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Welcome to hayayah’s page.
Contributor score: 1056

Comments ...

 +0  (step2ck_form7#15)

The symptoms of Wiskott-Aldrich syndrome may be remembered with the mnemonic "WATER":

W: Wiskott

A: Aldrich

T: Thrombocytopenia

E: Eczema

R: Recurrent (pyogenic) infections

UptoDate says IgG and IgM are notably low to normal and IgA and IgE are supposed to be high. So not sure why the labs are the way they are in this question.

 +0  (step2ck_form7#43)

Initial management for a small (< 2 cm), spontaneous pneumothorax: observation and supplemental O2

Initial management for a large pneumothorax in a hemodynamically stable patient: Needle decompression

 +0  (step2ck_form7#40)

Acute rheumatic fever --> mitral regurge

Chronic rheumatic fever --> mitral stenosis

 +0  (step2ck_form7#34)

Molluscum contagiosum is a poxvirus that causes localized skin infections.

Diffuse molluscum contagiosum infection in adults suggests HIV infection/immuno-suppression.

 +4  (nbme18#14)
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oMst olepbrms ihwt llec vdoisini occru in sanpahae of siMsoie .I

realfakedreams  @hayayah - made an account just to say thank you. I appreciate that you exist. +14

 +6  (nbme23#39)
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miFlfbizroe is a efiratb, udes for reoilnwg TG see.vll

mousie  I also chose Gemfibrozil too because its the best TG lowering drug listed but I can see where there might be some red flags for this drug in the way they asked the question... 40 year old obese woman with some upper abdominal pain ..... HELLO GALL STONES which is a common adverse outcome of Fibrates. +10
uslme123  Well I didn't wanna give a fat, forty, female, that smokes a fibrate. So a statin, for me, was the best next option. +9
whoissaad  Used same reasoning to choose statins. Fibrates are the main drug of choice for hypertriglyceridemia but given her symptoms, statins made more sense. Why do they do this to us... +
roaaaj  what a tricky question! there are multiple factors should be taken in consideration.. she has triglyceridemia which put her in risk of pancreatitis, and most importantly atherosclerotic disease, and all of that would outweigh the risk of giving her gallstone. +
paulkarr  Yeah I had statins selected initially because "statins are always the answer" but when I saw them stating first line "recently diagnosed with hyper TG" I figured this follow-up was purely to address that. So Fibrate is the best move. +2

 +34  (nbme23#43)
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lomboCoa is na eye ybmatolnair tath ruoscc efrbeo .ihbrt 'reTyeh sgminis eecspi fo siutse ni srreutucts ahtt form eht eey.

  • loCmoosba aecintfgf het ,rsii hciwh rtuesl in a lehye""ko aacpraeepn of eht upil,p aglenyelr do ont ldae to ivoisn sosl.

  • oaCsbomol nviiovgnl het terina leurts ni siovin slos in ecispfic atspr of the liuavs difel.

  • eLagr lraiten losabomoc ro sohet tacienffg teh ctpoi enrev cna cuaes owl viins,o ihhwc names ovisin sslo htat nantco eb tlpelmoecy eecodrrtc wtih alsegss or aocttcn slsnee.

mousie  thanks for this explanation! +
macrohphage95  can any one explain to me why not lens ? +
krewfoo99  @macrophage95 Lens are an interal part of the refractive power of the eye. Without the lens the image would not be formed on the retina, thus leading to visual loss +4
qfever  Do anyone know why not choroid? +1
adong  @qfever, no choroid would also be more detrimental to vision since it supplies blood to the retina +2
irgunner  That random zanki card with colobomas associated with a failure of the choroid fissure to close messed me up +11
mnemonicsfordayz  Seems like the key to this question is in what is omitted from the question stem: there is no mention of vision loss. If we assume there is no vision loss, then we can eliminate things associated with visual acuity (weird to think of in 2 week old but whatever): C, D, E, F. Also, by @hayayah 's reasoning, we eliminate E & F. If you reconsider the "asymmetric left pupil" then the only likely answer between A & B is B, Iris because the iris' central opening forms the pupil. I mistakenly put A because I was thinking of the choroid fissure and I read the question incorrectly - but it's a poorly worded question IMO. +
mamed  Key here is that it doesn't affect vision- the only thing would be the iris. All others are used in vision. Don't have to know what a coloboma actually is. +2
azibird  The extra section of that Zanki card specifically says that a coloboma "can be seen in the iris, retina, choroid, or optic disc." Don't you dare talk trash about Zanki! +1

 +23  (nbme23#11)
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He sah eflac icecnneionnt os hsi eanrxetl etnirhspc si ama,ddge ihwch si aivrnetedn yb teh apedduln .n .)-24SS( The epcvil nlchapncis nsevre, whihc ateidme the inteeroc secpos,r rea loas 2SS4.-

thomasburton  Why could this not be dysuria? +2
lilyo  I think that you are thinking about urinary incontinence. If we damage the pudendal nerve S2-S4, you can exhibit urinary and fecal incontinence since this nerve innervates both the urethral and the external anal sphincters. However since the pelvic splanchnic nerves also have roots that originate in S2-S4 a patient with pudendal nerve damage will also have impotence since these control the erection reflex. He wouldn't have dysuria which is painful urination. Most likely caused by a urethral infection or a blockade of the urinary tract. He would have urinary incontinence. I hope this helps. +16
alexxxx30  dysuria is painful urination...if it said urinary incontinence then you'd be right. But decreased innervation wouldn't cause pain (that would mores be associated with UTI) +3
peqmd  Another approach is fecal incontinence => parasympathetic nerve dysfunction => no boner +
dul071  ahhhhh fucked up with terminology again thinking dysuria was urinary incontinence +

 +9  (nbme23#39)
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brocniaC aynsarhed rioibtinhs e(g, elazmoeia)cdat dan olop dursciiet e,g( osdumefi)re aer thtghou to trexe htier tceeff no PIC yb diuenrcg iaelsrocrbenp dflui )(SCF drpocotuni at het ricdoho pe.sxlu

leoogG says ecnsmamhi si onwnukn .LLO

usmleuser007  Just FYI: Mannitol can also be used to reduce ICP by drawing free water out of CNS Howeveer, it can cause hypernatremia, pulmonary edema, and expansion of ECV can exacerbate heart failure +3
jimdooder  I think a good way to remember this is that CA inhibitors have very similar effects in the eye (reducing production of aqueous humor) as they do in the ventricles (decrease production of CSF). Can't say I totally understand the mechanisms but thats the connection I made. +2

 +21  (nbme22#15)
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sTih is a npaeitt sace of rumsopaptt .triihyiotds aCn reisa up ot a eary fetra dvleyier nad sah mhylpccoyti reitt.alinf

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

 +10  (nbme22#16)
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ncarngyeP + Hx of toshbmorsi t-;g-& tnhki snlpdpiiphotihao nrsymoed

The TP nad PTT ear eooprlgdn d/t teerenenicrf rofm teh tasbenidio to pssiphi.loohpd bmrniohT tmie lna.orm

adH ot fnid rcheresa acrleist toaub it os atek it romf eher dan tndo' astwe ruyo .t.em.i

monoloco  yeah, i’ve never heard of antiphospholipids increasing PT time ... +20
goldenwakosu  Not sure if that little detail was to throw us off. I think the point of the question was to ID antiphospholipid syndrome based on the clinical criteria (spontaneous abortion + thrombosis) +4
johnthurtjr  I actually went down a rabbit hole with this one recently - essentially in vitro findings =/= in vivo findings, clot-wise with anti-phospholipid antibodies. +3
link981  No mention of lupus anticoagulant, anticardiolipin, or anti Beta 2 antibodies. FA mentios prolonged PTT but nothing on PT. What a piece of shit question. But thanks to the dudes above who explained it +8
yb_26  UWorld mentioned "prolong aPTT (and sometimes PT)" in APS +3
oslerweberrendu  @yb_26 Can u please tell the QID because the one I have seen it says, "Although patients often have prolonged ptt (because the antiphospholipid interferes with ptt test), pt is normal." QID: 1298 +
kevin  just to clarify, lupus anticoag is in antiphospholipid and presents with paradoxical increased ptt +/- pt despite increase risk thrombosis +1

 +8  (nbme22#22)
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rGhowt mrnehoo egainsler rmooenh tcas iva oculG-edp ecpro.tesr G lpeoduc sopcrteer eend TPG to eceobm tdataveci dna GTsePa to eeobmc tneac.itaidv

oN sa-TGeP -t-;g& ylnarcliohc vatcie otgrhw norhemo rgaeelsin ormehno erotepcr -;&-tg cosatnnt iaaotctvni fo lylnyead asclcye / McPA wptahya nad eslreae fo hgtrwo

mcl  This figure is useful +
mcl  [link]( +
meningitis  How did you knkow it was GHRH and not GH perse? +4
meningitis  nevermind; I just read down below. Thank you +9

 +7  (nbme22#46)
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X ni eht iameg is het slmla tetnnesi.i tIs iicarrcshatetc ehfayter aceaareppn aeftr a imbrua lmea si edu ot nartpenem lcirucra fsdol dna eTh ivill igve het slmal ieninetst a etrga soauclm scueafr

nwinkelmann  Yes. The appearance of the mucosal folds depends upon the diameter of the bowel, and when they fold they appear feathery. Mucosal folds are largest and most numerous in the jejunum and tend to disappear in the lower part of the ileum. +

 +16  (nbme21#11)
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LPHLE edmn:orys esvma seyeitld EHlo Lrive nmwsy eLoez le.slttePa

A soitmientafan fo rseeev ai.erplacpsem ldooB esmra hwsos shst.cciyesot Can adel ot CDI nda aiehtcp asphmuml eorsaaabutsc Ž trpueru Ž versee pnheyisnto.o

mambaforstep  FA 2019 pg 629 +2
qball  One thing I find odd with this question is HELLP is a manifestation of severe preeclampsia but she has had an otherwise unremarkable pregnancy. Shouldn't she have hypertension/edema in regards to her pregnancy beforehand? +
demihesmisome  Pre-eclampsia, if not severe, can be entirely asymptomatic. +1
misterdoctor69  Her blood pressure is 164/102, which qualifies her as having preeclampsia. +

 +15  (nbme21#22)
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n-ietietcyeCnesys enceoikhm erercotp 5 (R5CC) si a teponir nuodf on teh sacefru fo D4C clls.e

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

 -5  (nbme21#28)
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exdiM usvneo eyognx aarstuiotn S(Ov2) is usamdree ni hte ymolaprun ae.rytr SvO2 seplmas eht etur dmixe sueonv lbodo avelngi the higtr at.rhe eMrunmaeets of diexm seovun ongyxe unitrtoasa Sv)O(2 frmo het mauynlrpo ryaert has bnee atdcoadve sa na nitdierc nxied fo essitu oot.yixnenga

nI gedcoriinac ohskc uoy evah daecserde OC ;--&tg erceedasd O2 eyrdvile -;&t-g srdecdeea S2.vO

 +4  (nbme21#8)
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akorisceKrfoen-kWf srdomy.en nD'to vaeh ot be an oillcaohc to teg ,shti jtsu uslyalu si retdael ot hoaillmsoc / nhemiati ncece.ifdiy

d_holles  Yeah the negative EtOH screen threw me off +3
dr_jan_itor  Why cant it be early alzheimers and hippocampus? She could easily have been a former prominent physician and member of city council. Am i supposed to assume that simply because shes disheveled and poor hygeine that she must be an alcoholic homeless person? It also mentions no symptoms of nystagmus, ataxia, etc. +2
kimcharito  it said broad based gait and nystagmus +9
lilmonkey  She is/was an alcoholic and appears pretty much homeless, just not drunk at this moment. +
fatboyslim  @ dr janitor. The question says "physical exam shows a broad-based gait and nystagmus." +
suckitnbme  NBME questions also stereotype the shit out of their patients +5

 +19  (nbme21#27)
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The hortidy is ldsuippe whti aalrietr oldbo from the prusreio droyhit rrea,ty a hbnrca of the exalnert itaocdr yerrat, adn the ionefrir ridyoht ,arrety a arcnhb fo eht ioelcraytvcrh nu.rkt

 +7  (nbme21#40)
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tNo:e heT baunescd n. is alaulytc eht veren mots lkliey to eb gadeamd by an egndpniax nlainetr crodait eurnasmy ni teh rvcosenua nussi ubt yhte igev yuo cepifsic 3NC tfocinnu in tshi .tqinsoeu

hungrybox  One pupil larger than the other indicates damage to the pupillary light reflex - afferent: CN II, efferent: CN III. +19
cienfuegos  A little more info regarding other sxs (via UW): -cavernous carotid aneurysm: small usually asx, enlargement can cause u/l throbbing HA &/or CN deficits. VI most common thus ipsilateral lateral rectus weakness, can cause esotropia = inward eye deviation & horizontal diplopia worse when looking toward lesion -can also damage III, IV and V1/2 -can occasionally compress optic nerve or chiasm thus ipsilateral monoocular vision loss or non-specific visual acuity decrease +2
lovebug  There are in FA2019, page 530. +

 +40  (nbme21#33)
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eht miyrtjao of cnraob deixodi elcueolsm aer rdcerai sa tapr fo teh oebarcnaitb uffrbe nI hist s,metys rbacno xoiddei sefsdiuf ntio teh sRC.B oainCrcb aasrenhyd C(A) whitni RBCs lqciyuk eosvtrcn het bnoacr oiexidd noit raoibcnc iadc 3O)C.H2( Cirnboca adic is an bnelaust tdimteeainre emulcelo atht aidymilmtee osacessdiit tion ticebaorbna nsoi O)-3HC( nad eryohngd +)(H .niso

hTe nlwye ntdseihzyes cobebrinaat oin is enotradrtsp uot of the RCB tnoi the psaaml ni cxaeeghn fro a cioelrdh oni −(lC); hist si cdeall the hrelcido tsi.hf nWeh hte doblo hsraeec eth ulgsn, teh bceaaibtrno ion si antprtesdro abck itno the BRC in ghcaeenx orf eht odlerich noi. hTe +H ion iscditasose rmfo the lnobhogmie dna ibdsn to het ncbaorbaeit shiT srpdoeuc eht rcocanib idca ,eniimeattder iwhch is etrdcnvoe back oint ocarnb eoiddxi hguhrot het yacimnzet cnaoit of CA. hTe naocrb xdoedii roddcepu is lpxeedle ghothur eht lusgn nrigud loaixeh.tan

hungrybox  Amazing explanation. Thank you!! +1
namira  in case anyone wants to visualize things... +5
ergogenic22  CO2 is carried in the blood is bound to hemoglobin, known as carbaminohemoglobin (HbCO2) (5%), dissolved CO2 (5%), bicarb is 90% +3
pg32  Nice explanation, but can anyone clarify how we know from the question that we are measuring HCO3 rather than dissolved CO2? +3
qball  @pg32 This question is asking about what accounts for the LARGER amount of co2 and the HCO3 buffer is about 85% of this transport and dissolved C02 is about 5-7%. +3
teepot123  fa 19 pg 656 +1

 +2  (nbme21#46)
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tMos umnha cnresca ear /td a sosl fo tncofnui of 5P3T g.nee

 +7  (nbme21#1)
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neIsviav ivcrcale raaincomc si acsoisteda hwti roopihhesysdnr nda eranl aeiufrl /dt AC gnpsaedri hougrth euientr wlla dan iont het aldd.reb

 -1  (nbme21#28)
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hhgtoAul fhla teseh mosroehn can aayclutl aols be rdeseetc rmof eht nmeodu,du teh edunumod si asditosace teh toms wtih CCK eserael.

didelphus  Gastrin, intrinsic factor, and pepsin are secreted by the stomach. VIP is synthesized in neurons, so CCK (from I cells of duodenum) would be most directly affected by a duodenectomy. +22
teepot123  fa 19 pg 365 +

 +18  (nbme21#23)
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ypmLh wflo arte is auyulls lwo. tI is idcunlenfe irpliaymr by eth aret of pmlhy fot.nraimo roF xae,lpme if bdolo claarpyli usersepr is ieradncse yb rirteaal ilaiosnvotda ro vosneu tso,ctirocinn eht wolf erat of mlhyp ssin.ecera ,oslA the wflo trea is dacefeft yb nsspoermcio fo chtlpiamsy by nctatniroco of rnebigigohn satuuluecrm adn yb itngeave ttaaroniirhcc pssreuer n)bhge(.airt

rnetiIsttail rersespu so( rseesupr in eth FC,E cwihh olwud sieancer if viegn IV naiesl) dna phmly fowl aer oyivspietl erel.tad A lslam ersineca in sliittinreat movlue lgyeart rsaeescni ist ur,eerpss rngimoopt pyhml owfl that tsca to eoterrs the aineititlrst vumelo to loanrm.

mroe on tshi :poict vobkb:i5stKB.o3wt//ch4hnw/n.Np.m/w8s4/.niolg

linwanrun1357  Do not understand the breathing (choice C and D) breath in and out are different? +
khanhluong  I don't know if it's correct or not but how I approached C & D was that they both cause vasoconstriction in the arterioles (because this is the lung where hypoxia causes vasoconstriction), which decreases hydrostatic pressure through the capillaries and eventually decreases lymph flow. Maybe I completely got this question right for wrong reason, but I felt that it works with all of the answers. For F) I was thinking that it would cause increased capillary oncotic pressure which causes more fluid to go into the capillary than into the lymph vessels... Here's a picture: +5

 +4  (nbme21#24)
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tceeuaprHy snrntatpla ionjteecr ccrsou inwhti tesmiun /td t-nxgseiepri nrepietci esidboatni taht recta to roodn ganenti yetp( II iestihrysvpytnie eo,)cairtn ttaiaecv mlopeencmt.

mcl  [Useful figures illustrating transplant rejection]( +
drdoom  ^ via @mcl [Useful figures illustrating transplant rejection]( +1

 +0  (nbme21#14)
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irmsCteni cngtla(ione hsdto)iypyhmoir is eht tosm mcnmoo csuae of abetrteal entmla a.ibytdisli Cesaus poor rbnai plmdtneeeov.

 +19  (nbme21#50)
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hrtteaeC c:elpenatm


lRalec htat het ugln pexa etnsdex ebova the sritf bi.r

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

 +14  (nbme21#26)
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retctSh ro adniolit of teh vixrec and invgaa ear togsnr stmuili fro iytoonxc eoesrt,nci madditee by eanlur apwhsaty celdla teh rgnoseuF lxe.ref

At:ircle tistsf/cmtdcrouep:wcr/swcrceueentwsi.seeefccnl.hroxnip//geoe-no/i

readit  This is also why ob-gyn's will massage the uterus (which is part of the birth canal) after delivery. It's to get the body to release oxytocin and cause the uterus to contract (to prevent postpartum hemorrhage) +5
jennybones  Please why is estrogen not the answer, I thought estrogen would upregulate oxytocin receptors and increase oxytocin secretion? +1
drzed  During pregnancy, oxytocin RECEPTORS are upregulated (by estrogen) as parturition approaches, but the ferugson reflex creates a positive feedback loop where the dilation of the cervix further releases more oxytocin. The inciting event that starts this feedback loop is the dilation of the cervix leading to a direct release of oxytocin, not the presence of more oxytocin receptors. +3
bbr  To add, the positive feedback loop here is pretty elegant. Basically, it seems like the cervix doesnt want anything in it. When its stretched --> oxytocin --> contract uterus --> push baby --> more stretch at cervix---> more oxytocin (and forward). The positive feedback loop aspect is that oxytocin-based contractions cause more dilation of the cervix (as the baby moves into it!). +

 +3  (nbme21#16)
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Thsi pt hsa an DAS chhwi si a el""oh eebnwte eht LA dan A.R Fnixig ti duclo mdgeaa teh AV s.ubnlde

sahusema  the atrioventricular bundle is also called the bundle of his +3
bbr  What if it had said "AV node", that's in the interaatrial septum as well, right? I'm wondering, that could be answer as well. (FA 2019 pg291) +

 +13  (nbme21#8)
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alenR eayrrt estsinos si gnigo to eescader oldob olfw to hte dy.enki JG clles eessn teh rseeaced in prnoisfeu urpesers adn ecrtsee i.nner

einRn si dpodcuer yb eht GJ lsle,c JG celsl rea in teh etrxco et(yh rae fidomdei mhoots eulscm of het rtefenfa iarltro).ee

 +10  (nbme21#47)
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yndScerao yimtadaoishrhryprep slau(ylu dt/ hoccinr rneal af.r)iuel

abL nidgsfni udeicln ↑ PHT poenesr(s ot lwo ,i)ualcmc ↓ meurs cilamcu (leanr lr)f,uiea ↑ erusm ephsohtap nrea(l ruife,)la dna ↑ anilkela ptosahphsea HT(P atiagvctni Boasslsto)te.

haliburton  also remember that in renal failure, 1-alpha-hydroxylase activity is down, so there will be less activation of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is a key mechanism causing hypocalcemia. +2
cr  why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain +
nala_ula  Increased phosphate, since the kidneys aren't working well, leads to the release of fibroblast growth factor 23 from bone, which decreases calcitriol production and decreased calcium absorption. The increase in phosphate and the decrease in calcium lead to secondary hyperparathyroidism. +1
privatejoker  Probably a dumb question but how do we definitively know that the ALP is elevated if they give us no reference range in the lab values or Q stem? Everything stated above definitely makes sense from a physiological standpoint, I was just curious. +1
fatboyslim  @cr the question asked "the patient's BONE PAIN is most likely caused by which of the following?" Increased levels of 25-hydroxycholecalciferol might exist in that patient, but it wouldn't cause bone pain. PTH causes bone pain because of bone resorption +1
suckitnbme  @privatejoker ALP is included in the standard lab values +
makinallkindzofgainz  @privatejoker ALP is listed under "Phosphatase (alkaline), serum" in the lab values +1
pg32  Why does AlkPhos increase in renal osteodystrophy? The PTH would be trying to stimulate bone resorption (increase osteoCLAST activity), not bone formation (osteoBLAST activity). +
drzed  @pg32 the only way to stimulate an osteoclast in this case (e.g. via PTH) is by stimulating osteoblasts first (thru RANKL/RANK interaction), thus ALP increases. +1

 +3  (nbme21#44)
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leowr ianq:uapantaord aparelit sielon

sv upepr rnqouatadaaipn = rolatepm esnloi

mcl  also, to differentiate whether it is the left or right parietal lobe, recall that stimuli from the left visual field hits the nasal side of the left retina and the temporal side of the right retina, then goes to the right side of the brain. [This figure]( is helpful. +6
d_holles  So you're saying that there's two crosses, making it ipsilateral? @mci +

 +16  (nbme21#29)
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P. 91 fo FA sha a qkcui lptnnxaoaie rof !siht

sliayBlac eocn ry'oeu in a rvstanig atste sethre' isllt cheitpa nuloegcneisoseg gniog on a(s lelw sa nuigs FF)A but eth negiuslsngeceoo is onicgm fmor rieelrapph etsius aceltat nad an.nelai

 +8  (nbme21#19)
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hiTs tp ahs claaaeooimts / cesritk n(sice eh's a koid).d dsauCe by eietecvfd toniiealzaimrn fo sidoeot ceaotali)ms(oa ro ctsrluinagoia rtowgh slatpe i,csrekt( ynol ni cndi.)rhel

tMso ylommnco /dt naiitVm D iieencdfyc.

Crnelidh tiwh crsiekt ehav igopthloca bow lseg ug(ne rmauv,) ke-ilabde toococdhrlsna jutinnsco tc(hicrai aors),yr sroaanbceti os(tf

  • tmniiaV D m(nalro ntuonfic is to robrebsa C2+a nda )4PO

  • cD.e usemr Ca+2

  • ec.D  rmues OP4

  • HTP

lovebug  FA2019 455pg !!! +

 +10  (nbme21#31)
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thWi htis ,suinetoq I tikhn hety tnwa uyo to ozeengirc hatt the ptnitea snit' vigahn chset aipn lareted to hte t.erah yehT sehempiaz eerlvas bir reuarcfst nda a emaprhtooxnu tub nod't ntiedaic any traeh megdaa lkc(a fo teuditasinov usodsn = on lrumnoyap edmea dcdiitnea ro a gunl esuis dtlerae to eatrh pem)lrob.

hTe isptdrcaerii is t'sahw ndaienervt yb eth cpirhne .n Segeni sa hwo hsi ehatr si nef,i eht cetrfaudr ibrs ear bblaroyp ahtw are csgiuna him pain vai eth oetsaicrnlt

didelphus  Visceral pain is typically poorly localized (heart attacks are usually described as "crushing pressure" that radiates to the shoulder or neck), so this patients "sharp" right-sided pain in the setting in multiple right-sided rib fractures is likely related to the ribs. The intercostals run with the ribs and provide sensation to the chest wall. +10

 +1  (nbme20#29)
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nA eresadv efetcf fo iynlcodeycx is itvph.eoositnstyi

rio19111  Why not Cipro? +1
raspushok  Which antibiotics increase photosensitivity? Several antibiotic classes commonly cause photosensitivity, including tetracyclines (doxycycline), quinolones (ciprofloxacin, norfloxacin), and sulphonamides (trimethoprim/sulfamethoxazole, sulfasalazine). The tetracycline minocycline is not generally associated with photosensitivity. WHY not damn cipro? +
medninja  I think it is because Cipro is not commonly used for acne treatment +3

 +3  (nbme20#48)
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tP. ash Fliialma dldpiay.esimis yTep ncymo—Hriyealih.mepcrIo

estefanyargueta  Lipoprotein lipase: degradation of TGs circulating in chylomicrons and VLDLs. +2
breis  FA 2019 pg 94 +4

 +1  (nbme20#15)
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livnetinytreopHa eucsas cededaesr 2COPa hchwi nlteusyubqes dlase to ltaaeirr noavtonsstorcici hsut ilnwegor clebarre bdool flow (BFC), rrbcleae odlob v,oluem nad .IPC

eH atwsn ot nicseera IPC lerarcb(e la)aniidsvoto chhwi he anc do by gdserancie hte rotprisryea trae yp)taihv(t.nolioen

 +9  (nbme20#21)
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Heeptynyriiissvt msmeunitx—eoniipd pyet IIVII/ vsthipytieyniser naoctire to mialorennvent ntan.ige Cuases dnpyes,a uhc,og chste ,tsehtgsni etnOf nese ni sremrfa adn hotse xpeeosd to .sibdr eblRierves ni lyare agstse fi slsuuitm si d.oaievd

s'tI a ptey fo sievctirrte lgun aei.essd

 +1  (nbme20#32)
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aoo:cngGaulm orTmu fo cacpireant α cllse Žngusaci an toveniucoodrrp fo logcagnu.

snetsPer iwht D:5s’

  • trtcsnrlm(atiecoDeiiy gimortrya e)ryathme
  • btieasDe )ea(peygriylmch
  • VTD
  • nnDlgceii etihwg
  • nerpsiDoes
killme  And the sixth D: Diarrhea +8
ergogenic22  a) CAT1 and CAT2 are important enzymes of fatty acid beta oxidation. Glucagon upregulates this process b) glycogen formation is inhibited by glucagon, so that glucose can be used by cells c) acetyl CoA carboxylase is used for fatty acid synthesis and thus decreased by increased glucagon d) glucagon increases ketogenesis +53
dermgirl  Basically, they want to know what is the function of glucagon. +1

 +3  (nbme20#18)
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-oeloEirllnilsZgn senordm:y girsenGtein-sacrt outrm togmi(a)anrs of rnascpae or demo.udun

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

 +1  (nbme20#10)
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Seh has a taiivnm C cdecfeini.y rvucyS ueafrest lwlosne sugm, esya u,igirsbn itphe,eeac llpcreoiufairl dna piusalbetorse marghr.seheo

 +6  (nbme20#31)
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ornI vodeeros si a cseua fo a ihgh noina pga tieolmbac osci.adsi

meningitis  I found this to add a little bit more explanation as to how it causes the acidosis if anyone needs it. 1. Mitochondrial toxicity - decreases aerobic respiration and shunts to lactic acid production 2. Cardio toxicity (Secondary to Mitochondrial toxicity) leads to cardiogenic shock (hypoperfusion), which causes lactic acidosis 3. Hepatotoxicity - Decreases lactate metabolism, causing lactic acidosis 4. When in trivalent form (Fe+3), it can react with 3 molecules of H2O --> FeOH3 + 3H+ This will then deplete Bicarb buffering system resulting in non-gap acidosis. Source: +17
sympathetikey  None of the other choices were even metabolic acidosis. They threw us a bone with this one. +21
imnotarobotbut  Don't changes in bicarb take a few days? How did his bicarb drop down to 8 in 12 hours? +2
charcot_bouchard  its met acidsis. not compensation +7
j44n  they did throw us a bone however I didnt catch it +1

 +11  (nbme20#7)
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shiT si a arirmpy cletnra vsrnuoe ysmtes omphmyal. stoM myocnlmo dtsescaaio whti VIAIHS/D; ghaepsetison lsoveivn EVB i.eninftoc

dndeeCoisr an ed-nfniSgADiI iblaaeVr seanroiepn:tt iofonscnu, oermym sol,s ziuresse. ssMa soi)snel( (mya be ngnagnncihei-r ni nmomcuordsmimoeip pitate)n no I,MR edsen ot eb gnedshitsduii from tmssxpiosoloa avi SCF lnsiasay or trhoe lab t.tess oxTo usullya ash peitllmu rgni nheciangn .iesnlso

peridot  For those who are curious, this is on p.422 of FA2019 +

 +15  (nbme20#17)
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sA,ol ouy snlotdu'h be nieegs nr-oadgen eaadgm or cieseadrn enrin / yendki seesonrp ithw a yposlueriv ehyatlh napeitt htat jtsu vdlodeepe ltesaensi THN. hTe body edtns'o wnta ot isarecne nnrei nwhe it ash HNT. ,owHeerv if ouy veah sestn,ios eht isnekyd karfe tuo bueesac rehy'et ont igtgnte hnuego ofwl dna khnti het eowhl ydob sn'it ither,e so yhet tvecaait eht SAAR ys.mtes ehnW oyu egvi temh na CI-A,E hte ninre is lstli nigeb oeudrpdc by eht ikedy,n it tusj 'snti engbi odevcrnte ot sIae.innngiIto-

To litineeam roteh ceoh:sic

  • He sah dnrsiceea ienrn tactiyiv os yuo can mieinelat mrypria eml.dtsonsoria haTt ahs cni. ldae,snroeto d.ce nrein.
  • No sgsni or xss fo ihCungss' so h'tast tdlin.emaei
  • -eshl1B-oxy1drya efeicidycn udowl sxs hitw teh gnlaaetii. Yduo' aevh .dec rinne ayvciitt reee(lkotidn-oasl ftecefs litls )s.enerpt
  • nseEatsil NTH: xnaepeldi oebva
sammyj98  I like you sticking up for the kidneys, thinking they're increasing Renin for the benefit of the whole body, but lets face it, the kidneys are a couple selfish dicks who want the high blood pressure all for themselves. LeftVentricularSolidarity +4

 +6  (nbme20#4)
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A dfrctaure iorcfmrbir tpeal atn(oeirr ksllu a)umatr nac erlsut in lgnkiea of iprcloneresba dfuli otni eht oens nad osls fo neses fo lm.sel lmlSe salyp a arelg orel ni the icotenrepp of ettsa. ,oS in cpc,reait a ttainep amy almopinc fo slos fo estta arhetr athn of mesll.

brownielove79  can it be a facial nerve??? with lateral head trauma (injury during passage through middle ear, or external auditory canal??) doubt!!! +1
doodimoodi  Olfaction is actually more important that tongue sensation in terms of food taste (think of how food tastes bland when you have a cold) +1
doodimoodi  than* +
champagnesupernova3  If taste is completely lost then it's an olfactory issue. If its lost only on a part of the tongue then the nerve that provides taste to that area is suspected. +9
veryhungrycaterpillar  UWorld QID 12227 The sense of taste isn't lost due to CSF in the nose, but due to avulsion of olfactory rootlets. +7

 +6  (nbme20#47)
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You evah a 2%5 ancech of ntneiirigh het eams HLA mkersar sa royu ngb.silis

masonkingcobra  Two siblings have a 25% chance of being genotypically HLA identical, a 50% chance of being HLA haploidentical (sharing one haplotype), and a 25% chance that they share no HLA haplotypes. +21
alimd  It looks exactly like an Autosomal recessive mode of inheritance. +1

 +3  (nbme20#36)
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gnBeni rutmso era lsyulua fd-ldfateiiwetenrel adn werlaldtae,d-ecm twhi low iotmitc yciaittv, no setmaea,tss nad no re.sncosi

alMnngita ousmrt acs(c)enr yam hwso poro erfnii,antifeodt ecairrt tgo,hwr local v,nionsia estatsmsi,a and ssoao.pitp hHig tcmioit yv.tiaict

tFa smo:utr

  • :Lapomi ,ningbe owl ititcom aivtityc
  • soLaioampr:c mat,gnilan dnicaeser tmictoi yitcaivt
whossayin  why can't it be a rhabdomyosarcoma? +
charcot_bouchard  Because of histology and gross appearance... very graphic description of fat cell tumor there +5
dr_cruceta  because the question said irregular vacuolated cells, describing fat cells. Rhabdomyosarcoma comes from skeletal muscle. +3

 +2  (nbme20#49)
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eaBt reoklcsb sa mhhicnrsyaritat pssrupse mroablan ckemerpaas by drgeeascni the sloep fo hepsa 4 ;t-g&- rnpglogoni pshea 4.

chandlerbas  piano player sliding the keys to the left ---> delays diastolic depolarization --> rate control +7

 +1  (nbme20#12)
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Pviecl nhiscnlapc ervens ear artp fo hte temaiyhsatpacpr

masonkingcobra  The inferior hypogastric plexus innervates internal pelvic viscera; has both sympathetic and parasympathetic components; parasympathetic contribution helps stimulate detrusor of bladder (along with pelvic splanchnic nerves), sympathetic contribution helps stimulate internal urethral sphincter +3

 +8  (nbme20#44)
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Down erndSyom sabL:

  • icn. lnuach cescrnualtny
  • cn.i ChG
  • in.c biniihn
  • rdecdease FPA
  • ecasddere PAAPP
celeste  I remember this as Down Syndrome has high HI (hCg and inhibit) +16
temmy  Thanks celeste. I'll remember Hi +1

 +0  (nbme20#44)
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 +6  (nbme20#19)
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It's talninsoirta cell oaicr,cnma whhci sikngmo si a nommco srki oaftcr fo;r ti nac linevvo hte ernal acilpecy.seslv/ The ohist emgai shwso hte arplplaiy taurne of teh oumrt e(whveor ti nca laso be atfl ro dounalr giroacndc ot htPm.)oaa

olAs owknn as ltaieorulh oan.raccmi sotM mmonco romtu fo rauiynr ttrac temsys n(ac cruco in rnlea cecy,asl laner pi,slev res,uret dan aer)b.dld nCa be estuggesd yb snpaelsi uaehmrait no( c).asts

usmlecrasher  i'm sorry guys it's bladder cancer blocking urine flow => reflux ureteral widening => reflux nephropathy. +6
hello_planet  FA 2019 pg 588 +2
kevin  Is the idea since that since the histology shows transitional cell cancer the most likely is smoking and that's the answer? The fact that this was unilateral really threw me off. Is it common to have unilateral carcinoma of the ureter (if that's what this case was, of the ureter) rather than bilateral? +
lovebug  I Choose F) vinyl chloride <- only liver angiosarcoma. :( about many Carcinogen FA2019, 226pg. +

 +11  (nbme20#13)
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isgDnoais of yS:hp diVzeaulsi by emucerefsimnulcoon or r-edladifk ocpiocr;mys lygoreso is piotarmnt – two pytse of eaditos:inb

  • bA bnisd ot idpolcaiirn: an egantni dfnou in amnmalaim itarmhodlnioc ebamemnsr dna ni t;meesenpro a chape ousecr of naingte si ocw e,htra hhiwc is sedu ni csneinerg s;estt vyer istvseine in yrapimr, ptceex r,aley dna aeyocnsrd shlipyis – teitr yam dleicen ni trayrtei adn whti ;artettnem but otn cisfipec – umts mfrnoci hiwt ABT.-FSA
  • sexaEmlp uecdlin aneerlVe esesDia saRcreeh aLb D(LVR,) iadRp slapam gRenia ,R)(PR mtaotdAeu niaeRg Test T),RA( ro nitcbeoamRn tinAeng steT )ECI(

  • icSfceip stset ofr enlaertomp boiatdyn rea emor en;spevixe aelirtes otisaibden nbid ot oth:siecpesr ehset ettss rae mreo csfpeiic and teiovsip lrer;iea uslluya raniem pvitsioe rof e,fli btu tviispoe n patitnes iwth ehtor nretepmloa saessdie nda aym be tpiieovs in ,Mono R,F psuLu, oLpsyre, im,eL adn Drgu .ssure

  • heT osmt diwely dsue is cFsnuoerlte mrnlTepoea oy-niAtbd Anisbprtoo ASF-)BA(T or opnareeTm uilapldm uihntniialmaotggcmero PMT(-HA)

 +15  (nbme20#17)
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isTh si cteirvea yotemyhiaclp ra,ve hchwi si due to gihh atiteuld ro lgnu ea.iedss O2Sa si low, dna EOP is ree.sdican

rnoethA yaw ot pahrcpoa teh queionst is klnigoo at eth oblod emrs.a sIt' tpeytr rolnam no( yargcsye,kameot on ceardnesi buermn fo elplsa,tte no s,odr ninhgto e,lub .t)ce A bodlo erams mfro a DPOC tepatin llwi eb aol.nmr utJs an eidcsrnea rnmube of RCBs ude to the idranesec OPE idnagel to ecndsreai Hgb.

mbourne  You shouldn't call it reactive polycythemia "vera", as polycythemia vera is a seperate disease with entirely different etiology. This is Reactive Polycythemia, or as another poster said, appropriate absolute polycythemia secondary to chronic hypoxia. +15
j44n  i jumped on myelodysplastic thinking it was PV due to the jak w mutation but you technically get elevated everything in that mutation so it would be more than just RBC's +
beetbox  I also thought it was PV. How can we tell reactive polycythemia from actual PV, if PV does not show other kinds of blood cell counts raised but just an isolate of RBC rise? +

 +9  (nbme20#30)
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s'He ton tgaein gu.hoen

Oen fo l'sootscir oufsictnn si to ernecsia oneeieoguncg,lss l,isylisop nad tsopsyer.loi

ankirin  Why wouldn't it be T3? Thyroid hormones also ↑blood sugar and break down lipids +1
waterloo  @ankirin his symptoms aren't really specific for T3. They don't mention tremors, exopthalmos etc. I think just in physiologic terms, you can bet cortisol is more increased. It's not a great question though imo +
rockodude  can someone comment on why his appetite is down, per first aid 2019, page 329, cortisol increases appetite. thank you +
lifeisruff  his daughter isnt there to bring him groceries +
medstudent22  T3 levels decrease in states of starvation in an attempt to preserve energy. T3 is incredibly metabolically potent - even more so than T4. By decreasing peripheral conversion of T4 to T3 (ie decreasing T3 levels), you are decreasing metabolic activity in "unnecessary tissues", decreasing ATP use, and increasing overall energy availability for necessary tissues (brain). On a side note, rT3 levels may increase but this is not metabolically active and will not be measured as an elevation of T3. Dr. Ryan had a great explanation of this in one of his thyroid videos. +

 +4  (nbme20#25)
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Tish is a etrtnanipeso of tmahorliincdo pyhytmoa. yheT etnof enrpset with ,poatyhmy iltacc sosiiadc, nda CSN saseied. °2 to relifua ni xiiotaved lhpoisyo.nrophta cesMul oysbip fnoet swsoh dgarge“ erd iefs”.rb

ehreT si arbleaiv oiexsnrspe ni a unppitoalo ro eevn nhtiwi a amilfy eud ot ytlpohmaseer in iomanchodrlit etharinn.cei

 +6  (nbme20#18)
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hTsi man is hownsig ssx fo na .IM

ilniatI hapse of darmcayloi oacirnnift dsael ot bisdeauclrdnoa siosrcen ivglinovn &;tl 50% fo eth oaridalycm sesitknch dsuor(adlabnice nticafi);orn GEK wssoh gsn-TmeSet rnpiosseed.

Cunntdoie ro svreee mcisaehi t0(&;g2 ut)simen sedal ot ramsunrlat oricssne onilgvnvi omst fo eth ayrdcmolia llaw rlanutmsar( ftrno);niiac GKE hswos tee-mTngsS evie.nolta

charcot_bouchard  May i know where do u read this +1
mbourne  @hayayah, Although this is a bit outside of the realm of Step 1, I want to clarify a point. Early MI does not typically lead to ST-depression. Early MI will typically present with hyperacute T-waves with straightening of the ST segment, and then evolve towards more familiar "STEMI" morphology. Great image representation of MI EKG changes: ST depression from subendocardial ischemia can occur with supply/demand mismatch --> ISCHEMIA, but not Myocardial INFARCTION. +1

 +8  (nbme20#37)
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veeeftcDi oogumolhos tmnroabniocei is eesn in eraibsota/vanr rsacnec ithw eht 1ARCB eegn tomtnuai.

johnthurtjr  Ashkenazi Jews have a higher risk of inheriting the BRCA1 and BRCA 2 gene mutations, just another tip! +2
lebron james  BRCA1/BRACA2 are involved in the repair of DNA double stranded breaks +5
samsam3711  Other answers: DNA Mismatch Repair: Lynch Syndrome (MLH1, MSH2) DNA Nucleotide Excision Repair: Xeroderma Pigmentosa +14
lovebug  not about this question but... Defective "Non"-homologous end joining is seen in Ataxia-telangiectasia. :) +1

 +8  (nbme20#18)
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aiimllaF stoomaunade opsoyilps si an atomsulao amtnnodi amutti.on uoTnahssd fo pslpoy riaes gtisrtan efart ;btuypre nianoopc;lc lswaay ivnlvose rcu.tem hcrpotiaPycl tyecolmoc or esel 100% spsrroeg to CR.C

osmoaAult niontadm sassedie h,eav no eegava,r %50 ehccna fo ibgen pseasd dnwo to ipnsff.gor

sympathetikey  I would say this is Lynch Syndrome (APC is usually thousands of polyps) but lynch syndrome would generally have a family history of other cancers as well, so you might be right. Either way, both autosomal dominant so win win. +2
smc213  uptodate states: Classic FAP is characterized by the presence of 100 or more adenomatous colorectal polyps +
dickass  @sympathetikey Lynch Syndrome is literally called "Hereditary NON-POLYPOSIS colorectal cancer" +9
fatboyslim  I think this actually is Lynch syndrome. Lynch syndrome can also develop colonic polyps but not nearly as bad as FAP. FAP has so many polyps you can't even see the normal mucosa. If you Google Lynch colonoscopy you can see that they develop a few polyps. +
rockodude  I forgot it was AD inheritance but regardless at the time I was confused because APC is a tumor suppressor so it needs two hits. I guess AD inheritance and then you need another hit to develop CRC kind of like familial retinoblastoma or li fraumeni syndrome +

 +25  (nbme20#32)
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A gbi hignt here too si ninigoct atht eht PAL si da.eeresdc stslteaobO viattcyi si srduemae yb obne .LAP I tihnk tath aws het mnia oucsf heer nad otn ttha oyu clyssrieane eedn to wnok eth FAB1C egne mnittu.oa

sympathetikey  Exactly. That's the only way I got to the answer. +3
pakimd  isnt increased alk phos consistent with increased osteoblastic activity? +
champagnesupernova3  A defect with chondrocytes would cause an short limbs like in achondroplasia so those are ruled out +
pg32  Exactly. Can also be helpful if you remember that the clavicles are formed by intramembranous ossification rather than endochondral; that allows you to rule out the chondroblast/cyte answer choices. +4

 +7  (nbme20#29)
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stoM mnritptao esauc of vlair coidarytsim is acxsCoike rros(piu)nci.av

 +4  (nbme20#3)
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Msot teinscroitr sezenym dinb eo.marinsdpl

So hobt GCC'G5 or 'CC3GG woldu haev eebn tceeapclab ni hist oeacr.sin

meningitis  Yes, correct. The 5'GGCC option could cause some confusion. +
guillo12  I really don't understand the question nor the answer. Can someone explain it for dummies like me? +8
whossayin  yes please.. I'm with guillo12 on this +
sugaplum  @guillo12 @whossayin questions says you've created a new cut site, 1. look at the region on the sick vs healthy. The C to G is the change 2. Write out the sick "CCGG" from 5'3'- you could write out the whole thing, but the answer only has 4 letters, so being lazy here 3. write under it, its complement, the dna base pair. So "GGCC" 4. remember both strands are going in opposite directions when you write them out on top of each other. 5. So the bottom strand actually reads 5' CCGG 3' so that is the answer I hope that clears it up +47
shirafune  To add to the palindrome part, many restriction endonucleases actually function as dimers. Each individual subunit usually has a nickase, so to create a double-stranded break in DNA, they must bind a palindrome so that each enzymatic domain creates a single-stranded break (thus a double-stranded break). +1
alimd  Why do we start from CCGG? Why not CGGG or TACC? +2
alimd  Why do we start from CCGG? Why not CGGG or TACC? +1
ssbhatti  I think its due to the palindrome requirement? +
bbr  Maybe I'm missing a part here, but the substrate that the enzyme will bind to will be the DNA. I went with the line that was from the questions stem, as it is the mtuated DNA will be recognized by the restriction enzyme. I didnt see the need to convert it into base pairing. Let me know what you guys think. +1
uloveboobs  @bbr I agree. I'm definitely not an expert in these lab tests, but the question asks "substrate specificity." I was thinking that it would recognize the abnormal DNA; nothing to do with RNA. I didn't know about the palindromic preference of restriction enzymes, but I don't think there's any need to figure out base-pairing and whatnot here. (At least for this question it didn't work out that way!) +
spaceboy98  sugaplum, I'd give you an award if this was Reddit +5

 +4  (nbme20#22)
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nI krcuotiaye lcsle, tow ajrmo yew—htspatha inuoesepqi-utormtbia hawtpya and oloaysmls eiteeydpsomat—orsil rpineot trga.doeniad

eTh orjam ayhtapw fo slieevetc peitron tiaoderdnag in aierotucky lcesl seus bnutiiqiu as a ramerk ahtt egtrats iysocloct and ecunral seonrtpi rof rdipa oryloisept.s

hTe rohet amjro yaawpht of trneiop eaordgtadni in uetaioycrk lcels onilevsv the tukape fo tiprnsoe yb oomssyesl dna oniigsdte yb

missi199  Could I ask why it is not Lysosomal protease +7
smc213  "Certain viruses have evolved to recruit the cellular E3 ligases to induce the degradation of cellular proteins that might have harmful effects on the viral life cycle. For instance, the protein E6 of Human papillomavirus (HPV) recruits the cellular E3 ubiquitin ligase E6-AP to induce ubiquitination and degradation of p53, thereby allowing viral replication." from: +3
smc213  USMLE Kaplan: A majority of cellular proteins are degraded via the ubiquitin proteasome pathway, including many proteins that play a role in maintaining cellular homeostasis. These include proteins that regulate the cell cycle, apoptosis, etc. +3

 +2  (nbme20#34)
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tP sah tdseabie idnpss.ui

fI niure ccsoterennta thiw odatnsarnmiiti fo AHD ,loanga the eynisdk aer veeposirsn nad hte robelpm is htiw AHD irucpootdn in the hahsamloyutp or elesaer in teh .ospt ripytuita.

hello_planet  FA 2019 pg. 344 +2
djeffs1  first aid (and my school) say if U-Osm doesnt increase by 50% or more, then its still nephrogenic. Not so according to NBME... +

 +4  (nbme20#24)
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atneitP sha ihcocrn aridrhea gianlde to baolmtcie sd.ocsiai Rpoyriestar tosonpnmeaci wlil lead to seeaedcdr O2C iaprrsrt(eyo ikolaalss iav rtle)poi.nahevtiny

usmleuser007  Aldo would increase b/c protons are anti-transported with potassium --> leads to hyperkalemia --> aldo activation ADH will also increase b/e of volume loss +1

 +3  (nbme20#40)
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Somuaqsu lecl carniamco acrhtis:eirtcacs vitn,aactio ryeaplcacimeh, sasectadoi hiwt mkigon.s

Sllam lelc may tycaaull rudopec nsaibeitod antaisg rtynpiepsac aC ns.acehln

smc213  Increased PTHrP seen in squamous cell lung cancer leads to increased Ca2+ levels +9

 +4  (nbme20#45)
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uAselotb rski: hte rdfeeefinc in rksi ont( hte orpnroipot) tuabttaiberl to the vienrtntnoei sa emdoaprc to a otc.olnr

2).1( - )(0.4 = 08.

RAR = %8

nwinkelmann  This isn't actually correct. Absolute risk is actually just the incidence, or the same as event rate. Absolute risk reduction = the difference in risk (not the proportion) attributable to the intervention as compared to the control, and thus ARR = incidence unexposed - incidence exposed x 100%. In this example, the incidence of exposed is the incidence in the new treatment group, and incidence unexposed is incidence in standard treatment group. +11

 +7  (nbme20#29)
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tcpeiS khosc is a eypt of tidveistubir oskch cwihh si admrke by msiavse nvtasidooial t/d( orayaintlmfm sseo)nrep aucgisn eascddeer V,RS dsceedrae ardelpo / PPWC, and ceeisdnar O.C

smc213  Septic shock can also present with hypothermia <36C +3
bethune  Why is it not gastrointestinal bleeding? +3
beanie368  GI bleeding would present with increased SVR as a response to hypovolemia +5
mysteriousmantyping  Why would this not be pulmonary embolism? +
step1passfail  Pulmonary embolism would cause a decrease in cardiac output. There is increased pressure in the high compliant RV which can bulge and compress the LV, decreasing its preload. CO=Heart rate x stroke volume and stroke volume is partially determined by preload. If the pulmonary embolism is large enough, it can also obstruct the pulmonary vessels and subsequently not have enough blood going to the LA and LV, ultimately making the cardiac output near 0. +1

 +2  (nbme20#2)
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looAlnrulip inibtshi anhniext doaeisx. It si uesd orf hrciocn toug as llew as nerivotepn of srms-toulyi castsdioae turea tonyhapherp.

betcher  I got confused because the question stem she was on an extensive chemotherapy regimen and got scared away from Xanthine Oxidase because of its potentially for interaction with 6MP/Azathioprene, but I guess since neither of those were directly stated in the question stem I should have gone with Xanthine Oxidase inhibitor to prevent tumor lysis as stated above +1

 +9  (nbme20#40)
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eTh olny tmei ouy ansfserut a evshh'aJo nesistW naeiptt si hwne eth taeiptn si a monri l1&(;8t ysrae do.l)

medstudent65  I get why the answer is not to proceed but simply stating at admissions you dont want blood products means nothing without proper paperwork being signed. +
md_caffeiner  @medstudent65 From what I recall paperwork is needed for example: if the pt is unconscious and wife says that he is Jehovah's Witness. +

 +16  (nbme20#20)
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istnyiiSvte tetss rea uesd fro igcennrse. cecpSiiityf ttess ear sdue orf trnimoocnfai afret eivtosip .cgniseensr

ytiiisSetvn tsets rea sued fro gnseie owh aynm lpepoe lytru ehva hte edissae. etpicfiiSyc ttess era ofr osteh how do ton evah hte .eesisad

A hilgyh nstvseeii ttes, enhw itgaene,v uelrs TUO .eessdia A ihyhlg icsifepc se,tt enhw oisie,ptv rusle NI ss.eiaed So, a etst hitw htiw lwo tyveintissi tonnac lure uot a e.adises A sett with lwo ipifiestccy 'nact lrue ni asidsee.

heT drcoto dna ptainte anwt ot ersenc for oconl ccarne nad erul ti out. The dcootr uowdl awtn a estt iwht ihhg yntistiesiv to eb blae ot od th.ta He nsokw htta gsettin reh otosl ofr odlob iwll tno elur otu the siiolistypb fo nolco A.C

sympathetikey  SeN Out (Snout) --> sensitive test; - test rules out SPec In (Specin) --> specific test; + test rules in +21
usmlecrasher  can anyone pls explain why it is not << potential false- positive results >> ??? +
almondbreeze  correct me if I'm wrong, but 'high FP (choice C)=low specificity (choice B)'. Whereas high specificity is required to rule in dz +2
almondbreeze  picked positive predictive value myself. can anyone explain why not PPV? +
williamfreakingosler  The principle @hayayah is talking about (a negative test being relied upon to reliably rule out) is negative predictive value ("NPV"). I don't see why "uncertain NPV" isn't the correct answer, particularly because NPV is predicated on the disease having the same base rate in the person(s) being tested as in the population that was characterized for the test statistic. Given that the patient has a strong family history of colon cancer, the NPV of FOBT is uncertain. Said another way, the sensitivity of a test does not change with the population, but the NPV does. The whole reason the doctor is denying FOBT is because of bayesian thinking (a priori information related to family history), and from my point of view bayesian logic is more relevant to PPV/NPV than to sensitivity, hence my confusion over why NPV isn't the right answer. +2
ibestalkinyo  I thought negative predictive value for the same reasoning +

 +6  (nbme20#46)
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yB aeg 75, hte suhmyt is iltetl mero htna yttfa isuest. noyltruta,eF eht myhtus roudpecs lla fo yuro T eclsl by eht ietm ouy caerh berpyut. They rae olligenv-d dna tsh'ta wyh uyo can osle oryu uymths whtutoi inpriemamt of yruo ummein sy.tmse

sweetmed  Memory T cells live for six months or less in healthy humans (Westera et al., 2013), whereas naive T cells can live for up to nine years +6
whossayin  so the bone marrow does not take the role of the thymus? +1
dr_jan_itor  @sweetmed, does that mean that if someone loses their thymus, they would develop imunodeficiencies appx 9 years later as the naive T cells have died off? +8
hpsbwz  @dr_jan_itor no, because once all of the thymocytes become T-lymphocytes, they are stored in lymphoid organs until they're needed. this is why removal of the thymus in MG does not cause any immune system deficiency. +6
peridot  @dr_jan_itor From wiki: "Thymic involution results in a decreased output of naïve T lymphocytes – mature T cells that are tolerant to self antigens, responsive to foreign antigens, but have not yet been stimulated by a foreign substance. In adults, naïve T-cells are hypothesized to be primarily maintained through homeostatic proliferation, or cell division of existing naïve T cells. Though homeostatic proliferation helps sustain TCR even with minimal to nearly absent thymic activity, it does not increase the receptor diversity." +3

 +7  (nbme20#22)
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nHGR gsasoitn keil iodpuLeelr rea etvceeiff ofr ttipensa with rbtase CA sbeauec fi gveni in a cuutniosno os,ahinf they ourelngweatd eht nGRH crorpete in het tiiupryat dna lmtlatyeiu aesrceed HFS nad .HL

md_caffeiner  Quick question: FA19 691 says Leuprolide ClINICAl USE is Uterine fibroids, endometriosis, precocious puberty, prostate cancer, infertility... I guess all except infetility(pulsatile?) are used as continuous? +1
usmlecrasher  GnRH is synthesized and released in pulsatile fashion , so if you give in pulsatile way you induce GnRH effect , and if given in continuous way it will suppress synthesis, depended the desired effect you want to achieve - infertility induce GnRH with pulsatile , stop synthesis for prostate cancer , testicular cancer , hormone dependent Breast cancer give continuous +1
djeffs1  I thought Gonadotropin was released by the Hypothalamus, not the pituitary gland. am I crazy? +
kevintkim4  ^ Gonadotropins are referring to LH/FSH; Gonadotropin-releasing hormone (GRH) is released by the hypothalamus +

 +2  (nbme20#37)
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Cilnilac ues of ang-riKsp usrectdi:i

  • serieaoldromHpstny
  • K+ dteipolne
  • HF
  • chieatp sectisa cna(lsropeoo)tni
  • nceprihogne DI l(oie)ridma
  • gdinaeronatn
redvelvet  Patients with hepatic ascites have hyperaldosteronism; because the intravascular volume is escaped to third space(ascites). So adding spironolactone is a good choice. +3
champagnesupernova3  Always combine a K+ losing diuretic with a K+ sparing diuretic +10
bryno20  My rational was a bit different. The patient likely has hepatorenal syndrome leading to a the ascites and decreased GFR. All diuretics, except for the steroids (eg, spironolactone), require secretion into the PCT in a GFR-dependent manner; for this reason, patient's with renal impairment show best success the steroid diuretics since their action is independent of renal function and GFR. +

 +1  (nbme20#15)
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acnteSsbu P PS() si an etaeuednpipcd epstner in eht CNS adn the pehelrripa vorsenu es.sytm A umopnocd tgtuhho to be ovdnviel ni teh iysptnca snsrnaitioms of nipa and othre rveen lpisemu.s

mambaforstep  also, apparently enkephalins attenuate substance p... so it would be dec her pain. +1

 +5  (nbme20#28)
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n-cHepnraiidued apeyotthboniormc I(T)H is eht edpteeovlnm of IGg tindioabes siganat pnirahe bonud teapletl ortcfa 4 P(4F). aedioihrFnyn-pb-4AtP clpoemx acaeitvst salteetpl Ž sbmhootsri nad opatethci.roynbom Hgthesi kisr itwh naicdnttaerfuo einrpah.

drw  could you also help to understand: 1) could anti-heparin-PF4 complex be also called anti-PLT antibody? 2) PLT reduction is due to both PLT thrombosis consumption and elimination in the spleen, then why hypersplenism is not correct? +
charcot_bouchard  hypersplenism means bigger spleen eating everything. thats not the case here. here spleen is normal. autoimmune cause +
benitezmena  Yes I dont understand why the called them Anti-platyelet antibodies and not specifically Anti-heparin bound to PF4 on platelets. Its just not the right antibody +2
benitezmena  Antiplatelet antibodies would be for ITP, but also anti-megakaryocyte antibodies would also be for ITP. +1
misterdoctor69  As an aside, pregnancy is a hypercoagulable state which caused her DVT in the first place +1
cport12  If anyone else was freaking out about the word hemodilution basically it just means that there is a decreased concentration of cells and solids in the blood resulting from some other gain of fluid. With normal pregnancy (not HIT), blood volume increases, which results in a hemodilution. +

 +30  (nbme20#44)
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VL eppsotd rgok,nwi rpsuesre ckebda up ntoi ulpm curtii.c umlP tiuccri ylrghou is dema fo 3 "rpa"ts - eht ,eraailsilcp lniaeirittts pasce, nda hte

In icgdcieoarn och,sk the ertxa odobl sscaneier aapcylilr rtasicydhot esrueprs, dinrvgi fdiul niot eht ltnetastiiri ceaps. ormpdCae ot eht ilvlao,e the ietaitrstiln sepac onw hsa rmoe ifudl (thsu oemr retatsniitil tsiychodtra sereprsu and essl octicno sspereur deu to taior of idflu to prt,io)en nad as a ulrtse of siht ncbgalunain of sefor,c ulfdi vemso tion hte eillvao -g&;t- nmypoular m.eade

 +8  (nbme20#8)
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tohrypA si deecresa in siuste assm eud ot radecees in zsie ines(caedr tsoyonceektl taredoniagd vai rqemn-aoueitbosputii apyawth nad athupyoag;  edraesced eoptnir sysniehs)t arod/n mnrueb of lclse o.ppatsos)i( aesuCs unidcle issu,de danie,vontre ssol fo bdool sppl,uy sols of oalnhomr it,lomtuisna oorp .titrnuoin

mambaforstep  FA 2019 pg 206 +1

 +8  (nbme20#25)
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sMto oocmmn ceuas of icsrgta ulotet soribuottnc ni nitnsfa. laaPbepl siedoa-vlphe msas ni reiciatspg ,gireno sbelvii estatpiicrl awsev, dna loosnnubii tjoiecerpl votgimni ta 2–∼6 weeks old.

snlotdaUru oshsw tichenked nad tnehegednl sryp.lou ematTetnr si suacglri nnsiiico l)yopoy.(tomomry

lovebug  Could you explain WHY NOT (B) Gastric volvulus?? bc I think it can share some clinical symptoms. +
calleocho305  This is what I put, wouldn't hps occur earlier than 4 weeks? +
ssc30  Gastric volvulus is very uncommon in general and almost never happens in infants. +
ssc30  Gastric Volvulus would also present with severe abdominal distention and pain due to incarceration. +

 +3  (nbme20#39)
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reoitsoIinnt si used ot ttrea rvseee itccsy a.ecn tI is a etatgrnoe. nCa ecuas llmitpeu reeesv hrbit tese.dfc retnCpotinaco is tm.daronay RXR is a tioedinr X rco.eretp


 +9  (nbme20#24)
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netaPti sha aoniglentc ptmyhrhdioiosy er(m).itnsci siFn:dign opt bl,yel lae,p efda-yfp,fcu ilicamlub iraehn, aogasoi,lrcms ohyoni,atp orop abirn dltnvmoeeep (CM sceau of tlbarteae taemln dn)iatreoar,t galre rtanoier .faeeotlslnn

whossayin  how can you differentiate the symptoms of cretinism from Down syndrome? +
step1soon  @whossayin Down Syndrome: upslanting palpebral fissures, atlantoaxial instability, bent little finger, congenital heart disease, displacement of the tongue, excess skin on the back of the neck, flaccid muscles, hearing loss, immune deficiency, low-set ears, mouth breathing, obesity, obstructive sleep apnea, polycythemia, seborrheic dermatitis, single line on palm, thickening of the skin of the palms and soles, thyroid disease, or vision disorder +3
ally123  I was confused about why the infant was jaundiced, and found this: "Hypothyroidism causes decreased rate of bilirubin conjugation, slows gut motility and impairs feeding, all contributing to jaundice." Source: +6

 +5  (nbme20#45)
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gLera nwlsole rcalte vesni &--;tg eptntia ash axenterl eoihsromr.hd nwloelS nad dfmilnea snvei in hte cmetru dna snua atth scuea ismfcotrod nda gb.ndeiel ehT mots ocnmom sceua of aextelrn rrhosimehdo si areeetdp tiasnirgn ihewl gvanhi a eblwo t.mnveeom

 +4  (nbme20#35)
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CMV si saticeosda ithw cegiitnnf oanrg pslnraantt nestpiat. MCV si asrtimnetdt avi lesuax tna,octc rgoan taal,rnstnp or aiveytllcr via na.epactl oaiicRevtatn of VMC cocrus ni het uds.ormpsnipeuems

graOn nlptrantas pinsetta rae at na drnesciae iskr fo MVC un.nopeami

 +14  (nbme20#23)
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In rroed rfo a gurd to eb eedacrl by het nek,ydi it mtus tisrf be etelirfd ni hte lo.geumrli rusDg htwi a hgih VD haev eomr fo teh udrg ni eht ssutei htat rea tno ealaabivl ot rtileedf yb eht .iydken surgD tihw gihh niteopr inbgnid 'ntow be liedertf ti.eehr So uyo wnat a drgu twhi wlo Vd and lwo gnibidn fi uyo want ti lrceade iav the ynikeds and nir.ue

zevvyt  But a low VD corresponds to high Plasma Binding Concentration(FA 233, 2019). That's my main confusion with this question. +2
kevin  If it's high plasma binding, then it's low Vd. But, low VD doesn't necessarily require high plasma binding. Low Vd can simply be due to it being a large polar molecule +

 +4  (nbme20#13)
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Atceu tirtailnseti raenl if.tanmlioanm yraPiu iclsllscy(aa o)hspisoilen dna izeamtoa rgcuornci aetfr imrnnatsiotiad of usrdg thta cat sa s,nptaeh niucndgi vreiytsphtniseiy e,g( dt,uisrcie SNIA,sD ieinplnilc eidtis,reavv rtpnoo upmp ohiirin,tbs mifni,rpa neuisooql,n se)mnafd.iouls

hungrybox  But how is a 2-year history acute? +4
jinzo  there is also " Chronic interstitial disease " +4
targetmle  i got it wrong because there wasnt rash, also there was proteinuria, doesnt it indicate glomerular involvement? +2
zevvyt  Got it wrong too cuz of that. But there can be proteinuria in nephritis, just not as much as in nephrotic syndrome. I guess that's confusing cuz this type of nephritis isn't grouped with the other nephritic conditions. +1
lovebug  FA 2019, Page 591. +

 +5  (nbme20#30)
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eTh rhtig nad eflt eicetvnrl aer rneidad yb eateraps rspta of hte rnoafme fo oomrn. tL(fe dsie is raidned yb eltf rmono, thrig desi by higrt .)onmro nA ttoisnoburc of teh hgirt onefmar of monor iwll gnraeel het rihtg tevilrce.n

hmorela  My mnemonic for CSF flow: "Little Infants Crying For Food. Sorry, All Done." Lateral ventricle - intraventricular foramen of monro - cerebral aqueduct - forth ventricle - foramen of lusaka/magendie - subarachnoid space - arachnoid granulations - dural venous sinuses +12
charcot_bouchard  u missed 3rd ventricle, how about " Little Igor the 3rd, Crying for..." +5
len49  "Little Infants Try Crying For Food. Sorry All done." Added the T (try) for third +1
caffeinequeen  Kind of a stretch but: LIT AFF to SAD Lateral ventricles -> Interventricular foramina of Monro -> Third Ventricle -> cerebral Aqueduct of Sylvius -> Fourth ventricle -> Foramina (luschka and magendie) -> Subarachnoid space -> Arachnoid granulations (reabsorbed) -> Dural venous sinuses (drains) +1
fatboyslim  Kind of dirty but: Monroe (foramen Monroe) likes to get on top of Sylvius (cerebral aqueduct AKA aqueduct of Sylvius). Then Luschka and Magendie are in alphabetical order. +1

 +1  (nbme20#27)
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tiSstan can ehva a ieds fcefte fo byydhooa.lmsirs

lilyo  Statins have an increased risk of myopathy, specially when combined with other medications like Fibrates. This patient presents with muscle pain along with an elevated CK and + myoglobin test in urine. Consistent with myopathy. +2

 +5  (nbme20#3)
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itantPe sah uldyeamlr .aracncimo nlaMiangt rlponifraoiet of lloriaaacfpulr "C" celsl ahtt rdueocp alicintcon adn vahe shtsee fo selcl ni an ioyldam

xxabi  Just to add - patient likely has MEN 2A or 2B with the presence of medullary thyroid cancer and pheochromocytoma +13
sympathetikey  @xxabi Was going to say the same thing. +
dermgirl  The patient have MEN 2B (Medullary thyroid carcinoma + Pheochromocytoma) Page 351 FA. +

 +15  (nbme20#34)
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riotntiAndimas of ilnnilPice orf Shyipils amy adle ot het emJxhrh-errescHaii ntirocae rosuh arfet nrtemtet.a sucrOc ued to ilyss fo rosecpitesh s(o ti anc urcco htiw lioareBr and poLostisreips as ).ellw eTh crntieao si raachrctzeide by efvre dna ch.llsi

eTh ilacalscs tnanexloaip fo hte ermxehHrie niroeatc si thta ttrtaemen lrstsue ni the eudsnd death dna cturodtensi of alerg nmusreb of me,sotenerp with het reainbotli fo tnoirep ucprsotd dna n.txsoi

almondbreeze  FA pg.148 +5

 +8  (nbme20#9)
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palmrFonotrtoe etemandi y(lrmerfo kwnon as kcPi e)adesis: l rayE hanesgc ni yaoeprtnils and ehvriabo albheiv(aro a)niratv, or spaiaah amrriyp( reogpvierss ).psaiaha ayM evah edtsisoaac eomntvme dssrdeoir ,(ge rimi)asnsnpo.k

heiWl thsi esretsnp vrey slyrimiail to unHogsnit,'ntg uyo nac etrfeetniidfa it eeabcus in shit mtse ti ssay ath"pryo fo teh nltoafr obsel br"lteylaail aerwseh iuntsnongHt' sah rtapohy of dcueata adn mtuenap itwh ex cvuao .ocviaeugynltlrem

dickass  and the patient has no chorea +1

 -7  (nbme20#23)
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uoimbctcMyera iumav clxmeop nefcitonis aer a ocmmno sctrnpiotpoiu ointcefin in enttspai wtih ecavadnd ISDA C(D4 cuotn .;50&)lt

realfakedreams  @hayayah you were being lazy.. smh.. Homie started anti-retroviral therapy. HIV infects CD4 T-Cells through either CCR5 or more commonly CXCR4. Because of anti-retrovirals start working, HIV isnt able to infect anymore CD4 T cells. Thus CD4 t lymphocytes levels start to rise and are able to active B cells. +13
myf1991  Why can't it be monocyte? macrophage eat MAC and interact with CD4 +1
weenathon  @myf1991 I also incorrectly chose monocytes, but if you look at the question carefully, it is specifically asking what cell is required for the lymph nodes to enlarge, not which cell is handling the mycobacterium avium infection. Since CD4 cells stimulate B cells to proliferate in lymph node follicles, which would make them bigger, CD4+ T cells is the answer. +2
j44n  macrophages dont enlarge nodes in fact they make them smaller, tingle body macs eat all the bad B cells in a node so improved mac fxn would decrease the node size +
mpel14  To add to @namira, an infectious disease doc described this concept in an HIV lecture where he said that prior to the Tx with antiretroviral therapy, the pt has such low CD4 count that their immune system cannot form a response to the infection, and after their immune system is given a slight boost with the drugs, their immune system can finally "see" the infection -> mount response -> causes S/S +

 +13  (nbme20#46)
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cN,toei the etms ssay rcsr"eporos ni eht ikns"

D3 eoerc)ifclhal(col rmfo ereoupxs fo ksin s(tmuart ebasa)l ot usn, nsonitgie of ishf, lmki, sa.tnpl

2D ogrcrfeaoel()cli ormf etgiisnno of sn,ltpa ,ifgnu staye.s

thoB eendcovtr to O52-H 3D aretgos( mr)fo in vreil dan to the taeciv fomr O,51(H22)- D3 lit)cirao(cl in d.eynik

sympathetikey  C is the 3rd letter in the alphabet. Hence, D3 = Cholecalciferol +4
karljeon  Thanks for the explanation. The question stem made it sound like "what future step will be decreased?" Actual question: "Decreased production of which... is most LIKELY TO OCCUR in this patient?" Maybe NBME needs a grammar Nazi working for them. +8
bharatpillai  question says "decreased production of which of the following precursors in skin is most likely to occur in this patient? the answer has to be 7-dehydrocholecalciferol! +4
bharatpillai  7 dehydrocholesterol +2
brbwhat  Yeah i did the same, but then realised acc to uw flowchart 7dehydrochole.. is converted to cholecalciferol in presence of uv rays. So the decreased precursor would be cholecalciferol since we already have 7 dehydrocholecalciferol not being converted by uvrays Tho the uw chart sites both ergo and chole as dietary sources. +2
drzed  Wouldn't 7-dehydrocholesterol build up in the skin? Since UV rays convert 7-dehydrocholesterol into cholecalciferol, if you are lacking the conversion, the reactant (7-dehydrocholesterol) should accumulate. +
brbwhat  They’re asking decreased production of which of the following precursor would occur? 7 dehydrocholestrol builds up, but decreased production of cholecalciferol takes place, which is a precursor in the pathway for vitamin d formation +1

 +9  (nbme20#1)
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'sTNRI aer aeistoadsc ihwt lbepsiso dsie fesfetc of aanie,m i,tpoguloycneraan adn leesp.mspoioyrnsu

sympathetikey  Especially zidovudine. +17
fmub  Nucleoside reverse transcriptase inhibitors (NRTIs) block reverse transcriptase (an HIV enzyme). HIV uses reverse transcriptase to convert its RNA into DNA (reverse transcription). Blocking reverse transcriptase and reverse transcription prevents HIV from replicating. +1

 +10  (nbme20#45)
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aFosnic'n is a zleeeniagrd saniorerobtp fecdte ni PTC gancisu idcneears rxoteicen of nimao saic,d gol,ecus –HCO3, and O–P,34 and all asstunescb eoabesdrbr yb eth TP.C

baja_blast  FA2019 p. 581. Fanconi syndrome causes a type 2 (proximal) renal tubular acidosis +1

 +10  (nbme20#25)
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oytOicxn sseu I3P giginansl htyapa.w

G,RnH nicOo,txy HAD )e(e1or,tVc-pr R,TH aneiHmtis c-p1oe,(H)retr tonseAiinng I,I itn.Gars

FA mnmnicoe: AT"GO "AHG

dickass  I figured "if Oxytocin can cause milk secretion and enough uterine contractions to expel a full baby, it's probably activating smooth muscle contraction through Gq coupled second messengers" +6
randi  signaling pathways in FA2019 p332 +1

 +5  (nbme20#30)
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teaCaitp and lutane era in hte rectne fo the tateapCi si ton na tpo,ion so eatuln is hte a.wnrse

oDcsnaitilo of natlue yma cesua tceau na lltunacrep .noyemrds

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

 +11  (nbme20#18)
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The etbus rae astcheter tup in orf riune to lwof tnoi a So eruni output is oging to eea.rcsni ehT ttinaep si laos kpharem.lceiy oseAotedlnr doenrpss ot kpremalaheiy by irisacgnen +K conriet.xe

elaerpmyHaik ilwl tslmtuiae tlsaoednoer eoiesncrt even if nnrei si seuesrdpsp eud to ihs t.ienhsernyop Althouhg +Na liwl be eboesrrda,b htis will be tinarsent ldusho( evlosre coen eth tusmspiao svleel mdnarloize) nda inecs hsi ieurn uttpuo iwll mots elkily nrrute ot ol,mrna shi oodlb rpessreu losuhd laso a.irnlzeom

charcot_bouchard  Postobstructive diuresis Postobstructive diuresis is a polyuric state in which copious amounts of salt and water are eliminated after the relief of a urinary tract obstruction. The incidence of POD is unclear but estimates suggest 0.5% to 52% of patients will experience POD after relief of obstruction.10 It generally occurs after relieving BOO, bilateral ureteric obstruction, or unilateral ureteric obstruction in a solitary kidney.11 Diuresis is a normal physiologic response to help eliminate excess volume and solutes accumulated during the prolonged obstruction. In most patients, the diuresis will resolve once the kidneys normalize the volume and solute status and homeostasis is achieved. Some patients will continue to eliminate salt and water even after homeostasis has been reached, referred to as pathologic POD. These patients are at risk of severe dehydration, electrolyte imbalances, hypovolemic shock, and even death if fluid and electrolyte replacement is not initiated.9 +7

 +13  (nbme20#49)
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Ceas of sl.oscaoieiterlorsr

eyipHlasprct slooetalserricrsio olivsevn ntcighknei of evsesl lalw yb yshpaealirp of thosom esmcul -on(nkions'i 'aapcnpeea)r

  • unoscCeenqe of gatminlna hniposeryetn /12(0108g;t& w/ caetu drngeao-n )eamadg
  • tlRssue ni ceeuddr vslsee lraebci hwit gn-nredoa saceihmi
  • May lade ot diibniorf ecsorisn of hte lvesse wlal wtih arehrg;ohme iacyssallcl easscu uctea elrna flaurie A(R)F hitw a hctareiistcrac bifa-''tnelte ecarepaapn
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. +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. +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 +

 +5  (nbme20#13)
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No m,iabrlsoetain onyl some mtnv,oiig solok lwel w/ on ulafrie to .hritve tosM lkleyi mareitum LS.E

masonkingcobra +13

 +3  (nbme20#50)
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Stohr trsacgi a. cranbh rfom teh isnecpl .a

Basnerhc fo teh celaic knrtu taht ioestttcun hte lbood suppyl ot eht htc:omsa ocnmom ecta,phi eps,cnil nad etfl rcg.tisa

 +6  (nbme20#37)
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tWhi noirhcc igvtio,nm you sloe lyoceesetlrt dna a otl of aicd. tI grtiersg ltbaicome ialsksalo ciwhh is hwy lla eht reusm lsavue rae wol o(r no the leorw den of eth omrlna gnrea) xtpece rfo ineraobtbc.a

ergogenic22  decreased K+ (from increased RAAS due to volume loss) and decreased Cl- (loss of HCl from the stomach), Alkalosis from loss of HCl and thus high bicarb. For this reason high to mid range K is wrong +4
sbryant6  Wouldn't increased RAAS lead to increased Na+? The answer shows decreased Na+. +3
sbryant6  Also, remember Bulimia Nervosa is associated with hypokalemia. +1
sugaplum  so the range they gave for K is 3-6? so 3.2 is WNL then? or are we just operating on "it is on the lower end of normal in peds" +2
dbg  sodium levels in pyloric stenosis vary, nothing really classic, can be high as in this case simply due to hydration, can low in other cases if aldosterone managed to reverse that to the other extreme +1

 +10  (nbme20#8)
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atireslE elcttbeeda dycnorase elsxua thciaasecrtcri is tebrsa bud emvpndleteo ni i,srlg tesuricatl taneelnmger ni byso.

pg32  How did you know this? The Tanner stages in FA simply list pubarche and breast buds developing in the same stage without stating which comes first. Thanks! +4
lynn  @pg32 look at the paragraph above the diagram, it says that exactly. Took me a minute too lol +4

 +5  (nbme20#28)
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liilnaCc :gnfsdnii itn,h wolelyn,rge-e lm,rudsoooa hfyotr ihrsgcaed nad laangiv afiniaoltmmn / ichtgni.

baL nsngd:ifi Hp .&g45;t dan lioemt iomca.dnotshr

 +15  (nbme20#4)
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lentaoMh is tcoxi by tow h:cnseismma

rtF,is omanhelt cna eb latfa ude to tsi CSN nrastdepes ptroeeirsp in the mase arenmn as hntoela sooipnni.g

neoSd,c ni a scpsore fo ,tiiaxncoot ti si eibadtmzeol to orcifm icda via emhyeodalrfd in a srcsope iitditaen by eth zmynee oloclah rodnhdaegyees in teh eaontlMh is eervcontd ot lmfeardodyhe iva laochol snheodeyardeg )DH(A nda meadyrfloehd is reotcvedn ot crfiom cdia omr)et(af vai eealhdyd yrenddgaoseeh L(.)HAD

ratFmoe is txioc bcuseea it isbhiitn hcdmiioloantr yrocctmeho c oae,sdxi sgicnua ipxoyah at teh ullrleac eellv, dan cloetibam caoss,iid gmano a irvaety fo ehrto itleomacb d.nusbrcsieat

sugaplum  Good pictograph comparing methanol, alcohol, and ethylene glycol. +9

 +15  (nbme20#38)
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tniPtae ahs a haiirgynaoacnprmo. sMto mmcono iohdlcohd pautelraornsit Derevdi fmor atnrsmne fo ahRetk cpuoh ol(ar d)eetc.mor ccnotaliiaCif si .mmcoon Cloeserloth rtsasylc funod ni t“moor llke-”ioi ulifd inhtwi m.ourt

A ctycis urllrspseaa smsa htiw oailncsfictcai dna enmahceetnn of eth wall or iodls pntoiosr ni a lhidc or eacetdnlos si lmosta saawly a nhcoaimniragpa.ryo

May be cunfdose iwth aupyrtiti amadone ob(th ceasu lmietropab anoia)h.epim

dickass  Cholesterol crystals in motor oil +
passfail  I also just thoughtL: failure to secrete GH = tumor affecting anterior pituitary hormone --> anterior pituitary is derived from Rathke's pouch +
ally123  "Due to the proximity of the tumor to the hormone-producing cells of the hypothalamus and the pituitary gland, there is significant endocrine dysfunction in most children and adolescents presenting with craniopharyngioma...Among the hormone deficiencies, growth hormone deficiency is the most common and is seen in approximately 75% of children with craniopharyngioma." Source: +

 +18  (nbme20#7)
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irloAyc,vc icamvf,ilrco cyalvvlocair ear sineuogna sgaan.ol Tehy rduogne sneroocvni ot yailcrcvo tepohoonhamsp iav isvur nddeoce einithsiednyam-.k ielmyattl,U htye thinbii lirav ADN lpyameoesr by ihanc anmioite.nrt

eaMudtt viral tinyheimd seknia acn auecs .tncsseaier

len49  Foscarnet and Cidofovir on the other hand do not require phosphorylation by viral kinase, therefore should be used in strains that are shown to be resistant. +3

 +7  (nbme20#39)
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ainulIng nraehis aer alulysu elbdierc,u feamlro irensah era nt.o

ishT is na citenrdi gnuanili e.hrani tI etesnr leannrit nnilagiu igrn ealtrla to rnfoiier rpeaiisgct sessvel dan si iureospr ot hte ualnniig mnie.tlag

Cedsua by ufaerli fo ucesopssr nvaslaiig to olces a(cn fmor .hdelco)rey aMy eb tdconie ni fntanis ro drisveoedc in uh.latoodd cuMh emro cmmnoo ni .msela

yotsubato  Heres a good picture to help with the concept. +4
sbryant6  Note that direct inguinal hernias typically happen in older adults. This question presents a younger baby, so it is more like to be indirect. +7
jawnmeechell  So a femoral hernia would be inferior to inguinal, but direct/indirect would be superior? +
azharhu786  The direct and indirect hernia are both superior to the inguinal ligament but the femoral hernia is basically inferior to the inguinal ligament. The direct hernia is medial to the inferior epigastric vessels whereas, the indirect is lateral to the epigastric vessels. An indirect hernia is seen in young people whereas, direct hernia happens in adults. +4

 +24  (nbme20#34)
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sniseMse iutmansto vlenivo a neduecolti usitnosubtti ungstirel ni echgdan naimo asdci. Smmstieeo eht ffescte of sniseesm ianstuomt mya be ylno paenptar duenr eracnit aonevnrnlitme oinoticn;sd usch sssneeim omitsuatn era aldlec ndoaitlnico tuisa.onmt ynaM smieness ntsutmaoi rseltu in nitrspoe ttah ear itlls fatliunc,on at easlt ot emos ere.edg

ls,oA all hte trhoe snreasw lwodu blaroypb eelva uyo ihwt hiteer a rtalyeg tledera ro nnacolntnfou-i npeo.rti

thefoggymist  I chose nonsense because I thought it'll make the enzyme shorter (since less bonds = more heat liable = can't work at 42 degrees) but yea, probably won't work even at 30 if it's an early nonsense. +6
joanmadd  A good clinically related example is HbC disease on electrophoresis. HbC disease is due to a missense mutation (glutamic acid (-) for valine (neutral)). The mutated hemoglobin is still fairly functional but when placed on gel electrophoresis the HbC migrates the least far from the negative electrode due to less negative propulsion (lack of wild type glutamic acid). +1
fatboyslim  @Joanmadd Just to clarify, glutamic acid substitution for valine occurs in sickle cell disease not HbC. HbC is glutamic acid substitution for lysine :) +6
rockodude  lyCCCCine for HbC +2

 -8  (nbme20#35)
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heT mdgeaa si in teh L dnrbmiai in the reaa cfnaetigf eth ioccsptanrloi t.actr usBcaee ti is ni eht ,badnmiir otuaesnidsc in eth pyidrsam leluad(m) os ti ilwl wsoh ileiartalps sayduncflinot mroto

otohP fo nbadimri adn moatntpri reaas: Hyrt/LalrRsu.tomh

masonkingcobra  Just for clarification, on the left side, you see where he had the infarction 7 years ago and the tissue is gone. +6
chefcurry  so is the dysfunction on the contralateral side? +
praderwilli  If the decussation is in the pyramids of the medulla, shouldn't it be contralateral hemiparesis if the damage is on the right? It confuses me because of the labeling right and left at the top of the pictures. +
endochondral1  that link isnt working @ there any good picture to look at to know where the tracts are on this section? +

 +6  (nbme20#10)
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tLtiel igfnre = lunra veen.r

TC81- rae hte trsoo of teh lnaru vener, wichh is a hacnbr of eth eildam cdor. The nalur eenrv is nto dfnou ni teh aapclr eunltn (the dlamie nvere )s.i

raUnl n. gdmaae nac lead ot ossl fo rtwis ienoxlf nad uoticda,dn onelixf fo ailemd eisrfng, coabuintd dna ddainoutc fo ifsrgne ies)noer,ti(s tnoicas fo iedlma 2 lcbliamur sLso fo isoeannts erov dialme 1 1/2 ger,isfn nudnicilg ypeahthrno ieen.menc

sugaplum  Also to add: since it is a bilateral sx it is more likely to be coming from the spinal cord then from equal compression of ulnar nerve (in guyons canal) on both sides. unless she is a cyclist +25
thefoggymist  shouldn't the other nerves of the same roots be affected? +
thefoggymist  shouldn't the other nerves of the same roots be affected? +
charcot_bouchard  Not really. In klumpeke paralysis ulnar nerve s/s dominates (Almost same cause) +

 +31  (nbme20#40)
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aaleNiosp is new usties wohtgr taht si elutd,rguean rvebisie,lrre dna l.ncmonaloo

tllCinaoy nac eb tmeenridde by clee-otshahosp6p-gu dysoehnadeerg G6)PD( nzeeym ms.oifros PG6D is -endXikl.

*Fro ermo otmioraninf echck uto .hC 3 paeoNlias in Pthmaoa

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! +

 +6  (nbme20#12)
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Teh felt ppeur iemtxrtye adn ebarst aer ddearin by teh xlilyara mlpyh d.neo eTh neydik is ineddra by eht irtoahcc udtc. heT ather hsa tis nwo pmlyh mysets iggon no sgronrinudu eth t.ahre

 +0  (nbme20#14)
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Of lla eth sotnpo,i pssao rojma si eht nlyo neo atth is leayrl tocsidsaea iwth hte albrmu eb.eeavrrt

Q. uLbmrumo vevnsoli hte raevnterss ecpssro fo 1L ubt osasP arjMo gteiniaors ofrm -L5L1

imnotarobotbut  QL is connected to L1-L5 vertebrae as well ( +

 +7  (nbme20#15)
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ontiifeDin fo jasndutemt s:deorrdi

Eltooainm ostmpmsy e,(g xnytaie, )seeisnpdor thta rccou ihtnwi 3 nohtsm fo na eeainifdltib oocsialhpcsy soetssrr (e,g drec,iov sns)ille nalistg &;lt 6 nhmots coen eth srerosst sha en.edd

If smopytms esrtspi ;&tg 6 hntsmo traef rtrsseso ,edns ti is 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. +

 +7  (nbme20#47)
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hTe owt msto poiatntrm MI iilcpotsmncoa atth curco iiwnth a 25- ady psan era ayappllri ucmles puturre dna tltiervrniarenuc tmpseu rut.rue

Plpyialra uemslc tupreru lsaed ot eveers irtlam rr,gietgiuanto rahde sa a sylotsic mruurm ta eht xap.e

dulxy071  I disagree. any sort of rupture is usually the result of the action of macrophages (to eat away dead, necrotic tissue) which come in on day 3. This was merely a word game to get the time line right. They said "TWO DAYS LATER" (keeping in mind our time line starts 16 hours after the first symptoms appeared in this stem) which actually turns out to be day 3 +4
leaf_house  Wouldn't necrosis of the interventricular septum create a VSD, which would also produce a loud, (holo)systolic apical murmur? I don't get how we're supposed to differentiate, here. +1
mangotango  A VSD produces a holosytolic, harsh-sounding murmur loudest at the tricuspid area, not the mitral (apex) area -- FA, pg. 288, 289. +3

 +15  (nbme20#20)
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toocinrCtaa fo the taora laesd ot dinrcseea LV deorlaov ascunig LV horyyretphp adn a L ixas .iaetidvon

hungrybox  Similarly, RV overload leads to R axis deviation. Could point to PAH. +1

 +7  (nbme20#19)
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Tsih iapettn ash allsm ellc siTh type of ercanc is satacdesoi twih pcratenalpisao rsesnomdy hcus sa: gishCun y,emSrnod SADHI, ro nibdoitesa ngaitas a2+C nhalscen t-(beaLn)omraEt or nsn.ureo noiimAipalctf of ymc gsneeoonc is aosl onm.omc

ASDIH redoSn(ym of petpaiinpoarr eiincaittudr eoonmhr ereoc)ntis is eracitdrhcaze b:y

  • vscexEesi efre rawet tiorneten
  • lmiuoEvce ehyomantpiar iwht ytr nciendaoinruu N+a reciteoxn
  • eiUrn iasoomlytl ;tg& uersm omatliosyl

doyB epdosnsr ot retaw ortieentn hwti eetrnsdolao nad NPA nda P.NB htaT is tawh ecssau the ceedinrsa ayrirun Na+ ntseieocr hwŽchi ldeas to loonnrziaiatm fo aetxrucrellla dluif volemu andŽ hte evoceimlu npy.meroahati

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. +

 +4  (nbme20#36)
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yioRlmsyhaodbs acn eersnpt ilonkgo iekl a dknyie urinjy t(i acn eadl to caetu tuaurbl sicosner sa e).wll Teh crloetyelet isnifgdn rae sjut ilek larne fleirua .(ncI +,K .nci 4-,OP edc. )aC

oT rfatitnfeeide eewbten soolyahmdbysri nda dynkie unyijr, uoy kcche teh nirue to ese if erhte are yan RCB.s In odiymybsosalhr there aer on eref RsCB ni the ruien.

ergogenic22  "Crush injury" is a buzz word for rhabdo +11
ibestalkinyo  The mechanism by which AKI occurs after rhabdomyolysis are due to free radical formation. Other urine finding include blood on dipstick, but as hayayah said, no frank RBCs. +1

 +11  (nbme20#2)
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heT ybab dsoe otn gte nay elnmtraa g,MI gIA ro IEg as they do tno ocssr hte eapcln,ta so fi gIM is fonud ti may gtegsus eth ybab ahs cetrndeeonu na ctionfnei ni or.teu

IGg is spsdea down to eht bbya as a sanem of ipsaves tnimiyum tluin het baby nca ofrm eihrt won bnasoitied fo fdnefeitr ep.tsy So if uoy see gtianyhn teohr atnh IGg (g..e I)Mg uyo kwon it umts eb t/d an ctoieifn.n

hungrybox  The baby gets IgA via breast milk. +4
mbourne  @hungrybox, this is true. However, IgM antibodies are the first antibodies endogenously produced before class-switching occurs. So IgM antibodies in a newborn suggests infection. +7

 -11  (nbme20#24)
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ddA on ot teh ertho tn:meocm KMCFEOSCSICA. (Ih wen mA kgnndiri rGaurpefit icjue) is het nmimenoc for gemembirnre hte YC54P0 tshriIb:ino

  • S idumo rploeavat
  • I adnizois
  • C ieidmient
  • K octzaneeloo
  • F cnllouozae
  • A cuet llchooa aseub
  • C hnemcihloorlpa
  • E nrociymiimcrrchyrynath/lto
  • S flsiedonmua
  • C lofpocxrnaii
  • O roeelpmaz
  • M aondoreietzl

  • A driemanoo

  • riGtruafpe cujei
charcot_bouchard  Its not a cytochrome question. IK because i go t it wrong +
waterloo  both azoles and PPI inhibit cytochrome P450. So one isn't causing the other's lack of effect. +8
stepwarrior  Nope. Inhibiting CYP450 would enhance the effect of itraconazole, so that can't be the mechanism. +1

 +9  (nbme20#6)
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nI cre,oyplnsa hrete is a crdtei itonairtns mfor keawsnelfus ot ERM es.elp saBlialcy sitande of noggi gohutrh eht yreal gsstea nda adaryulgl nallgif tnoi a peed l,epes you ujst sydleudn go rfmo inbeg awkae ot giebn in a pdee lsee.p

kamilia20  FA2020 P497(Sleep physiology): Changes in narcolepsy: decrease REM latency. +1
baja_blast  p. 485 for us plebs still using FA 2019 +
randi  FA2019 p. 556 "nocturnal and narcoleptic sleep episodes that start with REM sleep (sleep paralysis)" +

 +4  (nbme20#41)
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atPtotsirsi si aeiazchedrrct yb i,ysarud q,eyrncfeu guneyc,r lwo kbac .pian mrW,a e,dtnre nedalerg e.staprot

eAuct trailecba stiin—atptrois droel men osmt oonmcm eacbiutmr si .E

ergogenic22  In young men it could be chlamydia but the question stem makes no mention of sexual activity, so it is e. coli +11
charcot_bouchard  First this guy isnt older! He may incite Daddy issue but not older. At this age people tend to be more monogamous so E Coli the more likely answer. But again cont NBME 20 trend this one was pretty vague too. +1
monkey  They classify at 35 year old (<35 = Chlamydia or Neisseria and > 35 = E.coli) +3
mbourne  I put Pseudomonas, as that is a cause of prostatitis in older men, but it is less common than E. coli. Just keep that in mind, if E. coli wasn't an answer choice, the answer should have been Pseudomonas. If he was a younger male, then Chlamydia would have been acceptable. +3
brotherimodu  @mbourne I think Pseudomonas is the more common etiology for acute prostatitis in the elderly (>65ish for exams), whereas E.Coli is the more common etiology in adults 35-64yo +

 +4  (nbme20#5)
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oirnegF oybd oanriymtlfma iaflca skin iorsdred edairhtcazrce yb fmir, hirengpe-mpedyt apelpsu nda estluspu tath rae uanpilf dna rit.iucrp aLedtco on skech,e nwilja,e and nekc.

yComlnmo curcos as a rtlesu fo sivhnga (o“zrar ps,bum)” laymirpri fscteaf niccA-aairnmfeAr mael.s

:sgaemI rh/1.lottwpsufrYa

tyggles  A good way to remember this is that the word Barber comes from the French for beard (barbe) and these rashes will be in the distribution of a beard. +2
fatboyslim  Also, it is unlikely to be acne vulgaris beginning at the age of 24 with only a 3-month history +2

 +8  (nbme20#42)
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iThs tietanp has aehtr e.ualrfi laormN PJV is 6-8 H.mmg

Snigs of erath riluafe rae sdeba no iccarad uppm ,syifondtunc iooetgnn,Žcs nad wlo .urfpnsioe

Ssy:ptmom lndiuc e n,dseayp neorpha,ot tf;igeau gssni clinedu S3 trhae uod,sn alse,r raugjlu evnous dintsnieto D)(JV, nad ttigipn mdaee.

 +7  (nbme20#21)
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ihsT is an alpmexe of sgnieSl.h pHeres islxmep dan epsehr oeszrt usesirv uceas roamlnba clel sviiidno ni aedlmpeir slelc, nad shit reestac ucmueileldatnt tanig cs.lel

A kTazn msear wihngso lcdeetautimunl tniag lecls is htsraaicericct fo rallceVai tesroZ rsuiV nf.tnoiisec (VHS ilwl ehva iarilms sn)gifndi.

ergogenic22  other identifying terms for herpes: Single dermatome (does not cross the midline), painful (burning and itching),and lesions in multiple stages. +3
redvelvet  and why neutrophile infiltration, is it a thing? or just a distracting thing? +1
charcot_bouchard  Neutrophil comes into party always first. but it was distracting for me too. +6
dulxy071  Regardless if it can help resolve the issue, neutrophil will always be the first responder +2

 +5  (nbme20#44)
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eaovcRnasrlu dsaeeis is eht mtos conmmo aucse of 2° TNH in t.usald naC be /dt amiheisc ofrm leanr stsoeins or sucrliaarvmoc issd.eea aCn ehar nrael burtis altlaer ot bsiiumucl.

iMan cussae fo arnel rytaer nosisset:

  • trholsectAroeic —ioapxluelrqspam 1rd/3 earnlf o ,yrtaer lsuulya ni rdleo e,alms

  • cauboislmFrur sli—aldsataypsid 2r3/d flrneao raytre or seegmaltn eacn,hsbr usa yulloguny or gdla-ddmiee fem.esla

bLa vuesal sbeda :ffo

  1. eitnsSos dsacseere obdlo ofwl to .muglrlseuo
  2. lrmrxluJutegaoa arsautpap J(G)A sndopser yb egsnteicr nnire, cihwh tvnecors goieennoinsangt to agtnnnoseii .I
  3. getAinonsin I si oedtevcrn ot esinoagtnni II TAII() by nnnistaoieg retnvgcnoi meyezn CE(A -in- )lngus
  4. IATI saseir oblod reesuspr yb 1() ntcncagtroi raaoitlerr mshoot mcl,seu agnsincrei aottl leiaehrppr rnscietsea adn ()2 rogionptm ndrlaae eaelres fo on,deoaesrtl chihw sacsreeni abosrpteoinr of smodiu ew(ehr a+N sgeo H2O ilwl llwo)of ni eth sadlti lnuootcevd etulbu pdni(aexgn paamls o.uve)lm anC adel to elmkoaihypa s(ene in eth lbas rfo tish suoieq)nt
  5. Lased ot HNT tihw eceriansd aplmsa neinr adn lialtruena rypaoht de(u ot olw bdool )fwol of eth fecetafd dekyn;i trnheie tareefu si ense in mipayrr enhoepnsytri
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. +7
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

Subcomments ...

submitted by yotsubato(961),

Lactose Intolerant I guess? Not Celiac. Kind of a bullshit question.

study_dude_guy  Had the same reaction as you and then I learned that AA is a buzz word for lactose intolerance "African American and Asian ethnicities see a 75% - 95% lactose intolerance rate, while northern Europeans have a lower rate at 18% - 26% lactose intolerance" +  
seagull  I also choose Celiac's. "BuT RaCe AnD mEdICiNe DoN't Go ToGeThEr". +  
hayayah  I think a key part to differentiate between celiac's and lactose intolerance in this question isn't race, it's because of the part that says "he occasionally had diarrhea after meals since 12 years old and then it got worse since starting college". If he had celiac's he'd have GI symptoms (i.e. diarrhea) any time he ate something containing gluten (which would be every single time he had a meal) since he was 12. You'd also see signs of fat or vitamin malabsorption in celiac's patients and other autoimmune symptoms. Whereas in lactose intolerance, it's much more likely he'd once in a while eat a lot of dairy and have his symptoms triggered, and then he starts college and has even less of a well rounded diet and so his symptoms get worse. +2  

submitted by mousie(209),
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sI 45 mituesn too ongl to eb lhpiyaaactnc nad dwoul the sbneaec fo hras auractiir(, trr)puusi RO ayhcc?piaantl

hayayah  Yes! Allergic/anaphylactic blood transfusion reaction is within minutes to 2-3 hours. (pg 114 of the 2019 FA has a list of them ordered by time) +7  
hayayah  (also allergy / anaphylactic presents with more skin findings (urticaria, pruritus) +6  
seagull  The time through me off too. I though ABO mismatch since it occured around an hour. I thought TRALI would take a little longer. +7  
charcot_bouchard  Guys anaphylactic reaction to whole blood doesnt occur much except for selective IgA defi. so look out for prev history of mucosal infection. And it can have all feature of type 1 HS inclding bronchospasm. +5  
soph  I saw hypotension and though anaphylaxis........ -.- +  
usmile1  Chest Xray showed "bilateral diffuse airspace disease". This is much more indicative of TRALI than anaphylaxis which would have wheezing and possibly respiratory arrest but no actual damage to the lungs. Additionally there was no urticaria or pruritus one would expect to see with anaphylaxis. +5  

submitted by mousie(209),
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Is 45 nuisetm oot long to be yilcpacatahn nda udlwo het csebean of rahs a,irrutc(ia up)trsuri OR laaptinyhc?ac

hayayah  Yes! Allergic/anaphylactic blood transfusion reaction is within minutes to 2-3 hours. (pg 114 of the 2019 FA has a list of them ordered by time) +7  
hayayah  (also allergy / anaphylactic presents with more skin findings (urticaria, pruritus) +6  
seagull  The time through me off too. I though ABO mismatch since it occured around an hour. I thought TRALI would take a little longer. +7  
charcot_bouchard  Guys anaphylactic reaction to whole blood doesnt occur much except for selective IgA defi. so look out for prev history of mucosal infection. And it can have all feature of type 1 HS inclding bronchospasm. +5  
soph  I saw hypotension and though anaphylaxis........ -.- +  
usmile1  Chest Xray showed "bilateral diffuse airspace disease". This is much more indicative of TRALI than anaphylaxis which would have wheezing and possibly respiratory arrest but no actual damage to the lungs. Additionally there was no urticaria or pruritus one would expect to see with anaphylaxis. +5  

submitted by dubchak7(1),
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heyT sstggue oltMsopoisr ot otnuretcac s.DAIN.S. yhW nto ?PsIP

hayayah  PPI's don't have many side effects! If the question didn't involve the diarrhea side effect the answer would have been to give her a PPI. +1  
tsarcoidosis  I guess one takeaway is that PPIs don't directly cause diarrhea, but they do increase the risk for C-diff, which causes diarrhea. +12  
usmleuser007  PPI side-effects: + increased risk for C. diff + Increased risk for resp infections + can cause hypomagnesia + decrease absorption of (Ca2+, Mg2+, & iron) + increased risk of osteoporotic hip fractures (d/t low serum calcium) +1  
temmy  The patient got severe gastric burning and discomfort as an effect of the drug. My logic was since the patient was taking an NSAID it had to be a COX 1 inhibitor that destroys the protective barrier of the GI mucosa due to inhibition of prostaglandin so we needed to treat with a drug that will regenerate prostaglandin and prostaglandin is a vasodilation which might be the reason for the diarrhea. +  

submitted by docred123(6),
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Wyh si hte wenrsa to ihts ostqeuni tno hiveAsedi .l.spaC.tisui

hayayah  Adhesive capsulitis causes severe restriction of both active and passive range of movement of the glenohumeral joint in all planes (especially external rotation). +22  
catch-22  Adhesive capsulitis is aka "frozen shouder" so you can expect exactly that. The entire shoulder will be hard to move in all directions. +3  
meningitis  Since it says there is NO impingement sign, it cant be rotator cuff tendinitis correct? What other signs eliminate this option? +  

submitted by moloko270(64),
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nsormy"ed fo lta"onliudi omilolpas"thyyo- in ereevs etcvoigens tareh reafuil yma be adceus yb na piarloirayeptnp ghhi AHD oeesrtcin in ichhw the eromeorpotcs mtesys si manodtdei yb rnooamlson il"imsut

hayayah  Apparently, in chronic CHF you see hyponatremia. Because CHF causes a decrease in cardiac output and circulating blood volume, which in turn triggers a compensatory response aimed at preserving blood pressure. This stimulates the body to retain both water and sodium. +7  
seagull  i agree with Hayayah... the RAAS system is activated due to poor perfusion to the kidney due to decomp heart failure. +4  

submitted by sklawpirt(28),
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I hnkti the idae eher si sypiml htat noe dhouls kihnt uaotb weher isvecesl aer nmoigc mrof on hriet awy to hte gligo oexpmlc.

"woT tssep rwroadf nad oen estp "kc.ab lclcepyafiS eth stueiqno amy eb ergrnefri to a rrae iiccfloaraan d.eirrosd na seaawrness of atht eiasdes si ton rnsc.easye tahW si yessnerac si dsreanugnidnt the oigrni mrof hreew ceselsiv rea ktecidfra ot eth iglGo

ICOP intreop is ddeeen to oact lecevss fmor hte RER to ensd to .iglgo ,usTh ihtw a animoutt ni that iopre,tn the cgaapedk itpnores atth hdulos belb off nad eb stne to eht ,olgig iaendts cmuetaulac ni eht RER nda eltdai it. sTuh eht enra.sw


hayayah  pg. 47 on FA got the good visuals! +5  
notadoctor  COPII* proteins are needed to coat vesicles from the RER to Golgi. "Two(COPII) steps forward; one(COPI) step back." Anterograde goes RER -> Golgi -> Lysosomes/Secretory Vesicles -> Plasma membrane +22  
titanesxvi  why not small lysosomes? +3  
varunmehru  and I thought large lysosomes due to lack of enzymes to degrade +  
samsam3711  The size of the lysosome is not affected by the presence or absence of protein, but its function is compromised (eg. protein is getting stuck in the RER) +  
fattyacid  I hope this helps to whomever was lost like me Null mutation: A mutation (a change) in a gene that leads to its not being transcribed into RNA and/or translated into a functional protein product. For example, a null mutation in a gene that usually encodes a specific enzyme leads to the production of a nonfunctional enzyme or no enzyme at all. +2  
pingra  I think you made a typo: COPII (RER -> cis-Golgi); COPI (trans-golgi -> cis-golgi and cis-golgi -> RER), clathrin (endocytosis and trans-golgi -> lysosome) +  
kevin  So my thought process was if there is no COP signal then instead of going to Golgi it would be sent astray into cytoplasm, akin to how in I-cell Dx the enzymes get sent out of the cell since there is no trafficking signal (therefore I presumed large lysosome due to eating the aggregated protein). Are we saying without COP or Clathrin that the vesicle will simply stay put where it is? If I can get a reply before my exam (2 weeks) that'd be much appreciated +  

submitted by _pusheen_(6),
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I ithnk isth oen si atryllile stju gakins thwa trap of het ydikne lliw be hte otsm ryoolp despuref. Tath part oulwd aehv the otsm rnei.n slA,o teh admlelu ds’eton heva GJ clesl so I ugess ’tahts nrhteao rneaos why ti contd’lu ehav eht msto i.rnen

sklawpirt  Exactly, it has to do with where in the kidney renin is released and requires a bit of knowledge of the artery branches that give rise to the afferent arteriole in the first place and where this branch point is located. Where renin production occurs in JGA cells, EPO production occurs in the renal peritubular interstitium (especially the proximal renal tubule, corext and some of the outer medulla.) Thus with the same questions stem it might ask where is concentration of EPO the highest? [And it would still be the cortex, with lower concentrations in the outer medulla, lowest concentration in the inner medulla, and none found in the papilla or renal pelvis. +12  
hayayah  Actually, the renal medulla receives significantly less blood flow than renal cortex. So the medulla is the one that's very sensitive to hypoxia and vulnerable to ischemic damage. I don't think this question is related to "what area is the most poorly perfused." It's just knowing that renal artery stenosis is going to decrease blood flow to the kidney. JG cells sense the decrease in perfusion pressure and secrete renin. Knowing that renin is produced by the JG cells and that JG cells are in the cortex should be enough to answer this question. +6  
cry2mucheveryday  I thought all the renin would collect in the pelvis where the arteries whould drain into a common vein and changed my answer to pelvis ._. +2