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Welcome to cr’s page.
Contributor score: 3


Comments ...

 +0  (nbme24#37)
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hWihc etpy fo clel we r goign to fdin in t,elrsbs?i nuietohr?lsp

thotcandy  acute inflammation so i assume neutrophils to be replaced by macrophages -> granulation tissue -> fibrosis/scar formation +

 +1  (nbme21#47)
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yhw ton cesreinad cid-h?lolrchceyx5,yerlo2foa itwh het easm gocli ioluthnbra ianlpex +

usmle11a  i believe increase 25OHcholecalciferol indicates the storage capacity of vit D, which wont be affected in case of CKD. it goes like this, kidneys wont respond to regular PTH, loses Ca and cant execrete PO4, PTH gets made and tries to burn bone to produce Ca, resulting in elevated levels of Ca and PO4, Ca will bind the calcium and go to kidneys, yet same story all over. add to that the fact that 1 oh hydroxylase wont be able to function in a dead kidney. +1

 +0  (nbme21#21)
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why not ?.C I´st tno opsues htta ti oiprmev eth yttefvicei of nsinui?l

yb_26  thiazolidinediones (pioglitazone) increase insulin sensitivity (in muscles and liver) through activation of peroxisome proliferator-activated receptor-gamma (PPAR) I think they are asking about primarily mechanism of action, that's why it is E +
cienfuegos  UW explanation regarding the genes upregulated 1. GLUT4: insulin responsive on adipocytes/skeletal increases G uptake 2. adiponectin: cytokine secreted by adipocytes increases # of insulin responsive adipocytes and stims FA oxidation 3. PPAR family also plays significant role in pathogenesis of metabolic syndrome +1
poisonivy  Also, I think the word uptake shouldn't be right when speaking about insulin, it does increase insulin sensitivity and therefore glucose uptake +5
brotherimodu  @poisonivy That's why I didn't choose C and went with E since it was more specific +




Subcomments ...

submitted by i-de-liver(3),
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oseD aeoynn oknw wyh shit si cUri dAci not .N ?ronrageho lAl I see ni the rcarohipgm rea e.lsphtiuonr Is tath ewhit eiln in hte medldi fo het pecturi atht yrsalvoe hte ecymyphtol popuedss to be eth elsdnedeaeh-p rciu iac?d rO is it sabeecu hes's an old lady and usulyal pectis Atrthrisi is omfr .S sueurA, os it dwolu mero ielk yb ruic adci nad not hogrenaor ecisn 'hses lr?ode

maverick95  I struggled between those two answer choices as well. I thought that the large needle shape right in the middle was a uric acid crystal which helped push me towards Uric Acid as my answer. I also took into account that she was older (even though STIs are rampant among the elderly) she didn't really seem to have any other symptoms or history of STI/gonorrhea. I figured with her age that she just wasn't able to excrete Uric Acid enough, and got a gout. Something a pathologist told me one time was that they put the focus of the picture in the middle of the shot. So considering the uric acid-looking shape was right in the middle, I figured that's what they wanted us to focus on with the picture. Hope this helps. +10  
i-de-liver  Ah gotcha! I guess I shouldn't have thought that the thing in the middle was an artifact lol... thank you!! +2  
a1913  I believe it's because: 1) there is nothing given that would be risk factors for this woman to have N. gonorrhea 2) The thing in the middle is indeed an MSU crystal, just not under polarized light 3) apparently we get acute inflammation and increase in WBCs with crystal-induced arthropathies, per Table 11-2 on page 8 here (10 page document, top of page of interest will say p. 260) --> http://downloads.lww.com/wolterskluwer_vitalstream_com/sample-content/9781582558752_Mundt/samples/Chapter_11.pdf Also take a look at the pics on the previous page, left column for an example. I got this wrong as well, but I definitely won't again! lol +3  
cr  i had the same problem, Whats about the fever?, could be present in gout? +  
rainlad  I think this question mentioned the patient's temp was 100.4 which is consistent with mild fever in gout from inflammation. This photo was wack though +  
t123  The damage in gout is mediated by Neutrophils, so makes complete sense you see a bunch. +3  


submitted by ferrero(40),
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A yvre rsimila ostquien I heva nees ni baQkns ilwl aks hyw a ttiaenp hwit ihtrg arhte ulaierf eods otn opledev eeadm nda teh sewran si decnrseai aicmplthy dra.eigan I otg tish qisounte wgonr lonliyrgia seabcue I wdneesra gnlao shti ienl of nigernsoa ubt I iktnh in isht esac ti lla has to do hitw EWREH eht txrae essrrpeu is nomicg .fmro In this ntsqioue hte tp ahs iaocldsti nenhoeipryts os yuo can kntih aotub het rseurpes as niomgc o"wa"rdrf so iinrsogttccn rlaalcyperip tinepsscrh can rvteepn an rciensea ni pseuserr in teh yraalilpc deb. wroeevH orf rihtg rhtea aufeilr this atrex uildf is mcogni mfor eth IESPPOTO ieondcrti a(wdsakcrb omrf eth girth htare) nda icrnicottngs lpiaerralpcy iptrssnhce cna od nthinog n(o teoppsoi ieds fo licaypalr db)e - the noyl awy to pevtnre emdae is ot easicnre latymphci agrd.iaen

seagull  The question clearly lead us to think about Osmotic pressure by talking about protein and urine. I wonder how many people used that line of reasoning (like myself)? +15  
mousie  Great explanation, I chose lymphatic drainage for the same reasoning (similar Q on different bank) +5  
sympathetikey  My reasoning was much more simplistic (maybe too simple) but in my mind, systolic BP is determined by Cardiac Output and diastolic BP is determined by arterioles. Therefore, what comes before the capillary and regulates resistance? Arterioles. That's why I said that pre-capillary resistance. +31  
cr  the main difference between the 2 cases is that in this case the patient has high BP +1  
link981  So in kindergarten language the question is essentially asking how high pressure in the arterial system is NOT transmitted to the venous system (which is where EDEMA develops). But you know they have to add all this info to try confuse a basic principle and make you second guess yourself. (Got it wrong by the way) because of what @ferrero said of Qbank questions. +6  
hello  @ferrero what are you talking about? lymphatic drainage is the wrong answer... +1  
hello  ok never mind. i got it. hard to understand b/c it was a big block of text. +2  
asteroides  I think they may be talking about the myogenic compensatory mechanism: https://www.ncbi.nlm.nih.gov/books/NBK53445/figure/fig4.1/?report=objectonly "Increased arterial or venous pressure also induces myogenic constriction of arterioles and precapillary sphincters, which raises arteriolar resistance (thereby minimizing the increase in capillary pressure) and reduces the microvascular surface area available for fluid exchange. For example, because vascular smooth muscle in arterial and arteriolar walls contracts when exposed to elevated intravascular pressures, this myogenic response increases precapillary resistance and protects capillaries from a concomitant rise in their intravascular pressure." +3  


submitted by wired-in(67),
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tiMnncaenae sode mralfou is (sCs × Cl × ta)u ÷ F

rwhee sCs si eatst-eyatsd ttgaer almasp c.noc of ru,gd Cl si ,acnclaeer tua si sogdae tevnilra pa&m; F si labyba.oviitilia

hetNeir esagod inevrtal ron aoyblbiilivatia si g,envi so oiinnrgg toseh a;&mp lguggipn ni eht unmrbse u(clafre ot nrotcve niust to d:yg)gakm//

2 (=1 /mgLu × 1 00m1g/0 ug) × 9.0(0 //rhLkg × 0010 L1/m L × 42 hr/1 a)yd
= .5292 gkgay//md

..whci.h istn' nya of eth wasenr oihcsce ts.iedl hyeT smut vahe dournde 0.09 /khLgr/ to .10 kh,//grL nda dnigo os igsev alyetcx 8.82 mya/gd/kg iocch(e )C

lispectedwumbologist  That's so infuriating I stared at this question for 20 minutes thinking I did something wrong +69  
hyoid  ^^^^^ +11  
seagull  lol..my math never worked either. I also just chose the closest number. also, screw this question author for doing that. +9  
praderwilli  Big mad +9  
ht3  this is why you never waste 7 minutes on a question.... because of shit like this +8  
yotsubato  Why the FUCK did they not just give us a clearance of 0.1 if they're going to fuckin round it anyways... +18  
bigjimbo  JOKES +1  
cr  in ur maths, why did u put 24h/1day and not 1day/24h? if the given Cl was 0.09L/hr/kg. I know it just is a math question, but i´d appreciate if someone could explain it. +1  
d_holles  LMAO games NBME plays +2  
hyperfukus  magic math!!!!! how TF r we supposed to know when they round and when they don't like wtf im so pissed someone please tell me step isn't like this...with such precise decimal answers and a calculator fxn you would assume they wanted an actual answer! +1  
jean_young2019  OMG, I've got the 25.92 mg/kg/day, which isn't any of the answer choices listed. So I chose the D 51.8, because 51.8 is double of 25.9......I thought I must have make a mistake during the calculation ...... +6  
atbangura  They purposely did that so if you made a mistake with your conversion like I did, you might end up with 2.5 which was one of the answer choices. SMH +3  
titanesxvi  I did well, but I thought that my mistake was something to do with the conversion and end up choosing 2.5 because it is similar to 25.92 +2  
makinallkindzofgainz  The fact that we pay these people 60 dollars a pop for poorly formatted and written exams boggles my mind, and yet here I am, about to buy Form 24 +15  
qball  Me after plugging in the right numbers and not rounding down : https://i.kym-cdn.com/entries/icons/original/000/028/539/DyqSKoaX4AATc2G.jpg +1  
frustratedllama  Not only do you feel like you're doing sth wrong but then that feeling stays for other questions. sucks so baad +  
fexx  'here.. take 50mg of vyvanse.. I just rounded it up from 30.. dw you'll be fine' (totally doing this with my patients 8-)) +1  
cbreland  I was so close to picking 2.5 because I thought I did a conversion error. 5 minutes later and still didn't feel comfortable picking 28.8😡 +  


submitted by sgarzon15(11),
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ahknT yuo erittgl zeno fo hkecsyt aprm.h I lalsh rneve erftog uoy

cr  why not C?. It´s not supose that it improve the efectivity of insulin? +  
cr  why not C?. It´s not supose that it improve the efectivity of insulin? +  
divya  because insulin uptake by adipose and muscle tissue is not limited to thiazolidinediones but also and mainly by metformin. and glitazones' primary MOA is PPAR gamma stimulation which then increases insulin sensitivity to other tissues. +1  


submitted by haliburton(208),
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hits si a cvrciael nlsiap ordc ostenic. the tacneeu iscfucauls si ttacin )(UE iaornitvb nda irepoorni,ppcot tub the ewhti ictesno is the lacigre fsaliusccu EL() and si dmaeda.g I ikhtn hte arealtl oopntri atht si eveunn si ujst at.t/lnafacrrutia

arezpr  thorax section +3  
guillo12  How do you know the gracile fasciculus is damage?!?! +2  
cr  which parte of the image its damage?, the pink? or black? +  
usmile1  the pink park yes +2  
d_holles  If you look at https://en.wikipedia.org/wiki/Gracile_fasciculus#/media/File:Spinal_cord_tracts_-_English.svg you can see that the closer to the center = legs, while further away = arms. +3  
hyperfukus  i still don't see where the damage is lol! FML +  
hyperfukus  i finally figured it out lol that was a slow moment i hope im not this slow on step yikes! +  
angelaq11  @hyperfukus I had the same problem at first, marked it and then came back. If you remember, in the spinal cord the white matter and gray matter are "reversed" compared to the brain. That said, if the butterfly shaped region (ie, the gray matter) is colored (in this case) lilac and the rest (ie, white matter) is blackish, the only thing that is actually abnormal, is the region where the dorsal columns are, because it stains just like the normal gray matter. After that, you have to think about which fasciculus is damaged, the gracilis or the cuneatus. The gracilis is medial while the cuneatus is lateral (picture someone with glued legs and open arms). Hope this helped +12  
azharhu786  Gracilus Fasciculus = Graceful legs +  
icedcoffeeislyfe  Check out FA2020 pg 508 Put simply--> myelin= black --> color of the normal white matter no myelin= pink --> color of the normal gray matter and the damaged area Dorsal columns= vibration, proprioception, pressure fine touch F. graciLis= Lower body F. cUtaneous= Upper body +2  


submitted by sgarzon15(11),
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knTah ouy ilttger zeon fo sckethy h.mrpa I lshal nevre oretgf you

cr  why not C?. It´s not supose that it improve the efectivity of insulin? +  
cr  why not C?. It´s not supose that it improve the efectivity of insulin? +  
divya  because insulin uptake by adipose and muscle tissue is not limited to thiazolidinediones but also and mainly by metformin. and glitazones' primary MOA is PPAR gamma stimulation which then increases insulin sensitivity to other tissues. +1  


submitted by hayayah(1056),
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Srandyeco sdarthirmrayypiohep yls(uula /td iroccnh erlna )liu.efar

baL snfidnig uencdli ↑ PHT seeorp(sn ot wlo alm,cu)ci ↓ seumr clumiac enlr(a lafi),reu ↑ ersum sphehopta nl(ear felar)i,u nda ↑ nllekiaa aohtespashp (PTH ctvtaiagin aoels.sBots)t

haliburton  also remember that in renal failure, 1-alpha-hydroxylase activity is down, so there will be less activation of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is a key mechanism causing hypocalcemia. +2  
cr  why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain +  
nala_ula  Increased phosphate, since the kidneys aren't working well, leads to the release of fibroblast growth factor 23 from bone, which decreases calcitriol production and decreased calcium absorption. The increase in phosphate and the decrease in calcium lead to secondary hyperparathyroidism. +1  
privatejoker  Probably a dumb question but how do we definitively know that the ALP is elevated if they give us no reference range in the lab values or Q stem? Everything stated above definitely makes sense from a physiological standpoint, I was just curious. +1  
fatboyslim  @cr the question asked "the patient's BONE PAIN is most likely caused by which of the following?" Increased levels of 25-hydroxycholecalciferol might exist in that patient, but it wouldn't cause bone pain. PTH causes bone pain because of bone resorption +1  
suckitnbme  @privatejoker ALP is included in the standard lab values +  
makinallkindzofgainz  @privatejoker ALP is listed under "Phosphatase (alkaline), serum" in the lab values +1  
pg32  Why does AlkPhos increase in renal osteodystrophy? The PTH would be trying to stimulate bone resorption (increase osteoCLAST activity), not bone formation (osteoBLAST activity). +  
drzed  @pg32 the only way to stimulate an osteoclast in this case (e.g. via PTH) is by stimulating osteoblasts first (thru RANKL/RANK interaction), thus ALP increases. +1