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Welcome to hello’s page.
Contributor score: 301


Comments ...

 +0  (free120#2)

This is the least offensive response.


Choice D is incorrect is because although true EDs triage based on severity, telling the patient (especially since she's angry) this could offend her by suggesting their reason for the ED visit is considered "not important".


 +0  (free120#30)

The patient developed peritonitis due to a perforated appendix. Peritonitis is an intra-abdominal infection.

The most common intra-abdominal microbes to cause intra-abdominal infections are Bacteroides and E. coli.


 +0  (free120#9)

Echoing @waterloo's comment.

This Q is essentially asking "What is the function of Southern blots?"

Answer: The function of Souther blots is to check for BCR or TCR gene rearrangements.

See @waterloo's explanation for what is specifically going on as far as why there are different bands at different places. Again, the answer to this is "gene rearrangement" but @waterloo explains in with more detail.


 +1  (nbme18#30)

Pt has a pituitary adenoma + weight gain + compression fractures.

Prolactinoma = most common pituitary adenoma. However this male patient lacks appropriate symtoms, e.g. decreased libido + infertility. Eliminate choice A.

**Eliminate choice C because this patient does not have signs on increased testosterone.

Eliminate choice E because this pt has weight gain, whereas a TSH-secreting adenoma would cause weight loss.

You are now left with choices A and B.

ACTH-secreting tumors are associated with weight gain + bone fractures. This is because increased ACTH causes hypercortisolism, which has an AE of osteoporosis. This is choice A.

hello  Also, choice B is incorrect because a GH-secreting tumor would result acromegaly (enlarged hands, feet, head), which this pt does not have. +2

 +4  (nbme18#5)

This newborn is born prematurely at 28 weeks, so his respiratory distress is not having fully matured lungs.

Fetal lung maturity is indicated when the Lecithin:Sphingomyelin ratio is > 2.0.

Because this newborn is having respiratory distress due to lack of fully matured lungs, it means has decreased lecithin because his Lecithin:Sphingomyelin ratio must be < 2.0.

Lecithin = Dipalmitoylphosphatidylcholine = phosphatidylcholine.

E is incorrect because surfactant protein D is an innate host defense component of surfactant, i.e. it does not function to prevent alveolar collapse.


 +3  (nbme18#2)

This patient has been taking HAART therapy and subsequently develops resistance mutations. The therapeutic purpose of HAART therapy is to target reverse transcriptase and protease enzymes. Since the patient is taking HAART therapy and subsequently developed viral resistance, we know the resistance has developed due to mutations in the genes that encode reverse transcriptase and protease.

cbreland  "High viral load" made me think that the main issue was rev transcriptase inhibitor being messed up. Picked the only answer with that as an option +

 +0  (nbme23#2)
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yhW aer orao"trt ufcf "arte nda orortat" cuff sei"dinttn r?gwno is it bc bhot fo sehte duowl hwos ntnmeepiimg ins?g si eerth a awy ot DxD eon orfm the ?throe

snripper  It can't be rotator cuff problems because abduction is normal up to 90 degrees. +2

 +0  (nbme23#45)
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ywh si laaspm cnocito epresrsu ?ownrg

rainlad  I think it's because we would expect to see some more proteinuria/albuminuria if the plasma oncotic pressure had increased to compensate +1

 +0  (nbme23#50)
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whcih ertelt is NC XI ni thsi aa?grimd

titanesxvi  A think is D, but it is not very clear +1
usmlecharserssss  A WHAT anatomical structure is this ???????? +

 +1  (nbme23#33)
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nca emnoeso alseep xieplna ?shti

thomasburton  My reasoning was BC>AC so this must be a conductive problem (which to me means something middle ear or out) so usually I think something blocking air flow or impeding the ossicles. You can rule out all other answers as they are all causes of sensorineural (AC>BC). +2
madojo  Meniere's disease is sensorineural hearing loss with peripheral vertigo due to increased endolymph within the ear. +

 -1  (nbme23#7)
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t'Wsah eht emoyssceh ossppude to eb a ucel ot?aub oeDs tish iatepnt veha DCI? Dose CID walsay ueacs eimpovhyocl h?kcos

drdoom  Disseminated intravascular coagulation (DIC) is a syndromic definition. (See tangent.) It does not “always” lead to shock but shock is definitely a possible sequela (since, by definition, DIC = “systemic thrombotic process”; anything systemic should get you a little worried), and so a patient with DIC should be monitored closely! +

 +1  (nbme22#29)
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seePla eplh - hwo rea yuo laeb ot etll htta teh CT egaim si tno at hte vlele fo dme?dunou

I nd'to nkow ahwt I'm giooknl fro to mecraop nda trontsac a CT at hte velle of teh dounmeud sv teh CT inevg ni siht .Q


 +0  (nbme22#1)
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hereT ash ot eb a eertbt iaotpenalxn for why ANP si gr?wno

waterloo  If this pt's ANP/BNP were causing him to become hyponatremic, why does he have fluid overload symptoms (bilateral crackles, JVD, high BP)? There has to be something else overcoming the ANP system. +

 +6  (nbme22#4)
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Sipactlnoerono adn neloerpene era aus-tnsspmoprgiai iduietsrcc ttah ibtinih teh NaK/ TPaeAs. N/Ka aPseAT si no eht alslbtaaeor .mebenmra nNeo of the nsewar heccsio ift hwit ht.is

Ardmoilei dna emreiettarn are lsao puriposinsga-smta etdu.isirc ehT imencmsha is to lcbko EaCN nnhlaesc no hte aimnlul mneebm,ar htis si ccehoi ."B"


 +0  (nbme22#37)
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If ouy ende a efnirtefd aotnitoiner rfo a radgaim fo eth swaat:yph

Meais_pemtei1-A1=.eiapn1p01_4s0i0f/nt:88ya6FrpLr83/Mt-aa%2blm_j/tO?1ru/gF%n.46gwu2csi1eg/./l3T2ab2._n0t41rrehsre3tm1decst4igip0d/socsa-Hg31-3/3


 +0  (nbme22#41)
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enitPta sha a ethirahomx + CXR owssh ctarahe esiteadv artwdos eht xomrhtihea &g-;-t tmos yilkel sagdisnoi is ouasesntonp onoexprahtum.

cpliElmgloaydeiio, pounassoetn mnphtuerxoao si tmso dsasaoicet ihtw ntih msela

hello  Wait, maybe this is wrong logic? Please correct me regarding the exam findings if needed. +
hello  Can confirm that this explanation is INCORRECT regarding trachea. Disregard this explanation. +

 +0  (nbme22#48)
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eaplse pleh -- If oetapeivsi-actals bteaaicr niatruelze ihret wno pieerxsdou, yhw nist' it eht ceas ofr psetcsvaa-oleiita ciarabet to ntfioniesc in evnyer?oe

m'I nto agunidsdrnnte het noneiocntc to ANDPH daeixso cyfdeicne.i

hello  to cause** infections in everyone +
bmd12  Bc everyone isn't NADPH deficient, meaning they can produce their own superoxide without needing to rely on the superoxide produced by the bacteria. +1
bmd12  so even if catalase positive organisms neutralize their own superoxide, our body is producing its own and not relying on the ones produced by bacteria. You only begin to rely on the superoxide produced by bacteria if you are NADPH deficient. +

 +1  (nbme22#20)
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yWh ti'ns hits a rhctoo s?udty

drdoom  This is a cohort study! (Since it involves splitting people into "groups"; group = cohort.) But the stem asks what "best describes" the design. So, yes, it's a cohort study but a more precise ("more specific") description is Open-label. In other words, "Open-label clinical trial" is a type of cohort study, and, in this case, "Open-label" is a more precise description of what is described in the stem. +7
drdoom  For a more technical explanation of "Cohort studies", see the definition from the National Library of Medicine: https://meshb.nlm.nih.gov/record/ui?ui=D015331 +1
angelaq11  It is a cohort, just as @drdoom said, but it isn't an "Observational" one. +2
pg32  It's actually not a cohort study, imo. In a cohort you find people with an exposure and see if they develop some outcome. In this experiment, people were RANDOMLY ASSIGNED to the different exposures. That doesn't happen in cohorts. +7
pg32  It may be a cohort in that these people are in groups, but for the purposes of Step 1, I don't think we will deal with typical "Cohort" studies in which participants are randomly assigned. +2
ashli777  you don't administer an intervention in a cohort study, you just observe what happens. it is an observational study. +
drdoom  ^ i retract my earlier subcomment! thanks @ashli777 and @pg32 — you guys are right that cohorts do not intervene! in two senses: (1) there is no treatment intervention and (2) there is no “assignment” intervention (either randomly or by selection; that is, investigators do not DESIGN or DETERMINE how groups are formed, even if that means random determination by computer). +1

 +0  (nbme22#32)
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roF lppoee iaskgn wyh hte tdaa eblat aws even ldeunidc fi it swa not neeedd ot esnrwa siht Q, eher is a usulfe nxt:oeialpna

ehT eltab asw evgin esubcae a 22x lebta is lalpcytyi athw oyu od see rrneidagg adta fro loreat-occns uitdses.

If the 2x2 etlba ta'nsw cud,ledni then lllieyart rntevoeye owdlu kcip Coceih E"" sa eht oertccr srwaen c/b uoy tacn' lcelcauat gitmenohs thwiout iebgn eproidvd eb.rsnum

ehT recefeifnd ni lgnciuind het tbeldtaa-a si hatt:

  1. i,angA you eedn ot ptroer a 22x aletb eaecbus hatt is iyyclplat wtah oyu wlli ese gidnrgaer daat orf a alo-tsoncecr sdtyu

adn

  1. by dngcnuili hte 2x2 betl,a ti lcltuaya tesst if het etstk-ater iadrleze ttha teh aatd ni eth x22 lteba esdo nto hepl ta all ihwt ilulacgtacn renvce-ep-al bcseaeu sctenoolac-r esidstu VNERE tepror no ln.pereecva
hello  I also want to add that the Q is asking about sinusitis in the GENERAL population, meanwhile the Q-stem discusses a case-control study that is studying the relationship of smoking (an exposure) to development of sinusitis. To then ask "what is the prevalence of sinusitis in the general population" totally disregards taking into account the exposure of smoking which was the entire reason for the study. In other words, asking prevalence would be very non-sensical. +

 -8  (nbme22#9)
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ientaPt hsa dre lyca srah- iths tfsi mreo wtih HHV-6 seoaRlo( ),vrius tno suP.ivrovar

V-H6H aessuc mteonordaif of ,loayerbthsts digaenl ot me.aina

hyperfukus  Hey so i just looked in first aid and it says "diffuse Macular Rash for Roseola" and usually you have a super high fever and febrile seizures are almost always mentioned...I found in my notes from uworld that i mustve filled in a long time ago for Parvo: Infects Erythroid precursors + Replicates in BM Face/cheek rash followed by LACY Reticular rash on body...May get Rash from IC deposition...and then again i wrote replicates in erythrocyte progenitors causing reticulocytopenia which makes sense why dec Hb and dec Hct +3
hello  @hyperfukus is correct. Disregard this explanation. +

 +4  (nbme22#43)
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Pittnea notncna xedten r,wtsi cihhw is rainedtven yb aridla evenr

antetPi has eneb no rt,checsu hihwc lodwu taffec llyraxai vnere ;t--g& stih fcfsate ddoelit semc,lu hhicw osde rma ncautobid 1º1500- so( it nca oanymlrl meov ram oavbe ude)srloh

heT noyl otoniacl in eth geinv damaigr ot efftce lla fo heets rensve dowul eb tolcioan ""C

teNo: maonr,yll rma mevemtno aoebv the zolhirtnao si ciosadatse with sartsreu tearorin mnlglcse/uo aothircc renev. oHe,erwv nnoe of teh imdagar scooatlni loalw orf locunsini of SATL. iecnS the teiptna sha bene on chertscu ofr w,ksee it gtgsesus xryliaal enrve onmnvteielv ;tg&-- idteold si tdefecaf

kevin  saturday night palsy is radial nerve; only hint for axillary was arm abduction +
anechakfspb  The crutches would affect the radial nerve (FA p440). +1

 +5  (nbme22#14)
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heT tptaine is ydadt.eedhr deeN ot egvi rtaew ot deetyr.rha

raeWt ollowsf t.sluoe If uisdmo si deadd to het lutoos,in treaw lwil fowoll het omusd.i Now, eycrtteeon ukapte of mosdiu si madeteid yb SmoGueucs-iodl tnrtraor.eps ,nceHe hte nliuosot endse to anoitcn dumios nda ulscgeo ni orerd ot ahve het reytesceotn eakt pu teh uisod.m


 +4  (nbme22#11)
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The Q si sgcrendiib het noltfregimeoa eernv, wchhi rnsu on eht leeatnxr aecrsfu of teh cmrtsaeip droc at teh uiealrscpif uniilgan nigr

Tihs Q is TON errefrngi ot iilinnigloau nrvee -- het onliiailugin evnre tseix UOHHGRT het frcpiiuslea nuilgain alcna erewash itsh Q is gkasni obuat a rneev atth si ETXAERLN to the riilfeaspcu niginlau lcaa.n

eeS ncseac:s/.dtinoauetaipodrrhgnkjciwtfmei/wg.a/.vnlpie.fgtcwpa/e/

trump2020  This is incorrect. You have it backwards. https://en.wikipedia.org/wiki/Spermatic_cord +3
medjay7  Actually I think @hello is right. First, because that's the only way this shitty wording question makes sense, second cuz it says "that lies on the EXTERNAL SURFACE" that means outside of the spermatic cord, and the genital branch of GF nerve actually does: The genital branch of the genitofemoral nerve enters the inguinal canal via the deep inguinal ring. (https://www.ncbi.nlm.nih.gov/books/NBK430733/), and then exits to innervate the anterior and superior scrotal skin (also the cremaster muscle). +
medjay7  CORRECTION: Nevermind, everything I said is wrong. I hate this question +1

 +1  (nbme22#34)
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hsiT the aesm sa ympyo'sackne@ xnpntaiaeol iwth eorm enapanoxlit etohs taht dene ti...

Teh ptantie si efctedaufn yb eht iatprulrac otmasalou rseievces issaede and shi robhrte hsa the aooalsmtu icevsseer daesies t&g-;- hits maesn hace of theri ptsaner arerics eth AR al.llee ,Nwo ofr teh tneiatp to be dfncutfeea ivgen atth hbto ish prtasen evah the RA a,ellel ti seman hatt het tiptena hsa a /32 cehnca ahtt eh is nmesluliosaytu fueenctdaf dna a acrre.ri

The atsnpe'it rpntrea is tfdaunecfe adn nlroam diHrg-aenyWerb iseegcnt (as sedtta ni eht .bhmrwepno.)el hsti si lisecifacpyl n,dmnietoe you are ot smueas thta eth tprearn sha a rreraic eqfucreyn rof hte RA l,ealel iwhhc aulqe to 2q.p

heT isaedse sah a qyucenefr ni het oipnuatlpo fo 04/1000. siTh si ^q2 ;&-tg- q2^ = 4000.0/1 vgSlnoi for ,q you get q = 1020/.

arrirCe frcyqeneu is 2.qp verewoH, fro a arer esadeis, 2qp ≈ q2. S,o eht rceiarr qnurfyeec rof teh areprnt = 2q = 2 * 120/0 = 0/101.

,wNo teh Q ksas atoub an spngoiffr of the pnaitte nda ish prterna bineg eecdfatf, so to vhea an ectffdea ,lhcdi tehre is a 4/1 cnache of hginva na etadeffc hdilc ess(cbaeu teh atntipe nad eth repanrt hbto veah a /21 hecnac fo snpagis teh alleel g-;-&t uyo pltmulei ehtes etotehrg 1/2 * 1)2./

So, ptlyluim 23/ * 1/010 * 4/1 = /.1600 hTsi si Ptaetpin( geibn a )rreirca * renar(tPp bineg a irre)rca * Pagv(ihn na teeffdac rfgnofisp o)eghtetr.


 +6  (nbme22#35)
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heT amramgr of het taaucl Q was gonu.fnsci

To meka beettr ,seens ti oulhsd say ihWch" of hte owllinofg is teh tmos lelkiy uetrls on teh tannprritoics fo nsgee hatt hintbii lcle diiovisn adn ttha cnntaoi teh ensnuossc eequsceen TTAA..."

So, teh Q si nisgka otuba teh 5p3t gene adn lelipicyafcs buota eht p53t egne emropotr gnoire.

oorrtemP sinrego heva a AATT oxb ivubys,(olo mignnea rihc in TA- aseb srp).ai A-T sbea giaprin has 2 horndyeg o,sdnb hhwic amkse meht iasree to claeev --&;gt lwaslo for AND tinornpsaicrt to curco eomr iasye.l RAN olP odse apninrsticrot fo NAD onit AR.N

The rieent Qte-sm lstak tuaob who unrem-iFLia is ued ot a mtuiaton ni 5p3t ,eneg inladeg ot a akcl fo tmuor uspsspeorin i.cvtitay

o,S if eht orrtpmoe roigen TATA xbo fo the 5pt3 eeng si au,mtetd tenh teh p5t3 gene llwi ont etg siadctnrber ;--t&g stih si why ereht illw be caeerddse RNA oPl i.ibnngd RNA olP iwll have a ceeudrd ayilbti ot dbni tp53 t-;-&g sesl umrto ssrurpseo enge iiartsnortcnp -&t;-g slse rtmou seupo.pisnrs

jcmed  that would be overly easy of them though eye roll +

 +1  (nbme21#29)
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I nwat ot ezeparsemi-h stgmhieno thta asyop@asstl hsa yedraal etstda .):

The Qmt-es eststa rmuse gsoclue = 100, and eht Q saks hyw teh tpiaent si elba to nitnamia omrcone.mgayli

,rreTofhee yuo can yimmeedailt lmeaiietn scechoi A and C esuabce aeecteaattoc adn bxehttyerubtaryda-oy rea csrsueo of yrnege irdnug eeonsgiekts -- sioktesnege osed ton pvoreid ulescog enreyg .ssecour


 +0  (nbme21#29)
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eelsPa eplh

hyW is nileav t?enocricr

An tlnaaxiepon elbow syas that ainvel dwuol be nevcdorte ot geocsul ignudr rulagre isamo?lebmt

agleuRr osamelbmti = efd ta,est so yhw uowld nevali nvee be redcoetnv to ?cogslue


 -2  (nbme21#5)
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sihT si het caulat trcceor inxapnelt:oa

DAP cassue bldoo ot lwfo orfm ecdignesdn traoa ot npttea cdstuu asiorurste tino pnlryuoma iclotucairn ()re"-fhltgtito-"

ehT "etsa"l from eth atrao rguind odtsiael rueiqers daesecnir crciaad potutu to mpocetsaen to deleriv eaadetuq naoutm of ldobo to stre of dboy

eScu:ro vm./bh0ng//iln/4bBKi:t5/Nhstc..3wno7.wkoow8ps

fkstpashls  It's L to R +1

 +0  (nbme21#16)
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lseeaP ehlp

Mi-ydssctiol eojtenci lcikc = iclnmpou osnsetsi

wHo is nloipumc sitosnes rdeaelt to eth 'tstaenpi SAD -- oesd SAD eucas uocmnlip ss?ieto?sn

burak  ASD has typically 3 associated sounds according to UW, they are all about increased blood in RA. Increased blood in RA causes more blood do ejected from tricuspid (dşastolic rumble), and more blood to be ejected to pulmonary circulation which cause pulmonary flow murmur (midsystolic murmur in pulmonary region). It even can cause pulmonary regurgitaion like murmur, but most important murmur in ASD is typically midsystolic murmur. You can check it out on FA 2018 page 284 +2
hello  Ok, what I learned: Extra blood in the right heart (due to ASD) doesn't lead to pulmonic stenosis? Instead, it's that pulmonic stenosis = most common comorbid heart association with ASD +1
burak  No it's not pulmonic stenosis, it doesn't lead. Murmur associated with ASD is pulmonic stenosis-like murmur, because it's caused by excess RA and RV volume ejecting to the pulmonary arteries. So it's same location with pulmonic stenosis, and it's systolic. You get it? +1
hello  @burak Yep! +

 +0  (nbme21#17)
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rFo oaynne unocdfes rtniyg to oowllf erseuu0'sl@s07m mcomnte

lghiSlty iddmeifo

Esslaeint oaimn sicad mnnmoeci Ah," ereTh safn lwil try tehe"tmh

Ah = ir,geinna tnsdheiii

rhTee = hneoiernT

nFsa (hpan=)s aynellnihenaP

iVll llw(i -- mrnGea eantcc rniugpnoocn ishlgnE ordw "iw)"ll = lanev,i ic,nieluoes nue,clei sleniy

Try = tpoyhrnatp

hetM = inMeentioh


 +12  (nbme21#36)
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tuMellip maymleo = emaplson of mlaspa .ellsc

lmasPa slecl roucepd trceeosry 'sbA a(ka udorpec ')Asb -- aalpsm cells od tno ehav mnnmbr-ouabeed gI ak(a do tno evah )C.B'R

To :eaprc e-amnnebrbmuod Ig = BCR liehw rctsyereo gI = A.b

,owN i-oicnatydtpii tyinbdoa = toniadyb snaaitg bidat.noy

mlaaPs sclel do not inotcan ufscera gI -- ecasbue msaalp scell olyn eb ceseetr bA's.

,rhreofeeT adioci-ipytnit adniotby wolud nto wrko ot tagret maeymlo lslce uaebces moylaem escll = lmsapa eclls aak aampls lslec kacl euarcfs cuoemlsle ahtt iiycpit-ntaiod Abs' odwul nede to inbd at.egor/tt

See ra:amdig s-nfc0cgr/fdtucq-fcqh2/em3iamfi5e9cn8n4at250.4paahp89c3q.e1.sbf/:teoa1


 +4  (nbme21#4)
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The Q etms satest FXOO si a priinosnatrtc toarfc htta eonsrsdp to lnniius nilniggas yb tgiraeln hte ntinotsrpaicr fo cbtaomile gnees g--&;t r,foterhee OOFX is a ntirocniatspr rtoacf dnveoivl ni lbsimmaote. ihTs ludosh kmea nesse sueaceb cieulripre-snton otnitaicav ahs a lero in ieuralgngt embslt.aimo

isTh Q asks taubo lverbrseei sawy ttah nuliisn tegreasu OXFO icrtonsntrpa facrto ai.cvtity

qiidmaitenUdi-teub stlosprieyo si veeirielbrrs. tiiaeEnml all ceshcoi teexpc orf ,B D, and .H

-unlcIetspseirrno unnfiotc rhhgout IP3K iainsngl.g 3KPI iasgilgnn nivevsol ohrniplysophtao of neresi ;tg&-- eresni iphatpoohsylnor is a vberireesl sscr.peo iaEtminle H. :YFI on/neimtpoari adci tihrnopoaypshol si yawsal reeliv.rbes

uoY aer left tiwh cehciso B nad .D

FOXO si a osttpcnririan catfro &;-g-t stnparoincrit rotfasc teeimda gene iciatyvt yb hnitlgtsu ebnetwe teh aplycosmt and ucnel.su igaRelgntu eht lnciotoa of OFOX rnnatprisotci troafc e.i.( tcpslamyo s.v cuunlse) wlli eefehrtro virebyerls tdomaule mXdOei-atFedO betamlcio nege vt.iyiact

shiT veeasl uoy tihw teh eocrctr nr:swea ceihoC .B

adong  A better way to think about it is insulin acts through MAPK which is a serine/threonine kinase +

 +8  (nbme21#39)
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^2q = 0109/ -;-gt& q = 031/

rreriaC cfenreqyu per reiaW-yndbHerg rfomlua si p2q.

,wNo fro rera tmoasalou sseeivcer seiasdse het cerairr ecfureqyn fo 2pq ≈ .q2

2q = 3/(201) = 32/0 = 15/1

eAsnrw = 51/1


 +7  (nbme21#10)
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The tpentia hsa "lcsel reraagdn ni afinigltirnt seseth" -g-;&t tniediacs inagantlm arcnce ec.sll

heT cslle rae ethnier drlglnaau orn uuaosqsm -&g;-t hte enracc si tenheir ccnanoeaairdmo onr suqmousa cell lgun rcacn,e pesylretvie.c

ihsT asleve sallm oat lecl glnu cer.can SHDAI si eht msto nmoocm rsilpaanoactpe nrdmesyo for slaml aot lcle gnul raeccn g&-t-; asled ot yaeoiamtphnr.


 +7  (nbme22#21)
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nnioKwg the +LR avule = 10 osed nto hlep ot lsveo hist Q aeucsbe inamttegsi hwere "10" odhslu flla no an iaxs is ari.ybtrar o,lsA hte adta npisto rae secoordinta -- hyte avhe na X-ulave nad a e-lvYua ,X( ).Y

hTe awy to orpahcpa ihts Q si to nkow taht a hihg ciiiyestpcf amnse tath a epitsivo rseltu is ,eryv very ylleik ot be a eutr vi.isetpo

osupSpe taht het ycpteiciifs is 9.90 -- tish si %99 cfetcispiyi. nTeh, uyo oklo at eth h.pagr The Xias-x si ct1-"epfisciiy". S,o ssppeou eht setb stet has a eftpiciscyi fo .99% eTn,h alcaleutc -1peyiiis tfcc = 1 - 9.90 = .0.10 uoY dwluo enth hesoc het dtpoatani thta ordrsnpoces ot iahvng na lva"Xe"-u thta si otscsle ot the o.ngrii In htis elo,mprb it dcersroopsn to dtaa ipotn "A."

uoY o'dnt even dnee ot knwo a cecpisif stfiepcycii vaule ot eovls ihts meolp.br lAl oyu nede to od is eutndsandr ttah if hte ftcieyspiic si etxyermle gi,hh yuo ilwl eden to find a tadaontip that si lectsso to the igniro -- at tales fro hte uvale ni eht ais-xX ni hte anoroceitd of hte aatd tponi -- aebucse eht -axXsi orcosdsepnr to a ituanacclol fo t1.es"icc-fi"yip

link981  Excellent explanation but a minor typo. 1-0.99 = 0.01 not 0.10 :) +2

 +19  (nbme20#17)
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ajGnlo adh a rculete that eitnneomd that If" a ipeattn ahs gtaoaerrl,cha ewrive ryvee ugdr 'etyrhe iatnkg ncise mnya dgusr eascu lo"eaatra.cgrh

hTe olyn thgin of slesiopb vanleecre in ihts eQmts- si taht hes katse a idiet,oncam feoertrhe het reawsn of udgr" c"effet is eht omst liekyl oansre for erh lhcgr.atoaear

hungrybox  I still think this question is pretty BS. But having studied some more, I think it's less BS than I originally thought. Pathoma gives the three major causes of galactorrhea as nipple stimulation, prolactinoma of anterior pituitary, and drugs (see 16.1 - Breast Pathology). Only drug effect is an answer choice for this question. +5
hungrybox  To put another way - before you try to go through every answer choice, asking yourself "would this cause galactorrhea?" Instead, ask yourself, "What are the causes of galactorrhea?" According to Dr. Sattar, they are "nipple stimulation, prolactinoma of anterior pituitary, and drugs." +2
hungrybox  The question doesn't say anything that would point you toward nipple stimulation, like "it only seems to appear when she puts on a shirt/plays sports/runs/etc." It also makes no mention of bitemporal blindness (which would point you to an anterior pituitary tumor), so you can rule out prolactinoma. The only option left is drug effect. +2
drdoom  hungrybox’s full comment (below) here: https://nbmeanswers.com/exam/nbme20/410#3907 +1

 +10  (nbme20#24)
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nouGy lanaC erdnSyom si due ot an rlaUn Nevre oessiln adn si ossaietadc htiw ceclybi arlebnahd su.e

Also FGRIEN baudnoitc and ucdtdoani is dmeadite yb ualnr r.enev ehT aneittp si vanhgi bertolu whit RIGFEN ndictaobu and ac.tudiodn

Teh otmneFr igsn is tstegin TCURADDO IOSCPIL TITYVI,CA hhcwi si dmdeieat yb eth URLNA VEERN i.vitycat tI is NOT tgetnsi bmhtu pponoostii, hcihw ldwou eb eameditd yb eht nmiaed e.rnve

eSe omnFtre ings


 +2  (nbme20#50)
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eTh osaren do" ont biceprser nitcsioaibt lutin ngtesti eulsstr are lai"vbalea is ccirtrone is cseubae ew raeylda vaeh a rgma tisan that oshsw rgmvaeetin-ga pcoiocidcl ni .arpis shTi si Niesresia rge.hooernao o,S on ende to iwta rfo tset lsetrus oecm akbc.

heT mseQt- titasgn ttah si"ngeTt ofr reiNaisse adn hlymdaiaC" is rdedre"o earft adalyre iagnhv nedo eth mraG snati esesm to be a ttrrod.csai

misterdoctor69  I think even in a situation when you don't have the results yet, you'd still prescribe antibiotics just based on history and patient presentation. +
misterdoctor69  In THIS situation** +

 +24  (nbme20#44)
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st'Pienat ssmtmpoy gaebn 30 inm tefar moiwgn nawl e(..i aetrf giond hliapsyc iyva)c.itt eH ash everse techs iapn dna is loo,c m,myalc t.crdheoiapi He sha sdcnierae uplronmay ytrare persruse adn censidear flte ritaal rr.seupes kaTen a,rlgotehte shit si eoacricigdn .hcosk

rioacigendC kchso is a arthe mupp omebrlp -- het VL sin't .gnikrwo

hneW het V,L nts'i ok,wnirg ti causes a kcab pu in het ecdoiintr spoitpeo to owh obold oamnyllr f.sowl f,rTeeerho odblo wlli cabk up ni the l.usgn

ihsT ssauec inasdrece yalialrcp rtohcatydsi rresueps &-tg;- tsih isvder eorm idufl onti hte tsmiueiittrn g-;t-& tsih sasuce decrensia itsrlateinit ydotrtcahsi preurses t;&-g- rthee is own emor dulif naht omranl ni hte siintmuretti -g;t&- sthi tscfefa hte piotner atori hintiw teh uiittmtnres --g&t; tsih ssucea drdsaceee ntiaerltitis oioccnt repsurse.

targetusmle  awesomely explained :) +
lilyo  This was amazingly explained Thank you @Hello! +
pseudopseudopth  For edema to occur shouldn't interstitial oncotic pressure be increased?(when proteins are there, they can pull the fluid) +1
pseudopseudopth  And when increased interstitial hydrostatic pressure is pressure, shouldn't it oppose the edema by pushing against it? +1
pseudopseudopth  *when interstitial hydrostatic pressure is increased +2
pmofmalasia  You don't necessarily need to have increased oncotic pressure, you're correct in that decreased oncotic pressure would act against causing edema but as long as the net change in forces still acts "for" edema it will still occur. For example in this scenario, if the capillary hydrostatic pressure is greater than the change in interstitial hydrostatic and oncotic pressures. Also, the change in interstital hydrostatic and oncotic pressures is a direct result of the edema in this scenario, so it's more like they're responsible for setting the new equilibrium - if they didn't counteract it, you'd never come to a point where the leakage of fluid stops. +

 +2  (nbme20#42)
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etinaPt in looeyimhcvp cokhs - eth sucle aer wol PB dna COLO knis. lovyoemipcH kosch si eascdu by iufld sso.l

Teh tpainte ash seeradecd odrpela /cb of dfiul sol,s .ei. teehr si eeesdcdar obldo ovmeul tinnugrer to taerh t-&-g; thsu raedescde rad.pole

endochondral   why not dec SVR? +
sup  @endochondral w/ hypovolemic shock you would see increased systemic arterial resistance as arteries will constrict to try and bring BP back up. +1
eacv  @endochondral dec SVR it typicaly of septic shock. +

 +0  (nbme20#35)
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eeSpnl si eaed.ngrl Cropmea ti to TC sacn wshngoi il-nmzdeoras elensp:

p161qto4acwjbl.w5.thcowpot3/m/:dr/ut8///.ysaldsoiptoguilrhoargls





Subcomments ...

submitted by hello(301),

Pt has a pituitary adenoma + weight gain + compression fractures.

Prolactinoma = most common pituitary adenoma. However this male patient lacks appropriate symtoms, e.g. decreased libido + infertility. Eliminate choice A.

**Eliminate choice C because this patient does not have signs on increased testosterone.

Eliminate choice E because this pt has weight gain, whereas a TSH-secreting adenoma would cause weight loss.

You are now left with choices A and B.

ACTH-secreting tumors are associated with weight gain + bone fractures. This is because increased ACTH causes hypercortisolism, which has an AE of osteoporosis. This is choice A.

hello  Also, choice B is incorrect because a GH-secreting tumor would result acromegaly (enlarged hands, feet, head), which this pt does not have. +2  


submitted by wishmewell(30),
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I ntkhi hyte rea gnatikl atbuo Gbosatamillo euotmrlmif uesceab ti cosrses" rveo to het flte rpmieshhee" ihst si teh olyn NCS ormut ahtt deso atth and ti is radGe VI meangni hhgi ger.ad smbooiatGlal oimlutefmr is a yept fo samrcAttooy satht yhw sit APFG +p ega 015 AF 2081

hello  Correct, glioblastoma multiforme crosses through the corpus collosum. GBM is also known as a grade IV astrocytoma aka high-grade fibrillary astrocytoma +  


submitted by lae(19),
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eht tdronaiia atyerph sudaec fsiboirs nda teh airmssbbytlofo ttacronc"" gdunir si,bofsri isaucgn the ocuresl fo aswirya nda hust latcestsaei

hello  Adding part of @plummervinson's comment: Contraction atelecrasis occurs due to radiation therapy, necrotizing pneumonia, or granulomatous disease +1  
caitlyncloy  fa 19- 666 +  
leaf_house  FA2020 - p680 +  


submitted by 123ojm(7),

Specifically didn't choose coronavirus due to the evidence that COVID-19 is spread fecal-orally. How does it get through the GI tract if it's inactivated by pH < 6? Can someone explain why my thinking is wrong?

hello  ...COVID-19 is transmitted via respiratory droplets. +3  
123ojm  Right but some research has come out saying it's also spread fecal-orally. So I'm wondering what I'm missing in this question. +  
tyrionwill  Don't trust US CDC in this pandemic. They always downplayed the truth. Cronavirus does spread mainly by droplets, when they drop, they contaminate the surface, then fecal-oral could be a second pathway. Wearing mask, social distancing are both to prevent a droplet. +  
boostcap23  I thought covid used to be low yield when this test was made and they didn't mention helical so I didn't pick it smh I'm an idiot. +1  


submitted by hello(301),
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Paitent sha erd acly ahrs- iths fits eorm tihw V-6HH eRaloos( ,rvu)si tno vsri.aoPvru

6HVH- seaucs eoianmrotfd fo holset,rtaysb iaelgnd ot inmeaa.

hyperfukus  Hey so i just looked in first aid and it says "diffuse Macular Rash for Roseola" and usually you have a super high fever and febrile seizures are almost always mentioned...I found in my notes from uworld that i mustve filled in a long time ago for Parvo: Infects Erythroid precursors + Replicates in BM Face/cheek rash followed by LACY Reticular rash on body...May get Rash from IC deposition...and then again i wrote replicates in erythrocyte progenitors causing reticulocytopenia which makes sense why dec Hb and dec Hct +3  
hello  @hyperfukus is correct. Disregard this explanation. +  


submitted by nwinkelmann(284),
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urMusmr adn envras:emu 1st uohgtth = hwo oesd it cehagn tiwh a.olprde llA sruumrm cxepet COM,H PV,M dna aitlar mmaxyo yevesrti is ctredyli panoptlorroi ot angceh ni rapdoel e.i.( caiesernd oererawl=sdop rmrum,u ..c)te Bcseaeu fo ihts, xDD nca be rorawdne wond to ,HMOC PVM, dan alatir maomyx rgthi aawy cusaebe het rruumm dwernseo hwit decaderse erodapl e..i( adingsnt pu) hewn lal tub etnipxosec twhi orvem.ip

riaAlt ayxmom = CCM yriramp cadcira torum ude to fainreotiporl fo tveicocenn tussie scmen;hmeye a ucdaeupetlnd sasm ndetncceo vai sktla to rmutia pmetus atht si suedsnped in eth tlraai oldob oulmve dna semvo wthi het uelvom evenmmt.o

nPoetrsnta:ei rdait fo 1) liatrm vavle ttrunbicoos .i(e. aa,lsime spyotmms fo adcacri ei,lfrau sonepcy, t,.c)e 2) smytpoms fo olemsibm .(.ie cafial dan tirhg mra earsipiehsm ni )n,itaetp dna )3 ictulsntiotnao tmpmossy ei.(. rfv,ee ghtiew ls,so opmtsysm linemgbrse nntceecovi sisteu eisdes,a ceebuas omtur serelaes LI)6.- Otsehr ueicldn cgoirnoule mtssopm,y drpioa"tusle-m evval di"eases oytsrautaclu dnniisfg (i..e stoadilci ,urmrmu) dan ralita etelnnmreag hi(chw luodc esmscrpo guleiyndrn tuucrtsers dna ecuas tpymsosm as).lo

otN olyn oeds tnagsdni ereascde ,opadelr hiwhc eamns AL mveulo si rloew so msas st'ni as dp"edns"seu but moer emil,bo gnianstd olsa earessinc het ownwaddr ttoainairgv ,rofec hcwhi lwudo ieucorbntt to teh utomr oingvm aorwsdt het seba of eth rtaail rbh,meac oilgpp"p"n on teh mrliat avelv etlalfse, and nlyottelapi exnindetg hroghut dna uiagncs a tnocainulf epyt of mraitl esssnito ei(.. isrwoneng tloicasid u.r)mrmu Tshi idevo xneaplis ti arylel :ewll =gcw/o1=a?ust&/V4Lwtvns61..:sIpww6emibtput;h/ahlYotcym

dentist  Sorry, you narrowed it down to HOCM, MVP, and LA myoxma, but I only see LA myxoma as an answer choice. Wouldn't you have been able to stop right there? +2  
hello  @dentist, I appreciate this full answer b/c nwinkelmann is telling those of us that were wondering "how to ddx one from the other in case we need to"? +4  
hello  @dentist btw, HOCM is an answer choice (RVOT is part of HOCM) +3  
thotcandy  @hello but since that's pseudo-aortic stenosis, it would present with a systolic murmur, correct? +  


submitted by nwinkelmann(284),
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ursMmru dna earnusme:v 1st thohtgu = hwo dsoe ti eagnch twhi oar.dlep All usmurmr tpxcee MC,OH ,VPM dan itraal amxmyo ivtyseer is etcrldiy ntprplrooaoi to ehcgan in eroapld .i.(e adsencier rdelraoo=swep rrm,uum .etc). esBauec fo ith,s xDD nca be raondrwe nodw ot ,COMH MVP, and atrlai oxmaym rhgit wyaa esabecu eht mururm erwesndo twih sderaedec odelpar .e.(i sgindant pu) ewhn lal tub etxospicne ihtw .ropmevi

taArli momxya = MCC rpiamry craaidc mourt due ot irlorotepanif fo iceectovnn uietss mnecemheys; a uetudaclenpd ssam ccedtnnoe aiv klsat to taumir msetup ahtt si edpnsudse in teh iaalrt dbolo uovlem dan mvseo whti eht vomule emmvo.nte

eir:nensttoPa triad of 1) rtiaml vvela touoibntrcs .i(e. e,smilaa msoptmys fo airdcca ia,ufelr sopn,yce .,)tec )2 otsmmpsy of emmobils (e..i iaalcf dna itgrh mra meispshreai ni n)attiep, dna )3 ncaistniotolut ypotsmsm .ei.( reevf, tigwhe lss,o osystmpm gsmberlein nonevcicte eisuts sae,dsie becsuea rmuot ralseese -)6I.L rtOesh icnedul oenliucorg s,pmtymso p"diuoemr-ltas lveva "essiaed usruttoaycal nisifgnd ..ie( ctisdliao uu,rmrm) nad aarilt nemgnetalre (hhicw duocl scporems eydiunnrgl ucterstsur dan sauec yotsmmps s)ao.l

otN lnyo does atgindsn aederces l,aerpod hicwh aenms LA lvmoue si rwelo so asms 'sint as e"s"nedpuds btu reom m,ielob ndingsta olsa eaincerss eth wdrdwoan votitnariga fc,ero whhic odulw tincurotbe to eht rtmuo gvinom atsrowd het seba of eht ralait cbahr,em pp"ig"nolp on teh artiml lvvae f,laestle nad ineptollyat eengixdnt trohuhg dna agsnuci a nafutncloi etpy of riatml isessont e.i(. sorwennig caiitsldo uu)mrm.r shTi ivode senxpila it lrlaye e:wll cum1tp.ow&w;4uh/s.th6tLcwpa==wa//gYVsi1:ymb6Is?ovetlnt

dentist  Sorry, you narrowed it down to HOCM, MVP, and LA myoxma, but I only see LA myxoma as an answer choice. Wouldn't you have been able to stop right there? +2  
hello  @dentist, I appreciate this full answer b/c nwinkelmann is telling those of us that were wondering "how to ddx one from the other in case we need to"? +4  
hello  @dentist btw, HOCM is an answer choice (RVOT is part of HOCM) +3  
thotcandy  @hello but since that's pseudo-aortic stenosis, it would present with a systolic murmur, correct? +  


submitted by ferrero(40),
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A revy rlimias oinsuqet I ahev seen ni knbsQa lliw sak wyh a peniatt thiw hgirt retah fluaeri does ton deepvol aedem nad hte esrwan is cdrieenas tyamiphcl .naedirag I tog hsit iouetsqn ongrw iyllgonira euecsab I eenwrdas golna tsih leni of rsgonaeni tbu I nhtki in hits csea it all ahs to do htwi REHWE het xtaer rssrpeeu is ocmnig .mfor In tshi nsiuoteq teh pt has cldsoiait orniystpnhee os ouy anc kihtn oubta the eepsusrr as omgcni ad"r"wfor so sngctcniitor rlcpapialery rcsithespn cna eenrvpt an ceraiens in rseupesr ni het lialyacpr .ebd ovwreHe rfo gtihr rhate firlaeu tish xetra ulfid si gcnomi rfom het SOPTIOPE etiodircn daskb(wcra mofr teh gihtr th)rea dna tictnirncogs rrapyielapcl hintepsrsc can od gintohn (no topioesp edis fo ryapllcai bed) - eth only awy ot prneevt eedma is ot ciesnera cyilmhtap n.iraadge

seagull  The question clearly lead us to think about Osmotic pressure by talking about protein and urine. I wonder how many people used that line of reasoning (like myself)? +15  
mousie  Great explanation, I chose lymphatic drainage for the same reasoning (similar Q on different bank) +6  
sympathetikey  My reasoning was much more simplistic (maybe too simple) but in my mind, systolic BP is determined by Cardiac Output and diastolic BP is determined by arterioles. Therefore, what comes before the capillary and regulates resistance? Arterioles. That's why I said that pre-capillary resistance. +31  
cr  the main difference between the 2 cases is that in this case the patient has high BP +1  
link981  So in kindergarten language the question is essentially asking how high pressure in the arterial system is NOT transmitted to the venous system (which is where EDEMA develops). But you know they have to add all this info to try confuse a basic principle and make you second guess yourself. (Got it wrong by the way) because of what @ferrero said of Qbank questions. +6  
hello  @ferrero what are you talking about? lymphatic drainage is the wrong answer... +1  
hello  ok never mind. i got it. hard to understand b/c it was a big block of text. +2  
asteroides  I think they may be talking about the myogenic compensatory mechanism: https://www.ncbi.nlm.nih.gov/books/NBK53445/figure/fig4.1/?report=objectonly "Increased arterial or venous pressure also induces myogenic constriction of arterioles and precapillary sphincters, which raises arteriolar resistance (thereby minimizing the increase in capillary pressure) and reduces the microvascular surface area available for fluid exchange. For example, because vascular smooth muscle in arterial and arteriolar walls contracts when exposed to elevated intravascular pressures, this myogenic response increases precapillary resistance and protects capillaries from a concomitant rise in their intravascular pressure." +3  


submitted by ferrero(40),
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A eyrv rliisma euitsnoq I heav nees in asQbnk wlil ask hwy a ttniepa wtih tihgr ahret alfruie seod otn eldpove adeem and teh rwsnae is rdaeeicsn alpcymhit in.dagera I got thsi tuqsonie gownr irnigalylo uaebces I nweesrda galno hsit inle fo ronegnasi tub I knhit in sthi eacs ti all hsa to do hwti WREHE eht aetxr srruseep si ogmicn orf.m In tish qnouitse the pt sha aiilodtsc sirhtenpnoey os uoy nca ikthn autbo teh rreuspes as cimgno rofwrd"a" so tnotsriccngi rpielalraycp ctshnresip nca tvperne na iaecsern ni epresrus ni the lpyicraal .bde veorHew rfo rithg rhtea larfiue shti atexr diluf is ogimcn rmfo eth POTPISEO rtodicnei aaskrcb(wd rfom teh griht e)hrta adn ctinocnrgsit ealprlpaiyrc cestsnirhp acn od nthniog (no opsteipo ised of arclailpy be)d - the lyno ayw to eertvnp aemde si ot aensreic cpythamil eridagn.a

seagull  The question clearly lead us to think about Osmotic pressure by talking about protein and urine. I wonder how many people used that line of reasoning (like myself)? +15  
mousie  Great explanation, I chose lymphatic drainage for the same reasoning (similar Q on different bank) +6  
sympathetikey  My reasoning was much more simplistic (maybe too simple) but in my mind, systolic BP is determined by Cardiac Output and diastolic BP is determined by arterioles. Therefore, what comes before the capillary and regulates resistance? Arterioles. That's why I said that pre-capillary resistance. +31  
cr  the main difference between the 2 cases is that in this case the patient has high BP +1  
link981  So in kindergarten language the question is essentially asking how high pressure in the arterial system is NOT transmitted to the venous system (which is where EDEMA develops). But you know they have to add all this info to try confuse a basic principle and make you second guess yourself. (Got it wrong by the way) because of what @ferrero said of Qbank questions. +6  
hello  @ferrero what are you talking about? lymphatic drainage is the wrong answer... +1  
hello  ok never mind. i got it. hard to understand b/c it was a big block of text. +2  
asteroides  I think they may be talking about the myogenic compensatory mechanism: https://www.ncbi.nlm.nih.gov/books/NBK53445/figure/fig4.1/?report=objectonly "Increased arterial or venous pressure also induces myogenic constriction of arterioles and precapillary sphincters, which raises arteriolar resistance (thereby minimizing the increase in capillary pressure) and reduces the microvascular surface area available for fluid exchange. For example, because vascular smooth muscle in arterial and arteriolar walls contracts when exposed to elevated intravascular pressures, this myogenic response increases precapillary resistance and protects capillaries from a concomitant rise in their intravascular pressure." +3  


submitted by seagull(1405),
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Wtha a erbrlite eiutr.pc yheT htye evdcreo up rpta of ti htiw iel.ns WTF

sympathetikey  Agreed. +10  
catch-22  Start at the pontomedullary junction and count from superior to inferiorly (or medially to laterally): VI, VII, VIII, IX. +3  
yotsubato  I looked at the left side (cause the nerves arent frazzled up). Saw 7 and 8 come out together nicely. Then picked the right sided version of 8 +11  
lolmedlol  why is it not H or I on the right side; the stem says he has hearing loss on the right side, so the lesion should be ipsilateral no? +2  
catch-22  You're looking at the ventral aspect of the brainstem. +10  
catch-22  ^Also, you know it's the ventral aspect because you can see the medullary pyramids. +1  
amarousis  think of the belly of the pons as a pregnant lady. so you're looking at the front of her +4  
hello  which letter is CN IX in this diagram? +  
miriamp3  there is no VI nerve. That's the thing. The VI nerve should be in the angle between the pons and the medulla. Parallel to the pyramid. It goes V then VII and then VIII. I make the same mistake and I thought it was the picture but there is no VI par in the photo. They know We count from superior to inferior. +  
jesusisking  Don't G and H lowkey look like VII and VIII? I chose H b/c of that +  
ljennetten  G and H are CN VII and VIII on the left side, while this guy has right sided hearing loss. CN VI is not labeled in this photo, but is the smaller nerve that arises medial to CN VII and us cut most of the way up the pons. +1  
prolific_pygophilic  Mother Fuckers took this with a disposal camera then deep fried it. What is this grainy ass picture +1  
soccerfan23  There's over a million pics of the brainstem on the internet and of course, the NBME picked the worst quality, most blurry one for this Q. +  


submitted by seagull(1405),
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peinErehinp is hte yonl G dlcpeuo rpcotere titaaorcv hte .sitl The ters are eithre eiaenrcll-rltu or a rteinyos kiesan lusi(.nni)

hello  intracellular* correcting in case it trips someone up +8  


submitted by zpatel(23),
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all het osrhet a tivptnneocimoe niesc yeht ehav spey(iepffciisctciic dg)linas, MNAD is eth olyn isnvtccnoleeehene( tpcioetivme )epot,rerc hsa a ildang tesi dan ac , na nad cehem.ng.. iptecmoetvi

hello  the question says competitive interactions, i think this is different from competitive binding. +  


submitted by hello(301),
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seaPle phle

coldyi-iMsst jenoctei lcikc = umlopicn esstosni

wHo si clinmupo snseosit edrtlae to eht pntati'es SDA -- osde DSA ucsae iucopnml ?onts?sesi

burak  ASD has typically 3 associated sounds according to UW, they are all about increased blood in RA. Increased blood in RA causes more blood do ejected from tricuspid (dşastolic rumble), and more blood to be ejected to pulmonary circulation which cause pulmonary flow murmur (midsystolic murmur in pulmonary region). It even can cause pulmonary regurgitaion like murmur, but most important murmur in ASD is typically midsystolic murmur. You can check it out on FA 2018 page 284 +2  
hello  Ok, what I learned: Extra blood in the right heart (due to ASD) doesn't lead to pulmonic stenosis? Instead, it's that pulmonic stenosis = most common comorbid heart association with ASD +1  
burak  No it's not pulmonic stenosis, it doesn't lead. Murmur associated with ASD is pulmonic stenosis-like murmur, because it's caused by excess RA and RV volume ejecting to the pulmonary arteries. So it's same location with pulmonic stenosis, and it's systolic. You get it? +1  
hello  @burak Yep! +  


submitted by dr.xx(143),
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hTe alhalmrk of ITP si atelsido oca.pehymtotnbiro

8.mdeckeempoesptni//ar1ml2ai2/5e-:pw0cct/htdc.rsioue

jboud86  Refer to page 419 in FA2019. +2  
hello  @dr.xx Compared to what? +  


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.ecD ClaN - agrenle oeuvml eslcso .D K+ - trueicDi tos(m ,itdscreiu cxteep K+ ingarps ,sneo ueasc n )yIcKh.p+o HO;C-m3p&a Hp - mleoVu lsso t-;g& RAAS ;tg-& soeeldtanor cseaus K+ mp;&a H+ itnsgaw g&-t; mebiolcta ;ssolilaka She yma eb toiginmv as e,lwl ihwch si aehrotn pssbloei escau fo e.mt ncl a.Ik Ca2OP - pasoertriry oastieponmcn rof m.te alk.

hello  Patient has normal Na. +  
hello  Lab data indicates serum bicab not ABG bicarb. +  
hello  oops! just realized bicarb is never given as an ABG haha +  


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cDe. aNlC - renalge emlvuo lDe oss.c K+ - Duitcrie tmso( cedu,stiir pecetx +K iansgrp neo,s sucae Kony+ h).pcI m-C&Op;a3H Hp - ueolmV olss g;-t& ARAS -;tg& eesorotdanl suaesc +K &;apm H+ gsawnit gt;-& alecmoitb isllosaak; heS aym eb vnogimti sa e,llw wchih si honrtea blopises cesua fo t.me a.ncIkl COaP2 - sriotyarpre smpnootaince rfo mt.e ka.l

hello  Patient has normal Na. +  
hello  Lab data indicates serum bicab not ABG bicarb. +  
hello  oops! just realized bicarb is never given as an ABG haha +  


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Dec. ClaN - rgeelan vmuleo .s eoDcls K+ - tieDucir o(stm ,eiidcrtsu eetcpx K+ gnriasp nes,o ceaus pn c)yo+I.Kh amp;C&-O3H pH - ulemVo lsso &;gt- RSAA t;g-& sdelenoarot sacseu +K m&p;a +H sanigtw &;g-t cbileamot asaoll;ksi Seh yma be ivtnoigm as lle,w hchwi si rhoanet sslpbeio aecsu of t.me n.Iklca CaP2O - etiarrrspoy eoocistnmpan for .emt alk.

hello  Patient has normal Na. +  
hello  Lab data indicates serum bicab not ABG bicarb. +  
hello  oops! just realized bicarb is never given as an ABG haha +  


submitted by usmleuser007(370),
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hisT erom kylile ot eb cirtduise eratrh tahn tvsxileaa /cb

teh alb suytd shsow a anler fioynstdnuc N(UB ap&m; eieatnnCri rae eaevd)let

sotM leilky het ittnpea asdeub pool r;cdeiuist asol skonw to useca traiccontno ,ildasloka gonla ihwt nrela elsbmpro cshu as enatttiiisrl hnretipsi

endochondral1  would laxatives also have the low potassium? +1  
link981  My question exactly. And what if they were taking Potassium sparing diuretics? Then laxatives would be more likely or am I mistaken? +  
link981  Also creatine is normal, it's at the higher limit of normal so we can't say there is renal dysfunction. The BUN is elevated because patient has metabolic alkalosis with respiratory acidosis. +  
sweetmed  very important to Remember this: Diarrhea causes metabolic acidosis[from bicarb loss in stool], vomiting & loop diuretics cause metabolic alkalosis. +11  
hello  @usmleuser007 not sure your approach is the best way to think about it. The serum Cr is at the upper limit of normal (1.2). And, even if you calculate the ratio of BUN/Cr, it's 21, which would be a PRE-renal issue. +  


submitted by just_1more(0),
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I tgo htta it ededen to eb a imptsusoa pisnagr uic.dteri sI ehrte a nesaor it cannto be na ootldreeans ?anistnaotg I sehco locskb rlataoslbae +K lscnneah as seeth esreadce the blarlteaoas /aNTaK++PA/se ceabseu het grnwdio fo hte ctoerrc rsawne ddi ont kame sense to me -- ungamiss htye weer gongi rfo na NCEa oklbcre a(dn atth edcdsaree uamliln tlyeeprbimia iectdasin htta +aN dowlu eb eimrnngia ni het ml,une ton rigimnaen in eth anpiirpcl llce as I lgoaliinry otuh.h)tg

luckeroo  I think the reason it’s a potassium-sparing diuretic rather than an aldosterone antagonist has less to do with why the aldosterone antagonist cannot be used and more to do with the fact that a potassium-sparing diuretic would be more of a “first-line” adjunctive diuretic treatment. +1  
luckeroo  As for the answer choice, potassium sparing diuretics achieve their overall anti-aldosterone effect by competitively inhibiting aldosterone receptors on the interstitial side (decreasing the Na/K-ATPase effect of shunting Na into the blood), thereby decreasing the gradient for sodium to enter the cell from the luminal aspect, blocking ENaC. +6  
yotsubato  There is no such thing as "Basolateral K Channel" there is only basolateral Sodium Potassium Pumps which are controlled by aldosterone. FA pg 573 +9  
nwinkelmann  @yotsubato LOL.... why didn't I think of it that what?! (by the way, that LOL is for me). The only basolateral K channel is the nephron (based on the first aid picture) is in the thick ascending limb of the loop of henle. +  
hello  Spironolactone and eplerenone are potassium-sparing diurectics that inhibit the Na/K ATPase, so I'm not sure what @luckeroo is referring to. Spironolactone and aplerenone are both ALDO antagonists. Na/K ATPase is found on the basolateral membrane. None of the answer choices fit with this. Amiloride and triamterene are also potassium-sparing diuretics; their mechanism is to block ENaC channels on the luminal membrane, this is choice "B." +1  
rxfit  From Katzung Board Review: "Spironolactone and eplerenone are steroid derivatives and act as pharmacologic antagonists of aldosterone in the collecting tubules. By combining with and blocking the intracellular aldosterone receptor, these drugs reduce the expression of genes that code for the epithelial sodium ion channel (ENaC) and Na+/K+ ATPase. Amiloride and triamterene act by blocking the ENaC sodium channels (Figure 15–5). (These drugs do not block INa channels in excitable membranes.) Spironolactone and eplerenone have slow onsets and offsets of action (24–72 h). Amiloride and triamterene have durations of action of 12–24 h." So both K-sparing subtypes are technically correct. +  


submitted by hello(301),
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If uoy eend a erteffdin ntonoreaiti fro a agdmrai fo the htsaaw:yp

s4e/sdtg1srih4Tp_1eei886u3/2:4a%1a.1l.owg63at/H/n1a/r1pss2-i0eMi33ym1cbjlO=%ure_p.npc1e02-ramt/?i8neF0id1-_i/.0t_-2F3nLgms/tagt3rM4a0fecAsbgprt

hello  Oops meant https://imgur.com/pD4amBJ +  


submitted by drdoom(807),
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ceiN mtsciehca of owh zlhaorotin agze is icdraetodno throguh teh oncoFlub/tmra/MdoeoLucs pawhyat:

te.t/.s0rr/gtety:noue/c.ghonyrFj1/1l/a.eogn/oo7np//7lrgop5l7ueng

In eht rdi,maag eth ssemty si drocaitgoinn geza wotard pt’s lte,f hiwhc ol)nyic(nneevt is eth emas as in hte s.etm

ecoSur e:tlirca u7o.:e/y/1n.7oe/pngho/r/l75otntett0gncs/r

hello  Oops meant https://imgur.com/pD4amBJ +1  


submitted by drdoom(807),
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eNci ehmsctcia fo how ntoharozil eagz si tnidoaceodr rhuothg het oma/rstnFolccModL/oeuub aa:htwyp

/eue/o7jF7nltgors:71e1grtyhngonn.5/pgc/e0eoyulp//onttr../alr/og.

In eht ir,magad the ssetmy is tnrocignidoa aegz dwoatr pst’ ,flet hichw nce)lote(innyv si eth maes as ni hte sm.et

oecurS irle:cat ge/uo7oohn//.71tcstrr7y/.n/g50/ln:teonetp

hello  Oops meant https://imgur.com/pD4amBJ +1  


submitted by hello(301),
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eattnPi hsa a moxihhtear + XRC whsso chaetar eesvatid rdawtso eth mhaoixhter -g-;t& osmt illyek soadniisg si aeonpstnsou prxoenoatumh.

ayldiplcieoogEmli, anonoesputs nearopxmuhto si smto isaetsodca thwi nhit laesm

hello  Wait, maybe this is wrong logic? Please correct me regarding the exam findings if needed. +  
hello  Can confirm that this explanation is INCORRECT regarding trachea. Disregard this explanation. +  


submitted by hello(301),
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etiPatn has a omiaxhreth + XCR sshow rehacta diveatse atdosrw eth xehhrotmai g-&;-t toms kllyei diignasos is snpoaesuotn ehormauxtnpo.

eglamlodiiEclpiyo, eaosntosnup rxpoantuhmoe is osmt cdasaotsei ihtw htni mlesa

hello  Wait, maybe this is wrong logic? Please correct me regarding the exam findings if needed. +  
hello  Can confirm that this explanation is INCORRECT regarding trachea. Disregard this explanation. +  


submitted by hello(301),
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peslea elhp -- If seactspeotiiv-laa tbercaai tneuriaezl hrite nwo eo,rupxised yhw 'nsit it eth eacs rfo selvcaptstioeaia- btcaeiar ot eniicstnof in enreyveo?

'mI otn nnndedgsturai eht icnntoenoc ot DAHNP xasideo eicif.cnyed

hello  to cause** infections in everyone +  
bmd12  Bc everyone isn't NADPH deficient, meaning they can produce their own superoxide without needing to rely on the superoxide produced by the bacteria. +1  
bmd12  so even if catalase positive organisms neutralize their own superoxide, our body is producing its own and not relying on the ones produced by bacteria. You only begin to rely on the superoxide produced by bacteria if you are NADPH deficient. +  


submitted by meningitis(502),
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hertrdohhodoiyzlocai si COD fro noecregiNph easteDbi psiidisun eceaubs ti raoxldyacapil asecus an eicrsena ni PB by cienaginsr uomsdi norbptiaso adn usht atrwe ooprabtn,is aaoPhtm ispanxel shit n.yecil

eropmDsisnes si iocrntrec uasbeec oupn tinasfg ufi(dl niroettsi)rc DHA is indsarece amegnin HAD si geibn radeeesl nlartyeCl tub is nto gwniokr in eht sidyekn ta teh 2V csrreepto fo the ihpeatlile nrlae secll at tilCogencl cu.dt

On that n,eot lrAidiome si sdeu rof mitihLu uieddnc cgenipnheor .ID

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. +  


submitted by burak(52),
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st'nI ti nepnedetd no eht lo?aotcin I wdesarne it roonrcay snsui csubaee av deno is ocalted ni ochK g;enartil ciwhh msopdeoc of uC,Sins eonTnd of rToao,d rcTsiudpi nuuln?sa

hello  The correct answer was atrioventricular BUNDLE-- it's also known as the Bundle of His. AV Bundle ≠ AV Node. +2  
burak  Now it's more confusing to me:) because av bundle is more inferior to the av node. +  
hello  Patient has ASD --> need to repair interatrial septum. AV bundle aka bundle of His is located neart interatrial septum. Coronary sinus opens into atria but is not located near the interatrial septum +4  


submitted by keycompany(296),
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wloF eRat = lyVciote x sSoCoicesn-rlta eaAr

2 ^m2c x 02 mes/cc x 06 nsmci/e x 1 /000,1L 3mc^ = 42. n/Lmi

0010, c3m^ = 1 L

seagull  Well, I missed this one. I don't even feel bad. +55  
link981  @keycompany a small typo, 100 cm^3 = 1 L not 1000cm^3. 1000 mL^3= 1 L +  
hello  @keycompany how did you edit your original comment to fix your typo? +  
winelover777  Pretty sure @keycompany was correct. 1 L = 1000 cm^3. Otherwise the answer would be 24. +3  
drdoom  1 centimeter is a distance. (A line.) +  
drdoom  If we multiply a line by another line, we get a surface area. (A piece of paper.) +  
drdoom  If we multiply the piece of paper by another line, we get volume. (A cube. A box.) +  
drdoom  If we fill the box with a fluid, we will have 1 mL of this fluid. +  
drdoom  If we have a thousand of these boxes, we have 1 L of fluid. +  
drdoom  1,ooo mL = 1 Liter = 1,ooo centimeter³ +  


submitted by keycompany(296),
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cp69r5/gw2m/t8e.ni/.hln/hpcw:n.ato/wvcMs.s0i0bCPi/tml

lOser igSn si a eils-vtwit,soyin pccysi-toliewf gifndin fo keroMgnbec iiAorsotelscsorrel A)M( cierraehztcda yb a" elalpapb hoaglhut sselsl,pue airlda aryret ewlhi het PB fcuf si afndietl vbeoa icolsyst rprse"u.es

It is lobiesps that ee)ath :ir The oisccfpewliy-ti fo thsi stte smean it is olas clppielaba ot ocersilaehrtsos ont( ujst b )AM) eTh MBNE eolrcrcynti iespilm atht AM si gthecablennira thiw ortclisshaose.er

bubbles  This was my reasoning, too. I thought this was Mockenberg for sure +  
hello  I don't think think it's a type. According to 2 other comments: "It's atherosclerosis because it said “radial artery is NON-pulsatile BUT REMAINS PALPABLE even as the cuff is inflated”--> normally, you can’t feel the artery when the cuff is overinflated b/c overindlation occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!): "If if something were to not be palpable then it would have to collapse -- atheroclerosis prevents this vessel collapse." +17  
arcanumm  I agree, I just reasoned that atherosclerosis would not be thicker when the lumen is blocked. I don't think they were going for Mockenberg at all. +  
arcanumm  would be thicker +  
drzed  Atherosclerosis isn't common in the radial artery though... it's common in the abdominal aorta + coronary, popliteal, and carotid arteries. I am not going to assume a guy has radial artery atherosclerosis when he is in his 80s without a dyslipidemia syndrome over monckeberg calcification! +  
mdmikek89  This explanation is completely incorrect. Whoever upvoted this is dumb. Pseudohypertension. Pseudohypertension, also known as pseudohypertension in the elderly, noncompressibility artery syndrome, and Osler's sign of pseudohypertension is a falsely elevated blood pressure reading obtained through sphygmomanometry due to calcification of blood vessels which cannot be compressed. +1  
mdmikek89  This is a diffuse calcification. Monckenberg is like PAD with Calcium. Some places have it some places dont. The chance that there is a plaque at the same point as the doctor is feeling for palpation is...well low. Also Monckenberg is a complication of DM Type II. Not in this stem... +  
haydenelise  Would've thanked you for your explanation @mdmike if it hadn't included the "whoever upvoted this is dumb" comment. What a turd lol +4  


submitted by hello(301),
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oFr peeopl iaskng wyh eht aadt aeblt asw evne linecudd if it swa otn edeend ot werans tihs ,Q hree si a efuslu eanopnxlia:t

heT abtel asw nveig aubesce a x22 blaet si pacltyily twah yuo do see argindreg aadt fro cr-eoclanost ssdt.uie

If hte 22x taelb s'ntwa dudie,lcn hent lietllyra eytnroeev owudl pcki Chioce E"" sa hte rrcotce esrawn bc/ you 'atcn cecaatull hnsgitome owttuhi ibgne odvpride nub.mser

eTh iederfecfn in dgiucnlin het dtleta-aab si atht:

  1. inA,ag oyu eedn ot otrepr a 2x2 eltab aebsuec ttha si cpltlyiya awht uyo lwil ese diegnragr tada rfo a e-crtnaosloc usdyt

and

  1. yb undcgilni teh 22x etb,la it tyaacllu ttess fi teh a-stktetre daieelzr atth het atad ni eht x22 etlab osde ton pelh ta lla tihw tagnclaluic rcl-ee-napve aebucse oenoacc-stlr siedust EVREN rrepot on acereev.pnl
hello  I also want to add that the Q is asking about sinusitis in the GENERAL population, meanwhile the Q-stem discusses a case-control study that is studying the relationship of smoking (an exposure) to development of sinusitis. To then ask "what is the prevalence of sinusitis in the general population" totally disregards taking into account the exposure of smoking which was the entire reason for the study. In other words, asking prevalence would be very non-sensical. +  


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hWy s’antw hte etalb engouh ot edereintm cenrveealp in hte egranle un?aoplopit

sacredazn  For the case control question, it’s taking that principle that you can’t use case control studies to calculate relative risk and applying it to prevalence. Basically with case control studies we start by saying okay, I’m going to find 200 people with sinusitis and 400 without. Then, you go back and look at the number exposed/unexposed and calculate the odds ratio. So you can’t use case controls to calculate prevalence because it all depends on how many cases you picked in the first place. Might make more sense to think about it with a rare cancer like craniopharyngioma or something- let’s say you chose 10 cases and 10 controls and wanted to look at how many people smoked. It wouldn’t make sense to then say the prevalance of craniopharyngioma is 10/20 = 50%. +20  
dr_trazobone69  Thank you, that makes a lot of sense! So we can use relative risk (cohort studies) to calculate prevalence? +  
sacredazn  @trazobone Hmm I think the wording would be key, you could use a prospective cohort to calculate incidence, but you wouldn’t be able to find prevalence of the gen population unless you had more info. I think the concept is that really to calculate prevalence you need a proper ecologic study looking at population-level data. The way it was worded in the question was tricky though lol since when has “cannot be determined from the info given” ever been a right answer. +5  
nwinkelmann  @sacredazn thank you! this was the best explanation to use the rare disease comparison. Made everything make so much sense and hopefully I'll actually just remember it now, instead of learning the factoid and failing to recall it all the time. +1  
hyperfukus  i guess this makes sense but i don't understand why we are asked to calculate it from tables like this then? is there more info in those? +  
hello  @hyperfukus The table was given because that a 22 table is typically what you do see regarding data for case-control studies. If the 22 table wasn't include, then literally everytone would pick Choice "E" as the correct answer b/c you can't calculate something without being provided numbers. The difference in including the data-table is that 1. again, you need to report a 22 table because that is typically what you will see regarding data for a case-control study and 2. by including the 22 table, it actually tests if the test-taker realized that the data in the 2*2 table does not help at all with calculating prevalence-- because case-control studies NEVER report on prevalence. +  


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shTi noe wsa a tlielt itk.cyr roF ihts oen eht eyk is hte olw raiioeoddni autke.p hTsi inatpet hsa hihg 4T nad owl HST hwhic akmes eessn in a piohrtyryhed t,tipane ephasrp yruo sitrf tothguh is htat stih nttaeip sha re’vsGa seeids.a wHeo,erv in v’eraGs yruo rtyodih si ebngi aiustmtlde ot akem moer tirodhy rmeonoh mfro ahrtscc and as cush oduwl vahe na icasernde noidroeiaid aeptku ecebuas eht dtioyhr si rniibgng in eth duiqerer own( laedali)eordb i.iedno ihTs is hwy ti is ton raevGs seae“l(re fo oihrytd mhrenoo form a yhotird tutalmsedi yb .i”teobdan)is

So if sti tno vG’aers hawt ucdol ti ?eb orF siht duy’o ehav to onkw thta ta’hsomoiHs hsyiiodTrti (alos nwonk as cirhnCo ytLohcypcim yhisdtioTir dan si oefnt rderfree ot as schu on bdora amxes to hwtro you fo)f sah rethe sphsea - stfri ethy ear ohphyyirdte,r thne reiuotdy,h nhte hte accssli hoyopdhiyrt thta oyu odwlu cxteep twih wlo 4T adn high S.TH sihT wsa the yek to tsih qt.siueon ehT snorae ofr tihs is taht datnhitioyr opeidreaxs stneaidbio ni oHhsm’stiao ausce the thdryio ot elseare lal fo ist odesrt hdytoir onmohre kinamg eht eanitpt repyhdirtohy ofr a hotrs eioprd of emit. rfteA htis ieavssm ereaels of toiyhdr r,emhono hte eiandibots ekam meht nbealu to emka new HT dna toheeferr tyhe oemcbe eyurohdit rof a sthor edoirp dan nthe ithproyhydo hichw oyu owudl xtc!epe nSeic thye tnca’ kaem new T,H eth yrtohid liwl ont eakt up eth irodieoaind adn rofthreee tereh wlli be lwo enooiadidri kapu.et ,ceHne ra“eesle of eostrd idyhrot ohnorem orfm a idhyort gdaln entidiftlar yb cs”yopy.emthl kaa y“ypLoihcctm sa(hh)simtoo iot”sid.hyirt

I tinhk rsela“ee of hotridy nemrooh mfor a oltohuypamms irydtho lg”dna is nregerirf to esom dkin of rodithy rencca ni hchwi ecsa you oudlw tcexep hetm ot be gniirbcdes a ldoenu on inreiododai ueakt.p

uymrm​aS dvoie reeh dan salo a garte seit ni lngea:re oinqrsytnr/s/i.nce/latardte/cm/grpiiodpo/h:edueheendo

aesalmon  pg 338 of FA lists it under hypothyroidism but it does present as transient hyperthyroidism first +9  
hyperfukus  yep that was the key! Goiter is "HOT" but the remaining answer choices were still kind of bleh D was distracting the hell out of me i spent so long to convince myself to pick C and move on +3  
hello  Pasting nwinkelmann's comment as an addition: Choice "D" is wrong b/c "lymphomatous thyroid gland" = primary thyroid lymphoma (typically NHL, which is very rare) or Hashimoto's thyroid progression. Hashimoto's thyroiditis = lymphocytic infiltrate with germinal B cells and Hurthle cells, which upon continued stimulation, can lead to mutation/malignant transformation to B cell lymphoma. Both of these present with hypothyroidism with low T4 and high TSH (opposite of this patient). +1  
taediggity  I absolutely love your @liverdietrying, however the pathogenesis of postpartum thyroiditis is similar to Hashimoto's, so I think this person has postpartum thyroiditis and your explanation of transient thyrotoxicosis is spot on, which would also occur in postpartum thyroiditis +9  
pg32  I agree with @taediggity. Also note that women eventually recover from postpartum thyroiditis and typically become euthyroid again, which doesn't happen with Hashimoto's. +  
vulcania  In FA (2019 p. 338) it says that thyroid is usually normal size in postpartum thyroiditis, but the patient in this question had a thyroid "twice the normal size." I guess at the end of the day it doesn't matter which diagnosis is right for this question cause they both seem to lead to the same correct answer :) +2  


submitted by nwinkelmann(284),
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nCa oeoensm xielapn woh to eulr uot eht herto nsewar hrse?coci

warbyparker1  you can r/o SMA because as kidneys ascend they get stuck low in the INFERIOR MA (L3 level). So I guess there should be no problem w SMA +3  
hello  I think friability of vascular tissue would indicate in inflammatory process (the one I can think of is strawberry cervix) -- so i think that's why you can rule out choice C. +1  
avocadotoast  You can rule out multiple ureters with abnormal courses because the ureteral development relies on the ureteric bud. There will multiple ureters if the ureteric bud divides before it comes in contact with the metanephric blastema. Horseshoe kidneys are simply due to fusion of the lower poles and don't involve the embryonic tissues, so those two processes are not likely related. +  


submitted by pparalpha(83),
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anC onosmee spleae lxanipe hyw ti wodul nto be cyeogngl t?neiedplo I ghttouh teh nqotuies was nktgail toaub the bWarrgu n.eeno.hnmo.p os why nto bonwaerkd fo lnogygec ot gc?uleso

I sesgu it wuldo otn eipaxnl hte em?ead

hello  Glygocen stores are depleted within 24h. This person has signs and symptoms of longterm nutritional deficiences. +2  
raffff  it would not explain the edema, yes +  
drzed  Also the warburg phenomenon has to do with cancers preferentially taking up glucose; there is no indication that he has cancer. +  
haydenelise  The first sentence says that he has lung cancer. +2  


submitted by saifshaikh(13),
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I thnki iths erutcpi npsexila it lew:l

a.etic/evwu.lnfai/ns:t/wicgpendcgtiondaao.mpkrperascfiew//.gjht

hello  Adding to this... The Q is describing the GENIOFEMORAL nerve, which runs EXTERNAL TO of spermatic cord at the superficial inguinal ring This Q is NOT referring to ilioinguinal nerve, which exits THROUGH the superficial inguinal canal +  


submitted by keycompany(296),
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aendailMn iese:tncG

nMa has 2/3 hencac fo nbieg a .arirecr eH( dose ont veha the .aesid)se aWo nm rcreria rsik tsmu be aldclecuat itwh 2^p + p2q + .^2q 2 q^ = 100,0/40 q = ,0120/ p si guhrloy = pq21 = 011/0 = aCirrre eqceyfrun .

Rski of avnihg a ldihc htus aueqls 2/3 x 0110/ x 14/ = 10/06 uaces/Be3:2 = anM rCeriar irsk 11/00 = aeFmel irCaerr sR1/ ik4 = Ccaneh htye ehca asps no teh vseiecres eegn to hrtei .sogpirffn

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


submitted by burak(52),
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snIt' it ntneededp on the ocl?aonti I rdeeaswn it oorcaryn ussni ebceuas va edon si ldteoca in Kohc etran;lig whhci emooscdp of nuCisS, nnTedo fo Tdrao,o Tiscrupdi nauu?lsn

hello  The correct answer was atrioventricular BUNDLE-- it's also known as the Bundle of His. AV Bundle ≠ AV Node. +2  
burak  Now it's more confusing to me:) because av bundle is more inferior to the av node. +  
hello  Patient has ASD --> need to repair interatrial septum. AV bundle aka bundle of His is located neart interatrial septum. Coronary sinus opens into atria but is not located near the interatrial septum +4  


submitted by hello(301),
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Plseae lphe

-dytoslsMcii ioeetjcn kcilc = mnicupol sneiosst

Hwo is mciulonp seisstno lreedta ot the ptieas'nt DSA -- oesd ADS sueac olpicmnu ?tson?eiss

burak  ASD has typically 3 associated sounds according to UW, they are all about increased blood in RA. Increased blood in RA causes more blood do ejected from tricuspid (dşastolic rumble), and more blood to be ejected to pulmonary circulation which cause pulmonary flow murmur (midsystolic murmur in pulmonary region). It even can cause pulmonary regurgitaion like murmur, but most important murmur in ASD is typically midsystolic murmur. You can check it out on FA 2018 page 284 +2  
hello  Ok, what I learned: Extra blood in the right heart (due to ASD) doesn't lead to pulmonic stenosis? Instead, it's that pulmonic stenosis = most common comorbid heart association with ASD +1  
burak  No it's not pulmonic stenosis, it doesn't lead. Murmur associated with ASD is pulmonic stenosis-like murmur, because it's caused by excess RA and RV volume ejecting to the pulmonary arteries. So it's same location with pulmonic stenosis, and it's systolic. You get it? +1  
hello  @burak Yep! +  


submitted by assoplasty(92),
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atsF aer etceognki (pectxe ddo icahn ,)AF os yhte uoedrpc oensket orf nygree oridcutopn )C(oAl-cAyet earrht than ecug.sol fI the qeonusit eadks thaw teh ariympr erscuo fo egnyer idnrupocto ,saw it oluwd lilst eb neggycol and( nto eks)tnoe, easecub tish is nthiwi 42 s.uorh roeeHwv fatre 24 hsoru hte arwnse ulcdo eb noteek .isobde ael,Rdrgess teh usoeniqt ciylfiaceslp idas eht tp dha a erums coueslg fo 001, idtiignnca ttah we era onkilog rfo hmiosgent taht ideosrvp a asbrteuts rfo enngss.cgelioeuo

iurngD ireosdp of invsrtaoa,t etbstussra orf uossieeonglnegc ecom mfro wot :cssoeru 1() eronakdwb fo sxgneiti luse,cm or 2() via a-idcondh AF hghtruo oAnCpyro.o-lip l(*eVina osla fedes oitn rypoinolp A,Co tbu is otn niovelvd dugirn naiaovttsr --&t;g ees b)lwoe

()1 hTe auiyantvepanler- clecy dseoipvr siht ilgteua(mn ni lmsuec + yauvptre -&;tg- lnaaien -tg;&- seog to vleri -&tg-; tnmratsinaiaon ot huaaltlroattgke-epo ;g--&t rayuvtpe si prsdeaaet rmfo uimtanelg ;g--&t iagmunlet oesg ot ruae elccy, ueypratv goes no to .s)loingncugoseee cttaLae cna loas eb dseu hsit( uoldc eavh neeb a tgrih rnasew fi ti erew )lt.deis

(2) dOd icahn AFs era slao ogicg,eunlc ubt eaicrst acdi rddip(ove ni eth wnsaer eich)co t’sin ddo acnh,i os it is ylon knoceiteg dan acn be lrude u.to

htohgluA nileav nda( roeth nhrecabd a).a. efed iotn poo,AlynroC-Pi hyte aer not dseu ni airovtastn eeusabc orasnittva rctlyits rsleie no thapice gncgenusseoe.oil Teehs ..aa aer not loezimdbeta in teh lreiv acbuees teh eilrv ckasl -hrcedaainhcnb .aa. seaenasrrft nmeeyz. In striF ,dAi hmeociB no,tseic under vraotni,/tFniaatgsS ni obht the ia“sfngt t”saet c(hihw si ithwni eht item rafem of tihs uesoqn)ti, or the ttisr“oaanv ”a,tets btho ezliuti ciphaet loeeincoussngge. yM usspatmnoi is taht veainl is sude driugn erularg sliom,embta dna ton gudnir podsire fo iatoasr.tvn

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. +7  
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 +4  
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 +  


submitted by didelphus(54),
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nyA eadi wyh yplreehohiracm i'stn na eans?rw Teh reaahrdi wludo ausce na almron ninao pag erorhlciche()ypm eictmblao s.cdoisia

charcot_bouchard  this is the problem bet uw and nbme. in uw it would be for sure a gotcha ques. but in nbme they are usually looking for most obvious. also look what they are asking "most likely". baby would dev low Na before acidosis. Thats my 2 cents +21  
temmy  hyperchloremia will not account for the seizure that brought the patient to the hospital. seizures according to first aid is caused by hypocalcemia and hyponatremia +1  
cry2mucheveryday  Children with diarrhoea who drink large amounts of water or other hypotonic fluids containing very low concentrations of salt and other solutes, or who receive intravenous infusions of 50% glucose in water, may develop hyponatraemia. This occurs because water is absorbed from the gut while the loss of salt (NaCl) continues, causing net losses of sodium in excess of water. The principal features of hyponatraemic dehydration are: there is a deficit of water and sodium, but the deficit of sodium is greater; serum sodium concentration is low (<130 mmol/l); serum osmolality is low (<275 mOsmol/l); the child is lethargic; infrequently, there are seizures. https://rehydrate.org/diarrhoea/tmsdd/2med.htm#CONSEQUENCES%20OF%20WATERY%20DIARRHOEA +  
cry2mucheveryday  Also, why is this being given formula...? May be lactase deficiency...which leads to osmotic diarrhea...leads to hyponatremia(goljan) Aren't newborns supposed to be kept on exclusive breast milk till 6 months?? +  
hello  @cry2mucheveryday Don't read too much into it. The fact that the baby is receiving formula isn't relevant to answering the Q. Btw, not everyone breast feeds. Additionally, the Q wouldn't make much sense if it said "they ran out of breastmilk"... +1  
hello  @cry2mucheveryday Being on formula then the parents running out of formula is more of a clue for water intoxication. This is typically the scenario that water intoxication presents. However, I suppose if for some reason the baby was being breastfed and the parents switched to exclusively waterfeeding (and no other foods), then water intoxication would also result. +  


submitted by didelphus(54),
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nAy daei ywh oharmehplicery ns'ti an earws?n heT raehiard wduol uceas an rloamn ninao gap hreomcprihl)e(cy bteocilam c.sidoasi

charcot_bouchard  this is the problem bet uw and nbme. in uw it would be for sure a gotcha ques. but in nbme they are usually looking for most obvious. also look what they are asking "most likely". baby would dev low Na before acidosis. Thats my 2 cents +21  
temmy  hyperchloremia will not account for the seizure that brought the patient to the hospital. seizures according to first aid is caused by hypocalcemia and hyponatremia +1  
cry2mucheveryday  Children with diarrhoea who drink large amounts of water or other hypotonic fluids containing very low concentrations of salt and other solutes, or who receive intravenous infusions of 50% glucose in water, may develop hyponatraemia. This occurs because water is absorbed from the gut while the loss of salt (NaCl) continues, causing net losses of sodium in excess of water. The principal features of hyponatraemic dehydration are: there is a deficit of water and sodium, but the deficit of sodium is greater; serum sodium concentration is low (<130 mmol/l); serum osmolality is low (<275 mOsmol/l); the child is lethargic; infrequently, there are seizures. https://rehydrate.org/diarrhoea/tmsdd/2med.htm#CONSEQUENCES%20OF%20WATERY%20DIARRHOEA +  
cry2mucheveryday  Also, why is this being given formula...? May be lactase deficiency...which leads to osmotic diarrhea...leads to hyponatremia(goljan) Aren't newborns supposed to be kept on exclusive breast milk till 6 months?? +  
hello  @cry2mucheveryday Don't read too much into it. The fact that the baby is receiving formula isn't relevant to answering the Q. Btw, not everyone breast feeds. Additionally, the Q wouldn't make much sense if it said "they ran out of breastmilk"... +1  
hello  @cry2mucheveryday Being on formula then the parents running out of formula is more of a clue for water intoxication. This is typically the scenario that water intoxication presents. However, I suppose if for some reason the baby was being breastfed and the parents switched to exclusively waterfeeding (and no other foods), then water intoxication would also result. +  


submitted by jjubilee(-2),
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erP oegolg tsyspomm fo ehoalhoicpymr dna iempyatornha rea eyvr lrm;siai e,hwerov hyatpraomnei necslidu eerssiuz and spma.ss tuB erp my cuiqk goloeg ehrsca caoyhrmehlpio seod to.n mpyharHooilec aols anc etrsepn twih yrprisaoetr esf,fitiulicd but I dtni'd see ttha whti .yhaeoaripntm

hello  That answer choice is hypERchrloremia, not hypochloremia. +  


submitted by hayayah(1056),
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rheCaett tecnmepal:

a/6ao0yp2c/.p/heees.p0jiue00ntmpadg4cs/go8e0ks:tt/o1/n8lw/tm-n

eRlcal that the unlg pxae texensd aeovb hte rfsit ib.r

hungrybox  His expression is so blissful. U can tell they're shootin up some full u-opioid agonist codeine type of shit and not some shitty partial u-opioid agonist buprenorphine type of shit or some shit like loperamide that doesn't even act on the CNS +29  
rerdwins  even better, if you recall that the esophagus is RETROperitoneal ( its in like half the answer choices). hence, to get to it you have to go WAAYYYYY deep ( like rick and morty smuggling shit). after that, the lung option makes the most sense. +11  
hello  Also, pulmonary artery is way too far away to be damaged by internal jugular vein catherization. +  
makinallkindzofgainz  @hungrybox my mans just slipped in 3 high yield facts within a joke +3  
makinallkindzofgainz  @hayayah, I have an issue with that picture unless I'm missing something. In every other source I have, the internal jugular vein lies LATERAL to the common carotid artery. The picture you provided shows the internal jugular veins medial to the common carotid artery. +1  
cmun777  Look at the other side... I think it must be the manipulation of turning the head to the opposite side that better exposes the jugular for catheterization purposes +  


submitted by nosancuck(85),
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oY dwga ew lla butao PVT IMT LaHL

anlhyPeinl,ane Va,ieln ANpoT,DKrty onTeinhre, ,Iuelsoneci nMii,eotneh dinHse,iit iuLceen sLeiyn

meningitis  I don't understand what the question is asking... can someone please explain it to me? Patient doesnt eat protein, shes chubby. What does methionine have to do with this? +2  
charcot_bouchard  Just basically asking which is essential amino acids. +3  
usmleuser007  Essential amino acids (something i came up with) 1. "Three HAL fans will try meth" a. Threonine = Three b. Histidine; Arginine; Lysine = HAL c. Phenylalanine = fans d. Valine; Isoleucine; Leucine = will e. Tryptophan = try f. Methionine = meth +3  
nala_ula  They're saying there is a lack of good quality protein -> slight nutritional deficiency. She may have acquired weight but it's not because of protein. So they're specifically asking what amino acid she might be missing due to her subpar diet. Since essential amino acids are those that the body cannot make itself, out off those listed, methionine is the essential amino acid. It's on page 81 of FA 2019. +9  
nala_ula  correct me if I'm wrong please :) +  
hello  For anyone confused trying to follow @usmleuser007's comment -- slightly modified Essential amino acids mnemonic "Ah, Three fans will try meth" Ah = arginine, histidine Three = Threonine Fans (phans)= Phenylalanine Vil (Will -- German accent pronouncing English word 'will') = valine, isoleucine, leucine, lysine Try = tryptophan Meth = Methionine +1  
pg32  Why does @hello and @usmleuser007 mnemonic contain arginine? That isn't in the PVT TIM HaLL mnemonic for essential amino acids... +  
paperbackwriter  @pg32 arginine is semi-essential. It is essential in preterm infants who cannot synthesize it https://www.sciencedirect.com/science/article/pii/S0955286304000701?via%3Dihub +  


submitted by youssefa(124),
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otndWu'l uetac lachool nutmociopns even in eetmorad antuom caues leesvreibr hptiaec rclaellu ijyunr ethrrcdaeziac yb cllreual n?olnboglai It holuds be hte gthri narswe sunels hte otuienqs tmes eansm W"ekedesn"

hello  No. The order of liver damage due to alcohol is: fatty changes --> cellular swelling (cellular balooning) --> necrosis. This Q stem states to the patient consumed large amount of alcohol on a weekend -- he has acutely drank a large amount of alcohol on one weekend --> this corresponds with fatty changes +3  
et-tu-bromocriptine  It's not in pathoma, but I have it written in (so he or Dr. Ryan may have mentioned it) - Alcoholic hepatitis is generally seen in binge drinkers WITH A LONG HISTORY OF CONSUMPTION. +  
krisgsxr600  Its kind of in pathoma Chapter 1, "free radical Injury", Section 2 "examples of free radical injury" goes over how free radicals (caused by drinking) lead to fat accumulation +  
sallz  You can't get the steatohepatitis before getting the steatosis (fatty change). All the FAs caused by the alcohol consumption eventually lead to cytokine release, inflammation and finally the hepatitis seen in balloon swelling. +  


submitted by temmy(126),
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psleae lpeh ondgcirac to isenrwt ioqnuate the tenpiat sha a mlarno oainn pag

ergogenic22  winter's formula is to look at the compensation to see if it is appropriate. PCO2 = 1.5[HCO3-] + 8 +/- 2 In this case, 1.5* 10 (Pt's bicarb) +8 +/-2 = 21 to 25 Pt's PO2 is 23, so compensation is appropriate. If PCO2 was below 21, it would be concomitant respiratory alkalosis +5  
ergogenic22  in other words, winter's formula is not necessary for this question +2  
the_sacramento_kings  lol unless you want to make sure its not A. +1  
hello  @ergogenic22 Someone might use Winter's formula to rule out choice A. +  
maxillarythirdmolar  respiratory depression of alcohol should rule out "A" +  
baja_blast  Isn't the low pCO2 enough to rule out A? +1  


submitted by cantaloupe5(72),
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ootgisHly hsedwo taalecogviu sceionrs srpvee(dre iehuettrcacr fo mdroayicla sf)brei hwti oeplunihrt trianiolfitn ihcwh tndihe ttha teh IM swa tihwni 42 ohus.r Mots ileylk acsue fo tdeah nitihw sifrt 24 rhsuo of MI si ry.mahahrti lMiaaodryc uureprt luowd osal be vlisibe on srogs encaeaprpa fo teh r,heta ichhw hety eedsrdbic ni het esm.t

bighead478  in FA it shows softening of the myocardium to happen at 3-14 days. Do you think this was overly misleading people (like me) into choosing myocardial rupture? I understand the histo features are consistent with < 24 hours, but the stem should also match this in every detail +11  
sbryant6  Myocardial rupture would not happen until 3-14 days. Since this shows signs of <24 hrs, the answer is arrythmia. +3  
hello  @bighead478 You have to look at the whole picture. Histo shows preserved architecture, which indicates coagulative necrosis -- coagulative necrosis is a histo finding only in the first 24h. The most common causes of MI-related sudden death are: arrythmia > cardiogenic shock (heart pump problem) > rupture. +  
jcmed  I chose the rupture as well due to the timeline. Somebody gave me this advice the other day, NBME classically will give you an entire vignette leading you somewhere, and the what it asks will be something completely different; or in this case will give you a photo of something and will ask about the photo. They do what they want. +4  
athenathefirst  Anyone knows why it's not a cardiogenic shock if it was within 24 hours? +2  
zevvyt  It says "Mottling" which happens in the first day. If it was 3-14 days it would be yellow (p 302 2019). He can be having angina for 3 weeks leading up to an MI. +1  


submitted by dragon3(12),
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astWh' eth fnrediefec beentwe rtaivcee ntracgyoslosiu sv ?pmyioscsoyhtl

whossayin  Yes I’m at a loss for this one too. Still can’t figure out how we’re expected to differentiate those based on this slide shown. The only logical explanation that I can think of is that reactive lymphocytes may be seen in LYMPHOMAS as opposed to granulocytes which are seen in LEUKEMIAS Such a shitty way to trick us, hah! +  
henoch280  reactive lymphocytes are seen in EBV infection. you would see lymphocytes in the slide not neutrophils FA2018 pg 165 +3  
whossayin  That makes sense.. but was the question talking about EBV infections or hematological malignancies? Just a vague question I wasn’t really sure what exactly was it trying to teach us, I guess the reactive lymphocytosis just threw me off! Anyways, thanks for the clarification buddy! +  
ratadecalle  They way I thought about it was: Granulocytes: multi lobed nucleus Lymphocytes: single lobe +7  
hello  @whossayin - it's not reactive lymphocytosis because there are no buzzword type symtoms of EBV in the Q stem. Also, reactive lymphocytes look way different. +  


submitted by hungrybox(968),
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esom rnwog n:sersaw

sa*mek sesne cb/ styllbsmeao aer srreporsuc to gtalnoeursc,y hhiwc seu OMP to thigf fof citsnfieno

temmy  Hungrybox aka life saver +1  
hello  Thank you!!! +  
bbr  ....uh yeah im pretty sure we just call em "Auer Rods" now. Appreciate the answer tho! +6  


submitted by dr.xx(143),
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nI sss,adiiocor cpaeiahecylmr omyanlrl sseepsrspu eth lareees fo TPH nda rhretfeoe eth dprouocitn of iotllaiccr -olchfyhocxle(rocia1dly5)id,er,2 but ni soasosdiirc dan hrtoe gotauraslmuon ,ieesadss aceadtitv raoulncmoen escll curtilr(lyaap hceosga)pamr in eth ugln dan hylpm nedos pcuored iliccaorlt d1yr(eolfo)rxidaci5c,2ecoh-yllh frmo ioiclladc ceyoooclalycerdl(fh-2r)i5xh pndteidenen of .HTP

mssacetateup/ecp/id/mntt-sawn-seohtrgtolonwuaoicyriaas.lsnpew.t-mec:o/dhu

dr.xx  ~~In sarcoidosis,~~ +  
hello  Probably a typo in the first 2 words of the explanation -- not sure what they meant to say instead +  
drdoom  I believe @dr.xx meant to strikeout "In sarcoidosis" from his comment; double-tilde is the markdown plaintext that usually accomplishes that. +  


submitted by cantaloupe5(72),
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istpydoyrpi/merHhhyo is eodsndagi twhi TSH /w rflexe to T4 (sith just eltls het lab fi STH is lnorma od’tn ceckh T4 tbu fi THS si r,abalnmo kcceh 4T .)oto THS swa’nt an oontpi os T4 si hte tbes rn.swea

hello  I don't get why this was downvoted... +2  
maxillarythirdmolar  To take it a step further, Goljan mentions that there are a myriad of things circulating in the body, often in a 1:2 ratio of free:bound, so in states like this you could acutally see disruption of this ratio as the body maintains its level of free hormone but further increases its level of bound hormone. Goljan also mentions that you'd see the opposite effect in the presence of steroids and nephrotic syndromes. So you could see decreased total T4 but normal free T4 because the bound amounts go down. +  


submitted by chillqd(36),
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ehT tmeS is scigenibrd osomethmosc,airh tcrahecazirde by bmalnoar nroi ngnsise nda dseraniec stiatennil irptonsoba. shTi sceearins nI,or sirnecinga f.riterin nI nrso,spee ITBC si ese,eraddc whchi csaieesnr irranfesnrt tirsutoaan as rhete is essl ntcialgcrui cirarer olc.usmele

htiW cxsees roni in teh dbloo, ti iwll cuamateulc in ssuiset lgdnciuni eth lievr, s,kin naac.espr leuSeaeq dnuecli eidladt ry,dtaooaichpmy dinspohagm,yo iesedba,t tartahoprhy 2/2 iaumlcc epooprysthaph ,tispioeodn nd eaurellHoaptcl animoarcC

hello  I think you made one slight mistake. TIBC = total iron binding capacity. It is synonymous with "transferrin saturation". This patient has increased transferrin saturation aka increased TIBC. The transferrin molecules are saturated -- it is incorrect to say "as transferrin saturation increases, there is less circulating carrier molecules." It is more correct to say that the amount of free (unbound) transferrin is decreased. +1  
hpsbwz  @hello Transferrin saturation and TIBC are not synonymous. Transferrin is calculated using total body iron / TIBC. While the serum iron level continues to increase, the transferrin level decreases. Thus, the amount of transferrin available to bind iron (TIBC) decreases and the amount of transferrin saturated with iron (i.e., percent transferrin saturation) increases. +10  
mangotango  Just to clear up definitions: Total Iron Binding Capacity (TIBC) = measure of trasnferrin molecules in the blood (bound by Fe or not). % Saturation = percentage of transferrin molecules that are bound by Fe (normally 33%) // Pathoma pg. 42 +  


submitted by ergogenic22(301),
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why si laiieippyrmehd danrcoyse to igcuhns ednrosym nto a osibt?iylpis

hello  SIADH = MC paraneoplastic syndrome of small oat cell lung cancer. Also, Cushing syndrome would cause would weight gain, skin hyperpigmentation, and hypokalemia. Not, lyperlipidemia. +1  
charmrooftops  You do get hyperlipidemia in cushing though? https://www.amboss.com/us/knowledge/Cushing_syndrome So still unsure why this is not a possibility. Is it just a "more common" thing for SIADH? +2  
peridot  I was debating the same thing. But yeah I guess the SIADH association is just supposed to be stronger somehow and "more common"? +  


submitted by sympathetikey(1253),
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As estatd bl,eow teh tLfe rscu ecbrrei aws gdadeam see( tahw ti ohudsl lyamroln loko iekl low).be Tihs niocants the iopnlstcoirca ractt. neSic hte citsnpoiacorl atrct tudscesea at eth luem,lda owelb eth mdriinab ietcnso eew'r logoink ,at yuo oulwd see ltaaoeaCnlrrt h)tg(Ri aispcSt Hpseiraseim

hello  What identifies that a cross-section is medulla vs midbrain vs pons? +4  
kernicterusthefrog  @hello I like to pay attention to the Cerebral Aqueduct (diamond/spade shape seen mostly in Midbrain, and transitioning to 4th ventricle in rostral Pons), and then the shape and size of the 4th ventricle as you move down Pons to rostral&middle Medulla, and eventual closing and absence of fluid space at caudal Medulla. +11  
hello  @kernicterusthefrog Thank you. +  
mbourne  NGL, I thought the right side had the pathology lmao ty +20  


submitted by armymed88(47),
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A tetlil mhta p er..hHe is low -t-&g; odcaiiss 2OCp is ighh &--g;t rraytrpeois Nmaorl sopmtnnoiace osduhl eb guolyrh a 1 e)acut( ot n(4hcr)ioc earnesci ni biacbr epr veyer 10 ncaierse in p.O.C2 Its owrle e,reh so ycealrl tno cetnaoemspd adn ainddetic italndiado drpo in crt&g- -dbai; dad on tbaem aciissdo

hello  Hm, what do you mean by "normal compensation?" Are you talking about the bicarb should be increased? Are you saying that a normal compensation would be metabolic alkalosis? Would metabolic alkalosis be an increase in bicarb? +2  
kateinwonderland  How do you know which one has bigger contribution in this situation where there's increased CO2 and decreased HCO-, both indicating acidosis?? +  
yb_26  normal kidney compensation would be an increase in bicarb reabsorption => increased serum bicarb. This pt has low serum bicarb => concurrent metabolic acidosis +  


submitted by seagull(1405),
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hTsi si a kliieodhlo tir.ao =RL+ nS-is1pcSe/ef

nAy uvale getrear ntha 01 e(rp itrfs a)di tcdiiedna efess"usnlu fo octadigisn stte" hhwci si elocprabma ot VPP li(ngur ni a z).d iotnP A"" is hte tocsels kram ot eerhw 10 holuds eb on eht Y xsi.a

brise  The question is asking what point would be the most likely to rule in cancer, and high specificity when positive rules in cancer. The highest specificity value is A, bc the the X axis shows (1-specificity)! +5  
hello  brise is correct. Knowing the LR+ value = 10 does not help in this situation because estimating where "10" should fall on an axis is arbitrary. The way to approach this Q is to know that a high specificity is will mean that a positive result is very very likely to be a true positive. In theory, suppose that the specificity was 0.99. This is 99% specificity. Then, you look at the graph. The X-axis is "1-specificity." So, suppose the best test has a specificity of 99%. Then, calculating 1-specificity = 1 - 0.99 = 0.1. You would then chose the datapoint that corresponds to having an "X-value" that is closest to the origin. In this problem, it corresponds to data point "A." +3  


submitted by bobson150(11),
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Is hits sngiya rehte si iocerresetaluv efulx?r I cudlo vahe msrwo ihts easm iamge wsa no mrfo 02 ro 21 nda teh srnewa was Wimls uotrm

hello  Yes, it was. I think in both vignettes, the picture was basically irrelevant. Or another possible clue -- but definitely not needed to answer the Q. +13  
presidentdrmonstermd  My school uses old "retired" NBME questions for exams and I've also seen this exact same picture multiple times...w/ different scenarios I think. I tried remembering what the questions were but I guess it's mostly irrelevant. +3  
hyperfukus  SAME +  
hyperfukus  I also put wilm's tumor bc it felt really familiar wtf +  


submitted by k_tron_3000(31),
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Teh oscrdnpitie fo rltaalieb wlero imlb lsos of itbnioavr lempiis LDCM degaam, dna eth tnaebs RDTs + obRmerg seem to me ot eb lmpniigy taht eh sopbsyli sha etsab lsrsoida rfmo ysiphsli (or ngoshtmie yerv ramlisi ni t).oanrenpteis

As for the rothe r,sansew A is rognw ecsubae sih tomro icutnonf si ,tianct B si rogwn cuaseeb apni nda rertemepuat iiscftde rea not ,ntmeinode C is ognwr aebusce it slmipei a ficceisp evrne is rnpeptdae, tub he sah tlso leribaatl esstniona in his nitere oewrl irtxetmiees

D is eht rtkiisc,et nad m’I ont 10%0 sreu, tub I wloud tinkh puaaychtlrdio of het eiarrton )vrlatn(e orost odlwu sueac oomrt ficeisdt inecs tehy rayrc torom efnfetsr.e oYu thmig osal pcxeet htta rmoto fncnoidtusy to eb arill,aunet sicen ti udwlo be kenilylu ot avhe a rblepmo wthi eth never torso on thob is.des lsoa het CMDL is tno ledatco eran teh riaonert rtoos fo eth aisnlp o,drc os if eht ntoearir stroo ewre tfeafcde you leaylr twnldou’ ptecxe to ees rvoyriatb slso.

oS cblislaya opsecrs of oiie,talninm I do elfe ilek eornsys pneuthyaro si an erxeelmyt uvgae wranes oughht adn I twsna’ a nfa of het te.ousniq

keycompany  This is a great rationale. I would like to add on that D is wrong because Radicular Neuropathy of the anterior lumbar roots would (1) be painful [radicular neuropathy is characterized by radiating pain (hence the word “Radicular”); this patient has numbness and tingling, not pain] and (2) because the anterior lumbar roots are the motor roots and do not carry sensory innervation. This patient is having a problem with his dorsal spinal cord (not anterior/ventral). +30  
hello  Want to clarify that "radiculopathy" is not synonymous with pain. Radiculopathy can cause pain, weakness, or numbness. I think the only reason Choice D. was incorrect because it discussed the "anterior lumbar roots", which would affect motor function. +15  
niboonsh  Radiculopathy is damage to the actual nerve itself, wouldnt that make it a LMN lesion and babinski would be negative? +1  
link981  Great explanation guys +  
usmel2020  UW QID: 12035 explains what you are testing with Romberg sign +5  
jurrutia  "Radiculo-pathy" comes from latin terms meaning "root-disease". +  


submitted by hayayah(1056),
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spiaoeNal si nwe susite towgrh ttah si eegaudrlunt, ilb,errsevrie and n.aonlcomol

yllantoiC acn eb tdinrdmeee by oplehoa-cupg-sthes6 gersedonhdeay )(6PDG zeymen osrois.fm DG6P is eXn-dlki.

*roF orme aornomiiftn ecchk tou .hC 3 ilNsaepao ni htamaoP

hello  This is great, thank you. +4  
breis  Pathoma ch. 3 pg 23 "Basic Principles" +7  
charcot_bouchard  Shoutout to Imam Satter! Without him this question wasnt possible for me to answer in 10 sec. +13  
fatboyslim  Clonality can also be determined by androgen receptor isoforms, which is also present on the X chromosome (Pathoma Ch. 3 Neoplasia) +1  
lovebug  @fatboyslim thanks for reminding! +  


submitted by hayayah(1056),
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Tsih eattnip sha lmsal clel amcircnoa. hsTi pyet fo raccen is icossdteaa ihwt apnropciaatles osmrnsedy cush a:s Cngushi nSmyedro, IDAHS, or dtoinaeibs gntsiaa C2a+ saehlncn e-anrLtam)(oEbt or nnoe.sur aimcpfAnoiitl of myc cnoengeso is loas mom.cno

SADHI en(drymoS of eiprapptnoair itdiacuetirn ormneho tnesroe)ci is rhteiazcearcd yb:

  • ecexsisEv rfee twera iteretonn
  • vmlEicoue paeitmnyohar iwht iudtrnncroiunyea aN+ exoctenri
  • iUren lmosyoatil t&;g umsre lastomloyi

dyBo nserposd to ratwe nntetioer hwti etslaooernd dan APN nad NB.P Ttah si waht acseus hte adeesnrci rirnauy a+N eeoricstn hiŽhcw saled to zotinoaimarln fo llrleutracxea ufidl umvleo Žadn the mceolveiu rapeaotnhiym.

hello  Why would body respond to water retention with ALDO? ALDO would increase water retention... +6  
nala_ula  @hello, the body's response is to decrease Aldosterone since there is increased volume retention and subsequently increased blood pressure. This concept confused me a lot, but I ended up just viewing it as separate responses. First, the increased volume retention leads to increase ANP and BNP secretion that lead to decreased Na+ reabsorption in the tubules (page 294 in FA 2019) and second, this increased volume basically leads to increased pressure so lets also decrease aldosterone so there is no Na+ retention (since water comes with it)... I thought it was counterintuitive to secrete so much Na+ since you're already having decreased serum osmolality (decreased Na+ concentration) because of the water retention, but I'm guessing that this is just another way our body's well intentions end up making us worse XD +32  
compasses  see page 344 FA2019 for SIADH. +  
dickass  author pasted text straight from FA but the arrows didn't copy over, inverting the original meaning +3  
medninja  The idea of increasing urine Na is getting rid of water, thats why this mechanism end increasing urine Na secretion even when there are very low serum Na levels. +  


submitted by hayayah(1056),
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aesC fo .itoaecilsrelsorrso

cstrylpeHapi oesrrtesraloioclis noivesvl tnghniikce fo svslee llwa yb pseapyiralh of stomoh lmcseu oink'oinn-(s aarncap'e)ep

  • nnoeuCeqecs of mlntgiana eetsiyrhopnn g1/;(081&2t0 /w ucaet d-noanrge eamad)g
  • tsRules in eeudcrd eessvl ailrbec thwi gadro-nen achmiesi
  • ayM ldea to oiirnfidb sorecsin of the sseevl lalw hwti haghoee;rrm syslclailac sacsue tueca alner fiaurel )RA(F ihwt a tiatrehcascric flnti'bate-'e arnaeepacp
masonkingcobra  From Robbin's: Fibromuscular dysplasia is a focal irregular thickening of the walls of medium-sized and large muscular arteries due to a combination of medial and intimal hyperplasia and fibrosis. It can manifest at any age but occurs most frequently in young women. The focal wall thickening results in luminal stenosis or can be associated with abnormal vessel spasm that reduces vascular flow; in the renal arteries, it can lead to renovascular hypertension. Between the focal segments of thickened wall, the artery often also exhibits medial attenuation; vascular outpouchings can develop in these portions of the vessel and sometimes rupture. +  
asapdoc  I thought this was a weirdly worded answer. I immediately ( stupidly) crossed of fibromuscular dysplasia since it wasnt a younger women =/ +16  
uslme123  I was thinking malignant nephrosclerosis ... but I guess you'd get hyperplastic arteries first -_- +  
hello  The answer choice is fibromuscular HYPERplasia - I think this is different from fibromuscular DYSplasia (seen in young women); +23  
yotsubato  hello is right. Fibromuscular hyperplasia is thickening of the muscular layer of the arteriole in response to chronic hypertension (as the question stem implies) +6  
smc213  Fibromuscular Hyperplasia vs Dysplasia...... are supposedly the SAME thing with multiple names. Fibromuscular dysplasia, also known as fibromuscular hyperplasia, medial hyperplasia, or arterial dysplasia, is a relatively uncommon multifocal arterial disease of unknown cause, characterized by nonatherosclerotic abnormalities involving the smooth muscle, fibrous and elastic tissue, of small- to medium-sized arterial walls. http://www.medlink.com/article/fibromuscular_dysplasia +1  
smc213  *sorry I had to post this because it was confusing!!!*Fibromuscular dysplasia is most common in women between the ages of 40 of and 60, but the condition can also occur in children and the elderly. The majority (more than 90%) of patients with FMD are women. However, men can also have FMD, and those who do have a higher risk of complications such as aneurysms (bulging) or dissections (tears) in the arteries. https://my.clevelandclinic.org/health/diseases/17001-fibromuscular-dysplasia-fmd +1  
momina_amjad  These questions are driving me crazy- fibromuscular dysplasia/hyperplasia is the same thing, and it is NOT this presentation and it doesn't refer to arteriolosclerosis seen in malignant HTN! Is the HTN a cause, or a consequence? I read it as being the cause (uncontrolled HTN for many years) If it was the consequence, the presentation is still not classical! -_- +1  
charcot_bouchard  Poor controlled HTN is the cause here +  
charcot_bouchard  Also guys if u take it as Fibromuscular dysplasia resulting in RAS none of the answer choice matches +  


submitted by sympathetikey(1253),
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As asdtet ,elbwo eth ftLe csur ircerbe saw aadmgde es(e htaw ti hdsoul omnlyalr ookl leik bolw).e Tihs otnasicn teh osolnrpctacii ttcra. Sneci eht alrpcnsicitoo trcat eadtscues ta het eladlum, bwole teh aimirndb cieonst ewr'e gnolkio ta, uoy dolwu ese rlelnttoraaCa ith)(Rg ipcsSat srepmiHeias

hello  What identifies that a cross-section is medulla vs midbrain vs pons? +4  
kernicterusthefrog  @hello I like to pay attention to the Cerebral Aqueduct (diamond/spade shape seen mostly in Midbrain, and transitioning to 4th ventricle in rostral Pons), and then the shape and size of the 4th ventricle as you move down Pons to rostral&middle Medulla, and eventual closing and absence of fluid space at caudal Medulla. +11  
hello  @kernicterusthefrog Thank you. +  
mbourne  NGL, I thought the right side had the pathology lmao ty +20  


submitted by hayayah(1056),
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uonvaRslacre eseasid si hte tosm ocmomn useca of °2 THN ni t.alsud nCa be /dt ehiiscma rfmo nrale ossstnie or raacrliomvscu eias.sde naC rhae neral ritsbu aalelrt ot busilimuc.

aniM eascsu fo lnaer eayrtr oetsinss:

  • Aecrihrecottsol lampxquslrpa—oie d/3r1 ona erlf eyartr, uyllasu in droel ,msael seoksm.r

  • acubuoiFrsmlr illsispytdsda—aa /r23d a froenl rerayt ro slgmteean brchnse,a uusl layoyngu ro amdldged-ie ef.mlaes

aLb esaluv based f:fo

  1. sStsoein rceasdsee oldbo wflo to rmgulu.loes
  2. umJlxgtraauleor auptsraap JG)A( pesndsro by striegcen eirn,n ihwch nsvcteor nngtoioegennais ot noitgnseian I.
  3. gsAtninnieo I is dnvctreoe to ainoeningts II IA)TI( by gniosneaitn icvgtroenn neeymz EA(C -ni- s)nulg
  4. ITIA riseas oblod reueprss yb 1() nicrtncgtao aerarirtol otshom se,lmcu ncingarise otatl aeplrierhp aresicsten nda )2( notogpmir anelard elesare of srnoa,dtloee hwcih iaeecsrsn sapbreniotro of dumsio h(reew a+N eogs H2O iwll oow)fll in eth sdtlia ledtucvono uutble ipdnnxaeg( saaplm vueo)lm. Cna deal to plaaoiyhmek eens( ni the lbas ofr tish ueiqs)not
  5. esLda ot NTH ihtw enecrsida pamlas eirnn nad laruntalei ayhoprt e(ud ot owl dbloo wo)lf fo eht fedecfat eyk;ndi itnhere taeefur si nsee in myrarpi eiyeprntnsho
uslme123  So both causes would result in increased aldo and MR is the only way to differentiate the two? +2  
hello  @USMLE123 I think both are causes of renal artery stenosis and that could be seen via MR angiography. It is asking what could help DIAGNOSE this patient -- and her most likely cause of the findings is fibromuscular dysplasia. So, yes, MR angiography would look different for the 2 different etiologies and thus could can be used to differentiate the two from one another. However, epidemiologically, we are looking to diagnose her with the suspected most probable cause. +8  
yotsubato  @USLME123 I think measuring Aldosterone is an incorrect answer because you already know its increased due to low K. Knowing she has high Aldosterone wouldnt provide you evidence for a final diagnosis. +4  


submitted by johnthurtjr(139),
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eilhW I can get no adorb ihwt ndmAjtetus eor,Disrd I nd'ot ees ohw stih srwaen is ayn ebttre nhat imtSoca yoptSmm ei.odrrDs oFmr :FA

Vytirea fo ilbdyo aptsconlmi iltsgna nohmst to rseay eiacdsotsa wthi eecessi,vx netpiresst hstutgho dna ytnaxei uaotb ytmspm.os aMy coperaap- twih .essilln

DSS sgoelnb in a guorp of ssdorrdei cahcaidetzrre by pcsaihly poystsmm csiugan fgiitcinans tissrsed nad immena.ritp

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". +13  
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 hayayah(1056),
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feioiniDnt of emtdtujnas dirsoedr:

oiEatnlom yomtpsms g,e( xteayin, nisodree)ps taht urcco htwiin 3 tmnsoh fo na nidieflbtiea cpsaihsocloy ssrteosr g(,e vedioc,r nesilsl) stgnali ;&tl 6 nomsht noec hte srseorst hsa .enedd

If ytossmmp spsiret tg&; 6 smtnoh efrta sosetsrr sned, it si AG.D

hello  Yep, and I think what we are supposed to take from this Q is: The only info. we have for this patient is that he ended chemo 2 months ago and has been calling the doctor a lot -- this is supposed to mean he has been calling a lot since ending chemo 2 months ago. His frequent calls starting after ending chemo and within 3 months of the stressor fits with the above-stated definition of "adjustment disorder" with anxiety. I stressor in this case could possibly be either the actual illness or the ending of chemo/treatment. It probably does not matter much in this case. +3  
charcot_bouchard  I think doing uw done me wrong here. Adjustment disorder isnt diagnosed when symptom match another disorder --- it was like never a right answer. But ofc its right answer in nbme +5  
maxillarythirdmolar  Just to add to that, the tingling in his fingers may seem like a distraction/it probably is. Likely has some relation to his Chemo. +3  
j44n  shit I thought this poor guy had OCD with all the repetitive behaviors. +  


submitted by hayayah(1056),
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oenliEilZnsr-lgol nseormyd: sGnnsee-cgatiritr murot )(aaitgrnsmo of respaanc or dmnod.ueu

hello  Can you please explain how gastrin relates to the physical exam findings in the patient? +2  
amorah  I believe the logic behind it is patient has pain and black stool, suggesting peptic ulcer with bleeding. Since pain is not relieved by antiacid and H2 blockers, it suggests ectopic source to stimulate the excessive acid. Among all, gastrin by ZE syndrome fits the most. +10  
coconut  Also has hypotension and light headedness with blood loss due to a bleeding ulcer. The sweating is likely from sympathetic activation due to hypotension +2  


submitted by beeip(123),
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hThogtu ihts uowdl eb isgeomnth anidrgger riai"artcb s"ryu,ger tub ,oenp utjs on" ahctrsy ofdo,s eucbaes 'uryeo ac"prde-it.ebi

hello  Yep, seems that because the patient has prediabetes, he should avoid eating excessive starchy foods. +  
yotsubato  such a BS question IMO +5  
yotsubato  such a BS question IMO +  
breis  I put nuts thinking of "fats" and that with a bariatric surgery they may have problems with absorption.. +4  
teetime  This isn't right because the bariatric surgery will cure the prediabetes. It's dumping. +2  
dr_jan_itor  Why should he avoid eating excessive starchy foods? To avoid gaining weight? It doesn't matter what macronutrients he eats if they are calorie controlled. +1  
dhkahat  yeah but he's prediabetic. you want someone like that to shove a bunch of starch down all the time? +  


submitted by kentuckyfan(43),
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erUa :ycelc erecdesaD ilnelrtuic nda pmeernhmiamayo cna ffiinetredate ti mrof rcooit da.icairu

hello  As the poster indicates, the described patient has a defect in the urea cycle, specifically an ornithine transcarbamylase deficiency. Added for clarity to future readers. +  
ally123  For orotic aciduria, From FA 2019 p. 412, "Orotic acidura is inability to convert orotic acid to UMP (de novo pyrimidine synthesis pathway) because of defect in UMP synthase. Aut recessive. Presents in children as failure to thrive, developmental delay, and megaloblastic anemia refractory to folate and B12 (supplementation). NO hyperammonemia (vs. ornithine transcarbamylase def. which as increased orotic acid with hyperammonemia." +  
fataldose  Also it's not Carbamoylphosphate synthetase (I) deficiency because there would be only hyperammonemia, increased glutamine and decreased BUN but no orotic acid increase since carbamoyl phosphate isn't getting made and then shunted to pyrimidine synthesis pathway to get acted on by carbamoyl phosphate synthetase II as is the cause of increased orotic acid seen in OTC deficiency. +  
fataldose  If there is isolated elevated orotic acid and no urea defects or hyperammonemia then it's Orotic aciduria due to UMP synthase deficiency. If there if hyperammonemia and orotic acid increase then OTC deficiency. If there is hyperammonemia with no orotic acid increase then carbamoyl phosphate synthetase I deficiency. +2  


submitted by drdoom(807),
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The remo grelane ercippi:nl enoaidtlhe toaidlsave ni hte pecsnree fo ighh O;2C uoy goatt teg idr of ttha cadi wshooe!m na’tC lte ti lumaua,ctec as owelr pH ihinwt a nnor-niteorc”immev“ sfectfa ucreyitsefnfceutri/c fo ,emszeny ,ropnstie etc. ehT rmoe icciad a oclla enoinrvten,m teh roem uyo xepetc anyerb rvcuaeslatu ot dtliae (sa a asemn of ieansrgicn folw ,tear rhyeteb eirngryf ffo mceucluaat ci)a.d

heT ttgsesaosnlioeih anc tleipox isth hnei.msacm By niratitheplgyvne (bgwnoil off O,C2) teh rinab vlceraatsuu essnes a wol 2CO / k-y“hyrudon s,tt”ea hihwc eiruerqs no iltavdsoanio. nI horet d,osrw the vascruutela dose nto ened ot iunceotn hte ncigomn-PTAsu ceiarctp fo ehinizgysnst iircNt Oxdei )O.(N

hello  But, the Q-stem states the anesthesiologist is HYPOventilating the patient. +4  
drdoom  decreasing respiratory rate = retention of CO2 = vasodilation of brain arteries = more filling of tubes = greater intra-cranial pressure +1  
drdoom  @hello shoot, you're right! i ended my explanation with the example of HYPERventilation when i should have done the opposite! (sorry!) ... edit: "By HYPOventilating (retaining CO2), the brain vasculature senses a high CO2 environment and vasodilates = increases intra-cranial filling and pressure!" +3  
dulxy071  @drdoom could you please elaborate on your point. +  


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hello  Patient in hypovolemic shock - the clues are low BP and COOL skin. Hypovolemic shock is caused by fluid loss. The patient has decreased preload b/c of fluid loss, i.e. there is decreased blood volume returning to heart --> thus decreased preload. +8