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Welcome to gonyyong’s page.
Contributor score: 83


Comments ...

 +7  (nbme24#3)
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The kdi has eoatigaynsmc eud to pyutber csesxe( nrotteseetso → gsrhse eon)Tti gsoe awya uayralltn y(lpnearatp ni 12 ot 81 mtn)soh

I htink oyu t'nod hvae to od olodb tesst uabcsee eh ahs nlroma auexls toenemledpv rof sih eag nad erhte era no ehotr gis?sn

osler_weber_rendu  How does telling an "embarrassed kid" that he will have big tits for 12-18 months help?! +20
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. +6
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!" +2
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. +1

 +0  (nbme24#11)
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tn'Was seur btaou sero,th ubt ammpymrahgo fro enelagr untppoaoli ins't moecrdemdne tlnui 40

_yeetmasterflex  Also wouldn't mammography be secondary prevention since you'd look for asymptomatic disease already present? +16
suckitnbme  USPSTF recommends starting screening at age 50. 40 by patient choice if there's risk factors. +1

 +3  (nbme24#7)
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hTis saw ni ENMB 20 as tll sI.ew lpsnseia heamaruit + plapaliyr wgtrho si wgsnhoi airailnttson llce o Tcsamhcinari si saetcasoid tihw P"ee SA":C ,aehenntcpi nos,ikmg lnaiein ,yeds nad oecomhilshpadyc.p


 +5  (nbme24#37)
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I itkhn wath ewhrt em off whit shit etouinsq asw rsue"m 4"T - wt'ans seur if atth eamtn oaltt 4T ro sermu T4. yuck,iLl I 'dotn ntkih nya of hte rohte sneo fti orf rtihee so I ussmdae it enmta tlota T4 fro ichhw eht nsrwae kmesa snees





Subcomments ...

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yhW douwl ti not be manaei of ccnhior dssaeei htiw dscereead merus srreifnantr n?ntoicrceonta

lispectedwumbologist  Nevermind I'm stupid as fuck I see my mistake +  
drdoom  be kind to yourself, doc! (it's a long road we're on!) +17  
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 +18  
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... +5  
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 +  
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. +1  
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. +4  


submitted by ameanolacid(20),
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tecrelAsioorssh si eth TSOM monmoc asuce of nlrea taeryr tn.weso.h.iisst omubcafusirrl aadipsysl ibnge eth EOSNCD tmso nocmmo easuc eevn( tghohu ti si tntepmig to oohcse tsih npioto crnindsioeg hte ettanips' pmgd)hoica.re

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 +36  
gonyyong  Why is there ↓ size in both kidneys? This threw me off +2  
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. +6  
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 +5  
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. +2  
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. +1  


submitted by brethren_md(79),
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tiamVin 21B is teh tisotarcdr in itsh iuqsenot ebeusca it laso uscsea a s-rdbadeob,a xctaia igat dna eeedsarc ni nbrtviia.o utB - tVimain 2B1 wlil ton avhe msoytpms keli Hmyeioctl mAiean dearsde(ec ehbnom,igol isarendce .)LDH aniitVm E = nrawes, see lewob ofr nnpexl.otaai

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


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eThe’yr gviing a lot fo unsicfnog atrex itroonimafn hre,e abyem to rpit su .up heyT sjut nwta mulevo fo ,isbiiutnodrt eslmpi as tt.ha

dV = ur[gd eeidanrmtds]i ÷ lsm[aap dgru ctaicor]ennont

tiFrs vtonrec ti lla to g/L ucbease ihst si woh eth narwes lwli e:b

tm:ariisdndee 80 gm = 0.80 gpsaam l :oncoaintctner 4 /lmug = 00.04 L/g

Thu,s

Vd = .080 mrgsa ÷ 004.0 /Lg = 02 L

arCnclaee fo urgd si tno a uhge fatroc esbceua eht ahfl iefl is so gonl ttah hte ugrd si idbugtiitsrn boreef fninigctsia aecelrcna rso.ccu

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) +11  
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. +9  
corgilobacter  I hate NBME... I thought these stupid conversions were over after undergrad. Nope. +1  


submitted by seagull(1112),
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I gtouhht shti aws a pyet 1 TAR btu I wsa rong.w yAn nssgtsoeg?ui

seagull  It looks like it was a type II RTA. The difference is incredibly subtle from the info given in this question. +7  
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 +13  
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(348),
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PAC rsekto nca uaecs "ospspiaraogno" hwich is eht tibiyanli to onezcigre lfiaarim fe.csa dsauCe yb brlaltiae inlssoe of ilusav taocaiissno ra,ase chwih rae sadettui ni eht niirorfe ettlmcorooipacip xtcreo mosfuf(ri gy.rus) hTe ytiibla ot eman srtap fo het afce (,.e.g esn,o tmho)u ro etdyniif iidldvusani yb thoer ecsu .(e,g. tn,oglihc c)oevis is tlef nc.ttia

thutWoi wgnkoin ht,ta immebrgnree aictloicp bloe is onvvledi ni alusvi' ut'ffs adorly,b lnincudig iamge oregpscins adn shit ttaeinp is aingvh seusis wiht rgunnitnddaes gaisme ushdlo be onehug to get to eth rwea.ns

gonyyong  Lol I guessed it exactly because of that +2  
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! +2  
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. +  


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The nwesar si pyeeirlfoahx aesubec teh efrtfaen arc of the slucme etrcsth freexl hsa ot og grtohuh eth rsdola miar and lasdor troo iglgan.a bumD ,tuinseqo I nkow, tub ist’ the nylo wserna atth dema ss.een fI uyo rtuh eth ,GDR uyo tno lony sleo enreafft saiomct rysneso bf,sier yuo lsao olse het ersynos dbeosi ileovndv ni eht voaiusr lrsee.fxe

uoY anc aosl etg opealrefyihx frmo gnadmgai eth fnfeeter nrsuoen thta reinavent eth ecmslu iekl( a )LNM, but sa uoy know eshet aer in teh neatorri nrho and tarlnev am.ri

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 +4  
duat98  I'm confused about why it wouldn't cause muscle atrophy. Isn't that a fever of LMN damage? +2  
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 +1  


submitted by neonem(503),
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I nhtik the edia here is tath fi uoy teak eosmnoe off a IP,P fi e'resth no esapolnm ro any roblpme iwth ginstra pntcodoiru hnet ouy uldsho ese it go odwn orfm nabelsie ued ot mreo teaivgen cdekbefa fo tacgris aity.cid If to,n you lbbopray vhae a nelmopsa th'tas sjut gakinm nsto of isagtnr, suhc sa ni eth scae of loErZnislegloi-nl noy.semdr

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 +28