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Welcome to ls3076’s page.
Contributor score: 72


Comments ...

 +0  (nbme22#7)
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sI eaecserdd unnlarcto ietnoscre otn plbiesos deu to hte inoyingrcut etwbene ntsoe fo sopsmmty nad tokser (2 smo ssurve 3?) eAerg htta shete isonsqute rae vrye aveug dan tarnrguit.sf Not reus hrwee to egt a good sapgr no ihts .etilrama


 +0  (nbme22#47)
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can nynaeo lnieaxp hyw D)( aaspiemalt is octrrc?nie

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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rfetA ytneerivhg sit sjujt na edpeim sq.ue leBow 55 vs ovbeA 55 esyra

ls3076  can you elaborate please? +  


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heT sotm miroattpn ithsn to eth entiousq aer sa ,lflsowo iwth #2 iebgn het tsmo scip:eicf

1) ptieant osetprr anpi itwh ehovreda tnmoio adn portres rrrnetuce oehadrve tonmoi nurdgi wro.k hdeaOrev oomtni cna dgamea the sitasrppuausn cemlus edu ot iegntpnimme by hte am.coionr

)2 inaP is wsort hitw intalern inoratto of hte dosehlur - shit is cetontissn thiw teh nfdsinig of teh -ytpnceam t,ets icwhh sediictna a strausuipnasp u.yijrn

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 +34  
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 +1  


submitted by keycompany(301),
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ihTs souqeitn is i.issgeudd Wtha ehyt aer rlaely ngkias is "hwta is teh lseo mntreenaitd fo csispee vurasliv"? heT olyn nesrwa is hte tylaiib ot .ecarrepot uBecsea ADN omPryselae sah ofrog-ndpriea titciva,y gorpnye lwli eb tuefaednfc by NRA lresPmayoes aclk of rgnpoeadio-fr tiaicy.tv

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.. +  


submitted by keycompany(301),
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Tsih seioqunt is udegdsii.s hatW yeth era lyelar kgasni si "what is eht sleo emedrntniat fo pssiece urivvsla"? heT loyn wesrna is teh tiyabli ot r.peceoart euecsaB DAN esolrmPaey sha deorani-oprgf t,ciayvit yronpge lliw be autfeenfdc yb NRA alPryomssee kacl of ogdprnr-oeafi .vtiiacyt

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.. +  


submitted by colonelred_(99),
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bbeAiuattltr kris = cnidecien ni edspoxe – cienceind ni poeeudxns

= 30,0010/ )orke(sms - 030,/003 srk(mo)senon
= .300 - 00.1
= 0.02 (so teh rtbbitaluate srik si abuot 2%)

iAplyngp ti to a opaolitnpu of :01,000

= .200 * 00,001
= 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. +11  


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rieodDsrs nommoc in atse iaAs iacgrcnod to H tnijGtalisaeo:p BBEV ienoftnic - lsymot glaiedn ot neorhgsaaynpla AalhCpA aireasmholi taemiTsnsNa kledin ntInaestil etpy rctisag CA

nI shti q,uetisno eiscn eht pnattei is ytpmtmaaciso dna BEV ints etxaylc rseenedc" "fro, wetn iwth HBpe as eht nawres

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


submitted by sympathetikey(1265),
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Lukyc cdt,ieodnu utb niklgoo cb,ak I ebiveel htwa yeht eerw onigg rof is thaw seh uhlods hvae nebe caatevnicd for at 6 hsonmt fo gea c(sien rehet rea no pneptara )smmpstyo.

Hep B cniacev si salyulu gvnei ta ribht, 1 ot,nhm nad 6 shtomn of gea, so s'ti ertpyt niparttom taht seh be ctdeavainc sitnaag ,it slsenu esh rleayad hsa ti, ni hwhic eacs she houlsd eb eetdrta ot aidvo ri.ricoshs

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) +  
koko  Why does it have to be something with a vaccine? RSV Is extremely common in babies,shouldn’t screen for that? +  


submitted by welpdedelp(219),
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heT pt hda athams B(,SO kswea pu ta hnitg tuo fo atbhe,r ash le)esrilg.a It sekad for eht rpourscer of e,klsreeotuin hicwh is inoiraacdch a.cid heT pobr aveg mhi etaultknosM ro ldianhe coocrlosgictu.id

ls3076  wtf is up with the phrasing of this question +34  
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.. +4  


submitted by seagull(1443),
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out of citsiyour, hwo yma loppee nkew i?sht (todn eb shy ot ays uoy ddi or t?dd)in

My yrptveo nectidauo iddn't ganirin tish 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 +14  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +27  
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?" +7  
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 +21  
drschmoctor  Is it biochemistry? Then I do not know it. +4  
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 +1  
surfacegomd  no clue +  
schep  no idea. i could only safely eliminate carbamoyl phosphate because that's urea cycle +  
kernicteruscandycorn  NOPE! +  
chediakhigashi  nurp +  
kidokick  just adding in to say, nope. +  
flvent2120  Lol I didn't either. I think this is just critical thinking though. The amine has to come from somewhere. Glutamine/glutamate is known to transfer amines at the least +1  


submitted by niboonsh(338),
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siTh si a asce of tucea lrnsttnapa ceoni.tjer kwese to sonmht taefr eth a,npartsltn rieencpti 8cd n/raod d4c t eclls are atetdvcia iagnats eht nrodo a( ypte 4 S)HR nad teh doron sttsra mgknia neioadtibs gaisnta eht l.aatrnsptn Tish ensseptr as a tlsciisvau with dnees lnitaeirttsi mcoichyptyl taerti.infsl A0821F( 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(285),
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S,o I tuhogth tish otqiunes wsa resup ueavg dan nto .re.tag. hatt gnebi ais,d navhig nogtte ti gwron nda ont larlye ahvign a odog alntxeipano orf eht e,rwsan I ddi a ietltl ehcsarer dan dofnu htis acri:tle 3w/0la./oTas0.1/w.hodf7p.aRp11usgw1.itrSt.6n054.//j11h:r/od

isTh was het anim in:cconusol "heT tlseurs fo het erepsnt ,ystdu maeid at ssagssine het efcftse of skrtoe no uslxae inuicngon,tf verael a iiistnncagf edclien ni ilbd,io tclioa qre,ycfeun sauexl ,aosluar dna atonciaisstf thwi lsxeau efil in hbto krsote tintpaes dan threi essos.pu The enrptse tesuslr laso temsneortad htat srdsedoir fo sleaux cnonutsfi rae ostm islinyfcatnig doacsietsa wiht aosivur slhysiopcoca ,trocfsa chus sa taispnet’ aleenrg tuadetit rawotd uixatse,yl raef fo ete,oincmp dan iayibtl ot siucdss tse,iyxlau as lelw as tiwh hte reedeg fo skeoropstt uannftlcoi ditbaii.sly eMvrre,oo sxlaeu foyncdusnti was rletaed to hte enpersec dna edgere of psrn,oeides ebitaesd usei,ltlm nda rdauaclsorcavi .dmeacntioi Teh itgoeylo ro oolicatn fo eth rkseot dan hte deegnr or lrtmaia utssta of eth sipteatn eewr ont aadtoceiss hitw sehacgn ni oektrsostp ltayiuesx in ittensap ni hte sreeptn .t"sdyu

Lkogino ta het iqnsuteo nai,ga m'I snggeisu eth gau"itfe nda dntifuciigfl gesilnep nda tne"tcngicaonr tsetetmna aws puposdse ot eb a ucle rfo edripensso, elasliycep scnie it ttsared tfare ish korest. ,sAol no lyihaspc tliaimbreonsa segstgu cugfitnionn si anitct dan htus uaclonntr rtonseeic udowl eb sepredrev m.lnyolra ishT si usjt uidpst.

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(46),
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It eemss lkei a lot of the sscmtiey ueinouammt ssediase ear ci.uaforlttialm sI reeht a erlngea relu rof hi?ts

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)! +3  


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nrsIecdae westa nad +Na eccronntnioat lhduso pitno ot ytscic fsoiirbs ()CF. ehT plmrebo ihwt FC is ont ahtt the egne is gbein arestcbndri sle,s ubt atht hte reitnop ahtt hte geen dcseo rof is edelr,ta hicwh saeld ot the CF cleahnn eibgn dgaerdde eud to sfinmgo-dli t&-;-g esls CF roeectrsp no cell fasruec t;g&-- theipnyocp C.F

ls3076  why not membrane receptor? +7  
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 +7  
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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Oru tellti nedrif sha a iuaPsovrvr iitn,enocf whihc tfciesn yoiredtrh rcssoer,rpu cigusan tntriruinope of tyrceeyhtro udoopcrn.it ihTs si teh eams yaw it scaeus shroydp staeilf ni burnon bbseia adn tplicasa eaamin ni ekicls cl,le .ect

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. +23  
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. +  
mdmikek89  Honestly y'all lmao First line...RED CHEEKS AND RASH Malar Erythema --- Hello? Rash - Eventually it may extend to the arms, trunk, thighs and buttocks, where the rash has a pink, lacy, slightly raised appearance Hemoglobin is 1 g/dL below normal. This is Parvo B19 -- SLAPPED CHEEK. I swear man, y'all make this easy nonsence. WAY to hard. +1  


submitted by seagull(1443),
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If uoy dto'n know thwa coriumlDa oeds lkie any aorlmn .naumh eTh suocf on ahwt niairps n'odste ,do mylnae t'si sot'edn aftcfe PT meti nad osmt isllp ont'd esrecian ctlgoitn (yecaesplil tihw iira).nps hTsi is hwo I locig ot het trghi saw.ner

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT? +21  
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. +4  
snripper  yeah, it wouldn't work. We'll need to know with Dicumarol is. +4  
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 +3  
teepot123  di'coumarin'ol +