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Welcome to lsmarshall’s page.
Contributor score: 371


Comments ...

 +25  (nbme24#3)
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eTh tmso idertc apht, adn msto ielkyl p,ath for rsaebt cenacr to zasamitetse ot teh evrtabre aer eht lcsitenrtoa .viesn shiT aws no an erilrea MBEN tets as .elwl Brtesa erncca lwil esauc emid,x ictyl and aitbscl snoiles ocne in nb.eo

On an euanlrteda oetn; I flnlyia emac up twih a ectnde wya to mmrebree clyti vs. cabtsil saccenr ni e!bno

ekndIY nda dhoYtrI uacse ctlYI

eosarptt g&t; aaettlbs &;tg tilabsc

owT sretbsa ;> wto tsyep fo ilsenso ;gt& B trsea uscsea B oht

Two ungls &t;g two seytp of nssioel enpignded( no type fo guln ccenra)

ls-mllleac ulgn &tg; lsal"m "bsltsa

mln-nsoal lcle t;g& yiltc

artist90  VEINS: 1-Intercostal veins drain into Azygous vein which drains into SVC BUT some blood from this Azygous vein is also draining into BATSONS VERTEBRAL VENOUS PLEXUS how the breast cancer metastasizes to vertebral column. 2-Internal thoracic(mammary) vein drains directly into Brachiocephalic vein. 3-Lateral thoracic vein drains into Axillary vein which drains into Subclavian vein which drains into Brachiocephalic vein. ARTERIES ARE DIFFERENT: Subclavian artery----branches into---Internal thoracic(mammary) artery---Intercostal arteries. Internal thoracic artey is used for CABG if there is 1 vessel block. +12

 +18  (nbme24#16)
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rloFxe utiigmodr uonrsufpd is blprieesnso ofr fonlxei of .IPD idMeal tpcsea fo eth eumslc (wichh elsfex teh t4h nad th5 )igitd is lpiespdu by teh unalr renev C(8, )1T. heT llraaet psceat h(hcwi xlsefe eht dn2 and r3d dgii)t is nreivaentd by het eamndi rnvee cficpslialey teh nrieatro ostseurneiso bahcrn 8(C, 1T.) So teh teqoisnu is isibcendrg a tacneaoirl gmidagna eht enver spylup ot hte IPD flxreo fo eth nd2 giidt indx(e rf).ieng Tihs is gysina hte adlmie renve si engbi gadadem C(8 nda ;T1 werlo uktrn os.tor)

rsmLliacub d/1s2nt,( manid;e ,/h4rtd3 lua)nr rea a progu fo lssemcu ttah flxe at the MPC no,ijt dna etxend PIP dan PID o.istjn

lCoud brmrmeee sa xfo'erl ruimogdit uruodpnsf si fnouoyprdl nol'g isecn netdnos terins on PIs.D dopreaCm to rxoelf gitidormu rsuicfpesilai wsheo etnond arpsw dnuaro f'nusopdru flrulsipyecia btu tsnesir no IPPs.

toupvote  This is dumb but I remember FDP is needed for picking while FDS is need for scratching the superficial layer of the skin +10
whoissaad  @lsmarshall Flexor digitorum superficialis inserts at the middle phalanges to be more specific. +
aneurysmclip  shittt I remember it like this D for distal P for profundus > Double Penetration. and I know the PIP flexion from the other Flexor digitorum, which is superficialis. Extensors are lumbricals. (Lengthen your fingers with Lumbricals) +5
hungrybox  'flexor digitorum profundus is profoundly long' is such a good mnemonic, thanks bro +

 +19  (nbme24#27)
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lraaantPres" eevah ()itfl surocc dgnuri trghi runleivrcat prepyhhryot e(..i tnemnalee)gr or ryev aylrre ervees left airtla nlarenmg.t"ee RV yhptrheryop anc eb snee so aseily eseuabc the VR si ta the anrritoe rasucfe fo eht shec.t

In isth tpneiat obdlo rmof LA ot LV ceeadsrse in ,suiantraot so ti si oigng ee.rowmesh Fomr hte O2 sa.t ew anc eedcdu hetre is loybpbar a DVS sencd(irea RV rpsreseu wlduo suaec VHR dna arspalanrte a)ve.eh or,rmhtFuer the ieetgvtn si eykill idgnbrices alttyegor of loalft ucse(da yb oroiupenstrera inelcmtesapd fo the uuiabflrnndi e.t)supm nI Tte lsles,p VR wuftool si oot dtouscebrt and ptaeint steg oysinsca nad ;Lgt&R tnnguish sauqtS caseeirn SR,V deesigcnra g;tRL& tnghuns,i tntupgi rome lbdoo ghorhtu olnuapmyr cturici adn inlergeiv so.isycna

seagull  i'm pretty sure your a prof and not a student. +12
nor16  nevertheless, we are greatful for explanation! +
niboonsh  I remember seeing a question describe parasternal lift in the context of pulm htn. still got this wrong tho fml +
anotherstudent  Did my question have a typo? It says O2 saturation in the right ventricle is 70, which is equal to the Right atrium and vena cava. It says the O2 saturation in the left ventricle is 82%, which is a decrease from the LA (95) but not equal to the RV, which is why I thought there wasn't a VSD, I assumed there was a weird shunt from the LV to some other part. Will O2 saturation not always equalize? +1
pseudomonalisa  This is a right to left VSD due to the pulmonic stenosis present in Tetralogy of Fallot. O2 sat will be low (70) in the right ventricle, and from there it'll enter the left ventricle and mix with freshly oxygenated blood coming from the left atrium (95). Because of the mixing, the O2 sat of blood in the left ventricle will be somewhere in the middle of 70 and 95 (82 in this case). You're correct, though, that most other VSDs are left to right and you'd see greater O2 sat in the right ventricle in that case (not sure if it equalizes with the left ventricle though). +

 +32  (nbme24#20)
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nePatit has pnSia ibdafi lctoacu hchwi is a laruen bteu etcfde (eurlaif of nofsiu fo het sponeouer.r) eoresSocmlt era teh rtap fo ehca iemtos in a ebrrtveaet ymboer nvigig iesr ot enob or hoert talkseel uits.es cSnie a ptra fo ihst sp'ienatt ainps ibiadf cneduidl basne"cse of oisunsp "cpsroes enth a csleotemor swa dnvliev.o Konignw atht lueanr uetb dcftees rea an useis iwth osniuf uhosld eb ngehuo ot egt to teh gihrt anrs.we

fI eth ochortodn ldieaf ot edvlpeo enth eth neitre SNC dowlu otn epvloed as the onrdocoht seiundc faomnotri of lnareu .pelat

If eht ernula betu eaifdl ot poevlde neth hte wleoh NCS ouwdl ont vaeh eplevd.deo

Yklo sac is nervalreti ot thsi titnpa.e

heWn ruaeln sterc ellc ti has iefetnfdr eooucstm ni erfefntid u.esssit ieluFar fo ulaner csert to iaretmg in ather anc csuea pnTtoiarssoin fo atgre ,elevsss goealrTty fo lFal,ot or ssirPetten stncuur r.srisaouet ieualrF fo rauenl srstec to mageitr in GI anc uasec nipHrsghscru seedisa g(ltannioce m.locango)e raerTech Closlni mdyernoS nca rucco nehw uanrel stcer sclle ilaf to mrieagt ntoi ts1 ypahnargle .carh laeuNr ubet sdteefc ash gnihtno to do itwh uilafre fo eurnal tecrs miirtgnoa huhog.t

sympathetikey  Exactly. I knew it had to due with fusion of the neuropores but had never heard of sclerotomes. Thanks for the explanation. +8
hungrybox  Fuck I picked "Formation of neural tube" but yea that makes sense... that would affect the whole CNS +2
ruready4this  I also never heard of sclerotomes and I chose that and then switched it to formation of the neural tube because I thought that was close enough ugh close enough is not the right answer +

 +7  (nbme24#8)
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T"eh axect iemhnmcsa orf rmerot cutidonin yb -(2ercβgn)aidre goaitssn si ltsil u,knnonw utb hrete si oems nedvicee atth βdc)e-g(na2eirr nagotsis cta dyirtecl on ..mcs.elu erMo yree,tlcn rtoerm has nebe tcerralode cosleyl hwti iealoh".pyaamk - NHI atibnilcuop

Frtis Adi inotesnm ysydeitropmrihh gusican treomr omfr βiagnc-eredr latusntomi.i tI sola nemontsi 2-sisoβagtn ucsniag mtrero as a sedi .etfecf sFitr dAi lsao nesitonm stβno-2siga ivdrign tssamuoip iton selcl, hiwhc may rnutoibect ot orrem.t taTh ds,ia orem saicscl ypsmmots of mpelaakyoih are deiw QSR nad deaekp T evwas no CE,G th,mryhaasri nad esmclu .nwkseesa

ikongoL ruanod on het retinten ooskl ikel if erhtypa si cioetudnn hte otmrre orfm a anistβsg2-o soesverl rve.oimet

xxabi  Sketchy mentions tremor and arrhythmia as side effects! +1
drpatinoire  Hypokalemia is more associated with U waves, flattened T, muscle cramps/spasm, those symptoms you mentioned is more typical in hyperkalemia. (I guess you made a typo..?) +

 +13  (nbme24#1)
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nA mxipenrealet isendg or plemaxireetn dtyus stmu aveh na nvneoretniit, yb oeninditf.i locntraCo-es edisstu ear ibetlsvnooraa usidtse, ont nxtaeimeelr.p sTih tqoinesu is ncteyllhiac ieortrc.nc yhTe adwtne ot eakm a iotpn atht entlooaccs-r eduists aer imte and tcos cieftfeni necsi ethy tond' eeiruqr llonwoigf spteitan rvoe item or yna scersoure ebsdesi hi/naetrrvewiggegin if.anrtomino esCa eesisr uocdl ont tste hits stpho.esiyh

s,loA teh odrniwg siataocse"d twi an snacdeeri kis"r eatmhows uldesla ot oae-srncctol stdieus lnyo hngaiv hte ilbiayt ot ifnd ddso of na asiositncaos twnebee exusoper dna ou,tmcoe tbu nto hsesalbti sluaca arpstilih.noe

bigjimbo  classic nbme +1
poisonivy  totally agree, I dont understand why the right answer is Case control since that is not experimental +
howdywhat  am I subject to this kind of poor wording for the day of the exam? +
ajss  I bieleve so +

 +9  (nbme24#35)
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"sseomDeom calu(Ma ae)edrhns - A -l-oletcclel coetncnino hatt osdeipvr aulsrturtc oupprts ithw emttdnreiaei letmainfs, rclpluratiay ni ssiutse taht ueorngd aclemchnai essrts e.,.g( sn,ki scrgtia siest,u eabrdd).l Cncnteos tktysnieearco in eht rsmautt snspimuo of teh "esmei.dpir - SABMOS

sympathetikey  This is why I was looking for some answer indicating keratinocytes in the stratum spinosum...instead they just gave a bunch of bs choices. +25
roygbiv  I'm confused because I also know that S. aureus cleaves desmoglein in the stratum granulosum, so why is it specifically this answer? +2
duat98  desomosomes connects cells to cells. hemidesmosome connects cells to basement membrane. +2
medguru2295  I think what this is really asking is can you tell Pemphigus Vulgaris from Bullous Pemphigoid Vulgaris (question)- Attack on DESMOSOMES- this separates some keratinocytes from others (ie some in basal layer from ones above). Pemphigoid- attack on HEMIDESMOSOMES- this means separation of the keratinocytes from the basement membrane. +2

 +12  (nbme24#27)
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rpuyPntehyloao - A tiniconod lsivnveo gamead to llempuit elrappehir vener fisre.b snatietP plylacyit eptsrne wiht tmisycmre ldsati nsroeys loss or a rubnngi steoniasn dsosieaact tiwh mroot .saeewnks cCsasil npopyrthlaouye is rbingnu os iths uensotiq saw orem ssrcpoe fo .imanieolnit srteOh idd nto tfi .ewll


 +8  (nbme24#33)
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nnhItaal bsaue clodu eb noed htiw l,egu aptin isrte,nnh eulf, rsntiuo xod,ei or ylalk .eniristt ullyUas ni hocghihlos- egad ikds. Inlathans rea rdewon''s os awrethve itioatxnicno sfteefc etrhe era hulosd be tsdreanesp nad llyfu rsoelev tinhwi 03 mn.i to a lpouce hosru. sPitetna mya kool rkund hnew icoxdnteiat htwi annathis,l tbu lysulau uiqcylk re.esovl A hcitacsaecirtr "glue fnrisf'se hars" aduron the esno nad mthou si eimsmeost sene rtafe drngolope e.su


 +15  (nbme24#48)
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PAC esoktr nac acesu "ssnaorgaopiop" cwhih is het yibtlaiin ot ngeeoirzc faiariml f.sace suaCed yb raiebltal iosslne of uvasli niocaasiost aares, hiwch rae edtuasit in hte oerirfni cirpalooocpitmte otxrec (rfumfsio .u)srgy Teh lbiaity to amne tprsa fo the eafc e,.(.g o,nse mtou)h ro ynidetfi aiidvslnudi yb otreh secu (..ge, clt,ngiho oi)vces si ltfe iacntt.

iWotuht igkonwn ,ttah rmreeinmgeb pcoaltcii bleo is oivldnve in ul'siav f'ustf adro,lyb dciingnlu egiam igpenssocr nad shit titeapn is ghniav esuiss thwi ntsiudreadngn msieag luohsd be ogehun to teg ot het nwarse.

gonyyong  Lol I guessed it exactly because of that +3
sympathetikey  Never heard of that one before. Thanks! +1
karthvee  This is not prosopagnosia, but instead a case of apperceptive agnosia. Wiki: "...patients are more effective at naming two attributes from a single object than they are able to name one attribute on each of the two superimposed objects. In addition they are still able to describe objects in detail and recognize objects by touch." Although, lesions tend to be in the occipito-parietal area so PCA again is the answer! +3
misterdoctor69  I actually think it's both prosopagnosia AND apperceptive agnosia. She is neither able to recognize her mother's FACE nor is she able to recognize objects w/o the help of other senses (apperceptive agnosia) +
nifty95  Yea couldn't remember the exact name but I just thought of three pathways (visual, somatosensation, and auditory) all converging somewhere/processor (probably somewhere in the temporal lobe...hippocampus?). Beyond the point, the pathways converge to an area which culminates in recognition. Cut off one of the routes (in this case visual), the other two will still work. How is visual cut off? By the PCA not supplying the area leading to neuronal death resulting in varying loss of visual function depending on the area in the occipital lobe. +

 +36  (nbme24#8)
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Uear Ccley rrsioDsde ;&tg sIdeltoa eserve empaimenymrhao ;tg&( 010;0 ,i.e. no ohrte erevse cmatliboe sduitscbnrea

eihniOntr trcnrleaaayabmss ecifeycndi g;&t mso(t oommnc areu ecylc .is)d ictoor armdacaiuiai/eicd, nmehamyiapmeor

Onarcig Adacsimie ;g&t ynmarpHemao,emi noiag-nap o,sicaids eskstio r(mfo )oyyaehlcmipg

iheidu-cmMan A-alcyCo yednegsehraod ceinecfidy t&;g r,noammmpHeeiya ocepyttihko lamgyhoyipce ene(s ni aβno-tixodi dsori,edsr ECXETP erlk)eootnypaordusyhd

rveiL stfiyncundo &g;t aeamn,mHopmeyri sTFL dsemse p,u ldreo t.p

lsmarshall  Summary of metabolic issues relating to hyperammonemia +6
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +3
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria? +2
charcot_bouchard  if it was mitochondrial disorder no one would escape +2
wowo  figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB) + also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia +2
artist90  i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong +3
artist90  it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things 1-how does acidosis cause Hypoglycemia and Ketosis. 2-why is Ammonia elevated in these pts bc urea cycle will be fine? +
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld) +1
yex  According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA. +9

 +4  (nbme24#37)
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Ar"i sd"rtleop dussno ikel ertirposayr ivsl(aa ro )wtrea .rptledos onntilhaaI of poalsaxtmo tsyoosc in atc csefe sint' iteuq hte se;ma otn ot ays I wnok etcxlay wtha teh sooystc rea ehdianl as stj(u cprocmiocis ydr act poop i?l.crtsp)ae nesnIogti fo dcrdoeeounk tmea ot gte teh sytsc si antierlcy a TRO for lampo.aotxs

lTmsoxpaao as THCOR hsa itdra of rhehplcuodsay, balrrece ciniacacotsfli ,rrlc(terneabi)a and iiorici.htrsoetn tchnetirioirois acn eb ni oitenclnga MVC or spxooiost.mlas etiirveunPclarr sniaciialctfoc rae ni CV.M ateCninogl CMV lsayluu hsa nraiegh ,slos s,szrueei lpeaticeh rh,as y“rulreebb unmiff” sahr, teo,rsioirtihnic adn arnctrrlpiueeiv oicsiicanlaft.c

usmile1  also note that toxoplasma can cause the "blueberry muffin" rash (also rubella can as well) +
raddad  So looking at the CDC website, it looks like "accidental ingestion of oocysts after touching cat feces" is the route you were talking about in the first paragraph, so inhalation of air droplets is wrong inherently. +

 +27  (nbme24#49)
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engnrAod Issvtieiinynt drynSeom - teecDf ni rnaodeng rteprceo itluegrns ni ieaplrapogam-rnn meefal YX64(, SD).D ouintnniFcg ssttee csaues rsaeencdi rsottetnesoe at utryeb,p cwhhi si vdronceet to ngoseetr ia,pepylhlrre vnggii aelfme yaorcdnes lexasu crsircacattsieh ele(amf nratxlee in)laieagt. kaLc fo ndregoan eprcreto ofcuntin esdla ot stbnea ro ncsta lxyarali dan bciup riha. aetstPin hvae meryantiurd ,giavan tub ruestu dan apifanlol bteus s.neatb

ndernAog itiisvsyennit ormsnedy is het wnares btu oyu mihtg avhe desedirnoc rlnüilaeM nsegasei -oRyyara-s(kitMnke Hr-üuseKertsa ms)nr.ydoe

allrMeniu ssenaige illw heav lmnaor monreoh eellsv nad yma esptnre as 1° oaehmrearn d(eu ot a clka of ituenre mlepoe)devtn ni almefes twhi ylful eddlveeop 2° lsxeua ccitrheacisarst tnulc(nfiao oea.)rsvi aHir eoeptmnveld is onraml as wel.l ePtsanit oals ahve onralm .ehtigh

emsSe klei iths ueqstnoi ddi ont egiv su cmhu to hnssitidgui eesdbis higthe dna eatnrn seatg 1 ailpuxla/yicrb hai.r

dbg  100% agreed. Mullerian agenesis was on my mind too. The full breast development kept me fixed at this dx. Did not think how high testosterone at this age and insensitivity would push towards peripheral conversion to estrogen and hence breast development. Thanks. +

 +15  (nbme24#45)
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CHM lsacs 1 tdpepie tnneaig psorcsgnei &g;t ngnt"Aei etdespip dleoda noto MHC I in ERR ftear iyldreve avi TPA peranrtr(sto tisdaacseo hwit gnetina gnsics)reo"p - srtFi idA .9201

eBra hmtlpcyoye rdmnyoes eytp 2 SB(L I;I ctfefaing HCM )II si eud to tmatnusoi in enesg ttah deoc ofr ptnotasrcinir forscta ttah lymoalnr egrleuta the neepisorxs ge(ne nanptco)triisr of eth MCH II se.gen rBae ohcytyelmp snmydore tpey 1 SL(B ;I itfeanfcg HCM I), is uhmc moer rae,r dna is aiaostscde ithw TAP nfediisce.iec

tyrionwill  in the question, it says absence of MHC-I presenting cells. I guess the meaning is lack of MHC-I. IF TAP is missing or dysfunction (bare lym syn type-1), MHC-I should be there, however Ag cannot be loaded to the MHC-I. Can anyone help me to understand more. +
peridot  @tyrionwill From wiki: "The TAP proteins are involved in pumping degraded cytosolic peptides across the endoplasmic reticulum membrane so they can bind HLA class I. Once the peptide:HLA class I complex forms, it is transported to the membrane of the cell. However, a defect in the TAP proteins prevents pumping of peptides into the endoplasmic reticulum so no peptide:HLA class I complexes form, and therefore, no HLA class I is expressed on the membrane. Just like BLS II, the defect isn't in the MHC protein, but rather another accessory protein." +

 +17  (nbme24#22)
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lgreleeZw rnemdsoy - osmtlaauo reecssvei dsodrire fo piomsrexoe iobsesgnei ude ot etaudmt XEP es.gen i,poyHntoa zei,esurs tamo,eglepahy larye tdeha hnwt(ii 1 y).rae da-iβtoinxo fo LFVAC aenspph in seeoxrsmipo so hte idlhc iegelsynm aginvh osem srto of tingcalneo lbcaemtoi droiersd ihtw edtalvee AsCFVL sudlho eahv nebe egnhuo ot gte teh wnrsea wutioth owignkn abotu .rewlZlgee

jucapami  furthermore, FA 2019 pg 47 +2
tiredofstudying  Same page for FA 2020^ +3

 +17  (nbme24#25)
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rcAal estgiluoni is omts cmoomn etyp fo olmeanam ni Acfrain easicnmrA adn si on hte apslm or e.osls I sgues eth lcptiay nkgtiinh fo ceths dan abkc nu(s pdxse)oe si a tlteli eitfefdrn ni isth p?yte omAng lla a;pmgicseohdr aoslmaemn crcuo the omjiryta of mite no teh lsbmi ~6(3% oelrw and 91~% ;)puerp ruktn si ~7.%.2. oS asdeb on that nad mhi niegb fo Arnfica entsdec ew acn seocoh lma.sp


 +7  (nbme24#1)
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tluogAhh Csr'noh may vahe ,rcsleu ts,ufsali and eid;negbl ti yluasul edso nto cuaes noir ifeieydncc neiaam dna sha less nldeegib ntha C.U rrucltu"taS eartoaliimsbn of the atlinrem iuml,e chus as Cnrho seaieds nda ruglcasi so,rticene can csaue sceddeera rntpbsooia of vatmini .B21" - sirFt Adi lGnaree nrpPsieilc


 +3  (nbme24#24)
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ceiePdor"nb adn hid-sgohe iaactysslel iihtbin teoonpbrsira fo ircu ciad in mrlopxia clvoduonte btleuu saol( ibsithni stneecroi of ice.lnln"i)ip - stFir iAd 1209

uslme123  so ............... +8
adisdiadochokinetic  So probenecid is the best answer here because they only specified acetylsalicylic acid, not the dosage, and low-dose acetylsalicylic acid has the opposite effect. +8

 +7  (nbme24#31)
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trFglismai (C)-FGS si vyre ocomlmny seettd itsh w;ya rWdUol and e.wehsreel mhC.oe tpnitea itwh nebo rmraow ernsssoriup ;gt& vige S.F-GC


 +5  (nbme24#50)
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etapaasMli - A rrbeselevi petvaida oernseps ni ihwch trehe is ar"pnRerigmmog fo esmt lsmeecpenlaŽctelr fo oen cell ypte yb erathon ttah nca padat to a wen e"rs.sst hBto aer olmanr lelc.s pRotsraiyer eter soduhl not aveh amqssuou lslec inlut tieroayrrsp rebscolohni efbe(or th;ta obuacidl ni em.tr .nbor t&;g onarlmcu in obrhc.n > oespftsdaureitid ulnaocmr in argle. hcr.nb.)o

shayan  if its a metaplasia, then how it be normal ? I mean Metaplasia is not normal? +2
artist90  i got it confused bc the question stated that there was a mass in one lobe of lung and i didn't knew that squamous metaplasia also presents as a mass in lung. i missed that on biopsy they were clearly stating squamous metaplasia. +4
suckitnbme  @shayan The term "normal" in the answer is used to indicate that the cells appear normal (meaning appropriate size/architecture/appearance). Remember that metaplasia is a normal response to stress. +6

 +13  (nbme24#8)
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aeniSoybntpvr is hte argtet fo otisnaamtpnse seuattn( n;io)tx melscu msspsa era .tstraceiacrchi Olyn ehtro wrsane ouy gmthi rcoensdi si rsestoecllicAtahnyee ecnsi he is a mfrear nda szburowdz ftnoe crary us to eth pirosmed ..nlad. tbu tymsomsp fo a gernlhicoic mtors ear te.absn

vshummy  Synaptobrevin is a SNARE protein. Why they couldn’t just give us SNARE I’ll never know. +36
yotsubato  Cause they're dicks, and they watched sketchy to make sure our buzzwords were removed from the exam +36
yotsubato  Oh and they read FA and did UW to make sure its not in there either +29
soph  This toxin binds to the presynaptic membrane of the neuromuscular junction and is internalized and transported retroaxonally to the spinal cord. Enzymatically, tetanus toxin is a zinc metalloprotease that cleaves the protein synaptobrevin, an integral neurovesicle protein involved in membrane fusion. Without membrane fusion, the release of inhibitory neurotransmitters glycine and GABA is blocked. -rx questions! +5
qfever  So out of curiosity I checked out B) N-Acetylneuraminic acid It's sialic acid typical NBME +2
alexxxx30  shocked they haven't started calling a "farmworker" a "drudge" <-- word I pulled from thesaurus. +2
snripper  "You shouldn't memorize buzzwords. You gotta learn how to think." Lemme pick another random ass word that doesn't have anything to do with critical thinking skills and use it instead. +4
mw126  Just as an FYI, there are multiple "SNARE" Proteins. Syntaxin, SNAP 25, Synaptobrevin (VAMP). From google it looks like Tetanospasmin cleaves Synaptobrevin (VAMP). Botulism toxin has multiple serotypes that target any of the SNARE proteins. +2
wrongcareer69  Here's one fact I won't forget: Step 1 testwriters are incels +1
baja_blast  FML +

 +13  (nbme24#33)
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I"n het esray eeicgnpdr ihaypcls bpte,ury erbtoR M. yaBor rcieeovdds ahtt the oonrontdipag susple uccor lnyo girdun l,pees tbu sa bueyrpt sgrerespos htye can be tdeedcte unrigd the ayd. yB eht den of eprb,tyu ehret si ttleil ayi-thdng nfiedecefr ni hte dtipemlua dna nyerfucqe of prnnoiodatgo pus.lse

emSo ganvtssierito veah adttiubter eht soetn of yrueptb ot a cnreaseno fo latrosciosl ni teh ]9bia[.890n]][9[1r yB iths mmihcens,a eht angpooidortn euplss thta cocur ayiilprmr at tgnhi sutj bofeer yrbtuep pesrnrete sbet".a - ikiW

linwanrun1357  Who can explain, the 12-y boy with stanner stage 2?? I thought it should be stage 3.... +1

 +5  (nbme24#22)
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I hthtogu hsti wsa a icktr esnqutio scine knis cscnrae rea eth osmt omocmn eypt fo cenrsca vllaero. utB ylauactl onmag IVH t,isetapn rH-atlIeedV scnecar era hcum omre oomncm tahn Hanete-rdnoVlI- rnccsae (vene nksi ercs)nc.a dcuiE-denVB yrmpiar CSN ahmploym si hte olny tooinp thta si -gnfDeiindsAI /ceeslirnalscn.

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... +12
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

 +11  (nbme24#11)
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cognozyoMti laient"di()c" wtnsi vahe 0%5 of tignegt psnehociaizhr fi heirt niwt ash t.i izDgitcyo wtnis vhae ~ %20 cnahec o.utghh hiTs si teofn deinonmte ewnh hhceznoiSirpa eygiotlo is scdesuisd ,ie..( we tdo'n kown btu cnccrdoaeon idsutse egstgsu a gteenic )ilk.n M1DT hsa sesl fo a iencgte lkin tnah 2MDT tub it sola ahs 05% onrcecndoac btweene yiogomzoctn wtnis. siTh fact si tnimdeneo ni rtFis dAi 90,12 pega 4..63. I gto isht NEMB ineutoqs nwgor btu 'its nenttoc si ni ardob csuores.





Subcomments ...

submitted by medstudied(1),
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Cna mseneoo npliaex yhw hte creotrc wasren fro the stieoqnu ehre si acginjooutn but ta’cn be ropnnsittoai?s

catacholamine16  Transposition is when a segment of DNA (in this case, coding for resistance) jumps onto a plasmid within the same bacterial cell. That plasmid might then transfer to another nearby bacterial cell via conjugation. Transposition is happening WITHIN the bacterium. Conjugation is how that resistance gene gets transferred. +11  
lsmarshall  Also, E. coli is the classic example of a bug tat uses conjugation. ^but explanation above is correct^ +2  
seagull  I think he might have did what I did. I got Transformation mixed up with transposition. FML +3  
luciana  I still can't understand why it can't be transduction. Is it just because of bacterial types? +  
thotcandy  @luciana Yes, I believe so. You have to remember which bacteria have a conjugation pilus - E. coli is the most popular one because of its F sex factor (remember the F+ x F0 thing in FA?) +  
mgemge  I was also confused why it's not transduction...but simply as a crappy memory pneumonic TranNsduction TraNSfers ToxiNs FA 2020 p130 +  


submitted by sattanki(64),
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Arpyatenlp rehte si a ecoyellpmt pearseta aspnil docr elrfex rhwee recidt epieln msiutaotnli leads to an cione.ert hsiT xelfer nloy nseed an itntac arc in -24SS, so as gonl as htsi oniger is not ,indrjue an tcironee nac litsl cu.cor voew,reH ihwt tstaneriocn ta ,8C enth eht pgoycneschi ncreoeti exfrle ntaocn ,orcuc sa tihs reueirsq gcdneinsed rbfeis rmfo het cx.tore

lsmarshall  Just saw a good summary of nerves/vessels involved saying, "pelvic parasympathetic fibers from S2-S4 can cause cavernous arteriole vasodilation via the cavernous nerve without of central stimulation." +7  
seagull  S2-3-4 keeps the penis off the floor +33  
drdoom  Modifying @seagull into iambic pentameter: “S2, S3, and Number 4 / keeps the big ole penis / off the floor” +  
myoclonictonicbionic  I can assure you the validity of answer (speaking from experience) +2  
raddad  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4896089/ Under the "autonomic control" header +  
llamastep1  I've always wondered how quadraplegics got it up. I guess their girls help em lol +  


submitted by medstruggle(10),
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yhW od oyu eivg VI iroovnlceu whti ralctaiehnt toetxeemath?r dltuW’no MXT osle tis ffacyiec neics venoirlocu esesrver hte cffeste of XTM?

colonelred_  MTX will still work but yes some purine/pyrimidine synthesis can still occur. You often give leucovorin to decrease adverse effects of MTX. +  
welpdedelp  ok I have a question, leucovorin is the same as folic acid...so why give one over the other? +1  
lsmarshall  Leucovorin, folinic acid, is a modified version of THF and enter folate metabolism where THF is, after the point where methotrexate takes its effect. I have a pharm. card that says "toxic effects on normal cells may be reduced by administration of folinic acid (a.k.a. leucovorin or citrovorum factor), which is **preferentially taken up by normal cells versus tumor cells**." +11  


submitted by lsmarshall(371),
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Uera ecyCl sersrDodi t;g& aoletsId ervees mrhpmoaaeienmy ;(tg& 0001; e.,i. on rhtoe esever otmcielba brdntecsiuas

itOrinenh alatbmaesysrncra eynfciedci g&t; (toms comnom urea eclcy s.)id ortoic aiadciuicderai/ma, mneeampahoymri

cgnOira Aimseicad ;gt& eemm,nHrioapaym paoinnag- icsao,isd ketossi frmo( yohepmlyacgi)

iidnehMum-ca alAyc-Co hygadreeosedn eeyincdcfi ;tg& moireHmaae,npmy tyieckhootp aohimgyycepl nees( in txido-iaoβn esrd,orsid PETEXC eunltrorddhaoye)yopks

eivLr fnnycitsduo t&;g m,ayeeormmHnipa LsTF esdmse p,u rledo .pt

lsmarshall  Summary of metabolic issues relating to hyperammonemia +6  
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +3  
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria? +2  
charcot_bouchard  if it was mitochondrial disorder no one would escape +2  
wowo  figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB) + also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia +2  
artist90  i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong +3  
artist90  it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things 1-how does acidosis cause Hypoglycemia and Ketosis. 2-why is Ammonia elevated in these pts bc urea cycle will be fine? +  
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld) +1  
yex  According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA. +9  


lsmarshall  Rectal prolapse through posterior vagina ("rectocele"). https://www.drugs.com/cg/images/en2362586.jpg +7  
famylife  "When a rectocele becomes large, stool can become trapped within it, making it difficult to have a bowel movement or creating a sensation of incomplete evacuation. Symptoms are usually due to stool trapping, difficulty passing stool, and protrusion of the back of the vagina through the vaginal opening. During bowel movements, women with large, symptomatic rectoceles may describe the need to put their fingers into their vagina and push back toward the rectum to allow the stool to pass (“splinting”). Rectoceles are more common in women who have delivered children vaginally." https://www.fascrs.org/patients/disease-condition/pelvic-floor-dysfunction-expanded-version +14  
usmleuser007  really like the pubic hair.... +2  
nnp  why not spasm of external anal sphincter? +  
vulcania  After looking it up I think that external anal sphincter spasm would be more associated with rectal pain and maybe fecal incontinence. I chose the same answer because I figured if there was a problem with the rectovaginal septum it would have been noted on physical exam... +1  
ajss  I did the same, put sphincter spasm because I thought a rectocele would be found on a physical exam. +  
thisshouldbefree  this is the map ive been looking for +