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Welcome to gonyyong’s page.
Contributor score: 109

Comments ...

 +7  (nbme24#3)
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The dki ash ecsoaiatnymg due to uyrptbe sxecs(e esetroonttse → sn e)srhetogiT esgo aayw lauytlrna ray(ntleppa ni 12 to 81 )nsthom

I nhkti uoy tdno' vhae to od odlbo stest sbceuae eh sha aomlrn esxlau nvedometelp rfo hsi gae dna reeht are on terho sgns?i

osler_weber_rendu  How does telling an "embarrassed kid" that he will have big tits for 12-18 months help?! +29
howdywhat  my exact thought, telling him that it will last for somewhere around a year and a half doesnt seem so reassuring +1
suckitnbme  I thought it was reassuring in that the kid is being told this isn't permanent as well as that this isn't something serious. It's important to inform him about the prognosis. +8
thotcandy  "don't worry your gynecomastia isn't permanent, but the mental scars from the bullying you will receive in HS definitely will be :) good luck!" +4
therealslimshady  What is the gynecomastia is from a prolactinoma? +
misterdoctor69  @therealslimshady the gynecomastia is from the sudden surge of testosterone during puberty being converted into estrogen => more breast tissue. +3
mnunez187  My breasts are not rubbery nodules, thank you very much! +

 +0  (nbme24#11)
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t'sWan seru uoabt rse,oht btu rmmahpyaogm fro ralngee aunippotlo nti's romeddnecme lunit 04

_yeetmasterflex  Also wouldn't mammography be secondary prevention since you'd look for asymptomatic disease already present? +22
suckitnbme  USPSTF recommends starting screening at age 50. 40 by patient choice if there's risk factors. +2
j44n  @_yeetmasterflex thats a good point i didnt think about that +

 +3  (nbme24#7)
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Tshi was ni NEMB 20 sa Iewls. lt ispsnlae mhetuarai + ylialprap hrotwg si ihwgosn aiirttlnaosn lelc hcTm sincoarai si caotadessi ihtw ee"P "A:SC itenhnpeca, moni,kgs lnneiai ,edys dan smhaliccpdeohy.po

 +8  (nbme24#37)
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I ihtkn atwh ethwr em off hiwt sith neiusoqt saw eurms" 4"T - 'nastw suer fi atth tmane tolta T4 ro ursem T4. cLliuyk, I ton'd tikhn nya of het rteho noes itf rfo iethre so I dusasem ti maetn ltoat T4 ofr hhicw the waerns meksa nsese

Subcomments ...

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yWh doluw ti tno be imaena fo orncich iseased ihwt rdacesede mresu firranrnets ocnia?norentct

lispectedwumbologist  Nevermind I'm stupid as fuck I see my mistake +2  
drdoom  be kind to yourself, doc! (it's a long road we're on!) +21  
step1forthewin  Hi, can someone explain the blood smear? isn't it supposed to show hypersegmented neutrophils if it was B12 deficiency? +1  
loftybirdman  I think the blood smear is showing a lone lymphocyte, which should be the same size as a normal RBC. You can see the RBCs in this smear are bigger than that ->macrocytic ->B12 deficiency +23  
seagull  maybe i'm new to the game. but isn't the answer folate deficiency and not B12? Also, i though it was anemia of chronic disease as well. +  
vshummy  Lispectedwumbologist, please explain your mistake? Lol because that seems like a respectible answer to me... +9  
gonyyong  It's a B12 deficiency Ileum is where B12 is reabsorbed, folate is jejunum The blood smear is showing enlarged RBCs Methionine synthase does this conversion, using cofactor B12 +1  
uslme123  Anemia of chronic disease is a microcytic anemia -- I believe this is why they put a lymphocyte on the side -- so we could see that it was a macrocytic anemia. +3  
yotsubato  Thanks NBME, that really helped me.... +1  
keshvi  the question was relatively easy, but the picture was so misguiding i felt! i thought it looked like microcytic RBCs. I guess the key is, that they clearly mentioned distal ileum. and that is THE site for B12 absorption. +6  
sahusema  I didn't even register that was a lymphocyte. I thought I was seeing target cells so I was confused AF +  
drschmoctor  Leave it to NBME to find the palest macrocytes on the planet. +5  
zevvyt  so i guess size is more important than color cause those are hypochromatic as fuck +  
yesa  The NUCLEUS of a lymphocyte should be the same size as a normal RBC, which is not the case here. Under normal circumstances RBCs are not as big as lymphocytes, so this is truly extraordinary = megaloblastic anemia. +  

submitted by ameanolacid(26),
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elAosoestihrcrs si het SOMT cnommo seuca of ernla areytr ti.iotsn.h.swse rfbucirusomal dapisylas ibnge the NOECDS somt cnommo ueacs e(nve gothhu ti is ngetptim to ehosoc sith ointop incdrinsego the 'tetiansp rag)oheipcm.d

xxabi  Is there a situation where you would pick fibromuscular dysplasia over atherosclerosis if given both options? Thanks for your help! +5  
baconpies  Atherosclerosis affects PROXIMAL 1/3 of renal artery Fibromuscular dysplasia affects DISTAL 2/3 of renal artery +52  
gonyyong  Why is there ↓ size in both kidneys? This threw me off +3  
kateinwonderland  @gonyyong : Maybe because narrowed renal a. d/t atherosclerosis led to renal hypoperfusion and decrease in size? +1  
drdre  Fibromuscular dysplasia occurs in young females according to Sattar Pg 67, 2018. +12  
davidw  Normally you will see Fibromuscular dysplasia in a young female 18-35 with high or resistant hypertension. She is older has a history type II DM predispose you to vascular disease and normal to moderate elevation in BP +9  
suckitnbme  @gonyyong there's bilateral renal artery stenosis. The decrease in size of both kidneys should be from atrophy due to lack of renal blood flow. +3  
tyrionwill  1 year ago, she did not present any physical or Lab abnormalities. This means she must not suffer fibromuscular dysplasia, otherwise she must have presented renal abnormalities for a long long time, or even before DM-2. +2  
rockodude  a little surprised that atherosclerosis leading to bilateral renal artery stenosis and shrunken kidneys could happen that quickly after everything was A okay the year prior +1  

submitted by brethren_md(90),
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niaVmit 21B si het otdctaisrr ni this esiutqon ecauesb it lsao sasceu a daabsdbo-,er aiatxc tagi and eeadscre in rovta.ibin uBt - itVinam 2B1 illw not ahev tspmsymo kiel eilctymHo Aeinam serdda(cee lbomoegnhi, acedsnier )LH.D tmnaiiV E = wnr,aes ese lbweo for epla.ntnxoai

gonyyong  Also the MCV was normal, not megaloblastic like you would see in B12 deficiency +8  

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’yeehrT nvggii a lot fo sicfgnnou xetra niontmiorfa ,heer byema to tpir su u.p Tyhe ujst twan uvloem of iuistb,dinort islmep as

Vd = udrg[ einidertasmd] ÷ mlsaap[ rgud nonroanei]tcct

itrFs nrevotc it lal ot g/L bsuacee hits is how eth asernw lwli :be

nmdsreaii:det 08 gm = .008 g aslapm ntcaooiecrnt:n 4 /lmgu = 0.400 g/L


Vd = 800. marsg ÷ .0004 L/g = 02 L

leancCare fo durg is tno a gueh rtaofc cseueba teh fhal lefi si os nogl htat the urdg si sdbgrinutiti bferoe gifnsitcnai clnacaeer u.roscc

gonyyong  I think the distribution half-life and elimination half-life was saying that by the time you checked, it had fully distributed (10 half-lifes) and had not been cleared yet (super long half-life) +14  
soph  1000ug= 1mg and 1g=1000000ug so then 4ug/ml * 1g/ 1000000ug= 0.000004 g/ml 0.000004g/ml * 1000ml/L= 0.004 g/L 80mg*1g/1000mg= 0.08 g vd= 0.08g/ 0.04g/l =20L +4  
tiredofstudying  Or, like a normal human, convert 4ug/mL into mg/L ... which is 4 mg/L. 80mg/4mg/L is 20L. +20  
corgilobacter  I hate NBME... I thought these stupid conversions were over after undergrad. Nope. +1  
yesa  You do 1000000000s of these a day if you do any type of labwork o.O You just get used to it eventually +  

submitted by seagull(1573),
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I ttohghu sith saw a epty 1 RAT utb I saw nAy sin?ogussteg

seagull  It looks like it was a type II RTA. The difference is incredibly subtle from the info given in this question. +13  
gonyyong  He has Fanconi syndrome which is generalized reabsorption defect in PCT which leads to metabolic acidosis and hypophosphatemia → can lead to rickets Also, does lead to type II RTA +16  
duat98  Also the proximal tubule is the place with the highest phosphate absorption rate. That's why PTH works here mostly and a little bit in the distal tubule. +5  
boostcap23  Another easy way to go about this one is the question tells you he has metabolic acidosis, the only that can happen with is Fanconi/Type2 RTA. The rest will cause hypokalemia and metabolic ALKALOSIS. (pg 586 FA) Personally thought if they were going for Fanconi syndrome they would describe a lot more symptoms for the kid like growth failure or hypophosphatemic rickets but its NBME so. +1  

submitted by lsmarshall(417),
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APC krteso acn uscea "oaorgppasison" hiwch si hte iilnbtayi ot izceoerng alimifar afe.cs asduCe yb aelltbira issloen fo ualvis ascniaoisot ,aesar which rea auistdte ni het rirniofe cporpleotoacmiit corext rf(omfusi uyg.)sr Teh tiyilab ot nmea prtas fo the aefc .,e.(g ,oesn uoth)m ro ieydfint lnusidadivi by toehr csue .g(.e, i,othclng sceivo) is etlf inttca.

Wtothiu okigwnn ,that nbimerrmege tlcciopai lbeo si oilvednv in vusli'a s'utff ,labodyr dinngiclu agmei rsnopisceg dna stih naiptte is avihgn iessus wthi giedusrntadnn gmiaes ulhdso be eohgun to egt to teh nar.esw

gonyyong  Lol I guessed it exactly because of that +4  
sympathetikey  Never heard of that one before. Thanks! +1  
karthvee  This is not prosopagnosia, but instead a case of apperceptive agnosia. Wiki: "...patients are more effective at naming two attributes from a single object than they are able to name one attribute on each of the two superimposed objects. In addition they are still able to describe objects in detail and recognize objects by touch." Although, lesions tend to be in the occipito-parietal area so PCA again is the answer! +3  
misterdoctor69  I actually think it's both prosopagnosia AND apperceptive agnosia. She is neither able to recognize her mother's FACE nor is she able to recognize objects w/o the help of other senses (apperceptive agnosia) +  
nifty95  Yea couldn't remember the exact name but I just thought of three pathways (visual, somatosensation, and auditory) all converging somewhere/processor (probably somewhere in the temporal lobe...hippocampus?). Beyond the point, the pathways converge to an area which culminates in recognition. Cut off one of the routes (in this case visual), the other two will still work. How is visual cut off? By the PCA not supplying the area leading to neuronal death resulting in varying loss of visual function depending on the area in the occipital lobe. +1  

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The wrasen is loyehxiarfpe sueceab eth nftereaf arc fo the mesclu tercsth elerfx has ot go hhgtoru eht drolsa mrai dan sadlor ootr glaani.g uDbm uq,oeints I ,onkw but t’si the lyno asrwne thta eamd eses.n fI yuo hurt the ,RGD oyu nto olyn elso efatnrfe cmsitoa eryosns fr,esbi yuo olas soel teh snrosye boesid oidenvlv ni eht ivrsoua s.xfelere

You nac aosl gte epyariehxfol omfr gdmnaagi the refeftne enurons htta nertenvai the cusmle kl(ei a MNL,) but as yuo okwn eehst are in eht irotrean rohn nda rnaevlt

ankistruggles  Thanks! I agree with you. +  
brethren_md  Great explanation. +  
gonyyong  Agreed - I think I got this by thinking about tabes dorsalis (syphillis) and why it has hyporeflexia is due to dorsal root damage +6  
duat98  I'm confused about why it wouldn't cause muscle atrophy. Isn't that a fever of LMN damage? +6  
charcot_bouchard  Muscle atrophy wont occur because alpha motor neuron is intact. Motor control of Corticospinal tract on this is intact. so no atrophy. u can move shiti/ But remeber muscle spindle that is responsible for INITIATING stretach reflex send Ia fibre to DRG from where it synapse with Alpha motor neuron. if DRG is damage ur muscle is fine but u cant initiate strech reflex. areflexia +3  
zevvyt  DRG you lose DTR +1  

submitted by neonem(571),
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I tnhki the diae eher si atht fi ouy eatk eoosenm fof a ,IPP fi t'sreeh on poanlmse ro yna ombrlpe ithw rgstian dcutirnopo tnhe yuo dushlo ees ti go ownd rfom aneelisb eud ot rmoe aevengti ekfcdeab fo stirgca dici.ayt fI ,otn uyo yopalrbb heva a lmosnpea t'asth usjt anigmk nost of ngrista, hscu as in eht ceas fo neligl-lrolsZiEno od.neyrms

gonyyong  I thought it was that if you are taking a PPI, you will see elevated gastrin regardless of it you have a gastrinoma. Thus to confirm diagnosis, you make them stop taking it, then re-measure gastrin → if it's still high, you have confirmed. If it's normal, it's something else +39