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Welcome to notadoctor’s page.
Contributor score: 140


Comments ...

 +6  (nbme23#30)
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SEL si sdetcoasia htiw yficndeiec of elary lnmompcete tis.negrop(e C,q1 4C, C).2 AF( 91, .pg )462

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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cAridgonc to ,Gjnlao iaolhptcymey rvea is eon fo eht omts nommoc ssaeuc of CdBu-iaihdr sdymroe.n dcgorcAin to FA, aihdirBC-du si csoedaaits roem eayglrenl twhi huoaprelblgacey atste,s mteyhpacyoli r,vea tpapursotm stets,a adn HCC.

aeiptcH sicosrrih acn be dlreu uot ebasd no eht miet socreu fo eht aitens'pt rtianptonees - he wsa iefn 2 eskwe oag and eth mibaoadln pain taretds an ourh o.ag

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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emembrRe on gyolsthoi shtmasHio'o soiidhtyitr sah tow csiitdtn uetasrfe rĂĽHhelt sllwehcc(hi ear lehnspoioiic paimctatels lslce htat ilen feoclslli) and lphmoiyd artsgaegeg tiwh marnegli .pg.(crntsee 338, FA 190)2 ehT rteocrc enwrsa seesbcrdi hte ltatre ufrteea of soihmato.'Hs


 +0  (nbme23#39)
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laCcie urpse si a laoaibosrpntm ersdynom ttah lsetsur in threaseroat dan seurlst ni inro nedcecfiyi eaani.m sA raf sa m'I ea,raw none fo het teosrh eurlst ni onri cnieecdyfi mnaae.i I( dah eaBtricla ooterrhvwg sa a clsoe oscnde tub I 'dotn velbeie s'thta osasatcedi hitw nroi encfiyie.)dc

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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The dninofteii fo aog-iniDniMckes tiyaapcC gadicnorc to BB+ is ybiialt ot peemdnrcho fmrtoianion ubota lnisels adn ttmeaenrt tpioosn and kmae hesoicc in nikgpee twhi peornsal evalus.

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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Ive' eebn ngcasrehi rfo my serouc rof hits ubt nt'ca smee ot nifd .ti rveH,weo hte yaw I tgtuhho obtua it saw atth edema pspnaeh avi the ape.arlilisc fI hreet si draneecsi riseetcans aiv eth paelrarlipcy ictrhsnspe as uchm lbdoo ultnd'ow be leab to egt onit hte eslcaripai.l hTe dlobo ldwuo tsniaed gte dusnhte iav taonsasemos ot eht .vesni iThs lrtecia orfm s.oichypvglymoco lipaxens ti a ttllei teet:rb CV lgPyh:yoiso Teissu medEa dna alreGen eincslpriP fo asprTaialrlcyn iuldF neahEcxg


 +0  (nbme21#6)
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Tsih setoiqnu swa nakgis taubo teh daevesr eftscef fo rtpnoo pmpu obiristhni spclaleeiy evgin oruiespv eyidnk isesus. IPPs sdeeerac remsu Mg dna ursme aC asnboriopt nad anc seainrec eth irsk of aerrftuc e(aclsyliep in teh ledy.l)er

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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If uoy rewe kctsu ebntewe cgoadramitn)nsohmCaan(rlo nda eEanhnn)id(brcomnog memberre ocsarhdnoenm yam orede hte terocx tbu anc renev da/viptuiresdn the txcro.e I hkitn tihs was eht ointcsinitd hte ieqoutns asw stnite.g


 +29  (nbme21#32)
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uasUl seltitiirant mtinsionepu is the caltoogiilsh ednoifniti fo chtIdiipoa pyonumalr .brssfoii eW konw atth shit neatpti sha yanormlpu risobsfi aebscue het oqeusnti setsta atht treeh si obruifs kgcniehtin of eht earvlalo tas.pe shiT snuotieq aws tsju tsgneit htat ew enwk hte oetrh enmas for roPylmanu .iboFsisr

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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tacsiettaM esasedi si omer mconmo anht amiyprr oenb om.rtus

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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slAsyina fo eth slitaen ni the tonuiqse dweohs a redasdece rumnbe fo isomedens l-kso.scsinr eisnmoeDs is dmea up of rfou slyeni dsre.suei oeefhTrre anorlbam isatenl si ikylle sigsnim ynesil ssyncerea for eth oinartofm fo heste ieednossm ks.c-iorssln ikdWaieip italecr no snmeieDso.

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(347),
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Urae lCeyc issdDrroe g;&t telIdsoa eevser pmhmeomaraiyne ;gt&( ;0001 .ei., no ohrte veeesr bematlioc isrnteaucbsd

nthieinrO sanyeacabtsamlrr yindcfecie tg&; o(tms monocm uare cycel s).di rcoiot uaaeimicacdiirda/, pmyinaemaoremh

ciOrgan aeiAsmcid tg&; amemaym,reHpoin ano-ipgan sdaicsi,o sotikse om(rf )gemhoiylacyp

cnmiaude-Mhi cy-oClAa eredaoehgsndy dieneyfcci ;&tg ommpyir,aemeHna ottopkehcyi oapiylhegcmy esen( in x-ainoitodβ sodre,idsr XECTEP )outyhprdorlosyeaednk

ieLvr nsftcnioudy g;t& maHeyoaeimm,npr LTFs essedm pu, ledor 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(461),
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nme,saGoitcay idsrep gmtaoin,aa dna opihaymdnsgo (sa lelw as malarp )maeyrhet are lla ssnig fo sexecs s.rentgeo The irvel ni nptatise hwti iethapc eesisda si eirdapim and os actnon lreca setoregn funcietyisfl. xSi 12 zo beres ldiay 7(2 ,oz ro half a lnga)ol si oto um,ch and si ndysiotgre ihs e.virl

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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sThi ntsiqeuo was ksanig touba het eevsrda tecsfef of rnotop umpp nrhsibiiot secplaylei evngi ripeuovs einkdy usesi.s sPPI ersaeced rsemu Mg dna rusem aC trsaionopb adn anc ieacsner the isrk of rtcfaure ilal(pceyse ni the le).rleyd

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 ash areth rulfeia hchiw slead ot a eresaedc in reanl lodbo flwo dan rpaeelnr aom.aezit In ranlpree ze,taamoi :rUCBN tiaor is g&t;= 2;0 aAtonticiv fo hte AARS sstyem eud to the alrprene oeamiatz eamsn hatt the psec ragv si ihhg ta 125.0 and he si hnildgo toon odumis os uyairrn sdiuom llwi eb wlo l,(&2;0t FNEa ;1&%tl.)

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 eeoomns salpee pailxne isht to em? I ndto' adestrnndu wyh gartisnt eth etroh urdg dluwo otn nutco as xciulones ?cretiari

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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eTh iineidtnof fo ancDoMiei-knsgi tyaiCapc ciancgrod ot B+B si yilbtia ot pmhdonecer oifmnirotan tubao slilnes nad atemntert sntpioo nda emak iocsceh ni ipkegen twih rpneloas aelsvu.

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


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tihw CPT you rae psupedso ot aiodv esisexecv snuhgtli and VU r.esoxeup otnheealsMx esmak yuor nisk orme ltisupebcse ot UV ghi.tl

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 thnik eht edai reeh is ysmlpi hatt one hdulso kihtn ouabt eehwr sicvlees rea iconmg mrfo no rtihe ywa ot eth oiggl x.plmeoc

owT" espts frraodw nda noe teps ca.bk" cceypliSafl the uniqetos yam be ernfierrg ot a rare fraiaccilano ddoiers.r na esersawsna of htat adisees si tno scenyrsae. haWt si arcesyens si rnngiundatsed eth grioin ofrm rheew svlseeci ear rdeckatif ot het Ggoil .uaprtaasp

PICO opreint si needde to octa sescvle mfor het ERR to dnes ot il.ggo us,Th tiwh a tnuatmoi in ttha tn,peroi eht cdkaepag prnioset taht lusdoh lbeb off nad eb ntse to het gilo,g isaetdn macutaeluc in teh RER dan ealidt .it uhsT het re.nwas

(.2-datdl)t0w2-m/63j:/f7l0w/f14cs2e1/o9.2hpg09h0pw./pcS

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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etnaitP yma ehva edihetyrar ai,ndemeaog hhciw is aasicdetos with e"cetrrurn tkscaat fo nensi,te ms,esiva aceilzlod obunustcuase eadem iionvvgln hte xriitems,tee eingata,li ,feac ro tkr,un ro mbouucsasl eeadm fo upper yaawri ro ewo."lsb ehT etilcra soge on to say s-atreseCe"1 irnhiiobt kowrs riedcylt on teh cplmeetnmo and cctonat maplsa aacsdesc to eruedc nakdiibnry eselera" hwhic is also abblyopr godo ot wok.n

/e8wni.Pwnh.mnlh3i3ccgw/:cmiv/6CMstb/sa6r.1/.p6pl/tot

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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owh do yuo rwrnao dwon tath neetooetstsr iacesrned ilhobgmeno ?oatnrcninocet sjtu a nmaodr cfta to kow?n i ptu nlleakia ohshasaeptp esbceau i reugfdi ieecdsarn teosernsotet will cearisen nebo gwrtoh dan udlre otu ficoeastpsp-rteci aietngn bc ’tis a mnw.oa

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 +