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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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hWy aer "tororta ffuc ae"rt adn rotrat"o ucff ni"ndsteti owng?r is it bc ohtb of tehse loudw whos tnipgmneiem isng? si rehet a wya ot DxD neo fomr eht ?orteh

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

 +0  (nbme23#45)
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hyw si smapal occotin uresesrp ?gronw

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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hcihw lreett is CN IX in stih im?aadgr

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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nac moeoesn elpaes pleanix htsi?

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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s'thaW teh eoysemchs psupdseo ot be a cule bua?ot oDes htis atetinp veah C?ID esoD IDC slwaay seuac yoviecplhmo hokc?s

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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leaseP ephl - owh rae oyu leba to tlle atth het TC mgeia is ont at eht level of neo?dduum

I td'no nowk hwta m'I ikoogln fro to oapemrc nda crtnstoa a TC at hte vllee fo eth udemodnu sv eht CT eving in tihs .Q


 +0  (nbme22#1)
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rTehe sah ot be a etbrte teliananxop fro why PNA is wrnog?

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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tapoilSonncero dna ennleoreep rae ong-tssuiiapsarpm seurictcdi atth ibtnhii eth a/NK Ts.PAae /KaN TPeaAs is on eht laetlasrboa baer.enmm oenN fo teh aswnre hcsoeci ift htiw hs.ti

mdAiriloe and eimrteentar rea lsao niaipsrms-sguoatp cit.uidser eTh hcsaimenm is ot klbco CENa cahnesln no teh malulni mr,beeamn tihs si cheoci "."B


 +0  (nbme22#37)
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If uoy ndee a rnidfftee noirtnaotei fro a amairgd of the :aywastph

p-aawg43m221.pTg.8nsfar:/%a31ic0sFttcb_4ne12sF/iau4sAp3-O/mg8is1it1ngbe1/3e146rit1/i=ajdMLeled30tg?yh-n_3/pMec%rir.sH.80el6tr0o/pet2-_sma_r10/u


 +0  (nbme22#41)
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aePintt has a eiotrahmhx + XRC swosh hatarce aistvede wtodras teh rtiohhaemx -g;t-& omts lyeikl isngadiso si psouatonnes xmouoprthnea.

ipiolyalgdmEcoiel, pastsouneon oeoxhrpmanut si somt csadtoasie wiht niht masle

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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plaees hepl -- fI s-ivtspeecaaatlio rcebiata utrilzeaen hiret wno ,oerespiudx yhw ns'it ti teh eacs rfo lavtsei-sopeiaact ceiarbta ot icientosnf in nyev?eero

mI' tno gnndransuiedt hte onnctiocne to NDPHA oiaxsde .neiyifcedc

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'sn siht a coroht ?sduyt

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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oFr opplee gkasni why the aadt lbtae was evne ddeunilc if ti swa nto needde to erawns tihs Q, heer si a seuflu panno:axeitl

Teh abetl saw ginve cuseaeb a x22 taleb si iyyapllct awth oyu od ese rrgigdane atad rfo trneccsalo-o tieusds.

If teh 22x etlab tnw'as ,ucdeidln ehnt atyrliell reveteony luwod cpki ihcCoe "E" as het rerccto sanerw c/b ouy 'catn tlauacecl smhongtei tiwuhto ibneg peiodrdv ue.smbrn

heT nfrefceeid in undnligic eth aatt-bldae si tth:a

  1. i,gAan yuo eedn to oertrp a 22x lbeta eecbsau ahtt is tpialyylc thaw you illw see rgerndaig data for a ncsltoeroca- dytsu

nad

  1. by nilncgiud het x22 ,labte ti yltuacal stset fi the atte-kestr aeiezrld ttah teh taad in teh x22 atebl sedo ont pehl ta lla twhi tulcgncaali -elnrpaceve- asbceeu an-oelccorst ustdsei VEREN ertorp on lvnee.ecapr
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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Peittna ash edr lyca shar- tish sfti orem htiw VHH6- oaR(selo v,si)ur ont aPisvuorr.v

H6-HV sceuas oratmdineof fo rasyhs,lotetb anledig to nm.aaie

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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etatnPi aonnctn netdex iws,tr ichwh is editveannr by dlaria nrvee

Pentita ash bnee no thcc,user hwhic dlwuo caftfe lraaylix vener -tg-&; htis tafescf edoldit eslcum, iwhhc edos ram aibnodtuc 0º-0115 (so ti nca anolylmr vome rma ebaov s)hdorlue

hTe nylo coinaolt ni the eginv aradgmi to ecftfe lla fo htese nvsree dwolu be nitocalo "C"

oNt:e layonmrl, arm otenmvme beaov het onhlztoira is siasdetoca iwth rssrtuea onirtera ll/umenscgo iachoctr re.nve rHweove, oenn fo hte gardaim nostliaoc lowla ofr niouncsil fo T.ASL eincS het iteptna ahs enbe no srcetchu rof ksee,w it sestggus llairayx ernev nlveeviomnt -;&-gt iddotel si caeefftd

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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The tenatpi is ddtaheyrd.e eedN to vieg wreta to .trhrdyeea

erWat loosfwl lseto.u If imodus is edadd to eht o,stnuilo aretw will ololfw hte so.iudm ow,N oneyettrce ktupae of msoidu is ddtieaem by eSuloi-usdmcoG tp.onrestrar Hn,ece eth snotulio sndee to ocntina smiuod dan gcuosel ni erdro ot aehv eht cenretsotey kate pu the .doiums


 +4  (nbme22#11)
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The Q is denbriigcs het etlfoginmorae vrnee, whihc nusr on the xeaernlt faruces fo teh caritsemp rcdo at eth ciulespfrai alinguin nrgi

hisT Q si NOT einrfgrer ot ionialguilni ervne -- eth ioguinlnaiil erven xtesi GUTHROH the esiapulrcif niiglaun nalca eeahrsw sith Q si niksag tbaou a evrne atth is ERXTENLA ot eth ipicesaulrf iangunli nc.ala

eeS tdaaa/gposgc.rscceetgt.i:flteeav.njp/dcwpnnfeiikwu/n/rwo/iihm.a

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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ihTs hte esam as kpyyac@nse'mo tleoinaanpx hitw moer nopeainxalt shoet atht eedn ...ti

The anpiett si faedectnuf yb hte iparucralt stoloamau ersvceesi idsesea nad ish tbhreor has eth oatlumosa sivecsree eiadess g;--t& hist eamns hcea of hirte sprtena aicserr teh AR lleeal. Now, rof hte tpeaint to be uteeffancd givne ttha ohbt his tanrspe eavh the AR l,eella it mnaes hatt the atnitep ahs a /32 nechca ahtt eh is lltsaiesyunomu fantfdecue adn a r.rraiec

Teh ea'psttin antrper is funftdecae adn lronam WgaebHnidyerr- igecntes s(a dtesat ni teh wreon.lbmhpe). sith si lieyiacscflp tm,ideeonn uyo are to muases htat hte epnratr sha a crrirea neercfquy ofr hte RA ll,eael whhic aeluq ot .pq2

heT edaessi has a qfuneycre ni hte apoltpnoiu fo 0/00.140 Tshi is ^q2 t&;-g- q^2 = 0100/0.4 vngloSi for ,q uyo gte q = 00/2.1

erCrair eurnqyfce si q2p. ervwHoe, ofr a rare ssdeei,a q2p ≈ .q2 ,oS eth rrcreai ecnrfueqy for eht trenarp = 2q = 2 * 20/01 = 1/0.10

Now, eht Q sksa utboa an nprfsiogf of eht pitnaet and his nrerapt being aedfftce, so to veah na dtecfaef idl,ch theer si a 4/1 haccne fo ivhgan an tffdeace dihcl esbu(asce teh paitetn nda eht arenptr hobt ehva a 12/ chneca fo iansspg eth lleeal &--tg; uoy uilltmpe eehts grhttoee 2/1 * )/21.

,oS lpltuiym 32/ * /0110 * /14 = 6100./ sTih si atptiPen( being a riarr)ec * rntePpar( egnbi a arir)rec * avghnPi( na etcdefaf ffpionsrg gh.ert)eto


 +6  (nbme22#35)
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eTh agarrmm of eht tacual Q swa ngsuifcon.

oT meka retbet ssen,e it hsdulo ysa "chiWh of eht gwnlfiolo is hte mtso iylkle urlset no hte tcntoiarsirnp fo gnees htat hiinibt ecll odiinvsi dna thta ntacoin hte ssunsecon esueqecen "T.AT.A.

o,S the Q is iknasg oabut eht p3t5 ngee nda icfyilpsaecl uatob the 3p5t ngee prtromoe einogr.

etmororP neisgro ahve a AATT obx suloiv(y,bo emniagn irch in T-A sabe .)aisrp -AT bsea iprngia ahs 2 nhegdroy nbd,so hwchi esmka tehm aresie ot valece t-&-;g swloal fro NAD tairtscrinonp ot occur omer aleisy. RNA lPo deos snprotriictna of NAD into .ARN

The eneirt -etsQm lakts bauot who rumaiiL-neF is edu ot a tamutoni ni 3tp5 gen,e eagildn ot a ackl of rtumo ussosnrpipe tyt.aiivc

,So if eth mreptoro ngeior TAAT bxo fo hte 3pt5 ngee si eadutm,t etnh eth 5p3t gene iwll tno get atdrbeirncs --g&t; hsti si hwy teher llwi be drscedeae ANR olP ngdnb.ii RAN Plo illw aevh a ecduedr tibiayl ot nbid 3p5t -g-t&; ssel tmrou ossrpuser eneg pnrtisaitnrco --tg&; elss murot nreoups.ssip

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

 +1  (nbme21#29)
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I atwn ot pzrmhs-eeaie ignsetohm ttah aptaslsoys@ sha eradlya dtesat :).

hTe Qetsm- aetsst ruesm slgecou = 100, adn teh Q sask wyh the ntatpie is ebal ot tanminia oo.einmralgycm

e,orfeTehr uyo acn lmmtiaieyde leiemiant cehcsoi A and C cbeesau atcaeecoatet dna yrbetta-tybdxehrauoy era ureoscs of eryneg ugdrin eissnktgeoe -- iegesesotkn sedo nto pedrvio lscgeuo rneyeg soecs.ru


 +0  (nbme21#29)
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Pealse lhep

Why si navlie ri?ertccno

nA enaipxaotln blewo says ttha ilavne loudw be trcnveode to lseucgo runidg arrgleu ebt?amomsil

rRaeglu boemlsmtai = fed t,tsae so hyw wdlou ialvne nvee be rndevcteo to cgosl?ue


 -2  (nbme21#5)
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hTis is het taacul ecrtcor tiaolenx:pan

PAD uscaes oldbo ot lwfo form gniddcnese atora to entapt uusdct rsaiersout toni lmynuparo utilacironc iof)"l"-thr-t(etg

ehT ""letas fmro the aoatr udnrig iaeldots rusiqere eiaecsdrn criadca uottpu ot anemosctep ot lvrieed dteeauaq atnmou of dolbo to rtse fo doby

reoSc:u 03imsn4b5/h.kb//Bglwn.i7o://ch.ttKpwvns.8oNwo

fkstpashls  It's L to R +1

 +0  (nbme21#16)
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Pesael plhe

itilM-socsyd jnetioce kcicl = puiolncm stnsoise

woH is numlopic tiossnes daeeltr to hte ntsaip'et ADS -- dose DSA ecusa inmucopl ne?os?itss

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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For nonyae nusocedf ygtrni ot lfloow u07emr0'ss@slue tneocmm

tgyhllSi emdidoif

slteaEnis niamo asdic ominmenc ,"hA Terhe ansf lwli try thehemt"

Ah = inenaig,r etiishind

Trhee = erneThnio

sFan (pha)sn= nhlnayeeniPla

illV lwi(l -- Gmanre cceant cpnnrogunio inEglhs odwr l"l"w)i = vla,ein ensceoiui,l iunlee,c elysin

yTr = ptoyphatnr

hMet = Mnhieeoitn


 +12  (nbme21#36)
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llMtupei maomeyl = omalspen of spmlaa e.sllc

aamslP lcsle uporecd rerotycse 'bAs ak(a dorcpeu b'A)s -- malaps lscel do ton have banebmormu-nde Ig a(ka od nto aevh .C'RB)

To a:pcer obubmear-nnemd gI = RBC ewilh erctrsoye Ig = .bA

o,Nw ipcino-dytitia obindayt = iadtnyob taasing t.oabdyni

alasmP lslce od not ocniant eufscra gI -- uaebcse apamls secll lnyo eb rstceee bA.s'

eerrThoe,f tiaid-pctoiyni nbiaodyt lowud tno wrko ot gratte lmeoyma escll sbceaeu eaomlym clles = lapsma lelcs kaa salapm lclse aklc uarcesf ulcolmsee atth iinpi-todaytci bs'A ulwdo deen ot bnid t.atoegtr/

eeS d:argima u2oseff4c/h1qa:n/83fef95.ctqbhqcn3.e-dae.9pccama80c1tsig/t2-4fa0primn5


 +4  (nbme21#4)
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hTe Q setm tasets FOOX si a ianprroscntit actofr tath sosndrep ot iislunn ggnisalin by nrlieatg teh ircotinstnpar fo mcatilebo egnes ;--> eeoet,rhfr OOXF is a natcritnoispr otrfca odvlivne ni stbeoa.mmli iThs hoduls aekm essen basceeu npcoilsuiternre- iactvotani ahs a eorl in artnggleiu .oailmebstm

shTi Q sska uobat eierlerbvs sway atth uinnlsi rseaegtu OXOF rnnartspctio fctoar iyi.tvatc

q-denmuUdatiitbiei sseooriyptl is rvlerbesiier. mieilatnE lal cscihoe cxptee rof B, ,D dan H.

tiso-lrnresenpucI foicnntu grhouht IP3K ilgiag.nns KPI3 ninagslgi vvosleni ypsnopholiarhto of nsriee --g&t; rsniee ranoslhiphoypto is a ilebevrsre osrcsep. teliaiEmn H. YFI: potenmii/noar idac ooyosrhtpphanli is lsayaw .ereevilsrb

oYu aer eltf twhi csheoci B adn D.

XOOF is a icoaitnrntrsp arcotf &t--g; iarponnirctst trfcoas maetied eneg cyiatvit yb ttlhiusng twneebe the talcyosmp and uesuc.nl Ralgugenti hte ocantoil of FXOO spnitcrtanrio otafcr e.i(. syoamcplt .vs culnu)es ilwl tehreefor eelsrrbyvi uemadlot OFi-aedmOXtde ciabtlemo ngee yitcat.vi

shTi seaelv oyu wtih hte trorcce nas:ewr hCeoci 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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^q2 = 190/0 ;->- q = 01/3

rirrCea feeunycrq rep eWrHbeid-ngary larfomu is pq.2

,woN rof aerr ausoamotl ecreisevs sdseeais the iaercrr cryeeunfq fo 2qp ≈ .q2

2q = 13/)(20 = 30/2 = /151

wnAers = 11/5


 +7  (nbme21#10)
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heT einaptt sha "lelcs rdrganea ni ngntritfiali "hestes -&g-;t nsdaeciti lmgnitana cnraec ll.ces

Teh cells are eneihrt lrundalag ron suqumaso -&t;g- the ranecc si eehntri acmnaeocaondri orn suamosqu ecll nlgu erc,cna et.relepvyics

hiTs evsale mlsla ota ellc ulgn nce.rac ISADH si het mtos oomcnm oplnseaactarip mseorynd rfo llsam oat ellc lgnu raencc gt;-&- saedl ot tpiaomh.naeyr


 +7  (nbme22#21)
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owKginn eht R+L alevu = 10 oeds otn lphe to velos isth Q usebeca stiametgni herew 10"" sldhou flla no na isax si atryi.rarb Aol,s hte tada posint era eaoscinotdr -- ehty aevh an aue-lvX nda a uevla-Y X,( Y.)

heT way ot papracoh tsih Q is to wkno hatt a gihh tcpsicieyif anmes hatt a vtoisepi lsuetr is e,vyr veyr lklyei ot eb a reut iistvop.e

eosupSp atth teh ytcfipseiic si 9.90 -- isth si %99 fipy.tsiiecc ,heTn you look ta teh .pahgr eTh ai-Xxs si tciic"-p.esif1"y o,S ppessuo hte sbet tets sah a ciisitefpyc of .9%9 Th,ne ulacetlac it1secifyc- pi = 1 - 9.09 = 001.. uYo wlodu ehnt hcose het doiatpnta tath resdnsproco ot gahinv an avule"-X" ttah si ssoltec ot eth goir.ni In sthi mlop,erb ti oseodscnrrp ot tada niotp .A""

You ndto' neve eden to oknw a pecsific ecisctyiifp vealu ot losev stih peoblr.m All you ndee to do is sraenddunt taht if the eifctpcsyii si eyemtlrxe hhig, ouy wlli need ot idfn a iatptaond ttha si tclssoe ot hte ogiinr -- ta alets fro het vaeul ni eth -iasXx in the taocnrioed fo teh tada ntoip -- ebceuas eht iax-sX oesrnorcspd ot a tlcaiolunac of -"csefyp."cii1it

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

 +19  (nbme20#17)
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lGajon dah a ectuelr atth eoiemntdn ttha I"f a tpiaent ahs ala,rhgocater ierevw vryee rdug rh'teye kntgai csien myna grdsu uaces toagrlrce.ha"a

The only ignth fo oiesblsp ecrvenlae in ihst s-Qetm si atht hse ektas a ctidmnoa,ei eererfhot het arwnes of rg"ud "ecftef is het omts leilyk nosrae fro ehr eahgrtlo.caar

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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onGyu nalaC mnSdoyer is due to na rlanU eerNv osensli adn si adsaosicet thiw ecbylci halenbadr seu.

oslA GENFIR nbitdacuo dan cudnatoid is ieamtedd yb luran .verne Teh attpnei is anigvh oebrtlu ihtw FINREG uctonidab nad uaditn.cdo

The moeFrnt gisn is tingste RDTCDOAU CIOSLIP YVIATTCI, hiwhc is etdidmae yb hte NURLA NRVEE .acviyitt It is TON teitgns hubtm oopi,snpoti ihhwc dwlou be miadtede by eth anedim re.evn

eeS rmnFoet nsig


 +2  (nbme20#50)
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eTh saoern od" ton cpibsrere ontticiaibs nilut tntsegi uslrtes rea aaebl"vlai is rcoteicnr is sabeceu ew adaleyr evah a amgr tnsia tath hssow tmvgrgi-aeaen cocipdlioc ni rsi.pa sThi is seNeisrai ho.gornoeare oS, no need to iawt rfo tset ssrtleu oemc kb.ca

eTh -Qsetm gtsntai atth ge"Tsnti fro ssrNeiaie dan i"maCalyhd si re"edord ftaer deraaly hinavg dneo eht Grma snita eesms to be a caitd.tsrro

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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nPtaeit's tmysmops bnage 03 min feart gwmion alnw .ie(. rtefa odgni lhacypis tt.iy)vaci eH sah eveser hscet pina adn is co,lo cmlamy, dihroapit.ec eH has ednceiasr puraylmon ryerta eeurprss nda neirdsaec flet ralait s.rrupsee kTean taogeltehr, tihs is idgcnrieaco cok.sh

iCceianodgr cohks is a retha umpp brmlpeo -- eth LV 'tsni gowrn.ik

When teh ,LV n'ist norwi,kg ti uescas a bkca up ni het eircditno poseiopt to who oobld ryamolnl f.wlos e,hfrTeero lbood ilwl bkac up ni eht l.sngu

isTh saesuc danscreie iaacpllyr rsdatcthyio sperurse &g-t-; isht vedisr more flidu toin hte iistemirttnu ;--t&g itsh saescu nsdceaeir atsitlteniir yhdstoaritc serpreus t-;g-& erthe si nwo emro ludfi nath omarln ni eth enmistutirit g-t-;& tshi esfcaft the enroitp raoti itihnw the tttnsuiriem t-&g;- hits scasue eradeedsc lsritttainie ccnooti ssreurpe.

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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inatePt ni hoyvcoplmie kchso - teh suecl rae wol BP nad COLO .skin epoviyomlHc kcohs is uacsed yb ldufi lsos.

eTh intatpe has carsedeed apedlor cb/ of fliud so,ls e.i. eehtr is eadsdecer lodbo lvmeou euninrgrt ot ahtre -&-tg; shtu reeeaddcs par.olde

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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epelSn is ldge.eran amCoerp it to CT cnas gohswni lzinaros-dme lse:pen

rtswialgsmhosoo6tdtpc.bh4u1or3//pj1t.aqoa//yuric.8wgdll/o/tl:5wp





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 khint yeth rea tkgianl uoabt atasGmoiolbl iolrtmmuef eceuasb it sc"rsose oerv to het flet h"pheiremse tihs is eht noyl SCN outrm tath deso atth and it is adGer IV iennmga ghhi edgra. itlbmooasalG mtroufeilm is a ytep fo mrtoytaAsco shtta ywh sit PGFA g+ eap 015 FA 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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hte aordtaiin yeaphrt sducea ssboirif and eth rilsbfmyootbas "ctoc"tnra udgnri rbisf,ois usnagic eth coursel fo isarwya dna usth lctaeasties

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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nPeiatt ahs der alyc rsah- hsit itfs mroe ithw -6VHH ooelRas( s,vir)u not auorvrvs.iP

V6H-H sscaeu oarndmeofit fo syhte,lotasbr ineglad ot aamni.e

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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usMurrm nda n:evureasm 1st hugthot = hwo soed it caheng iwht odlrepa. llA umrsurm tepecx ,HMCO V,PM nda aliatr ymmxao vietsrey is ctyilred aortonpiolpr ot cehnga ni reloadp e.(.i neradecsi eao=dwpslreor ,murmru ..ce)t ceBaeus fo i,hst DDx anc eb weradron donw ot HCM,O V,PM nda taairl mmxaoy girth ayaw ueecbsa eht uurrmm deeowrsn hitw drcdeeaes adlrpeo i.e(. tgdnasni )pu nhew lal but xtcisneeop twih opvmie.r

Aiatlr myxoma = CCM praryim aiadcrc outrm due to firoeitrlnapo fo teveocnnci estsui eysh;nmcmee a alectuudpdne msas oeetcnncd iav slkta to timuar umtpse ttah is seudnpsde in the iatlra obdol velmuo nad somev tiwh eth olvume ovnmeet.m

inarsePotnet: trdai of )1 ialmrt vleva tbstucnoori i.(.e mia,slea mtossypm of crcaaid ule,afri soepcny, .),cte 2) ssotmpym of bmismoel .ie(. alcfia adn igrth rma pmhsieisrae in nip,t)eta nad 3) ootctilninsatu pmtmoyss .i(.e vree,f giwteh lsos, smypostm eisrlengmb icvenetcon tiuess d,seieas sceubae turmo lseresea .-6I)L rheOst cinuled lounoregci m,ypomsts ratluisme"od-p lveav "aeiesds actusorayutl dsfngiin .(e.i cidtaosli r,rum)mu dan larait emrtgenenal cwhi(h duclo rmecosps ynrngdueil ureurtssct dan sacue typosmms ol.as)

Not lyon edos dningsat reeacdse peld,rao ihchw nsmea AL lvoeum si wrole so msas is'tn sa e"suen"pdsd tub reom eboim,l tgidnsna sola eiacesrsn eth wdwdnora tiiagonravt fe,cro hwcih uwdol ubtcnoietr to het urmto vingmo adsrwot het abes of het irltaa hbera,cm noip"gpp"l on teh rtilam lavve eftasle,l adn yplotieatnl itdnngeex ouhghtr nda gcsuian a aoctfnlinu type of mirtal inesosts (.ie. oerinwsgn iliosatdc .umumrr) Thsi diove snialexp ti elayrl lw:el :om=yt1c6s14tugohlh.w/?6et&a;v=ms//pVsbcttLp.iuIwnwwaY

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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sumMrur and unavm:esre 1ts tthouhg = owh sdoe ti ancehg thiw .ldrpaeo lAl umrsmru xeepct OMC,H ,MVP nda tlarai momxay syrievte is ltidceyr nrrootplaopi ot ecangh ni earlpod i(..e nrdieseac eedro=poaslrw ,urrumm c.te). eseaBuc fo ist,h xDD anc be nrrweoda down to OHC,M VMP, dna laairt maxyom tgrhi waya bauscee the mrruum wsdeorne wiht dceeaedrs daelpro (.i.e nsgtidan u)p nhwe lal tbu intcoxpees htwi e.ipvomr

Aliart ymxaom = CMC rmapiry cdracia tourm edu ot operlariotfni fo teecvoncin stuesi mcsmhey;een a eudacldputen mass dcceteonn via tlksa ot tarium pmuste taht si despundes ni hte traali olbod muvoel nda sveom hitw eth muvloe o.neevmtm

arietnsPetn:o ritda of 1) rialmt vlaev untscroiotb i..e( ei,slama soptmmsy of dcrcaai ae,fluir c,nspoye .,t)ec 2) motpysms of mlbomsie i.(e. alfcia dna itghr amr hmaisseiepr in n)itte,ap dna )3 tocltnntouiais symtsmop i..e( re,evf hewtgi los,s motssypm irblgnemes icecntonve itsuse s,eadsei scabuee otmur sreslaee I6L.-) treshO ueldnci engriocluo stmops,my mtrd"sulaio-ep velva esdesia" tslcurytaoua sndingfi .e(i. dctilisoa )r,umrum dna liraat lenmtneegra (hwhci doclu rsscopem eigrdylnnu csrtuusrte adn euasc pomtysms ).lsoa

oNt olny edos nngtdais daeecres doepa,rl hcwih seman LA oemulv is lewro os sasm 'ntsi sa p"nedd"essu tub ermo mlb,ioe stnadign saol rssiacnee eht dndoawrw riatnaiovtg ro,fec hhwic dwolu beuitrntoc to het urotm omnigv awsodrt the abse fo het aiatrl ,rbhceam oig""npppl on eht tarmli avelv ,tleelafs nad oiplaentytl negdxneit horutgh dna sanucgi a otfilnunca type fo itmarl ssoinste i..e( gnoswenir ascilodti )rmrmuu. iTsh ioevd spxealni ti rallye lel:w gms/pw:;no1t1ae6wt.c/stu.t4y&6=upYli=tLoc/wwvbs?mVahhI

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 evyr limrais qseuntio I heva snee in skabQn wlil ksa why a iptneat htwi hitrg etarh raulefi edos nto oevlepd eamed nda the wnrsae si sreaiednc acmltphyi renaigda. I tog this uqitsneo gorwn iiglrlnyoa baceues I wndsaree nolag this inle fo ainengros utb I thnki in hsti saec ti lal sah ot do ithw WRHEE eth texar srreupse si ngoicm morf. In sthi noequits hte pt sha asolcitdi hyeepnrnoist os you acn khnti baout het reeuspsr sa oingcm rroadw""f so nigrsctciont yprerllcapia crinshtpes anc vpnrete na eirnasec ni reusserp ni eth lilaarcpy deb. rweoeHv fro irgth rtahe rauelif isth etarx uldif is igcomn fmor hte POOIEPST todeiicnr cabwrdask( romf eht tihrg )threa nda tricigsconnt ycaapprelril snirhsetcp nca od ontginh no( piptoeos deis of pliaalrcy de)b - the onyl ywa ot vntpeer eaedm si ot cnsierea lyhatmpic adner.gia

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 yerv irmilsa stiuoqne I avhe nese ni aQksnb ilwl ska yhw a ptitane twih tihrg haret elifrua sdoe not pelevod eamde adn het wanrse si esncaierd mthlypcai eani.drga I gto thsi eqontius rnowg logyriianl ceausbe I eeasdwnr olnga shit nlie fo neoianrsg but I ikthn in sthi scea ti lal sha ot od whti EEWRH het retax erspesur si ongimc r.mof In isth tsoniueq hte pt ash ldtiascoi npisteryohne so uoy nca hntki tobua hte epsuserr as cmngio ora"drf"w os stcrgiinocnt leppriaacyrl tspihecnsr can eevnptr na srcenaei in sperseur ni eht rpiyallac d.be ewervHo rfo igrth rteha ulfraei iths etrax ldufi si ngoimc mfro eth PTEOPOIS icerondti sb(kcdawar ofmr eth tgihr hte)ar and ortgsncincit yrliraepaclp srshicpetn can do gtnonhi no( oetpsopi sedi of yplaiarlc d)eb - eth yoln ywa to vertpen edeam si to esarcien chpatmyli rdiaegn.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(1404),
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aWth a eteilrbr cprteu.i yeTh hety vceedro up ptar fo ti htiw esin.l FTW

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(1404),
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einrnipheEp si teh ylno G lduocep tcpeorre rtvaotcai eht li.ts Teh tres aer eiehtr llreui-lnaretc or a tersoniy kaisen ins(ilu)n.

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


submitted by zpatel(23),
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lla the rothse a nnoeomivtcitep csein etyh aveh cefsfipi(icycctespii )gns,laid MDAN si eht nyol hnneecoetlcev(eisn teeiivopcmt e,orpc)etr sah a agndil ties adn ca , an dna nceh.e.g.m tcvteoimpie

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


submitted by hello(301),
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Pseeal pehl

-yoiscMsdtil ceenjtio click = mnilcpou stseonsi

How is nolicmpu stsioesn ldetaer to eht pn'steiat SAD -- esdo ASD eacus plomunic io?st?essn

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(142),
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hTe klhlmara fo PIT is eiltsado iro.mnheoopayttcb

/..oktseecc-appmhe8ms/eactie/i2re2mdnrdwpoi5c0/1u:tl

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


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ec.D lNCa - legaern eoluvm cslD. eos +K - icDtreui sm(to ,studiirec ptecxe K+ rsipgan ,noes uesac ho+nyI)Kcp. mpO;-3C&aH Hp - Vuemol sols t&g-; ASAR tg&;- ralsdneoeto ucasse K+ &;pam +H agiwsnt tg&;- omibceatl lioasa;lsk eSh mya eb gtvnmioi sa w,lel ichhw is enohart lsoiebps caeus fo met. k cnIa.l Pa2OC - eirasrpyort ocpoenisnmta for .emt lk.a

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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e.cD NaCl - lganeer mvoeul Doscl e.s +K - eDitciru omt(s scued,riti txecep K+ arpsing n,eos ucaes )h nKoI+pyc. C-Hp&3amO; pH - melouV sslo t-;g& ARAS g;t-& nelraoetsod eascsu +K ;m&ap +H sngtawi g;-t& mebitaclo slo;ailska hSe yam be tonmvgii as lw,le wchih si ateronh sblosiep acseu fo tm.e cnIa lk. CPaO2 - atyrrisoepr ooepscmnnait rof e.mt lak.

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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.Dce lCNa - renegal eumvlo slD.s eoc +K - cirituDe tsmo( ucisted,ir cetxpe K+ rsaipgn o,sne asuec +ny)I.opKch ap3;OmHC&- pH - Vomuel sols >- SAAR ;&-tg nlrsotodeea asuces K+ ;am&p H+ ngsiwta g;t&- elcotbima lalko;ssia heS amy eb tgimoniv as ,ellw wcihh is tnehora lossiebp seuac fo emt. Ilcakn. C2PaO - eirrtsroypa tpnsecamnoio orf m.te .akl

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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hiTs emro ykllie ot be iiusdetcr artrhe hatn atsaixlev c/b

het alb tsyud sshwo a leanr uityndonscf NU(B p&am; eateinrnCi ear eadevetl)

Mtso llykie het ttipena dseabu oolp ted;usicri olsa ksnwo ot seuac rtincnotcoa as,ildokal oangl hitw lanre erbslpom cuhs sa itrnlsaetiti ihnepsrit

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 tog ahtt ti enedde to eb a ptaoussim snirpag itecidu.r Is heetr a nsorea it ntoacn eb na eletnordaso n?tatgnsoia I cohse lsobck lbsaoaaelrt K+ ahelnsnc sa htees eedecrsa het aoabslertal a+Na+Ks/e/TPA sbeecua the nodriwg of the orercct sanrew ddi tno akme neess ot me -- niamugss ehty erwe gogin for na NCaE erclkbo (adn hatt eeradesdc uilnaml ryemlpiiebta icidnseat htat a+N wdlou be naiminrge ni the enl,mu tno giranmnei ni eth ircnilapp lecl as I iilrlangoy ut)thgoh.

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 ouy eden a irfeetfdn ritanoneoti for a aagirdm fo het h:awpsayt

3.iM0c-a_yagsi4.f83e3egi/stj6TA0/?a2mlgFdre1c/rmrn8rseO3%gu1Lngndeuhso4/M40pp4bwa1pm6ct-3tere2npe-ir//t21_b:_=si11/8iatl0a21ti.pFssa1_0-/1%.Ht3

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


submitted by drdoom(806),
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eicN tiamshecc fo hwo hzrnltoaoi zgea is adindrtceoo ouhgrht teh seMoublancF/uLdtmoo/roc p:aytwha

ptp.cot7/j1/oeu5ogl:goeon//rnr1uenngl/y7.g.erFgy/herl7n/tto/.0as

nI the ,aradmgi het mtesys si ginontcridao agze awtrdo ’pst eflt, hhiwc (nnn)iecvoelty si het esma sa ni eht etm.s

Sceoru eilac:rt noun5:/onr.l7c1t/tptg7y/ose/hne7/eg.or/t0

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


submitted by drdoom(806),
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Neci mcsahetic of hwo ooatzlrnih zage si oedidnoatcr tohhrug hte /rLsao/moMdteFobulcuocn :aphywat

n0/rpes/hoorF7o/rjrpe.le:7uglgg/ttc71t5/lgneytogeun/a/n1n./.o.yo

nI eth ,mrgaida het tmeyss is actriongdino egza doratw ’spt lte,f cihwh vt)y(icenonnle is eht aems as in the e.tms

reucSo ercitl:a tr7o:/lnrnst.noenou/7/otgc//gpee0.15yh7/t

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


submitted by hello(301),
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Pnietta has a athhroxeim + XCR owshs aehatcr sdeitave wdstora eht miaothxehr ;-t-&g stom yelkil ssaiongid is poauoenstsn htnpomeourxa.

llipodceEiymloaig, enoatnsuops huotroamnpex si stmo aisctasode htwi itnh slema

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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niPteta ash a thxhmoeair + XRC sshow aactrhe veeiatds dtwsoar het xhemhaitor ;--g&t omst illyek iogsisdan si sneuasonpot pmuanoxethor.

elmdioogiyilEplca, nusenoopsta aenoxhurtopm is tsmo scodsteiaa hiwt tnih esmla

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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aelsep hlep -- If easstetocaiivpla- etibarac lniautezer itrhe own xuosep,dier hwy ti'sn ti het asce for iesvaeact-pastloi riabetac to nnstiefico in ven?yeroe

m'I ton rsanddguninte the onneionctc to DAPHN diosxae cfdei.nyeci

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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eozhhdioodtyaocihrlr si OCD orf incrgepoheN btieDesa isduspnii asueecb it llpdyraoacixa susaec na necirase ni PB by ncaigsreni iomsdu inoptbarso dna thus wtare tanobp,rios atamhPo xisaelnp this ecln.yi

ssenosDiprme is otrceincr secbaeu unpo iftsagn uf(dil )crnsieoirtt DHA is rciesnaed ainnemg DHA si ibneg ersaeedl rlyClntae btu is otn worgkni in hte kiydsen ta eht 2V osetrrcpe of the tlehplaiei anrle lelsc ta ntlcCleiog t.ucd

nO atht oten, erdAoimil si dues orf mtuiLih idcuend norhnpigeec .DI

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


submitted by burak(52),
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'sntI ti penndteed no the io?oanlct I wdrseean ti rryoaonc ssniu acsebue va enod is caelotd ni hKoc egtali;rn hwhic odopcems fo uCSisn, Tndeon fo doaoT,r cduriispT lsuanu?n

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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wolF etaR = iotcyVel x -oClnicessaStor rAea

2 ^c2m x 20 s/ccme x 06 esm/icn x 1 L,/1000 ^3cm = 24. mni/L

01,00 ^3cm = 1 L

seagull  Well, I missed this one. I don't even feel bad. +54  
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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a86:lb2/ciss/e/9hmvwt//Ptnrp.C.cM/0.igtpoh5cnw.0mwnil

eOrsl giSn si a vywsisttli-o,nie clitp-ewyofcis ginnfdi of beoMgkrenc soroloierltiAscres AM)( iczcetdeararh yb "a pblalaep tgulhhoa es,seulpls ldiaar eyrtra lhewi teh PB cfuf is daelifnt aoevb syiclost eu"ssper.r

tI is pobssile htta ea :irhe)t hTe iecsflpcwiyti-o fo tihs estt asmne it si oasl lalpicaebp ot isharetsoolcers no(t utsj )A) bM The EMBN celiynrtcro milipse ahtt MA is traicnnehaeblg iwht rrecoh.itssealso

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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orF eoppel ngaski why het tada tbale was nvee cednldui fi it was tno eededn to aewnsr isth Q, rhee is a usleuf xiaoelp:tnna

The ablet swa egvin auecebs a 22x bleat si tlyypacli hatw uoy do ees driagngre aadt for tcnoearcls-o .edustis

fI teh 22x tbela was'nt l,ndcedui ethn lityralle yeevteron wdluo cpik cioeCh E"" sa het rcrtceo asnerw b/c uoy c'ant lacteaclu onmtgiseh htuwoti ibnge dvdiorpe .mesnrub

hTe ecrfideefn ni digucnnli eth -ttaaldbae si ht:ta

  1. Agia,n yuo ened to trrope a x22 bealt esecuba tath si tipylcayl twha uoy llwi see geadrignr atad for a ocso-ctaenrl tdsuy

adn

  1. yb uinlcignd teh 2x2 be,tal ti clayltua esstt if het tke-etsrta eairlzed taht hte aatd ni eth x22 blaet seod ton hepl ta lal twih tcnllagauic lvape--cerne eucaseb octoarlnces- ssidute VENER prreot on .alcenrvpee
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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Why nt’swa eth abelt hgeoun to eniertmed erpeavnlce in teh elngare aputnipo?ol

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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Tish oen saw a leiltt kcti.ry rFo ihts one hte yek is eht wlo rioidinadeo utpaek. Tish aepnitt hsa ighh T4 and wol SHT chwhi kmsae essne in a rtedyhpyroih npte,tai rhspepa uyro ifstr utohhgt si htat sith piettan has sv’areG sed.aies v,Heowre ni ears’Gv ryou ohytird is beign tdmsilaute ot emak emro odhyrit merhoon orfm thacrsc adn sa scuh duwlo aevh an nrdaiecse oididroaein taeukp ubecesa teh odhrtyi si irgngnbi in eht rerideuq n(wo rleaob)ailedd idio.en ihsT is hwy ti si tno Gresva leree(s“a fo rydthoi oehronm orfm a rdyhiot sttliaeudm yb ”itid)oa.ebsn

So if ist nto arseGv’ hatw locdu ti be? rFo hsti ’ouyd ahve to know htat o’siHostmha rsdTihyioti (oasl wonnk sa inchrCo mcotcypLiyh Tyihitosrid dna si ntefo rrdeefre ot sa cush no adrob xmesa to rtohw ouy off) ash terhe easshp - sitfr ehyt ear ,ohihreyyrdtp hten hu,rideyto ethn hte ccssali dryphioyhot ahtt uyo dowul xpctee wiht lwo T4 dan ighh .SHT hTis was the yek ot ihst ieou.nqts ehT aerosn rfo hits is ahtt onitraiydht adioserpex oibestdnai in aht’isHmoos sueca eth doyithr ot eerlsea all of ist serdot yoidhtr mhnreoo ankigm teh atinept oyptiedhrrhy for a shtor perdoi of m.eit teAfr sith saveims resaele of ydhtori nom,rohe the odsieiabtn kema them lnubae to kaem enw TH nda fterheroe yhet moebce oruiethdy for a ortsh odiepr adn enht troohiydhyp ihwhc yuo louwd epcx!te icenS tyeh cat’n emak wne H,T teh yohirdt wlil not aket up het addoineroii adn oeetrhrfe rhtee wlil be owl dniodaroeii .pekuat ecn,eH leeae“rs of dresto hotidyr ermhoon fmor a ytordhi agndl iflatrdtnei by ymyoct”lhse.p aka cyi“ocLthmyp hmha)o(oitss doiti”yhi.srt

I nikth esle“rae of hdotriy hoornme ormf a ayslhtoopmmu yoithdr dlng”a si gfrreeinr ot soem dkni of hoydirt carnec ni ichwh seac uoy udlwo eecpxt hmte to be segindicrb a oludne no roiednoiadi ak.pute

Su​amrmy oediv eher adn laos a eartg eits in g:lreaen got//.tsrmorpeqdha/reny:uiirih/nntioslddedeopncee/c/a

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 emnosoe nlpeixa how to relu tuo het eorth raswen iheoccrs?

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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aCn moneose espela inxpale yhw ti owldu not be ygnolegc e?iotepnld I uhogtht hte nsitqoue asw lnaktig btaou eth uWbrrag no...nhnemepo os ywh nto norebkdaw of cgngloye to og?clues

I essgu ti wldou nto xlnaipe het made?e

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 ihknt tish reiputc lnxseiap it :lwel

td/dwmcip/e/iptoaekwige.ihrcsnaflfnn:jwrt/unieaat.gcao.pg.vc/se

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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leMaindan :eGcesnit

anM hsa 3/2 hecnca of engib a era.irrc He( osed ont haev hte eia)sesd. W mona riarrce rkis sutm be dlatauccel thiw 2^p + qp2 + 2^q. 2^q = 01/,4000 q = 00/2,1 p si ghruloy = p 21q = 0011/ = eCarirr urefnyqec .

Rksi fo ghniav a hildc shtu esualq /23 x /0110 x /14 = 001/6Bas2 e: u3e/c = naM Cearrri rski /100 1 = Feamel Ciaerrr 4ks 1Ri/ = nechCa teyh ecah pass on eht eeesscivr ngee to rthei .fsfgpniro

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


submitted by burak(52),
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Ins't ti npdetened no het atooi?nlc I rsneewda ti oocryarn uinss eeuabcs va deon si tclaeod ni ohcK ltanrgie; whcih cmdoopes of CSn,usi nnTedo of oor,daT cidTrpius una?nlsu

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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elPase elhp

-iilscoMytsd ijetcone kclic = mocpunil osiesstn

owH is lciuomnp istsenos teadler ot hte sp'nettia DAS -- odse ASD casue mplionuc e?sts?snio

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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aFst ear igcketoen p(xtece dod ainch ,)AF os hety cdopure eketons rfo greney codotpinru eto-CcAly()A threra tahn eg.cusol fI the tuenisqo ekads awth teh aryrpim creuso of gynree dirocotpnu ,aws ti wuldo tlils be ogcgenyl a(nd nto toesn,ek) aeceubs ihts is twhiin 42 u.shor eHrowve artfe 42 shoru teh nesawr coldu eb noekte sbdoie. ,gsdaRrlese the eqtisoun pilleafscicy dasi eht tp dah a usemr uogcles fo 01,0 cagiiidtnn htta ew rea kloonig for hmtnegsoi that osirpvde a utssebtra fro e.snluecnosogegi

uDrign oieprds fo istaaovtn,r uasebtsrts for scoligneeeunogs mceo from two sre:oscu (1) ebkwdonra of sxigenit sucem,l ro )2( vai cnoi-hdda FA ghuhtor AClio-po.ynopr Vilna*(e lsao sedfe into iropnlopy ACo, tbu is otn nvdolevi nigrdu itvrsnoaat -;t&-g ees olwbe)

)1( eTh vntpulaaerenai-y ccyle sieopdvr isth lginuea(mt ni lsuecm + tauvrpey &;-tg- inalaen &t--g; gose ot leirv ;g&--t atonrnmiiatasn to eahoot-erlaagtuptlk t-&-;g uyvpreat si eadaerpts orfm nltuaimge t&g;-- iantmulge gose to uera ,ecylc aretvpuy oegs on to e.selncug)soignoe eaacLtt nac lsao eb esud sth(i lduco evha eebn a gtirh areswn if it rewe ed.sil)t

()2 Odd hcian sAF aer sola nlicg,ecgou tub siaertc dcai iedd(povr ni teh narwes hoceic) i’snt dod hn,cia os ti is olyn eotngkice and anc be udelr u.to

tguohhlA alivne adn( ehotr edrcbhna .a).a fede itno ,Pnopo-olCyirA ethy era nto sdue ni vtnataisro sbaceue vtartianso ycsittrl leeris on ptaeihc ocssglign.neouee eTseh a..a rea ont imabedtlzoe in hte rilve eascube hte lvier kslca arcdnacbhnih-e .aa. teaeanfssrr .zmnyee In irtFs i,Ad ohcieBm nceis,ot neudr ttt,noaiigaFrnSv/sa ni hbot teh tgsi“naf tat”es hwi(ch is iithwn teh mtei eamrf fo hsti ,ensqtio)u ro eht tst“oarnavi astet,” tohb iteizul eiatphc oeicnnusegesglo. yM omsnspuiat si atth vleani is seud iugrdn ruergal bemmotalsi, dna nto uringd isrpedo fo iat.trnsoav

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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nAy idae why criemalhohprye 'sint na n?reasw eTh hrardaie uldow cueas na oarlmn niona pga c(l)heycpriorhem ioecbtmal .sidaoisc

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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Any iead yhw yoihelmcahrpre is'tn an ?nrewsa heT eaihrard would caseu na nolrma noian agp irreohmhcyp)e(lc eitbaomcl s.dociisa

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 elgoog mtpsysom of yorhcmahloeip dan ympoanitareh era yvre lamiir;s v,reehow ranipyomhate ciudlnes srezieus nad mas.sps tuB rep my qcuik ggeolo eahcsr elmorahpihyoc sedo ot.n locmhierapoHy aosl can rpseent ihwt ertiraysrop fclut,ifeidis btu I 'dtind see ttha wiht p.yhnaaeimrot

hello  That answer choice is hypERchrloremia, not hypochloremia. +  


submitted by hayayah(1056),
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Cttehare pcenmal:et

sn1mep6ohtd2np/-/j8/0pomtlogsg00yasc0..te:ct4ke/ia0ae/n/pu8e/w

cllaeR htat het gunl epxa dsetxen evboa the isftr br.i

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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Yo adwg we all utoab VTP TIM LaLH

aneyPhnealil,n eVain,l opKDNTryt,A noreT,hnei ,siueoecInl in,hMteoein dstHei,nii uceeinL isenyL

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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tWn'doul uceat clhloao ipmsconount evne ni odamreet ontmua seauc srlierebev hapiect rlualcel ijuynr heaedcaticzrr yb arulllce niolgoa?lbn tI oshdul be het rghit neasrw nlseus hte eiuntsqo mtes esnma "es"edknWe

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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easlpe phel aigordccn to swrtnei enquoita teh ntpaiet sha a nmorla nioan gap

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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iogtHsloy ewdsoh lcietagoauv reinsocs eedp(vesrr tcetrruechia fo ialoryadcm frbesi) whit putlronieh tonintfiialr hwich hndite htta eht IM aws tnwhii 42 r.usoh oMts eklliy seuac of aetdh ntwiih fstir 24 hsrou fo IM is a.tayhmihrr rcMaidyalo pruutre ulowd aols be evilibs no sgrso raecppanae fo eth retah, chiwh teyh esddcbrei ni teh m.est

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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h'tWsa teh cridfnfeee eeebwnt cetariev rsytugniacsool sv scpsymtohiy?lo

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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smoe owrng snwa:ers

*eskma sesen cb/ tlymsselboa era roeprrsucs to eynoac,trusgl cwihh seu POM ot ifgth ffo sintocnfei

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(142),
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nI rdossi,soica alchircypemae oralynlm espsusepsr eht eslerae fo TPH nad eerfohter eth tuicnoorpd of cllriiaoct 5e(cer)1lf2-ialxolyohodc,hic,yrd ubt ni caiosidsros dan eohrt otogsauaurnlm eadisses, avtdetcai lnauoorcemn eclsl arayulclitp(r msehapocga)r in teh ugnl dna lhpmy endos urcoedp tillicoarc )cdldaifri5rc(ohlhoyc2e,yxo-l1e mofr liicolcda c(lroela5hyeo-c2royiclxfh)d neeenitndpd of .HPT

orits/ppeu/anweheau/hgn-tnos/dpwtcnwm-ee:c.ruacmsllytmaie.-dtscastoooiast

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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/oyyimtpireHhrphsydo si adeigodns iwht STH /w xeferl ot T4 sith( sujt letsl eht abl fi SHT si mnarol o’ntd cechk 4T utb if HST si banolar,m hkcce T4 too.) TSH astnw’ na tpnioo so T4 is eth bset wnars.e

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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heT teSm is dirbgceisn otm,iohcomsashre erahercicdzta by robmanal inro esginsn nad searcedin ilesitnant iptasnobro. Thsi eiasescrn In,or ngesaiincr .iinterrf nI seos,eprn ITCB is ceda,esrde hchiw nesrcseai esfrrinantr ntuasiraot sa etreh is sles ltaigcircnu crrirea .elceomsul

tWhi sxecse ionr ni teh lbod,o ti liwl ccuataemul in tusssie cniindlgu eht lev,ir k,nis pca.ranse leSqeae u iuedlcn dlideta ,yhmordictaoayp ,ongsadyhomip asedt,bie tthayrorhap 2/2 ccaluim yhoatpsrheppo pdtoesin,io dn ulaclHetoaplre acoinamrC

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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yhw si ieihimlyrapedp asnyocerd ot nghsiuc ymrosned not a is?pibtliosy

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(1252),
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As staedt eblow, hte etLf scru ecrerbi saw gaemadd ese( atwh it odlhus rnymallo kool leik e)l.wob shiT isntcaon eth pcsotlicriano tatrc. neciS teh itsprcnaciolo atcrt deussetca at eht lme,dula wloeb the nibrdmai iotcnse 'rwee olngkio at, you udwlo see oatlCaanrrlte Rt(ih)g tSaicsp piemissHaer

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 lettil tamh hr..pHe e si lwo ;--t&g daisosci 2pOC si hghi -&g-t; oyireptrsar Nromal mcpooanients slhudo be olhyrgu a 1 euc)at( ot chn4)rci(o eecnsari ni ciabbr rep eyver 01 eaeirsnc in .O.pC2 tsI worle her,e so yrallce ont pocedamsnte and iiatdcdne tlodnadiai podr ni dgi-c;-at&br dda no etabm idasicso

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(1404),
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iTsh is a eodlihokil riot.a +=RL /pfesi-ec1SnS

ynA lvaue egreatr htna 10 p(re itfsr di)a cdeitanid fesu"snsleu fo acgintiosd tet"s ihwhc is oaebmlaprc ot PPV u(glnir ni a ).dz tioPn "A" si eht scotles ramk to rwhee 01 sholud be no eth Y sxia.

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 tihs insgay eetrh si viruelsoertcae rfx?leu I olcud veha rmwos ihts esam iaegm wsa on mrfo 20 or 21 nad hte wnaesr asw lmiWs otrmu

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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hTe pridoetsinc fo leaatirbl lewor mlbi lsso fo ainvbtior pelsmii LDMC aagdm,e adn het benats RsTD + rbmegoR emes ot em ot eb gympliin htta eh sboslpiy hsa tbaes arsodsil mrof ssplyihi (or segmiohnt yver mslraii in senatri)np.eot

As ofr het threo swrn,aes A is ogwrn cubseae his tormo niunoftc is cntta,i B is norwg sebecau niap dan pemretretua tsifiecd aer ont in,medeotn C is wnrgo uesaecb it mielsip a iicfpsec never is tredpenp,a ubt he has lots laitrelab tsinnsaeo in his ieenrt eolrw iesmetixert

D is eht kritcetis, adn mI’ nto 001% rs,ue but I oulwd khtin udypatahicrlo fo eth narrtieo env)trla( otrso uwdlo sauec otmor diisecft csine yhte rryac omtor efrsenef.t uYo hmgti laso eectxp htat ortmo isunfodynct to be utairnall,e seinc ti ldwou eb enullkyi ot vhea a rpmloeb hitw teh renve tosor on hotb sds.ie osla eht DLCM si not aldceot anre teh anetrori ootsr of teh slianp oc,dr os if hte neraiort srtoo ewer efcedfta uoy lrleay ’dtnwolu xetecp ot ees rorbaivyt sol.s

oS iylsalcba soprcse fo amel,ionniti I od fele ilek yersson ernapythuo si an xleyrtmee geavu reanws hgthou dan I a’sntw a fan of the usetin.qo

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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laiespaoN si ewn siuest rtowhg htat si ,ugldenutaer rvsieib,reelr dan nm.oanlloco

lalCyiont acn be ieenmtdrde yb ae-os6plsotphhucg-e ahroenegesydd 6D)G(P ynzeem ofriossm. 6GDP is Xliknde-.

*For mero afnrnimoito hccek out .Ch 3 aoelpsaNi ni oamtaPh

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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Tshi etaptin ash sllma lelc cmcaarn.oi hsTi eytp fo cernca is secastiaod twih lraspoinceatpa ynmosders chsu a:s nshuCig y,enromdS HIDAS, or esoiinbatd isganat 2aC+ cheslnan t-btmaEroLena)( ro rneo.uns mAptiflanioci of mcy nenooecgs is olas mom.ocn

ADISH S(rnmyode fo apaptonirpeir entrdiuiaict oerhonm )tsenoicre si hicazrdaceert b:y

  • scxeivEes eerf rewta rotneietn
  • locuEeivm mhpteoaaynri with uiictynnnar oderu N+a trnoxiece
  • enrUi mylaitosol gt;& eurms sloyilaomt

Bdyo sonrdpse to trewa eirotentn wthi oesdaernolt and PNA dna NPB. Ttah is wtha seacus the eeacsnrid uyriarn N+a nroiecets wihcŽh aelsd to ootnaiilrzmna fo aurltrlcleexa iudlf vleomu Žand the meilucove atamphiyn.oer

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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Case fo oritereals.isocsorl

preHypalstic tisieassocrrloorel oivnselv nntigeichk fo ssleve lwla yb ylppaerasih fo mhsoot scmeul nsonnki-oi(' a)p'enaecrpa

  • neeqCeuocsn fo ntalaignm nrtenyshopei 0;t/&(81g120 /w eutca ga-onrned ea)mgad
  • sRslteu ni uedercd lsseve barlice thiw gneranod- iiecmahs
  • Mya dlea to nfidiobir eincsosr fo hte slvees lalw hwti rhm;erhgoea laylccsslia escsau acuet anerl arieufl )(AFR ithw a tcriitrceahacs litfa''e-tenb aacrpanepe
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(1252),
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sA dttaes b,lewo teh eLtf urcs erbcier swa adgmeda ees( hwta it uhdlos orlaymln olko keli o.el)bw siTh ascnoint het caiintcloorsp trtac. nceSi hte lnricsocoatip rtact sdastecue ta hte melld,au oelwb teh rdbanmii tisoecn 'erew gliknoo t,a uoy dwoul see terCataronlla )g(iRth itpSacs eeprssiHmia

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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Rcaalsnuerov easides si eht osmt ocmomn csuea fo °2 HTN in lst.uad Cna be dt/ caimshie mfro aenlr esisstno or uasciaovclmrr is.esaed Cna hare arnle utsirb tarlale to milbsicuu.

Mani uassec of nalre rteyar tnssosie:

  • cAerhltterscoio lrieopls—apuqxam r3d1/ nr leofa aye,rrt usluyal ni odler aeml,s som.sekr

  • laFiucuorrbms ipla—dsiaaydstsl 2r/3d aef olrn eayrrt ro eelgmastn ,hecarnsb yallsu uoyugn ro imdelgedad- sl.mefea

aLb aesulv desab o:ff

  1. Sseotisn ercessead ldboo flwo to ueuolrsm.lg
  2. uJtgoxaluemrrla rpusatapa (JA)G pdonsres by tneegcirs en,rni hwcih csoretvn naonnignsegiteo to isntgaennoi I.
  3. ngsAinoneit I si edtrvonec to inianosegnt II AI(IT) yb aegnstnnioi eorntigvcn zeemny AEC( n--i su)lgn
  4. TAII iesrsa obodl resrupes by )(1 gntianortcc eortarilra thomso musc,le gnsrianiec atlto arhileeprp centsseria and ()2 oritnompg dlenara eerseal of teeslroon,da hichw srneceisa isoenroptrba fo iuomds hwr(ee N+a gsoe HO2 will )ollfow in eht distla vteconloud ulbtue ip(edgnaxn pslaam .lu)mveo anC aeld to amelpihkayo nee(s ni hte slab ofr isth eoinutqs)
  5. edLsa to HTN hwit irsencaed maalps nnire adn ualrtlenai ahyrtpo de(u ot low bodol o)fwl of teh feafcdet i;ydekn treihen aftruee is enes in iypramr ripsneythnoe
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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ieWhl I nac teg on rabdo hwit jdmtnsueAt r,rsDdioe I ont'd ese owh isht srwane si ayn eebtrt ahtn acStmoi Sotmypm id.rsDore omrF F:A

aVtyrei fo lboyid osimatclnp ginaslt stmhno to eyasr datoicasse thiw ,csisevxee etissrntpe guthoths adn xnityae abtou s.pytomms Mya acrp-eaop twhi e.sisnll

SDS enbslgo in a ugrop fo dsdesrori eziceartrdcah by lcpahyis mmsoytps gncuias iafstcnnigi sidsrset nda .miapimrnet

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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inoeftiDin of esjamtdtun s:reodidr

lmnooaEti sympmtos g(,e iexatyn, r)sdsiepeno atth cruoc twniih 3 onmths of na enatifiebdil pcaoolihycss etrosssr g,e( ocivrd,e )ielsnsl gaistnl l;t& 6 stnhmo ecno het otrsesrs sha nede.d

If msypostm srtesip &tg; 6 smohnt eatrf esrosstr s,ned ti si .GDA

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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lnongrllZoeli-Eis r:domseny Grer-nicnitssaget rmuto ri(otasn)amg of cnaprase or n.mdeudou

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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uohhgtT shti dulow eb gsotnhime aenrggrdi ictabrar"i yr",esgur but oe,pn tujs "on hcarsty ofso,d esceabu yore'u adbcri".tp-eie

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 c:lecy esaeDecdr euilrlictn and immmpaoeayenrh can tfeetafinerdi it rfmo otcoir auricaid.

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(806),
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hTe ermo eaerngl cilnrippe: ieadohntel oialvteads ni eth ecesnrpe of ghih C2;O oyu tagto egt ird of tath cdai whose!om a’Cnt lte ti letca,aumcu sa loerw Hp htwini a om”“r-trioncnmevien stfcaef cyitscifue/furctnree of ne,mezys sitp,rnoe ct.e ehT mreo aiccid a cllao emvrnntioen, the meor you pxeetc nrebya suvtlreauca to iteadl as( a nmsae of airgeninsc lofw ,trae ethbrey nyfgerir ffo utceaamluc id)a.c

eTh aissogioethtensl nac oepxlti shti emcmhsa.ni By nleiihatpyngrtev i(ngwlbo ffo ,2O)C teh ibanr rualtscaevu ssseen a owl 2CO / rudnokh“-yy t,aes”t cwhhi ieqruesr on dnoa.lsvitiao nI horet r,sdwo het tcresuuvaal esod otn dene to tuenocin the ucgP-nnmoTsAi tieapccr fo hetngszisiyn Nriitc dxiOe NO.()

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