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Welcome to lsmarshall’s page.
Contributor score: 348


Comments ...

 +24  (nbme24#3)
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hTe tsmo tedirc htap, dna ostm eilkly thp,a ofr arebst acecrn to tiesesztmaa ot eht vetaebrr rae het loteisnartc .ivsne Tihs aws no na erlaier NMEB stet as llw.e erstaB earncc wlil ascue ,demix iylct nda lbictas iessonl ceno ni .ebon

On na rtauedlaen et;no I inalfly amec up tihw a cednte awy to ebmreerm tcily v.s sitlcab crneacs in oe!bn

nIYedk nda IorYthd csuae tIlcY

estrapot g;&t abtalest &tg; sbtlcai

oTw esbstar g;&t wot pytes of lssineo tg;& B strae sausec B oth

owT lngsu &;tg two etysp fo lionsse eedinpg(dn on ytpe of ugnl ce)cnar

llelalc-sm nglu t;g& l"lsam ltbs"as

nll-nmoas elcl &;tg yclti

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. +10

 +18  (nbme24#16)
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rlexFo umotdrgii fdsurpoun is rebeospinsl orf loxefni fo PI.D eaidlM tcaspe fo teh lmseuc (ihhcw xsleef het t4h and h5t gtdii) si plepdisu yb het lranu enver C(8, 1)T. The altlare tcapse hwcih( lsfeex the nd2 and dr3 td)iig si tnvineerda by eht maneid rneve lepcifialcsy eth rraineto siseueontsor cnbarh ,(8C T)1. So het uqeintso si dcgierbnis a raocatlien maanggdi teh envre pylsup to teh IPD rlfeox of hte nd2 idtgi d(exni .)ingefr siTh is iysnag het deimla neerv si ngbie aaedgdm (C8 dna T;1 wrloe nrkut r)s.oto

urLmibcsla /2td,sn1( min;aed h4dt,3/r uarn)l rae a puorg fo slscume ahtt elxf ta hte PMC jnoi,t adn netexd PIP adn DIP tojsi.n

oudCl rerememb sa lr'eoxf imtroidgu rupdsunfo si pfynorluod ogl'n cnsei estdnon teirns no PD.Is maordeCp to rlxofe ritdiuomg fisiursleacpi seowh tdoenn sparw drnuao rnodfp'usu fiuislleyacpr ubt estsirn on IP.sP

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) +3
hungrybox  'flexor digitorum profundus is profoundly long' is such a good mnemonic, thanks bro +

 +17  (nbme24#27)
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aaarPsnr"etl vheae tl()if occsru idgnur rgtih tecrnliauvr rpheyhoytpr e(.i. eergenlt)man ro eryv rlraey rseeve tlfe rialta teemng."alner RV orphpheryyt anc eb sene so aeyils beeacus the VR si at teh eoairntr searfuc of the cte.sh

nI hist etinpta lodbo fmro LA ot VL caerdeess in t,stnrouaai so it si gogin eowsher.em Fmor eth 2O .sat ew anc dceude tereh si poyablrb a VDS ri(adeencs RV resureps uowld eascu RHV nad nsapltearra e)e.hva turmorh,Fre eth eitvetgn is eklyli bnsciedigr loagrytte fo afllto sa(udce yb errtsipornoeau ctmildaspene of the arbdnulinuif .)mepust nI teT slpsle, VR tulofow si oto ttbcruesod nad eatnpit stge iyscsnoa dna t&R;gL histnngu sSqaut aesincre VRS, egnseaircd ;LtgR& in,tnhsgu utigptn eorm dbolo ohgturh maurynopl icructi adn liegivren aoys.icns

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). +

 +30  (nbme24#20)
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Ptetani sah apSni aibdfi ltoucca cihhw is a ernlua ebut tfdeec ru(aifle fo fiunos fo eht roes.opneur) ecmlsoeSotr rae teh tarp fo ehca ismoet ni a vterbetaer yrebmo gniigv eirs to eobn or threo kaelslet .itusse ciSen a aptr of isht nttapie's insap ibidaf necddilu aessbcen" fo suispno rp"oscse ehnt a looemtsrce saw dnv.eovil gwinnKo atht urlane uteb deescft rae na susei hitw foinus sohuld eb noeghu to egt to eth trgih rean.ws

fI the dtrhcoono aelfid to leedpov tneh the etneir SCN dlwuo ont lvedpoe sa the ootdonhrc dnsicue anofimtro of erlnau tpl.ea

fI teh aenrul betu eidlaf ot voedelp nteh eht weloh SNC dwoul nto aehv v.oleepdde

oYkl sca si rnralivete ot this e.atntip

hWne aneurl sectr llec ti ash fdefentir ouetsocm in nfedifter iuts.ses alieurF of rnuale setrc to temriga ni threa anc caseu nsTioiarsntop of etgar selsesv, Tagteolyr fo t,lloFa ro Pnerssitet untrcsu erro.uaisst Flaueri of nureal erscts ot taregmi in GI anc uaesc rruhssHipngc eadssie oa(gincltne alno.)ecgom errehaTc niColls dnrmyoeS nca crouc when nalrue tescr eclsl fila ot ieagrtm ntio 1ts rgpelahnay ahr.c arNlue bute sefcetd ash githnno ot od twhi eiulafr of runlae rcets riatomgni hgo.hut

sympathetikey  Exactly. I knew it had to due with fusion of the neuropores but had never heard of sclerotomes. Thanks for the explanation. +7
hungrybox  Fuck I picked "Formation of neural tube" but yea that makes sense... that would affect the whole CNS +1
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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heT" aexct mcinmseha rof rremto ndiintuoc by di(nee)2-rcgβar nsgitsao si ltlis o,nwnnuk ubt eethr is omse niedvece taht -a)drcr(egβ2ien noaigsts atc rcyleitd no u.l.me.cs oeMr ,tcenyelr rermot hsa neeb aerdloertc ocslyle thwi "maoipaye.hkla - NHI loibipctanu

rsiFt idA nonmsiet hidstpreihymryo igcnaus otmrre ofrm βa-ncirerdge naiumsilot.t tI aslo osteimnn βnoagsti2-s sgcnaiu romtre sa a dise ff.ceet sFirt iAd saol nmsniteo otg2-naissβ niivgdr iatsmspuo tnio ,eslcl chwhi yam ncbrtoetiu to ret.mor tahT isad, erom alsiscc soysmtpm of ylpihmkoaae ear deiw QSR dna kaepde T aswve on CE,G h,sayrthiamr nda elsumc ekawss.en

kogoiLn noduar on eth entenrti kloos iekl if terhyap si tundeocni the ermort romf a sn2t-oβasig reselvos ov.ertime

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 eretixplnmea seidgn ro anxliepeetrm tsudy umts veah na etnineoitrvn, by .enntdiofii aotClnseorc- estusid are asvaeinootrlb sitused, otn lmpien.extaer Tsih eousntiq si elcyiahltcn or.nricetc yhTe tdeanw to kaem a intop that -nclctrsoeao utiedss rea iemt adn otsc finecetfi cnsei yeth tdon' reuiqer lgnolwfoi pnaetsit ovre imte or any rsceruose eebsdis tgivnrgihengeawire/ ifaroimonn.t seaC srisee lcuod not test isth pe.htyhssio

sAol, eth gnwirod aads"icteso itw an dciaeners "irks atehswom lasdleu ot -ocratnoelsc suesdit ylno nhgiva teh biltiya to ifnd dosd of an oiascastniso wbneete oueepxsr adn cuoemot, utb not lstiabshe luacsa n.leopiitashr

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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"oeoemmssD aMclua( dnrees)ah - A o-leeclltc-l cncntoonei hatt epiodvrs uursattlcr rpsoput tiwh eitiemaerntd fmnl,isate auiyrcrpaltl ni esistus htta ouedgnr claamnceih rsesst (g,e.. kn,is tgcrais tus,ies edb).rald ecConnst ckitrynseaoet in teh amrtust nmsoispu fo teh mrpee"id.is - SOSBMA

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. +23
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. +1

 +12  (nbme24#27)
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npeaylrPutoohy - A ninciotdo eivvonsl dgamae ot mllteupi irlpeearph neerv f.ebsir inPattse cptyiylal espntre hitw tmyermcsi aidstl yesnosr slso or a nibunrg sesnntoai astdiaseoc hwti oortm wessk.ane saCsilc tpyaolpneouyrh si nurgnib os sith oqstieun swa omre socespr of enomit.liain strheO did ton tfi l.lwe


 +8  (nbme24#33)
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nnhalatI uaseb odclu be oedn whti ,eugl itnap riesnh,tn uel,f iunsotr ,oexdi ro kayll rnt.iiets lsluayU ni oshol-ighhc dage .idks laIasnnth rae 'esndwor' so atweevhr itxnniotacoi tsfefce there rea loudhs be stsepradne nda uflly leoresv iwinht 03 i.mn to a epluco uoshr. tetsniPa yma lkoo krdun when tndiiacetxo ihtw lnht,saain but saulyul yucqlki ose.erlv A seiaatihrcccrt "lgeu ns'irseff rahs" rudaon eth oesn dna uotmh is smotemise eens eatrf noogpdler ue.s


 +13  (nbme24#48)
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PAC rkoset acn cusea "asosappginoro" wihch si teh tbyanliii to oncregezi ilfiraam .feasc euCdas yb iealrbalt eonliss of viasul aoinoacsits ar,ase hhcwi rea atiusetd in eht frnreoii clperoatcmotiiop xorcet rus(fmfoi gu)syr. heT labtiiy ot mane rapst fo hte faec eg.(., seon, tmoh)u ro ntdyeiif luiisinadvd yb tohre seuc .ge(., ht,olicng vc)isoe si flte tac.nit

ttWoiuh iwongkn t,tha rrgmneibeem cctoiialp bloe is dvnolevi ni 'lvsuia tffu's ,oyldbra nulcigndi gemia gcipssreno nad isth iatpnte si gvhina sesuis iwht gdendritnusna esimga olsdhu eb heuogn to teg ot hte wsean.r

gonyyong  Lol I guessed it exactly because of that +2
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! +2
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. +

 +35  (nbme24#8)
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eUra ecCly Ddsseorir gt&; tsdleaIo seeevr hrinmamayepome gt&;( 00;10 ,i..e no otehr eresev cmalbtioe anisesudrbtc

Ontiienhr aelsbntsaarycrma yedccnifei ;gt& ost(m mcnomo aure yccle s.d)i tcrooi iemaid/raaciuidca, prmiymeoamhnae

gcOrani smaiiAced &;tg aim,amoHreeynpm nipao-nag osiida,sc eisstko or(fm yglhcmpiy)oae

h-aicmueiMnd cloyC-Aa sdeeahrdeynog dcefyenici gt&; Haempmr,aniyemo hocttikyeop hyemyilogpac e(sen in β-nxadootii dsirrsd,oe EETPXC ryyoodauldens)tpkorhe

eivLr ufyidnscont tg&; Heanrmipe,ymmao TsFL eedmss up, deolr tp.

lsmarshall  Summary of metabolic issues relating to hyperammonemia +5
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +2
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. +7

 +4  (nbme24#37)
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"Ari r"dpolste onssud klie iysrprroaet lavsi(a or )erwta rsoe.dptl tIlaoanihn fo pamtaosoxl ytscoso in cat sefce int's utqei eth s;aem tno to asy I ownk etylcxa awht het ooycsst aer hadnlie sa sut(j ocpmicirsoc rdy tac oopp rciepl?ts).a tsoIeingn of ncrkdeeooud tame ot egt eth ssyct is lreycaitn a ROT for t.aoxlapsmo

asxoTaompl sa OTHRC hsa riadt of dsh,rupcoehlya rebalcer ficoclatsnacii ea,)iranrteblrc( nda nierrso.tictohii iroitsinocethir nac eb in lningeacto CMV or xosa.lpitoosms ecireilarPuvrtn iolfaiccsticna rea ni .MVC nCgoantiel VCM lluuyas sah neahgir ols,s ,rzieessu plheeatic sh,ra bybule“rre ff”nmiu hrsa, i,strtoerihiiocn and trauceirnilerpv asloc.itacnfici

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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Agdorenn ttissnnviieyI onreySmd - eDctef ni nonagdre oertrpce telsinrgu ni ameairno-rgnlapp lmefae (,XY64 SD)D. iugcnitonnF stsete secasu easdrenic trneosetteso at btup,yer ihhcw si toevcndre to eegrotns ,aryelrepplhi ginvgi emefal caesryodn axuels atestschcrriica (lafeme xenatrle it)ia.aelng cLak of aodnegnr rtepecro ounitncf sdela to bsenta ro antcs lrlyaiax adn bupci irha. iePantts evha nirrtamydue va,aing ubt euturs dna pialnlfao sbute bsn.tae

Aedrngno nyetitisiinsv yrsnmdoe is teh rsnwea tbu uyo hgtim vahe icsedronde nirMüalle eeigsnsa ria-Reoysyntkka-M( srturKeaesHü- sdnr.mye)o

eunlMarli neeaigss iwll heav omrlna omhenor elvlse nda may nprseet sa 1° oamreenahr (eud ot a ckla fo eietnur evempletndo) in sleafem iwht ylflu vdedeploe 2° slaxue srriacacicshtte iatcunol(nf e.ris)avo iHra odventmlpee si lmnaro as .lwle tatnPesi also eavh omalnr ieg.hth

seeSm ilek iths iqtnuseo did not egiv su hcmu to ihsigtdnusi sisdebe ihgeht dan rnaten egtas 1 ilxcyabualrip/ iah.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. +

 +13  (nbme24#45)
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HMC cslsa 1 tpeepid inanegt psnercosig ;gt& iAgn"tne petipesd dldeoa onot CMH I in ERR ratfe ydilvere iav ATP ero(rrpntast seastdaioc htiw itgnnea cogpnie"rss) - First iAd 910.2

reaB hypylcomte nmdoyesr epyt 2 BS(L ;II acefngfti CMH I)I si eud ot atonumtis in ngsee ahtt code for otiptnrcrnais tocasrf ahtt ramnloly geurelta hte ronxespsie (gnee ntaciitorsp)rn of eth HCM II e.egsn areB pyyoelmhtc smdeoynr ypte 1 BLS( I; neftacgfi CMH ),I is ucmh emro er,ra nda si asesitaodc iwht PAT eeife.dccisni

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." +

 +15  (nbme24#22)
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relelZewg nreosdym - otmsuloaa essircvee iordrsed of eriopmxseo sneogseiib deu ot eumtatd EPX .gense tH,oyipaon izsesr,ue olayhemp,tage larey daeth i(niwht 1 ).yaer ad-iintβxoo of FALVC nhpaspe ni eoremxoissp os teh dhcli eilsmyneg nivhag smeo sotr fo gitcanlneo aloectbim rdeidors ithw etelvade CAsVLF hodusl veah nebe ogehun to etg hte answer iutwhto iwnonkg toabu leerwelZ.g

jucapami  furthermore, FA 2019 pg 47 +1
tiredofstudying  Same page for FA 2020^ +3

 +16  (nbme24#25)
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Aalcr inutsolgei si mots momnco etpy of aonelmma ni iacfrnA eAmsrnica nad si no hte aplms or oe.sls I uesgs het ltyacip tigkinnh of stech and abck (usn )oeesdpx si a etitll fnirfedet in ihts tpe?y Amgon lla ocisdemrgah;p eaalonmms crocu hte rjyioatm of meit on eth lbsmi (3%~6 eorlw nda 1%~9 pe)upr; krtnu is %72..~. So sabed on taht dna mih being of nrcifaA ecnetsd ew can sechoo .mpsal


 +7  (nbme24#1)
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htglouhA s'rnoCh yma hvea eucls,r lsutfas,i nad dlgibe;en ti suually sdeo not aeusc onir dcycneeiif niamae and sha slse ligebedn nath C.U "urtrcluSta etoibanailsmr of het miaeltnr ,mulie hcsu as oCnhr saidese nda rgasluci cesiteorn, nac seauc crdeaseed ntairposbo of iatvmin B2".1 - rtFis iAd rleGane lrciPispen


 +3  (nbme24#24)
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cnedPe"ibor nad hdigseho- letscilsyaa iitibhn ntprrisoebao of cuir daci ni poaxilmr utoclvdnoe lutbeu a(los ntiihbsi citesrnoe fo lin.)e"lpcini - Fisrt Adi 9120

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. +6

 +6  (nbme24#31)
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aiimFstglr GC-(F)S is rvye ynolcmom ettsde isht ;wya rdUWol dna hse.erlewe C.ohem inaettp with neob mrrwao oesrpssirun > ievg C.GF-S


 +5  (nbme24#50)
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eaislapMat - A evlsieerbr teaivadp resospen ni hchiw tehre is oemgrpmin"Ragr fo etsm lmetŽccpnlelaeesr of one lcel epty by netroah hatt acn ptdaa to a wne "rse.tss Btoh era anlomr sll.ce triRroypesa etre ouhsld tno eahv oqausmsu lslec litun rrrtapoiyse olonsbheric e(refob ;taht boicudal ni mt.re nb.ro ;gt& nulcraom ni o.crnhb g;&t sdfotteepisdurai rmcanoul ni .eglar .c)bh.nor

shayan  if its a metaplasia, then how it be normal ? I mean Metaplasia is not normal? +1
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. +4

 +11  (nbme24#8)
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atyinSnbeprov is teh tgarte fo maspottnaneis ean(tsut i);tnxo mucsel mssspa ear aichertcracist. Onyl htreo sneawr yuo hmtgi eisdconr si oahAeyeesctscrinllet sinec eh si a armref nad wdrszobzu tonef ayrcr su ot eth rpsmiode n..l.ad but ysommpst of a riehgcilnoc tmsro era .tensba

vshummy  Synaptobrevin is a SNARE protein. Why they couldn’t just give us SNARE I’ll never know. +34
yotsubato  Cause they're dicks, and they watched sketchy to make sure our buzzwords were removed from the exam +32
yotsubato  Oh and they read FA and did UW to make sure its not in there either +28
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! +4
qfever  So out of curiosity I checked out B) N-Acetylneuraminic acid It's sialic acid typical NBME +1
alexxxx30  shocked they haven't started calling a "farmworker" a "drudge" <-- word I pulled from thesaurus. +
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. +2
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. +
wrongcareer69  Here's one fact I won't forget: Step 1 testwriters are incels +1

 +13  (nbme24#33)
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In" eht asrey gdrepenic ihlapysc ypebt,ru btoRre .M yBaro svdcdreieo ahtt the oitnoanorpgd puessl corcu nyol rungdi les,ep tub as ptbreuy srospreesg ehty cna eb ddtceete ridngu eth yd.a yB eht end fo reu,tpyb eethr si tlltie ihgny-atd ecifdnfree ni eht lauipedtm nda yuqerfenc of odroinoatpgn epl.ssu

Semo inrgosaivtste vahe uetdittarb eth setno of uypbetr ot a ecseroann fo asliotsrolc in hte 89].[9n9[a[0]ri1b] yB tshi ehnmi,acsm eht ooiontapnrdg uspsel htta crcou miirparly ta thgni juts efrebo yepurbt rterenspe a.st"be - iiWk

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

 +5  (nbme24#22)
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I hgtthou sith aws a citkr quenotis iecsn nski nsccera era het tsom monmoc epty fo cncares la.oelrv uBt ylacutla amngo HVI tsaitpen, eead-HtVIlr arcncse rea mhuc oemr oomcnm thna renoI-HlntdVa-e asnrecc (neev snik nc.sr)cea dEcindBe-Vu iaprymr NCS oymlamhp si eht ylon notipo ttah is dDisgfn-IniAe aei.slcle/ncnsr

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...?) +1
yotsubato  God damn this is such BULLSHIT... +11
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 +

 +11  (nbme24#11)
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oyticogzoMn dnlaic)ie(""t iwnts ehva 5%0 fo gteingt ozsnphahreici if rhtie nitw has .it gticyDoiz itwsn vhea ~ %20 ceahcn hogtu.h Tihs si otefn nmedoinet nehw enzhhpaoicSri tygeiolo is cdseissdu (.e,i. ew otnd' onwk utb ceronndocca iedstus gegusts a geentci n.)lki MD1T ash less of a ncegite inkl ntah D2MT btu ti osal sha 0%5 cadcocornne bteenew ziocmnotgoy ins.tw iThs tfac is notendemi in risFt Adi 9,102 egpa ..36.4 I tgo htis BNME eqniotus wnorg tbu 'sit netonct is ni darob seorsc.u





Subcomments ...

submitted by medstudied(1),
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naC emsooen nplaxei hyw eth rercoct srneaw ofr the eoqustin reeh is ajinctoonug tub nac’t be si?sioptnoanrt

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. +10  
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 +2  
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(56),
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Areptyapln ehtre is a llecmtopye tsaeerpa ilsapn rocd elexfr hrwee tidecr ilpnee iiolautstmn easdl ot an ct.rneioe ishT eerxfl yoln esden na ainttc rca in ,-4S2S os as lgno as tshi negori is not erjdun,i an eoencirt anc tslil oucrc. ,Hewevor wthi tnestaciorn at C,8 hnet het yhnsgoipecc rconetei flxeer cotnan ucro,c sa hsti sqrriuee gseedinncd ifsebr mrof eht cxeo.tr

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." +6  
seagull  S2-3-4 keeps the penis off the floor +30  
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 +  


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hWy do uyo vieg IV oenulivorc htwi raniacetthl ta?etrteehoxm lnu’Wdto XMT lseo tsi iycfaecf nseci cvirleunoo erevress the cfeestf fo TM?X

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? +  
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**." +7  


submitted by lsmarshall(348),
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eraU ceyCl sdoiDerrs &t;g etIdolas everes arayommehpeimn &(t;g 0100; ,i..e on treho eresve aitblocem cdbisresatnu

rhetOnini nsmrbaaacleytras iefydcecni &;gt tm(so ncoomm arue yccel ids.) otocir eauaiiaidcacr/mdi, eyenraimpohmam

inrOcga sdaiAemic ;gt& mamo,aeHnryempi gnpioaan- isaoc,isd tsikeso f(rmo poiyyclamhg)e

iMehumna-icd Aa-Clocy hrgeyeddsaoen ineeicfdyc tg&; mmpmaoye,rHniea itkpyohtoec iolhypeygcam (nees in iotdoxaβi-n sesdorird, TEECXP eyyoeldrk)shoptunaord

vierL ntiysndocfu &t;g opHaairmmmee,yn LsTF eesmds ,pu oelrd p.t

lsmarshall  Summary of metabolic issues relating to hyperammonemia +5  
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +2  
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. +7  


lsmarshall  Rectal prolapse through posterior vagina ("rectocele"). https://www.drugs.com/cg/images/en2362586.jpg +6  
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 +13  
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 +