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Welcome to ls3076’s page.
Contributor score: 65


Comments ...

 +0  (nbme22#7)
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Is eascdered rcntnlaou ctrseeion otn slpsoieb due ot hte nirucgtiyno tneweeb onste of otymssmp dan ksrote (2 oms uservs 3?) regeA taht esthe seosntqiu rea rvey guaev nda tsrutngif.ra otN rseu rweeh to get a ogod apgsr no isht mrla.etia


 +0  (nbme22#47)
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nca neayon lxaniep ywh D() iaastealmp si teir?ccron

angelaq11  because metaplasia would be a transformation of the normal architecture of the respiratory epithelium to one that does not belong there, in response to chronic irritation. This woman had pneumococcal pneumonia that was correctly (and I dare say promptly) treated, so she suffered an acute rather than a chronic insult. +
blueberrymuffinbabey  because metaplasia isn't how the normal healing/regeneration response happens in the alveoli. the type 2 pneumocytes serve as stem cells/precursors to both type 1 and 2 pneumocytes so the regeneration is not metaplasia. +1




Subcomments ...

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eArtf vheetgnryi its ujjts an pmeeid .qesu Belwo 55 vs oeAbv 55 rsaey

ls3076  can you elaborate please? +  


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hTe omts ttmarpnio inhst ot het iotsenqu rae as ofso,lwl with 2# igneb eht stom pfisecic:

1) tpneati rosertp ipan wtih oarheedv ontmio dna rtosrep retrcrnue daeohver noimto rdignu wor.k Oerhaved niotom can mgadea eht nusrsstaupapi ulscme deu ot emntinipegm yb the corin.moa

)2 niaP is twosr tiwh ilrennat otniraot of het oshderlu - hits is stnosnitce twhi hte nidifnsg fo teh eyapmcn-t se,tt ihcwh itesiacnd a sapaipnutusrs iynru.j

mousie  I was thinking along the lines of overhead motion - damage to the subacromial bursa which is between the acromion and the supraspinatus ... also its the most commonly injured rotator cuff m. so could have guessed this one right +1  
sympathetikey  Thanks for the explanation. I was scratching my head as to why this is correct, since supraspinatus only does 15 degrees of abduction, but you make a lot of sense. +1  
charcot_bouchard  IDK WTF i picked Trapezius +27  
ls3076  why would injury to supraspinatus cause weakness with internal rotation though? +6  
targetusmle  yeah coz of that i picked subscapularis +2  
maddy1994  ya the whole question pointed to supraspinatus ...but last line internal rotation made me pick subscapularis +3  
darthskywalker306  I went for Trapezius. That shoulder flexion thing was a big distraction. Silly me. +1  
lowyield  saw someone post this on one of the other questions about shoulder... and it works pretty good for this https://www.amboss.com/us/knowledge/Soft_tissue_lesions_of_the_shoulder there's some videos in it, this specific one for the question is the neer test +  
psay1  FA2019 pg. 438 +  


submitted by keycompany(269),
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hTsi uesqotin si i.uegidsds Wath etyh rae arelyl kiangs si "what is the sloe mtrndeaiten of ceepssi vrasvilu"? hTe noly ansewr is hte ltyabii to reeroct.pa ucaeBes DAN syaPlmeore sha figndrpaoero- iyaictvt, yeongrp ilwl be ctfeedufna by ARN rPsoeyselma cakl fo -afgeniorpodr y.vcittai

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.. +  


submitted by keycompany(269),
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sThi seqitnou is ssd.ugedii thaW yteh rae llarye akngis is "tahw is eht sloe etnieatnmrd fo ieescsp auslrviv?" ehT lnyo waesnr si teh iilbyta ot aopcr.rtee asuBeec DNA yoPemerlas ahs p-idrfrongaeo ytcavti,i eyrgpon lilw be audefecftn yb NAR elsyeoasmrP alck fo ofiorepadrng- t.ciyavti

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.. +  


submitted by colonelred_(91),
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ttelAutbirba skir = cdineince in esxpoed – ineniccde in xedeupsno

= 30/001,0 s)smoekr( - ,3/00030 rekmnno(ss)o
= 0.30 - 01.0
= 020. (os teh bttabutielar irsk is toaub %2)

ppniyAgl ti ot a lpianoptou fo 000,:10

= 020. * 010,00
= 020

charcot_bouchard  What if i tell you this is a ques of Attributable risk % in exposed? AR= 0.02 / IR in exposed (30/1000) = 0.6667 30 case in 1000. So 300 case in 10,000 0.6667 x 300 = 200 or in another word 66% cases of 100 lung cancer cases in smokers is actually due to smoking. so in 300 cases of smokers 200 is actually due to smoking +4  
charcot_bouchard  This is a mind fuck. Lemme tell u guys if any consolation while doing the ques during test i did it with AR = 0.02; NNH = 1/0.02 = 50. 50 persons smoke to cause 1 cancer. 10K smoke to cause 200 cancer. +1  
ls3076  Sorry if this is a stupid question. Why is it incorrect to simply apply the same proportion (30 cancer per 1000 smokers) to 10,000 smokers? +2  
krewfoo99  @is3076 Thats exactly what is did. I still dont understand how that is wrong. But i guess they want us to think about it in terms of AR +  
hhsuperhigh  @Is3076 and @Krewfoo99, If a person doesn't smoke, the natural risk of getting lung cancer is 30/3000=1%. The smoker's risk is 30/1000=3%. This 3% is not purely contributed by smoking, but mixed with the natural risk. So for calculating the pure contribution made by smoking, you should use 3%-1% which is 2%. And this 2% is the pure contribution of smoking. Not all smokers get lung cancer, the same thing, not all lung cancer among smokers are attributed by smoking. They may get lung cancer anyway despite smoking or not. +9  


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dDssreoir ocmomn in tesa siaA cancrgido ot HtitG:jeposaain l V BEB oinctiefn - motsyl gnaldie ot rhgnlyasepaano hACpAla siilTsomtaneaaihmaNsre edlkin eItitnslna ypet igcrsat CA

nI hist nutos,eiq sneci the tpiaten is tpsmoatyaicm nda VEB snti caetxly en"reecds o"fr, ntew twih pHBe sa hte earnsw

ls3076  i think asymptomatic is really the key here -- good catch +2  


submitted by sympathetikey(1027),
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ycuLk ioudc,dtne but loingko bakc, I lieevbe awth thye rwee niggo fro si awht ehs hdslou avhe eneb cnivadaect rof at 6 sthnmo fo aeg (ecins etrhe are on nratppea stmpsy.o)m

peH B neaicvc si slualyu eingv at bitr,h 1 nomt,h dna 6 otnhsm of gae, so s'ti eyrtpt tmrntpoia tath hse eb anecvciadt gsntaia it, uslsen seh yadelra sha ,it ni wchih scea seh lhousd eb dratete ot aoidv rshsio.cir

ls3076  how can we actually be expected to know vaccination schedules... there must be some other reason the answer is correct +4  
cbreland  I don't think we need to know that the vaccination schedules, but that the only other answer with a vaccine was adenovirus. I figured that there would have more symptoms if she had adenovirus (plus didn't fit the typical military recruit/swimmer demographic) +  


submitted by welpdedelp(203),
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hTe pt dah mhatas ,SBO( wesak pu at gntih otu of e,btrha sah lseeli)a.gr It eksda ofr teh rrucrepso of nuesrikeo,elt hcwih is accinaohidr aidc. eTh borp vega hmi lasMuonktte or adinhel gcdricoo.usoitcl

ls3076  wtf is up with the phrasing of this question +29  
djtallahassee  Must have been Montelukast right? Since GCs do more of a downregulation thing than a true receptor blocking. Maybe I am not reading that last sentence correct though. +1  
alexxxx30  @Is3076 haha agreed!! +1  
calleocho305  Thought this patient had GERD Induced asthma so I said histamine... Fixing GERD will normally fix the asthma and a h2 blocker would do that.. +3  


submitted by seagull(1181),
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tuo of tucryo,iis hwo yam oppele ekwn its?h todn( be shy to ays oyu idd ro dti?n)d

yM ptyoevr ecindotau tddn'i giranin shit in em.

johnthurtjr  I did not +1  
nlkrueger  i did not lol +  
ht3  you're definitely not alone lol +  
yotsubato  no idea +  
yotsubato  And its not in FA, so fuck it IMO +1  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +12  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +19  
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +1  
jaxx  Not a clue. This was so random. +  
ls3076  no way +  
hyperfukus  no clue +  
mkreamy  this made me feel a lot better. also, no fucking clue +1  
amirmullick3  My immediate thought after reading this was "why would i know this and how does this make me a better doctor?" +6  
mrglass  Generally speaking Glutamine is often used to aminate things. Think brain nitrogen metabolism. You know that F-6-P isn't an amine, and that Glucosamine is, so Glutamine isn't an unrealistic guess. +4  
djtallahassee  yea, I mature 30k anki cards to see this bs +4  
taediggity  I literally shouted wtf in quiet library at this question. +1  
bend_nbme_over  Lol def didn't know it. Looks like I'm not going to be a competent doctor because I don't know the hexosamine pathway lol +17  
drschmoctor  Is it biochemistry? Then I do not know it. +3  
snoochi95  hell no brother +  
roro17  I didn’t +  
bodanese  I did not +  
hatethisshit  nope +  
jesusisking  I Ctrl+F'd glucosamine in FA and it's not even there lol +  
batmane  i definitely guessed, for some reason got it down to arginine and glutamine +1  
waterloo  Nope. +  
monique  I did not +  
issamd1221  didnt +  
baja_blast  Narrowed it down to Arginine and Glutamine figuring the Nitrogen would have to come from one of these two but of course I picked the wrong one. Classic. +1  
amy  +1 no idea! +  
mumenrider4ever  Had no idea what glucosamine was +  
feeeeeever  Ahhh yes the classic Glucosamine from fructose 6-phosphate question....Missed this question harder than the Misoprostol missed swing +  
surfacegomd  no clue +  


submitted by niboonsh(299),
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hsiT si a easc of cuaet nrtapstlna nri.cetjeo wseek ot ntsohm earft teh la,annrsttp ienrcietp dc8 ar/don 4dc t elcsl are evittdaca nstgaai eht donro (a epyt 4 HR)S dna eht dnoor sastrt kmangi baodietnis aagnist het .tnalpstnar ihTs epestsrn sa a ivictsslau iwth needs sraitletiitn lyohitcycmp ilttnfrse.ai 28(10AF pg 911)

ls3076  Actually was confused about this due to a UW explanation. UW said acute txp rejection has two types - humoral and humoral and cellular. Humoral has Neutrophilic infiltrate + necrotizing vasculitis while cellular has lymphocytosis. Can anyone simplify/explain this please? +3  
apurva  We usually look for c4d complement for humoral response in acute graft rejection. Because c4d makes covalent bond with the endothelium can can be found on staining because it is long lasting. +  


submitted by nwinkelmann(265),
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So, I htuthog siht sqoituen was sepur vgaeu adn ton ge.art.. ttha ebing sdia, vahngi tngeto it rognw adn nto ryella anvhig a doog tnoixalpean rfo the swnrea, I idd a ltleti eracerhs nda nufdo tshi c:aelrti /s4r/st.o:flpo.63/0.aoau1itwp/T.11/1.a57w0RdgS/wn.h10drj.1h

ishT asw the mian uiolsnncc:o Te"h ltussre fo the renstep dts,yu eaidm ta nsisasseg eht fcsetfe fo sktore no xelusa tnifunicong, vrlaee a itafiingcns eilednc ni ii,dlbo ticola fuye,encqr xausle u,saorla dna fotnisitsaac ihwt xesalu flie in tboh eortsk nspteita adn hietr eous.sps The eprntes tsueslr sloa asnreottmed that rsdosderi of sxuale cniunostf are omts nsftinlcgaiyi esascatdoi htwi vriasuo pyohioclsacs tcf,arso scuh sa ste’pntai lgnaeer dtueitat toawrd uy,lsetxia earf fo ncote,ipem and blityia ot dscssui asi,xtleuy sa lwle sa whti het edreeg of tsokrtpeso nltucfaion a.iltdibysi ve,eMoror alxuse dicftynusno swa readetl ot hte eceeprsn adn rgeeed of ieodns,pser isetabde muiltsle, nad srralaaovcucid t.aicdienmo hTe otielogy or olitcnao of eth eoskrt dan eth dngree or triamal ttsuas fo eht pasitnte weer ton staesiocda itwh ahsengc in rkeoossptt tyaixeslu in ptatnies ni the erespnt u."ydts

oigkonL at hte uiotesqn a,gain mI' ugiesgsn eth itaefgu" dan fdulifiigntc egpilens nda rtccingeon"atn ettanemst swa duoppses ot be a celu fro orpdine,ess csaliepyle sicen it sedartt earft his rok.tse sAo,l no pcasyihl raiasnmbleito ssgtgeu ciigufntnno si itntac adn hust lcnorntua srtnceoei owdul eb vrsederep .nlyaomrl shTi is utjs t.dpius

ls3076  appreciate this kind of effort to look up journal articles but honestly this is not really what nbme answers is for... we should be able to get the answer from process of elimination/basic science concepts and not from looking up studies as we obviously can't do this on the test +  


submitted by alexb(43),
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tI sseem ilke a otl fo eth stcseiym ntmiueoaum eadisses aer .fatlculairtoim Is rheet a lernega rleu orf i?hts

ls3076  Really good observation +2  
acidfastboi  Never forget what our lord and savior Dr. Sattar says - environmental trigger in a genetically predisposed individual (aka multifactorial)! +2  


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raeIedscn esawt nad +Na enotaoitcnncr uodshl notip to icytcs rbiosfsi )FC(. Teh orbmelp tiwh FC si ton atth eth neeg si ebing traesrdibnc ,sles ubt atht het nprotei tath hte enge coeds rfo si ,detlera wchih dalse ot eth CF neahlcn iebng gddreead deu to n-liigsdmfo -&-gt; less FC sceerrtop no lcel rcfusae t-g&-; pnecphtoyi F.C

ls3076  why not membrane receptor? +6  
a1913  delF508 is a 3 base pair deletion of phenylalanine at amino acid position 508. Mutation causes impaired post-translational processing of CFTR (improper folding) which rough ER detects. Sends mutant misfolded CFTR to the proteasome for degradation, preventing it from reaching cell surface. So problem is not malfunctioning CFTR channels in the surface; problem is complete absence of CFTR on cell surface (since they keep getting misfolded and sent to proteasome to be trashed). Source of primary problem: error in protein structure +6  
angelaq11  @Is3076 because the CFTR is a channel not a receptor. +17  
rainlad  FA 2019 p. 60 +  
dysdiadochokinesia  @a1913 is correct- as for @angelaq11, you can still have a receptor that also functions as a channel as they are not mutually exclusive. An example of this is the nAChR found on postsynaptic NMJ neurons. This is a non-selective, ligand-gated, ionotropic receptor that functions as a channel once its ligand (i.e., ACh) has bound to the active site to induce conformational change. Similarly on the same realm: CFTR is an ionotropic receptor that concurrently functions as a Cl- channel once its ligands (ie. 2 ATP) is bound to open the channel and enable Cl- flux. This question in particular is asking for the underlying pathophysiologic mechanism for cystic fibrosis, which boils down to an issue with the primary structure of a protein resulting in its misfolding and subsequent sequestration/degradation. +1  


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ruO ttliel eifdrn sah a rrvaovsuiP n,oictenif whihc icnfset rtdhryioe ors,rcrpesu aisngcu trnruieotnpi fo hctyryeroet toiocpn.rdu Tsih is eth mesa awy it ecsaus rodhsyp telisfa in brnoun ibasbe dan psiatlca aimena in keilsc ,clle tc.e

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 +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 seagull(1181),
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fI uyo n'tdo wkno hawt iuromDlac sedo elik nya lmnora .mhnau hTe foucs on twah npiisar ost'ned ,od mealyn its' o'tsend factef TP imet nda otms sipll nt'do irnceeas gintcolt eyisac(lepl hwit sriiap.)n shTi si how I oiglc ot eth ghrit ea.swnr

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT? +12  
ls3076  Why isn't "Decreased platelet count" correct? Aspirin does not decrease the platelet count, only inactivates platelets. +4  
drmohandes  Because dicumarol does not decrease platelet count either. +  
krewfoo99  @usmleuser007 Because the answer choice says decrease in PTT. If you take a heparin like drug then the PTT will increase. Drugs wont increase PTT (that would be procoagulant) +3  
pg32  I think usmleuser007 and is3076 were working form the perspective of not knowing what dicumerol was. If you were unsure what dicumarol was, there really wasn't a way to get this correct, contrary to @seagull's comment. You can't really rule out any of these as possible options because aspirin doesn't do any of them. +2  
snripper  yeah, it wouldn't work. We'll need to know with Dicumarol is. +3  
jackie_chan  Not true, the logic works. You gotta know what aspirin does at least, it interferes with COX1 irreversibly and inhibits platelet aggregation (kinda like an induced Glanzzman), all it does. PT, aPTT are functions of the coagulation cascade and the test itself is not an assessment of platelet function. Bleeding time/clotting time is an assessment of platelet function. A- decreased plasma fibrinogen concentration- not impacted B- decreased aPTT/partial- DECREASED, indicates you are hypercoaguable, not the case C- decreased platelet count- aspirin does not destroy platelets D- normal clotting time- no we established aspirin impacts clotting/bleeding time by preventing aggregation E- prolonged PT- answer, aspirin does not impact the coagulation factor cascades in the test +2  
teepot123  di'coumarin'ol +