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Welcome to trichotillomaniac’s page.
Contributor score: 104


Comments ...

 +5  (nbme18#30)
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sit tsbe to htikn baotu iyuapttir msodneaa sa eno fo htere gbi tos,poin clrnapoit en,secrtig HTAC sne,grtiec or GH nrect.iges Teh oyln riiatyput mtoru ttha usacse rospsoositoe adn hetereorf eht cnssioomepr rasrcfeut nese in teh iueqtsosn olcdu eb a ATHC rteisncge iruaptyti eadanom (otne: aodmranmaeco utjs senma taht teh mruot si 1;0mmg&t ni ie.sz) rnaecsied CAHT lesad ot riedensca socltoir dna eehorrtfe ecdesedra csbtotosaile vaiyctti enbo( rman)iotfo = tssooisoreop

nnp  even prolactin causes reduced bone density +2
jmangels  I was thinking the same thing about the prolactin, but the weight gain made me lean toward ACTH +2
jurrutia  Prolactinoma reduces bone density due to suppression of estrogen. However, that wouldn't explain weight gain. +

 +7  (nbme22#25)
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ayliblcas ulosegc matiesuslt tBae llsec to toxeyosce ni.ilnus yAn eopsscr inolgivvn xsiyotosec ivsvonel unifso fo an llalncrrieuat lveices wiht eht apmlsa rae.embnm


 +0  (nbme22#25)
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lybliasca useoclg iuttasmsle aetB llsce ot oseyxtoc sii.nnlu nA pcessro ninlgvvoi tysoioexcs novlsiev sunfoi do an lratlnclaiuer vislece wthi het amslap bnreeamm.


 +0  (nbme22#23)
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dobiestnia morf aagstni teh rtsieanpevyp Ca+2 ehnlsacn ta het -oJMNsmt cyonlmmo eesn in tteipasn htwi slmla lcle lgun ecacrn


 +0  (nbme22#23)
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neidabiots rfom tgaisan hte yearpevsitnp 2a+C nnhlaesc at eht -MmJsNot ylnocmmo sene in tiaetsnp thwi lmlsa llce ugnl cecrna


 +6  (nbme24#44)
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corpi is a quneoo.ruoolifnl eth MAO fo qiolofouolnunres si ot binihit ckayotrropi oporsemotsi II (DAN )seyarG nlcsaoaicoly rmGa (-) gosinarsm keil lce-io doveple escaetsnri yb ngmtiuat threi NAD gesyar os gsdru keil porci tnncoa ibhiint





Subcomments ...

submitted by lsmarshall(396),
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I toghuht isth saw a tcikr tsnoeuqi cinse iskn cecrnsa era hte tsmo cmnmoo tpey fo ccarsen oar.evll tBu ylaautlc nagom IVH sttn,peia VaHtee-dIlr ccnsera are cuhm meor cmonom ahtn HIedroe--ntnaVl anseccr e(nev sink necs).acr cEedu-nBVdi arymirp SCN mmaolpyh is eht nloy itnoop that is DinfgsdAIni-e le.snnsaceirlc/

medskool123  why not hep B? i guess another whats the better answer ones... Just rem reading that it was more common with aids pts.. anyone have an idea about this? +1  
haliburton  Yes, I think CNS lymphoma as an AIDS defining illness wins the day. My thought was since SHE has AIDS it is most likely from IVDA, which has a high risk of HBV that could go undiagnosed for a long time. at 32, that might not be long enough to have HBV and get HCC (but with no immune system...?) +3  
yotsubato  God damn this is such BULLSHIT... +13  
trichotillomaniac  Why you gotta do me dirty like this NBME +2  
sars  My thought process, usually wrong all the time, was that HBV (IVDU) can occur to anyone. Acute hepatitis to Chronic occurs when HBV incorporates its DNA into host and releases mutagenic proteins. This is regardless of immunosuppresion. Primary CNS Lymphoma reappears primarily when you are immunosuppressed (organ transplant, immunodeficiency, HIV/AIDS). +  
syoung07  Hep C is far more likely to become HCC than hep B +1  
jurrutia  Even if you were thinking skin cancer is more common, that's only true for basal cell and squamous. Melanoma is rare. EBV much more likely in aids patient. Even H pylori was a better answer. +  


submitted by lauri(-2),
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I OATNCN EWIV TEH RITENE QUSOITN.E SI STIH NMAOL?R

trichotillomaniac  Hi Lauri, this is normal. We can't post the whole question due to copy right laws but you can almost always find the question you are looking for and the answer to by going to the form and then Ctrl + find -ing the age of the patient and other key words or the answer! +6  
drdoom  HI LAURI. THANK YOU FOR DEMONSTRATING YOUR PROFICIENCY WITH ALL-CAP COMPOSITION! +4  


submitted by bubbles(67),
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stuJ sa racntaifiilc,o yrpialalc rhaditcysto seeupsrr odlwu sadceeer ueebacs of csmtiesy ntitvoranciscoso in sesenopr to itrcao uupet/yirsestmrc inoth?npyoes

lolmedlol  i believe you get peripheral vasoconstriction and central vasodilation in the first stages of shock, which would cause stasis in the capillary beds, which would mean decreased capillary hydrostatic pressure, despite interstital hydrostatic pressure going down as well. https://www.sciencedirect.com/topics/medicine-and-dentistry/vasoconstriction and amboss shock description +1  
trichotillomaniac  ^ this type of question is really hard for me to conceptualize. the link above walks you through it step by step with pictures. Theres not much of an explanation in FA. +  
trichotillomaniac  Overall is has to do with osmotic vs hydrostatic pressure. osmotic pressure stays the same and hydrostatic decreases. Hydrostatic pressure is the pressure pushing fluid out of the capillary and in the setting of blood loss this would decrease in efforts to keep as much fluid in the intravascular compartment as possible +2  


submitted by bubbles(67),
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stJu as cotacalf,iiirn lrlycaiap ahtystcodri suprrsee ulowd dreeeacs seabeuc of ecytssmi ntrosiovoiccsnta ni sesrpeon ot ocairt uetspseymuirr/tc yte?nnhspoio

lolmedlol  i believe you get peripheral vasoconstriction and central vasodilation in the first stages of shock, which would cause stasis in the capillary beds, which would mean decreased capillary hydrostatic pressure, despite interstital hydrostatic pressure going down as well. https://www.sciencedirect.com/topics/medicine-and-dentistry/vasoconstriction and amboss shock description +1  
trichotillomaniac  ^ this type of question is really hard for me to conceptualize. the link above walks you through it step by step with pictures. Theres not much of an explanation in FA. +  
trichotillomaniac  Overall is has to do with osmotic vs hydrostatic pressure. osmotic pressure stays the same and hydrostatic decreases. Hydrostatic pressure is the pressure pushing fluid out of the capillary and in the setting of blood loss this would decrease in efforts to keep as much fluid in the intravascular compartment as possible +2  


submitted by bubbles(67),
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tsuJ sa lt,frciiacoian acpaliryl tasoictryhd seeprrus wdlou sedrcaee usabeec of setimycs ovicctsstninooar ni rpsoeesn to tiaorc t/tyrcpsrsuemieu h?nyosontepi

lolmedlol  i believe you get peripheral vasoconstriction and central vasodilation in the first stages of shock, which would cause stasis in the capillary beds, which would mean decreased capillary hydrostatic pressure, despite interstital hydrostatic pressure going down as well. https://www.sciencedirect.com/topics/medicine-and-dentistry/vasoconstriction and amboss shock description +1  
trichotillomaniac  ^ this type of question is really hard for me to conceptualize. the link above walks you through it step by step with pictures. Theres not much of an explanation in FA. +  
trichotillomaniac  Overall is has to do with osmotic vs hydrostatic pressure. osmotic pressure stays the same and hydrostatic decreases. Hydrostatic pressure is the pressure pushing fluid out of the capillary and in the setting of blood loss this would decrease in efforts to keep as much fluid in the intravascular compartment as possible +2  


submitted by sacredazn(80),
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The cptcnoe is a ocldvnutoe way fo sigakn if yuo eknw woh VDJ meoconrinatib wkso,r hchwi is atht ti si uatlylac an apxmeel of tenrgila eht DNA of hte BT/ emctyhlyp.o

oSruthen lotb qi:utcnhee So ewhn teyh esu a boepr atsigna semo ,rgonie adn tuontiutgp a zsei of 15. bk ro 6 kb, hits is llnietg uyo eth sezi fo eth NAD mfrateng ni ehca ecll dnot’e(s etratm if yhte ays J obepr ro ctnnotsa ieonrg erp,ob ryeth’e just yisnag r’yhtee girgtaent seom nceiutoled eqesnuec ndufo in het Ig cRTulCo/s abet cinha oucls lepeviytescr orf /TB l)c.lse

I ktinh the ncfgiusno tpar udolc eb irnownedg ohw oyu nokw hhewert ourye’ ypltra ohrutgh renramtngreea narsew( hciceos B hrut D) ro if ti sna’ht cocuerdr at lla tey ocr(tecr ns)a.wre ,reHe teh otpnecc si htta B leslc gourdne (DV)J mnrnareeargte in the oebn worm,ar hwile T slcel od it ni hte my,shtu dna it lal pasphne at n.ceo So a paaslm cell ni eth blood kiel ni ilupltMe ymaMelo wulod avhe ulyfl nuereodng iornt,mbaocnei eiwlh a T lcle in eth bdolo dlcuo tehire eb fylul edeuactd n(da have hinsfide DJV aneb)initocmor or umirmtea n’(htsa stdeart ).DJV

Seicn the T lcel eneg aws 6 bk nad nietdiyfel grigeb htna het 51. bk ene,g teh T ellc astn’h ugednenro obnricntioaem .eyt

trichotillomaniac  very nice explanation! +27  
nwinkelmann  This was awesome! Made so much sense and hopefully I will be able to think that critically about questions in the future (because I NEVER would have come up with this on my own, hah). +4  
eacv  OMG! THANK YOU. I DIDNT KNOW ANYTHING about this!! Hope this is not testesd on real examen :p +4  
ajss  wow! this explanation was awesome! thanks! +  
mrglass  Also the T-cell V-D-J segments are not the same as the B-cell V-D-J segments. Therefore a B-cell J segment southern blot would look for whether the B-cell site VDJ segment in a T-cell, which would always non-rearranged. +6  
mynamejeff  Thank you! So is this because multiple myeloma produces excessive monoclonal light chain Ig? Is this the 1.5 kb gene? Whereas, T-cells that have not gone through differentiation yet and their J region includes everything (VDJ) vs. just VJ in the light chain? (FA 2020 pg 104) +  
peridot  This explanation is amazing! However, to fully understand another step of what the question is getting at, please take a look at @highyieldboardswards's and/or @mrglass' explanation as well - a very important addition!! +  


submitted by airhead5(2),
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seDo aonyne nkow hte deaessi ehyt aer taknlgi tau?bo I saw ntinkghi plsuu wihhc seakm eenss ithw eht a,srwen tbu i c’ant find ihygnant on oatirnre hrbcmea of eey dan ciohdor l.sxeup

liverdietrying  It's lupus, all the symptoms listed are classic especially the serositis. Anterior chamber of the eye = uveitis. Choroid plexus = cerebritis. For a great overview, check out this (free) video: https://onlinemeded.org/spa/rheumatology/lupus/acquire +5  
in_a_pass_life  I think this was reactive arthritis, not lupus. Choroid plexus not just in the brain, also in eye (can’t see, can’t pee, can’t climb a tree). Mechanism of reactive arthritis is immune complex deposition, per UWorld, which was correct answer. +5  
trichotillomaniac  The inside of the eye is divided into two chambers: the anterior chamber and the posterior chamber. Both chambers contain fluid, and when there’s inflammation in the eye, a specialist can often see inflammatory cells in the fluid. https://www.hss.edu/conditions_eye-problems-lupus.asp +  
trichotillomaniac  I agree that this is Lupus after doing some more research! +1  
nwinkelmann  I find this article describing the SLE ocular manifestations, including uveitis and cerebritis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4908056/ Also this talks about the lupus cerebritis (choroid plexus inflammation): https://en.wikipedia.org/wiki/Cerebritis +  
medulla  every time I read about Lupus there is something new!! +1  
aakb  woman of child bearing age + serositis + arthralgias/arthritis >=2 +  
aakb  kidney issues (main cause of death in sle) +  


submitted by airhead5(2),
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Does oynane wkon hte aseseid ehty ear ktngial bt?uoa I aws tnkginih lupsu chihw kesma esnse ihtw teh rsen,wa ubt i atnc’ nfid nhnityga on nreoarit bemarch fo eye nad crhiood lu.esxp

liverdietrying  It's lupus, all the symptoms listed are classic especially the serositis. Anterior chamber of the eye = uveitis. Choroid plexus = cerebritis. For a great overview, check out this (free) video: https://onlinemeded.org/spa/rheumatology/lupus/acquire +5  
in_a_pass_life  I think this was reactive arthritis, not lupus. Choroid plexus not just in the brain, also in eye (can’t see, can’t pee, can’t climb a tree). Mechanism of reactive arthritis is immune complex deposition, per UWorld, which was correct answer. +5  
trichotillomaniac  The inside of the eye is divided into two chambers: the anterior chamber and the posterior chamber. Both chambers contain fluid, and when there’s inflammation in the eye, a specialist can often see inflammatory cells in the fluid. https://www.hss.edu/conditions_eye-problems-lupus.asp +  
trichotillomaniac  I agree that this is Lupus after doing some more research! +1  
nwinkelmann  I find this article describing the SLE ocular manifestations, including uveitis and cerebritis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4908056/ Also this talks about the lupus cerebritis (choroid plexus inflammation): https://en.wikipedia.org/wiki/Cerebritis +  
medulla  every time I read about Lupus there is something new!! +1  
aakb  woman of child bearing age + serositis + arthralgias/arthritis >=2 +  
aakb  kidney issues (main cause of death in sle) +  


submitted by m-ice(326),
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hTsi ilrg ahs noMo aseduc by petrrEB-nias uVirs. ehT ymstpsmo aer vlyetriael aevgu, ubt hlepomypdhaynta klie sith owldu eb mmocno orf noMo. Teh BCC owhss eateelvd yhleo,smtcpy gimnpliy siht is nto a abircltea elni,sls so rvial is ykll.ie Cdiboemn iwht hte tenmpayoalyhd,hp htsi aeskm su orywr tbaou noo.M ehT tooSn-Mop sett for BVE is hwat het nuiqetos si eriegrrnf ot wenh ercdngbisi teh eesph ceysttrhyero atnigig.gatnlu rmoF ,rtehe htis ioqesunt equiresr tath uoy know atht in EVB tcfinnei,o BEV ftecsni B ls,elc tbu odse tno ueacs emth to beomce oaanb.lmr Isntde,a DC8 cell,s which ear cleiytva gytirn ot kill the B e,lscl eeocbm nab.omral

medskool123  NBME does trick now and then.. when they zig you zag. then when you think they are going to zag, they zig just to destroy yourself confidence. +17  
kylemax  The abnormal T-cells are known as Downey type II cells (Sketchy) +3  
haliburton  I was recognized EBV, then knew EBV infects Bc, and the atypical lymphocytes are Tc. Then I said CD8 are MHC1 for virii, and bingo bango, boom. +6  
trichotillomaniac  congrats you played yourself +3  
lilyo  Soooooooo EBV infested B- cells is not considered atypical WTFF?? +  
med4fun  They are atypical b/c usually you do not see a super high amount of CD8+ in peripheral blood. Now there are a ton to try to stop the infected cells. +  
aneurysmclip  oh and primary CNS lymphoma caused by EBV has T cells NOT B cells. I just try to remember the peripheral blood has atypical lymphocytes which are CD8+ T cells, and the CNS lymphoma is the opposite, ie; B cells +  


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I locud eb owrn.g. tub the marnol ACN et(lsaoub tupnelrhoi cn)otu sgnare fmor 0(510, ot 030m)8/m,0 sith nptteia si way owbel het omrnal ANC earg,n tsuh a CMFGS ulcdo ephl oobts tnushroelip ichwh rea cngosuetay!lr

mgoyo89  I think there are two questions with this answer!!I was so scared :( +4  
trichotillomaniac  yep ---not IL-2 bc that stimulates Tcells and NK cells- I think I blacked out when I answered this question +  


submitted by famylife(87),
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tNo a lluf aewnrs but i'st a srtat (in teh txnteco fo na :ntou)ritsboc otibnctrOus" of ienur olwf ersulst in na cisnaree in dhoticrsyta sereusspr praixlmo ot eht esit fo nstitc.rboou It si sith duublpi of surepres htta eslda ot teh aoypncmcaing n,api eth seonntiitd fo the locgentlic ssymte ni the nyei,kd adn vleeadet taublauntirr epserssru htta niiettai brautul idnotys.ncfu In the tsirf ydsa fo cr,bonsottiu teh ndaiiltato of het oplyro ltaoimcnp cctgilelno sytesm aym eb m.inalim sA eth enseriadc tayctohsdri prerusse is ssxdreeep ni hte nruryai pscea fo the rillue,mog hfturre fanirtitol aecdresse ro ostsp mllpc.t"eoye ,arH'i(ssonr 0e,2 aprtCeh 133)

trichotillomaniac  the key here is the term hydronephrotic kidney. anytime there is that, there is a post renal obstruction of some sort. The fact that he has progressive renal failure just contributes to the idea that his kidneys have seen damage before and are not able to withstand the pressure from the back up as well. I got tripped up on this. The important thing to note is that Hydronephrosis and dilation = back up = increased in volume pressure (hydrostatic) +5  


submitted by medstruggle(12),
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hWy is hte ewrsan urnoln“agita siues?”t I hhtgtou eratf 14 ydas uoy veha a lfluy mfedor rcsa.

colonelred_  If you go back and look at the image you can see that it was highly vascular which is characteristic of granulation tissue. Scar tissue formation will be closer to 1 month, plus you will see lots of fibrosis on histology. +13  
sympathetikey  It's a bit misleading, for me, since you do see fibrosis intermixed with the granulation tissue, but granulation tissue was a better answer. +2  
haliburton  According to FA 2017: 3-14d: Macrophages, then granulation tissue at margins. 2wk to several months: Contracted scar complete. Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus). i'm getting pretty frustrated with NBME contradictions to FA, and FA omissions of content. this stuff is hard enough to get straight as it is. +1  
yotsubato  Thats cause the NBME exam writers read FA, then make questions not fit in with FA +6  
trichotillomaniac  This fits the timeline laid out in Pathoma! 1-3 wks = granulation tissue with plump fibroblasts, collagen, and blood vessels +10  
alimd  never look at the image in the beginning. They dont want you to success. Most of the time images are made to ditract +1  


submitted by seagull(1443),
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hTe einscatms of sthi ntoqsieu eadm me ovtmi o.bdol

Oen yda a npteati llwi ookl em in eht seey and aks, er"Weh aer trpditiees enbkor "dwon? I illw mslei at mhet and sy,a eh"t esitlanitn smauoc nad tno teh muuodnd."e heTy'll smeil cakb and lI'l lkaw waya and ihknt of this ntmeom sa I pmuj ofmr het .odnwwi

sympathetikey  Too real. +3  
mcl  how do i upvote multiple times +16  
trichotillomaniac  I made an account solely so I could upvote this. +30  
dragon3  ty for the chuckle +6  
cinnapie  @trichotillomaniac Same +3  
thedeadly96  XD made my day! +  
hardly43  RIP legend @seagull +  
seagull  A legend never die +1