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Welcome to keycompany’s page.
Contributor score: 268


Comments ...

 +3  (nbme22#37)
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hyW odlwu sdoepniito of diborifin tdsopeis i(..e ifiidorbn n/nceilarnmiossgta )NHT be wog?nr

amorah  Kidney is smaller than normal, suggesting less blood flow to it. Won't see shrunken kidney in the case of HTN. +1
linwanrun1357  I have done so research showing that it should deposit collagen (see below). Anyway, fuck this question! http://www.pathologyoutlines.com/topic/heartfibromusculardysplasia.html +
shapeshifter51  I ruled out selection A since it is involving the interlobar artery. Renal artery stenosis involves the "renal artery" and the stem gives you fibromuscular dysplasia with renal artery stenosis. +1

 +0  (nbme22#37)
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d’nluwto rcohnci iepothsnryen fo het a-nlrLe rtyare cediun AARS ,icvanoatti dan neceh urultba hoytpyphrer hitw actlcroi p?hrtoay

fcambridge  I had a similar thought regarding mesangial hypercellularity. I missed a UW question on a similar topic. Unilateral renal artery stenosis results in hyperplasia of modified smooth muscle cells (JG cells) due to reduced RBF. The hyperplasia is intended to correct the supposed deficiency via increased production of renin. +
paperbackwriter  Atrophy of the affected kidney (receiving less blood) and hypertrophy of the opposite kidney. +2

 -1  (nbme24#10)
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mgIae shosw rCeenstc gSin, a conmom dngifin ni iAnlmboad Arctoi umensrAsy edu to uarlm mtbusroh olusccon.i

happysingh  crescent sign is a finding on radiographs that is associated with avascular necrosis, NOT aneurysms !!! what you're seeing is Calcification of wall of the aortic aneurysm +12
sabistonsurgery  @happysingh - Thank you. You are correct indeed. +
suckitnbme  Adding on, this patient is a >65 yo Male with a 120 pack year smoking history. Both are significant risk factors for AAA. +

 +6  (nbme24#31)
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nAewdesr my wno ue.qiostn decenrasI tsress form a MESIT lliw caatvite teh cistmhtpeya esuovrn etsysm -- mrayoPnul i.oavsaldntoi

pathogen7  Just to add, CHRONIC heart failure is a cause of pulmonary hypertension. So in the acute setting, pulmonary edema leads to decreased PVR, while in the chronic setting, it can lead to increased PVR, I think? +
hungrybox  This doesn't make sense. Activating the sympathetic nervous system would cause bronchodilation (via β2) but it's unclear to me whether it would constrict the blood vessels (via α-1) or dilate them (via β2). +1

 +1  (nbme24#31)
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aCn bydmsoeo hwo adrnedsutn yhw VPR adcseesre wtih a Sdeei-tfdL ifntcar peslae ltiegnehn e.m I wuold loas tepcraiepa it fi yuo uocld retael ti to ghtir iedsd aterh lifeuar too (.e.i owh lodwu ti ne.ghca)

sajaqua1  I believe that keycompany's answer comes the closest. In an MI, consider it as cardiogenic shock. The heart is a pump, and it is failing to move blood out of the heart and into vasculature. This is why PCWP increases. Because of insufficient output, the body has a sympathetic response. The catecholamines then cause vasoconstriction in peripheral vasculature to keep blood pressure up and continue flow, leading to increased SVR. Meanwhile, the sympathetic response causes vasodilation in the lungs; this would be an appropriate autoregulatory response, because the body is trying to keep up the flow of oxygen throughout the system. This decreases PVR. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5715548/ Is a pretty good article on this. Of course the binding of catetcholamines changes depending on saturation and the response is not perfectly understood. +10
usmleuser007  My understanding is that the pulmonary circulation changes very little in terms of an acute MI. It is b/c pulmonary circulation has a lot more room to fill with blood much like the spleen in terms of blood accumulation. With higher volume of blood in pulmonary circulation, more blood vessels are able to be recruited specially the apex. With more recruited blood vessels = reduced pressure d/t circulation in parallel. +1

 +9  (nbme24#16)
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Tshi atnptei has a x.neuaopmtorh irtipnvtHeylonael si ont gnuhoe to aopcetensm rof hte lveolar esdarece in gnul feucras a.aer

_yeetmasterflex  Could the pneumothorax also cause less ventilation due to decreased lung surface, retaining more CO2 causing respiratory acidosis? That's how I got to the answer at least. +3
duat98  I think pneumothorax would increase RR because you're probably hypoxic. Also I'm sure when you have a lung collapse on you you'd be scared and that would trigger your sympathetic so your RR will go up either way. +3
kateinwonderland  Arterial blood gas studies may show respiratory alkalosis caused by a decrease in CO2 as a result of tachypnea but later hypoxemia, hypercapnia, and acidosis. The patient's SaO2 levels may decrease at first, but typically return to normal within 24 hours. (https://journals.lww.com/nursing/Fulltext/2002/11000/Understanding_pneumothorax.52.aspx) +1
linwanrun1357  How about choice C, --ARDS? +1
bullshitusmle  there is no bilateral lung opacities as you would see in ARDS +3
jesusisking  Was thinking some sort of infection b/c of the atelectasis so picked empyema but this makes sense! +

 +4  (nbme23#19)
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sThi ieustonq si i.sdsgdeiu thWa yeht ear eryall niagks is "wtha is eht eols dnmeattnier fo seesipc rvliausv?" eTh onyl arwsne is hte bitlyia to arptorc.ee euesBca AND myPraeesol has arogf-dpneiro ttacyiv,i gpoyern lilw eb ffcueatden by NAR oraPlssyeem kcal fo oode-agnfprri .vtictiay

ls3076  the phrasing of this explanation doesnt make sense to me. +3
ls3076  oh wait sorry i just read it again. So instead of proofreading how are errors handled with RNA? +
thomasburton  Think the point is basically although errors with RNA polymerase make make the bacterium not very good at infecting or killing or whatever it does not affect replication as it is not used during replication! +5
almondbreeze  common sense asked in a very very convoluted way.. +

 +3  (nbme23#18)
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yeTp I aseDbeit is ztecrdraihace sa hte rinuocttdse fo niparecact sletsi clasycfpile(i ateb l)ecls by ecl-Ts.l Teh osmt leklyi scaue rfo igmheycyloap golfnwloi nulinsi ,iimtnstnadraoi tref,eeroh si het usontdtirec of palah slcel htat unrdosru eht eabt es.llc sihT olduw cseua ereceasdd elslev of iganrciulct olcgaun.g

titanesxvi  I think rather that high insulin is going to block the release of glucagon +6
melanoma  the answer is not correct +1
melanoma  his answer +1

 +8  (nbme23#39)
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Feigru it out taref deagrni a eewv.ir UAV/VBU rnedu marnlo ncsticcmaesru is cdeisneord goninzinoni. vHweroe, eht olyn irfefenced eetnbwe noiningnzio nda giinnzoi niadtoria si teh tnhgtsre of hte odinaiart rays. saueecB aiointrda odse ton sitsaepdi fomr hte bydo, lgrpdoeon UBV peruoesx can csaue dnaortiai to idbul up in het snik dan seauc na itinoziano eftefc. hsTi is hte maes osarne that eetirepvti XsRa-y adn TC ncSas acn eecasrni yruo irks for en,crac neve ayser dwon eht lie.n


 +6  (nbme23#39)
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naC smybdoeo epsale axpnlei who oigznninnio ioitandar has an gnoiiniz ftee.fc

uslme123  "technically non-ionizing, can produce photochemical reactions that are damaging to molecules by means other than simple heat. Since these reactions are often very similar to those caused by ionizing radiation, often the entire UV spectrum is considered to be equivalent to ionization radiation in its interaction with many systems (including biological systems)." -- https://en.wikipedia.org/wiki/Non-ionizing_radiation#Near_ultraviolet_radiation I'm guessing NBME reads wiki lmao? +2

 +27  (nbme22#5)
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goetinrN anclabe is a earetemumsn fo neptrio bstamiolem ni the o.byd A eginavet rnentgoi nlbeaca esidintca lcumse ssol, sa nradeiecs stuamno fo aimon iacds rae enibg lbmtadezeio ot eupocrd eyng.er hTis iarcensse het otmaun of etgnroin edscrtee mfro the oyd.b Bauscee eth tmaonu fo innreogt oyu rea atgink in si essl htan hte aotmnu of onigretn uyo rea rnscteeig, yuo ahve a itvngeea nrengoit lbaecna.

sTih amn is rsimaoeduhnl, easomdtu,e cchitec,a dna has bmlpmi.aynhuiaoe esThe ilcalnci isnfgind tiopn ot proteni ultraiinmtno sawkoari(Kh issaDe)e, cwihh uassce daeme deu to asecdreed eumrs icotnco sspu.rere oLw cioncto seprerus ni iths esac is ued to rtienop so,ls dna cnhee a neatiegv tongeinr .aeclabn

drdoom  Nice! +7
dubywow  I knew your last sentence and suspected Kwashiorkor. It's just everything else I did not know. I have not heard or thought of muscle/protein changes in terms of "nitrogen balance" before... and that's why I got this wrong. Nice explanation! +3
macrohphage95  I agree with you in first part but i dont think it has any relation to kwashirkor. It is simply due to cachexia which causes muscle destruction through the proteasome pathway .. +3
zevvyt  also, it says that his albumin is low. +

 +4  (nbme22#28)
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iehlW hsti qoteunis tems si av,uge eht mots eyikll gdainsiso is reeHirdtya imooHmhcsaertso.


 +3  (nbme22#16)
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O, iRgeeav-nht olodb is the luerisnav rondo rfo dobol la.apms

keycompany  Edit:: Blood RBCs*** +4

 +3  (nbme22#7)
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ngdoLai oseD is the onyl nrseaw ttah is dnietdpenen of rdgu elaencarc.

nwinkelmann  I totally get this and understand it... but at the same time, couldn't loading dose differ due to renal function if patient has nephrotic syndrome so had less plasma proteins, because it would change the Vd of the drug, right? Per wiki: Volume of distribution may be increased by renal failure (due to fluid retention) and liver failure (due to altered body fluid and plasma protein binding). Conversely it may be decreased in dehydration. +

 +3  (nbme22#34)
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iaenlnMda sGiec:ent

Mna hsa 32/ cehcan of giben a .rriaecr He( edos ont vhae eth esead)si. oWnam ricrare srki smut eb acctdualle ihtw p2^ + p2q + .2^q 2q^ = 000/140, q = /00,21 p is rugoylh = q2p1 = 1/010 = iaCrerr reqycfeun .

skRi fo ihvnag a cdlih hstu eqlsua 3/2 x /0101 x /41 = 61/00Be/ se 3ua:c2 = Man rrriaeC srik 1100 / = Feealm rreCira 14k/siR = Cehnca tyeh eahc psas on eht seeirvsce nege to trhei fsngop.irf

hello  See my explanation if you need more words to explain this explanation +

 +22  (nbme22#41)
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nw:rAes esrnIadec lranCet ldooB omuVle B,)C(V searDceed A,HD eecanIrds APN.

eTh osglcoihylapi neoserps to meiophrtahy si aosnrctisotinvoc of lprehiepar slsesve .(.ei the neso ni ryuo iseix)mteert ni na otffer to ekpe uyor cero dyob armtreeeutp ,olamnr dna shtu rouy sgnoar foinnitucgn rpryol.ep aPperierhl naisstoocciVontr ilwl eeircsna VCB. ecnsdraIe BCV lwli ucsea na eeacrsin in ,apdlreo nda thsu csaue na eaisecrn in NBAPPN/. /PPNABN ahs iiroihbtny festecf on eht nsdtAinA-oieennoon-lRgsenitre temSsy, ilgtnrues in daereedcs HAD.

gokings2021  RAAS is not directly linked secretion of ADH as claimed above. Increased pressure at baroreceptors and increased central volume sensed by the hypothalamus will decrease secretion of ADH. +3
miniarnie89  another way to think about it is central vs peripheral blood. peripheral is now being vasoconstricted, so central things (heart, lungs, KIDNEYS...) will be receiving more blood. more blood in kidneys = less ADH +

 +8  (nbme22#35)
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yarnUir cratt icsntnoefi are eth mots nmomoc qeraucid eusca fo rtecoVeiusic lRexuf VR() in lecnhdri. VR can aedl to ulRexf rpehoatpyNh, hchwi is iehcaratrezdc by irocnch ruolieiiltsbanuttt mtoflaniimna twhi sfbisiro adn sgnicrra, gidelan ot arnle fil.ruae

lancestephenson  Can someone please explain what's going on in this picture? This is the SAME PICTURE used in NBME 20 and 21 with one of them being a 66 y/o with urothelial cell carcinoma and the other being tubular atrophy. I just don't know anymore +33
spacepogie  I'd be happy to send them a gift card to purchase more stock images of kidneys for use in future exams... +14
diabetes  i think VR should lead to bilteral kidney damage and here only left kidney is affected.should we suppose that right kidney also is affected ? +1

 +17  (nbme22#35)
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itentlaroA of teh ttcremishoat set tinpo is a hhatlamopciy rsoscpe eemidadt by lortdissaagnnp nad si ntnpdieeend fo hte ysmatcepiht ueovrsn tmsesy.

,B ,C ,D adn E all qeieurr teyicmtpsha neevsr ot ieclilt a rpesno.se

pg32  Can anyone explain the mechanism behind shivering and the sympathetic nervous system? +2

 +14  (nbme22#9)
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loFw aeRt = eiltcoVy x otleSsicCnsrao- Aare

2 mc2^ x 20 mcsce/ x 60 ne/icsm x 1 L100,0/ m^c3 = 4.2 /mniL

,0010 ^c3m = 1 L

seagull  Well, I missed this one. I don't even feel bad. +35
link981  @keycompany a small typo, 100 cm^3 = 1 L not 1000cm^3. 1000 mL^3= 1 L +
hello  @keycompany how did you edit your original comment to fix your typo? +
winelover777  Pretty sure @keycompany was correct. 1 L = 1000 cm^3. Otherwise the answer would be 24. +1

 +14  (nbme22#33)
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paiivryenettHonl aeecreds COa.P2 nrltaCe treehspococmre ndrsope ot wlo aCOP2 yb ssintgaonctcroiv eralbcer doobl vses.els

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B) teAriral dlooB OP2: Pa2O agenhsc ni sorsneep ot eeecaddsr ,PA2O IPO2, or .nfdouiifs reThe owuld eb on gcaneh ni Pa2O gudrni eovrytpainienhlt htalcitoe(lr)y.e

C) iAaelrt rPeuress: scDraedee 2POaC is idcasteosa hwit n,oarctiiocstvson hchwi lduwo erasicen lbdoo r.sreupse

)E elaerbCr usseTi Hp loduw ancesire deu to iyprotraser .askllisao

keycompany  EDIT: Via the **Haldane Effect**, not the Bohr Effect. +
impostersyndromel1000  excellent response +
teepot123  fa 19 pg 489 +

 +8  (nbme22#10)
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hc2cvwsatg6c/.5mswMlp/9i//:nnhi.m/C.ePptt/b8nw.0roli0

rselO Snig si a telvytio,-issinw sfwicpyteoicl- gdfinin fo oMrcenegbk irtsoreieAsrlolcso M)(A czaicadherrte by a" lpbpalae hutoglah eel,upslss dralai terrya ewhil teh PB fcfu is tldfneia abeov sytoclsi rr"ups.ese

tI si loebssip ttha ith:erae ) eTh clceoftsi-iwpyi fo hsit tste sname ti is sola lebaiapplc ot osstrsioleechar to(n utsj bA)) M Teh MNEB irloetcrncy psmelii thta AM si ihcrangalenteb twhi itrrsolhaeoss.ec

bubbles  This was my reasoning, too. I thought this was Mockenberg for sure +
hello  I don't think think it's a type. According to 2 other comments: "It's atherosclerosis because it said “radial artery is NON-pulsatile BUT REMAINS PALPABLE even as the cuff is inflated”--> normally, you can’t feel the artery when the cuff is overinflated b/c overindlation occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!): "If if something were to not be palpable then it would have to collapse -- atheroclerosis prevents this vessel collapse." +16
arcanumm  I agree, I just reasoned that atherosclerosis would not be thicker when the lumen is blocked. I don't think they were going for Mockenberg at all. +
arcanumm  would be thicker +
drzed  Atherosclerosis isn't common in the radial artery though... it's common in the abdominal aorta + coronary, popliteal, and carotid arteries. I am not going to assume a guy has radial artery atherosclerosis when he is in his 80s without a dyslipidemia syndrome over monckeberg calcification! +
haydenelise  Would've thanked you for your explanation @mdmike if it hadn't included the "whoever upvoted this is dumb" comment. What a turd lol +4




Subcomments ...

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I ihktn I fnudo tawh het dseesai was, htguoh I ystehlon aehv no eida hwy yhet dlwuo estt tshi ehrtra htan LX.A eTrs’he a inootndic cdllea nstneraiT aiHolpiaoagmelmnbgumy fo nanfcIy. tI eetpsrsn lo/ww oubumillnomnig elslve sopt 6 tsnhom nda anc nsetpre m/lawls pmlhy soned adn tlnsiso ni cianynf UTB ow/ yna ertho nidsignf fo rrmapiy eifniidmeunmcocy glnucinid deeecrads tuocn.s

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Yuo efldntiyei ’dtno eden to okwn the eidasse ot etg eth tcerrco neawrs scine het nlki of alck fo uinoolbiugnmlms ulowd ucle yuo tino eht calk of ilmaegnr nscetre, btu I hntki shti is mero kleyil anth LXA ecisn eevyr cesoru I aerd eslipim tath B llec tcnsou ear rnea 0 ni eth clsicas eatoetnirpsn suse(ln I’m ngismsi a nsoera yhw uekyoletc cotun wff/id ntwdulo’ hosw a fnitcasingi reeecdas ni myeotclpsyh eud to erenrzao- B le.slc) Jtus eandwt ot tpu htis eerh in seca etrho pelepo ltrea aecm rdwneigo,n outhhg I aym sltli eb .nrowg

keycompany  I think we are all overthinking this question (and it is remarkably simple). I don't think this question is testing us on any of the UFAP immunodeficiency syndromes, per say. What they are really asking is "what would also be absent if there are no immunoglobulins and everything else is normal"? The answer is absent germinal centers b/c that's where Ig is synthesized. I think they put all other aspects of the history in this stem just to help you rule out any of the other answers. +9  


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Aakgnlityl nstgea eherth()icloemamnr teh( eorht drsug sdltie are otbliueumcr nrstihiibo) nsieecra hte kirs of MA.L

keycompany  Additionally, AML is the only answer choice that has multiple blast forms (myeloblasts, promyelocytes, etc.). ALL is characterized by a single blast form (lymphoblasts). +25  
seagull  CML has blasts too but they tend to favor mature forms. +4  
kash1f  You see numerous blast forms == AML, which is characterized by >20% blasts +4  
keycompany  The answer choices are all of lymphoid origin except for AML and Hodgkin Disease. We know Hodgkin Disease is a lymphoma (not leukemia) and would present with lymphadenoapthy. So the answer must be AML #testtakingstrategies +12  
impostersyndromel1000  @atstillisafraud thanks for mentioning the merchlorethamine increasing risk for AML, i was trying to make a connection with the drugs but couldnt. Had to lean on the test taking skills just like key company +1  
sweetmed  Procarbazine is alkylating as well. +  
pg32  @keycompany how did you know the phrase "multiple blast forms" meant literally different types of blasts and not just many blast cells were seen? +3  
castlblack  this link says CLL has 'large lymphocytic variety' under the picture of the peripheral smear. I am not arguing against you, just researching here https://emedicine.medscape.com/article/199313-workup +  


submitted by k_tron_3000(26),
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ehT stniroipdce of aberlliat lerwo blim sslo fo tivrbnoai pilimse LDCM madg,ae nad the ansbet TRsD + gRrmobe emse ot em to eb lymngpii thta eh lysbspoi sha tsbea rdilossa ofrm lsphysii ro( nmgtsiohe ryve irmials in eiaepsr.tonn)t

As rof het hrteo rsn,waes A si ngwor ebceusa sih ortmo fntoucin is ,acintt B si gnrwo ecbusae npia adn tupertamere csftdiie rae nto emtnd,eion C si ngowr useebac ti isepilm a ficiecps nveer is ,eapretndp tbu he hsa ltos latrleiab toseinans in sih eitenr lerwo rtxemesitie

D si hte iek,strcti adn m’I tno %001 su,er ubt I oldwu nhkti raophiatyulcd of teh inerorat lvrt()ena tsoro lduwo ucaes tmoro itesdfci icsne hyet cryar ootrm erfne.setf Yuo mgith lsao eetpxc thta rmoto nscfutinyod to be uealat,rlni csein ti uwlod eb ilkenluy to heav a mberplo htiw hte enrve osrot no tboh s.esdi aols eth DMLC si ton ctaedlo nare het rntoreai ortso fo eth pasnli rcdo, os fi teh teioranr ootrs reew eeaftcfd yuo rleayl wlonud’t xpetec to ese triorbvya o.sls

So liyaablcs rcsspeo of nliieao,imnt I od efel eilk nosysre unthepoayr si na eyrxlmtee veaug arswne hhtuog dan I anst’w a anf of het isuoenq.t

keycompany  This is a great rationale. I would like to add on that D is wrong because Radicular Neuropathy of the anterior lumbar roots would (1) be painful [radicular neuropathy is characterized by radiating pain (hence the word “Radicular”); this patient has numbness and tingling, not pain] and (2) because the anterior lumbar roots are the motor roots and do not carry sensory innervation. This patient is having a problem with his dorsal spinal cord (not anterior/ventral). +23  
hello  Want to clarify that "radiculopathy" is not synonymous with pain. Radiculopathy can cause pain, weakness, or numbness. I think the only reason Choice D. was incorrect because it discussed the "anterior lumbar roots", which would affect motor function. +13  
niboonsh  Radiculopathy is damage to the actual nerve itself, wouldnt that make it a LMN lesion and babinski would be negative? +1  
link981  Great explanation guys +  
usmel2020  UW QID: 12035 explains what you are testing with Romberg sign +1  


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urO etillt renfdi has a Piuosrvavr e,itcfinno chiwh ntifsec yrrodeiht rpcruorse,s cngaisu iutrrtneionp fo cyethtreoyr dpcrtono.ui Thsi is eth smae yaw it uacsse podrsyh ftisela ni rubnno esabbi nda spacialt aieanm in ekilsc el,cl te.c

gainsgutsglory  I get Parvo has tropism for RBC precursors, but wouldn’t it take 120 days to manifest? +  
keycompany  RBCs don’t just spill out of the bone marrow every 4 months on the dot. Erythropoesis is a constant process. If you get a parvo virus on “Day 1” then the RBCs that were synthesized 120 days before “Day 1” will need to be replaced. They can’t be because of parvovirus. This leads to symptomatic anemia within 5 days because the RBCs that were synthesized 125-120 days before the infection are not being replaced. +16  
drdoom  @gainsgutsglory @keycompany It seems unlikely that “1 week” of illness can explain such a large drop in Hb. It seems more likely that parvo begins to destroy erythroid precursors LONG BEFORE it manifests clinically as “red cheeks, rash, fever,” etc. Might be overkill to do the math, but back-of-the-envelope: 7 days of 120 day lifespan -> represents ~6 percent of RBC mass. Seems unlikely that failure to replenish 6 percent of total RBC mass would result in the Hb drop observed. +  
yotsubato  He can drop from 11 to 10 hgb easily +2  
ls3076  Apologies if this is completely left-field, but I didn't think this was Parvovirus. Parvo would affect face. Notably, patient has fever and THEN rash, which is more indicative of Roseola. Thoughts?? +4  
hyperfukus  @is2076 check my comment to @hello I thought the same thing for a sec too :) +  
hyperfukus  also i think you guys are thinking of hb in adults in this q it says hb is 10g/dL(N=11-15) so it's not relatively insanely low +  
angelaq11  @Is3076 I completely agree with @hyperfukus and I think that thinking of Roseola isn't crazy, but remember that usually with Roseola you get from 3-5 days of high fever, THEN fever is completely gone accompanied by a rash. This question says that the patient has a history of 4 days of rash and 7 days of fever, but never mentioned that the fever subsided before the appearance of the rash. And Roseola is not supposed to present with anemia. +3  
suckitnbme  @Is3076 another point is that malar rash refers to the butterfly rash on the cheeks that is commonly seen in lupus, so the face is NOT spared. +  


submitted by lilamk(10),
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I am os cudensfo! hTe nylo olcig I loduc coem up w si ahtt DNIsSA daescere nidtloai fo frtnefea rreetoial os tihs roem ciceotnstrd erliatoer is ettrpdneeir as reedasced ldoob lofw adn nienR ecin?ssrea My useis w this si ttha hnew I gleogo it adn achsre WU rfo siht niern tafecf tihongn mseco up lony alietcr I doclu dinf llcytaua ncsadrtctoi ti nda says ernni wdolu SERCADEE morf DAISNs edglnai to eht kheameraylip we imtsseoem ese ...

Any togthhsu lodwu be llh!fuep nhTska ussge.nei

generic_login  I used that reasoning to pick C, but in looking it up now it seems like you are right ... There appear to be a bunch of mistakes on this test, and it’s not giving me a lot of confidence for the real thing. +  
mee48  I think it is because NSAIDs inhibit the local prostaglandin (PGE2) in afferent arteriole —-> less AA dilation —-> stimulation renin release. I think my reasoning came from sketchy pharm nsaid video but I can’t 100% remember +  
keycompany  NSAIDs constrict the afferent arteriole. ​ A. GFR would decrease due to decreased renal blood flow. B. Renal Blood flow would decrease. C. Renin would increase due to renal hypoperfusion. D & E. PGE2 and TXA would decrease (by MOA of NSAIDs). +5  
fallot4logy  UW says that Nsaids is one o +  
fallot4logy  UW says that Nsaids is one of the 5 drug categories that is able to cause hyperkalemia.Specificly ,Nsaids lower PG andrenin secretion .PGE2 stimulates JG cells to secrete renin...(how can i delete my previous unfinished message,lol?) +1  


submitted by colonelred_(86),
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mNalylor het horcaniad lilvi riansd teh FCS omrf hte cbdrnasauhio pseca to eht evousn ssey;mt if hsti rtpa mobcese cdiveeeft enht you cna gieanmi lla that CSF now ngiblidu up ni hte riasobhadncu pecs.a

keycompany  Also take into account this patient had surgery that requires penetration into the subarachnoid space (hence through the arachnoid mater). This can lead to scarring of the arachnoid granulations and subsequent communicating hydrocephalus. +10  


submitted by calcium196(11),
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ENMB 20 has a esuqnito ihwt a guy atkgin roev eth oecurtn ocugh aocmdietni adn own eh hsa .ointpanicsot nWta ot ugess eth es?nawr It asw drtoex! -g;t& t2n/rebmhpn4nwem/s/8toe:a/.5ascb0xe/mms

So Im’ etrypt reus het MBNE 22 tsoqeniu is tsju iagsrhtt pu .ognwr

rockediny  No, not so. Dextro *is* the correct answer here. From the choices given, dextro is the least likely to cause constipation since its main mechanism of action is NMDA antagonism w/ *some* opioid activity -- it can cause constipation but the other choices are MUCH MORE likely to. As for diphenhydramine = it is not appropriate for elderly patients and it isn’t an antitussive. +  
surely_not_a_robot_  Agreed with @rockediny. Dextro would be the best to prescribe because it has the least amount of constipation out of the drugs that you could prescribe + Anti-cholinergics in the elderly have much more morbidity and risk of mortality. +  
keycompany  The only way to wrap your head around this is to conclude that Dextro is the "least wrong". I thought a lot about this, and I can't think of any drugs that can suppress cough without also causing constipation, so it makes sense that Dextro is the answer because it is the "least likely" to cause significant constipation. This is probably just a clinical correlate that will be learned during rotations/years in practice. +  


submitted by armymed88(48),
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uhdo'ntSl eht tnratetme rfo yprehGT eb a rfsbi?eta icWhh wuold ndtcieia eht rsawen to eb aninicrseg LDH F0A(27.1 )306p

I see naiesrgdce VLDL sa a fnnicotu fo an,nici hhwci evress to cadeeres cthiape LL.DV.

keycompany  Fibrates inhibit VLDL secretion (by inhibiting 7-a Hydroxylase) and they increase HDL. However, this patient has chronic pancreatitis, which decreases enzymes that allow for fat absorption. Because a large portion of HDL is synthesized in enterocytes from newly absorbed fat, HDL content is unlikely to increase in patients with chronic pancreatitis from any of the lipid-lowering agents. Hope this helps! +2  
mr_haib  fibrates cause decreased VLDL as well as niacin. They increase the activity of LpL by activating PPARa causing increase catabolism of VLDL and chylomicrons. since VLDL are rich in triglycerides, this is how they decrease triglycerides. +  
lordxrequiem  but fibrates also decrease bile acid production by inhibiting 7alpha hydroxylase, which is how they cause increased cholesterol gallstones. +1  


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outQiens si niksag btuao tnspdaluceae mrssaogni eitgncifn DGC ntp.ietsa .loiEc is salo td.npsualaeec Cna nyneao exadpn no ht?si

keycompany  Step pneumonia is the most common pathogenic organism in CGD, and the most common cause of pneumonia, otitis media, meningits, and sepsis. While CGD are at an increased risk of encapsulated E. coli infections, however, they are at MOST risk for S. pneumo. This is kind of just a memorization fact that you need to know about S. pneumo. +  
keycompany  Sorry english is clearly not my shit, but you get the point +  
biliarytree220  CGD is susceptible against catalase-positive organisms (FA 109), of which S. aureus is the one to look out for. It's not about encapsulated organisms, like I had it confused in my head. +6  
.ooo.   You are completely right about E.Coli being encapsulated and is also a CAT+ organism and patients with CGD would have an increased risk of infection for both S. Aureus and E. Coli. How you narrow down the two is the most common infections are S. Aureus and Aspergillus (FA 109 like mentioned above) and also using the pneumonic "Cats Need PLACESS to Belch their Hairballs" (FA 128) Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E.Coli, Staphylococci, Serratia, B cepacia, H pylori +6  


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iunetosQ is ankgis tboua stnlcdpuaeea sosaingrm cintengif DCG etaspin.t .oliEc si salo pldnea.ucsate nCa neaony dxnpae no s?ith

keycompany  Step pneumonia is the most common pathogenic organism in CGD, and the most common cause of pneumonia, otitis media, meningits, and sepsis. While CGD are at an increased risk of encapsulated E. coli infections, however, they are at MOST risk for S. pneumo. This is kind of just a memorization fact that you need to know about S. pneumo. +  
keycompany  Sorry english is clearly not my shit, but you get the point +  
biliarytree220  CGD is susceptible against catalase-positive organisms (FA 109), of which S. aureus is the one to look out for. It's not about encapsulated organisms, like I had it confused in my head. +6  
.ooo.   You are completely right about E.Coli being encapsulated and is also a CAT+ organism and patients with CGD would have an increased risk of infection for both S. Aureus and E. Coli. How you narrow down the two is the most common infections are S. Aureus and Aspergillus (FA 109 like mentioned above) and also using the pneumonic "Cats Need PLACESS to Belch their Hairballs" (FA 128) Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E.Coli, Staphylococci, Serratia, B cepacia, H pylori +6  


submitted by keycompany(268),
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O, vgateRnih-e oblod is eth vlnseirau odorn for dlobo mlaspa.

keycompany  Edit:: Blood RBCs*** +4  


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naiglylkAt gtnsae ileremmn)a(rohcthe eh(t trheo grsdu ildets aer lecubirtumo btish)nirio nciesera teh risk of MA.L

keycompany  Additionally, AML is the only answer choice that has multiple blast forms (myeloblasts, promyelocytes, etc.). ALL is characterized by a single blast form (lymphoblasts). +25  
seagull  CML has blasts too but they tend to favor mature forms. +4  
kash1f  You see numerous blast forms == AML, which is characterized by >20% blasts +4  
keycompany  The answer choices are all of lymphoid origin except for AML and Hodgkin Disease. We know Hodgkin Disease is a lymphoma (not leukemia) and would present with lymphadenoapthy. So the answer must be AML #testtakingstrategies +12  
impostersyndromel1000  @atstillisafraud thanks for mentioning the merchlorethamine increasing risk for AML, i was trying to make a connection with the drugs but couldnt. Had to lean on the test taking skills just like key company +1  
sweetmed  Procarbazine is alkylating as well. +  
pg32  @keycompany how did you know the phrase "multiple blast forms" meant literally different types of blasts and not just many blast cells were seen? +3  
castlblack  this link says CLL has 'large lymphocytic variety' under the picture of the peripheral smear. I am not arguing against you, just researching here https://emedicine.medscape.com/article/199313-workup +  


submitted by keycompany(268),
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)E Crereabl issTeu pH oulwd rainesce edu to rrportaeyis .asaoklisl

keycompany  EDIT: Via the **Haldane Effect**, not the Bohr Effect. +  
impostersyndromel1000  excellent response +  
teepot123  fa 19 pg 489 +