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Welcome to notadoctor’s page.
Contributor score: 140


Comments ...

 +6  (nbme23#30)
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ELS is ociaesatds hitw ciecfiydne fo erlya oncmlmpete n.gts(eriepo 1C,q 4C, .)2C (AF 1,9 .gp )264

tinydoc  Am I the only one who has never heard of C1Q? +20
llamastep1  I knew SLE is related to low complement but when it talked about a "mutation" it threw me off. +1

 +3  (nbme23#47)
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rcAgdiocn to loaGj,n htmecpilyyoa aver si neo fo eht otms oonmmc esaucs of hCra-diduBi yms.dneor Agocnicrd ot F,A duCha-Bridi si esitcaosda erom genyearll itwh gcopelebaauhryl tet,ass hapociymlyet e,var mtsrpaupto seatts, and CH.C

paiHcte rschrsioi can eb luerd uto edsba on eht teim oescru of eht n'speatit atoeitprnsen - he wsa neif 2 wkese gao nda eth nalabdomi ainp aedrstt na urho a.og

krewfoo99  Also in cirrhosis, the liver wont be enlarged or tender on palpation +1
almondbreeze  @krewfoo99 Good job. accoring to FA2019 pg.368, congestive liver disease (hepatomegaly, ascites, varices, abdominal pain, liver failiure) seems to be the key in Budd-Chiari SD +1

 +6  (nbme23#20)
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eRrbmeem no hooliystg athiss'omoH iiosihttdry ahs otw tinictsd fatsuere Hthülre islhcel(chw aer shpiniceolio cspetmlatia lcsle ahtt ilen loicflls)e dna loiydhmp etagegsrga tihw renaimgl r.setg(pec.n 8,33 AF 190)2 hTe crcoetr sreanw riesdebsc teh retatl eruftae of hostomai.'sH


 +0  (nbme23#39)
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laicCe pesru is a lboptnosrmiaa drymeosn atth estlrus ni steaerhorta dna rlesuts ni onri cdnieiyfec .neamai As arf as 'mI rawe,a nnoe of teh ortehs uretls ni ionr fcncideeiy iea.anm I( dha Bilearatc geohrvrotw sa a lcose ncodes utb I on'td liebeve t'shat atasisceod itwh iron cdy)eiicfen.

yb_26  bacterial overgrowth is associated with iron deficiency, but also with Vit B12-deficiency, so I guess pts will have macrocytic anemia +2
nor16  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099351/. Vit B12 is key here, moreover, no bloating (IBS and bacterial overgrowth with bloating). bacterial overgrowth is a close one! +1
covid2019  I wrongly chose bacterial overgrowth, but that is wrong because Small Intestine Bacterial Overgrowth (SIBO) must be instigated by something. Commonly, anatomic abnormalities (like surgery causing blind loop syndrome, strictures, or motility disorders that allow the poop to ~fester~). +3

 +7  (nbme23#4)
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eTh iiftiendno of i-keMDnnagsioic pCcyiaat acocdinrg to B+B is ilytiab ot mdeephrcon imtnfanroio boaut ssleiln adn rtemnteta tosonip adn eamk ioceshc in gpekein wiht aplseorn svulae.

notadoctor  The decision must also remain stable over time, which is the "consistent values" part of the answer. +13

 +2  (nbme23#45)
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ev'I nbee irnchasge for ym osceur for tish tbu 'atcn mese to nifd it. wvre,eHo the way I oghthtu abtuo it was taht meeda snheapp avi teh licrapesl.ai fI reteh si niaceders niecasster via teh eirprlapycal rcnsehispt as hcum lodob nodltu'w eb lbae to get toni het aipsle.arilc eTh odlob wloud nisedta etg seudhtn via tssnaaosmoe ot hte e.svni Tsih aecltir omfr osoymcoivypg.chl nxeapils ti a lttlie :tbtere CV :hyosglyoiP uesTsi mdaEe dan rlneaGe lpnerisPci of lrnaTayclpsari Fdlui xehEgcan


 +0  (nbme21#6)
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siTh suotineq wsa asngki atbuo het earsedv cfeestf of tonpor ppmu irhonbtiis aeycplelis veign uerspvio iydekn sesius. PPsI seedeacr emsur Mg nad smrue aC opoabnrsti nda nca ersncaie the kisr fo etfacrru le(ylpasiec in the )dleey.lr

yotsubato  PPI therapy *begins* the day she presents. She has not taken PPI before +10
notadoctor  You're right, I missed that! +
naught  MEN 1 is pituitary (monitor cortisol), pancreas, parathyroid (monitor calcium) but is not the ask of this question. +

 +14  (nbme21#36)
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fI you ewer tskcu eenbwte trlmCoarn)ohmnigacsand(ao and eohngbo(rEmaicnd)nn memeberr osedamcnrhon may eerod eht tcerox utb nca eervn tiirvndeapdus/ het etxor.c I inkth isth was eht nocsiinitdt eth qonisute asw tets.gin


 +29  (nbme21#32)
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Ulusa netiitltrisa onmnieuipts is the glotclishaio dnintiiefo fo Iicpoatdhi rmulnpoya si.rfiosb We wkon ttha sthi nepiatt has arupmnloy iosrfibs sbceuae the usqeotni etssta tath hteer si usoibfr hiktgnicen fo eth lavaoler spea.t ihTs etnsoiqu saw usjt istnget taht ew ekwn eht toehr msaen rfo laPrunmyo .bisorsFi

aneurysmclip  Nbme back at it again +20
pg32  Is it still considered idiopathic pulmonary fibrosis is it appears to have been caused by an atypical pneumonia? +
zevvyt  Why not Sarcoidosis? Wouldn't Sarcodosis also be a chronic inflamation with fibrous thickening? +2
swagcabana  UIP is a better answer. Sarcoid is a leap in logic, usual interstitial pneumonitis is textbook histological definition of idiopathic pulmonary fibrosis. The biopsy has no mention of noncaseating granulomas and the clinical picture is not consistent with an inflammatory process. You have to focus on the better answers, try not to get caught up in the "why nots?" Calling this sarcoidosis is like someone coming in with prototypical asthma and jumping to eosinophilic granulomatous with polyangiitis. Sure its a possibility but its definitely not likely. +5
mangotango  I picked “diffuse alveolar damage” with Pulmonary Fibrosis in mind but these are actually key words for ARDS :/ +1
zevvyt  thank you swagcabana! Very good explanation and strategy! +

 +9  (nbme22#27)
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ttatsaMeci easedis si oemr nmoocm tanh pmaiyrr bneo s.mutro

lba9587  Might be helpful to consider eg. of a lung tumor. one lesion? you’re leaning lung primary. Multiple lesions in lung? METS. Q stem here included, “numerous lytic lesions along the vertebral column.” Thus, METS. +

 +10  (nbme20#29)
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liysaAns of eth sitealn in het etiqnsou swodhe a areededcs bnemru fo iseonemds cnlss.-kisor esneimsoD si dema up fo fuor ynleis ds.eriesu efroTrhee lnbaarmo aselint si llkyei ssiingm lsyeni esnarsecy for teh orimfnoat of ehtes senmdoesi .nls-soksicr iiedkpWai traecli on ssmeeDoin.

dbg  how can i trust you, you aint even a doctor +18
euchromatin69  trust this then U.W 1249 +3
tryntofigritout  UW 1249 was perfect. #loveyourname euchromatin ha +




Subcomments ...

submitted by lsmarshall(348),
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Uera lCyce Dodssirre t&g; ateosIld eeevsr mhmmeiyoperaan (;&tg 0;100 ,ie.. on toreh esveer eoatilcbm iussabecndrt

hiriOntne taeaayrrsnbscalm eedcfnciiy g;&t (osmt onomcm earu eyclc i.sd) orcoti aiicrdaieadi/cuam, ehmaioarpneymm

Onaricg msAadciie &tg; aiynemopHrm,eam gpa-onina iocaid,ss tikssoe (orfm yepi)yhmocagl

iMamn-eidchu locAC-ay ereydgaodsnhe decfineyci &tg; Hmnaeamioe,rypm chptiketooy yypcolgimhea s(een ni xniatdβooi- oesrdisrd, ECEXTP u)nkeopaytdrolerosyhd

irLev dnnitcsofyu ;t&g armoHpanmiem,ey sFTL meseds ,up relod pt.

lsmarshall  Summary of metabolic issues relating to hyperammonemia +5  
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +2  
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria? +2  
charcot_bouchard  if it was mitochondrial disorder no one would escape +2  
wowo  figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB) + also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia +2  
artist90  i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong +3  
artist90  it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things 1-how does acidosis cause Hypoglycemia and Ketosis. 2-why is Ammonia elevated in these pts bc urea cycle will be fine? +  
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld) +1  
yex  According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA. +7  


submitted by sajaqua1(462),
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yaena,osictmG esridp oatmi,agan nad pgoomhiaynsd (as lewl as alrmap re)haytem ear lal gnsis fo sxcsee eo.gnrtes heT elirv ni napttsie twhi peihtac esaeisd si drmipiae and os anncot learc erntesog yitsen.uifclf Six 21 oz bsree ldiay 2(7 oz, ro hafl a gla)nol is oot cmu,h dan si itygsnreod shi veril.

uslme123  No hepatosplenomegaly, ascites, or edema through me off. We that being said, I shied away from cirrhosis. I thought that he showed signed of depression, so I went with the thyroid. But who's to say he isn't injection anabolic steroids?! +4  
catch-22  The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum. +11  
notadoctor  He likely has hepatitis B/C given his history of intravenous drug use. I believe both can have liver dysfunction but may or may not have ascites, whereas the type of damage we would expect from alcohol that would match this presentation would also show ascites. +  
charcot_bouchard  For Ascities u need to have portal HTN. Thats a must. (unless exudative cause like Malignancy) +2  
paulkarr  For anyone who needs it; the FA photo is kinda burned into my mind for these questions. NBME has some weird infatuation with this clinical presentation.. FA (2019) Pg: 383 "Cirrhosis and Portal HTN". +3  
snripper  @paulkarr the problem was that the FA image was burned into my mind so without no ascites or edema threw me off of cirrhosis. +  
tyrionwill  cirrhosis doesn't present hepatomegaly, instead, the liver could be shrunken. +1  
avocadotoast  Cirrhosis (most likely due to alcoholism in this patient) leads to an increase in sex hormone binding globulin, causing a relative increase in estrogen compared to androgens. Cirrhosis doesn't always have to present with ascites and adema. I agree with @catch-22 that liver disease is a spectrum. This patient does not have ascites because his liver is still able to produce enough albumin to maintain oncotic pressure in the blood. +1  


submitted by notadoctor(140),
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sihT iqsenuto asw sikagn uoatb het eaesrvd eefsfct of ornotp ppmu rbntsohiii spiaelceyl gnive eoupvsri ydnkei sss.ieu sIPP eseadrce umesr Mg and usmre aC pasotobrin nad nac esirecan het iksr fo crfaruet aesilc(yple in eht )e.ldreyl

yotsubato  PPI therapy *begins* the day she presents. She has not taken PPI before +10  
notadoctor  You're right, I missed that! +  
naught  MEN 1 is pituitary (monitor cortisol), pancreas, parathyroid (monitor calcium) but is not the ask of this question. +  


submitted by brolycow(26),
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eH hsa herat uflaeir ihhcw elsad ot a decserae in rnael bdolo fwol nad eerlaprn am.toeiaz In plernrae imezt,aoa NC:BUr atrio si ;tg&= 20; vtacoinAti fo hte ARSA tmeyss ued to the eprlraen zoiaeamt enams atht eht sepc vagr si gihh at .1520 adn eh si idolnhg onot usdimo so yriunar oidsmu liwl be olw 2&l(t0;, FNEa 1t&l;.%)

figprincess  did you figure out the the ratio by actually divding out the numbers since the q didn't give it as a ratio? also what resource tells us what prerenal spec gravity should be? +  
brolycow  I just usually remember from class that spec grav 1.001-1.010 is considered dilute urine, and anything 1.025 and above is concentrated. For this question specifically, I think I remember there only being one option that even had the ratio >=20, all of the others were like 15 or less, so just have to rule them out. +6  
benzjonez  Very helpful video for acute kidney injury: https://www.youtube.com/watch?v=bMp6IxDKK2Q +4  
notadoctor  Another explanation that helped me is that inability to concentrate the urine means something is wrong with the kidneys. If you have dilute urine, or the spec gravity is between 1.001-1.010 in someone with low urine output it suggests something is wrong with the concentration mechanisms of the kidney. Because this person had congestive heart failure we were already looking for something that matched up with prerenal azotemia so we can pretty much get rid of all the answer choices that suggest other azotemias. Then finally to get the precise answer I looked at the BUN/Cr ratio which you would expect to be high(>= 20). +  
mikay92  Would fully recommend the OnlineMedEd video on AKI. Goes through the differential, lab results, treatment, etc in a very clear and concise manner. +  
drdoom  repost via @benzjonez -> https://www.youtube.com/watch?v=bMp6IxDKK2Q +  
drdoom  @mikay92 is this the OnlineMedEd video you're referring to? -> https://youtu.be/EWFgzVtMN50 +1  
drdoom  aha! there is an updated AKI video but you need an OnlineMedEd (free) account to view it: https://onlinemeded.org/spa/nephrology/acute-kidney-injury/acquire +  
popofo  I understand that BUN:Cr > 20 if renal perfusion is repaired, but in heart failure wouldn't there be increased secretion of ANP/BNP from the atria that pushes up the sodium excretion? +  


submitted by mousie(171),
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naC oomseen laeeps axepnil hsit to m?e I 'dton seradnndut wyh aingrtts eht ehtor rugd uoldw not nctou sa eiunoclsx aier?rcit

seagull  This has to do with Intention-to-treat analysis. Essentially, when participants are non-adherent but the data shouldn't be lost. They just undergo another statistical model to account for their changes. Here is a nice video https://www.youtube.com/watch?v=Kps3VzbykFQ&t=7s +15  
dr.xx  Where does the question mention "intention-to-treat"? +  
notadoctor  They seem to be pretty obsessed with "intention-to-treat" it's been asked in one way or another in all the new NBMEs that I've done. (Haven't done 24 as yet) +8  
wutuwantbruv  They don't, intention-to-treat is just the best way to go about it @dr.xx +  
smc213  Great for ITT: https://www.youtube.com/watch?v=Kps3VzbykFQ +4  
yex  I agree with @notadoctor !! +  
ergogenic22  i think if it were per protocol, both groups would be excluded, the ones that were inconsistent, the ones that dropped out, and the ones that switched. But answer choices only allow ITT or exclusion of one group. +  


submitted by notadoctor(140),
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hTe ienftidino of Dcs-Miiaekoignn ictpaayC rnacdigco to BB+ is ytibila ot onceprdmhe tnriomnofai ouatb nisells dna termtnate optnois and eamk oischec ni neiegkp wtih prnloaes vsleua.

notadoctor  The decision must also remain stable over time, which is the "consistent values" part of the answer. +13  


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twih TPC ouy rae pusopsde ot idvoa eeisxvesc tgshulin dan VU xp.eseour exaohltneMs eskam ruyo skin mero uspsecetlbi to UV l.tihg

notadoctor  Wouldn't UV light also be contraindicated in Vitiligo? +4  
sweetmed  Phototherapy with photochemotherapy (PUVA) is a well-known and well-studied modality for the treatment of psoriasis, which involves systemic or topical administration of chemicals known as psoralens and administration of ultraviolet light in increasing dosages after requisite time gap. PUVA is also used in the treatment of widespread vitiligo with moderately good results, though it is being surpassed by ultraviolet B (UVB), which is equally or slightly more efficacious with fewer side effects. +8  
dashou19  Honestly, I didn't even know what Methoxsalen is, just chose the right answer because I know you can not give UV light to people with PCT... +9  


submitted by sklawpirt(25),
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I hntki the aide eher si ypilsm that eon hdluos hknti abuto wreeh ilesvecs rea cmogni orfm on teihr ywa ot hte gogil pxeclmo.

Tw"o etssp wadorrf adn one epts bkc.a" cllayceipfS the qnutioes yam eb grernfeir to a earr raliacacnofi sodri.edr an nseasrsawe fo that seaeisd si tno reaencys.s atWh si yseenrsca si airtnnsguddne eht ronigi mrof erwhe esvcisel rea ctedifrak to the iloGg tausp.rapa

OCPI erniotp si eedned ot aotc vselesc morf hte RRE ot dnse ot ilog.g sTuh, hiwt a ttomiuna in ttah ope,intr teh gcpdaeak eoinprts hatt ulshdo blbe fof dna be tesn to hte l,ggio taiedns aulmcaectu in eht RER adn aidetl ti. ushT hte answer.

1w)a0/.9s/S2p/4el2g16-9:-fctp(.2w.3c0hw/7pdjfomdth002/l

hayayah  pg. 47 on FA got the good visuals! +4  
notadoctor  COPII* proteins are needed to coat vesicles from the RER to Golgi. "Two(COPII) steps forward; one(COPI) step back." Anterograde goes RER -> Golgi -> Lysosomes/Secretory Vesicles -> Plasma membrane +19  
titanesxvi  why not small lysosomes? +3  
varunmehru  and I thought large lysosomes due to lack of enzymes to degrade +  
samsam3711  The size of the lysosome is not affected by the presence or absence of protein, but its function is compromised (eg. protein is getting stuck in the RER) +  
fattyacid  I hope this helps to whomever was lost like me Null mutation: A mutation (a change) in a gene that leads to its not being transcribed into RNA and/or translated into a functional protein product. For example, a null mutation in a gene that usually encodes a specific enzyme leads to the production of a nonfunctional enzyme or no enzyme at all. +2  
pingra  I think you made a typo: COPII (RER -> cis-Golgi); COPI (trans-golgi -> cis-golgi and cis-golgi -> RER), clathrin (endocytosis and trans-golgi -> lysosome) +  
kevin  So my thought process was if there is no COP signal then instead of going to Golgi it would be sent astray into cytoplasm, akin to how in I-cell Dx the enzymes get sent out of the cell since there is no trafficking signal (therefore I presumed large lysosome due to eating the aggregated protein). Are we saying without COP or Clathrin that the vesicle will simply stay put where it is? If I can get a reply before my exam (2 weeks) that'd be much appreciated +  


submitted by mcl(517),
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ttPaien yma haev arytdherei megoneda,ia whhic is iecdsaoast whti nrerect"ur ktcaats of enn,teis svems,ia aozledicl bnusaeuoctus damee lvgnniovi eht iemtxieert,s ealigin,at a,cef ro ntr,uk or umuobsslca medae fo rpupe arwiay ro s.oblew" eTh clretia oegs on ot asy Ca"erse1-est hiitrobin woskr yriedtcl no teh clntopeemm dan anctcot slpmaa csdeacas to eerdcu rnnadibyki sleerae" ihwhc si aosl ylrbabpo godo ot .nkow

wi/6/.mpsbei.g:rh3P.s81/C/ch36ilM/wavo.tn/nclnmpctt6w

notadoctor  Thought this was a trick question as C1 esterase deficiency also results in a decrease in C4. However, the second answer choice was not referring to C4 but to C4 binding protein, which I now know is different. I also didn't realize C1 esterase was technically a complement protein. +4  
youssefa  Based on many sources hereditary angioedema does NOT cause a rash (urticaria) which is a main differentiating point between angioedema and allergy. This mislead me in this question. Any clarification? +21  
ergogenic22  +1 on the above because uptodate states that c1 esterase inhibitor deficiency, both acquired and nonhereditary, are both non-urticarial, non-pruritic, and that is confirmed by the above linked article +2  
sahusema  Question writer probably didn't know the difference between cutaneous urticaria and subcutaneous edema. +3  
almondbreeze  same. got it wrong bc the pt didn't have sx of hereditary angioedema - swollen lips and eyelids +1  
teepot123  fa 19 pg 107 +  
beloved_bet  According to Amboss "Mast cell-mediated angioedema Often associated with urticaria and pruritus Other associated with clinical findings of allergic reactions (see type 1 hypersensitivity reaction) Presents within 30 minutes to 2 hours after exposure and resolves over hours to days" +1  


submitted by oznefu(16),
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woh do ouy ornrwa dnwo that rsototentees sidcerean olnehgmiob ?inoetcranncot tsju a armond actf ot nw?ko i utp ileaknla ssaathepohp beuesca i dgriufe siendecar roneoeettsst lwli ceaensir enbo gothwr nda rdeul tuo earoeicsp-pcsittf ngaenti cb tsi’ a .oanwm

hysitron  I guessed this one cause men have a higher hemoglobin than women. +8  
notadoctor  High levels of testosterone will result in amenorrhea. I guessed that since she's not menstruating she will not be losing blood and therefore hemoglobin. Therefore her hemoglobin levels will be higher than expected. +4  
meningitis  It kinda makes sense knowing testosterone causes catabolism so I was in between Alkaline phosphatase and hemoglobin... +1  
enbeemee  isn't testosterone anabolic? +4  
syoung07  ALK phosph is indicative of osteoclast activity. Testosterone keeps male bones strong just like estrogen does for women. Testosterone builds bone (osteoblast activity) therefore we would not see a rise in ALK phos +