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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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sMto pmlsbroe ihwt elcl sidviino rcouc ni aehapnsa of osieisM .I

realfakedreams  @hayayah - made an account just to say thank you. I appreciate that you exist. +15

 +6  (nbme23#39)
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eofbrlzFiim si a fr,teaib euds for rioelgwn TG .eesvll

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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moaboCol si an eey ylamarontbi htat scrcou bfreeo thirb. er'hyeT snimsgi eeipcs fo iesstu ni rrtsscuetu atth form teh ye.e

  • laooCbosm atgncfief teh r,isi whihc rtulse ni a ylekh"o"e nacrpepaae of eth upipl, egrnyella do ton aled ot sioivn sosl.

  • oaboosmlC vovnniilg hte aenrti reults in vonisi loss ni cfiiepsc aptsr of hte suliav fld.ei

  • regaL aelirtn bsoolmoac or sohte icnfgtefa het tciop neerv cna acseu wol iionvs, hcihw mensa isvnoi lsso tath nncoat eb etpmlleyco credoecrt iwht ssgelsa or tntocac sels.en

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 hsa celfa nccnenioneit os ish atenxrle esihcrtnp si e,mdaadg chhiw is trvineaned by eht pdunaedl n. )(.-S4S2 ehT pevicl lciaphnsnc vsn,ere cihhw meiedat het trecinoe oerscp,s ear osla -.SS42

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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ibocCarn hsrndyeaa hirnbitiso ge(, aetoecamial)dz adn lpoo rusideict ,(ge r)osdifumee aer totuhgh ot xeetr thire effcte on PCI yb rdenicgu aclserbprieno iufld )C(SF ocutnprodi ta teh drhcooi pxsl.ue

oGgoel says ahicmmsne si unnkwon L.LO

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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hisT is a tetpian ceas of apurtotpsm dttsoihyiir. Cna isare pu ot a reya aetrf iyeevrld nda sah thpyccmlyio lnriittfae.

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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enPycgarn + xH fo itsmhboosr -;t-g& thnki oliphndppishotia neosdrmy

heT TP adn TTP rea opongdrle d/t freicrnnteee fmor the tioeisdanb ot ooidihs.hlppsp iTnmrbho tmei orlnma.

aHd ot fnid heasercr rlictesa otuab it os ktae ti rmfo hree nda nt'do wesat ryuo .tm.i.e

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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owGhrt ooermnh aneersigl nroomhe cats vai pucdloe-G rtseceor.p G deopucl trrecsoep edne PGT to boeecm eaticavtd adn sPaGTe to cemboe d.vtieaitacn

No TsPa-eG &;--gt rlacicnohyl taivce htwgro omrhneo isralnege nromohe reroeptc --g;&t otntsacn nicaaovtti of nalyyled sylccea / MPAc wpyhaat and eeerlsa of towghr .hroemon

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 in eht eamgi is hte aslml tenn.esiit stI itcahcrsaecirt fhareyet raneappaec etfar a aurbim aeml si ude ot npertmean iuccalrr dslfo and iiv.ll ehT vllii gvie teh lalms tetesinin a trgea acuomsl ueacsfr arae.

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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PHLLE n:rseoymd leoH mdvss iaetlEey vrieL enwzoeLsm y .ttlseaePl

A stniemanfatio fo eseevr pac.esarmeipl oodlB mears sshwo Cna elad ot IDC nda eitphac bsacmshleamrutaasupo Ž puuerrt Ž veeesr yhsoe.tnoipn

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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nsttC-icsenieyeey ocmenhiek trroepec 5 5R)C(C si a pionrte nduof no eth raufces of D4C slelc.

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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idxMe oeuvsn eongxy tsraoiuatn O2(S)v is udeamers ni eth pnraumoyl .artery O2Sv epmsals eth rtue exdmi usvneo blood ainvelg eth htigr ahret. arumtneseeM fo xdime veuons xgneoy otitunaras )(SO2v ormf teh rlmpoyaun ertayr has eenb acedtavod sa na ertdiicn ndixe fo tessiu gnxo.iyteaon

In cdiincaerog shkoc ouy aevh aedscdree OC tg--&; areecddes O2 ldvreeiy -t&-;g seacerdde OSv.2

 +4  (nbme21#8)
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sKoW-kinofrefackre onyrm.sde 'otnD eavh ot eb an lcihaoocl ot tge hi,ts tujs uuyalsl is rtlaede to smhacoolil / aetmnihi ciyidn.efec

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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ehT oytihdr si pdsepiul thwi trelaria odbol mrfo eht rrupeosi yhdiort ryarte, a arbcnh of hte laerenxt tciorad yrraet, and eth roirnife htyiodr rtrea,y a bnarhc of teh arvtycorlhice tunr.k

 +7  (nbme21#40)
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o:teN ehT dcnebusa n. si catuyall eth vreen tsom lkeily ot be aadgmde yb an xpngeiadn rltaenni ricadot nmsayeru ni the vonuacres sunis btu tyhe egvi uoy cpicfesi 3NC uiotcnnf in sthi n.ouqiste

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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eth iarjtmyo of robanc oixidde coellsume ear eaidcrr sa rtap of het tiocrabnbae fruebf ss.tmye nI tsih se,smty boracn eiidodx udfeifss toin eth RsC.B Crcbonia ysreaadnh (CA) iihwtn BRCs luqkciy ntsoecvr teh onrcba diioxde tnio niabcrco ciad )HO32C(. iCnarcbo acid si an tlaesnub inimreedeatt uleloecm htat demmtiliaye ticoisesdas ntio ntcbairaoeb nsoi HO(C-3) dna dyegnhor H+() s.ino

Teh wenly nhydestizes natiebracob oin si tptraerndos tuo fo eht RCB otin teh salpam in chgeanex orf a rodhclei nio l(−;)C sith si cdllae eth hlcoeird ht.fis eWhn eht obldo aheecsr teh ,lgsun hte eoaabtnrbic noi si oarpetsrntd kcab tnoi eth RCB ni xgeacnhe rof eht hecldori nio. Teh +H ion ceadistosis form hte bhoelnogmi adn sndbi to eht bibacaretno oni. iThs spdecruo het bainoccr adic tneiiera,temd cwhih is cteodrenv ckab oint aorncb ixdiode tohurhg the eaicmyztn ctniao fo CA. Teh brnaoc oiexdid roueddpc si epldelex roguhth hte nlsug guindr iloh.taxean

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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otMs hmuna snraecc aer t/d a olss of ointnfuc of P5T3

 +7  (nbme21#1)
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aseivnvI lcceriva mcnaocrai is atcioedass hwit irndhhpesyoros dna areln aiuflre t/d CA anieprgsd hghrtuo nteirue lalw nad ntoi het .ardbeld

 -1  (nbme21#28)
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oAuhthlg alhf eshet sonreomh anc autcalyl alos be seertced mfor eht udodmun,e eht emdundou si oitaadscse eth somt whit KCC rs.eleea

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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pyLmh olfw tear si lyusalu lo.w It is dleenfiucn pimiarylr by het aetr fo hmpyl nfo.otraim Fro aeexlp,m fi lbodo apycrlali prrseuse is cndeesira yb raetrila oavsoliinatd or osuven c,stooincitrn eht oflw aert of mhpyl racssnee.i lsoA, the olwf eart is etadceff by oioscpenmsr of syaihmtlcp by rcnocoattin of iiohgennrgb uaclesruumt nad by aniegevt ihcinaoatrrct epuerrss )inhtbe.a(rg

aiItittlersn usepresr (os rsuprsee in het E,FC hihwc wdolu nsareice if iengv VI slnea)i dan hlpym ofwl era seyliovtip latedre. A amsll csrenaei in eritttilsain veouml trlagye ssrcaneie its sesrrp,ue pmtgirnoo mhply oflw thta cats ot retrseo het itatieltnsri volume ot rnalo.m

oerm on isth iopt:c .//nic.sBo.thht5wgmK//pi8b:lsno3b44nwN.ov/wk

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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acrtueeypH aslaptnrtn tocierenj rccsou nitwih seumnit dt/ ngiexseptri- iiecenptr bsdnioetai taht reatc ot doonr tnieagn pyet( II tishnsyeiyvrptie i,treao)nc tetviaca ptl.noemecm

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

 +0  (nbme21#14)
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itmresniC gncloae(itn yrmyiop)dthisho si teh tsmo oommcn escau of ttbraeael tmalne ybsaidtli.i eCusas opor bnira v.letempeodn

 +19  (nbme21#50)
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eathrCte ecpmn:ltea


alelcR htat het guln epxa tnsdeex ovbea eth sirtf .irb

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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Schrtte ro tonaliid fo eht cvrxei dan aaving era gosntr iitlusm for tnxcioyo sieenoctr, ddeeimat yb leunar aasypwht declal the neFougrs x.rleef

lercit:A chpe/uw//roc:nxpiwso-/itocdefweecei.rlcnesof/.erctrtngmsesiucsnte

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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hsTi pt ash na DSA hchwi is a ""hoel neetweb eht AL dna AR. xnFgii it dcoul aagemd the AV .nsuelbd

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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eRlna terrya tnsoessi is igong to cdseeera odbol oflw ot eth idneky. JG lescl snsee eht eaesrcde in oupienfrs urserspe nad erescet rn.ien

eniRn si ueopcdrd yb the GJ c,lels JG sllec ear in eht coxtre (etyh are fmdieido hoosmt umecls fo het aftfrnee oaeir)elt.r

 +10  (nbme21#47)
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enSaycord odtpyaayrehprsmihri (yslluau t/d ichorcn erlna rul)afe.i

Lba ingfnsid udeinlc ↑ HPT ps(snoree to owl m)uilac,c ↓ resmu iucmlca al(nre uie)ral,f ↑ semru eotpahshp nelar( ,iraleu)f nda ↑ ikalealn shhepsoatpa THP( aitvctagin ltsaootBs.)se

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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eowrl anortnduaipqaa: eliraatp soneli

vs ueppr nadapnaruqatio = raeotmpl isnoel

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. 19 fo FA sha a qkuic ennxtlpaaoi rof s!thi

llayicBas oecn ye'rou ni a antsgirv taest et'hesr itsll chpetai gusgelioeoncsne igong no as( llwe as sinug FAF) tub eth sionesenoeglugc si ongmci mrof lrpiheerpa iestsu ecalatt dan n.ianale

 +8  (nbme21#19)
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shTi tp sah oselaaimotca / kiercts csien( s'eh a dk)iod. deuCas yb edeecfvti nmntailiziorea of dotseio caiaas)oloem(t ro ngcitraailsuo ghtwor tslpea ikrstec,( oynl in hi.lcd)ren

tosM oolncmmy d/t iminaVt D e.eiicdcnfy

hCrenlid whti eitcksr hvae gotcpolahi obw lsge egun( )urm,av -kdieaebl nscoodotahcrl unoticnjs icrh(tica as)rryo, rnasbaoctie tofs( kl.uls)

  • c.De inaitmV D anlo(rm ofnictun si ot oaerrbbs 2aC+ nda )4OP

  • .ceD ersmu 2C+a

  • Dc.e  mseur 4PO

  • cI.n HPT

lovebug  FA2019 455pg !!! +

 +10  (nbme21#31)
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ihtW htis sneqt,iuo I tiknh they nwta oyu to rzgcoeein ttha the ttaepin snt'i vianhg cehts apni tdleare to teh rath.e heTy shepizema arevles ibr raftcersu and a xemrnoopuhta tub dno't tiaindec nay ertha eaagmd clka( fo doiatstuienv odnssu = no olnmyupra madee ddatineci or a gnul ssiue lderate to htare lmpor)eb.

hTe reitdaspicir is ahtw's rideenntav by the ipnrhce n. geeSni sa hwo ihs ehtar si ,enfi the atdfeucrr ibrs era olbrpbya ahtw aer isanucg him ainp aiv teh aseotilntcr envsr.e

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 edesarv ceftfe of exnydclyico is pniivty.stoesihot

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. sha iFalliam ldsdiyiipe.sma pyTe l.ymyac—nHrcohemepirIoi

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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annvitlrpeHoteiy saeusc redeadces aC2OP wichh ebtqenyuslus asdle ot aelrtari conassotivtionrc uths wegnoril elbrcrea oodlb flwo C,B)(F lrebcear odlob l,mevou and .PCI

He tnaws ot iscnaree PIC albreec(r aidloi)ovtsna hhicw eh nca do yb eedargcnsi the trrispreaoy atre tytehlinao.p()inov

 +9  (nbme20#21)
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sptiiyHerestniyv —moimdiiepsxuentn ptye IVI/II ypyhtveeiisstinr cinarote to iatmrvnoneenl tgei.nan esusaC ,pandsye gho,uc thesc snhs,egtti .headheac Ontef eens in msferra nda eohst eexpdos ot reRivebels in leyra atessg fi tlsusmiu is

st'I a pyte of rteicersvit glnu edaess.i

 +1  (nbme20#32)
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Gugoaan:lomc mourT of nipatecrca α lelcs igcŽnaus an tveournrpooidc fo c.ulongga

ssnterPe hwti 5s’D:

  • lsteoyamcii(itntrcreD gtramrioy rhety)mea
  • biDeetsa per)meic(yyaglh
  • TVD
  • Dngenlcii heigtw
  • psroeiensD
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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lnoornZellgii-Esl eoyrsdnm: trerieiGsn-cagnst morut sm(r)tnoaiag of carapesn ro .dndueumo

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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heS hsa a nitmvia C yfeciicn.ed cryuvS eruetfsa nlsewlo gus,m ysae uisgirnb, teehe,cpai rcioaelufplrli adn rtaosulsbeepi re.rahemohgs

 +6  (nbme20#31)
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onIr odevsoer is a auces fo a ghih nioan pga itbmoclea i.oidsacs

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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ihsT si a riympar tnaercl envrsuo msstey mlapmo.hy otsM nylomcom tdsaecsaio wthi IHD;VSIA/ oesaphnegits ivsevnol BVE ncio.fietn

eidrsondeC an ieISnAid-gDfn .lnsisel bVarleai p:soneitarten cnuosni,of meymor slo,s .uesresiz assM n(loseis) m(ya be gnrannehcn-iig in iopidsmrcmunoomem atn)itpe no M,RI eends ot be dsiinueishtgd romf islxsmoatposo via FCS snsilaya or oerth abl Toxo uusylal ahs lielputm nrgi ainencghn neil.oss

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

 +15  (nbme20#17)
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As,lo uoy 'onusthld eb isngee nnadorg-e aegmad or adrnieecs rnine / dneiky nrpesose ithw a luprvyoesi eahythl ttpnaie ttha utjs dedplveeo eainstesl NTH. Teh dboy estdon' atnw ot icaeresn nneir ewhn ti ash T.HN ,reeoHvw if you vhea is,esnsot eht knydies kerfa otu cubaees r'teyeh tno igntetg guneho wlfo nda tihnk the whoel yobd nts'i iee,thr os eyht eiacttva the SARA sy.esmt nWhe uyo egvi hemt an ,AC-IE the rnine si ltisl gnibe ruepdcod by het edk,iyn it juts sn'ti ngbie rdvencoet ot ie-ntosIinI.nag

To ianteelmi tehor :scciohe

  • eH has dsiernace innre itcytiva so oyu nca leetmaiin rimrpay enrtsoa.oidlsm hatT sha oonldt,raese d.ce nn.rie
  • No ngssi or ssx of hCniss'ug so athst'
  • 1xs-y1-reaBoylhd eiyidencfc woudl ssx hiwt hte ligitaena. o'udY veah edc. rneni aivtiytc -ei(olrtadeenloks tcsfefe lslit n.seepr)t
  • eslEsiant T:HN ieaenxlpd abeov
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 rcfaedtru mrbocriifr petal netr(roai lslku ata)rum anc utrles ni kilaegn of snepriocbrlea dlifu iton teh onse nad olss of ssene of leml.s mSell saypl a elrga reol in teh orciptenpe of seta.t o,S ni ccaptri,e a aepnitt yam nmloapic of slos fo ttaes rehtra hant of .slmel

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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uoY hvea a 5%2 ceahnc fo treinihign the msea LAH smrkear as yuro nlis.gibs

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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eingnB tumsor aer lusayul eldldnwefirf-titeae nad lecra,le-wdetdma whti owl tmociit yt,cvtiai on ms,setasaet nda on nesc.sori

lainnMgat outmsr c)enrc(as amy swoh rpoo iar,tdneifitefno iarctre rotg,hw caoll inaionvs, mtasesis,ta nda i.papostos Hhig titiomc vitic.tya

Fat tmsou:r

  • :mpoLai bn,gnie wlo ictmito ctaytivi
  • isaamcoLpor: mltaaingn, rneiedacs iocmitt vyittcai
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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Bate keobrscl as rtcaihisatmynrh rsspspue bmanolar prcmaeaesk by riacnseegd eht soepl of eahps 4 -gt&-; rglpgonnoi apehs 4.

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

 +1  (nbme20#12)
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ePvlic nnpsihccla nresve ear ptra of eth tiphaayctmaesrp smyest.

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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Donw dnmeoSry asbL:

  • inc. luhacn lnercnutsacy
  • nc.i ChG
  • .nci nbniihi
  • cesrddeae PFA
  • rddcseaee PPAPA
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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s'tI atnstnlarioi lcle cn,marioac hwihc noikgsm is a onomcm kirs crfato of;r it acn ioenvvl the nalre capsi/eelv.cyls eTh toish meiag hossw the piralylpa netura fo hte rtomu evr(wohe it nac oasl eb aftl or danorlu ncodcirag ot mP.oth)aa

Also konnw as hutreliola ocaimrnac. tsMo omcnom tumro of nrauryi ctart tysesm n(ac uorcc in arenl ye,asccl nlear ,slvepi e,sterur dna d)la.dbre anC eb etudgessg yb enssplai heruamati no(

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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gsaDinsio fo h:pyS usleiVidaz by flneonresuumcmoiec ro eriad-kfdl ym;sicocrpo oeyrlgso si mtrinptao – owt espty of :otnsedbiai

  • bA sbndi ot cinaipidorl: na niegnta fudno ni mnaamimla iodlrntiaomch bemnsmear and in sremt;epone a aehpc sreuoc of gntneia si cow ahtr,e ihwhc is dseu in ncegsinre ;sstte evry sisvnieet ni mriay,rp ctxeep e,aylr nda secadonyr iilhpssy – eitrt mya eniclde in tirteayr and htwi tnee;mtart ubt otn ficspiec – umts cformin hitw A.-BFAST
  • selaEmxp dilecnu leraVeen essieDa Rhreseac Lab ,L)(VDR adiRp apmsla ngiaeR R(,PR) atmdtouAe negRai Ttes (R)A,T ro eabnciRotnm nenitAg Test C()IE

  • Scicpife estst fro rmalpeeont bytiadno rae omer esxneevip; saetleir ntdeioibsa dnbi ot sioteshcrp:e eehst sestt are eorm iefpcics nad etpiovis erilare; asluluy irname seitivpo fro fie,l tub tivopsie n eansptti iwth eorth emeroapnlt adiseses dan mya eb ietopvsi in oo,Mn ,RF u,upsL ,seyrpoL mieL, dan ugrD

  • eTh tmos weldyi dseu si Fetneocslur Tpoernleam Atoibdyn- oAbptrsnio -ABA(FTS) ro Tmneeoarp adimllup glamionoagihinrtumetc PHTM-A()

 +15  (nbme20#17)
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Tsih si tieeacrv ctaiylohyepm vra,e ciwhh is due ot hihg ultditea ro nglu sed.asei O2aS si ol,w dna PEO si ercea.sdin

Anhoret ywa ot rapochpa eth netqiuos is nlkooig at the ldboo .amres tI's yptert rolamn no( erays,ceokmyagt no eaicesndr meburn of ,lelaesptt no rdos, nitohng leub, )cte. A ldboo smrae rmof a OPCD ieptatn llwi be a.nrolm Juts na nrdcaseie rneumb of BsCR due ot hte idaerensc POE indelga to irsceedan bg.H

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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eHs' not egniat uneog.h

nOe of 'cirsltsoo fscnotuin is to eeirscna s,nueoecgisnelgo ilyols,pis and osptoeisrly.

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 si a tiroenaepnts fo andoichmrotil .yophmtya eyTh tofne prsntee with yya,pmhot ctlcia cisdasoi, nda NCS iadeess. 2° ot rufeila in eaxdiivot tohliahppysoro.n Mlcsue yopsib nfeot ohssw daegrg“ rde rf”si.eb

ehTre si brelavia isxpesoern in a nplotuioap ro eevn nwtihi a yimalf edu to moaspteyehrl ni rhcimnitldoao neriencihta.

 +6  (nbme20#18)
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ihsT man si ihsngwo ssx of an .MI

iitalnI pshea of aomyidalrc riconatnif esdla ot cuenlodasbrdai rsnceios onnvligiv t;l& 05% fo the araymdicol cetsikhns easirolcba(dndu i)icnnt;faro EGK soswh Sse-eTmgnt sepsneorid.

Citnuonde or erevse scheaimi &t;g(02 tisumen) adlse to rlasnumrat snsrcoie vnnigoivl mtos of teh damicylaro lawl rtsmnurala( i)not;cfnari EKG swhos TeteSnsm-g litona.vee

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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vcDfeiete hmouloosog oobnnmatcerii is snee ni aoteiarsarnbv/ cnercsa whit eth RC1AB enge uaotm.nti

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 +6
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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mFlliiaa ooedastmuan polssoyip si na tuosmalao ntndioam otu.tamin sohdnTaus of slpypo sriea rtigntas ertfa uytbper; al;cnoonicp yaswla vvloisen ucetr.m ctiPrlchpyao myelocotc or lese %010 rrspgeso to CCR.

osutmloaA otdanmni esisaeds vh,ae no gea,arev 50% ncheca fo gebni essadp dwno ot isrfo.pnfg

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 gib tnhgi eerh too si icontign htta het APL is c.dareedes Osltstbaoe iicttvay si drmseaeu yb oneb APL. I iknth hatt wsa eht aimn fucso here and tno ahtt ouy esneyslacri ndee ot nkow eth ABC1F eneg a.inmttou

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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ostM tnartimpo auesc fo ilvar dicmyarotsi is ieaCscxko pir.uisoncv(a)r

 +4  (nbme20#3)
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Most orsriitcent eznyesm nbid m.nldaproise

So obht CCG'G5 ro GCC3'G dowul aehv nbee cacpeabetl in htsi asrocen.i

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 oeicurkyat ,lcsel tow mrjao saeptaywhht— auequinosb-ptimoeitr tyaahpw dna mloasyosl epodt—tesmylairieos oepinrt dgardt.ioena

Teh ajorm ptwhaya of cilesvtee eoipntr rtadiogenad ni cuioteyrak lclse sesu buqnuitii sa a maekrr ahtt trteasg ioylosctc nad cualner oriesptn for padir

ehT heort roajm haaptwy of tpirneo adrtongidea in yeaucritok clsel ivnsevol het pkutae of einorpts yb oosslmesy nad gtesindio yb oresptaes.

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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Pt hsa dbetiase dspi.suin

If inreu enrtctconase tiwh otadanrnmsiiit fo DHA ag,laon teh eidksyn rea seonsrveip dan teh pboelrm si tihw ADH rtndcooupi ni eth hhaouplasymt ro eeresal in the otps. utrypi.tia

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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iPtaten sah rnccoih drahaire galdeni ot lbetcmoai oiis.dcsa rRorasiyetp tnaipomnsceo will elda ot erdcaeeds C2O rpr(iratyeso laassokli avi nhpo).yanerteliivt

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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uuqaSmos ecll oaacircmn cserthaisaict:cr tit,anciaov laaichmercype, atdceossai whit nmiskog.

malSl lecl may cllytaua edroupc oeiadsbnit ngatasi ripepsyacnt aC sl.nnheca

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

 +4  (nbme20#45)
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utleAsbo k:sir the ffniecdeer in rsik nt(o eht npopior)rot ttbtuaerabil ot the nevioitretnn as dreapomc ot a nootcrl.

.1)(2 - 40)(. = .80

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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epiStc hsokc si a tpye of dvusetriiitb hsock hcwhi is mdekra by smiaves iotinvdolsaa d(t/ yrmtaifmolan )spnresoe isngcau rsedecead R,SV eacddseer alerpdo / C,WPP nad adnesceir .OC

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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Alpiluoornl isinbthi netxnhai ixdos.ea It is dsue rof rhcinoc toug sa ellw as nviepentro fo utrs-molisy sadstocaie atrue horhepntapy.

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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Teh nyol temi you strnauesf a h'vhaseJo eitWsns taietpn is wehn teh pantite si a imron t8;&l1( yeasr d.)ol

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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ntiysSviite estts are sdeu rfo i.cnesenrg yitipeccfSi sttse era sude orf actrnifmnioo artef oiptvsei c.gnnreeiss

tyiivtenSis ettss era deus for sigene owh anmy oeelpp ltury ehva the siasede. eypciSitifc sestt aer rof oshet woh do otn ehav the

A hlhiyg visienste ett,s nehw ti,evagne ueslr TUO sedesa.i A yglhhi iicfecsp t,ets wnhe ipi,vstoe eulsr NI oS, a tets wthi with low sititineyvs nocnta urel uot a as.idese A sett whti olw ficyesitcpi cnat' reul in asdesie.

ehT roctod nad aiettpn ntwa to snreec orf nocol naercc nda eurl it .tuo The coordt loduw nwat a estt iwht ghih etssyitivin ot be aelb ot do a.tth eH snwko thta eitnsgt hre otosl orf olbod will ton eulr otu eht itpbosyliis fo onclo CA.

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 gea ,75 the hutmys is elltti rmoe ahtn tyaft tess.ui lytFuntearo, teh tyhmus pcdeours all fo royu T celsl by the mtie you cahre brtu.ype ehyT rea dlevloni-g nda att'hs wyh yuo cna lsoe yoru utysmh uhtwtoi atminrmipe fo yuro ueimmn e.smsyt

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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HRnG osagtnsi kile oleipLrdeu are eeiftecfv ofr sneitatp iwht tbears AC saebecu fi vgnie ni a intcsunoou sfh,inao they wurdtelonaeg eht HnRG rceopter ni eht tpairyitu and mteuiyltal sdecreae SHF nad .LH

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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anCllici sue of r-gaispnK i:rcediust

  • oinpedayrstremslHo
  • +K nlepietdo
  • FH
  • piacteh icssaet eaos)iroc(olnntp
  • ipnnoceehgr ID e()ioaidlrm
  • aogdnrnteani
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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bStnsceua P (SP) si an puaepneicetdd sepretn ni eth NCS dna teh hlirpreape ruovsen ms.esty A moupncod tgtuhho to be ndevliov in eth yctpaisn snrmsinstioa fo iapn dan oerht neevr epsl.sumi

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

 +5  (nbme20#28)
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anHddr-iicuneep neotmioychatpbor H)IT( is eth epltmdeevno fo gIG sbteniadio aiastng harenip udbon etaeltpl rfocta 4 FP.)4( tpyoie-nF4nAibrPh-da clxepom etcaaistv ellpttaes Ž iotssbrmoh dan crbhinatpeomtoy.o Htgseih iksr htiw ttaioufnrdcnea pahei.rn

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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LV etppdos wg,nrkio serresup dabcke up onit pulm uPlm iurctci oghulyr is adme of 3 as"p"tr - eth lspa,icilear itseitiranlt ,paecs and eht evloia.l

nI aeocricingd hco,ks the atrex obldo ecsaisenr lpyarilca oirthayscdt psesruer, idngirv iufdl onit hte iisnltrateti a.ceps apdeCorm ot the iavll,oe hte isitleitnatr apcse now hsa mroe lifdu ut(sh oerm ltiirsetntai scryadthtoi useerpsr and ssle oiccont rsesreup eud to riota fo fuidl to r,opietn) dna sa a utlres fo htis annbanucigl fo eof,crs fduli moves into the olialev -tg;&- yrmpnoalu e.adme

 +8  (nbme20#8)
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pyhrAto si csaeerde ni issetu asms eud ot rdeeseca in zise r(diaescne tyknetsoocle igadratndoe iav qirnom-ibtetaouiepsu ywtapah nda uayohpgat;  drecedsae ipotern hsnyssi)te rodn/a erumbn fo clels )tso(pis.apo eussCa dculnie dei,ssu ed,vrannoiet slos fo boold ppu,yls osls fo lohmaron ,ittonilamsu orpo

mambaforstep  FA 2019 pg 206 +1

 +8  (nbme20#25)
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Mtos ommnco acues fo rsciagt uleott obtruiostcn in nsatn.if Palebpal io-vadhpeesl mssa ni rcipgseiat onire,g vieblsi rasptitielc savew, adn oblinisuon oicrlejtep ovgmiint ta 6–2∼ kesew old.

taslnorUud hswos tdinehkec adn glenndhete y.psrulo tmTreenta si alsriguc ocniniis yoytrpy(omml).oo

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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isrntitoeIno is esdu ot ratte eersve sticyc cean. It si a n.arteetgo aCn csuea uilptmle eevser trbhi ceedtfs. Ceotianpntcro si t.aamodyrn RXR is a dnortiei X ept.orrec


 +9  (nbme20#24)
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itPnate sha olegcnnati mhrpohdoisyyit .i(mcent)irs nsnig:diF tpo ,eyllb eal,p d,fuyf-ecfap lcuiibalm rihnae, aaosmirc,olgs hptianooy, poro rianb eltmvnedoep (CM uasec fo bearttlae neamlt airdeaon)t,rt eargl ionaetrr lnsto.laefne

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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agLer owelnsl raltce nsvie --;&tg pantiet hsa aeetrnlx eshrm.dihoor lnoewlS dan imenlfad inesv in eth tcurme nda unsa tath aeusc roctsidmof dan heT omst ocnomm suaec fo xeenarlt smdhrooheri is drpeteae naisitnrg wlehi gnivha a bewol

 +4  (nbme20#35)
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CVM is daeotcsias thiw fecnitgin nrago lanptasntr snp.ieatt VMC is atsinmetrdt aiv xelsua ctnctao, ronag pnslant,atr ro ltacirvyel avi .lncteapa eavtRiintaco of CMV socucr in eth mmrsdsseuponpuei.

gnrOa nnlsttraap nsettiap are at na rnaeisedc krsi of MVC .ionaenpum

 +14  (nbme20#23)
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In reord fro a udrg to eb rlaecde by teh dkiey,n it tums stfir eb refditle ni eht lil.mgueor Dusgr ihwt a hhig DV eahv omer fo the ugrd ni het sstieu hatt aer not laeabaliv ot fidetler yb eht dki.nye rsugD thiw high otnerip gbnndii wton' eb dirtfeel eeit.rh oS uyo anwt a ugdr whti wol dV nad low nbdiign if uoy wnat ti redaecl via teh enydski and en.uir

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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tAceu ieitiartstnl nlrae namilinto.fma auriyP clsycaals(li sl)inpoihoes dan aoamizet nircrgocu faret tnotnrdismaiai of udrgs thta cat as nhtepsa, gcindnui vtrpiehyyieinsts (,eg srt,cdiieu SNIsD,A inplecinli ivrsevdait,e torpno pupm si,boiihrtn p,irfnmai uoennil,oqs aesds)mufniol.

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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hTe girth adn flte revetlicn ear daeidrn by sereptaa satpr fo hte fenmaro of onorm. Letf( dies is ddiaenr by felt orno,m gihrt ides by trgih rn.o)mo An tusbtoroicn of hte hrtgi raoemfn fo onrmo lwil leneagr eth grtih tcreeiv.ln

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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ttiasSn cna ehva a esdi teefcf fo dos.rbhlyimysao

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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enatPti hsa rllyademu .oacrancmi Mtnglania pnritiroeoafl fo rplalrlfuaaioc ""C ellsc that crodepu ciotliacnn adn heva hetsse of ellsc ni na yimdaol .atmors

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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iotdnsmiitnarA fo ncneliiPil rof isShpliy amy aeld ot het acxJerrsemieirhh-H naetorci hruso fatre e.nertmatt cuscrO ude to yslsi fo iprsshteeco os( it anc rucoc itwh roreBali adn oeisspLirpost sa llw.)e Teh nrtoicea is rzerhicadacte yb fveer dan lhcil.s

eTh saalcilsc tanelxionpa of hte mxrreeeiHh tineaocr is htat ttnaetrme elsstur ni het enusdd hatde nad teidnucostr of leagr mrubesn of emnroesetp, with hte balnirieot of eontipr tpscurdo nad .oxntsi

almondbreeze  FA pg.148 +5

 +8  (nbme20#9)
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poalmtFonetorr nedaeimt lemofy(rr nnkwo sa kPic as)edse:i aEy rl eashngc in ltpoesiryan nda iaevbroh ve(aboihrla vit,n)ara or haiaspa yiamrr(p sgvsrieerop )apa.ahsi ayM aehv saiedacost etenmvom dioressrd (,eg kiimn)

eilWh tish tpesrnse rvey liismialyr ot g'nisouH,nttgn you anc eritdffeaenit ti aceebsu ni stih emst it asys pohry"ta fo hte foarntl lboes "llrbalaitye eahwres ot'nuginHsnt has taphroy fo deaucta nad eutamnp wtih ex uaovc regtvclyelnuamio.

dickass  and the patient has no chorea +1

 -7  (nbme20#23)
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bceioumtMacyr uvima mxelopc ncioeintfs ear a momnoc uttspnicoipor iefctnnoi in sepintta hwti vadcedan DSAI 4D(C octun 0.t5&l);

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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c,etioN hte tsme yssa srro"rcsepo in eht snki"

3D rcaheeloil)fco(lc rmfo xpursoee of inks (taturms ea)basl ot nus, stonniige fo h,sif ,lmki

2D clagel(riofro)ec rmfo tginseino fo tpnsl,a ifngu, tayess.

oBht rvcdneeto ot 25OH- 3D rogt(esa r)fom ni vriel nda ot hte avcite ofmr 2(5-)1H,O2 3D il)atlocicr( ni .dnkeyi

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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NRT'sI aer tscaosedia thiw esbsiolp eids cffetse of aa,imen tinnroplay,ogaceu dan esispronopey.smlu

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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sn'ioFcna si a dgnzealreie tipesorrboan tedefc ni TPC ncugsai ceasndrei enoixerct of animo isd,ca coelgsu, 3–OCH, dan O–3,4P and all esnasbcuts erebodrsba yb hte CP.T

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

 +10  (nbme20#25)
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yctoxOni sesu 3PI nagilsing taahw.yp

RnH,G ntcyiOx,o DAH -tpcorr)V,ee(1 THR, smtaiHien pHec)oer1,-rt( tisngennoAi I,I .Gtinars

FA c:onnemim TAGO" HGA"

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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Cpiteata and neulta era ni eth ecnert of eth mapl. pCeaatti is tno na option, os uneatl is eht ans.rew

iicoDlotasn of utaeln yam cueas cueta cpraatlelnnu

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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heT setbu era srhceteta ptu ni fro urnei to lofw noti a bag. oS uenir tupuot is iggon to rce.inesa Teh apitent is losa phlryemia.eck doneoAlerts enpdrsos to mheiaapklyre yb seaginrnic +K ecixortn.e

mHyailekrape illw uielsmtat eoradolenst rcniestoe neev if rnnei is eedpsrspsu eud ot hsi nhotpy.ieerns Ahuhtlog N+a lilw be rasebroeb,d sthi wlli eb nitnesatr dl(osuh oreselv cneo hte ositmausp eslelv )edmalzinro nda cnise shi nriue uottup will stom llikey eruntr to nrlmo,a shi oobdl uresespr odshul oals rna.ilomze

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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sCae of esacsooe.isloiltrrr

reslyHpapcit leiresooloctssrrai enlivsov ktgniechni of eevlss alwl yb siapryaehpl fo sthmoo slumce -ikiosnnon'( 'rppanee)caa

  • nunqeoceesC of atniglman hsrnypeteoni gt1;201(/08& w/ ctaue ondrnaeg- )gdeama
  • stsuRle in rceudde elvses liaerbc thiw eogn-dnra meachiis
  • yaM laed ot rnfoiidbi rsnoesci fo the vslsee lalw with heaermroh;g ylcsaiallcs ecauss caeut nrlea riufael A(F)R iwth a creitasaicrcht 'l-atfetnei'b apaearnpce
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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oN sbtiaeol,namir noyl osem ,nvmgiito solok llew /w on uairlfe ot etvihr. tMos lelyik timrmuea S.LE

masonkingcobra +13

 +3  (nbme20#50)
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trSoh iatsgcr a. crahnb fomr het incples .a

rnsBcaeh fo eth icacel ktunr ttha nsouettcti hte olobd uppyls ot hte cma:tsoh monocm tcpiah,e i,peclns nad ltfe tics.rga

 +6  (nbme20#37)
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ithW nohircc img,ntovi uoy sole clytesertole adn a lot of cid.a tI rrgtsieg mlaoebtci lisakolas cihhw si why all het rsmue lausve rea owl o(r on the reolw dne of eth nrmloa aner)g texcpe fro biraeonbtac.

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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ieEatlsr acttedeelb aocsenydr xluesa ictcrrsiahtcea si asertb dub plveeomndte in gilsr, ucsraettil eemnarlgten ni yosb.

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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ilailCnc ngdsf:ini nhti, yowlleg-,eern ,uamooolrds yoftrh isagchder and agvlnia itlmfanmonai / citgnih.

Lab n:igdnfsi pH 5;tg&.4 and tloime ratcdhso.mion

 +15  (nbme20#4)
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alhtMone is ioxtc by wot nsmecah:ims

F,isrt nlahtmoe nca eb fltaa eud ot tis SCN ndsseeartp srppoeerti in het mase rnmaen sa olnteah s.ngpiooin

coe,Snd in a srepsco fo cixnoat,tio ti si ildmzeobtae to cirfom dcai aiv aydfrehmdole in a osepcsr einiitdta by het emezyn laoohcl dsedhgroyaeen in teh .elriv teMnlhao is erdenvcot to dmyfadhlroee via oollahc edysgeonhread )(HAD dna mdyadhelefro is eotcdvnre to focirm cadi etmfor()a iav lyddhaee hngdeaoeredys (A.LHD)

oFmreta si itcox eseabuc it tnsiibhi cdaotnrhlmiio ooretcmyhc c x,eadosi nsciaug ixyopah at the lluecral e,evll dan eoatlbicm sio,idcas agmno a yiaevrt fo torhe eolticmba sncedtu.srbia

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

 +15  (nbme20#38)
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tPeanit has a angihpoamorcriayn. otMs conmom hdodiolch aetstnliuarpor u.rmot Didveer form ernstnma of Rahket opcuh o(lra .mr)deotec ifiioCaalctcn si .moocmn oshlelroCet ylctsras onudf ni “otmro l”-leiiko dfilu witihn tmour.

A ictycs slsalrauper amss itwh iniacciaftlcos dan echeatnennm fo eth wlal ro dlsio nsooiptr in a ichdl or stndealceo is sotalm lwasay a inahrpamngcao.yiro

yMa eb cdosneuf hwti uittpryia aaenmdo htob( aesuc romtleapib anap)

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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rlAiycvo,c mrfcvoial,ci ayivlrocclav rea iunoseang ognasal. yehT dgoeurn nrvoseionc ot aovicclyr posepthnaomoh aiv irvsu oendced siimh-ke.nedyaitn laUmyti,elt tyhe iinbiht ilrav NAD osyamepler by haicn trnoia.nmtei

Mtduaet vairl iiemhytdn akisen acn uasce c.earitesns

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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aIguinnl iehnsar era llsuauy decbu,riel olrmafe nahirse rae no.t

siTh is na rdicteni gulnniia ri.ahne It nstree irnatlen iulinagn rngi ealrlta ot inirreof precisgtia velssse dan is risreopu to eht nlnigaui atgeinml.

dsCeua by efariul fo sssorucep gansliiav to soelc cn(a mfor rleoec)d.hy ayM eb icedotn ni fninsta ro dserivcedo ni hdotodla.u cuMh mroe ocmmno in

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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nseisMes omitunast nvivloe a idcleoeutn usotbutnsiit niruestgl ni ahdcgne moain ac.ids memeSiost eht eftfesc of essiemsn atosnmuti yam eb nloy rntapaep udrne rniatce rmnialeoenvnt doc;ntisoni chsu eesmnsis tmatoinsu rae cellad diantoloinc inautstmo. naMy emesnssi iustntoma utelrs ni poestinr ttah ear ltsli ncontlfau,i ta selta to semo .gereed

s,Alo lla the otreh nswaesr wdolu yblaropb laeev oyu thwi threie a geayltr rteleda or -infautnonocln

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. +7
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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Teh aegmad is ni teh L anrimibd ni the eraa fintcfega hte ncclsotoriapi .ttcra usaBeec it si in eht nmia,rdib aduonssicte in the ypiamdsr la)mlu(de so it lwli swoh tapilsialer fcainulsytdon motro .sisgn

ohotP of dbnaimri nad rotntipam a:raes rHausRl.rtohL/mty

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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eitlLt rnfegi = nualr

8-TC1 ear hte troos of teh ruanl rev,ne hwich is a hnacrb fo eht ilmdea r.odc hTe uarnl ervne si not undfo ni the aalcpr tleunn (het leamdi reenv si.)

nUalr n. eagdma anc deal ot sols of witrs lefonxi nda cudidnaot, xnoilfe fo lmiade ngesirf, ondbaucti dna ctdnoduia of gisfren (oesr,sintei) tsacion of amdile 2 lmcbriual sle.cmus sLos fo ntaeosnis eorv emladi 1 /12 eirgfsn, icudginnl ehhtarnopy emnience.

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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iaeplNaso is enw setsui gowhrt hatt si t,garunledeu er,eiblievrrs dna noomcl.nola

laConlity can be imderteden by atespeuhpoo--6gshlc hyadeseoengdr (PG6)D mneeyz oosmi.fsr 6GPD is lekdi-nX.

*rFo rome ianrnftmooi chkec uot Ch. 3 aoeNslaip in hotPama

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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eTh tlef pperu etyemitxr nda tsrbea rea anrddei yb teh rxaliyla hmlyp o.nde heT yiednk is dendari yb eth richtoca ct.du Teh thare sha tsi now phylm tseyms inogg no ogridrunusn teh .haret

 +0  (nbme20#14)
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fO lal the o,potnsi spaos ramoj si eht olny neo htta is arlyle itcasdeaos ihtw the umbalr evrarbee.t

Q. uLmobmru lvivnoes het rvnstasere sorpecs of 1L utb ssoaP Morja iaisotgern orfm -1L5L

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

 +7  (nbme20#15)
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nitfinDieo fo etjtamdnsu ddeosri:r

mooEintal spsymomt ,e(g einyatx, de)eorssipn tath ocrcu tihwin 3 homstn fo na ibneeilifatd hlocipyosasc tsrosrse g,(e dorevi,c lns)seil ilnagts t&l; 6 stonhm ceno teh sesrrots ahs dned.e

fI spsotmym etrsips ;g&t 6 mhsotn rtfae sserrsot des,n it is GAD.

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 osmt impatotnr MI tcaolpcoinsmi htta cocur iitwnh a -25 ayd snap ear lryiapalp mlcues rretuup nda lrauntetnreiirvc uetspm rue.urt

liPyplaar sumelc reutrpu easld ot eseerv mtilar tiogur,ntearig dehar sa a ssytolic muurmr at teh

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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oaraiocttCn fo the arato deals ot eicdnaers LV ervodoal asgnicu LV yhypeotprhr adn a L xsia neivoiadt.

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

 +7  (nbme20#19)
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shTi eattnip ash lalms clle n.cmaicaor hsTi epyt fo enracc si cssoatidae wiht aansrceaotpilp orseydnsm chsu :sa Ciusgnh roe,dSmyn HDISA, or diotisneab tniaags +2Ca cnahesln tn(Lra)Etbaoe-m or en.ousnr npoiitAmalfci fo ycm ocnesegon is sola .oommnc

SIDAH d(remySon of peppnotriiraa uadittiiecrn oonhmer cstie)roen si rdhzcaitaeecr by:

  • esvxseicE efer etarw rnioentte
  • uoclmiEev paniaermhoty ithw ycd nnritauorienu +aN rcxenoeti
  • iUern loitaoysml ;&tg serum tmaoioslyl

ydBo rpesnsdo to eawtr oenttnire hwti edoanoserlt nda NPA adn PN.B aTth si thaw aucses het nscieraed rrinuya Na+ ritnocese whchŽi adesl to tanaizlnimoor fo eecrlrxtlalua fduil ovlume ndaŽ teh ciueemvol .mpoeyritnhaa

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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oyhaRlsibmosdy anc tnperse gnookil ekli a ndeyki inurjy i(t acn dlea to cutae ublutra orcnssei as el.wl) hTe certlyetelo fdiisngn era jtsu leik earln iafrlue (cI.n ,+K ci.n O4P-, .ecd )aC

oT taieeteindffr beentew hlrbyaiodssomy and nkdiey rinjyu, uyo hkcec eth reinu ot ese if trehe ear nya BsCR. In irsmaodloybshy ethre rea on efre sRCB in eth

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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Teh byab eods not get nay arnmleta MIg, IAg or gEI sa ehty od otn scros teh aancltp,e os if IMg is unfdo it aym sgstuge eth bbay hsa uceeentonrd an otfiinecn in .treou

gIG si esasdp dnow ot eth aybb sa a seamn of eipsvsa iyuimnmt nltiu eth byab acn romf etrih own eniiadbost fo ifrdtfeen .yptse oS fi ouy see gnnaythi otreh naht IgG ge..( IgM) ouy nokw ti sumt eb /td an fnciino.te

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. +8

 -11  (nbme20#24)
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ddA on to hte ehtro ometmnc: C.SAKISCEOCMF nhIwe( mA kigdrnni utGripearf uijec) is het enmcmoni for eermgbiemrn eth 054PYC binritsIoh:

  • S idmuo ptrlaaeov
  • I onszaidi
  • C iiinedtme
  • K ltzocaoeoen
  • F neuolalzco
  • A utec alhoocl ebsau
  • C npoacrimheholl
  • E rtchoilryynirmcyirco/mtanh
  • S fldaisomenu
  • C licporfixaon
  • O mzpelerao
  • M eoeldizanotr

  • A rmodienoa

  • rirftGaeup eicuj
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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In yslrepaco,n treeh si a dtreic riaitnsnot ormf asnwuksflee ot EMR .eslep ciasalBly tasedin fo ogngi ohruhgt teh ealyr taegss dan aluyrglda gnlfail iton a eedp eep,sl uoy tjus sdedynlu go ofmr ebign akwae ot nibge ni a edep sl.pee

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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otrttasiPsi si rteeacazdhicr by siur,ady nfcue,qyre gceurn,y owl ckab maWr, r,etedn greandel torae.tps

teAcu ieblcrata poitisstani—tr drloe nem msot moncom rebamicut si E. .cilo

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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onriFeg bdyo iomnftmaryla laicaf insk irsdodre tezrcirchaade yb rim,f hetepgin-mdeypr uealspp dan stuusepl that ear liupafn nda aecdoLt on c,ekhes jnwa,eli dna kecn.

Colmmnoy rsccuo as a erults of aghivns “oarrz( ),u”pmbs ripryiaml casefft nfnmiA-irAacacer

egasmI: ouf1htt.sarlpYr/w

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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iTsh ptaeitn ash thera ulfaie.r lmoraN VJP si 68- mmHg.

gisSn of ahter eafliur aer ebasd no dcaicra ppum dsitf,uonnyc engŽotnios,c dan lwo frusno.pei

tSm:ysopm iulecdn de,sapny p,onaeorth gteaiuf; sgnsi liucden S3 reath sodnu, sel,ar juuglar uensov tnnitideos J(V)D, dan nttiigp em.ead

 +7  (nbme20#21)
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hiTs is an maeelpx fo lghsSne.i eHsepr mslpiex and prseeh srzteo suvsire saeuc amaonrlb clle vsindioi in pialmerde cls,el nad isth eertcsa uclaednmutetli niatg sec.ll

A Tznka emars hogsnwi ueltunatdcmiel taign lescl si rteriasccthaci fo craleVlai tsZreo uVirs (SVH lwli ahev lsmaiir snndgfi)i.

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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svrcelnaaoRu seadesi is het tmos mcnoom sauce of °2 HTN ni s.uladt Cna eb d/t eamsiich omrf leran essinots or raricscvuaoml ds.ieaes Can areh enlra uisbrt alrleta ot iiculmusb.

aiMn sauecs fo alrne tyrear se:osisnt

  • roccthtrseloeiA or—ueppaxqlsilma 31r/d alen orf r,yreta suaulyl ni eolrd aml,se .rmsseok

  • cularbusormFi s—apsadiyiadlslt 3r/d2 ol rafen rtyrea ro naglsteme rhcasbn,e ylulua snougy ro igdmdaeled- .meaefls

abL suleva bseda ffo:

  1. eosiSsnt dssereace odbol olfw ot ulosr.gulme
  2. ualgmruaxeoJrlt astuaparp JGA)( pdrnsose by rsentcgie inn,re hwhic rsonctve nsnioanngeetiog ot oignnstaein I.
  3. igesntinonA I si tcodeenvr to sgnaeininot II T)IAI( by ngaseonniit iroegnvntc zeyenm E(CA -in- nus)lg
  4. TIIA saesri blodo espurres by (1) atncoitcgnr arrielraot soohtm ue,lsmc asnrgicien ttola arpehrilep sancirseet dna )(2 nrpogmiot ealrdna seerale of ,ltoarnseedo hwcih nsaeersci airnsrtbeopo fo iosdmu hwe(re +Na oegs H2O illw l)lowof in eht itadsl oeudcnotlv tlueub de(gixanpn paamls o.)meluv aCn eald ot yhmloeipkaa en(es in hte abls for isth usnot)ieq
  5. eLsda ot HTN ihwt earcednis aaslmp innre and auletialrn pytorha deu( to lwo dobol lfo)w of hte tcfefdae ky;nide heinetr rtfeaeu is eesn ni mrrpayi ineserpyotnh
uslme123  So both causes would result in increased aldo and MR is the only way to differentiate the two? +2
hello  @USMLE123 I think both are causes of renal artery stenosis and that could be seen via MR angiography. It is asking what could help DIAGNOSE this patient -- and her most likely cause of the findings is fibromuscular dysplasia. So, yes, MR angiography would look different for the 2 different etiologies and thus could can be used to differentiate the two from one another. However, epidemiologically, we are looking to diagnose her with the suspected most probable cause. +8
yotsubato  @USLME123 I think measuring Aldosterone is an incorrect answer because you already know its increased due to low K. Knowing she has high Aldosterone wouldnt provide you evidence for a final diagnosis. +4

Subcomments ...

submitted by yotsubato(968),

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(210),
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sI 45 meusitn too glon ot be clancaihpyat adn udowl teh bsneaec fo ahsr ,(iatraurci isuptr)ru RO hpanccaalt?iy

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(210),
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Is 45 mueistn too gnlo to be ichtpyncaala dna oldwu eth eeasbnc fo hrsa tiri(aa,rcu sruu)tpri OR a?cpyahltncia

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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ehTy tsegsug sMtosoriolp ot noactuetrc S.NIAs..D yhW nto ?PIsP

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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hyW si hte rsnewa ot itsh osenqtui nto vehidisAe C.lpiis..satu

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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osremdny" fo o"llntuadii aoyi-hpll"sootmy ni revsee ivctnesoeg htare uliafre mya eb dcesau by na ntoplrapriepyia hhgi AHD snoricete in wihch eht remosopteorc tyssme is niedmdtoa by rmnooalsno smlu"iit

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 nkthi eth idae ehre is piymsl thta one dlshou nikth aotbu wrehe selcevsi rae mogicn rmof on their ywa ot eht loggi xmo.lcpe

"Tow tssep arrodfw nad one ptes .ab"kc llafcieypSc eht itnqesou amy eb enirrregf to a arre rnifcaacoali .ridseord an wsaseansre of tath seesdai is ton .raessecny thWa si aerscneys is driadgnesunnt the onigir rfmo hreew scesivle era tacedfkri to het ogiGl appraa.tus

OCIP tinrepo is ndeeed ot taoc scvsele omfr het RRE ot neds to i.lgog hsu,T hwti a mttinoau ni thta rotnip,e eht ecagapkd iprnesot htta hosldu bbel ffo nad eb ntes to eht lgog,i stnidae cmeutcalau ni het RRE nda dleait .it usTh eth


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 tnhik stih oen is llryatile jsut askign whta atrp fo eth ynkedi wlli be het stmo ryploo defuprse. tTha tapr oludw heav teh mtos ne.rni sAol, het llueadm s’onedt vhea GJ scell os I segsu s’atth atonher eorsna hwy it utcn’dol ahev eth tmos ien.rn

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