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Welcome to lsmarshall’s page.
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Comments ...

 +29  (nbme24#3)
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Teh msto ceitrd h,tap and omts eylilk ,taph fro trbeas cnacer ot temtaaissez to eht tvrebrea rae the esnrctiotla viens. hiTs wsa on an leaierr BMNE sett sa lew.l tresBa cacern lilw aescu ixm,ed lcyti nda balcsit nlseiso econ in .bone

nO an eunldaraet ;note I lfaylin emac up wtih a ecdetn ayw ot bmrmeree cltyi sv. tbclsai secancr in o!ebn

ndkeIY nad YrItohd cuase tcIYl

rteaospt gt;& aaebtlst &;tg cbiaslt

owT sarebst t;g& otw eptys fo senoils ;g&t B rtase scsaue B toh

woT ulnsg ;gt& wto septy of eioslsn dndp(negei on eytp fo lgun )ercacn

lmall-lecs gunl g;&t "sllma stab"ls

on-lmlnsa llce ;&tg tliyc

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. +17

 +22  (nbme24#16)
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lrexoF gitdoimru dnurpuosf si neprelsibso rfo nfexiol of .DIP aMiled cspeat fo teh smuelc h(iwhc exlesf het ht4 nad th5 di)itg si lsuiedpp by eht launr vreen 8,C( 1)T. The artalle stepca icw(hh fselex het nd2 nda 3rd ditg)i si inveetrnad by teh eidanm nvere ialpcylesfic teh aiteronr esotouenssir acrbhn 8C(, T1.) So the osineuqt si inirgbceds a oaratneilc magdiagn eht nveer ulpsyp ot eht DIP efxlor of eth n2d tgdii en(ixd gfeni.)r hTsi si nisgay het mliade reven si ebnig gaamedd (C8 dna T;1 lweor tnrku tsoo)r.

mriascLblu tsd,12n(/ admei;n ,3tdr4/h nural) rea a rpgou of eslmusc atht lfex ta eth PMC jto,in nda neextd PIP dan PID sio.jtn

lodCu mmreeebr sa elxof'r tgiodrmiu orfnsudpu si funorlydpo lngo' since ntsndeo iretns on D.IPs dCmeapor ot forxel igtuirodm prifisiuaelcs wshoe nndoet sarwp roadun u'fosurpnd pelcsyiafuilr but nesirst on I.PPs

toupvote  This is dumb but I remember FDP is needed for picking while FDS is need for scratching the superficial layer of the skin +13
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) +8
hungrybox  'flexor digitorum profundus is profoundly long' is such a good mnemonic, thanks bro +

 +22  (nbme24#27)
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aa"taePsnrrl aeveh )l(fti uccros rdugin ithgr venrriltuca ehpyyophrrt .(ei. mnanlg)eteer ro ervy erylra vsreee etfl aartil nr.etne"mlega RV hprpehrotyy acn be sene so ayiesl esbucae the VR is ta teh oriraetn fucrase of hte e.scth

In tsih einaptt odbol mofr AL to LV ascreseed in oauinasrtt, os it is gogin ehmwose.re mFro teh 2O ta.s we nca dducee htree si oablrbpy a VSD cneeis(dar VR essurerp dowul secau HRV nda nelrtaasrpa h).veae rr,rFuemoht the vegttine is eillky isdgnibcre ttaylorge of lofalt d(ecusa yb eorarnpeitrsou lcdmesanipte of teh banrifidluun ).spmteu nI teT lsels,p RV ofluotw is oto brscttodeu nad ptntaei segt nascoyis dna ;&tRgL nnigtsuh atusSq ecresnai VR,S eaiedrsgnc L;&tRg nnu,tgsih tiputgn emro obldo uogrthh oupmrnaly rtciuic nda eegnirvil iano.sycs

seagull  i'm pretty sure your a prof and not a student. +20
nor16  nevertheless, we are greatful for explanation! +1
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). +

 +39  (nbme24#20)
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teintaP sah nSpai adfiib ctcuoal icwhh is a rlenua utbe fdceet iel(faur fo nsifuo fo teh rnrspo)oue.e emoSolescrt ear eht trap of ahec oiestm ni a bertrtevea ryboem igvnig rsie to eobn or eothr etlsleka eiutss. Scien a ratp fo tish nte'astpi aipns ifiadb iudlndec bseanecs" of iposnus "rcsepso thne a oltrescoem wsa envolv.di wionKgn that anerul buet sfectde rea na susie whit soifun lodsuh eb gnhueo ot gte ot eth irhtg nseawr.

fI the rohtndoco deailf ot eepvlod ehnt eht ierent CNS dwluo tno lodpvee as eht dcrhotono ecidsun itomforan fo naurel a.tepl

If eth lnauer eutb fedail ot podeelv tenh eht olehw NSC udwol ton aveh eddl.oeevp

olkY sca si eanrvteirl ot shti pt.ntaie

hnWe lurnae rtecs ecll ti has deifneftr ecmouots ni rneifdeft tsess.ui uaFielr fo luerna setrc ot remiatg ni taehr cna aseuc risaoTsonntpi fo aetgr e,essvsl goatTyrel of Fltoa,l ro nrtesPstie crsntuu rrsst.uoeai aFlreiu fo laneru tsrces ot etirmga in IG acn eusca scHgphursrin seiaesd glet(noiacn ).eacoglnmo hreceTra Colsinl ryndemSo nca ucorc henw nleura scetr sllce ailf ot gaemrit into s1t arpgneylah ha.cr Nuelar bteu tsefdec ash ntihogn ot od htwi eruafli of aunelr etrcs imngoatir hotuhg.

sympathetikey  Exactly. I knew it had to due with fusion of the neuropores but had never heard of sclerotomes. Thanks for the explanation. +14
hungrybox  Fuck I picked "Formation of neural tube" but yea that makes sense... that would affect the whole CNS +4
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 +1

 +7  (nbme24#8)
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Th"e txace ahcsmmein for eormtr ntiiocdun yb ad2-c)(regenriβ gisstnoa si listl non,nwku utb rheet is eosm vieneedc ttah 2ardc(neerg-βi) sitganos act rcdyelti no .clmsue.. oeMr tcnyerl,e rmtore has been rteocedarl elyocls hwti "a.omleahiakpy - NIH ocipliatnub

iFstr dAi nosmtine ypishmidtyrohre sngaciu mroetr orfm de-grercnβia mnito.iltsau It slao nitmonse goβati2ssn- gniaucs reomrt sa a sedi fcte.fe tisFr dAi olas insmntoe agonβss-it2 idirgnv pssamuoit noit s,clel wcihh amy nteibucrto ot r.otrem aTht adis, oerm iccssal poysmtsm fo lohayaeipkm ear ewid QRS nda pedeka T esvwa on ,ECG im,ayhtrashr and emlusc swe.nesak

onogiLk raodun on teh tirtenne ooslk eikl if pyrahte is etcdionun the errmot mfro a ssio-g2tnβa esreslov tiorevme.

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..?) +1

 +15  (nbme24#1)
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An aptelneimrxe geidns ro epixrnaeltme udyts ustm ahev na nrnoiteienvt, by .oindfnitie cte-lCaosorn dusteis are tebraoinvlosa sdteusi, otn pxiren.amtlee sihT ieontsqu si hllycetcian rre.ticnco Tyeh wanted ot amek a nitpo thta rosnotclec-a esusdit rea mite dan stco tifeicnfe nisce they dt'on reirque onlofwlgi ntepstai reov imet ro ayn uroresces sbdeise whi/iigeervnggartne mrfnt.aooiin aCes ssriee lodcu ton test sith yosithehp.s

s,Alo hte wndgroi sa"ieactsod tiw an ndsierace "riks etoshawm uelsald to coecna-sorlt situesd lnoy nivgah the ilytiab ot fdni ddos fo an ooisctsnaais tnbewee psoueerx dna tocu,emo utb ton lehissabt scaula sitlpeonar.ih

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

 +9  (nbme24#35)
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"Dossmmoee uaM(cla seadr)nhe - A --tlecoellcl cotcnenion thta ovirpeds tulrtruacs upsotpr iwth eeiedrntaimt lftim,anes caylilpraurt ni esissut ttha rgneduo ahlnicaemc etsrss ,(eg.. isn,k csgarit iuess,t eda.r)bdl ctoCnsen attneosericyk ni eht tsartmu nmuspois fo eth ms.drei"pei - ASOBMS

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. +29
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. +3
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

 +14  (nbme24#27)
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oPpyyruonhelta - A niotcondi eslovvni aegadm ot ullipmte hpeprreial vrnee sbei.fr iPtatens cpyilytla nrsepte thiw yimsmtrec tsldai norsyse sslo ro a ibnunrg estniaosn aoadsciset iwht mroot wne.askse aCcilss npoteahpryuylo si nrubign os hsti sqitnoue aws rmoe srecspo of limo.niniate Orshet did not ift .elwl


 +8  (nbme24#33)
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lhnatIan eabus lcdou be doen whit lu,eg atipn retsnn,ih l,feu utsorin xeido, or alylk i.ittsrne lUauyls in -hlcohgiohs aged .dsik naInsltah aer n'r'esodw os rvewahte aiocoittinnx fctfese ereth are lsuhod be nesdsptrea nad luylf sorveel tinhiw 03 .min to a lcpueo uhosr. tePitans yma oklo ukrdn when tndxoiceita tiwh hlsania,tn tub aslyuul iukqlyc ve.oelsr A hsticirtcecaar "ugle n'ssfierf rhsa" ndorua teh eons adn tuhom is stomiemes enes efatr penodgorl e.su


 +16  (nbme24#48)
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PCA oterks cna ausce "poaropnasigos" hhiwc is eht byinlitai to gerenoczi armiiafl sc.eaf seuaCd yb llaribeta oslnies fo salviu oiciassaotn aear,s hcwih are itstadue in het frreniio ecpottlrompacioi tecxro fs(uformi g).rsuy eTh aybliti ot emna astrp fo eht efca e.(.g, ,soen m)ohut or iedinyft liisiduavdn by herto cesu (g.,.e nghcloit, i)sovec is ftel tcatn.i

uthWoit nignwko ,ttah rmmigeneerb aocliitcp beol si ilvvnedo ni uvis'la fs'uft orylbda, nluidcgin imgea regcpissno nad siht natipet si ihganv ssiesu thiw nritguednnsad mgisae hlduos eb uogehn ot tge ot the wernas.

gonyyong  Lol I guessed it exactly because of that +4
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. +1

 +39  (nbme24#8)
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eraU lyCce sdseDorri ;g&t odstaIle seevre nryimmhaepeoam g&t(; 0;010 e,..i no erhot sereve aemobilct eidstrbucnas

eiinhrtOn etabynasrmalcsar icndeefyci g&;t m(ost nomcmo earu ccely )id.s oicotr cimiruea/ddiacaai, yrmanmhoapmeie

iargncO iesAmadic t&;g menapam,yomeriH -ainoapng cda,issio ssteiko (rfom y)iycmolahgep

mhiM-icanude A-yCoacl gesdadoenrhye neyciiedcf t&;g emeyi,omnHpamra ptyetciohok comagehlyyip esne( in aoiβi-dnoxt doe,dirssr EEXPCT dypkndayrretooohl)use

erLiv iscftndoynu t&g; rmnHpeoiyema,am FLTs dsseem p,u dlore tp.

lsmarshall  Summary of metabolic issues relating to hyperammonemia +8
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 +3
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 +4
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. +11

 +4  (nbme24#37)
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"irA oeplrsd"t sosudn kile eoyitrraspr avsal(i or ae)trw rlsopedt. anIailhont fo xsapaltomo oscyost in atc ecfes ist'n uiqte eht mea;s otn ot yas I nwko lcyatxe athw the yososct rea inlehda sa jt(us rpcmisoccio yrd tca opop aisrl?).ctpe ntoesingI fo ednedokucor emta to egt eth cysts is rencyltai a ORT ofr lx.aoasopmt

osxaamTplo sa THCRO hsa rdait of ulhys,oapechdr eercalrb canifacitolics ran(c)ribrtele,a nad sec.iorottrnihii ortiriihtecosin cna eb in anignecolt CVM ro ssplot.mxooias eveilrtPinracur aifiitcosclnac aer in VC.M nCtalngioe VCM usulayl sha ngrhaie ,slso ,eusseizr hcatepeil ha,rs “burlreybe ufnif”m asr,h oinoitchsreri,it dna uearvtpenirrlci na.oicifiatcslc

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. +2
zevvyt  is his small head common is Toxoplasma? +

 +32  (nbme24#49)
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noneAgdr isItnveiinsyt Seyrndom - etfcDe in ngaonedr erceptor ugestirnl in rao-legnarmapnpi fmelae Y(,X46 D).SD unFnoictgin ttsese acssue riscnaeed sroetettenso at rebup,ty cwhhi si nvocretde ot esegntor rapyirlhe,lpe vniggi faelme ynorsaedc uasxle ssaacreicrticht (mlfaee xlenerat agietn.ial) kacL of deragnno rrptceoe ciunfnto easld to esatnb ro astcn iyaxllar dna ucibp ihra. stantePi hvea ytriudmeanr gni,ava but sutrue adn lfolanaip tuesb bt.anse

ogdnerAn ysennisiititv dnomesyr si hte eanrsw but ouy igthm veah eddnscorei laMüilner eenigssa t--(yokMkersyaaiRn ars-HsüeterKu o.sn)eydmr

alnrlMiue gisseaen lilw ahve marnlo rnhmoeo sveell nda mya nseertp sa °1 eranhoemar du(e to a calk of eeturin )eldvpneoemt ni lefmeas thwi fyllu eopdvleed °2 ulxeas tarasirccithces oniu(acfnlt )osear.vi riaH tlepodevnem si nmlrao sa wl.el aestitPn salo haev lamrno ti.hghe

smeeS leik sthi eositqun idd nto gvei us uchm ot iiuhdnsigst esdebis hitghe dan atnrne asget 1 yiibaul/lcxrap .arhi

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. +
makingstrides  Mullerian agenesis: absent vagina, uterus/cervix because no mullerian system. Yet, still has secondary characteristics ie: breast, pubic hair, normal hormone levels (normal ovaries). Also check to break down the different subtypes of DSD: CAIS, 5alpha reductase deficiency, and swyer syndrome all for XY DSD. Where as for XX DSD, overproduction of gestational androgenism and placental aromatase deficiency. Bc in CAIS the testosterone receptor is dysfunctional, no external / internal male organs are going to form in an XY fetus, but you will have an extra production testosterone (like explained above) leading to increased estrogen (breast growth), but since no ovaries, you dont have the mullerian system. You are left with a vagina with a blind pouch (from lack of functioning receptors) +
makingstrides  Also to add, there are testes that produce the MIH, so you have degeneration of the mullerian system. From B&B +

 +16  (nbme24#45)
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MCH cslsa 1 ptediep natnegi gisrsnopce g;t& Aengtn"i ptspeide doedla tono MCH I in ERR erfta rledveiy iva TAP atptsro(rrne esasocdait htiw tnigane cnrp)"ssoegi - rFtis dAi 1902.

eBar yhployemct yedomrsn teyp 2 S(LB I;I efcinfgat CHM )II si edu to numaotsti in esnge tath oecd orf stniriaptcrno arctfso tath yalnomrl aelretgu the spnxesiroe gnee( )icoipnrnatstr of teh MHC II eengs. Bear ycmlthypoe rnomsdey ypte 1 SB(L I; ngaicffet HMC I,) si hcum eomr erra, nda is dcosaeisat whti ATP sei.idfeccien

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." +
j44n  i hate this question because MHCI is on all nucleated cells. So this person is literally a bag of RBC's +1
soccerfan23  @j44n Not quite. It's true that MHC I is on all nucleated cells. Because of the TAP mutation, these cells don't express MHC I on their membranes. But these cells still exist. That is what is meant when the vignette says "flow cytometry shows absence of class I MHC-expressing cells. +

 +17  (nbme24#22)
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gereelwZl medsnroy - lomtusaoa eesvsriec ersriodd of romxosepei inbeigesso ued to eautmdt PEX eegs.n y,Htoapion i,zsreuse ,yaepgelhamot yelra tehda iw(tnhi 1 raey). ndooiitβ-xa of FVCAL epnashp ni mprssieeoxo so het chdil elsnmygei anvhgi semo rost fo ongtaclnei cabotlime eorddisr twhi vaeedetl ACFVsL uoldhs evah eneb eguohn to get teh ewnars whiutto ioknwng oubat g.weZrelel

jucapami  furthermore, FA 2019 pg 47 +4
tiredofstudying  Same page for FA 2020^ +4

 +18  (nbme24#25)
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calAr iosiguteln is otms cmoomn yetp fo nmaloema ni arncfAi eraimnscA dna si no eht psmal or .osels I egsus the laiytcp hnignitk fo thecs adn cakb sun( eodsexp) si a ellitt fdnrfitee ni htsi y?ept gmAon lla crspahi;meogd moamnsela cucro the yoitamjr fo emti no eth smlbi 6%(~3 oewlr and %91~ ;rpu)pe nkutr si 2.~..7% oS asdeb on tath and hmi binge of aAcfirn stdeecn ew nac coehos lm.pas


 +7  (nbme24#1)
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uhgotlhA 'sCrnho mya ehav ,ureslc astuls,fi dna ;lgeeidnb ti uuyalls dseo ton ausec nior yeicfinced aemani dna sah lses gendblie hatn UC. cua"tStrurl oanisbletarmi fo hte eilrnamt ,lueim chus as hoCrn eiassed dna urlgaics reosctni,e acn ceasu radsecdee sonaprotib of intivma .21"B - rsiFt Adi nlarGee lPnsrieicp


 +4  (nbme24#24)
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brcePeoid"n and -ohdhseig yceillsaast niiithb bronrsioaept of urci cdia ni oirxlmap ultocevndo uubetl aol(s thiisnbi tinsereco of ien)ll"pci.ni - itsrF Aid 1209

uslme123  so ............... +10
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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Ftriiasglm CG-(FS) is vrey molmoycn teesdt iths ;wya WoUrdl nda weseer.lhe hm.oeC ttpaeni twhi obne orrawm sseinospurr &t;g igev CGS.-F


 +5  (nbme24#50)
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Maatpiasle - A beirlvrese idvaetpa soepsern in which ehrte is rg"prmaoemgiRn fo stem lerneelecptcslmaŽ of oen clle tpey yb noherta atth anc atdap to a ewn tss."sre ohtB are marnol els.cl sryiReorapt rtee lhodsu otn veha auusmoqs cesll utinl ryeatsirpor bonolrecsih beerf(o tha;t obucidla in mert. rnb.o gt;& cnlmuaor ni h.nbcor ;&tg ddesueaptrstioif anroclum in .rlega ch.)b.orn

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. +8
jurrutia  Metaplasia is not normal (in the sense that you only have metaplasia as a reaction to stress, but under not under normal circumstances), but the cells in metaplasia are normal. When they become abnormal, you get dysplasia. +

 +14  (nbme24#8)
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bvtSeynoprnai si het agtert of eaopnmitsnats tns(aetu oi;txn) mseulc ssmspa are .trhtaracisiecc yOln hoert ewsarn uoy imtgh sncedoir si cyhlAlinasetrscteeoe ncsie he si a ermarf dan rszzdbwou tofen rcyar us to hte rmospide ln.ad.. utb ytmsspom fo a nolghcerici tsmor rea bet.san

vshummy  Synaptobrevin is a SNARE protein. Why they couldn’t just give us SNARE I’ll never know. +45
yotsubato  Cause they're dicks, and they watched sketchy to make sure our buzzwords were removed from the exam +46
yotsubato  Oh and they read FA and did UW to make sure its not in there either +37
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! +6
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. +3
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. +5
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 +2
baja_blast  FML +
j44n  its not an ACH-E inhib because he doesnt have dumbell signs +
flvent2120  I'm not even mad I got this wrong +

 +14  (nbme24#33)
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"In hte asrey enecgpidr lscpihya rtbu,pye otbeRr M. roBay veddieorsc taht het ootndgiaonrp psslue ccrou lyon irnugd ,peels ubt sa epyturb sgsesprore heyt can eb dcttedee idunrg het y.da By hte ned of teuybrp, ethre si tlleti dhnya-git eedfencirf in eht peludmita dan ycureqfne fo odnnirogoapt sp.ules

Some sgiavrensttio hvea dtitetabur eth oetsn fo brteuyp to a rnnaeseco fo stosrclaiol ni teh ][a9i]]9[n.0b19r[8 yB hsit eani,mhcsm het piagortodnno elsusp ahtt uccro rrypmilia ta itnhg tjus oerfbe rpybetu etenerpsr b"east. - iWik

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

 +7  (nbme24#22)
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I tgutohh hist swa a trick touneisq insce knsi ernsacc rae the tosm comomn ytep of ccnsare ralov.le tuB atluclay onmag VIH ,tipsenta IdrleVt-Hae screanc aer hcum oemr coonmm naht dnetl-HVorIa-en arcnsec env(e nkis s.cerca)n d-VeuiBEndc pimrrya CNS mpoyahml si teh nylo ootpni tath si AnifnI-seDdgi rse.cslcean/nli

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
jurrutia  Even if you were thinking skin cancer is more common, that's only true for basal cell and squamous. Melanoma is rare. EBV much more likely in aids patient. Even H pylori was a better answer. +

 +14  (nbme24#11)
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ygnczMoitoo tl"c(iae)"nid tiswn ehav 0%5 fo gingtet ezcrhsanpoiih fi ehtir niwt has it. ycgDoztii wisnt aevh ~ 0%2 ncheca .tuhogh Tish is efnot noeeditmn enwh czrahhoniSipe goleytio is esddcssiu e,(i.. ew dot'n know tbu noaccnreodc ssdteui ssgetug a cgnetei .n)kil M1TD ahs ssel fo a ieencgt link ahtn DTM2 tbu ti losa hsa 0%5 rncdaecoocn enetbew cmoitoynzog ntwi.s hTis caft is onndmeeit ni tisFr Adi 1029, gpea ..3.64 I otg hsti MBEN qtoniuse ngowr but i'st cnetton is in boadr ruoes.cs





Subcomments ...

submitted by medstudied(0),
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naC oesemno lpienax wyh eth etcrcor nerasw ofr eth snieqtuo rhee si tguoonianjc tbu atn’c be ostsiano?print

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. +12  
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(71),
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eyarpptAln hteer is a ctoeepllym pteasear lipsna codr efrxel hweer icedrt ielpen tsnoitauilm sedal ot na intee.cor Tish xfrele nylo dsnee an itctna rca ni 2,-SS4 os as lgno as hits negori is ton urnd,eji na tieoecnr nca ltlis couc.r wveHro,e hwit inerstotacn ta C,8 hten eht cihspgeycon eocnerti fxlere nocnta cro,uc sa sith irqeseru csinenedgd feirsb omrf teh .rexoct

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 +37  
drdoom  Modifying @seagull into iambic pentameter: “S2, S3, and Number 4 / keeps the big ole penis / off the floor” +2  
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 +2  
llamastep1  I've always wondered how quadraplegics got it up. I guess their girls help em lol +  
jj375  This article is shockingly helpful. Scroll down to the 3 types of erections (psychogenic, reflexogenic, nocturnal) https://craighospital.org/resources/sexual-function-for-men-after-spinal-cord-injury +1  


submitted by medstruggle(12),
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hyW do yuo gvei VI cnoiurevol wthi aeatltchrin heaerm?otxett ’oWltdun MTX sleo sti fiefcyac esinc creoulnoiv rvesseer hte esftecf fo XMT?

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**." +13  
jj375  @welpdedelp I also struggled with that and chose the wrong one, but then I remembered something from biochem that I think is helpful:I think the good thing about leucovorin is that it doesn't need to be activated by dihydrofolate reductase. Methotrexate is directly blocking Dihydrofolate reductase, so folate can't be activated to help, but leucovorin doesnt need the activation, it is turned into Tetrahydrofolate and rescues the cell! +  


submitted by lsmarshall(417),
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eUar ecCly ieDdsrsro g&t; tdoaelIs rveese mmranmpeyhiaoe ;&t(g ;1000 ei.., no rteho evrees ematobilc raniecusbsdt

iinthenrO blcnsaryemtraaas iicdeecfny t;&g ms(ot onmmoc arue yeclc .)isd oortci muicidae/daraiiac, nmaremapmeyohi

gcnriOa Aieimasdc g;&t ieHre,momaanmpy nogan-iap ,idcaisso sstekoi rofm( )pcymaihgyeol

hcinuiame-Md CAy-oacl anedehdygroes ficcyednie g&t; amyHripo,neemma ehptokiycot ycmpieolhgay es(ne ni odβo-ntxiia oddesrsri, PECXET akdrhroelnsuotp)ydoey

vreiL tsudnioycnf > eperyHmmnioaa,m FsTL meesds ,up erldo tp.

lsmarshall  Summary of metabolic issues relating to hyperammonemia +8  
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 +3  
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 +4  
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. +11  


submitted by beeip(124),
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uYo can see hte oeandifrmoente scuttreru ni tshi idrg.aam

lsmarshall  Rectal prolapse through posterior vagina ("rectocele"). https://www.drugs.com/cg/images/en2362586.jpg +8  
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 +17  
usmleuser007  really like the pubic hair.... +4  
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 +1  
mnunez187  I didn't choose spasm because the stem says there the rectal tone is normal +1