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Welcome to bubbles’s page.
Contributor score: 63


Comments ...

 +2  (nbme22#40)
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ekTa a lkoo ta atht eaisvms tetallpe tncou -- vore a lioinlm erp 3mm! That hdolus oiptn uyo otardsw a iemalrofvtloeeipyr sdioedrr of oesm osrt ecnis tshi ealfl 'istn eldngbei out sa arf as ew acn llet rofm hte olbdo lepna i(whhc uwdol put civaetre issbtmorhtyoco on teh dxd).

oNw lt'se look ta otehs .ytyerotresch Namlro -- os sit' ont yothlmiapyec rae,v dan dsrgnnoieic eht klca of osi,keulsyotc apbbyorl ont MCL or odimlye tmpaeisaa.l

oS oru rasnew smut be telsaeins htoorham!ceimbyt


 +4  (nbme22#23)
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aCn oemeson aexpnil rppyeolr owh ew onwk taht shti riatt olfswol Mdielnena nsigtece nad si amuaolost scvseeire dan trmerefourh woh teh anetsrp rwee ?reygstzehoou

I euegdss a olt on hsit oqueisnt adn tgo yluck (:

niboonsh  Autosomal Dominant disorders usually present as defects in structural genes, where as Autosomal Recessive disorders usually present as enzyme deficiencies. P450 is an enzyme, so we are probably dealing with an autosomal recessive disorder. furthermore, the question states there was a "homozygous presence of p450.....". In autosomal recessive problemos, parents are usually heterozygous, meaning that 1/4 of their kiddos will be affected (aka homozygous), 1/2 of the kids will be carriers, and 1/4 of their kids will be unaffected. +27
nwinkelmann  Is this how we should attack this probelm?: First clue stating endoxifen is active metabolite of Tamoxifen should make us recognize this undering first pass hepatic CYP450 metabolism? Once we know that, the fact that the metabolite is decrease suggests an enzyme defect, which is supported by patient's homozygous enzyme alleles. Then use the general rule that enzyme defects are AR whereas structural protein defects are AD inheritance patters. Once we know the pattern, think that most common transmission of AR comes from two carrier parents. So offspring alleles = 25% homozygous normal, 50% heterozygous carrier, and 25% homozygous affected, thus sister has a 25% of having the same alleles as patient (i.e. homozygous CYP450 2D6*4)? +6
impostersyndromel1000  we had the exact same thought process, so i too am hoping this is the correct way to approach it get reasoning friend +
ajss  thanks for this explanation, I totally forgot about AR patterns are most likely enzymes deficiencies, this kind of make the question easier if you approach it that way, thanks +

 +0  (nbme22#2)
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sJut sa ana,irfcoliitc ypliclara ohtyrasidtc surpeesr odwul sceedrea cubaese of istemscy norcoicsttsaniov ni sesreopn ot tcioar emicytt/ruesspru eptoo?niysnh

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

 +13  (nbme22#42)
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oihcCnr alren ffnyisnci:ieuc

)1 opro toppasehh cnaceearl --;t&g hgih rmuse iocngairn suhhopoopsr

2) ihgh serum hphpsaote &t-g-; plcoesxem ihtw altvndie tcioan Ca -;tg&- aC fasll

)3 aC alsfl --g;t& trgegris PHT ixas

)4 kdieny flraeui g--&;t serededac civaiytt of e-hxlydao1yrs at hte dyekni t&;--g sesl ciloltcrai

makinallkindzofgainz  this guy renals +4
paperbackwriter  Someone please help me with this (always trips me up): PTH causes increased vit D production in kidney... are we assuming the increased PTH can't catch up with the kidney failure? Is it the level prior to PTH compensation that they want? D: +
miriamp3  @paperbackwriter what it works for me ;;;; is find the first abnormality so CKD low calcitriol (no D vit) ---> is gonna increase PTH ---> the kidney are not working (chronic, they don't tell u recently- you can;t revert a CKD so the kidney never going to catch up) --> increase inorganic phosphorus.--> always start with the problem. I also use this for celiac and types of shocks. start with the problem, and trust yourself. +2
paperbackwriter  @miriamp3 thank you! I will try out your strategy next time!! :) +1
snripper  I thought renal insufficiency -> inability to reabsorb phosphate at PCT -> decreased phosphate? +2

 +3  (nbme22#1)
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sThi snteuioq oducfnes me a tol eaesubc os nmya qsutnoeis vahe edlrdil me on hte rnpcemitao of hte NPA seepca nmsaemihc ni mitse of dufil rdvaoeol s(a in HC).F

I totghhu PAN asw a huge apelyr ni het lsso fo Na in smnetruiscacc fo evlmuo loraeodv as ni this teanipt iwch(h is hyw uoy ese vucloeime ynrOeiahtpam in stintepa htwi HSIAD or ivecyoravtti of eht RAAS as ni F.)CH

Why si DAH won ebngi ndema sa the plssrenobei ?gntae

jooceman739  My thinking is that ANP causes natriuresis, so you're losing salt and water at the same time (isoosmotic fluid?). Meanwhile, ADH absorbs only free water, so it would dilute the serum. Correct me if i'm wrong. +9
bubbles  Ohhh you are right. Thank you for the explanation! I got so fixated on that one mechanism haha. +3

 +12  (nbme22#47)
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Bemnseta arneebmm getitiynr si eth dtienamtenr of lflu nugl vcyoeerr lwfiloogn mlypaonru iultsn.

ymmSaru:

)1( sols of metbneas meberamn tyngtriei is ialcictr in nmtnedgieri eht n“opit of no ”e,rrnut nda ctibetrnuos to eth ytabiliin to lseartehisb nroaml guln ertucetcarhi htiw iooorpntm of sobriif;s

)2( slso fo laipteehil el,scl thilaoledne esllc, dan nesmaetb baeenmrm ryitgiten ni aulsu ltsiatnrtiei omapnineu ecsoitaads iwht phaioidcit umnpayrlo siisrobf ldsea to yeoddsret ugln turrehiactec adn retupapel is;orfbsi

)3( nmsrgftaiorn tghorw otacfβr- si sae,cyerns utb nto ltreiyen inticsfufe, to otroepm enrntapme r;ssibifo

)(4 rteintspse tjnytninir/gaetuinr/iar is iiatlccr ofr eht otiarnopgpa of isi;osfbr

()5 ipioadhtci apmyunolr fbiisrso si an xmapeel fo a sorsepc reatedl to teh tcesrpneesi fo an n(ngs”,ea)t“i ohriccn ,faanomimitln dan srfbisoi; nad

6() euinuq lescl are ctilaicr lelalcru epraysl ni hte nrioegltau of i.sofribs

ctant oi:io.s4p/clmwl/nthw/cs/4t5MPivr.i/gae2.nmpn.C2b/1:ic6thw

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

 +0  (nbme22#41)
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dtunWol' iontrtoscnic fo hplairpree sessvel laos egtrgri hpnlascnci ssvn,raocntcotiio chhiw isuealtms nrlea eiscmiah nad aeucss cdsneaeir RASA i?ytitcva

drdoom  Constriction of peripheral (cutaneous) arterioles/capillaries in response to cold surroundings is an attempt to reduce heat loss & maintain internal body temp; it is not at all coupled with splanchnic vasoconstriction. In fact, the peripheral vasoconstriction is trying to “re-route” blood to more internal/visceral compartments; simultaneous splanchnic vasoconstriction would impede that very process! +35
bubbles  Ah, okay! I got led off track because I had a bunch of super hard practice questions asking about hepatorenal syndrome and how the constriction of sphlancnic vessels might trigger renal ischemia. Do you know if there would ever be a time when sphlancnic vasoconstriction occur outside of hepatorenal syndrome? +
drdoom  @bubbles i would think only in cases of catastrophic shock (when the body is doing everything it can to maintain central tension; pressure to vital organs like heart,kidneys); in those cases, i could see the body sacrificing visceral flow as an "option of last resort" +

 +0  (nbme22#50)
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anC enmsoeo lucdo neailxp ot em how isht si uulelnyoqivac srubutoe iseorcsls sipeted -1NF nda rbgeuet-SerW oasl sgpniernte ithw knis soinels, pmtpinhoyeedg ,lceasmu dan zeur?essi

nAd ciigsdronen the aenvitge falimy siythr,o I udwol aehv dsesmau that a dscoapir mnatouti kile( SW) uwlod be rmeo l..iyekl.

cocoxaurus  This question was tricky! Tuberous sclerosis= Hypopigmented= Ash leaf spot (The skin lesion in NF is Hyperpigmented- Cafe au lait and in Sturge Weber it's a port wine stain (also not hypopigmented). I'm assuming that the SINGLE raised flesh colored lesion is a Hamartoma (The angiofibromas in NF1 are typically multiple). Although both Tuberous Sclerosis and Sturge Weber are both associated with seizures, I used all the other stuff to narrow it down to the correct answer. Also, don't forget that there is Incomplete penetrance and variable expressivity in Tuberous Sclerosis. So I think the lack of family history of "seizure or major medical illness" was there to throw us off. +18
bubbles  Thank you! :) I thought I really knew my congenital disorders, so I was a little annoyed when they trotted this question out +7
pg32  @cocoxaurus I believe the single raised flesh-colored lesion is actually a Shagreen patch, which helps you arrive at TSC as the diagnosis. +1

 +2  (nbme22#33)
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uJts to be ctsalyr clare escuaeb( eIv' eottng emro yrhoitd saxi uqtoissne gwonr tnha I :us)ohdl

T4 -t-g;& 3T is piolessb tbu T3 ;-gt&- 4T 'sint?

meningitis  Exactly. I know there are papers saying there is some conversion of T3 to T4 but I try to keep it simple and think of it as once you break it apart (T4->T3), you cant put it back together. Only thyroglobin etc can put another I on it, so any T3 cant become T4 because you need it to be done in thyroid. +8
angelaq11  I honestly don't know about this, but the way I reasoned this was: she is taking a whole lot of T3, so on top of already having hypothyroidism, she is just making things worse, so TSH is going to be decreased because of feedback inhibition, and hence T4 (Which is the main one produced by the thyroid) is also going to be decreased. I think the high T3 is the exogenous T3. +

 +21  (nbme22#13)
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oFr the speep ohw tog ecunofds no htis ouenitqs bc of l'soUdrW dweri seiqotnu on IVH ivarl aldo:

aeuct IHV-1 nite:cniof HIGH vlair do,al wlo -AHI2 Vb fno:itienc LWO lariv ,lado wlo Ab c(b rdasatnd VHI yssasa tedtec p,24 hwchi si tno rsptene on I2-H)V

Kinda aeonynd I iesdsm an ysae monglumyio cteopnc esuonqti /:

eacv  I feel you my friend! same stupid mistake over here -.- +3
step1soon  FA 2019 pg 176 +2

 -7  (nbme22#3)
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Soryr fi mI' negbi we.n.yh.sed edso htis monwa haev ahdrriea ude ot ,tntaiss ,tied adn rees?eixc I ddnt'i rlaely tsrnedunad ahwt heyt wree nagsik rof eher ot eb .tnsheo

.ooo.   I believe they were asking what the most common effect of statins, which is GI upset (including diarrhea). Rarely you can have hepatotoxicity and myopathy but neither of these are a side effect in the answer choices. Hopefully this helps! +1
niboonsh  Theyre asking about the most common side effect of Orlistat - which is really fatty diarrhea +2
asharm10  Orlistat is not a statin drug, it basically inhibits pancreatic lipase so that you absorb less fatm drug is used for weight loss. So when you are not absorbing fat you are inviting diarrhea. +2

 +1  (nbme22#33)
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saH bnodayy onduf a ogdo itanealopxn for tish g?oshtoyli I eenigyuln aehv no iade thwa m'I glkooin ta.

meningitis  This is common in Klinefelter.. think of the equivalent of Streaked ovaries seen in Turners. White streaks, red/pink material of hyaline, and hyperplasia of Leydig cells. Just remember: It doesn't look like normal structured testicle histology (No organized seminiferous tubules with Sertoli cells around) +9

 -1  (nbme22#34)
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.Sso.al.nct-roeoc teudssi ecmproa a oupgr of poeple htiw eth seiseda dna a pgoru fo polepe huttoiw the sdisee.a mI' ton eurs I durnasndet hyw ouy nac allc eoppel onydmalr nad alcl that a tncorol p.uorg tahW if mngao ohtse lacdel o,rlmdyna moes fo thme ehva sola dah orecahhmirg trsko?es

impostersyndromel1000  this is one of those Qs where you just dont over think it and focus on your first point, that they are comparing a group with the disease vs (potentially) one without it. Thats what i took from it at least (sorry fi this is too late) +3
tiagob  Why is not Cohort ? since it compares groups exposed to drug X? +
djinn  Cohort studies determines end of disease and CC determines begins +2




Subcomments ...

submitted by mcl(517),
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To dpaxen on s,tih tlolhaoigsuepntyo eberidssc eth hisoyoltg fo pioaswk acamsor sa lepd"nsi lecsl iormngf lssti htwi saaetravxetd dre oldob s"elcl

mcl  lul i don't know why i spell kaposi like that, my b +8  
bubbles  This site is super helpful. Thanks for sharing :) +  
mcl  yesssssss ofc <3 I love path outlines +  
usmleuser007  Just realize that spindle cells are similar to the endothelial cells of blood vessels. Anything that have vessel association might have spindle-shaped cells. a. NF-1 b. NF-2 ~ Schwannoma (Antoni A) = Cutaneous neurofibroma ~ high cellularity (w/ palisading patterns with interspersing nuclear-free zones called Verocay bodies c. Leiomyoma (uterus & esophagus) d. Mesothelioma (cytokeratin positive) e. Anaplastic Thyroid cancer (biphasic & along with giant cells) f. Medullary Thyroid cancer (can also have polygonal cells) g. Primary cardiac angiosarcoma (malignant vascular spindle cells) h. Osteosarcoma (bone cancer) (pleomorphic cells) i. Meningioma j. Kaposi's Sarcoma (HHV-8) = Slit-like vascular spaces with plump spindle-shaped stromal cells +4  


submitted by bubbles(63),
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Thsi iqseutno oesdcnuf me a tol esacbue so myna ntsioqsue avhe ddlelri me on eht eiocatnmrp fo the APN peesac cnismhmea in emtis of dlfiu odeloarv sa( ni CH).F

I gtohthu PAN wsa a gehu ylpaer in teh loss fo Na in imcrassucetcn fo uoevml oveoldra as ni itsh patnite hh(cwi si ywh uyo see emoveclui miyhnpetraaO in tpsiaten whit ADSIH or ravictityoev fo eth RSAA sa ni .HCF)

hWy is ADH wno gebin dmaen sa the sorleinspeb gea?nt

jooceman739  My thinking is that ANP causes natriuresis, so you're losing salt and water at the same time (isoosmotic fluid?). Meanwhile, ADH absorbs only free water, so it would dilute the serum. Correct me if i'm wrong. +9  
bubbles  Ohhh you are right. Thank you for the explanation! I got so fixated on that one mechanism haha. +3  


submitted by bubbles(63),
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nuld'Wto notinccitsor fo hraelrpeip sseslve oals rggriet hnscainplc osinvntotora,ccsi whchi iselmasut alren mihicaes adn sseacu eiacrdnes ARSA ctiyv?iat

drdoom  Constriction of peripheral (cutaneous) arterioles/capillaries in response to cold surroundings is an attempt to reduce heat loss & maintain internal body temp; it is not at all coupled with splanchnic vasoconstriction. In fact, the peripheral vasoconstriction is trying to “re-route” blood to more internal/visceral compartments; simultaneous splanchnic vasoconstriction would impede that very process! +35  
bubbles  Ah, okay! I got led off track because I had a bunch of super hard practice questions asking about hepatorenal syndrome and how the constriction of sphlancnic vessels might trigger renal ischemia. Do you know if there would ever be a time when sphlancnic vasoconstriction occur outside of hepatorenal syndrome? +  
drdoom  @bubbles i would think only in cases of catastrophic shock (when the body is doing everything it can to maintain central tension; pressure to vital organs like heart,kidneys); in those cases, i could see the body sacrificing visceral flow as an "option of last resort" +  


submitted by bubbles(63),
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aCn onoesme ludoc ileapxn to em hwo shit is eiquunclvylao ousrbuet slsoirces ipeedst -FN1 nad W-Seureerbtg aslo ipenntsger tihw kisn enslio,s dtyeoppeminhg lscuea,m nda sieers?zu

Adn idnecgriosn hte tgeeaivn aliyfm osy,itrh I odlwu evha asedmus that a pdaisocr monutait ikl(e WS) ldowu be rmoe .lke.yl.i

cocoxaurus  This question was tricky! Tuberous sclerosis= Hypopigmented= Ash leaf spot (The skin lesion in NF is Hyperpigmented- Cafe au lait and in Sturge Weber it's a port wine stain (also not hypopigmented). I'm assuming that the SINGLE raised flesh colored lesion is a Hamartoma (The angiofibromas in NF1 are typically multiple). Although both Tuberous Sclerosis and Sturge Weber are both associated with seizures, I used all the other stuff to narrow it down to the correct answer. Also, don't forget that there is Incomplete penetrance and variable expressivity in Tuberous Sclerosis. So I think the lack of family history of "seizure or major medical illness" was there to throw us off. +18  
bubbles  Thank you! :) I thought I really knew my congenital disorders, so I was a little annoyed when they trotted this question out +7  
pg32  @cocoxaurus I believe the single raised flesh-colored lesion is actually a Shagreen patch, which helps you arrive at TSC as the diagnosis. +1  


submitted by shaydawn88(8),
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I ulwdo hntik ruslontoie vlinevso eth smet elscl tpey( II ypemsceo.tun) sI hte iattnc eeanmbst mebemnar the nsaerw auesecb ti tmliis prsead?

aesalmon  I would also like to know if anyone can answer this question - I saw it as a Sattar "one day, one week, one month" kind of question. Its probably very simple but I still don't get it +  
bubbles  I posted a new comment explaining: basement membrane integrity is the strongest determinant of full fx recovery following pulmonary insult :) +3  
drdoom  You have to think about it this way: the basement membrane is the “scaffolding” on which [restorative] healing occurs. So, yes, stem cells (type II pneumocytes) would be involved in that healing process but they couldn’t restore the *normal* architecture (“no abnormalities”) without the ‘skeleton’ of the basement membrane telling them where to go, in what direction to grow, which way is “up”, etc. If the basement membrane is destroyed, you can still get healing, but it won’t be organized healing -- it’ll be *disorganized* healing, which does not appear as normal tissue. (Disorganized healing is better than no healing, but without a BM, the regenerating cells don’t have any “direction” and therefore can’t restore the normal architecture.) +7  
nwinkelmann  Yes, this a great summary to the post by @bubbles and the article he posted! Another way to think of the question is not, what causes repair, but what causes irreversible injury/fibrosis. That article explained an experiment that showed TGF-beta was necessary to initiate fibrosis, but if BM was intact and TGF-beta was removed, the fibrosis didn't persist, i.e. intact BM is protective against TGF-beta. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/ +  


submitted by keycompany(268),
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mwchC8s0elpgn2/:ioi./.rw.cbwi95lM/6nt/hc/n0v/spatmP.t

rsOel iSgn si a tlivesiiswyt-,on liyoecptis-wfc dfining fo keborMceng rteiessisAroorlcol MA)( cziretahderac by a" aplabpel tgloauhh lsseeulps, ailrad rteayr eiwhl eht BP fufc si enafltdi vaobe itlsysoc pr.e"sresu

It si olspeisb tath reth: e)ia The lioweiic-fcpyst fo tshi stet nmsae it is laos cpallaibep ot seirlsreotcsaho to(n ustj A )b)M ehT ENBM trrlncyieoc isimepl atht MA is regaihcbnlenta htiw ehtsoiassrore.lc

bubbles  This was my reasoning, too. I thought this was Mockenberg for sure +  
hello  I don't think think it's a type. According to 2 other comments: "It's atherosclerosis because it said “radial artery is NON-pulsatile BUT REMAINS PALPABLE even as the cuff is inflated”--> normally, you can’t feel the artery when the cuff is overinflated b/c overindlation occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!): "If if something were to not be palpable then it would have to collapse -- atheroclerosis prevents this vessel collapse." +16  
arcanumm  I agree, I just reasoned that atherosclerosis would not be thicker when the lumen is blocked. I don't think they were going for Mockenberg at all. +  
arcanumm  would be thicker +  
drzed  Atherosclerosis isn't common in the radial artery though... it's common in the abdominal aorta + coronary, popliteal, and carotid arteries. I am not going to assume a guy has radial artery atherosclerosis when he is in his 80s without a dyslipidemia syndrome over monckeberg calcification! +  
haydenelise  Would've thanked you for your explanation @mdmike if it hadn't included the "whoever upvoted this is dumb" comment. What a turd lol +4  


submitted by skraniotis(9),
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ndayidlzeU nlare iufealr sdlae to olbtcaime o,adisisc adn as a tsruel cbbria sgte detdeelp sa ti seitr to ebffur hte lumnoicatuac of incagor ic.asd

bubbles  Thanks for the explanation! Do you know why Mg would not be a potential answer? Phosphate also accumulates in those with undialyzed renal failure, so I was thinking that maybe magnesium as a divalent cation would complex with PO3 (in a mechanism similar to Ca). +  
nwinkelmann  From the little bit of research I just did (because I didn't learn anything about dialysis at my medical school), ESRD can be associated with either low or high Mg levels, so the dialysate can cause either increased or decreased Mg levels depending on the patient's serum content, therefore I don't think based on this question, would could determine if removal of dialysis would lead to elevated or decreased magnesium. The end of the first article seems to favor ESRD leading to hypermagnesemia, so if that's the case, then removal of dialysis would cause Mg to increase as well. https://www.karger.com/Article/FullText/452725 and https://www.karger.com/Article/FullText/485212 +1  
hyperfukus  why is it that we aren't learning this stuff and they r just throwing it on step there's barely a blurb in FA about ckd/eskd +1  
hyperfukus  does uremia potentially have to do with this? +  
medulla  ESRD and not getting dialysis -> he is uremic -> met acidosis -> dec bic +6  
angelaq11  @medulla this is the best and simplest explanation. I got it wrong and chose Mg, wish I had made that connection. +