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Contributor score: 84


Comments ...

 -2  (nbme24#29)

Up to 80 percent of aortic aneurysms are caused by "hardening of the arteries" (atherosclerosis). Atherosclerosis can develop when cholesterol and fat build up inside the arteries. ... Elevated blood pressure through the aorta can then cause the aortic wall to expand and bulge.

https://www.uwhealth.org/heart-cardiovascular/aortic-aneurysm-causes-symptoms-and-concerns/10971

Also, FA 2019 pg300 says complications of atherosclerosis includes aneurysm

almondbreeze  I was dumb and went for marfan.. +1
llamastep1  Wrong question lol +4

 +2  (nbme23#4)

FA2019 pg.479 + spina bifida occulta: failure of cudal neuropore to close, but no herniation + anencephaly: failure of rostral peuropore to close --> no forebrain, open calvarium


 +1  (nbme23#49)

Testosterone--> dihydrotestosterone (DHT)

DHT + early - differentiation of penis, scrotum, prostate + late - prostate growth balding, sebaceous gland activity


 +4  (nbme23#22)

other answer choices

black fly - onchocera volvulus (river blindness) tsetse fly - trypanosoma brucei (african sleepling sickness) deer fly - F. tularensis

peridot  Also, deer fly can transmit loa loa (FA 2019 p.159) in addition to F. tularensis +

 +1  (nbme22#20)
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FA 0912 gp 545 no avsraluac nseicors of tb o:eonrInafnic of bneo nda rrwo,am lluyaus very fan.uilp otMs mnmcoo etis si remaofl dahe w(rdehesta )zone (deu ot cnncysifiefui fo emliad xrilfumcec rlafmeo )ye.ratr seaCus ledciun erdotr,istoiocCs coihllsAom, kcleiS llce ed,iasse rT,amua EL,S t"he ns"Bde iorssom(onepcssae/dnic as,ede)si vg-EgLlaC-e ehstPre easdise cho(d,ita)ipi uhaGcer eias,des elpSipd tclaiap marlfoe ip-seyiphs SASCT endB G.LSE


 +1  (nbme22#34)
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:uw EVB momlnoyc csnteif B leslc, tlainitgmus ehtm to eertn eth lelc eylcc nad rtiolfrpeea lcuosytionun afaornsotnrmti"( or t"liionmizarmt"oa). thsi is cisldmhocape whne VeBndE-code ctvaeait itrevrliaeopf and tatioapctop-ni ngigisanl haatpyws i/w hte eecnfdit B cell. ... eth ziammirelotd B lscle aniatimn hte ilyatib ot tsreece Ig and l-Belc vinocttaia tuocrpsd eg.( ,D)3C2 htwi reyv fwe of htme elgnaires isrvu ciatplers at ayn neo emi.t


 +2  (nbme22#28)
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W:U eht thsor tisgcar vv rinad boldo fmro teh cigasrt fnuds tino het pcesinl ne,vi natapeccri nalmotmaiifn .eg(. e,asaicrintpt acciatnepr ac.) can uecsa a boldo clto /iw hte cnilspe env,i cihhw can ecasrien rsuserep ni eth hrsto irstagc esvin and dael ot irtcags eiarvs noly in eth sudnf

almondbreeze  b/c pancreatic causes can form blood clot in splenic v, b/c splenic v runs behind pancreas +

 +10  (nbme22#19)
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a doog icp iwsghon amnsoaulo traerise ni oeorhsesh ykedin

/nesoiesw_reorcorsthcsPt9-.r-3teahwda-e-onrfe-l1Aaorr-sw:7o2ik-hc-cw9ea-cge_eaneayfe9pret-ghsio/t-1sfishsf-3rus3ei//rettgahetpey.it


 +2  (nbme20#14)
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d'ounr, asrnrptieetasmn suelnod'

F0912A .374p says CCsB rea yaxw, ,nkip prlyae odulens





Subcomments ...

submitted by karljeon(118),
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A amn ithw a Hx of EtOH dpneeedecn nda honcric dba npia as lwel as aXry- igdnifns of tcacnisaii"lofc in eht emupi-pdr enbdoma" is tosm llkyei fnierrgre to a nocihrc sittr.npaaiec

sTih asedl to a ckal of peisal sotcinree ece,nh eapl, ugnesflliml-o ostlso hwti ilo toespdlr erp pt Hx. hTsi tps' csenarap oals onte'ds eectser herto ymzen,es uhcs as a,lsmyesa opetes,ras rno tingerpnoys t(o vieaattc rothe s)meyzn,e os eht srnwea is ee"dnizaeglr oasb".omlrtnipa

karljeon  p. 367 (FA 2018) +11  
usmlecrasherss  pancreatic insufficiency FA 2019 p375 , +2  
almondbreeze  FA 2019 p391 on chronic pancreatitis +  
almondbreeze  UW: in chronic alcoholic pancreatitis, alcohol induced secretion of protein rich fluid precipitates in pancreatic duct--> forms ductal plugs that calcify +3  


submitted by karljeon(118),
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A nma iwht a xH of tEHO pncededene dan icnrcho bad ianp sa llwe as y-Xra ingndfis fo oain"cctafcisil ni hte rmpipe-du ao"bedmn is toms ielykl enfirrger to a ochnric ntrceapaitsi.

shiT alsde ot a kalc fo paleis irnotcsee ehe,cn ,plea film-lgsnloeu oltsos thiw loi stopldre epr pt H.x hiTs ps't prcnseaa aslo o'setdn resctee ehrot eensm,yz hucs sa asysemla, rosa,eptse nor syertnipong ot( tvaectai erhot smz)yeen, so eth wasnre si rzieaedln"eg bamronoip"al.ts

karljeon  p. 367 (FA 2018) +11  
usmlecrasherss  pancreatic insufficiency FA 2019 p375 , +2  
almondbreeze  FA 2019 p391 on chronic pancreatitis +  
almondbreeze  UW: in chronic alcoholic pancreatitis, alcohol induced secretion of protein rich fluid precipitates in pancreatic duct--> forms ductal plugs that calcify +3  


submitted by mousie(220),
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ndsr"ea"ot ear aooss,pspntBehhi mmcylnoo dues to ertatpvt/enre rotspeso.osoi otsM ocmomn redesav tesfefc aer sEiatpsgoih pantties( losdhu etka with aewtr adn be hrpiutg rfo ta stale is,mu30ent) itorscnOessoe fo het aw,j adn taacilpy eflarom ertsss .srfuearct e-katn ghtir rfom AF 2108 pg 147

almondbreeze  FA 2019 pg 248 pill-induced esophagitis : bisphosphonates, ferrous sulfate, NSAIDs, potassium chloroide, tetracyclines +3  


submitted by neonem(572),
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I nihkt mstaeasist swa hte tsbe toinop eerh eeucsba ehret rea etullmip lintmgnaa eo..lmss.pan arrpiym rneascc dnte ot start sa a lgeisn msas in the ssietu fo irogni. In eht l,gun ssteataems ear emro mmncoo anth rrmypia .snplmoase

dbg  I seriously could not figure out whether those white opacities were actual lesions or reflections from the actual picture (flash light) ... mind went all the way maybe this is the shiny pleura so they're going after mesothelioma. smh +6  
dbg  shiny pleura with tiiiiny granulations if you look closely. but obviously was far off +  
et-tu-bromocriptine  "Multiple cannonball lesions" is indicative of a metastatic cancer. I think if they were leaning towards a mesothelioma, they'd show the border/edge of the lung ensheathed by a malignant neoplasm (see image): https://library.med.utah.edu/WebPath/jpeg1/LUNG081.jpg +4  
bullshitusmle  guys something I learned from NBMEs is that if there is a clinical vignette dont even look at the images they give you ,they are all useless and time-consuming +1  
goaiable  The way i narrowed it down was that the patient had signs of weight loss since three months whereas her cough developed recently (3 weeks). If the cancer arose in the lung then I think the cough or other pulmonary symptoms should emerge earlier. +1  
almondbreeze  FA2019 pg 669 in the lung, metastasis (usually multiple lesions) are more common the primary neoplasms. most often from breast, colon, prostate, and bladder ca. +1  


submitted by colonelred_(107),
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odeoLk ti up nad odufn ahtt uesaebc yu’roe ni a sipneu sinitpoo for a long teim eru’yo gnogi ot hvae adinersce vsneou nrtuer whcih dlsea to crsdneeia .OC hsTi tavengiyel kfebdscea on ASR,A aneldgi to arcsdeeed dolnersoeat. sA a tu,lsre euo’ry iggon to veha eraisndec eiissrud iwhch eslad ot edcseerda bodlo nda laaspm e.umvlo

medstruggle  Doesn’t supine position compress IVC leading to decreased venous return? (This is the pathophys of supine hypotension syndrome.) There was a UWorld questions about this ... +4  
tea-cats-biscuits  @medstruggle *Supine position* decreases blood pooling in the legs and decreases the effect of gravity. *Supine hypotension syndrome*, on the other hand, seems specific to a pregnant female, since the gravid uterus will compress the IVC; in an average pt, there wouldn’t be the same postural compression. +8  
welpdedelp  this was the exact same reasoning I used, but I thought the RAAS would inactivate which would lead to less aldosterone and less sodium retention +3  
yotsubato  You gotta be preggers to compress your IVC +5  
nwinkelmann  Could you also think of it in a purely "rest/digest" vs "fight/fright/flight" response, i.e. you're PNS is active, so your HR and subsequently your CO is less? But the explanation given above does make sense. Also because I think just saying someone is one bed rest leaves a lot up for interpretation, maybe not with this patient because his pelvis is broken, but lots of people on bed rest aren't lying flat.... ? +1  
urachus  wouldnt low aldosterone cause low plasma sodium? choice B +5  
kpjk  could it be that, while low aldosterone levels decrease plasma sodium levels- there is also decrease in blood volume(plasma),so there wont be a decrease in the "concentration" of sodium +4  
almondbreeze  FA 2019 pg 306 on Lt heart failure induced orthopnea - Shortness of breath when supine: increased venous return from redistribution of blood +  
almondbreeze  if there was no HF, it would lead to increased CO --> decreased aldosterone +  
theunscrambler  @peqmd thanks for sharing that. According to the presentation, the diuresis via ANP occurs (along with sodium), which is followed up by an increased in RAAS --> maintains sodium levels. This cycle can then continue. Slide 13. +  
jj375  @urachus - Either BB or Sattar taught me this but I feel like it is often forgotten. "RAAS/Aldosterone affects blood volume, and ADH affects Na level". So Increasing aldosterone will increase blood levels however water follows the sodium so you will not get a change in sodium levels. ADH however does affect Na since aquaporins are bringing in water without affecting sodium levels. +  


submitted by colonelred_(107),
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eoodLk it up adn unfod htat besaeuc uroy’e ni a uesnpi siontpio fro a gnlo time ’eoryu ginog to aehv esdareicn ouvens euntrr hichw dslea to eridenasc O.C sihT geyanltiev dsecaekfb no ,RSAA nialged ot daderscee tdslenoeor.a As a ,tsuerl y’roue ggoni ot ahve ercidanse usiedsri ihhwc eslad to secrdeead boldo nad mpsala eomv.ul

medstruggle  Doesn’t supine position compress IVC leading to decreased venous return? (This is the pathophys of supine hypotension syndrome.) There was a UWorld questions about this ... +4  
tea-cats-biscuits  @medstruggle *Supine position* decreases blood pooling in the legs and decreases the effect of gravity. *Supine hypotension syndrome*, on the other hand, seems specific to a pregnant female, since the gravid uterus will compress the IVC; in an average pt, there wouldn’t be the same postural compression. +8  
welpdedelp  this was the exact same reasoning I used, but I thought the RAAS would inactivate which would lead to less aldosterone and less sodium retention +3  
yotsubato  You gotta be preggers to compress your IVC +5  
nwinkelmann  Could you also think of it in a purely "rest/digest" vs "fight/fright/flight" response, i.e. you're PNS is active, so your HR and subsequently your CO is less? But the explanation given above does make sense. Also because I think just saying someone is one bed rest leaves a lot up for interpretation, maybe not with this patient because his pelvis is broken, but lots of people on bed rest aren't lying flat.... ? +1  
urachus  wouldnt low aldosterone cause low plasma sodium? choice B +5  
kpjk  could it be that, while low aldosterone levels decrease plasma sodium levels- there is also decrease in blood volume(plasma),so there wont be a decrease in the "concentration" of sodium +4  
almondbreeze  FA 2019 pg 306 on Lt heart failure induced orthopnea - Shortness of breath when supine: increased venous return from redistribution of blood +  
almondbreeze  if there was no HF, it would lead to increased CO --> decreased aldosterone +  
theunscrambler  @peqmd thanks for sharing that. According to the presentation, the diuresis via ANP occurs (along with sodium), which is followed up by an increased in RAAS --> maintains sodium levels. This cycle can then continue. Slide 13. +  
jj375  @urachus - Either BB or Sattar taught me this but I feel like it is often forgotten. "RAAS/Aldosterone affects blood volume, and ADH affects Na level". So Increasing aldosterone will increase blood levels however water follows the sodium so you will not get a change in sodium levels. ADH however does affect Na since aquaporins are bringing in water without affecting sodium levels. +  


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eiFocbrtnni is an lleetrxaruacl arximt ry,pgenoticol eihwl iamln is an ieimattednre mfiteanl that iialyelpfcsc vseidrpo utrppso ot teh lcel ne.uucsl no’tD usnoefc minal ithw inilnam cc(seine hstea su )ll;ycrea naimiln si ikel n,tcfiboenir na CEM egoyponltrci nda a oarjm meonotnpc fo eth albsa mniala fo tbanemes .reeabnsmm

masonkingcobra  Lamin looks like a "cross" and held up Jesus and the basal lamina is super important just like jesus (you bet there are people who believe this) https://answersingenesis.org/biology/microbiology/laminin-and-the-cross/ +35  
dr.xx  blasphemy @masonkingcobra +1  
luciana  I clearly confused lamin with laminin, now I know +3  
almondbreeze  FA 2019 pg 48 lamin +1  
almondbreeze  picked tubulin but i guess tubulin makes up microtubules and therefore is spherical +  
abkapoor  Also remember progeria is due to lamin a dysfunction, and progeria patients have messed up nuclei +  
brise  @abkapoor the f is progeria? and do we need to know it for step? +  
brise  @abkapoor omg jk jk wow +  


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inoebncirtF is na rlleuaxareltc rmtaxi yclopinto,egr iwhle lmian is an idetentmaire emaltfin taht flaylpciices erovspdi otsrpup ot het llce s.luneuc nDo’t efcsnou laimn twih miannli en(sceci heats us ;lay)lcre nnialim is ielk tf,onrniebci na ECM yilcprogtneo adn a jmaor nencoopmt fo teh lsaba iaalnm fo eabemsnt ae.mrbemsn

masonkingcobra  Lamin looks like a "cross" and held up Jesus and the basal lamina is super important just like jesus (you bet there are people who believe this) https://answersingenesis.org/biology/microbiology/laminin-and-the-cross/ +35  
dr.xx  blasphemy @masonkingcobra +1  
luciana  I clearly confused lamin with laminin, now I know +3  
almondbreeze  FA 2019 pg 48 lamin +1  
almondbreeze  picked tubulin but i guess tubulin makes up microtubules and therefore is spherical +  
abkapoor  Also remember progeria is due to lamin a dysfunction, and progeria patients have messed up nuclei +  
brise  @abkapoor the f is progeria? and do we need to know it for step? +  
brise  @abkapoor omg jk jk wow +  


Up to 80 percent of aortic aneurysms are caused by "hardening of the arteries" (atherosclerosis). Atherosclerosis can develop when cholesterol and fat build up inside the arteries. ... Elevated blood pressure through the aorta can then cause the aortic wall to expand and bulge.

https://www.uwhealth.org/heart-cardiovascular/aortic-aneurysm-causes-symptoms-and-concerns/10971

Also, FA 2019 pg300 says complications of atherosclerosis includes aneurysm

almondbreeze  I was dumb and went for marfan.. +1  
llamastep1  Wrong question lol +4  


submitted by famylife(94),
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entsnIevra" hte sluemcs of het elmaid cteprtmnamo of eht gihht trr(abuoto sutrnexe, oadrdctu onsl,gu uratocdd vib,esr dtarcoud ausngm and gl"sr)iiac.

err-tnotomoveol/hue.trisl-/ireesarfc///b:wntepaant/myntmaevhbo

almondbreeze  FA 2019 pg 444 +2  


submitted by docred123(7),
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Can yenoan utherfr xeinapl hti!s? I lduco amitlneie a ewf ietm cecshoi dna I geuedss olctcr,yer sjtu edne mreo nt!roiinfmao snhkaT

wired-in  Patient has 5 yr h/o hep C, so it is chronic. Chronic inflammation is characterized by presence of lymphocytes & plasma cells while neutrophils is more characteristic of acute inflammation (Pathoma Ch. 2). AFP is within reference range so probably not HCC. Choice D, palisading lymphocytes & giant cells suggests granuloma which isn't typical of hep C. +42  
almondbreeze  Fa2019 pg 215, 217 on acute/chronic inflammation +1  
popofo  But doesn't AFP has not-so-high sensitivity for hepatocellular carcinoma (HCC)? If so, a negative result shouldn't be able to rule out HCC? +  
popofo  But doesn't AFP has not-so-high sensitivity for hepatocellular carcinoma (HCC)? If so, a negative result shouldn't be able to rule out HCC? +  


submitted by notadoctor(159),
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docicgrAn to ,olGjna tiayeoypcmhl vear is oen fo eht tsom oocnmm esusac of iCBaduhid-r ny.rmdsoe cogndcrAi to F,A iBddhiu-arC si iacdeastso rome lgelnryae twhi aglbcypeeulrhoa tsst,ea oahyplitmeyc vae,r aoptsrupmt ,tastse dna CH.C

iHtcepa ihrisoscr acn be rulde out bdsea no het emti uoercs of hte e'sttpina notiepatersn - eh saw neif 2 sweek aog nda het nomlabida apin atedrst na hour ao.g

krewfoo99  Also in cirrhosis, the liver wont be enlarged or tender on palpation +1  
almondbreeze  @krewfoo99 Good job. accoring to FA2019 pg.368, congestive liver disease (hepatomegaly, ascites, varices, abdominal pain, liver failiure) seems to be the key in Budd-Chiari SD +2  


submitted by sajaqua1(535),
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i-CdhBradui oendysrm orcscu whne three si uiconoslc of hte hiapect vnei or hte eacthpi ivne saifl ot anrid ntoi het VI.C Tihs nca be dausce yb sobhotmsri of the etapchi nvei, ro yb gtirh eddis ethar ieurfal sunig(ca oodbl ot c'akb u'p e,rreewyehv ubt ist tanmsonaeifit tgrhhou eth theiacp inve ear lal het isgsn fo h-rduCiaBdi .de)osyrmn ninyhAgt ahtt nac sncireea eth rksi of omtbsiorhs anc tenh aeiescrn the krsi of CurBdad-hii m.noeyrsd Tshi iudlsecn chlayeompyit erva, a eaaohprcbyleulg sa.ett Oru ieatnpt nad PV tbu idesms sih epnoaptnmit wot wseek .gao eH onw stneerps ihtw eslcrla uic,rset na ergdanel irvl,e adn mseo sngsi fo tlrpoa ehe.pnyniostr issmTboohr of hte yonl caaotamlin npitoo rtnseepde atht socrve all fo tshi si het iceahtp niev ie ruo ttnipea sha -u.dariiCBhd meRrembe tath uCBdia-hdri will veha a gme"tnu "reilv acrneappea no rsgso hp.laoytgo

)B tiHaecp crih-ssoir ti's nlieteyr soplbise uor tiatnep esdo heav hapteic ohcrisisr orf erlneudta o,nrsaes rvhewoe het ecaut tsoen asekm itsh esls lkeiy.l )C cePiratnca manoc-cira iecanctrap anicmoarc ttocbrnusoi fo the oncmom iebl tduc clodu secua a a'bkc 'pu of ibel, yltiemtlau scaingu moes rielv eadamg nad rcselal eiutsrc. Hveerwo oenc nagai hte intimg keams isht lu.yieknl D) arPtol evni rm-obsostih trlpoa neiv tsrosmbiho ldocu sceua emos lnpsiec eleamnntrge adn arolpt .pinesrohenty vrHo,eew sit oiotrtncsub dwoul otn seuca a de,entr lnderaeg veril subeeac ti si ema.rpsut E) raPrmyi ioomtcmhhsaeos-r due to a eetdcf ni ehndpici coon,iptdur itsh orni dvroloae reptessn thiw raekendd si,kn suliinn lag,sonrutdeii aciphte admeag wit(h hte ntolaitep fro crueotlpllaahe onraia)ccm nda aterh eesdais (rscivtreeit or eitldad ayrhocmiytpoda, dengidenp no yoru r)ou.esc The olny eno of ehest nigss tath our aineptt hsa is na aredenlg .lvier

almondbreeze  FA 2019 pg 386 +  


submitted by defalty98(3),
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hWy rea we mipiolgatncc si?ghtn agenhC ni eht ebssa ilwl dtsorey the adiloinpmrc uenesceq urdierqe fro nya soretitcrin celsdeanneou ot .rwok tMleinathyo is eth nlyo ooptin ahtt akmse seens.

arcanumm  This makes sense have reading what your comment. I overlooked this and just assumed the GATC was a mutation that allowed the restriction enzyme to work on the mutant only. +2  
arcanumm  it makes even more sense when looking at "numerous small fragments." Methylation is truly the obvious answer here in retrospect. +1  
bgiri  DNAse can also cause a change in base by breaking down dna at the GATC sequence? +  
almondbreeze  @bgiri Had the same reasoning - according to wiki, DNase catalyzes the hydrolytic cleavage of phosphodiester linkages in the DNA backbone, thus degrading DNA. +  


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tPaneti si entrruc bed-srafet, os we acn lmieentai tfcoeusr ucsft(reo si fduon ni nyheo dna sutfri nda osme auomlrf, tub not in estabr m)ikl. atPtnie hsa guirdnec ecsbsusant tub on lsuocge ni teh ei,nru os he usmt smeo guslcoonen- sgaru. yM daerfiefltin ofr iunrdgec -uconlsngoe rugass ni het eruin is riserodds sefurotc lbmteaomis ro aegastloc blmae.moits We ahve mdetelnaii sofuer,tc so tath eeavsl su hiwt nieatakgsoacl fdceniiyec ro sclacsi .clsatoageami

sympathetikey  & Galactokinase deficiency would be much milder. +7  
smc213  Big was soybean formula not giving any issues. Soy-milk can be used as a substitute formula in patients with Classic Galactosemia since it contains sucrose (->fructose and glucose). +1  
oslerweberenu  Why can't this be glucose 6 phosphatase deficiency Confused me +  
almondbreeze  @oslerweberenu G6PD - increased RBC susceptibility to oxidant stress (eg, sulfa drugs, antimalarials, infections, fava beans) -> hemolysis; has nothing to do with presence of reducing sugar +1  
makinallkindzofgainz  @almondbreeze; Glucose-6-phosphatase deficiency is Von Gierke disease, they are not referring to G6PD deficiency (an entirely seperate disease) +7  


submitted by lfsuarez(143),
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hTsi onsteuiq asks aobtu teh micsheamn of hroteapoytph as it reelsat ot otaennal audin.jec hWti htrhtoaepo,yp iniulbirb si limspy nvtordcee to awetr lsebuol ireosms ahtt are ehtn albe ot eb etrxceed yb hte ndykie. hsTi eohervw odes ont natugeocj het u.liirnbbi

almondbreeze  FA 2019 pg 387 +  
abhishek021196  Physiologic neonatal jaundice At birth, immature UDP-glucuronosyltransferase = unconjugated hyperbilirubinemia = jaundice/ kernicterus (deposition of unconjugated, lipid-soluble bilirubin in the brain, particularly basal ganglia). Occurs after first 24 hours of life and usually resolves without treatment in 1–2 weeks. Treatment: phototherapy (non-UV) isomerizes unconjugated bilirubin to water-soluble form. +  


submitted by nwinkelmann(297),
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h89@g8 ceu"Besa het ottosncibur si eovba eth lloavaer oensigr ereth is a craeseed ni iar o,lwf not nugl ,voseulm ciwhh luodw emak sith an vbstuorecit altop"ogyh si het tmos pluehlf xlnn.iaeapot If you kwno hte stom asibc hondtyopaegopoiisiy/filhtn fo trveitusocb vs eesicrivttr hihc(w I d,o tsju dti'dn in that ostm pilsefidim w,)ya ethn oyu cna uregif ginhnyta .otu fI emigsnhot is tngmiicap rawiya owfl = ,sriotvetubc fi sothmngei si ngictmpia yawair luoevm = vster.ieritc KTNAH !YOU

burningmoon  How about emphysema? airway volume changed but it's obstructive. +2  
almondbreeze  i think OP meant to say that something DECREASING airway volume = restrictive +3  
jgraham3  I think they mean if something is impacting LUNG volume (ie. expansion/compliance) = restrictive Airway disorder --> obs. / Parenchymal disorder --> res. With emphysema the airway collapses (obs.) before they are able to exhale fully thus the air is trapped +  
dna_at  Just to be clear, this is not a classical obstructive lung disease affecting the small airways, as it is above the carina (trachea). This is better classified as a fixed upper airway obstruction. See the flow loop here for "fixed obstruction" - it came up in IMED UWorld so maybe familiarize yourself with the image since it is unique! https://www.grepmed.com/images/2948 +4  


submitted by asapdoc(64),
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.aronlDjG lpsinaex ti rlylea llew on het ia.udo I iwll tjus eigv the icsab .aide llA the hmooesilgnb hvea lhapa in ti erterohfe ouy noantc tcoien it no ingeolmboh stileeohrpersco

someduck3  Just to add to this; a-thal is due to a deletion. While b-thal is due to a mutation. If they had a b-thal there would be target cells. a-thal just presents as microcytic & hypochromic. +9  
almondbreeze  looks like a-thal can have target cells too. Individuals with alpha thalassemia trait (-α/-α or --/αα) are asymptomatic, with a normal CBC. The peripheral blood smear typically shows hypochromia, microcytosis, and target cells. (emedicine.medscape.com › article › 955496-clinical) +  


submitted by krewfoo99(93),
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oS aisabclly hwta isth si aignys taht AND lliw eb ertidntmast ot hte eygrnpo otn SoN R.A DAN iwll ticalpere in het 2G haeps nda anrrseft of ADN ailamret to peyrogn will cucor ni eth M hspa.e ehT RAN yam eb umedtta dna nkmiga edeevitfc pc,sudrto utb iths lwli ton nratsmit onit hte onp,gyre uhst not eigctafnf sseicep ivlsruav abdse no NRA tna.tsumio

bk2458  makes sense!! +  
almondbreeze  good work +1  
tyrionwill  the question asks the reason of no impact on its survival. if a protein translated from a wrong mRNA loses its function, how can we say the bacteria will still survive well? if there is always fatal error happened during mRNA transcription, and always leading to fatal dysfunctional protein, how can the bacteria and its progeny still survive? so the point will be whether the fatal errors will always happen during transcription? I dont know... +  
tyrionwill  actually FA and NBME seem to have made a wrong statement that RNA polymerase has no proofreading function. RNA polymerase has more fidelity to DNA than DNA polymerase by 2 ways: 1) highly selection of correct nucleotide, and 2) proofreading. (Jasmin F Sydow and Patrick Cramer, RNA polymerase fidelity and transcriptional proofreading: https://pure.mpg.de/rest/items/item_1940413/component/file_1940417/content) however, if survival of the species refers only to the reproduction of progeny, mRNA mutation has nothing with the progeny. +1  


submitted by keycompany(311),
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sihT oeqstnui si diisdes.gu thaW ehty rea erlayl iagkns is "what si teh oels etneidnrmat of sepesci lasvurvi?" The nyol aesrnw is het liitaby ot apto.reecr easueBc ADN Peslmyaore ash oi-apdgreonrf iv,tiayct pryngoe wlli eb udffceante by RNA elseoymrPsa aklc fo nrfodoar-pgei tvcyia.it

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 monkd(18),
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Am I ryzac or ddi loUwdr ont vhae a neustoqi ttha tadtes nisttSa aer eth otsm feceftevi rudg rlgesdsaer of alsbeein ilsdpi. sThi ilcgo trewh my f.of

adisdiadochokinetic  You are not crazy. I got this question wrong for the same reason but here's why I think NBME was going with fibrates. You can use the Friedewald equation to calculate LDL cholesterol from the values they give. This equation is LDL= Total Cholesterol-HDL Cholesterol-(Triglycerides/5). The Triglycerides/5 term is an estimate for VLDL. If you calculate it in this case you get an LDL of 120 which is firmly normal and thus the patient would ostensibly not benefit from statin therapy. +14  
hello36654  omg when the hell am I going to remember this equation? Jesuusssssss, this kind of details makes me want to give up on STEP +4  
almondbreeze  Her goal LDL should still be <100, bc she has 3 CHD risk equivalents (https://www.aafp.org/afp/2002/0301/p871.html#afp20020301p871-t3) CHD risk equivalent=the major risk factors that modify LDL goals 1) age(M>45, F>55), 2) smoking status, 3) hypertension(>140/90), 4) ow HDL level (<40), and 5) family history. (https://www.aafp.org/afp/2002/0301/p871.html#sec-4) +  
almondbreeze  *low HDL level (refer to table 3 of the article) +  
makinallkindzofgainz  These guys are hitting up attending-level cardiovascular risk factor calculations, meanwhile I picked statins because I think I remember that they help the heart +12  
jimdooder  So I ended up going with fibrates because of her age (39). I vaguely remember being taught that statins are really only recommended for patients >40 because the big study that came out about them was in the 40-75 age group. I think this might contribute to the question but I'm not totally sure. https://en.wikipedia.org/wiki/Statin#Primary_prevention +  
ytho  This question inspired my screen name +2  
cbreland  "Statins are always the answer", "Fat Female 40 Fertile", "Fibrates can cause gallstones". I feel lied to +  
brise  I'm not sure if this question is correct. I chose statins according to what an attending told me and UWOLRD 2, I just went back to check and on uworld 2, you only consider giving fibrates if their TG levels are above 1,000. So idk what the nbme is smoking. Or if doctors actually write these questions. +  


submitted by monkd(18),
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mA I zaryc ro idd lwdUor otn veah a oeniutsq taht dtaets sinSatt aer het omts cveeifeft gudr lsrsedgear of leinesab ips.lid hiTs olicg rwteh ym .fof

adisdiadochokinetic  You are not crazy. I got this question wrong for the same reason but here's why I think NBME was going with fibrates. You can use the Friedewald equation to calculate LDL cholesterol from the values they give. This equation is LDL= Total Cholesterol-HDL Cholesterol-(Triglycerides/5). The Triglycerides/5 term is an estimate for VLDL. If you calculate it in this case you get an LDL of 120 which is firmly normal and thus the patient would ostensibly not benefit from statin therapy. +14  
hello36654  omg when the hell am I going to remember this equation? Jesuusssssss, this kind of details makes me want to give up on STEP +4  
almondbreeze  Her goal LDL should still be <100, bc she has 3 CHD risk equivalents (https://www.aafp.org/afp/2002/0301/p871.html#afp20020301p871-t3) CHD risk equivalent=the major risk factors that modify LDL goals 1) age(M>45, F>55), 2) smoking status, 3) hypertension(>140/90), 4) ow HDL level (<40), and 5) family history. (https://www.aafp.org/afp/2002/0301/p871.html#sec-4) +  
almondbreeze  *low HDL level (refer to table 3 of the article) +  
makinallkindzofgainz  These guys are hitting up attending-level cardiovascular risk factor calculations, meanwhile I picked statins because I think I remember that they help the heart +12  
jimdooder  So I ended up going with fibrates because of her age (39). I vaguely remember being taught that statins are really only recommended for patients >40 because the big study that came out about them was in the 40-75 age group. I think this might contribute to the question but I'm not totally sure. https://en.wikipedia.org/wiki/Statin#Primary_prevention +  
ytho  This question inspired my screen name +2  
cbreland  "Statins are always the answer", "Fat Female 40 Fertile", "Fibrates can cause gallstones". I feel lied to +  
brise  I'm not sure if this question is correct. I chose statins according to what an attending told me and UWOLRD 2, I just went back to check and on uworld 2, you only consider giving fibrates if their TG levels are above 1,000. So idk what the nbme is smoking. Or if doctors actually write these questions. +  


submitted by hipster_do(6),
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mI’ ingog ot sya it’s X kdneil eoanmmgmlablguaiai rertha nath DS,IC tbu the rfdneceeif enebwte eesth tow aer ynti tub stih is wyh I iknht i’st teh ofrmre:

  • yoB ars(eincde kris btu obht BA nad ISDC era x nleid)k
  • crunerteR taalbceir cinnsoitfe utb ond’t omeitnn eraraihd ro thushr hhiwc is in CSID
  • iTeenmil is after 6 nts,moh os hte otsmrh’e iitneaodbs eowr .off

IDSC dsholu be tiemaledimy eucebsa heyt tsuj d’otn aveh het 2IL rpetcres.o CIDV shosw up nhwe ythe’er 2004- sarye ldo. oYu get nbsate grmnalie certsen ni o.htb oN ennimto fo sbaetn ytchim aswodh hcwhi si ni D.ICS

placebo079  “Uniformly” low is also a clue; in CVID they are not. +4  
tea-cats-biscuits  This makes sense, though what really threw me off was that in Classic Bruton’s Agammaglobulinemia there’s near-zero B counts though (or at least that’s what FA and UTD says, “Absent B cells in peripheral blood” FA 116, 2018). The Q says the leukocyte count was normal though. Wouldn’t the leukocyte count include lymphocytes in the differential? And wouldn’t lymphocytes be low due to the near complete lack of B cells in peripheral circulation if it was BA? +2  
partybrockk  @tea-cats-biscuits Bruton’s is a failure of B cells to /MATURE/. So you get normal lymphocyte counts, decreased levels of immunoglobulins, and absent germinal centers. +5  
tea-cats-biscuits  @partybrockk That makes sense to me, but I keep getting hung up on how that’s not what either FA or UTD says about the classic lab findings of XLA. UTD specifically says this: “Laboratory findings include hypogammaglobulinemia/agammaglobulinemia, deficient antibody responses to immunizations, and absent or markedly reduced B cells in the blood,” and I previously quoted FA. I suppose it doesn’t really matter, but it’s definitely a bit frustrating unless I’m missing something about how absent B cells in the blood wouldn’t correlate to a decreased lymphocyte count ... +3  
temmy  please correct me if i am wrong cos i might be but my logic was there is decreases immunoglobulin uniformly meaning the B cells are uniformly absent and since they develop in the germinal center, the germinal center will be absent. +2  
almondbreeze  Picked 'decreased # of CD4 lymphocytes'.. ->Both CD4 and CD8 T lymphocytes were affected; the decrease was most pronounced for naïve T cells. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809006/) +  


submitted by meningitis(546),
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iocatelihrdzooyhordh is DCO rfo Ncehreogpni tiseDaeb ipnsiusid cbsauee ti oaalayxrcilpd cssaeu na escerina ni PB yb igncsnriea dsimou niarptsobo dna tuhs tarwe btropn,soia athPoma sxinelap tish .yiecnl

Dessionrmsep is ercrctoni ebasuec noup isgafnt u(ldfi riicots)ntre DAH si dnaiseerc minneag HAD si nigeb relaesed tarllCnye ubt si ont ogrwnik in teh iesnydk ta eth 2V errcoetsp fo the pithialeel naerl lslce at tcgneoClil cdut.

On atht n,oet ildoimAer is dseu rfo itmLihu duicned rchnipgonee DI.

hello  Where in Pathoma? I couldn't find it. +1  
almondbreeze  also sketchy says that thiazide s decrease the amount of lithium cleared--> lithium toxicity +1  
paperbackwriter  Agh confused as well because FA2019 (pg 562) says that thiazides are implicated in lithium toxicity D: +  
paperbackwriter  OOPS, please ignore last comment. I just realized that this Q stem never mentioned lithium. And on top of that @meningitis mentioned that amiloride is used if lithium induced. Apologies. +  
jaramaiha  Question is nephrogenic DI. ADH is increased but kidney's aren't reacting, mutated receptors. In which the Tx is HCTZ +  


submitted by gh889(129),
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arcniocgd ot patduoet zhiiadtes eucsa a mild hyopoilecmv ttsae utsh oryu PCT will see emor aN dan 2OH --;t&g yb rnpcpelii thta eth TCP sywlaa orsresabb 6%0 of hwat it ssee, ti liwl aobsberr eomr aerwt adn aN.

almondbreeze  in sketchy as well +  


submitted by imgdoc(135),
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I hknit tola fo oeplpe mhtgi aveh orev zdaehpiems hwo otratnpmi PNA and NPB lrleya rea, esy ti is tontprima to kwon ehtse piptsede get tcesdere by the tai/ltrarraiecvuln omicamyudr drnuig athre lui.frea roeHwev rthie lraoelv fenetfsescive ni tgnretai retah lirfuae si lihz,c a rtperpoce ltod em hatt if PNA adn NPB rewe so luuefs ni iaetsurnsir ethn wyh od we eigv icursted?i 'Its eesbcua ARSA woorvrepse tshi mstesy ceenh nsaicug aevignte estfcfe dan het leesnds oopl of etrah eurli.af AKA hyw we gevi EAC srbhito.nii

nonKgiw tath PAN estg truezalined by teh ASAR mytess, ew acn ftish our socuf bkca to ehrat eifalur ni tihs eap,nitt reweh rcdcaia otptuu si ,erdedseca ielndag ot DAH ireeotscn nad iallnyf iiltnuolad pomaatnhyier.

almondbreeze  a concept continuously emphasized by uw, but I get always wrong :'( +2  
almondbreeze  good work done! +  
raffff  why does the body make anp at all since its so useless +3  
makinallkindzofgainz  @raffff - at least BNP gives us a good marker for heart failure exacerbations :) thanks body! +  
mannan  Yeah it's important clinically because it has a high sensitivity (if negative, rule out) for Heart failure. +  
alimd  At the same time ANP inhibits renin release? +  


submitted by imgdoc(135),
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I knhti aotl fo eplpoe htigm heav eorv pdiehezmas hwo pnotimtar NAP adn PBN laryle rea, yse it is ortnpimat to konw thsee pepseidt gte steeecdr by het naairlarlvteu/crti myiomadcru ndurig rhtae .aelufir wvHeeor tihre rlveaol eeistesevnfcf ni rtgentai ahert arfileu si c,zlhi a ptpecrore ldot em atth if APN dna BNP erew os ufleus in ntsiuarrsie hnte why do we vgei ucs?rtdiie 'Its aucesbe ASRA srpoeweovr isht temssy chene agcunis agevtnie fecestf nda het edsesnl lpoo of areth ieru.lfa KAA yhw ew iegv ECA .rioitsnihb

wogiKnn tath ANP estg tezridnaelu by eht AASR yms,ste ew nac htfis rou sucfo bakc ot reaht ieurlfa in tish ,iatpnet wrehe icracda touput is eedr,csade ildeagn to AHD isrcntoee dan lnayifl oiatdnluli tpmiayohear.n

almondbreeze  a concept continuously emphasized by uw, but I get always wrong :'( +2  
almondbreeze  good work done! +  
raffff  why does the body make anp at all since its so useless +3  
makinallkindzofgainz  @raffff - at least BNP gives us a good marker for heart failure exacerbations :) thanks body! +  
mannan  Yeah it's important clinically because it has a high sensitivity (if negative, rule out) for Heart failure. +  
alimd  At the same time ANP inhibits renin release? +  


submitted by hayayah(1081),
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ihsT si a tnteipa easc fo uopmrtstap yo.ditiihrts Cna rasie up to a ryae eaftr erlyeivd and hsa lpctyychmio tti.aefrnli

almondbreeze  FA 2019 pg 338 +1  
waterloo  Although history seems to point towards that, she has an enlarged thyroid, and in postpartum thyroiditis, thyroid usually normal in size (from FA). regardless either would have lymphocytes infiltrating. +  


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W:U het sthor gacitrs vv dainr lobod fmor eht gitrsac snduf tnio hte splnice ven,i ercpacntai nilomatfmain ..eg( ,ratactisiepn riapacnect a.c) cna eucsa a bodlo tlco /iw eht enlpcis en,vi hwihc acn senicera epsusrre in het sothr taigsrc nevis nda lead to cstairg ieasrv ylon in the usdfn

almondbreeze  b/c pancreatic causes can form blood clot in splenic v, b/c splenic v runs behind pancreas +  


submitted by welpdedelp(229),
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It asw a ugoernrFuis -i&gd-;sotbe bsiasts.eso nueoursigrF sedbio are leviebde to be eormdf yb orcmaphegas ttha heav oogetphcydas dna tpetatedm to esgidt the e.sfibr

almondbreeze  info about ferruginous bodies being mf can't be found on FA/UW :'( they just say it's 'material' +  
taediggity  FA 2020 677, FA 2019 659... mf?? mofos?? +3  
69_nbme_420  Just to add: The question asks what cell type initiated the Fibrosis → Alveolar macrophages engulf the particles and induce fibrosis (same pathophys for all Pneumoconiosis). Pathoma 2019 Pg 92 +7  


submitted by rogeliogs(9),
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My ahopcpra to tsih enstiquo swa emro jstu gscifonu ni het ofni tyhe ear gv.gnii Noen fo hte teroh tpiono easmk nsese eucsbea teehr is not eniveecd to atkl buato th.em I saw vrye dtmpeet ot ikpc eht rdsaceee" ipelnt ptu"ocroind but I erermemebd rD Gloajn iyagsn iTh"kn ,seilpm hknti chpea, yteh ear nto gtrnyi ot trcik y".uo oS, bubhcy speantr = cuybhb k.dsi

almondbreeze  thought his words on "think cheap" had to do with treatments - i.e. exercise +  
alimd  Yes they are. There are so many trick questions +  
skuutnasty  I chose leptin deficiency cuz I was tryna get fancy with it. For anyone who is interested, however... according to UpToDate: "Most people with obesity do not have any abnormalities in the leptin gene, their serum leptin concentrations are high reflecting their increased fat mass..." Peace +  


submitted by jooceman739(27),
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:Rtialaobseontm

The yhaicnsip dais hte yob is llyneuik to pveodel yan erhto sneoals,mp os he 'sdenot ehva eht needrihti Rb tua.iomnt

nI siht aes,c eh has eth daroiscp or.otmteiasblan rpaoScid tmerbatsonilao riqsreeu owt csmaiot instmtauo fo bR ni hte msea ilrante ell.c

utJs as a side net:o eItinherd olmoaniaerstsbt entd ot be tar.ebilal Sdiocpar rae ae.alrltnui

carls14  aren't retinal cells a type of somatic cell? Why not is the mutation not considered in the somatic cell of the child? +9  
omerta  Although this mutation would be considered somatic, I believe the question is just asking you to be specific as to which cells. If you answered "somatic cells of the child," that's quite broad and could apply to almost anything. +12  
kernicterusthefrog  I had the same struggle and thought process. +1  
eacv  There is a Uworld qx that explain this in detail> ID: 863 +3  
arcanumm  I read the answer options too fast so got this wrong. It is a somatic cell type, but somatic in general implies a higher risk for developing other cancers. The hint here is that the physician stated he is unlikely to develop any other neoplasms, so it is a specific double hit mutation in the retina. +7  
almondbreeze  wouldn't she have any possibility of developing osteosarcoma as well? :( +  
almondbreeze  did some reading and it seems like osteosarcoma only occurs in familial retinoblastoma with RB mutation +  
brise  But how can a 5 year old get two mutations to get retinoblastoma? In 5 years?! Obviously doctor is probably wrong LOL +  
jaramaiha  The difference between familial and sporadic mutations dealing with Rb is that in this case he only had one hit so that only one eye is affected. In other words, if he would have been born with the familial type, he would present with Rb in both eyes and also be predisposed to osteosarcoma. In this instance he only has Rb in one eye having only a one hit mutation in his right eye. When the stem says this is the first mutation it's implying that he wasn't born with the familial type so to obtain a second mutation over the course of his lifetime would be rare. +  
brise  @jaramiaha I believe it still falls into a two hit mutation, but both were sporadic. But you are right about being unilateral. +  


submitted by jooceman739(27),
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ote:boRltnaimas

hTe iinhyapcs asid hte yob is eulynlki to oelpved yna toehr enap,slsom os he edso'tn veha hte endtreiih Rb otant.umi

nI tshi e,asc he sah eth cradsipo mtsaor.obinleta ricpaSod ostnmblreaiaot uesreiqr wot cioamst ttianosum of Rb ni hte smea elaitnr l.cel

utsJ sa a sdie nto:e eIhterdin taeatossbmoirln ntde ot be .arillateb rSicaopd are il.autlaern

carls14  aren't retinal cells a type of somatic cell? Why not is the mutation not considered in the somatic cell of the child? +9  
omerta  Although this mutation would be considered somatic, I believe the question is just asking you to be specific as to which cells. If you answered "somatic cells of the child," that's quite broad and could apply to almost anything. +12  
kernicterusthefrog  I had the same struggle and thought process. +1  
eacv  There is a Uworld qx that explain this in detail> ID: 863 +3  
arcanumm  I read the answer options too fast so got this wrong. It is a somatic cell type, but somatic in general implies a higher risk for developing other cancers. The hint here is that the physician stated he is unlikely to develop any other neoplasms, so it is a specific double hit mutation in the retina. +7  
almondbreeze  wouldn't she have any possibility of developing osteosarcoma as well? :( +  
almondbreeze  did some reading and it seems like osteosarcoma only occurs in familial retinoblastoma with RB mutation +  
brise  But how can a 5 year old get two mutations to get retinoblastoma? In 5 years?! Obviously doctor is probably wrong LOL +  
jaramaiha  The difference between familial and sporadic mutations dealing with Rb is that in this case he only had one hit so that only one eye is affected. In other words, if he would have been born with the familial type, he would present with Rb in both eyes and also be predisposed to osteosarcoma. In this instance he only has Rb in one eye having only a one hit mutation in his right eye. When the stem says this is the first mutation it's implying that he wasn't born with the familial type so to obtain a second mutation over the course of his lifetime would be rare. +  
brise  @jaramiaha I believe it still falls into a two hit mutation, but both were sporadic. But you are right about being unilateral. +  


submitted by armymed88(47),
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undoW nagelhi trnoifmlmyaa orf pu ilt 3 ayds sl(cto, P,NsM lcrei)oaiPstv emorafr 3ydas lti ekwes- notglnaiaru eus,sti enw ee,svsls ewn umethpiiel, rooccnintta piaerr( nad )noieetngearr dem eRol 1kw lti m6- ecrpela ogecllna III tihw ,I ancriese tgehntrs p(u ot -7%600 giailnro engttsrh peilsobs)

john055  it looks like the patient has new onset erythema which points to infection and I think neutrophils make sense. I myself have marked angiogenesis but I did it offline. Is angiogenesis the right answer ? +1  
almondbreeze  yup +  
almondbreeze  according to FA 2019 pg217, neutrophil is present during inflammatory phase- i.e. only up to 3d after the wound. After that we have the proliferative phase with granulation tiss. and angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction (involved cells: fibroblasts, myofibroblasts, endothelial cells, keratinocytes, mf) +  
mitchell_to_lakers  why not fibrosis? +  
waterloo  mitchell_to_lakers They are asking why is the incision erythematous and slightly warm. When someone is red, Dr. Sattar says that's because blood is going there. Fibrosis isn't a mechanism where someone's tissue will appear red and warm, it's collagen deposition. +4  
juanca10  Very good! +  
srmtn  is not infected, is healing. normally when healing is a little warm and erythematous because of angiogenesis. +1  


submitted by armymed88(47),
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nodWu eanlhig ifoyrtlnmaam rfo up lti 3 asyd ,(olsct sNPM, )ecorri aPeostlarmfvi 3adys itl sewek- aanngltroiu si,stue new esssev,l wne m,uheilietp anrotnictco rar(ipe nda eeniterna)org emo ldeR 1wk tli m6- praleec oclglane III ihwt I, rsceenai ehtgtsrn up( to 70%6-0 ignolari tsegnhrt )lispbseo

john055  it looks like the patient has new onset erythema which points to infection and I think neutrophils make sense. I myself have marked angiogenesis but I did it offline. Is angiogenesis the right answer ? +1  
almondbreeze  yup +  
almondbreeze  according to FA 2019 pg217, neutrophil is present during inflammatory phase- i.e. only up to 3d after the wound. After that we have the proliferative phase with granulation tiss. and angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction (involved cells: fibroblasts, myofibroblasts, endothelial cells, keratinocytes, mf) +  
mitchell_to_lakers  why not fibrosis? +  
waterloo  mitchell_to_lakers They are asking why is the incision erythematous and slightly warm. When someone is red, Dr. Sattar says that's because blood is going there. Fibrosis isn't a mechanism where someone's tissue will appear red and warm, it's collagen deposition. +4  
juanca10  Very good! +  
srmtn  is not infected, is healing. normally when healing is a little warm and erythematous because of angiogenesis. +1  


submitted by calcium196(11),
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U-eiqeidduatnibtim lotoseiprys is ont ebleirysrv edftcfea yb siilunn. The qsetonui sask for evreebrsil sway ttha snilinu csfatfe ,ti dna iniiuuttanoqbi udlow aedl ot eaidnargdot vai ,petraoses cwihh is otn rvseilrb.ee utlNeccasprclio/aym tghusnin kemsa eessn ubcseae OOFX si a tnornastcriip oarc,ft so it nta’c do tsi boj if ti si in het tolyapcms!

meningitis  Thank you for your explanation! One question: How about the serine phosphorylation? Is it answered by pure memorization that the FOXO TF is serine phosphorylated, or is it a general fact that all TF's are serine-threonine phosphorylated? +  
tsl19  I'm not sure, but it may be as simple as this: ubiquitin-mediated proteolysis is irreversible, but both N/C shuttling and phosphorylation are generally reversible processes. +  
didelphus  I also guessed that FOXO must be a part of the PI3K pathway, since insulin regulates metabolism through PI3K and the question stem specifically mentions that. Phosphorylation is a major part of that pathway, so even indirectly phosphorylation would regulate FOXO. Frustrating question. +19  
niboonsh  yes, FOXO is affected downstream of the activation of PI3K. This is a really good video that explains the whole cascade https://www.youtube.com/watch?v=ewgLd9N3s-4 +2  
alexb  According to wikipedia (https://en.wikipedia.org/wiki/FOXO1) phosphorylation of FOXO1 is irreversible. This is referring to phosphorylation of serine residues on FOXO by Akt, which occurs in response to insulin. But the NBME answer suggests it's reversible. What's up? +1  
almondbreeze  could wiki be wrong on phosphorylation being irreversible? according to this article, it is a reversible process: regulation of FoxO transcription factors by reversible phosphorylation and acetylation (https://www.sciencedirect.com/science/article/pii/S0167488911000735#s0010) some wiki info, however, is helpful : In its un-phosphorylated state, FOXO1 is localized to the nucleus, where it binds to the insulin response sequence located in the promoter for glucose 6-phosphatase and increases its rate of transcription. FOXO1, through increasing transcription of glucose-6-phosphatase, indirectly increases the rate of hepatic glucose production.[19] However, when FOXO1 is phosphorylated by Akt on Thr-24, Ser-256, and Ser-319, it is excluded from the nucleus, where it is then ubiquitinated and degraded. The phosphorylation of FOXO1 by Akt subsequently decreases the hepatic glucose production through a decrease in transcription of glucose 6-phosphatase. +  
leaf_house  It seems like the phosphorylation from Akt leads to destruction, but maybe the assumption is that that phosphorylation step (excluding every other step of ubiquitin-proteosome pathway) is reversible, where proteolysis is final. @niboonsh video is good but doesn't split this one. +  


submitted by assoplasty(95),
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tasF rea eiokegtnc pxt(ece odd ncahi ,AF) so yhet percuod etsekno rof yngeer iouptcrond tAc-o(CAey)l hetrra anht c.segluo If teh touisenq eadsk whta eth myirrap soucer fo eyngre cpnuortoid w,as ti wloud ltsli eb gnelycgo dan( ton )esk,eont asceebu this si wintih 42 rshou. Hvwreeo ftear 24 shoru teh nawrse udloc eb enteok .sdbeio sRrla,gdees hte oisueqnt lypiesacfcil dsai hte tp dah a murse ucogsel of 100, inaicdgtin taht we rae nokolgi for geihsnomt taht veridpos a testbursa ofr nesnl.cogosueegi

rnguiD sidpoer of atrntsvoi,a sseastbtur fro eoniegslngucsoe cmeo orfm owt :ocusers 1() kedobanwr of gseinixt sul,cme or 2() via idcodna-h AF hotugrh oA-iony.pClorp *enilaV( saol deesf tnio ilrnoppoy AC,o ubt si tno inodevlv ingurd osnatvirat t--g;& ees oebl)w

1() hTe liaevtpna-nreayu leycc ordvesip hsti negma(iltu ni elusmc + uapvytre ;-t&g- eainaln -tg&-; eosg ot ilrve -t;&-g onnntaiatrmsia to gu-atlheaotkleptaor &tg--; teavpuyr si tsdereapa morf tlangmeiu ;t--g& mitunealg oegs ot aeur ,lycce tuapyerv ogse on ot )neesgoocgnls.uei ctaaeLt nac olas eb udes sih(t uocld vhae enbe a rgiht nwsrae fi it eerw )de.ilst

2() Odd ianch FsA era losa un,gegciloc utb ericast iacd ierpdvo(d ni the rwsaen c)heico sn’ti odd ,incah os it is olyn ginekecot and nac be delru t.uo

hAouglth elniva n(da hoert hearbndc .aa). fdee toni PlioCoo-yAn,rp they aer nto seud ni tnitvoaasr aeuesbc rvastotnai csitytrl eiserl on tpaiceh eeo.soelgnsguinc shTee a..a are tno lbdeaztoiem in eht rilve asecebu het evlri sclka hacbinna-hdcer aa.. seansaetrrf nyzem.e In riFst iA,d ehBcmio eino,tcs rduen t/sa,toanirainvtSFg ni htob eth “fnsgtia tsa”et ch(ihw si whinti het iemt rmafe fo iths ti)nqeos,u or eht t“toravains ”teas,t otbh tieliuz aptheci cunonegl.igseseo yM snamsuipot is ahtt naeivl si dues niugdr rluerag tolaimb,sme dna tno drignu sordipe of nvart.asiot

hello  I want to re-emphasize something that @assoplasty has already stated :). The Q-stem states serum glucose = 100, and the Q asks why the patient is able to maintain normoglycemia. Therefore, you can immediately eliminate choices A and C because acetoacetate and beta-hydroxybutyrate are sources of energy during ketogenesis -- ketogenesis does not provide glucose energy sources. +8  
chandlerbas  ^ this checks out: valine and isoleucine are broken down in the muscle into branched chain 2 oxo acid via branched chain aminotransferase (reversible) then the valine and isoleucine leave the muscle and swims to the liver to be acted on by branched chain 2 oxo acid DH (irreversible). So bascially the process from taking BCAA valine and isoleucine requires 2 enzymes. the first enzyme is in the muscle, and the second enzyme is in the liver (for simplification purposes --> both organs contain both enzymes but dont have the same affinity for their substrate). source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1147506/?page=4 so you're right to say that the liver +5  
toxoplasmabartonella  Thank you for such a great explanation. Isn't it glutamate instead of glutamine that combines with pyruvate in muscle to yield alanine for Cahill cycle? +1  
almondbreeze  @ toxoplasmabartonella think you are right +  
revanthshanmukh  its given that methionine histidine and valine are glucogenic AA.nso why not these form the glucose in the body first compared to alanine? +  


submitted by hayayah(1081),
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-eesnesiticyeyCnt cemnheoki eperrtco 5 )(RCC5 is a itnpoer dounf on eth uacerfs fo DC4 ce.lsl

yotsubato  Note, this is NOT in FA +2  
sbryant6  It is in UWorld. +3  
almondbreeze  it's in FA2019 pg.110 +1  
almondbreeze  but missing the full name for CCR5 +4  
demihesmisome  CXCR4 is also a chemokine receptor. +2  
sononono  Uworld ID 953 +1  


submitted by hayayah(1081),
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sceCeieityyn-tnse nmkeocieh petorerc 5 (5C)RC si a nptroei foudn no eth ufecras fo CD4 llc.se

yotsubato  Note, this is NOT in FA +2  
sbryant6  It is in UWorld. +3  
almondbreeze  it's in FA2019 pg.110 +1  
almondbreeze  but missing the full name for CCR5 +4  
demihesmisome  CXCR4 is also a chemokine receptor. +2  
sononono  Uworld ID 953 +1  


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Qntosuie sdkae ofr amgr veoitips oiccc in CAI.SNH S. uuaser fsorm rluecss,t gimanlineit it. sTih evasel nococEtusrec efaaicsl adn Goupr A strep. .E casiafle si acodsaetsi hitw s.TIU

almondbreeze  get the clinicals but got thrown off by 'chain'. FA2019 pg.137 also says coccus = berry, strepto =twisted (chain), differentiating the two:( +2  


submitted by mcl(601),
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eiatPnt mya ehva ihadytrree gonma,adeie which is scaisedtao whti eunertr"rc aactstk of stennie, v,missae loaeizdcl csbsuaouuten edaem igovnvlni the iirte,extmse nag,etliia cfa,e ro ktnru, ro sucambusol emaed of ppuer araywi ro .eswbol" The citlare seog no ot sya "saesrCt1-ee hiriibtno kwros etcildyr on the metcmpoenl nad cncttoa mapasl adcsseca ot edrecu inybdriank lseeare" whhci is olas labbopyr doog ot won.k

wit3stc/ilhilC6.p.c/m6n1r//tM:.ceahwnpn/ws/vmbP63.8go

notadoctor  Thought this was a trick question as C1 esterase deficiency also results in a decrease in C4. However, the second answer choice was not referring to C4 but to C4 binding protein, which I now know is different. I also didn't realize C1 esterase was technically a complement protein. +4  
youssefa  Based on many sources hereditary angioedema does NOT cause a rash (urticaria) which is a main differentiating point between angioedema and allergy. This mislead me in this question. Any clarification? +22  
ergogenic22  +1 on the above because uptodate states that c1 esterase inhibitor deficiency, both acquired and nonhereditary, are both non-urticarial, non-pruritic, and that is confirmed by the above linked article +2  
sahusema  Question writer probably didn't know the difference between cutaneous urticaria and subcutaneous edema. +3  
almondbreeze  same. got it wrong bc the pt didn't have sx of hereditary angioedema - swollen lips and eyelids +2  
teepot123  fa 19 pg 107 +  
beloved_bet  According to Amboss "Mast cell-mediated angioedema Often associated with urticaria and pruritus Other associated with clinical findings of allergic reactions (see type 1 hypersensitivity reaction) Presents within 30 minutes to 2 hours after exposure and resolves over hours to days" +1  


submitted by readit(14),
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yhW si si nto opdesu snaumr?ye

otcir"A eaysdumrssuneop yylapilct ucrco as a tulsre fo araumt -+/ reneitv,noint a rddeseconi essutb of mtiautarc aritco ryinju in teh ytrmaoji fo eas.cs eyTh cna be uatce or .oich"rcn

ag/pmotpal.yo?ugao/sirt=ns:cred/decasdturlsthueaaasrr-iiopien/

readit  *same goes for saccular aneurysm, which also is usually 2/2 trauma +  
samsam3711  In the question stem there is no indication of trauma so it would be hard to just assume that +  
almondbreeze  see my comment above for marfan syndrome. might help +  
drzed  This is because a pseudoaneurysm is between the media and adventitia, and is incited by trauma; a dissection is between the intima and the media and is a result of hypertension causing an intimal tear. The history points toward cocaine -> hypertension rather than penetrating trauma. +  


submitted by neonem(572),
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Mjora sirk fartoc rof tiroca seiitconsd si hsrietyonnep, dan ni tihs ecas tmgih be due to anceoic ,esu hichw scuesa edmark ohtyninserp.e Dtossceniis caesu a rtae in teh iautnc timian -- lbodo cna wflo rskadabcw niot the paicemrudir nda useac mt.eoanpda iTsh tsmnseaif as escrkcal in eth nglu eud to proo ftel inteuclvrra octfunni iigfc/ltldiilnsao( plbemro eud to soemos.cnipr)

forerofore  there is another clue, the man has diminished pulses in just one arm, which means that the left subclavian artery must be involved somehow, and an aortic dissection would be the best answer explaining this. +9  
temmy  please why is there where a diastolic mumur? +1  
whoissaad  @temmy Aortic dissection especially near the root of aorta can lead to dilatation of the aortic valves, which can lead to Aortic regurgitation (diastoic murmur at left sternal border) +8  
garibay92  Does anyone know why is this patient's tepmerature elevated? +1  
ratadecalle  @garibay92, not important for this question I think but cocaine can cause malignant hyperthermia +1  
almondbreeze  judging by his heart murmur, he probably has marfan syndrome. that's the only place where FA talks about dissecting aneurysm +  
almondbreeze  he's only 28 - another clue for marfan? +  
turtlepenlight  did anyone else think it was weird his only sx was SOB? I always think of radiating pain as being a good clue for dissection +2  
cmun777  @almondbreeze his heart murmur is at the LSB (aortic regurg) and not consistent with MVP plus no other sx/indication of Marfan. I think the only association of RF you should think about in this question is the cocaine use and consequent HTN. +1  
ibestalkinyo  @turtlepenlight I agree. I chose another answer because I was like, there's no way this guy doesn't hurt if he's got a dissection. +1  


submitted by neonem(572),
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rMjao rksi taocfr orf iaortc tdsenciois si t,shroeniyenp nad ni tish ecas higmt be due to aonecic es,u whchi uacsse kadrme nytihn.eeospr setisnicDso acesu a ater in the acutni intima -- lobdo nac folw bcdrskaaw oitn het crupmaeirid dna csuae ptoea.mdna sihT imsfasetn sa ccaserkl ni teh glnu ued to roop telf nvrlrctaieu fnitocnu c/ildloga(ntfiisil peorblm eud ot smnec)oorisp.

forerofore  there is another clue, the man has diminished pulses in just one arm, which means that the left subclavian artery must be involved somehow, and an aortic dissection would be the best answer explaining this. +9  
temmy  please why is there where a diastolic mumur? +1  
whoissaad  @temmy Aortic dissection especially near the root of aorta can lead to dilatation of the aortic valves, which can lead to Aortic regurgitation (diastoic murmur at left sternal border) +8  
garibay92  Does anyone know why is this patient's tepmerature elevated? +1  
ratadecalle  @garibay92, not important for this question I think but cocaine can cause malignant hyperthermia +1  
almondbreeze  judging by his heart murmur, he probably has marfan syndrome. that's the only place where FA talks about dissecting aneurysm +  
almondbreeze  he's only 28 - another clue for marfan? +  
turtlepenlight  did anyone else think it was weird his only sx was SOB? I always think of radiating pain as being a good clue for dissection +2  
cmun777  @almondbreeze his heart murmur is at the LSB (aortic regurg) and not consistent with MVP plus no other sx/indication of Marfan. I think the only association of RF you should think about in this question is the cocaine use and consequent HTN. +1  
ibestalkinyo  @turtlepenlight I agree. I chose another answer because I was like, there's no way this guy doesn't hurt if he's got a dissection. +1  


submitted by tissue creep(114),
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rohrdpAto rfo eu,sr btu ofr eht oedrcr 'Im rttyep sreu hsti aws hinykuagnuC Vri.us lnOy tog itsh from a WUodlr iouentsq as I dnhat' seen ti utinl etn,h tbu ynatprpela eht hglaatairr is rlelya abd, chhiw si whta rwed me ot eht are.wns

hdt/hgmda./ih/gwwup.wn:inl.etyouxccvsck/nt

meningitis  More like Zika Virus (Same a. aegypti vector) since it says she has rash associated to her bone and muscle pain. I had Zika one time (i live in Puerto Rico). Remember also dengue and Zika are Flavivirus. Dengue can cause hemolysis (hemorrhagic), and Zika is associated with Guillen Barre and fetal abnormalities. +12  
nala_ula  I'm shocked that I found a fellow puerto rican on this site! Good luck on your test! +2  
namira  dont be shocked! me too! exito! +2  
niboonsh  Dengue is also known as "bone break fever" which makes me think its more likely to be dengue due to the "excruciating pains in joints and muscles". https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4242787/ +21  
dr_jan_itor  I was thinking that its Murine typhus transmitted by fleas +  
monique  I would say this is more likely scenario of either Dengue or Chikungunya, not Zika virus. Excruciating pain is common in those, not in Zika. Zika has milder symptoms of those three infection. +2  
jakeperalta  Can confirm that Chikungunya's arthralgia is pretty horrible, from personal experience. +  
almondbreeze  UW: co-infection with chikungunya virus with dengue virus can occure bc Aedes mosquito is a vector of both Chiungunya, dengue, and zika +  
lovebug  FA2019, page 167 RNA virusesy. +  
lovebug  Found that Chikungunya also have Rash./// An erythematous macular or maculopapular rash usually appears in the first 2–3 days of the illness and subsides within 7–10 days. It can be patchy or diffuse on the face, trunk and limbs. It is typically asymptomatic but may be pruritic (Taubitz W, Cramer JP, Kapaun A, et al. Chikungunya fever in travelers: clinical presentation and course. Clin Infect Dis. 2007; 45: e1. ) +1  
beto  it is chikungunya->fever, polyarthralgia, diffuse macular rash, dengue has retro-orbital pain mostly +1  


submitted by fatboyslim(46),
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(moFr UW 8152)1 eSmo eaomitcsnid undgcilni ,sidopoi aistodtarcrno d,sey dna oesm aibctstoini .(.eg ncvaic)nyom nca udienc dan gIE-PDENNETINDE atms clel entoiaaulngrd yb tnoaitaivc fo printoe nkaies A nad PI3 sika,ne hwchi urestls in aseerel of ,tshniaemi nkibayn,dir adn ehrto tmtoachcice tfrscoa ;&tg- iudfesf cng,tiih pan,i ,nmposcshobra nad cdellzaio =giweesnll (cutra)iri.a

almondbreeze  just to add : more agents causing such reaction - beta-lactams, sulfonamide, aminoglycoside +  
drzed  Are those IgE dependent, or just allergic reactions (asking because the sketchy for beta-lactam penicillins mention acute interstitial nephritis as an allergic reaction)? +  


submitted by hayayah(1081),
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isytiveiSnt sstet rea sued ofr c.snereing fiySicctipe etsts era deus rfo moaitnrifcon trfae pstoevii sns.gecnrei

etiSivsityn ettss are dsue ofr eensig owh nmya opeepl ytulr vaeh eht dsseeia. ceScypiftii stets are fro ohset hwo do ton avhe het ssieeda.

A lhihgy tisvsieen t,set hwne naegvi,te urles OTU esis.ade A gyhilh scceifpi test, henw vsti,eipo rsuel IN iasse.ed ,So a sett thwi itwh wlo ittviisenys tncano uerl tuo a s.adisee A sett twhi owl eiyptficsic 'catn uler ni iadsese.

ehT octrod and tniatep antw to ercnse rof nocol acercn nda eurl ti out. hTe dcootr ouldw wtna a tset ihtw ighh vnityiteiss ot be aebl ot od .ttah He wnsok atth isettng erh sloot for dolbo wlil ton leur uot teh osbyisiiltp fo oonlc .AC

sympathetikey  SeN Out (Snout) --> sensitive test; - test rules out SPec In (Specin) --> specific test; + test rules in +23  
usmlecrasher  can anyone pls explain why it is not << potential false- positive results >> ??? +  
almondbreeze  correct me if I'm wrong, but 'high FP (choice C)=low specificity (choice B)'. Whereas high specificity is required to rule in dz +2  
almondbreeze  picked positive predictive value myself. can anyone explain why not PPV? +  
williamfreakingosler  The principle @hayayah is talking about (a negative test being relied upon to reliably rule out) is negative predictive value ("NPV"). I don't see why "uncertain NPV" isn't the correct answer, particularly because NPV is predicated on the disease having the same base rate in the person(s) being tested as in the population that was characterized for the test statistic. Given that the patient has a strong family history of colon cancer, the NPV of FOBT is uncertain. Said another way, the sensitivity of a test does not change with the population, but the NPV does. The whole reason the doctor is denying FOBT is because of bayesian thinking (a priori information related to family history), and from my point of view bayesian logic is more relevant to PPV/NPV than to sensitivity, hence my confusion over why NPV isn't the right answer. +2  
ibestalkinyo  I thought negative predictive value for the same reasoning +  
raga7  AFTER THE RESULT OF TEST WE CAN USED PPV OR PPN, BUT FOR TEH FIRST TIME LOOKING ANY DESEASE USE SENSITIVITY OR SPECIFICITY. +  


submitted by hayayah(1081),
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isetiinyvtS tetss ear sedu for ig.eesnncr ciecpiyitfS stest are dseu for ctimoariofnn rtfea iviotspe gnsrsce.nie

Sytetnisvii esstt era duse fro sneige ohw mnya elopep yurlt evah hte .eideass tcyiSiifpce sttes ear for ehsot who do otn veha the idsae.es

A ilhhgy eeviinsst tset, henw ievgan,et uslre UTO de.siesa A hlyigh pieisfcc ts,te hwne pset,ioiv srleu IN e.ssdeai ,So a tset iwht hwti lwo eittisyvnsi tcanon rule uot a ds.aeeis A stte hiwt wlo fyistceipic ntc'a urel in edsiea.s

Teh oorctd nad ipttnea wnta ot reensc fro lcoon ecnacr dan eulr it .otu The dctoro dulow watn a sett thwi hgih isyiintetvs ot eb aleb to od t.hat eH nwkso htat tsetgin reh tlsoo ofr lbodo will not elru tou hte iboiltisspy of olcon CA.

sympathetikey  SeN Out (Snout) --> sensitive test; - test rules out SPec In (Specin) --> specific test; + test rules in +23  
usmlecrasher  can anyone pls explain why it is not << potential false- positive results >> ??? +  
almondbreeze  correct me if I'm wrong, but 'high FP (choice C)=low specificity (choice B)'. Whereas high specificity is required to rule in dz +2  
almondbreeze  picked positive predictive value myself. can anyone explain why not PPV? +  
williamfreakingosler  The principle @hayayah is talking about (a negative test being relied upon to reliably rule out) is negative predictive value ("NPV"). I don't see why "uncertain NPV" isn't the correct answer, particularly because NPV is predicated on the disease having the same base rate in the person(s) being tested as in the population that was characterized for the test statistic. Given that the patient has a strong family history of colon cancer, the NPV of FOBT is uncertain. Said another way, the sensitivity of a test does not change with the population, but the NPV does. The whole reason the doctor is denying FOBT is because of bayesian thinking (a priori information related to family history), and from my point of view bayesian logic is more relevant to PPV/NPV than to sensitivity, hence my confusion over why NPV isn't the right answer. +2  
ibestalkinyo  I thought negative predictive value for the same reasoning +  
raga7  AFTER THE RESULT OF TEST WE CAN USED PPV OR PPN, BUT FOR TEH FIRST TIME LOOKING ANY DESEASE USE SENSITIVITY OR SPECIFICITY. +  


submitted by laminin(15),
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accesyeltTinr heva a ihhg nfaitfiy to rmof elsahtec whit yvntllpoea etacillm oasinct scuh sa eF+,++ F,e++ +A,+l+ ++gM adn C++a. anyM fo etseh laecntettlaryimc-e mepecloxs are rehtei euinlolsb ro weoesirht plrooy lrobbabsae ormf the -intiaontssgatlre .tctar Mikl adn ohetr rydia sutprodc, actdisna gintoannic yvpeloalnt ac,tosin as ewll as vausroi onri asslt sniteegd usolsuntlymiea htiw yeitralencct ievvrtseid,a thgmi eiefnrert htwi hetri ipantsboor by 50 ot 9%0 or vnee e.rmo ousec:r u.9g4hb/h.w:t8n9/vlmd/sw5i.p6bontcm.wi/enp

almondbreeze  FA 2019 pg. 192: Do not take tetracyclines with milk (Ca2+), antacids (eg. Ca2+ or Mg2+), or iron-containing preparations b/c divalent cations inhibit drugs' absorption in the gut +1  
fatboyslim  This is also why tetracyclines are teratogenic and should not be given to children because tetracyclines chelate with the calcium in the teeth and cause tooth discoloration and inhibit bone growth in the fetus/growing child (Source: SketchyPharm) +  
kevin  just remember fluoroquinolones also are prone to chelation. you know it's gonna pop up on the real one +  


submitted by hayayah(1081),
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Aaitdtrionmisn of cilnePnili fro ipsiShly yma aeld to hte ermHrsxrhaJhiece-i coitraen uhrso ftare .eenttmart uscrcO ued ot yissl of pioersctshe (so it acn curco wiht reorliaB adn sriiepstsopLo sa lwe.)l hTe nocireta is reacadzcehirt yb ervef nad lsl.hic

The lailcascs axoliapentn of hte Hmhreexeir itceanor is atth ttaneemtr reslstu in teh eddnus dthae dna idrtecotnsu of ralge reumnsb fo rpmo,snteee twhi het onebtiirla of opintre sdpurcot dna toxis.n

almondbreeze  FA pg.148 +6  


submitted by hayayah(1081),
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iepaattC adn atnlue rae in teh netrec fo teh a.pml pCaatiet is ont an t,oopni so uleatn is eht wan.res

onaiiltDosc of natuel yma asuec euatc n teunrlalacp rsomedny.

yotsubato  Lunate is the only carpal bone that is frequently dislocated. Scaphoid is frequently fractured. Hook of hamate is also frequently fractured. +3  
redvelvet  and also point tenderness in the anatomical snuffbox may indicate a scaphoid fracture. +3  
chandlerbas  yes lunate is the most common dislunated carpal bone ;) +4  
almondbreeze  FA 2019 pg. 439 : dislocation of lunate may cause acute carpal tunnel syndrome +  


submitted by monoloco(136),
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ishT si hte nylo ceoihc tath soecm oscel ot kngicin the ihatoccr cud,t fpceiycillsa ta sti nt,ile het ftle aciasub.lvn

kpjk  why not midsternal thoracotomy? +3  
wuagbe  because the thoracic duct ascends the thorax posteriorly, and enters venous circulation from behind. link to image: https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/thoracic-duct +5  


submitted by johnthurtjr(145),
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ehWli I acn tge on dbaor htwi dnutAjtems sird,orDe I ndot' see hwo shti esanwr si yan eterbt hant cSmtiao Symtmpo Drori.dse ormF :FA

ryitaVe fo boiyld lnctaspimo nilgtsa hotsmn ot yersa ditsosecaa ihwt exi,vsseec pstsreeitn thhogust dna aiyxnte btauo s.myopsmt aMy ppecar-ao twih i.selnls

DSS beolgns ni a grupo fo rsrsddeio rcezreiadhtac by cpiylash oypsmmts nugscia sgiaicnfitn dsetsrsi dan prnammte.ii

savdaddy  I think part of it stems from the fact that this patients symptoms are occurring within the time-frame for adjustment disorder while SSD seems to have a longer timeline. Aside from that I find it difficult to see why SSD wasn't a possible answer. +4  
chillqd  To add to that, I inferred that the obsession with checking temp and with the tingling sensation were signs provided to him by the physicians of recurrence. He is anxious over his cancer recurring, and they are more specific than a variety of body complaints +1  
hello  In somatic symptom disorder, the motivation is unconscious. I think for the patient in this Q-stem, his motivation is conscious -- he wants to make sure that recurrence of cancer is not going "undetected". +15  
cienfuegos  I also had issues differentiating these two and ultimately went with SSD, but upon further review it seems that a key differentiating feature was the timeline. His somatic symptoms would have had to have been present for at least 6 months per the DSM criteria https://www.ncbi.nlm.nih.gov/books/NBK519704/table/ch3.t31/ +3  
almondbreeze  @chillqd Same! Why not OCD? He's fearful that something bad might happen (=cancer relapse; obsession) and calling his doc (=compulsion) +  
kevin  great reasoning @hello, this was confusing me but that makes perfect sense +  


submitted by sympathetikey(1376),
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Ceoihc .A oudwl ehav bnee tcecrro fi htsi tnetaip wsa d.mcmsomriimoupeon erP trisF dAi, If" DC4 00t,l&1; Fn:intdgsoneB.r..ailal iclpoNhrutei nmmiIna.toalf

evoe,wrH sa sthi aetpnti ash a entcmtepo mieumn syme,ts buzz wosdr rae tatleels ticnrioezng aralsmognu.

yotsubato  Everyones choice A is different. +  
sugaplum  they mean- Diffuse neutrophil infiltration +1  
macrohphage95  what does stellate necrotizng granuloma means ? +1  
krisgsxr600  always with the details! losing dumb points :( +1  
futuredoc12345  @sympathetikey Doesn't the biopsy finding vary with the biopsy location: Lymph nodes have stellate granulomas and Bacillary Angiomatosis (skin lesion) has neutrophilic inflammation. What do you think? +  
chextra  @sympathetikey Pathoma chapter 2 says cat scratch disease forms non-caseating granulomas +1  
almondbreeze  @ chextra Same with FA 2019 pg. 218 +2  
almondbreeze  Sketchy micro: Immunocompetent: regional LN in axilla in one arm (like our pt here) Immunocompromised: bacillary angiomatsis is transmitted by cat scratches +  


submitted by sympathetikey(1376),
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iohCce .A lowud heva eenb tcrceor fi tihs iaettnp swa nmciimosruomed.mpo ePr Frtis i,Ad f"I D4C 10lt0,&; ngaeaF:dsonrlit..i.nlB tlcieoiuNhpr nato.fmamInil

vH,weeor sa sthi inpteta ahs a emptcenot umnemi metsys, ubzz rodsw rae llsteeat inztcionger uglrmnaaos.

yotsubato  Everyones choice A is different. +  
sugaplum  they mean- Diffuse neutrophil infiltration +1  
macrohphage95  what does stellate necrotizng granuloma means ? +1  
krisgsxr600  always with the details! losing dumb points :( +1  
futuredoc12345  @sympathetikey Doesn't the biopsy finding vary with the biopsy location: Lymph nodes have stellate granulomas and Bacillary Angiomatosis (skin lesion) has neutrophilic inflammation. What do you think? +  
chextra  @sympathetikey Pathoma chapter 2 says cat scratch disease forms non-caseating granulomas +1  
almondbreeze  @ chextra Same with FA 2019 pg. 218 +2  
almondbreeze  Sketchy micro: Immunocompetent: regional LN in axilla in one arm (like our pt here) Immunocompromised: bacillary angiomatsis is transmitted by cat scratches +  


submitted by sugaplum(382),
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B enHle-es aCt htrcSca in cm-nmoeotiunotpm - lytnpyw.o:/otccopulitghsct/tncell/i./ohaashaommstmettc.wphhrdwpoe oalrt lBna hsaeelne ni op-modecsommImr-uin lcBiriaya mitnasgiosota L ksoo like pksiao saocamr ffDusie " ornchuitplei litrafe"tin FA 2190 717

almondbreeze  FA 177 says Kaposi has lymphocytic inflammation whereas Bartonella spp has neutrophilic inflammation. I guess this does not apply when immunocompromised? But doesn't Bartonella usually affect the immunocompromised ppl? +  
almondbreeze  Got it after seeing that she's immunocompetent +  


submitted by sugaplum(382),
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B e-elsHen Cta cracSth ni pimnoot-mmenouct - adaoacnosihgrlwt/ptc/iconh.uwptclyhtpts:lopmc/hosteeottwmh/l.my.ta rlnalBe o sheenael ni rodnmemIim-ms-opouc aiilByrac mastsgoitoain Looks lkei aioskp camsoar suffiD"e piteoihurcln attrfleni"i F A 0921 771

almondbreeze  FA 177 says Kaposi has lymphocytic inflammation whereas Bartonella spp has neutrophilic inflammation. I guess this does not apply when immunocompromised? But doesn't Bartonella usually affect the immunocompromised ppl? +  
almondbreeze  Got it after seeing that she's immunocompetent +  


submitted by xxabi(261),
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s’oBacr ais:haap ersseevxpi oo(rtm )pahaias iwth ramastigmma stp( rawea taht hety ’ndot akem seesn) - reaa neiecAkW rs’ pasi:aha eertcpiev erso)syn( aahaisp htwi emidiapr snoirhenoepcm t(ps lack )tgsnhii

breis  Why would B be incorrect? I realize Broca is "technically lower" but A seems too low to be causing weakness of the lower 2/3 of the face? Am I missing something? +  
shaeking  @breis B is incorrect because of the lower 2/3 of the face weakness. B isn't located on the motor cortex but in the premotor cortex, plus it isn't low enough for the lower two thirds of the face. https://thebrain.mcgill.ca/flash/a/a_06/a_06_cr/a_06_cr_mou/a_06_cr_mou.html https://www.sciencenews.org/blog/science-ticker/homunculus-reimagined +1  
cienfuegos  @breis, per UW: "a/w r. hemiparesis (face & UE) bc close to primary motor cortex" +  
almondbreeze  B is close to premotor cortex which is involved in learned or patterned skills & in planning movements. (i.e. two-hand coordination) slide 25/37 :https://www.slideserve.com/hal/the-motor-system-and-its-disorders +  
almondbreeze  B is also close to frontal eye field; eyes look toward the lesion FA pg. 499 +  
frijoles  I incorrectly picked C. When answering this, Broca's "broken speech" was my first thought, but I figured a lesion causing a facial droop would have to involve the motor strip so I prioritized that and chalked up the speech issue to dysarthria (I understand this is more of a "slurred speech" than broken, abrupt speech, but again, I simply misprioritized concepts.). So for the record, Broca area is part of the motor cortex? +1  


submitted by xxabi(261),
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csrBoa’ a:aiphas veieperssx mr(oot ispah)aa hitw atagmasrimm pt(s rewaa taht tyhe tndo’ ekam ees)ns - aera esenkcA’ Wir psh:aiaa crpteeevi rs)sonye( paasiah iwth mpeardii smeooprncnhei pt(s klac ihtnigs)

breis  Why would B be incorrect? I realize Broca is "technically lower" but A seems too low to be causing weakness of the lower 2/3 of the face? Am I missing something? +  
shaeking  @breis B is incorrect because of the lower 2/3 of the face weakness. B isn't located on the motor cortex but in the premotor cortex, plus it isn't low enough for the lower two thirds of the face. https://thebrain.mcgill.ca/flash/a/a_06/a_06_cr/a_06_cr_mou/a_06_cr_mou.html https://www.sciencenews.org/blog/science-ticker/homunculus-reimagined +1  
cienfuegos  @breis, per UW: "a/w r. hemiparesis (face & UE) bc close to primary motor cortex" +  
almondbreeze  B is close to premotor cortex which is involved in learned or patterned skills & in planning movements. (i.e. two-hand coordination) slide 25/37 :https://www.slideserve.com/hal/the-motor-system-and-its-disorders +  
almondbreeze  B is also close to frontal eye field; eyes look toward the lesion FA pg. 499 +  
frijoles  I incorrectly picked C. When answering this, Broca's "broken speech" was my first thought, but I figured a lesion causing a facial droop would have to involve the motor strip so I prioritized that and chalked up the speech issue to dysarthria (I understand this is more of a "slurred speech" than broken, abrupt speech, but again, I simply misprioritized concepts.). So for the record, Broca area is part of the motor cortex? +1