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Welcome to endochondral1’s page.
Contributor score: 16


Comments ...

 +0  (step2ck_form7#41)

why not myastehnia for this one? They put some LE weakness in the stem as well so that before respiratory depression made me skeptical of it being a pure descending paralysis and I went with MG instead .

study_dude_guy  I think the history just points more towards Botulism or GBS. Tbh I'm not even entirely sure why this was Botulism and not GBS +
seagull  The nausea, vomiting, and diarrhea are also good cues that this is a foodborne illness. Then the DTR are mildly dulled which won't happen in myasthenia gravis +
derpymd  The confusion for me is the timeline. She consumed the food 32 hours prior and symptoms started at around 24 hours. I figured with preformed toxins, the timeline would be more similar to Staph aureus (i.e. just a few hours). The learning point for me here was that it can take 12-72 hours for symptoms to occur depending on dose. +

 +0  (step2ck_form7#34)

why could the answer not be G6PD (also unconjugated) Or abnormal synthesis (what does this one even refer to?)

komodo  G6PD causes hemolysis in response to oxidative stress (infection, foods, meds, etc.) which seems unlikely in this case. It also is not as severe as this case. Abnormal synthesis refers to thalassemia or sickle cell. Sickle cell doesn't present at birth due to high HbF levels. Alpha thalassemia could cause hydrops as well but would likely present in utero, so would have been detected during the pregnancy. +

 +0  (nbme22#24)
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si isth iostequn kinasg wtah ew cpllyyhsai psas uotrhgh ro yb?

impostersyndromel1000  no, basically the question is testing if you know the branches of the abdominal aorta and which is closest to the renal (in this case, inferior to the renal arteries) +1
impostersyndromel1000  what you are passing by would better answer your question actually +1

 +0  (nbme23#41)
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I hhtutgo tibalnoa fo het va ndoe saw a tx for a ibf ton taehr o?kbcl

underd0g  The question asks for the CAUSE of the heart block, not treatment. +

 +0  (nbme20#21)
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cdoagcnri ot oluwdr irypsvnthtsiyeie inmpetnusio si due ot dstu nad ahtt was asol an i.p..ntoo.

amarousis  so it's definitely dust but the specific type of dust was the most important in this question. the fact that they mentioned the birds is important. the dusty books would cause it but the bird dust is more important -.- +
charcot_bouchard  Hypersensitivity Pneumonitis - Organic dust (like moldy hay) Pneumocniosis - Inorganic dust none help here though because both will present with same restrictive lung disease picture. i think since dust in library arent neither organic or inorganic and also u dont see many librarians with lung disease but bird ownership is specifically mentioned as cause of HP disease. +

 +0  (nbme20#21)
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how od ew knwo ekasaprte euasc snvtiseehyypri eutonminisp

smc213  FA18 p.657 bird exposure--> HSN pneumonitis (restrictive lung disease) and FA18 p.214 granulomatous diseases: foreign material-->HSN pneumonitis. I had to make sense of it since I didn't know it was HSN pneumonitis at first. +5




Subcomments ...

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sHi ildat euvmol swa 500 m.L en-xrEpriydtoa saw 5+ cm nda yr-asnioitdpenr was 5+2. We erew psedosup to ues eht cerednfeif ni yawira ure,esrps nda nto hte ndnpoatysei-rir elrlupa eprusser )(+20.

imnpCaleco = VΔP/Δ = 005 / 20 = 52 Lm/cm H2O

some-zheimers  Great explanation. In general, also a great idea to pay attention to the units. I studied Physics in undergrad and have got one or two questions based purely on following the units, when the formula slips. +23  
endochondral1  is that equation in FA? +  
redvelvet  yes @endochondral1, at page 651 in 2019FA +12  


submitted by bubbles(69),
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Bsaeentm maeenrbm yeirtitgn si het netdinmraet fo lufl gnul orveycer wfonlolgi ynplmuoar .inlsut

u:mmSrya

(1) loss of ebtsmnea mrnebame iyegrtint si larcctii ni egmtniiredn eht pt“nio of no tne,rur” and etuonsrtbci to the iltiiabny ot abeethrlssi mlnrao nlgu ttuharecierc ihtw omnorptoi of sibfo;isr

2() olss of htiipaelel lsel,c aeiodllhnte sclle, nda emstnaeb bnareemm igytnetir in ualus sireatittinl ionnaeupm dstcioseaa twhi idicaithpo rnoulaymp siisbfor dasle ot eydtderso nugl ttchreecairu and etepauplr ofsb;irsi

)(3 fstmrnoairgn roghwt otβrac-f is neaess,cry tbu otn elteryni setcfii,unf ot pteomor enamrpnte rbsis;fio

4() tnsesiterp ri/yg/atraninnnjttieiur is ctlriica rfo het goapnrtoapi of rossbifi;

5() thoadipici lynpraoum sobsirif is na epmlxae fo a osesrpc eeatldr to eth treesiscenp fo an i“”)tsg(en,na hcorcin li,amitfnnmoa nda sfois;rbi nad

)6( unique lcels are arliictc laellcru aresylp ni eht unoitgaelr of r.fsoiisb

ot:nci aitw5g:w/.ht6nCi2n.tc1oa/peihPc/..4sir/Mlnpmlw/t/bcvm2s4

kernicterusthefrog  Lovely +  
endochondral1  any FA or pathoma or uworld correlation? +  
endochondral1  or was this a random? +  
taediggity  Type II pneumocytes serve as the stem cell precursors, w/out those you're more or less fucked: FA 2020 pg 661 +4  


submitted by bubbles(69),
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amBesnte mernmeba ngitetyri is hte amndrtenite fo fllu glun oeryrecv lglofoniw mnuaroypl iu.ntls

uy:mmraS

1)( loss fo ameetbns nmeermab teginyrit is aliirtcc ni gmreintedin hte topn“i of on ”nruer,t nda obuettnirsc to teh tinibliya ot eraesbilsht rlnoma ngul hictrareucte with omtoprnio fo s;riofsbi

(2) ossl of eliilhptea elcl,s tnahedlloei ellsc, nda smnatebe ambernme iegitrnyt ni aluus artilneitsti enipnamuo asdacoiset tiwh tohiaiipdc rmoynupla sfsiobir lased ot ddoersyte ungl eeruhaicrttc adn palruteep oibifrss;

3() tsnronifrmag ogrwth -cfaβrto is ce,srnyase but ton yrtelnei tniiffe,scu ot roepomt reanmtnep fosr;sbii

4() rsetteipns natuirneyritr/atgn/iinj is ilicctar fro teh topapgaroni of ;bsofiirs

5)( hpaiotidci pnauyrmol oibsrfis is an leeapxm fo a rscepso drtelae ot teh eespicnrste of na i(ngt,ae“)”ns croicnh imlatnmnifa,o dna ;bfosisri nda

(6) eiuqun csell are accrliti ulearlcl pselary ni eth nituaogelr of i.iosfbrs

ni ct:ioatn4hwnlp.pPnbtc//.l56w/i/4tsm12csCetm/.iwr:ocaMhv.g2i/

kernicterusthefrog  Lovely +  
endochondral1  any FA or pathoma or uworld correlation? +  
endochondral1  or was this a random? +  
taediggity  Type II pneumocytes serve as the stem cell precursors, w/out those you're more or less fucked: FA 2020 pg 661 +4  


submitted by drdoom(874),
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eres’H erothna ryve ince noe thta msppieuroses het aphwtay noot a iflpiiedms ntaebsmir garidwn c(ine fro het aalcoanitm snrl:oitae)

spaecIgioaeeeh/2piL:uome-2s/.c/f-hNtueRorb.dnuy25pw/ytst/Ois./eFheg-wG.a

eoSruc etr:lcai

m2caewhaate5ehlo.hy-w/hhf:-up2o//ypreiumr/sehlreotacnet/eoi..ianstoeedtgutmpu.bpsl

To ese neve m,roe tyr oleggo eamig rsache no maei“ld ldnitonglaui cfcsusul”ai:

wmb:intpoghh/dtsegah?eapelouilonfcs=&ocustti/waicau.m.si;cgq++lml=ra/csmwld

endochondral1  what is A and B in this pic? i knew it was dorsal pons ipsilateral but i just didn't know what part that was on the pic? +  
nwinkelmann  A and B are the superior cerebellar peduncles.http://what-when-how.com/wp-content/uploads/2012/04/tmp15F2.jpg +  


submitted by usmleuser007(395),
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1) peSaclirfui grr(e-isdetf)e = pEirmdsei ~ rpseesnt as dre uniotkhs itw ibtsserl

)2 ialipruScef raitalp csnthkeis or)(dgneees-ced = nedtEsx into uriecisplaf )ppim(siraaldyl re ~ rPsestne twhi enrdses htwi lcreeriab tls p;m&a wctsbhain leh usrperse

3) eeDp pilaart sckitshen g-)eeecdsoen(rd = Edxesnt tnoi epde rl(riute)ca edrsim ~ ssrentep sa yweoll or tihew snik twih lses glc.ahninb aMy be n.regsiiblt

4) lluF estikhnsc ig-(tedrderh)e = stEexnd ruhghto etrein iedmsr ~ psesrent sa tffsi nda b/htwreniwo .nski No ahgin.cbln

)5 gdrure-tehoeF = tsdxeEn uhtghor tnieer knis, nad onit uleiyndgrn at,f umlecs dna ebno ~ stnpseer sa akbcl s;kin edrarch she ahrwcit

endochondral1  what is rhus dermis? +4  
endochondral1  nvm its urshiol +  
btl_nyc  Allergic contact dermatitis because of contact with poison ivy. +  
abhishek021196  Urushiol-induced contact dermatitis (also called Toxicodendron dermatitis or Rhus dermatitis is a type of allergic contact dermatitis caused by the oil urushiol found in various plants, most notably species of the genus Toxicodendron: poison ivy, poison oak, poison sumac, and the Chinese lacquer tree. +2  


submitted by usmleuser007(395),
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)1 cepuSfailir g(s-)trreeifde = rEiesdpim ~ epnrsest as red nwitt shukio sebrilst

2) culiiafSper lrpitaa enkchitss c(-nedoeedesgr) = xnEdste onti rsiufaicelp deypsllp iarri)ma( ~ sretPsen hitw drensse whti lesicbltrrea  pm&;a tawih sebnlhc puresrse

3) pDee artlaip teicsnhks sdrd-c)(egoenee = Etsenxd into eedp )criuetr(la rdimse ~ stpeensr as welyol ro hwiet skin tihw ssle galc.ninbh yaM eb sg.ebtinril

)4 lluF ichnkstes rd)e-id(ehrgte = xsEnedt hhuogrt eneitr seimdr ~ serptens as tifsf adn ewn/boriwht kns.i oN n.icnalbhg

)5 egreue-Ftrohd = dxEnets routghh rieetn n,kis dna tino lierduynng fta, meslcu dan eonb ~ tesepnsr sa lbkac ;snik dcharre at swihehcr

endochondral1  what is rhus dermis? +4  
endochondral1  nvm its urshiol +  
btl_nyc  Allergic contact dermatitis because of contact with poison ivy. +  
abhishek021196  Urushiol-induced contact dermatitis (also called Toxicodendron dermatitis or Rhus dermatitis is a type of allergic contact dermatitis caused by the oil urushiol found in various plants, most notably species of the genus Toxicodendron: poison ivy, poison oak, poison sumac, and the Chinese lacquer tree. +2  


submitted by meningitis(537),
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Taennr seastg strta at TNE ersya dlo

agteS I:

  • I si lf,at sa ni alft etch;s
  • I is e,noal sa ni no uelaxs airhs.

gaeSt II :2() tsgae II ttsars ta 11 yo/ II( olko ilke )1 1

  • 2 lslab tetlirua(cs r)eneglamtne
  • 2 ashir (buicp iarsh nwo ppare)agin
  • 2 atsber usdb fmor

eStga III )(:3 rtasst ta 13 yo /

  • fI oyu rtoeta ,3 it kolos klei mllas betsrsa as(Bret dnsoum );fomr
  • fI uyo glgsquei hte III htye oolk klie rurcceloys+a cupib irah
  • Icnarsede ipens ntlgeh dan sezi acn eb nterdpesere y:b II -t-;g& III
    uor(y seinp was ihnt II tbu won tis cetkhir III)

etSag IV 4(:) ssrtat at 14 o y/

  • triFs n:iaegim Teh I in IV esetprnesr eth ihhg,t nad eht V ni VI sloko like hte nsom ibups tebewen oury e:sgl
    IGAN NE:M yuo vhea irha ni mnso sibpu (V) but uoy eavh a rdoebr niigatnde teh arhi rfom ngworgi onti gihsth.
  • The V si ytp,noi sa in won the sbasret aer npytoi re(dias eaarlo or unmod no o)udnm

agSet V 5:() 15 y/o

  • V has on odrbesr eitnidang irah ofmr nggoiwr tion shgtih icbup( aihr + hhtgi ahi)r
  • 5 irsga(nsfe in shadn) ntatelnfig eth laserao hnew rgibgbna htem aerol(a antlfte ta siht gstae adn on rome dmon"u no nu")omd

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +19  
gh889  According to FA2019, stage 2 ends at 11, stage 3 starts 11.5-13, and stage 4 starts at 13-15, where did you get your info from? +  
meningitis  You can change it to ENDS at 11, ENDS at 13, ENDS at 14... I simply have it as a range just like you stated in a couple of them. The importance is in how the kid presents because he/she will have some things mature but others not, the age will vary in questions. +  
endochondral1  stage 3 breast mound is for females not males btw +2  
endochondral1  see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females +  
angelaq11  this is just too funny, I LOVE it! xD +2  
snripper  While this is impressive, this doesn't help with answering the question. +1  
yng  Pseudogynecomastia (False gynecomastia): this has nothing to do with puberty or hormones. Simple d/t the fast some guys have extra fat in chest area, making it look like they have breasts. The boy weight at 60 percentile while height at 50 percentile. +  


submitted by meningitis(537),
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Tranen gaesst trtsa ta TEN resay lod

gSeat I:

  • I si ,talf as in fatl stceh;
  • I si el,aon sa in no ulaxes sriha.

eagtS II (:2) tgaes II tatsrs at 11 oy/ I(I lkoo kiel 1) 1

  • 2 aslbl ecrtstiu(la rlgntmaeeen)
  • 2 hirsa ibp(cu sairh now pinar)epga
  • 2 breast buds rfmo

Setag III ):3( atrsts at 13 o/y

  • If uyo tetaro ,3 ti lkoos eilk sllam ebtrsas (sBrtae suonmd rf)m;o
  • If uyo eguiqlgs hte III hyte look ilek +rusrcolecay cuibp hria
  • eacndeIsr eisnp nltegh adn ezsi nac eb rntereseedp yb: II -;-gt& III
    uyr(o pneis aws hnti II tub own sit chetirk I)II

gaSet VI 4):( ssttra at 14 o/y

  • isrFt iaie:gmn The I in VI seerpernst hte htgi,h nda the V in VI oklso klei eht msno usbip weeenbt uryo gl:es
    GME:ANN I uyo avhe arih ni onsm sbpiu V() but oyu vhea a drerbo agnieintd eth ahir fomr riowggn noti gsih.th
  • hTe V is ,iyntop sa in wno eth setarsb rea tnyopi aid(res aalore or odumn no unmdo)

tSaeg V (5:) 15 yo/

  • V ash no srbdero idngitnae hiar fomr wgonrgi tnoi tgihsh (ciupb arih + gthih )rhia
  • 5 frnsgaie(s in a)dnhs tngialetfn het raaoels ehnw igabgbnr emth ala(roe fnttlae ta isht etsag dna on remo "udmno on )odnum"

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +19  
gh889  According to FA2019, stage 2 ends at 11, stage 3 starts 11.5-13, and stage 4 starts at 13-15, where did you get your info from? +  
meningitis  You can change it to ENDS at 11, ENDS at 13, ENDS at 14... I simply have it as a range just like you stated in a couple of them. The importance is in how the kid presents because he/she will have some things mature but others not, the age will vary in questions. +  
endochondral1  stage 3 breast mound is for females not males btw +2  
endochondral1  see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females +  
angelaq11  this is just too funny, I LOVE it! xD +2  
snripper  While this is impressive, this doesn't help with answering the question. +1  
yng  Pseudogynecomastia (False gynecomastia): this has nothing to do with puberty or hormones. Simple d/t the fast some guys have extra fat in chest area, making it look like they have breasts. The boy weight at 60 percentile while height at 50 percentile. +  


submitted by usmleuser007(395),
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siTh eomr kyllie ot eb euicrisdt ahtrre naht lteaavxsi /bc

eht bal tusyd wohss a rlane outiyncfdns B(NU ;& Ciatreenin era ve)dtaeel

stMo kylile the tpnaeit ueabds loop tdsc;ureii asol onkws to eucsa riattoccnno lsi,koalad longa itwh rnlae mreopslb ucsh sa litntetsairi ipsnthrei

endochondral1  would laxatives also have the low potassium? +1  
link981  My question exactly. And what if they were taking Potassium sparing diuretics? Then laxatives would be more likely or am I mistaken? +  
link981  Also creatine is normal, it's at the higher limit of normal so we can't say there is renal dysfunction. The BUN is elevated because patient has metabolic alkalosis with respiratory acidosis. +  
sweetmed  very important to Remember this: Diarrhea causes metabolic acidosis[from bicarb loss in stool], vomiting & loop diuretics cause metabolic alkalosis. +12  
hello  @usmleuser007 not sure your approach is the best way to think about it. The serum Cr is at the upper limit of normal (1.2). And, even if you calculate the ratio of BUN/Cr, it's 21, which would be a PRE-renal issue. +  


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ermPie ash no traaftusnc

enignoisntA II - ngteaeerd ni lavpyoheimo

pyailolmitD lieintch aka hhitllpstalipoahidnpmyeicydolo nulg ttruncafas

adPtpilolisynoshtioh osps4,-h5iaphteb aak IPP2 Gq ptecrreo aahytwp

adryiPtolhpshenesi dvve-olin in nitirincs toosappis whne pexsdeo no luetrlxealcra cuaferss

gSoeiynnhpmil - eospmcos nliyme dan osla sah oserl ni sanilg snc,iurtadton .sppoosita i:tLecnih lnmgihioSynpe oatir g&2t; tacnidise mrutea aflet l.ngsu

endochondral1  how are we supposed to know that dipalmitoyl lecithin is the same thing as dipalmitorylphosphatidylcholine +6  
qfever  FA 2019 page 647 Pulmonary surfactant is a complex mix of lecithins, the most important of which is dipalmitoylphosphatidylcholine (DPPC). Also: Screening tests for fetal lung maturity: lecithin- sphingomyelin (L/S) ratio in amniotic fluid (≥ 2 is healthy; < 1.5 predictive of NRDS) +18  


submitted by hayayah(1074),
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heT aedgam si ni hte L aidbimrn ni hte raea ffaeicngt teh tiniclsacorpo ctar.t scauBee ti is ni the andbrmii, sotunescdai ni hte rdapmsyi (ldmauel) os it iwll ohsw iltalisrpae lsyudnfntoaci otorm .isgsn

htoPo fo idmbinar dan rantomtpi se:aar ./huaLostmlrHyrRt

masonkingcobra  Just for clarification, on the left side, you see where he had the infarction 7 years ago and the tissue is gone. +8  
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 @ hayayah....is there any good picture to look at to know where the tracts are on this section? +1  


submitted by xxabi(257),
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lnweoig ef ltSh lelcg,opceidhyr. . ( icenarsden se hiigse oa→tmi)etu: end pcdAurroisotTP deeca sTAedeea→Pn+ ca/sKa  r+Ned ad a2p+mCup u ftcnidtsyfo fi →aiovi a+ aNnd erawt etit hon  →elcl lelgel wscrluinal

endochondral1  can someone explain how to cross out the other choices> +1  
endochondral1  what is hydropic degneration and where do i learn about it? why is it not the loss of plasma membrane integrity? +1  
shaeking  Endochondral1, I had the same question. I tried figuring it out and this is what I came up with. The CHF and congestion of the lungs is reducing the amount of oxygen getting to the renal cells. With hypoxia there is decreased aerobic resp in mitochondria with decreased ATP. Without ATPase Na builds up and water follows. As far as the loss of membrane integrity. I think it would cause cellular destruction not just hydropic changes. This is my best guess. +2  
charcot_bouchard  Membrane damage is irreversible stage of cellular injury. if membrane is damaged cell is dying & it will shrink. or totally destroyed by inflammation. they are specifically asking hydropic changes ie cellular swelling. which is the 1st sign of reversible cell injury due to failure of Na/K pump +1  
winelover777  @endochondral1 Chapter 1 of Pathoma. Also FA 2019 p207 describes hydropic degeneration without saying those exact words in the first bullet under reversible cell injury. +1  


submitted by xxabi(257),
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to Swfhng eelil e,l. l.cghcyde(o ipr uearss)im→gtse e dioia tencnh:ie opdeeardcPiTs uoectrndA  K/esredP aTcAd sea→d e+N aa+n Cpum2+ap f→dou f tivfa iicotniys N+ada n taewr oihnett   c→ell ulanllw lcgeriels

endochondral1  can someone explain how to cross out the other choices> +1  
endochondral1  what is hydropic degneration and where do i learn about it? why is it not the loss of plasma membrane integrity? +1  
shaeking  Endochondral1, I had the same question. I tried figuring it out and this is what I came up with. The CHF and congestion of the lungs is reducing the amount of oxygen getting to the renal cells. With hypoxia there is decreased aerobic resp in mitochondria with decreased ATP. Without ATPase Na builds up and water follows. As far as the loss of membrane integrity. I think it would cause cellular destruction not just hydropic changes. This is my best guess. +2  
charcot_bouchard  Membrane damage is irreversible stage of cellular injury. if membrane is damaged cell is dying & it will shrink. or totally destroyed by inflammation. they are specifically asking hydropic changes ie cellular swelling. which is the 1st sign of reversible cell injury due to failure of Na/K pump +1  
winelover777  @endochondral1 Chapter 1 of Pathoma. Also FA 2019 p207 describes hydropic degeneration without saying those exact words in the first bullet under reversible cell injury. +1