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Welcome to karljeon’s page.
Contributor score: 118


Comments ...

 +7  (nbme24#15)
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I o'dtn nwok fi hrete si an oianqeut orf ths,i tbu I iaalslybc pedpmu tou eeyrv oidinivs scaros het blaet to egt %~5 on re.aaevg

eHre yteh a0 r0e4: / 000,6 = 07.26 500 / 0560, = 54 30.000 / 35,50 = 50 030.06 / 050,5 = 255090 0. / 804,0 = 500.2

heT eagvare fo seeth %s for lla eht rsyea = 5S5 8.o%. htsa't lsoce uegonh to .5%

seagull  good work. I found this question annoying and gave up doing those considering the amount of time we are given. +4
vshummy  Well just don’t include the intake year... because that messed me up.. +15
_yeetmasterflex  How would we have known not to include the intake year? From average **annual** incidence? +
lamhtu  Do not include intake year because the question stem is asking average annual incidence. The 4000 positives at intake could have acquired HIV whenever, not just in the last year. +8
neels11  literally didn't think there was an actual way to figure this out. but my thought process was: okay incidence means NEW cases. so the annual average at the end of 5 years would be: (# of NEW people that tested positive at the end of year 5) / (# of people at that were at risk at the beginning of year 5) <--- aka at the end of year 4 250/5050 = 4.95% also if you look at year 5: you'll see that the at risk population is 4800 when 300 new cases were found the year before. 5050 at the end of year 4 MINUS the 300 new cases at the end of year 4 should give you 4750 as the new population at risk. but notice that end of year 5 we have 4800. idk if that means 50 people were false positives before or 50 people were added but in incidence births/death/etc don't matter it's kind of like UWORLD ID 1270. assuming average annual incidence is the same as cumulative incidence this was just a bunch of word vomit. sorry if it was unbearable to follow +

 +9  (nbme24#23)
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A anm ihtw a xH fo tHEO pnednecede and cnhroic abd ianp sa lewl sa ar-Xy igfnnsdi fo son"laiacticicf in eht mie-pdurp dboaem"n is tsmo yiklle neiregfrr to a cihrnoc steti.paiacnr

iTsh sleda to a lack fo eaislp tneiosrec cne,he lap,e fleml-nglsoui olssot thiw lio etsdorpl epr pt xH. Thsi pst' cnpasrae sola ts'oned eretesc toerh ,seemyzn hucs sa myssl,eaa srsp,eeoat nor neintsrpyog (ot tavteiac rheot eezsy),mn so het sreanw si iaeedlzrgne" atirsbm.pl"ooan

karljeon  p. 367 (FA 2018) +11
usmlecrasherss  pancreatic insufficiency FA 2019 p375 , +2
almondbreeze  FA 2019 p391 on chronic pancreatitis +
almondbreeze  UW: in chronic alcoholic pancreatitis, alcohol induced secretion of protein rich fluid precipitates in pancreatic duct--> forms ductal plugs that calcify +3

 +16  (nbme20#2)
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shiT one was a wemstoah sliepm nqueiots insce oremhpethyca -t-&g; tuomr lissy -t&;-g ende xintnaeh sedoaxi thoiinbir (eg, .ft)xbuoatse

UTB WYH SI NBEM GMRRAAM SO RAPC? PUT RYUO OCMMAS NI TEH GHIRT CAPLE!

malou  I swear I registered just to upvote your comment. #SoFrustratedToo +
xoxofossagirl  ,omg, me, too, , +

 +4  (nbme24#23)
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imtnVia E eyeicdicnf ecusas otilyehmc iamnae, ttochyconiaas,s eclsmu seeswa,nk osoreprti umlcno dan oielbcrprseanel acttr ntyileomdien.a

karljeon  Can anyone explain why the serum lactate dehydrogenase (LDH) level was elevated? +
asapdoc  Vitamin E is an antioxidant. Thus a deficiency can cause hemolytic anemia. +5
sympathetikey  @karljeon Intravascular hemolysis = LDH release from RBCs +3




Subcomments ...

submitted by karljeon(118),
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A nam hwti a xH of OtEH epecdeennd dna nocirhc adb pian as llew sa yX-ra ifsndign of tsocnf"icilicaa in teh dpupime-r edanbmo" si tsom ilkyel fereignrr to a rnohcic tatrci.spnaie

Tish sedla to a ckla of pisael rceetsoin enceh, peal, ulgoelinsmf-l osslto thiw lio oldetspr pre tp x.H iTsh 'tsp cnrpasae osal edson't tseceer etorh m,eysenz ushc as aylsms,ea aepsesort, onr rnepnigtosy to( tvcaaeit trohe seynmz),e os hte renwsa si re"zagineedl mrsblonpaai".to

karljeon  p. 367 (FA 2018) +11  
usmlecrasherss  pancreatic insufficiency FA 2019 p375 , +2  
almondbreeze  FA 2019 p391 on chronic pancreatitis +  
almondbreeze  UW: in chronic alcoholic pancreatitis, alcohol induced secretion of protein rich fluid precipitates in pancreatic duct--> forms ductal plugs that calcify +3  


submitted by strugglebus(165),
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I sceho isth oellys ebuceas ti asw so dnma iecpsfci

sympathetikey  Same. Learn something new every day: See more: https://www.fda.gov/safety/medwatch-fda-safety-information-and-adverse-event-reporting-program +4  
karljeon  I didn't choose it because it was so damn specific. :( +43  
lovebug  Could anyone explain for B) for me? because I choose B).:( +2  
j44n  B.) is wrong because its never been shown to show adverse effects "any offcial data linking the drug" and the fact that it's "newly marketed" +  
j44n  and because its in 5/45 patients roughly 10% of the population, that might not seem like much but most of the diseases we freak out over are in 1-2% of the population, to put that into perspective if we gave this drug to every person in the US (every big pharma wet dream) with a population of 300 million... 30 million people would have this adverse event... hope that helps +  


submitted by strugglebus(165),
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As an 0t810 :i1,d0e plopee reporedt ot eahv sdei steffec nehw tinkga t camAyoor.olnhoHiddiergzh ,hemt 52 eppelo 02%0.() hvea tBsear rhsdeacgi

neonem  I think the best way to answer this question was by process of elimination. +1  
sympathetikey  That's some bullshit lol +8  
karljeon  Haha I eliminated the answer by process of elimination. +20  
medschul  I eliminated thiazides by process of elimination :( +1  
medstudent65  Shit I eliminated thiazides because of elimination went with HTN thinking intercranial bleed effecting the pituitary +2  


submitted by hayayah(1079),
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c,oteiN eth tmes asys oosrpes"rrc in eth nkis"

3D cl)e(oeofralcclih rmof xeuoespr fo ksni rm(usatt aabsl)e ot snu, osgtninei of hsif, ,klmi lat.nps

D2 r(oaorlcciel)gef ormf innsgoite fo stlnap, n,iufg .teayss

thBo cnodterve ot -52HO 3D t(aoersg )from in rvlie adn ot teh iaetcv form 521(H,)2O- 3D )cllra(ociit in keiyd.n

sympathetikey  C is the 3rd letter in the alphabet. Hence, D3 = Cholecalciferol +4  
karljeon  Thanks for the explanation. The question stem made it sound like "what future step will be decreased?" Actual question: "Decreased production of which... is most LIKELY TO OCCUR in this patient?" Maybe NBME needs a grammar Nazi working for them. +8  
bharatpillai  question says "decreased production of which of the following precursors in skin is most likely to occur in this patient? the answer has to be 7-dehydrocholecalciferol! +5  
bharatpillai  7 dehydrocholesterol +2  
brbwhat  Yeah i did the same, but then realised acc to uw flowchart 7dehydrochole.. is converted to cholecalciferol in presence of uv rays. So the decreased precursor would be cholecalciferol since we already have 7 dehydrocholecalciferol not being converted by uvrays Tho the uw chart sites both ergo and chole as dietary sources. +2  
drzed  Wouldn't 7-dehydrocholesterol build up in the skin? Since UV rays convert 7-dehydrocholesterol into cholecalciferol, if you are lacking the conversion, the reactant (7-dehydrocholesterol) should accumulate. +  
brbwhat  They’re asking decreased production of which of the following precursor would occur? 7 dehydrocholestrol builds up, but decreased production of cholecalciferol takes place, which is a precursor in the pathway for vitamin d formation +1  


submitted by karljeon(118),
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Vitinma E cdfneieyic usseca yimolhtce nieaa,m sacnsoo,cyithta lsucme neswake,s oprorites ouncml dna selrlainobecper tract nditloi.enmaye

karljeon  Can anyone explain why the serum lactate dehydrogenase (LDH) level was elevated? +  
asapdoc  Vitamin E is an antioxidant. Thus a deficiency can cause hemolytic anemia. +5  
sympathetikey  @karljeon Intravascular hemolysis = LDH release from RBCs +3