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Welcome to lsmarshall’s page.
Contributor score: 415


Comments ...

 +29  (nbme24#3)
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heT toms citred ptah, and toms ylliek t,ahp for bersat nercca to sizasmtaete to eht rbtevear ear eht oltnsecirta vs.ine hiTs aws on na leriaer MEBN sett as we.ll etasBr naccre lilw asecu ,imdxe cilyt dna iltbsac osnlise oenc ni b.eon

On an rnatedluae e;tno I llafnyi aecm pu iwht a eedctn yaw ot mrmeeber tyicl .vs abislct ascrcen ni oe!nb

kIdYen and rYohtdI uaces IctlY

oetrstap g&t; talsaebt g&;t lsctabi

Tow sstreba g&t; two tepys fo seoinls g;t& B aerts usaces B oth

woT slgun &g;t tow ptsye of esolins geeddnp(ni no teyp of guln cnare)c

cml-lealsl ulgn &;gt "sllam "slatsb

nsm-aolln lecl ;t&g cylti

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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elrFxo idtgmoiur rfusopdun si eserbnpilos fro inofelx of DP.I eldaiM satecp fo eht lcuesm (iwhch elxfes hte 4th and h5t igit)d is pudpslei yb the nuarl evnre (,C8 .1)T heT tlreala aseptc wcih(h xfeles teh d2n and 3dr )itgid is nveendrita yb eth ndmeia eevnr cfliaeplcysi hte rriaonte uinoresostse ahrcbn ,(C8 T.1) So teh qnsueito si snrgbeciid a ilaroaetcn mngaiadg eth nreev lppuys ot eth PDI olrexf of teh dn2 igtid xe(ind .rfg)ein sTih is yngias hte leimda eevrn is nebig madeagd 8(C adn T;1 lrwoe unktr s)o.tor

maiLcubslr /n,dt(21s ;inmdae d3,tr/4h r)lanu rae a guopr fo esmlusc hatt xlfe ta teh PCM jinot, and xneted PIP nda IDP .ijotns

luodC bemermer as e'rxflo tidormigu unorpdufs is ondrfplouy lngo' encsi donsetn tsnrei on .sDIP Cmdraeop ot lxofer tomirudig fseiiulpcsiar hewso dneont wsapr undaro fpuosurn'd pfycuarilleis tub treinss on .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 +12
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) +7
hungrybox  'flexor digitorum profundus is profoundly long' is such a good mnemonic, thanks bro +

 +21  (nbme24#27)
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P"teaarrsanl haeev )(lift crucso ugidnr itgrh tiunrvecral hoppyyretrh (i.e. nmtge)lneare or rvey lyerra eersev eflt ratial mrgleeen.nt"a VR hrpyreyhtop nac eb sene os aseily eubaecs the RV si at het rroneiat easrucf of hte eht.sc

In shti pinteat boodl mfor AL ot LV sdcsareee in onrsia,autt so ti si ogngi ee.owreshm omFr teh O2 s.ta we can euddec three si ryplobba a SDV cen(aerdsi RV usrerspe ouldw asecu VRH and ptnaasrrale )aehev. oturmFher,r teh gneeitvt is likely bindcgrsei orayttlge of ltalfo cduae(s by ertoroierpnsau eaipesclmntd of eht funadlbuinir .smtpu)e In etT elspls, RV owofult is too ttoduecsbr and attpein setg sysniaco dna gR;Lt& usigthnn qSauts nracesei VRS, erdnecgias t;&LgR ,nhtsngiu ittnugp mroe odobl hgutrho amnuoyprl ccituir nad vegielrni soys.ican

seagull  i'm pretty sure your a prof and not a student. +19
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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ienPatt sah npSai afdibi ucatocl hihcw si a uerlna uebt edcfet lfri(uea of usfnoi of het poe)sro.uren Seocrslemot are het patr of aceh omseti in a tbreraveet yoebrm igivng iser to eonb or hoert alsleekt e.istsu eiSnc a artp of hsit itet'nspa npsai badiif ceudnild "casesnbe of poiussn escsp"ro ethn a lteoosermc saw .ionvldve nwginKo ttha leranu uebt teecdfs era an ussei hwit fsiuon ouldsh eb uohneg ot tge ot the ghirt nserwa.

fI the dhnoootcr dalief to oelvepd enth eht inerte SCN ouwdl not opledev sa the orodotnhc cundsei atroofmni fo naeulr .epalt

If het arueln ebtu faeldi ot epdelov etnh het howle NCS dluwo nto heva e.polevdde

loYk acs si enrvetalri ot hist .ntiptae

Wnhe nurela ertsc lcle it ahs fniedfetr teoomucs ni efridtfne .stsesiu laierFu of lanuer crtse to taemigr ni ahter nca ecsua npintoTssairo fo targe eesv,sls eoTrytlag fo al,tloF or senretsiPt tsrcunu asrtresoui. uirelFa fo lanrue rsecst to riagemt in IG acn eacsu urHpngsrisch esdieas ot(nlagneci mncl.o)goae rrcehTae nlolsCi reomdySn acn ocruc wenh eunlra rcset slecl lfai ot atemgri tino s1t lapneygahr cha.r erNlua bute etsfecd sha ihtgnon ot do hwit feliaru of leaurn rtesc oamtirign .thguoh

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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eT"h cxeat nsmhcamie for erortm coidtunni yb deg(a2-βce)rnir ngoistsa si istll kwnu,nno tbu erhet is omes nedievce hatt n-regacde(i2)rβ nstgoasi tca edyrcilt no c.sm.lue. reoM tce,rylen orertm sha nebe alcrteroed llcyoes wtih i."yahpmeaaolk - IHN aibtuonlipc

rtisF iAd eostnimn iiyemohrthpsdyr igcusna trorem rofm drarc-eβgein uinalottsm.i It laos emotinns ansβ-soigt2 gunscia mreotr as a esdi ce.ffte First iAd asol otnsnmie βsn2-isaogt nrdigvi imtspuaso ntoi ,lelcs hwcih aym rbteictuon to tmrro.e athT ai,ds erom isacslc ptsoysmm fo iapahoelkym are diwe RSQ dan paedke T esawv on C,EG hyasmth,airr nda cmules eswsaek.n

ikngooL urdnoa no het eretintn oksol ikle fi tpaeyhr is tednnicuo hte roetmr mfro a togsβi2sn-a reeslosv ieoet.mvr

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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nA rmailpxnteee dnigse ro aeiexlpemtrn dystu utms eahv na etninorenivt, yb fi.ionitned roa-oCtlecsn suedsit rae leovotnaabrsi duiesst, ont exneia.ltermp ihsT uonsteiq si llacichteny tcnrer.oci ehyT edwant to kmea a opnit ahtt notlccr-saoe sueitds rae tiem dna tosc ecentfifi ceins htey dtno' rqieure flnowiolg etptians oerv time or nay ercrsusoe sedbesi giwerignaei/hvtreng nofitar.nimo Case esersi doluc ton tets isth .teshypisho

olsA, hte worgndi oeia"catssd tiw an edrsniace ik"sr asehtowm suealld ot clc-tnorosae steuisd ylon vnhgai hte aibyilt ot fdin sddo fo na saonisscoita nweeteb repuexos dna ,ecutomo but nto lshetisba usaalc elast.ohriipn

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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"msomeoDes alMcu(a easdenhr) - A ce-oel-cltll otcnconien tath dsoeirpv tuuclartrs posuprt thwi reietaimdent stlmenf,ai rlpaulcriayt ni ssestiu tath uergodn mihaecnlca estrss (e..,g i,nsk aitgrsc esuits, ddae).blr tsCocnne yeateoriscknt in teh sartmut usnmoips fo teh ier.mspied" - MSOSBA

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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yplhyaoeoPrunt - A iotnniocd sloinvev eaamgd ot mulpelit laeeirhppr evern irebf.s Pstnaiet yctliaylp rneestp thiw eysmmitcr dstlai roessyn sols ro a grniubn esstoinna sdtceioasa htwi rtmoo sea.eswkn sCilsac pyaeyhutopnolr is unnbrgi os siht tousqeni aws emor esposrc fo oalninei.itm rtheOs ddi tno ift .lewl


 +8  (nbme24#33)
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atIlnnha sbeua oucld be oend ithw u,egl nitap t,esnhrin e,flu osturin xoie,d or lklya .snttiire aslUuyl in loshihgoh-c edga .isdk hsanaItln aer ds'oer'wn os ehatrewv itaincootnix fcfetes ehret aer houlds eb atpnesesdr nda fyllu eolrsev wtinhi 03 imn. to a elpuco usroh. nstiateP aym oklo nudkr wenh onetdciixta ihwt s,ltinnhaa tub asuully yciuqkl eler.ovs A ttrsaicceraihc "gleu nsefis'fr hsar" orudan teh enos adn htumo si smmtsieeo esne tarfe nogdroepl eus.


 +16  (nbme24#48)
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CPA teskor nca auesc "gosnopoapsari" cwihh si eht tyaliiinb ot eczoigern lrfmiaai cfae.s dauesC yb arleatilb snelsoi fo uvisla astcoainios a,rsea wchhi era edtatsiu ni hte ernforii loemipctticpoaro xercot fs(froimu g)ysur. The ityabli ot emna strpa fo het face g(,.e. n,ose ohmu)t or fieidnyt niidvdalusi yb otrhe csue ,.(.ge hongt,cli )vcesoi is tefl cnat.it

uoWitth nnokiwg at,ht bemnrremgei oicciaptl oble si vlonivde ni va'usli fufs't l,oardby cudinlnig maeig sgesprnioc dna ihts tnipate is hvniga essius tiwh driteadugnnsn asmegi ousldh eb nougeh ot tge ot hte na.esrw

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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Urae yceCl Drsreodis g;&t Iosaltde ereevs ymaerieoammnph t(;g& 00;10 e,i.. on hreto erseve mtalecboi adrstiscbune

hOerinnit ascyrnsmbaaltera ieynifecdc g&;t t(som nomcmo aeru cyecl s.di) tooric /cidmaderciuaiaai, nmhyeaoierampm

rnaigcO miecdsaiA tg;& yaepmo,aHirnemm ngainap-o di,iascos itsskeo o(fmr lhygmoceyipa)

dihMn-ciemua ycl-CAao hyrdsgeonadee ccieydfeni &g;t ,rmemHyanampioe ytpeochkiot aycepmogihly (sene in nxdo-toiiaβ drosde,sir PECXET dhds)noourlyptayekero

Levir ntncsfoidyu &t;g naameoHeyrpmi,m TsLF eedmss ,up rleod p.t

lsmarshall  Summary of metabolic issues relating to hyperammonemia +7
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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"riA dsropl"et sdsuno ikel ioeatpryrsr sl(vaai ro )artwe .lptsedor anonihaltI of pltmxsaoao csotyso in act esfce ti'sn tqeiu eht e;mas ton to ays I nwok cxtyael ahtw the stsoocy ear eianhld sa tju(s opsrcmoicic rdy tca oopp tescapr.?)li sginoentI of orucddneeko tame to teg het scsty is tynrceail a ROT rfo la.saotpoxm

olamaxposT as OTRCH hsa atrdi fo h,olhaesudpcry ealcerrb iiclftccaoiasn rtrbie)ral,n(cea dan cnsetoi.hriroiti toritoiienricsh can eb in ogaicnlnte MCV ro pasltosoxs.oim tilaiecrrenruvP ciafsoccniliat rea ni VC.M iConenltag CMV yuuasll sah eahnrgi s,slo erzisus,e itlcpheae s,rha ebrbl“yrue fnmuf”i rs,ah iro,isihrnieoctt dan lartinruecvipre oi.aiscncictlfa

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. +1
zevvyt  is his small head common is Toxoplasma? +

 +32  (nbme24#49)
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nAngorde isnyvsIeittin ynmSedor - eefcDt in noragden eeortrpc iruglnets in nnopi-eaaagmprrl mfeale ,46(XY DDS.) ntgFuoncnii etesst eucssa aircensed toeoeentsrst ta ,bueyptr whhci si vecnotdre to rtegseon lyeep,aplrhri ingvgi fealme aodynscer easlxu taeircscchtrisa mafeel( ntaxrele g.)aieaitnl ckaL fo ndongear cetrrpeo iunotfcn elads to ansteb or stnca rillayax nda cupib hair. taiePsnt eavh tudmranyrei g,anvia btu etusru dna inpoflala stbeu tebsn.a

gnrAonde tiseytisniinv dnsmeryo si hte searwn tbu you gmhti veha csrnedoeid allüMneir easgsein -aesa-RkkinyMroy(t rHKetr-ueasüs oy.n)srdme

rulaileMn iagssnee illw vaeh orlnam mroehno lveels and yam senetpr as 1° aemraonerh deu( to a lack fo eurient le)tdpmvoeen ni smafeel hwit flylu ledevdoep 2° uxelsa saeirrtcctcashi tonlunc(ifa ev)oa.sir iraH dletpmneoev si nrmola sa wlle. Pnitsate osla avhe anorml .tgiheh

mSees ielk tish uniseotq did nto giev su umhc to isiisutgdhn essbide thhieg nad ntenra etasg 1 rclpaaiy/xilbu .iahr

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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CMH asslc 1 pdtepie gianent piogrscnse g;&t nit"ngeA esipdetp oaeldd oont MHC I ni RER eatfr eyveidrl vai PAT rron(esprtat asidescaot hwti nnegati rgneicpso"s) - iFsrt Aid 1209.

areB etypymclho serdnmyo tepy 2 B(LS I;I cfgeftina CMH II) is due ot uatmosnit in gense taht cedo for tiitcpoannrsr rosatfc ahtt lmalnyor lguertea het onressiepx e(eng ttraii)rnpcnso of teh HCM II es.neg eBar tmyplcoyhe enrdymos tpye 1 (SLB I; enicaffgt CHM ),I is cmuh orem arr,e nda is astiedscao iwth PAT ceeiifcdns.ie

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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rweeglleZ dsoymrne - laootuasm rsveiseec dersdoir of sopreeiomx igoebinses due to dmtateu PEX geesn. ,iapnHtyoo z,isseeru gomelhetpya,a aelyr daeht iht(iwn 1 ey).ar -idxoβtaino fo AVFCL shepanp in eersmosipxo so hte icdlh neylmesgi anigvh meos tosr of ntanoegcil obaeiclmt sdrideor iwth eevetdla FVCsLA hlsuod aehv neeb oeghnu ot gte het nsewra otuitwh nigokwn bauot llewreeg.Z

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

 +18  (nbme24#25)
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aAlcr nugteliiso is msot ommocn peyt of mmanlaeo ni fncariA manArsice dan is on het lmaps or lss.oe I essgu het ialytpc tnihgkni of thsec and kbca snu( dexspe)o is a titell eiftenfrd ni isht te?yp mongA lal iserph;gdomac smmaoalen coucr teh yjomirat fo imte on the limbs (%3~6 werol adn 9%~1 r;)pupe rnkut si 7%...2~ So eabds no atth dan mih engbi fo ricnafA necdtes we cna hoeosc mlaps.


 +7  (nbme24#1)
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hotgluAh 'hsoCrn mya vahe re,culs itf,sausl dna ;eibnldeg it lslayuu odse otn sucae nroi iyiccnedfe naemai adn sah lsse lniebegd tanh C.U tuau"rltScr itlemriaansob fo hte eralmnit imu,le ushc sa honrC seaeisd dan rlacusig in,tocsere nac aseuc rdedeseac spnboriaot of tiivnma B1"2. - sFitr Adi eaGnelr islrePpcni


 +4  (nbme24#24)
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boirPceen"d dna -ieodsghh aytacllssie tiinhbi pnaotebsrior of iurc cadi ni lraoxmip oulcdeovtn eutulb (oals instiibh nreceotis of nlncpi).iiel" - Fsitr Aid 2190

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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rFisaimlgt S)(FC-G si veyr mnocolym eesttd tish wy;a roWdlU adn weresele.h .Cmeho ntipeta itwh beno oarwrm nrpsoiusesr tg&; evig .-GSFC


 +5  (nbme24#50)
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italMapaes - A eeebisrvlr pdiaevat esrnspoe in hhicw reeht is oaRinmmperr"gg of mset mnlŽlcteeclseerpa fo oen lelc tpye yb artheon thta acn pdtaa ot a ewn srs.es"t hBot aer onalrm .ellsc riyetoparsR eert oudshl ont ehav muqsousa cesll utinl eyiarostrpr bsihceornlo eebofr( tht;a dbiolacu in .trem on.br ;t&g ocunarlm ni orhcb.n g&;t dsurftoasepetidi ulmaocnr in aegrl. co).nr.bh

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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eoabrypvntniS si eth teatgr of tietsnaspmoan au(tents tonx;i) emulcs mpasss rea acci.rttreiachs Onyl orteh swenar ouy hmgti docenris is srhaeeyoltcesclitenA ecsin eh si a rfmrea nad wzdsourzb fetno arryc su ot the sdeporim .na..ld tub tmopsmys of a rhliiecgonc srtom aer ean.tsb

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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nI" het ryeas edripcgne hiasylpc rp,byuet etRrbo M. Braoy eevcsdrodi htta teh pooaonndtrgi slespu rcocu oynl nigrud lspee, tub as yteprub oerpegsssr eyht can eb tdtedcee igrnud eht y.ad yB eht end fo tr,yupbe eetrh is etiltl -ytdinahg fencieedfr in het pmaulitde dna yerfqucen fo raidgnootnpo .plsuse

meSo raosetvtinisg have rittdtabeu teh nstoe of yurbpte ot a enroescan fo stlloasoric ni eht r]n9b9]1a8[0.][9i[ yB stih mmhnesca,i the onpdrtoagoni eslusp thta orccu ripayrlmi ta gnthi tusj reofbe pbetruy ernpetrse b"as.te - kiiW

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 tuhhotg ihts asw a ictrk snetiouq cinse nkis ercscna ear hte omts mmocno yept fo scrcnae olvler.a But tulcayla gomna VHI pit,tesan VId-leetrHa aecscrn era umhc oemr omnmco tahn enIVern-tHad-lo scecanr nee(v knsi nesr.c)ac nidBEed-Vcu riypram SCN pymhlmao is eht ylno ptooin tath is fAiesIgDnind- snacleie/cs.nrl

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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coMotizgoyn e)"iil"cad(nt twsin have 5%0 of gnietgt achezoprsiihn if terih iwtn hsa it. toziicDgy intsw aveh ~ 2%0 ncceah utghoh. sThi si fenot mdnoiente wneh onzhhciaiSrpe gtoylieo is sdcssudie e..(,i ew on'dt wonk utb daorenconcc dssiteu gugtses a gicteen ik.)ln DT1M ash sles of a gntieec ilnk anth DMT2 ubt it aosl sah 50% odcerncaocn eeewbnt tomogiyonzc iwtn.s Tshi cfta is meenoidtn ni Fsirt idA 19,02 pgae 63.4.. I tgo ihts EBMN qnisuoet rongw tbu st'i etntnco is ni obrad sruecso.





Subcomments ...

submitted by medstudied(1),
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aCn emenoso anexlip hwy teh cortcre rsenwa ofr eht nsioutqe eerh is actingojnuo but tnc’a be paisoitnsront?

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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ltAprpnaye ehrte si a lpceomeytl perstaea pislan crod fleexr ehrew rcidet eipenl sltimuiotan lsdea to na cetrein.o hiTs exlfre only dnsee na icttna rac in S2S-,4 os sa gnlo sa shti rngoie is ont nirudje, na ecrneiot nca slitl u.rcoc r,oveeHw wiht rniottsecan at C,8 neth het snchcgyoepi eocrtein lxerfe aontnc orcuc, as this rseerqui dcsnidenge irsfbe orfm eth cxr.eot

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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Why od uyo veig VI rilceonouv tihw rnehattical ethxoter?etam Wt’dnoul XTM leso tis eciayffc senci roiunovcle sreveser eht cseteff fo M?XT

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(415),
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aerU Cylec ireosDrds ;> odaltsIe evrsee imemnrheyapmao g;(&t 00;10 ..,ie on threo rseeev oicletamb ecsinatsrubd

nrhienOit lmeyabaaastcrsnr yidcfencie &;tg s(omt ncomom erau cylce dis). iootrc riddieiaacaacmu/i, enamiomaeymhrp

icngrOa mieidAcsa t;g& morinemHa,ypema nia-ponag d,soicsai esistko (ormf lymyhocg)ipae

Meiha-munidc alA-Cocy dgeysdnreehao yccnieidef &;gt amrHpyanio,emme yitthepkoco loycymeaihpg seen( in oniio-dβtax rs,soddire TCEEXP lneuoaeyo)yrdprdthsok

Lreiv dounisnyctf ;> oaayiepemmH,mnr FLTs messed pu, ldroe pt.

lsmarshall  Summary of metabolic issues relating to hyperammonemia +7  
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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You nca see hte enfratiooemdne teurctusr ni isht i.mgaadr

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 +16  
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