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submitted by assoplasty(92),
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I nhtki eth eoctpnc hteer’y sgnteit is eht areedcins GTB eelvsl in apy,nnercg nda nto tsju misdeopiyhtryhr ni .nrleeag

heWn ninsceegr rof eim,yhypd/roripthyosh TSH slleve era WLYAAS lenlfyipearter cheeckd saeeubc yteh ear roem eiivtessn ot nieumt sdcreefifen ni T/34T. efOnt emist THS vlesle cna ensdmoaertt a ehacgn veen ehwn 3/TT4 lseevl rae ni the ulaiiblncsc ea.ngr heT lnoy cnxtiopee to htis uoldw be in reygcapnn d(na I gusse amyeb ilvre fula?rei I dbtou heyt uowdl sak tsih hu)ot.hg Hhig sgonrete lselev srpenvet the veirl rmfo iekbganr wndo TBG, eidlgan to inercadse GBT elvsle in the .rseum sThi sidbn ot rfee ,4T desaregnic hte otnuma of laaeavilb feer 4.T As a amesrptycoon meanic,hsm SHT lsvlee era tatlieynnsr daescrein and eth ATRE fo T4 idctopuorn si iseadrcen ot hesnirepl saleeibn feer 4T sveel.l ovrweHe teh LAOTT ontuam of T4 is ais.dcener

hTe eqitouns si igaksn how to fcomrni rhmoiedtypirysh ni a ngtnpaer nwoam ;g-t-& uoy ndee ot hccek FEER 4T vlesle esaceub( hety uodhsl eb oanmrl eud ot rcsoymaoepnt )psoer.sen uYo anoctn ccekh STH ll(suuay levdaeet ni erapnncyg ot mocpneseat ofr aredecsni BTG,) nad you acnton kcech totla T4 evslle lil(w eb .adie)cresn uoY gto the raenws tghir irhete way but I ktihn isht si a detefnfri gansronie wthor iongd,escinr ebasceu ehty nca sak isth nctcpeo in eotrh xesocttn fo neogrytmisere-,psh dna fi htye stleid HS“T” sa an wrsane heccoi thta wodul be ortcicner.

hungrybox  Extremely thorough answer holy shit thank u so much I hope you ACE Step 1 +7  
arkmoses  great answer assoplasty, I remember goljan talking about this in his endo lecture (dudes a flippin legend holy shit) but it kinda flew over my head! thanks for the break down! +2  
whoissaad  you mean total amount of T4 is "not changed"? 2nd para last sentence. +  
ratadecalle  @whoissaad, in a normal pregnancy total T4 is increased, but the free T4 will be normal and rest of T4 bound to TBG. If patient is hyperthyroid, total T4 would still be increased but the free T4 would now be increased as well. +1  
maxillarythirdmolar  To take it a step further, Goljan mentions that there are a myriad of things circulating in the body, often in a 1:2 ratio of free:bound, so in states like this you could acutally see disruption of this ratio as the body maintains its level of free hormone but further increases its level of bound hormone. Goljan also mentions that you'd see the opposite effect in the presence of steroids and nephrotic syndromes. So you could see decreased total T4 but normal free T4 because the bound amounts go down. +1  
lovebug  Amazing answer! THX +  


submitted by taway(29),
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ustJ sa a noet rfo dayobny eels owh swa WFT at owh 3203)030/()(/92 = a1/.51.. lto of eqinouts ksban udonr /9023 ro( nay lryamisli alreg tarnfoic) uot to 1

gh889  I think you meant 2(29/30)(1/30) just to clarify! +7  
niboonsh  i am confusion +2  
arkmoses  You have to use the hardy weinberg formula (1=p^2+2qp+q^2)and p + q = 1 they basically tell you that q^2=1/900 which makes q=1/30 now you can figure out (p=1-q) so p=1-(1/30), p=29/30 then to figure out carrier you solve for 2qp, 2(29/30)(1/30)=1/15 I got it wrong cuz I forgot how to figure out p but hopefully wont happen on the real deal. +5  
garibay92  2pq= 2(29/30)(1/30).... Transform this to 2 1 1 2 1 x x = _ = ____ 1 1 30 30 15 +  
garibay92  Nevermind :/ It didn't come out as planned :( +  
garibay92  /Users/carlosgutierrez/Desktop/IMG_2423.jpg +  
pg32  How do we know this disease is autosomal recessive? I assumed it was just because they love these carrier frequency questions with AR diseases, but how do we know it's AR? +  
turtlepenlight  Sounds like Gaucher (ish?) if i'm remembering correctly +5  


submitted by nosancuck(85),
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oY ids B tog ON NRNILTEA LAEEMF NOSGAR

Wyh ?ad!??t

We be klioon ta onmoees wtih na YRS romf rede Y io ceehrm!Dy be a Y recmoih Heomi os tyeh eb mkina osem siteTs mitnnDieer tocraF ihchw I eb ersu samke mose niec lli AINT NUELLIARM FTACOR so eyd tani got ttha Faeelm tIneraln actrT u onwk hwta i be syani

Adn scien immizwn si ad AEDLFUT yhte stil eb teitgn edso psysu psli adn resatbes

meningitis  The above explanation is correct (disregarding the hard to read and unprofessional dialect) but just in case anyone was wondering: chromatin-negative= Just a quick way of knowing it was a boy. The term applies to the nuclei of cells in normal males as well as those in individuals with certain chromosomal abnormalities +16  
yotsubato  Turner syndrome patients are also chromatin negative as well though.... +5  
sympathetikey  I didn't know a complication post-meningitis was lack of humor. +5  
sympathetikey  Ah, didn't read the last line. Yeah, that is taking it a bit far +18  
niboonsh  yall are haters. this is the first explanation that has ever made sense to me +5  
arkmoses  https://www.youtube.com/watch?v=yuXL-3eoB-o&t=77s Interesting syndrome watching this helped me to put it into real life perspective, interesting points they have no pubic hair/body hair, they apparently also dont smell, and breast size is usually increased... +1  
whoissaad  How does chormatin-negative indicate a normal cell? Isn't chormatin just condensed DNA? +1  
cienfuegos  According to this paper most individuals with Turner Syndrome are chromatin negative: "One of the initial laboratory procedures used to confirm or rule out this diagnosis involves a sex chromatin determination from a buccal smear. Cells from the lining of the mouth are stained for the presence or absence of X-chromatin or Barr bodies, which represent a portion of an inactivated X chromosome. The typical Turner’s syndrome patient, who has 45 chromosomes and only one sex chromosome (an X), has no Barr bodies and is, therefore, X-chromatin negative. This abnormal X-chromatin negative finding in the majority of Turner’s syndrome females is similar to the result found in a normal male, who also has only one X chromosome, and differs from the X-chromatin positive condition observed in the normal female, who has two X chromosomes. Occasionally, the patient with features of Turner’s syndrome is found to be X-chromatin positive." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6233891/ +1  
hyperfukus  i really hate haters this is awesome! +1  
selectuw  to add to the above, free testosterone is aromatized to estrogen leading to breast development +  
misrao  Is the free testosterone not creating male internal or external gentalia because of the defect in androgen receptors? +  


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tI asid ti asw laatf to mslae ni eotru, dna het unostiqe seadk atbuo ielv bonr psfifng.or ecinS eth emasl nerat’ gnebi obrn in het frits calep, I sida 05% afemels nad 0% lesma.

hungrybox  fuck i got baited +30  
jcrll  "live-born offspring" ← baited +20  
sympathetikey  Same :/ +  
arkmoses  smh +  
niboonsh  why is it 50% females tho? +2  
imgdoc  felt like an idiot after i figured out why i got this wrong. +1  
temmy  oh shit! +  
suckitnbme  This isn't exactly right as males can still be born as evidenced by individuals III 6,9,11. This basically an x-linked recessive disease. A carrier mother can still pass her normal X chromosome to a son (50% chance). It's just that the other 50% chance of passing an affected X chromosome results in death of the fetus in utero. Thus all males actually born will not be affected. +2  
makinallkindzofgainz  @suckitnbme, Correct, but if you're a live-born male, you 100% for sure do NOT have the disease, so the chance of a live-born male "being affected" is 0. +3  
spow  @suckitnbme it's not X-linked recessive, otherwise every single son would be affected and therefore have died in utero. It's X-linked dominant +2  
qball  Jail-baited +