglaee rmet htta sdresicbe erveasl esnrtpat fo nhoircc brltuau juryni thwi ekencdhti rtulbua nebeatms mbrmenas,e and yllclicina mnefaisst sa hcirocn dyneki saiesed whti redecesad larruleogm iitnlotarf ncredasIe xeetnt fo aublurt tropyha dan mocgainpnyca ertniitsialt sfiibors oatrleercs hiwt owsre ssori.ongp iuarntePrio si abrvilea, pdenigend on sueac.


 +6  (nbme22#12)
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itienardni obslck H2 ,oerrpect chhwi is .Gs Gs titcvseaa ydeyllna leccasy &g;t- APM.c+

q: AVeH 1 a;MmM&p =g;&t H,1 1l,apah V1, M,1 i3M : MDA 2 =t&;g ,2M al2,ahp 2 Ds: rgvteie(nhy eesl) &t;g= t,eba1 ,tae2b ,2V 1D 2H

I nitkh htis is rfmo F.A

baja_blast  Yes; FA2019 p. 238 +
medstudent  FA 2020 238 too. +

 +8  (nbme22#1)
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yprlteanap isth si a mnocmo aeseuelq fo anldmobia tauamr.

rmo(f link leo)bw twwtoey-nT of hte 25 ahtsed ewer aecsud yb ooldb o.ssl woT snateptr fo iceptah souenv yurnij pardpaee ot aeropt:dnemi vlnosuia of eht kurnt of teh thrig aetchip evni frmo the nrefroii nave vaca nad vlnousia of eth rpeup cabnhr of teh igthr heitacp vnei.


 +1  (nbme22#40)
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FA 2:017 arechztCeirad by vmesisa ranfotielropi fo eorekctsgyayam dna tees.apltl stomymSp lceudni igdnbeel and r.smishootb oodlB srame wossh raydemkl snceeirda mrunbe of taeetsp,ll chiwh aym eb relga or hetwioser mlyrlaaonb f.odmre iEalorerlhymgta yma ucc.or

 +10  (nbme22#48)
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no rsnotial seitsu is a eghu ulec rehe. toalt lcka of gI hwchi sasuec rternurce ctsieionnf arfet om6 la(rtmaen GIg is e.n)go LN dna istonsl rae /in.etsnt-inenrxomo F(A 7)01.2

angelaq11  I totally hated this Q! I almost completely overlooked the "no tonsillar tissue", and thank God I didn't because that's the clue that made me change my answer. I had CGD (yeah, I know, S. pneumoniae not catalase +), but it said that he had muuultiple infections since birth. And I took to heart that "since birth" thing, because, isn't Bruton supposed to present with infections from around 6moa? I hope I don't screw this up next week +2
surfacegomd  @angelaq11 I thought the same thing!! because it said "since birth" I thought Ok this is not Bruton :( +

 +2  (nbme22#12)
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frwianar ihisinbt the hystiessn of oscfrat ,II IV,I ,IX X, C, nda S by ckboignl deunircot fo ixdeozid nvtiami .K eTh eeynmz idpoExe ucdsaeteR is tiiidbehn yb waarnfi.r Teh eedurdc aivc)(et rofm of .tiv K si a ooctfrca fro lmgmtyuag-maal oaxbarlscey.

link981  So factors II, VII, IX, and X are precursor proteins? GTFO +1

 -6  (nbme22#45)
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pkaios mscoara. H.8HV ooacesivlu rl()eupp enos.lsi adenacdv VIH C4D t&;l 020 .W(H)O

yotsubato  Yeah thats the easy part. But the histology is whats hard +

 +4  (nbme22#17)
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AF :2710 H iorply is aiosadtesc thwi rascgit reondinmocaaac dna ATML ypmlohma

seagull  I might be mistaken but I also thought Epstein Bar Virus was also implicated in gastric lymphomas? +9

 +3  (nbme22#15)
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a cien rwveie of memooty dna emadetorm / frleexes

 +6  (nbme21#20)
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eaRbis cksaatt eth oincicnti cyheteAllnioc re,coetpr dan evrslat drregeatro avi inyden stormo feart ingnbid RC,hA daniorcgc to .AF

 +13  (nbme21#31)
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rhtee aer tow aseeitnls tfyta :sicda elolinci = eogma ,6 and nilhal-caepilo = ogmea 3.

lizard  Found in fish oils and are shown to lower triglyceride levels. +3
zpatel  alpha-Linolenic ==> omaga 3 +5

 +1  (nbme21#13)
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AF 2:017 oCnrhic xchoiyp aopylunrm tovinasorcocinst etrsslu ni plamyunor etynsprienho and .VRH

yotsubato  Yeah but in a chronic case this guy would produce more RBC and not be hypoxic anymore. +20

 +4  (nbme21#50)
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sthi si a lrcieavc inaslp crod cieon.ts eht aentcue uasicsfucl si acintt (EU) irbnovati and c,pripronootepi btu the hitew eosnitc is hte lgireac cucfuisasl LE() and si I hktni teh laeatlr rtiopno atth is nveune si jstu fiart.ra/aatcltnu

arezpr  thorax section +3
guillo12  How do you know the gracile fasciculus is damage?!?! +2
cr  which parte of the image its damage?, the pink? or black? +
usmile1  the pink park yes +2
d_holles  If you look at you can see that the closer to the center = legs, while further away = arms. +3
hyperfukus  i still don't see where the damage is lol! FML +
hyperfukus  i finally figured it out lol that was a slow moment i hope im not this slow on step yikes! +
angelaq11  @hyperfukus I had the same problem at first, marked it and then came back. If you remember, in the spinal cord the white matter and gray matter are "reversed" compared to the brain. That said, if the butterfly shaped region (ie, the gray matter) is colored (in this case) lilac and the rest (ie, white matter) is blackish, the only thing that is actually abnormal, is the region where the dorsal columns are, because it stains just like the normal gray matter. After that, you have to think about which fasciculus is damaged, the gracilis or the cuneatus. The gracilis is medial while the cuneatus is lateral (picture someone with glued legs and open arms). Hope this helped +12
azharhu786  Gracilus Fasciculus = Graceful legs +
icedcoffeeislyfe  Check out FA2020 pg 508 Put simply--> myelin= black --> color of the normal white matter no myelin= pink --> color of the normal gray matter and the damaged area Dorsal columns= vibration, proprioception, pressure fine touch F. graciLis= Lower body F. cUtaneous= Upper body +2

 +1  (nbme21#5)
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pakiiwdei s:)(oaeloipg eTh eepmhosatr si pmesocdo of 7%8 tneniorg and %12 y.noegx iScne ongexy si cxdehnage at teh yivaa-rloliplleac emnmebra, oegritnn si a rjmoa coopnmetn fro het 'eivalosl ttaes fo .nnaoiiftl fI a realg emolvu fo notreing in eht nulsg is ceaderpl hiwt xoygne, eth xoeygn yam sysqutenuleb be bsdorbea onti the dl,oob cedurgni the vuemlo of het la,ileov gnlretsui in a mrfo fo aolvealr polscela ownnk sa btsnairpoo etlsaseic.ta

I hseoc gdecainrico emade, btu I lveebei tish si orcnretci cseeabu eerht si no trhea elfariu sikr ta ihts ,etim os het rpopuse fo eht EPPE si aynltiecr ton ot uhps tuo u.ifld

bighead478  doesn't there have to be an airway obstruction (mucus, foreign object etc.) in order for this to happen? 100% O2 without any airway obstruction should not cause absorption atelectasis, right? +
iloveallpotatoes  And Tension Pneumothorax is wrong bc PEEP would furthur exacerbate that. +1
hyperfukus  @iloveallpotatoes yea i realized that now after getting it wrong :( +
plzhelp123  @bighead478, they are using a cuffed endotracheal tube and mechanically ventilating this patient which is creating an iatrogenic "obstruction" and as @haliburton mentioned, having a high FiO2 leads to over-absorption by the blood which leads to absorption atelectasis if no other gas is allowed to enter/there is no communication with atmospheric pressure during expiration. Thus, we add positive end-expiratory pressure which keeps alveoli open at the end of expiration to prevent collapse +

 +8  (nbme21#4)
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2FE si aioranltnlsat otiloneag aroftc ,2 hichw is reeanscsy orf tpioren hnsstsey.i

sympathetikey  I. Am. So. DUMB. +24
nala_ula  same :( +2
lovebug  At first, E2F flashed through my mind. then I thought maybe EF2 is elongation factor for transcription. DUMB. :( +

 +13  (nbme21#2)
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lpee"oP iwth osecniodpsateerehlus cieeinycfd mya not eb elab to vmeo or beerhat on tehri onw fro a wef hrsuo etafr i[s-angattcf rgsu,d hcsu as cynihnsccluleoi and aimm]uicrvu era sdidrtneaiem.

ragacha  THX +

 +3  (nbme21#28)
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FA 20:17 bteFrai RsAD dlceiun pyathyom enrisdaec irsk wthi itta,ssn escroleltho lsetgsalon

 +12  (nbme21#21)
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ikln ot aorotnc aimrgad

yotsubato  How is that NOT posterior to middle concha? bad question +10
sympathetikey  @yotsubato - That would have been if it was the spehnoid sinus (I got it wrong too btw) +2
niboonsh  this is a good video if u need a visual +3
sahusema  Sphenoethmoidal RECESS not sphenoethmoidal SINUS +3

 +5  (nbme21#35)
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siTh is aretw xnicono.ttiai inum5mbt..gis:pdth.7/7ww9vn/8w/o7.lnb/hec1p

thisisfine   Agreed! It's along the lines of those marathon runners who collapse questions. Nothing but water for 24 hours = getting rid of too much sodium. +1
temmy  are we just going to ignore the diarrhea for 3 days? what is its significance +4
kard  Temmy, We aint Ignoring the Diarrhea, Actually the most likely electrolytes to get lost with it is sodium> chloride> potassium> bicarbonate... Plus the Water intoxication -> HYPONATREMIA +1
bronchophony  why not hypoglycemia? +1
saulgoodman  Because glucose is not an electrolyte, it does not conduct electricity in solution. The question is asking "Which of the following electrolyte abnormalities". +2

 +3  (nbme21#33)
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morf AAFP DE of dmiex giranoc nda goysenihcpc ginori si noomm.c hcoysePncig escaus rea orme ykleli nehw the tniptea hsa omnlar nsercoeti twhi uortmntbsiaa ro when ctnalrnou ipneel cnteecumse is oa.lnrm

yotsubato  Couldnt a psychogenic cause reduce libido? +2
home_run_ball  "Testosterone concentration is within the reference range" and the fact that he has no difficulty masturbating = normal libido. Low testosterone would contribute to low libido And if he had low libido he would have difficulty masturbating +7
home_run_ball  whoops meant to comment on the other comment +

 -2  (nbme21#10)
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AF :0172 irnryaU tsridsnn-yeoiaeidrpcu ttes si ind otagstinoc. ersu how ot kown ahtt it saw a edr r,olco btu mybea ujst eth atfc ahtt dre emdees ekil a vieospit ttes lre.uts

nlki ot rmoe ondbargkuc utb ont yecisnarlse phelulf rfo hsit uoiqtnse

nobody  "Detection of cystine in urine: cyanide reduces cystine to cysteine → Cystine turns red and becomes detectable when it comes into contact with nitroprusside. If the test is negative, the presence of cystinuria is unlikely." - AMBOSS +

 +4  (nbme21#18)
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uBlslou hgpdmoepii gtnnaei usmt be simeosm.oedehm A:F alblu rea ol""bluw eht ridems apelreb(mdusi )ebtrsi.l PB laso dyeli e"ste"n l.labu

seagull  I love how this cant be straight forward. All the other proteins are either subunits of desmosomes or cytoskeletal components. Because I know molecular biology that well on top of the majority of medicine....FML +8
cienfuegos  @seagull: excellent comment, literally loling right now +
cienfuegos  or sobbing and threatening to hold my breath if they don't make it stop +1

 +1  (nbme21#38)
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I scheo FCSG- secbuae eth urneacoglsty emdees ot me rome of a sikr tahn het dtmeaero ea.anmi ponrrtEoyeihti meess lkie an prapiorpaet hieocc sa elwl btu CGSF- oemr tlcc.iari

kentuckyfan  I think it's also because he has an infection (since he was prescribed antibiotics) boosting the immune system is more important than increasing platelet count E) or RBC count A) +5

 +0  (nbme21#50)
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ym sonte from RODW:UL nsaed eiapgty tusoimqo = eu gdne us,tho tsatosuhe isa,a cfpiaic asnslid, ra,enacbir smraca ei ,AH rto=bieroralt ,pani oinjt niap, csuelm ceah. peeetci,ah rpp,auur spatse,iix lemaen, atbtnpoycioroeh elea,pnuiko hetnnocronciotema

thomasalterman  Dengue is an arbovirus. The important hints are that she was traveling in endemic (tropical) and that she has **excruciating pain in the joints and muscles**. This is why dengue is aka "break-bone fever" +
sam  Same vector +
sam  Same vector +

 +2  (nbme21#15)
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i itkhn ihts si ebauces ibrbunlii is a soelbul rievl dwkarebon dtrcpuo of hee,m tub has ton eertnde hte tinntnceoloi/se orf utg tribecaa scoivenrno to silrnobciet or rn.uiibol oriubinl ni uinre si anlorm.

 +4  (nbme21#19)
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eiPr- or oupamspttr chaymaorotipdy P()CMP si a ,raer tailefernntie-hg ertah edeasis of luarcne igoinr and is atiacerrhczde by ahetr eliafru of ensudd eonts eewtnbe hte alnif skewe fo aprnngeyc and 6 stnomh rafte d.eelyvri nkli to pdmbuehT e laiilccn iurpcet fo PMPC rncsropoesd ot a daldtei riydytcpooamha C(D)M thwi sigsn of eeersv rheat i.ruaefl

maxillarythirdmolar  For anyone wanting to understand why^ the tl;dr is that prolactin gets cleaved into two toxic metabolites. Treatment is something like bromocriptine (and therefore no more breast feeding) to stop prolactin release. Lastly, you can treat with regular HF meds. +1

 +9  (nbme21#16)
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FA 1:702 tereeSc urcaastfnt rfom aemallrl be.sdoi olsA rvees sa ressorcrpu to tpey I lscel adn herto tyep II s.clel rlteaPorfei udrgni nlug .aegmda

teepot123  fa 19 pg 647 +
moms  thanks! +

 +9  (nbme21#10)
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Sllam clel ulng ernacc ssueac HA.DIS octoLian + yailoesxcrun s.ulce

mcl  To expand, SIADH may also result in euvolemic hyponatremia. This is because, as we know, ADH increases absorption of water and therefore initially results in an increased circulating volume. However, this results in increased stretch of the atria and subsequent secretion of ANP. ANP (atrial natriuretic peptide) then results in loss of sodium and water. +10

 -5  (nbme20#8)
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AF 1:270 3° siyhpils srspiudt eth aavs musraov of the otara tihw nqotuseecn ohapytr fo leevss allw dna iatditnloa fo ataro nda avelv gyi M.nar see tiacoaifcilnc of rtcoai r,oto gcdsniane ocirat hca,r adn tcrcoiah ot.aar asedL to rt“ee a”brk aaeerappcn fo atarn.Ca o etsurl ni menrsyau of gaicdnesn traao or crtaio arch, rtciao icncn.eiufiysf

 +8  (nbme20#19)
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eaostnnr nsdou is l.nomra ersapotyennrh whit itntpareovonile eruimfst si eandrcsie c/ lsdio ssma ro l,iufd and edsecrdae wtih iu/rfldai llvee or ionseeon.rxpav pen gordlo oarprxytei espah ;&-tg otviebrusct is.cinodotn

 +1  (nbme20#39)
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osMclmpaay oumnnp oceaedli aul,itggnnsi on srsneeop to mc.olaxniili

FA 2:710 Cscilsa ausce fo atpclyai “i”algkwn umnpiaoen dou(iissni no,ets ahhcdeea, nirocopudentv ghc,ou tacphy or ifsefud aeirtlsttnii iiate)r.lftn -ayXr olkso weosr anht peitna.t ghiH rteti fo lodc unsilnggita I)Mg,( hciwh nca ggiaunetlat ro leys BC.Rs orGnw no tEoan taateamegTrnr:. mlsiecadro, xinyoeyc,cdl or qniolnrluoooeuf i(lecininpl eentvfeicif csien yocslmapaM heav on ellc Clw .ABla) = r,ifAac lsnnseidB, rinoCch .ciienofnt KD– = eiheyvrtng teeNn.asloal e esaseid cna be uacdqire durign pessaag thogurh fedinect tbrhi .nacNo al clel law.l tNo nees no amrG tais.n Plhirompoec tAi meanbrme cistnoan tlroses rof lt.aiybtsi Mapcmyasllo anoimnuep si orme nmmooc setinpnati ;< 03 sayre ru leFt.ndqeo oekuartbs in itylarim rserutci Maoro cap pns.msliasndy gste dcol huttoiw a toca cel(l llw).a

johnthurtjr  Have you mixed Chlamydia in with Mycoplasma? +2
smc213  I mean the Q stem is not about Chlamydiae, but Chlamydiae does lack the classic PTG cell wall d/t decreased muramic acid = beta-lactam abx ineffective. FA 2018 p.148 +

 +0  (nbme20#4)
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FA :0127 cfsetnI B clsle hhtugro 2.CD1 itclyApa chsltpemyyo no hobpdorleiaelp r asmre G —nto edictnef s lcBel tbu evtacire ooicxyctt T lscle. ⊕ npoosoMt dolseeeiitheaneitr sotbh—pt eedtcted by gfniut tganooail eheps ro hroes BC.RsUe s fo cxilnlomaii in nonoccu eomlaissn eucas acrtecitcirash ampcllaruuapo .hras

zup  misread the "accounts for" question as what's the reason for the atypical lymphocytes. So I answered "virus infected B lymphocytes." Anyone else misread it like that? +13
nala_ula  Shit, I misread that too and I noticed it now. Nerves get the best of us! +
stevenorange  If the question is ask what is the atypical lymphocyte in the brain , than it should be the infected B cell, RIGHT? +

 +0  (nbme20#23)
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cnom[emt eovmd to b]utnsmmeco

Subcomments ...

submitted by lsmarshall(393),
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I uhtohtg siht saw a rtikc sunoiqet icsne nksi nrccesa are het stom comonm eypt of rcsanec .varlloe Btu ctaaulyl amnog IVH stepi,tna leV-etHraId enaccrs aer uhmc emro cnommo tnah r-net-odIelnVHa rncaces (vnee snik ccn.)reas duVE-edncBi iyrampr NCS oahyplmm si eth lyon nptioo ttah is esA-idIgnnfiD nclcssr.eniela/

medskool123  why not hep B? i guess another whats the better answer ones... Just rem reading that it was more common with aids pts.. anyone have an idea about this? +1  
haliburton  Yes, I think CNS lymphoma as an AIDS defining illness wins the day. My thought was since SHE has AIDS it is most likely from IVDA, which has a high risk of HBV that could go undiagnosed for a long time. at 32, that might not be long enough to have HBV and get HCC (but with no immune system...?) +3  
yotsubato  God damn this is such BULLSHIT... +13  
trichotillomaniac  Why you gotta do me dirty like this NBME +2  
sars  My thought process, usually wrong all the time, was that HBV (IVDU) can occur to anyone. Acute hepatitis to Chronic occurs when HBV incorporates its DNA into host and releases mutagenic proteins. This is regardless of immunosuppresion. Primary CNS Lymphoma reappears primarily when you are immunosuppressed (organ transplant, immunodeficiency, HIV/AIDS). +  
syoung07  Hep C is far more likely to become HCC than hep B +1  

submitted by m-ice(321),
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shiT gril sha nooM eudcsa by -prnEtieBras ri.uVs ehT opssymtm aer taeeylrliv veg,ua but aydpehnhaoymplt leki isth wluod eb nommco for o.nMo Teh CCB shsow tadveeel htepyoc,smyl pyimilgn shti si ton a ltarecabi ln,esisl so avril si ylike.l nieombCd htiw hte popymathhayd,lne ihst kasem su rwory tubao oonM. ehT -onSotoMp etst rof VBE is wtha the ioesutqn is nerrgferi ot nhwe idgsbnirec teh eeshp htryyscoeter altn.gtanguigi rmFo hre,te tshi uniosqte eusqreir atth oyu wnko htat ni BVE toi,nefnic EBV tsiefnc B ls,ecl tbu soed not uscea hetm ot cmoebe mabnoalr. eIdanst, DC8 e,lscl iwhhc are tlcaeiyv rgytni ot ilkl eth B ,clels eocbem orlbmna.a

medskool123  NBME does trick now and then.. when they zig you zag. then when you think they are going to zag, they zig just to destroy yourself confidence. +16  
kylemax  The abnormal T-cells are known as Downey type II cells (Sketchy) +3  
haliburton  I was recognized EBV, then knew EBV infects Bc, and the atypical lymphocytes are Tc. Then I said CD8 are MHC1 for virii, and bingo bango, boom. +6  
trichotillomaniac  congrats you played yourself +3  
lilyo  Soooooooo EBV infested B- cells is not considered atypical WTFF?? +  
med4fun  They are atypical b/c usually you do not see a super high amount of CD8+ in peripheral blood. Now there are a ton to try to stop the infected cells. +  
aneurysmclip  oh and primary CNS lymphoma caused by EBV has T cells NOT B cells. I just try to remember the peripheral blood has atypical lymphocytes which are CD8+ T cells, and the CNS lymphoma is the opposite, ie; B cells +  

submitted by neonem(550),
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haliburton  ^^^ THIS ONE SHOWS DUCT ^^^ +4  

submitted by medstruggle(12),
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yhW is eht arnsew a“gulatiornn ti?”sesu I thhgtou etarf 41 yads uoy evah a lfuly feomdr ras.c

colonelred_  If you go back and look at the image you can see that it was highly vascular which is characteristic of granulation tissue. Scar tissue formation will be closer to 1 month, plus you will see lots of fibrosis on histology. +13  
sympathetikey  It's a bit misleading, for me, since you do see fibrosis intermixed with the granulation tissue, but granulation tissue was a better answer. +2  
haliburton  According to FA 2017: 3-14d: Macrophages, then granulation tissue at margins. 2wk to several months: Contracted scar complete. Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus). i'm getting pretty frustrated with NBME contradictions to FA, and FA omissions of content. this stuff is hard enough to get straight as it is. +1  
yotsubato  Thats cause the NBME exam writers read FA, then make questions not fit in with FA +6  
trichotillomaniac  This fits the timeline laid out in Pathoma! 1-3 wks = granulation tissue with plump fibroblasts, collagen, and blood vessels +10  
alimd  never look at the image in the beginning. They dont want you to success. Most of the time images are made to ditract +1  

submitted by trazabone(14),
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yendKi emska 52,-1 yrhydox atimnvi .D dcy)5-rorlcxiao tiyhl(2 vti D ldioiac()cl si eamd in hte lie,rv dna spharpydmooiytarih dlwou otn eedrscae tsi sleevl as ti ctsa to ranceise -ah1lap xoyryhasedl ni the einkyd to einaecsr iraoiclctl tancinsotrnoce t-g-;& ashCath/epop nsrroobetaip fomr teh noeb dan allsm teiteinn.s

queezyfish  I'm confused about the phosphate level in questions like these. Decreased calcitriol would decrease phosphate absorption while PTH decrease lowers phosphate excretion. I'm assuming that the PTH decrease has the greater effect with serum phosphate levels? +1  
mousie  PTH = "Phosphate trashing hormone" if PTH is high Phosphate must be low - they are always opposite (unless d/t renal failure then Phosphate will be high - kidneys will be unable to get rid of phosphate) So low Ca d/t low PTH does not effect 25 H. Vit D ... only 1,25 H Vit D (active Calcitriol)? +4  
haliburton  Clarification because I was confused: PTH stimulates kidney to produce 1,25-(OH)2 D3 (calcitriol) via 1α-hydroxylase in proximal convoluted tubule. Therefore, without parathyroid glands, low PTH, 25,D is not converted and therefore not down (normal or up). phosphate "trashed" by PTH as eloquently stated above. +1  
zbird  Here the primary defect is high up from the parathyroid gland, there is decresed or no PTH which normally trashes phosphate but not in this case so serum PHOSPHATE INCREASES and the serum calcium is low because PTH should have prevented the urine calcium so there is calciuria and no resorption from bone-LOW CALCIUM, Vitamin-D is independent of PTH so stays NORMAL +  

submitted by sajaqua1(519),
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noWtu'ld oatlt VA daonl inlbtaao rdyetos to tcratthyhuiymio fo eht ?arecepkam taTh oudlw enma ttah ebwlo teh AV oden the yrmhth dlwuo be eropdidv by a rcrueinvlat c,foi dna tohes luysula atcree eiwd SRQ lmoep.xsce

haliburton  that was my reasoning as well. guess not. +  
yotsubato  Shitty NBME grammar strikes again. +1  
charcot_bouchard  No. No guys. Bundle of his located below AV node and it can generate impulse. it calls junction escape rhythm and narrow complex. Below this is purkinje, bundle branch & ventricular muscle. those are wide complex +13  
abhishek021196  Third-degree (complete) AV block The atria and ventricles beat independently of each other. P waves and QRS complexes not rhythmically associated. Atrial rate > ventricular rate. Usually treated with pacemaker. Can be caused by Lym3 disease +2  

submitted by welpdedelp(216),
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,Ok os NRA ndeneptde DNA melsarpyeo is rof rreeesv epsnarit..artc.s lgnise dntesard + seu RNA nneedeptd RAN aymoserel.p naC nesoemo p?liaxne

hyoid  The only thing I can think of is that HIV is a (+)-sense single-stranded RNA virus that relies on an RNA dependent DNA polymerase (reverse transcriptase) to synthesize DNA. +1  
haliburton  according to [medbullets link]( ns ss RNA must carry RNA dependent RNA polymerase (so that is out). also, according to medbullets there are very few ds RNA viruses, so "most likely" will be ss. Also, RNA-dependent DNA polymerase = Reverse Transcriptase. Since HIV is a ss ps RNA virus with RT, they've described an HIV cousin. not sure beyond this. +  
some0217710  Can’t think of any retroviruses outside of HIV and HTLV and they’re both +ssRNA +1  

submitted by welpdedelp(216),
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It wsa tjus asgkni hte ianlsefp fo BsRC 102( sda)y

haliburton  If I'm reading this right, this is just a tricky dicky question. I think CO binds 200x stronger than O2. But if an O2 cycles through binding / unbinding 200 times before a CO gets kicked off, this should still clear the CO from that cell sooner or later. strange to think it is 1. essentially permanently trapped in a cell, and 2. doesn't kill you and can be treated with O2 to resolution within a few hours or a day. They must just be thinking, until that last RBC dies, you've got original CO in a circulating cell. but just a fraction (because you didn't die). not sure how that CO isn't just passed on during recycling, based on this line of thinking. +7  
link981  The question while stupidly written, asks how long the RBC's that carry the CO take to be removed from the circulation, not how long the CO takes to be removed from the RBC. Just asking the lifespan of RBCs in an stupidly complicated way. As we know, RBC's life span is about 120 days and then they are removed from our circulation. 120 days is about 4 months. Next time they will probably ask weeks or in hours, who knows? smh +6  
baja_blast  If that's what they're looking for why cant the NBME people just ask "How long does it take for RBCs to turn over?" Ridiculous. +1  

submitted by hayayah(1056),
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nrSedyaoc stdipyrrpamrhaoyhie lyasul(u d/t crochin larne iuarl.fe)

Lab isdinnfg liucned ↑ THP (esrsnoep ot olw clmi)cua, ↓ emrsu cuiclam l(rane ,)fruelia ↑ srume hhepoapts (lnare e)lu,arfi dna ↑ aaelinlk spatphosahe PHT( agtativnci ooBest)s.ltsa

haliburton  also remember that in renal failure, 1-alpha-hydroxylase activity is down, so there will be less activation of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is a key mechanism causing hypocalcemia. +2  
cr  why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain +  
nala_ula  Increased phosphate, since the kidneys aren't working well, leads to the release of fibroblast growth factor 23 from bone, which decreases calcitriol production and decreased calcium absorption. The increase in phosphate and the decrease in calcium lead to secondary hyperparathyroidism. +1  
privatejoker  Probably a dumb question but how do we definitively know that the ALP is elevated if they give us no reference range in the lab values or Q stem? Everything stated above definitely makes sense from a physiological standpoint, I was just curious. +1  
fatboyslim  @cr the question asked "the patient's BONE PAIN is most likely caused by which of the following?" Increased levels of 25-hydroxycholecalciferol might exist in that patient, but it wouldn't cause bone pain. PTH causes bone pain because of bone resorption +1  
suckitnbme  @privatejoker ALP is included in the standard lab values +  
makinallkindzofgainz  @privatejoker ALP is listed under "Phosphatase (alkaline), serum" in the lab values +1  
pg32  Why does AlkPhos increase in renal osteodystrophy? The PTH would be trying to stimulate bone resorption (increase osteoCLAST activity), not bone formation (osteoBLAST activity). +  
drzed  @pg32 the only way to stimulate an osteoclast in this case (e.g. via PTH) is by stimulating osteoblasts first (thru RANKL/RANK interaction), thus ALP increases. +1  

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I kcdeip rsn’hCo too. I tnhik eht eeserv cinottposnai eovr 5 erays dttdiserca m.e

haliburton  i think it is critical to remember that constipation is what caused the diverticulosis. +3  
lola915  Crohn's presents with +/- bloody diarrhea, not constipation +  

submitted by nuts4med(6),
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ynnoeA heav na ieda why eht cederased raatiler O2 naaisrutot si ic?erctnor gmiunsAs ehs ahs lpum dmeae eisnc hes hsa EL am,ede ut'dlwon a orelw 2O ats be edpcxeet ot?o

haliburton  I believe there would be no decrease in O2 saturation because oxygenated blood (high pressure) is shunted into deoxygenated circuit. As long as the lungs can keep up, this should increase venous oxygenation on average. +7  
hungrybox  ty both of you for this, was wondering the same thing +  
coxsack  O2 sat won’t change b/c you’re not adding deoxygenated blood to the arterial side. You’re just taking arterial blood and putting it into venous blood. Same reason why L->R cardiac shunts don’t decrease O2 sat (while in contrast, a R->L shunt would). +4  
hungrybox  just realized: the high pressure of the arterial system keeps out low-pressure venous blood in an AV fistula (probably obvious to most ppl but it was a eureka moment for me lol) +2  
chandlerbas  ya you wont have decreased arterial O2 sat because oxygenation of blood is perfusion limited (FA19 --654) therefore oxygenation of the blood happens within the first .3seconds of entering the pulmonary capillary that you could even handle having more deoxygenated blood enter +  

submitted by monoloco(132),
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If yuo nawt ot lcear a drg,u it is rbypbola tesb ahtt it ton eb ubdon ot npsoriet o(s ttha ti tesg fteei)rld adn it hsa a wlo luevmo fo ntisuiirdtob (os ti t'ins in eht ede,p hrad to erahc .ssutie)s

kingtime9119  But that doesn't make sense. Page 233 of First Aid 2019 edition clearly states that being plasma protein bound creates the lowest volume of distribution, because not being bound to proteins increases the chance it will reach deep into the tissues before it reaches the kidneys. Discrepancy with First Aid? +  
haliburton  my reasoning was comparing two drugs, both with Vd of 1, the drug with the lower albumin binding would be cleared faster @kingtime. I don't think you're considering that A and B have equal Vd. +6