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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 htis suqtione snkiag thaw ew hcpyiylasl pssa hhtogru 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 hotgthu lobnaita fo hte va deon aws a tx rfo a fbi ont rthae obl?kc

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

 +0  (nbme20#21)
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gnocdraic ot udowrl esyypnhestvitrii seonmpiutni si eud ot sudt dna taht swa lsoa na o.tp...oin

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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who do ew wkon keaaterps ucaes ssyriptnviyhee oesiiutnmpn

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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siH itdla muolev saw 050 Lm. iE-trpxoradeny asw +5 cm dna srni-ieotdynapr wsa 2.+5 We were ouspepds ot eus hte reindeefcf ni wyaair ,rpsersue and tno the eosynpaind-rirt elrapul seerursp .(+)02

peoCncalim = PΔ/VΔ = 050 / 20 = 52 c/mmL HO2

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 +14  


submitted by bubbles(70),
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mBeensat bemmrnae yrngetiti si teh deenmanrtti fo ulfl nglu creroyev owiofngll anomyprlu tl.suin

ymuSm:ra

(1) loss fo atbmseen rmbemnae yttrniegi si rcalciti ni dintirgmeen eth “ipnto fo on nur,r”te dna ibtuocnrset to hte atlybiini to hitarblssee aornml nlug ctatuheriecr ihtw ipomnoort fo bsfoisir;

)2( lsos of teplieilah scl,el atlodleeihn ,llecs dna bemantse brnammee etnirygit ni usula tesiaitirltn ompunaein sidcastoae ithw diphcioati upmyaroln ofssbiir dales ot teyosrded lung ccethtauerri adn eprpautel o;srbfisi

)(3 amogrsnitrfn owghrt tf-acβor is srnceya,se btu otn nlyeeitr ifisef,cunt to poomrte eanrtmpen os;riisfb

()4 rpsntstiee iuntgtjy/nnarn/rtareiii si raitclci rfo het taropgpinao of sifo;srbi

(5) ipicdhatio ranlmyopu osibrisf is na epamelx fo a sercpso tarlede to eth cnieerstpse fo an inans,()e“tg” orcnchi mninlmitafao, nad f;soirbis dan

)(6 qiuneu llesc rae trciialc ercalllu ylsepar in teh utgnelraio fo ss.oifbir

nta:otcii tpn/ilct.6Carvomcc1/wmb.//2/n.twhsil5hnw.pPi4gs:2M/e4

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(70),
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atnseBme ambeemrn rnittyige is eht eieatdrnntm of llfu ugln recerovy lfooiwngl mnouapryl iuns.lt

au:mmryS

()1 olss fo mnebstae mbmaener ttygirien is iicarclt ni nirgnidemet hte noitp“ fo on u,rnr”et dna biesottuncr to teh inbiayitl to ihsrbeealst rmlnoa nlug uirtetehcacr ihwt torpiomno of rifssib;o

()2 sosl of ealhipelit c,lels elltoindeha ,elslc dna eetabmns mmaeenrb ygeirtnit in asluu srltitatniie nienpaumo aasoitecsd itwh doihcipait lrpaumyon sirfibso aseld ot dydseorte ugln eacretricuth adn aerptulpe fb;ioirss

)(3 rrtmnagsfion wrthgo βaofr-tc si reync,eass but nto irnlteey ef,cfintusi to ptoroem eeamrnpnt bif;srois

)4( sseipnrtte rainjirteyign/nnrttia/u is lirticca fro eth npropaiagot of fissi;rob

)5( ihadiiotpc lrmopanuy ibsrisof si an elpmxea of a ecsrosp rdltaee ot hte tnercspisee fo an n”(),iaeg“snt oircchn mmlnoiania,tf adn ifosrsbi; dna

(6) uqneiu lslce rae aitlicrc lrlucela eralpys in teh ogearnitul of i.rbsifos

tiaon: ctiwmp4ace2tlw:i/M.n/.tccP5nbg/rC6hhi/i/s2ot.s4m/1pwvn.l

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(892),
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He’ser eranhot vyre ceni one taht uoppesemrsis the haawytp otno a ledmipisfi nreiabsmt ingwdar ce(in ofr the mlcnoaaati l):inaostre

.esFuiisawe-2cd/e-./o5eyceoutepLuhOot/Gseg.sp2h//.a2fwNIp-gmy/iRahbtern:

rSuoec eartc:li

she.eauom2oplh2-/erutgwiodantapu.aechreifntyt/5hprmbeus:eweyhme./o/hip/clt-al.soet

To ese eevn r,emo ryt oelogg gmiae hrasce on edam“il tgdilonanlui luci:uac”fss

op.cs&dowacuiutstsaw/qaigd=s/melperftwcloblcius?h+;.ao+mmhlmelna/n:hcit=igg

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(397),
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1) eifcilpraSu dseitreeg()-fr = iemrEpdis ~ nsretesp sa erd  skuwiinttoh rbelstsi

2) iSflucipera tarapil csnhsitek cn(doeere)ed-sg = edEtxsn niot prafsiulice  i(esalarlryppd)mi ~ nserPste tiwh eenrssd tihw leirabecstl r pma&;  nctbawislheh erpressu

)3 eeDp liaatpr hsctiksen eseee-dnr)o(cgd = enEdtxs onti peed )lraurec(ti sedmir ~ tsnserep sa lleywo or thewi nski wtih sesl lbc.ghnina yMa be etsir.inblg

)4 lluF eikcstnhs rgee-td)h(deir = tdxsenE hgoturh tneier desmir ~ etnsepsr as ftsfi dna onhww/berti nki.s No algbnhn.ic

5) F-gordethruee = nteEdsx ohhtrgu rteien nks,i and oint reniudnlyg at,f uclems nad onbe ~ esespnrt sa lbkac ;niks rhadrec  shecirtwha

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(397),
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)1 ciaSfiulrep )rfdseegetir-( = diempsEri ~ sentpsre as edr noisttwukih  lisbtser

)2 elapifcruSi lraaitp ssinechkt (eg-ee)csoednrd = txEedsn niot afieprlcisu sm)pa (aillderipry ~ tsenPrse with eesdnrs wiht itrecrae llsb &apm; lhwet inchbas speruser

3) eDpe paitlar istkecnhs e-s(ecrndegode) = steEdxn iont pdee liar)t(ucer srdeim ~ sptneesr as woylel ro weiht inks thiw sesl inn.cahbgl yMa eb elribnit.sg

)4 Full iseskcnht dr()teerg-iedh = sxtEend rhgutho rintee siremd ~ spstener as ftfsi and rwwi/ehontb .kins oN h.labcgnin

5) rtuFr-hegeedo = Etdsenx ohutghr terine ,nisk dan iont neguyrnlid ,taf uemscl dan nebo ~ ssnteerp as bcakl ;ksin cradehr  hhitcwasre

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(545),
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Taennr segsta sttra at TEN easry old

gteSa :I

  • I is l,fta as in alft ;etchs
  • I is nl,eoa sa ni no suxale .arish

aetSg II :)(2 egtsa II stsatr at 11 /oy II( olok leki )11

  • 2 llbas utlirceas(t enmalenetr)g
  • 2 rhasi p(ibuc hiras onw praep)iagn
  • 2 rbtaes ubds fomr

gaetS III :3)( ttsras ta 13 oy/

  • fI uyo toatre ,3 ti lokos ilek lsalm staerbs rBe(tas udmons or)mf;
  • If uoy egluisgq eht III eyht look ilek rcrosae+lcyu bcpiu hari
  • edrnacsIe senip thglen and zsie nca eb teeepsdnrer yb: II ;-g-t& III
    (ouyr nipse saw nhti II tbu own its ikcrthe III)

geatS IV 4:)( sratst at 14 oy/

  • iFstr aeii:mgn The I ni IV sptreeresn teh g,hhit dan hte V ni IV oolsk leki het smno ipbsu entbeew uryo lg:se
    ING AEM:N uyo hvae irha in nsmo bispu ()V tub yuo hvea a doebrr eindnigta the irha morf grnwgoi toni gthhi.s
  • The V is yin,pto sa in wno the etsrasb are iypnto eari(sd aalroe or nmdou no uodnm)

gteSa V ()5: 15 oy/

  • V ahs no bordesr gideinnta riha frmo irggown iotn sghthi pucib( iahr + gthih ar)ih
  • 5 aeg(snsifr ni d)hnas ttalfnnieg teh aoleras when bigbrnga htme (oalrae lenattf at iths tgsae dan on ermo "noumd on "md)onu

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +20  
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 +3  
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(545),
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Tnnrae atgsse rsatt at TNE yeasr dlo

eagtS : I

  • I si ,ltfa sa ni aflt ecth;s
  • I is anle,o as in no saxlue hsri.a

gteSa II 2:() tagse II ttrass ta 11 y/o I(I olok elik 1) 1

  • 2 lsabl itulcate(sr rteg)mnelane
  • 2 hsair i(bupc rhisa nwo aapir)nepg
  • 2 erbast dbus mfor

aSetg III 3)(: srttsa ta 13 o/y

  • fI yuo rttaoe 3, it looks ielk llams ebtsrsa raBe(st ndumos fom)r;
  • If you glsugieq teh III yhet kolo elki erouyl+sccra ibpuc hari
  • nIesdrace einsp egtlnh dan size anc eb eepeserdrnt :by II -;&tg- III
    (oyru neips aws hnti II ubt nwo sit hceritk )III

tSega VI (:4) trtssa ta 14 oy/

  • Ftris gniimea: eTh I in VI esrprenest eth t,hgih dan hte V ni VI okslo ikle het onms supbi newtebe uryo l:ges
    I A:GEMNN uyo ehav irha ni nsom buisp )(V btu ouy ehav a reobdr deaitngin het iahr morf gwrnigo tion h.tsigh
  • The V si y,topni as in won eth astsber rea ypiton saed(ri aerlao ro mound on nud)mo

egatS V ()5: 15 /yo

  • V hsa no rdrboes iaedingnt airh rofm rnggiow tnio htigsh (pcuib rahi + hhgti i)har
  • 5 (gsarsinfe in dhsn)a litnefgnta teh aersaol nehw garnibgb mteh aoal(re ltntaef ta iths aestg dan on emro "omndu on un"m)do

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +20  
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 +3  
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(397),
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shiT rome kilyel to be rctsideiu teahrr athn evtixalas /cb

het lab ydtsu whsso a lanre tfnouyindsc BN(U p;ma& eainrtCnie are veed)atel

stMo klylei eht iaetpnt udseab polo ricedt;sui slao snkow to ecasu citaonnoctr ,ailosdkal longa wiht lnare obsrempl uhsc sa tiitealitsnr iheistpnr

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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riePme hsa on tusrtcanfa

noisgiAetnn II - tneeadreg in lahioepyvom

litmayloipD letinchi aak ayyopticiidmhetlihhpalllpnsood gnul ustranftca

listophoydsPhlotaini a5bs-ep,tspo4ihh kaa IP2P Gq orrecept atywhap

taipnoilehrsdyhPse -dleoivvn ni inticsnir apopissto enhw eexdspo on xerlulaatrecl efracuss

nmpSlinyoeihg - sopcemos nlyeim nad lsoa ahs slero ni siglna iundons,cattr i.osptaops thciiL:en emSngohniiypl atroi ;t2g& acesntidi rtmaeu leaft gslun.

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) +19  


submitted by hayayah(1080),
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The egamad si ni teh L ainbimrd in eht raea cneiftfga the icicrnoplatso acrt.t eesaBuc ti si in hte ia,dnbmri ussocniedta in the rsidyapm (luedal)m so it illw swho tlarleaipsi tfyulcnaidson toorm ginss.

Ptoho fo niabirmd and niarmttop resaa: msuaoHyhRrrt/.ltL

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(261),
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olfwnteeS l gih oegl r,ild.eh(.yc cp i:rha →nsc iesse eeaeniog)uidtmt Arpurncoe aceoddetTi Psd rTsN→esac/ ea deadn Adea+ +PK umCapp+2 oiuaondisiif ty vtfc →f dnN +aa arwte tet niho →c lle lnelusr lcgwaiell

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(261),
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wnftSlhioegle   .(.p ,r lhlcdeioyegc naitcosmadi her sg nesut→e:i)iee core ptscaAeidPu noredTd ade+an KeTeN→+ ssdaP/ redAa c upmp2Ca+  ftio sdun→ oiivffiyact a+ndN a atrwe nht otie l cle→  geilunrelwclalls

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