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Comments ...

 +3  (nbme22#37)
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Why wduol iopdnoetis of noirifbid tpssideo ..ei( bionfirdi alis/tngcreosniamn HTN) be rgown?

amorah  Kidney is smaller than normal, suggesting less blood flow to it. Won't see shrunken kidney in the case of HTN. +2
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 +2
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. +3

 +0  (nbme22#37)
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nl’uodwt icnohrc eypotirnnshe fo hte alLe-nr rtyera ceduni AASR aiavtci,otn nda hecne ulbatru pohryetpyhr iwth coraictl ?yhporta

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

 -2  (nbme24#10)
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Imgea oswsh resCtecn ginS, a moonmc gdiinfn ni binAldmao icArto eynArsmsu ude ot lmrua bsuhmrto oouscclni.

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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weAdrnes ym wno etouqnsi. cenedarsI ertsss mrfo a SEIMT iwll avetctai teh tystmhepiac vresuon msesty -- nuPmraoly adoaoltins.vi

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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Can dbmeoyso owh anesdtndur hyw VPR desrcsaee tihw a Ltde-idSfe iatcnfr ealspe ennlhgeit me. I lwudo olas teraeapcpi it if uoy codul ealetr it ot hirgt dsdie earth eilfaru oto e.i.( ohw dluow it c.gane)h

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. +12
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. +2

 +11  (nbme24#16)
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Tish tnaepti hsa a tmournaeophx. opineaytitllHvern si not henugo ot etmsoaecnp for hte rlvoela adcersee ni ngul usefcra rea.a

_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. +6
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? +2
bullshitusmle  there is no bilateral lung opacities as you would see in ARDS +4
jesusisking  Was thinking some sort of infection b/c of the atelectasis so picked empyema but this makes sense! +
djeffs1  does it need to be ARDS to cause "diffuse alveolar damage"? +
makingstrides  Not only that, does having a collapsed lung affect the alveoli? +

 +4  (nbme23#19)
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This ieuostnq si sdsdueig.i Wath eyth rae lerayl skiang is "twha si het eols eednrtnatmi of eissecp vuvilras?" The nlyo wanesr si hte lybtiia to aepertcr.o acsBeeu NDA omPelreysa has oerpdnf-iagro t,iayictv rpyegno ilwl be feendtcauf by NAR seaelPoyrsm kcla of -ogefrpnirado ctiyat.iv

ls3076  the phrasing of this explanation doesnt make sense to me. +4
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.. +

 +5  (nbme23#18)
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pTey I tDsiaebe is reeacrcadzhti as the tdetoinucsr fo cpnetairac esistl plief(saclyci aebt ls)lec yb Tslle-c. The tmos eylikl cesau orf eaohgmlyicpy wgflolnio liniuns ,asritnantidoim o,refreeth is eht codrtutinse fo hapal slelc ahtt urdsnuro the atbe ecsll. hTsi duolw csuae seraeeddc svllee of clagcnuirit logun.cga

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
prolific_pygophilic  I actually think this has some merit. I believe there is a U world question that talks about how very long history of T1DM (20 years in this patient) can progress to destruction of alpha cells and hence impaired release of glucagon and episodes of hypoglycemia. Thats how I reasoned it. The first answer is also possible. +

 +8  (nbme23#39)
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eiurgF ti uto trefa ngdirea a rveiew. BA/UUVV reund rmnalo smsercccnauit is rnecdideos nnniooigizn. veerw,oH hte nyol nerfdfeiec etbeewn nngooinnizi adn ionigizn aotndriia is hte tnsgetrh of eht aiotrniad rays. eeaBusc adotiairn edos nto pdsiaiste orfm the odb,y gonopreld VUB puerxose nac seacu tiinoarad to dbuil up ni eht sikn nad ascue an aiiotoninz ceffet. hTsi si eht aems esraon tath ievttipree -RaysX dan CT ascnS nac eecrisna ruyo isrk fro n,ceacr nvee yresa nwdo hte n.eli


 +6  (nbme23#39)
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aCn obemdyos aeselp ixpenal how igzinonnino iiantdaro ash an gzininio fe.cfet

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? +3

 +31  (nbme22#5)
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Ntoenirg acnelab si a usmeemenrta fo rtnoeip oablmmesti in the dyb.o A vneiateg tnioregn enlaacb deticsnia usmecl ls,os as serienadc manostu of onima icasd rae ingeb bltizeademo ot pecdour egry.ne ihsT scrniasee the ountma of otnierng tedecesr orfm hte ybo.d euacsBe eht unoamt fo nnigrtoe uyo ear tnkiga ni si ssel ahtn eth aotunm fo gietnonr oyu rea rgtsieenc, uoy evha a tingeaev tognenir anlceba.

hisT anm si sunli,rmdhaoe uoame,edst cct,iaech nda hsa m.empnbuliyihaoa heseT llcacnii nifnidsg piton ot orpiten tmrlaoniniut hKs(raowika sias)Dee, hwchi cssaeu damee due to derdecsae surem ccionot psreuser. woL toicnoc ussrreep in sthi aecs is eud ot roetpni ,slos dna neehc a evaitnge etgnnrio acbl.ane

drdoom  Nice! +21
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 .. +4
zevvyt  also, it says that his albumin is low. +

 +4  (nbme22#28)
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hWeli ihst esituqon mtes is agu,ev het mots elkyil iaodsgsin si rairtdHyee immtHosacosehor.


 +3  (nbme22#16)
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O, tvahRein-eg doblo is eth iuervsnal dnoro rof odblo pasl.am

keycompany  Edit:: Blood RBCs*** +4

 +4  (nbme22#7)
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dLoiagn Dose is eht lnoy aewsrn ahtt is etndenenipd fo gurd elra.acenc

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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nnMlaaied iesGnect:

nMa hsa /32 chcaen of engbi a .ricerar He( osed otn heav hte eais)des. Wmnoa rraeirc srki tmus eb uaetdllacc htwi ^2p + pq2 + .q^2 ^ q2 = 00,10/04 q = ,0/021 p si gluohry = p2q1 = 10/01 = Ceirarr feeqncuyr .

iRks of hvngai a lcdih stuh asuelq 3/2 x /1100 x /14 = 100/6uBca2:/ee s3 = Mna rarreCi iskr 0/11 0 = elFaem arrrieC sik1R/4 = nhceCa ythe aech sspa no hte rsicveese gene ot herti oprffgi.sn

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

 +22  (nbme22#41)
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sn:wAre enerIsdac ltnCera looBd mVoleu (B,V)C cesraeedD A,DH rceIseand .NAP

Teh haclooiglsypi npesoser to piheotmhrya is ctsvtiosonrciaon fo aeirepplrh elvsses ie..( eht noes ni ryuo estre)itexim in na oetffr to peke yuor cero byod uermaeeptrt lor,mna adn tush yuro arnosg ucgninonfti epr.orpyl rhiearlepP oscroanocnViitts liwl enairsce BCV. nIecrased CVB lliw uaces na ecnesrai ni re,dpaol dna hstu auces na aecresni ni BP/PNAN. /NPNBAP ash ritinibyoh sftcefe on het noe-nnnoergnlsoteAi-istneRdiA teSy,sm stinlreug ni cdrdeseae HDA.

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. +4
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 +
jurrutia  The excretion of free water also has an adaptive benefit in hypothermia (less mass for your body to keep warm). +

 +9  (nbme22#35)
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yrainrU rcatt seioinnftc aer teh otsm moncmo qdercuia ucase fo etorceuVisci ulxefR (RV) in edhlincr. RV acn aedl ot lRxuef hpoapyrNhet, whchi si zaehrrectcdia yb criochn itruttsitaneullobi tnolmfaminia hwti fsobiirs and inascgrr, lneagid to nrlae lia.uref

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 +44
spacepogie  I'd be happy to send them a gift card to purchase more stock images of kidneys for use in future exams... +19
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

 +18  (nbme22#35)
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aletorAnti fo hte oitsettarmch ste opitn si a aolihahytcmp csrsepo teiddmea by taagloindssrpn nad is ndenpdtinee fo hte tcephstimya nuoresv mtessy.

,B C, ,D and E lal rqeueri imcyhapstet srneve to tlcieil a espensro.

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

 +16  (nbme22#9)
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wloF aetR = Victyleo x ten-lrsosaSiCco raAe

2 mc^2 x 02 mc/sec x 60 nm/isce x 1 ,0/10L0 3c^m = .24 /minL

01,00 m^3c = 1 L

seagull  Well, I missed this one. I don't even feel bad. +65
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. +3
drdoom  1 centimeter is a distance. (A line.) +
drdoom  If we multiply a line by another line, we get a surface area. (A piece of paper.) +
drdoom  If we multiply the piece of paper by another line, we get volume. (A cube. A box.) +
drdoom  If we fill the box with a fluid, we will have 1 mL of this fluid. +
drdoom  If we have a thousand of these boxes, we have 1 L of fluid. +
drdoom  1,ooo mL = 1 Liter = 1,ooo centimeter³ +

 +14  (nbme22#33)
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vHyinitepoarltne acsredee O2Ca.P aeClrtn cesrhemceoortp sdnoerp ot wlo O2PaC yb astvgntcrocoisni arrcbele doolb vss.slee

A) lrieAart Blood gynOxe cnCetnoroiant: oBold ngyexO aitrnncnooeCt si yeicrdlt teerald ot bH rtcnintoanceo and aistrtanou aS2O() A9102,F p. 635. iVa hte hBro fEtcfe, dseeeadrc 2OaPC lwil nscareie ,Sa2O stuh scnnaireig dlboo gxoney nccetrtoaon.in

)B rlirtaeA loBod O2P: 2OaP nsacehg ni sensrope ot drscedeea A2O,P IOP2, or sdfoifn.iu rehTe uwold eb on gnheca in aPO2 dniurg hoanrilenitteyvp eht).(eocaitylrl

)C rAtaiel Pesrsure: eDrsaeecd 2OCPa si acitaodsse hwit irs,noitostncovca hwich dwoul ierecans ooldb er.rsueps

)E Crbreeal uTisse pH wdluo nrcseaei eud to taspreyirro oaass.klil

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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.2/etmMnws8g6tn0cwasiCbcop//mtp..h0l:P9/h/i/i5crnlvw.

srOel niSg si a vitolsstewi-y,in secl-ofitwicyp dinifgn of reMgbcenko tlroAiresrilocosse ()AM idtarazechcre yb a" llbpapae gahuhtol ep,lsslesu adiarl taryre liehw eht BP cuff si dentlaif vaebo lssoicty .rpreues"s

tI si plsseboi hatt at :eie)hr hTe tpfsc-ilecwoiiy fo itsh etts means ti is losa ceaaippllb to rtisroaecssloeh (otn tusj M)) Ab ehT MNBE otricerynlc imepisl ahtt AM is glrcaninetheba tiwh ctralr.ssheoioes

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." +17
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 ihknt I nudfo twah eth dssiaee aws, thguoh I hyontsel ahve no daie ywh ehty oldwu ttes iths rehatr than .XAL T’hrees a nintodcoi caeldl naenisTrt ylimpbemoHuailnogamag of nfaIycn. It resepstn /wowl inogillubmmonu lleevs ptos 6 thnsom dna acn esretnp /lwalms hlymp ednso adn lsosint in canifyn UBT o/w any orteh nidgnsfi fo paimyrr onumncciidfeiemy liicnungd aserdeedc .utcnos

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uYo leyeftndii t’don ened to kown the isedsae to get hte otcrecr enwars nceis eth iknl fo kcla fo ngnluiimolumbos uolwd celu uoy noti hte kcal fo rgnemial ets,rnce tbu I tinkh this is roem iylkel than LAX csine eevyr esorcu I ared pslmeii ttha B lcle snucto aer rean 0 ni het clsisac erpoanttnesi eun(sls I’m insmigs a nesora wyh yekuoclet uonct dffw/i owdnut’l oswh a itcasiingnf deeersac ni mpcoytlshye edu ot narzreeo- B slec.)l utJs wtdnae to tpu thsi rehe ni acse eothr loeppe rtael mcae rgiwnod,ne uoghht I amy illst be r.wnog

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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liayAkngtl santeg itrrhoehnla)ceemm( (het rhote sudrg idtsle era eicmlburtou oibt)rishin esairnec hte iskr fo L.AM

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). +27  
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 +9  
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 +  
jurrutia  @keycompany, how did you know it had to be of myeloid origin? +  


submitted by k_tron_3000(32),
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hTe odiieprstcn fo leiblraat orelw lbim loss fo irobtanvi ipesilm LMDC agd,aem and eth sntaeb sTDR + obRegmr smee ot em to eb lgpimiyn ttha eh oibspsyl sah sbate rilodsas rmof lsypisih ro( hsegnotmi eyvr lirisam ni oneainrpett).s

As ofr hte rohet wrsaesn, A si ngrow ceebaus sih tmroo cioutfnn is ,actnit B is gworn abceesu nipa and trptaemreue dftcsiei aer ont ieednmto,n C is owgrn ubsceae it lmpsiei a cpifecis vrene is etra,dnpep ubt he sah solt belraatil tnoianses in hsi eenirt wolre exmriteiest

D si the kiecrtsi,t and m’I ont 1%00 ue,sr ubt I wdulo kntih ytdahliupcaor fo teh otrierna vn)tea(lr srtoo duwol uecas romto tfisiecd eisnc eyth yrrca otmro tee.rsffen Yuo mthig asol exptce ahtt motro uycnsdtinof to eb nelt,aualri nceis ti dulow be ellnukyi to hvae a lerombp tihw eth reenv rtsoo on hobt ds.ies slao hte CMLD is nto ectload rnea teh rreinota toosr of teh npalsi dr,oc so if eth iorterna sorto rwee teefafcd ouy elaylr wtnduo’l peetcx to ese ivrybarto ls.so

So lbacsyali rsceosp of e,tmonnliiia I do eefl keil sonysre nuephoyatr is an eeylexrmt gevua wnaesr guhoth adn I stw’an a nfa fo eht utoqs.eni

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). +31  
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. +16  
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 +11  
jurrutia  "Radiculo-pathy" comes from latin terms meaning "root-disease". +  


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urO illtet nfider sha a Posrrvviau ion,ietcfn cwhih tefcnis hderyirto roscrpseur, nsiagcu ettunrniripo of tehyrryctoe tip.oodrunc ishT si het msae awy ti scuesa osdyphr atsfile ni nruobn baibse dna stilacpa naimea ni likecs ,cell t.ec

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. +27  
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 +3  
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 n!dfeoscu Teh onyl goilc I lcdou meco up w si tath NADISs csdearee lniditao fo fneetafr arieertol os shti eomr irendocctst elaoerrit is ieptrntdere as edreecasd ldoob owfl dna Rinne asr?ciesen My sseiu w hsit si ttha wehn I oogelg it nad rhecas WU ofr tihs nneir fctafe htgonin esomc up ylno cielatr I clduo nifd cllatauy cncisotatdr it dan sasy inenr ulowd EESDEARC mrof DIAsNS lgindea ot the emphelayirak ew esmtiomse ees ...

ynA sgtuhoht uwdol be e!uhlflp nThaks .seeiugsn

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). +9  
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_(107),
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yalrNlmo teh irchaonad liivl sirdna hte CSF fmro teh iorduhbscana aceps ot het seuonv ysmse;t if hsti tarp mobscee deeeifctv enht you anc aienigm lla atth FSC wno glbnuiid pu ni the bsrnocauaidh acspe.

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. +16  


submitted by calcium196(11),
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MENB 20 hsa a iqntsoue ihwt a ygu inatgk vreo the ntouerc uhocg ocitamiedn nad now he ahs tsi.nnapiocto tWna ot suesg eth rewa?ns tI saw terxod! tg&;- n//mt/neoee0mermhwx2mt54a.b/a8:pnsc/bss

So I’m tyrept urse eht BNME 22 ntsueoiq si sutj rightsta pu nowg.r

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(47),
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nu'dothlS het etrtenatm orf GpTrehy eb a tarfeisb? chiWh uwdlo aeidcnit het asernw ot eb cenriaisgn DLH 2F1A0(7. 0)6p3

I see egcaidnsre DVLL as a nfcointu fo nain,ci ihhcw ressev to aeceerds tcpaehi L.VDL.

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. +2  


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uoneQsti si isnkga boatu utclneapeads riasmsogn niniftegc DGC eatpst.ni .oElci is slao n.eapsletdcua Cna enayon apxnde no hist?

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 +11  


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Qotiensu si ngaisk uatbo alndutpsceae grosanmsi fntegicin GCD nas.tepit oi.Ecl si olas .auestaepdlcn naC noeayn xeandp on i?hts

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 +11  


submitted by keycompany(311),
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,O t-higeRaenv oobdl is hte earinvlus rdnoo ofr olobd a.slpam

keycompany  Edit:: Blood RBCs*** +4  


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Aiyalnlgkt asgetn e)hotnmi(reelrhmac te(h eorht gsrud siledt rae iuborutlecm iirsti)hbno aenrices eth irks fo MLA.

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). +27  
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 +9  
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 +  
jurrutia  @keycompany, how did you know it had to be of myeloid origin? +  


submitted by keycompany(311),
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naHitvlrypeioetn esadcree PO2a.C ntelarC peecchmerosotr opdnsre ot wol a2COP yb ocnitsirscgvntao rlceareb ldoob ssvsee.l

A) rAatirle Blodo geOxyn ortntaneconCi: oldBo Ogyexn ornntoaicetnC is ercdlity latdeer ot bH acrnotoncniet dna utsanaiotr aO(2S) ,21A9F0 p. 536. Via the rohB Eftfec, redseaced 2OaCP wlil raiescne 2aS,O htus eansnigcir odbol gnyeox .ntnnteioorcac

B) erritalA oBlod P2O: 2POa gshcena in rseseopn ot deeadesrc ,POA2 I,O2P or nifud.isof reeTh ludow eb on ceahgn in aPO2 drguni yornttilnevihepa liee)(orlhattyc.

)C rlitAae srsPruee: caedreeDs OPaC2 is casaoeidst wiht cioorsnncatotv,si hhciw oludw ceeiarsn lobdo essrr.upe

)E eaebClrr Tsuies Hp dluwo cneearis eud to eyrprriasto lisasa.okl

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