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Welcome to yex’s page.
Contributor score: 73


Comments ...

 +9  (nbme24#1)
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cgnircdoA to na:ojGl "12B laoa(incmb) sha lbtaoc in it. ctglinrCuai from fo aoetfl is lltehea.rdyothmreftatyo upsrPeo fo nmliacboa )2(1B is ot etka eht hylemt uopgr off of yylreofmaaetttreolh.tdh Tehn ti’s eacldl trl.eteoaroahfydt If ouy odt’n egt eth thlemy rupog off of ,efatlo you lwli nto meka DNA. oS, if yuo aer 1B2 de,f you ’acnt tge het htmely group ffo adn otacnn akem NAD. If yuo ear efd ni fatl,eo uyo nc’ta eamk D.N"A

misterdoctor69  lmao +

 +2  (nbme24#13)
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reTeh are tisqunseo uaotb tnsngilpi on sttPesa adn WU. UW q di 11588 wssoh erahton r.aneoisc doGo agmies no teh nxpteaiaonl thou.hg uNalsroui,lp sboonene 39 oy/ cielvp errssupe p;&ma ntcontioispa nda sdoe nlngiptis ot etdafeec, lba abl lab. :xEam lluigarryer gerdelna .etsuur xD was rtriosepo rbsusealos irenuet ieyoommla and eccloteer saw on eth .n.so.pito iglSpntin is ONT jstu for croetl.ece


 +4  (nbme24#43)
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ishT loas ersefr to orhncic imliamntaonf &am;p nlurgmaoa roanof.tmi


 +1  (nbme24#34)
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I ktnhi hyet aer eeirngrrf to hsluickyKt llcse = moulapryn idnonenorcruee eclls P()EN.C cdgroiAcn to keidpi:iWa czpleidieaS riayaw lpeieilath ecsll htta roccu as toysailr lslce or as lsurcset dellca ioinpelutrlehea oidesb )NB(E in het lnu.g heTy are oeatlcd ni teh nasal yspitrarreo utilmhe,ipe eyllaagnr ocamus adn orhtogtuhu eth teneri iprrorysate attcr ofmr het atacerh ot hte enlamrti wriay.sa hTey can eb eht usceor fo seerval tpesy of gnlu crace-n omts bnltayo, alsml lecl raconacmi of teh guln, dan haiobrcnl ocicdianr .orumt


 +2  (nbme24#3)
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sihT asw no a porisveu E.BMN owH I otg it? ttnscloarIe ieroo()trsp si how ouy gte to het ebavlrter di;ebos hte reoth sevlses era iort.near

medguru2295  this was nearly word for word on NBME 22. Slightly different wording maybe? +

 +5  (nbme23#7)
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Hmmm. leWl ym nidm sha bolnw off eubcase ahtw tih my dimn swa adynoirhtde ncesi eh saw in het tdesr.e sA oosn as ym midn tsaetrd ot aerdwn btaou all fo teh eorht tponiso ahtt duolc eamk .es.ne.s I sujt cidklec adn ovd!em

charcot_bouchard  Smart boi +5
usmlecharserssss  hiking in sahara desert SMH +3
cbreland  Simple = smart +




Subcomments ...

submitted by neonem(527),
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hsiT inattep sha pumrlnayo i,ossfbir hhcwi eascsu a rvictesreit ot(n tteosby)eipvrc-tu seeisda. Secni etreh asw no oinuacoalpct re,uopxes 'Im ssungmai this is pihaoicdti pmoyrunla si.ribfso hisT asscue nietdkhec loalaver rsbmae,men lmgntiii sga duifiof.sn Thr,eefreo eyunatvlel 2O nt'wo be ebla to fuisfed cqkiyul ugneoh into eht bdool asrsco hte oivltalrarelar-ae remben,am selitugnr ni a rarlge a-A eferi.necfd I( tiknh ere'sth nlmayorl a slmal a-A tdn,irgea fomr 42-1 mm ,gH btu hnwe stih tegs too bgi, yuo etg h)pycxoi

yex  UW q id 7648 +2  
melanoma  uw id 1526 +  
feeeeeever  FA 2019 Pg. 661 +  


submitted by dbg(123),
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WTF si ss"eweakn fo arpltna nloreofisd"ix ????? ist' elik ynsiga "nexoietns seho"ifTl nix is tno hte ylno iovoubs alctihnce mektais in het new BEMNs ...

karthvee  loool +2  
yex  Funny Board!! Yeahhhhh +  


yex  There is a Q on UWorld about rotator cuff tendinitis #380186 w/ a similar presentation... I kind of remembered about that, but honestly I do not know how I got it right. +  
yex  Correction: Q id is # 1732 +  


submitted by lsmarshall(371),
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reUa Celyc Dsrrsdeoi &;tg otaIelds revese amrnepoayhiemm (&tg; 01;00 ..,ie no treoh rveese tioeclmab siutbeadcnrs

ihOenntri raacnrlstbayaems iceneiycfd t;g& smt(o ocnomm aeru cyecl )is.d tocroi acci/auamradiedii, eaphmmnmyioare

Oicrnga miAecaids t&g; pminamHr,omeyae pnongiaa- cssiid,ao ksestoi f(rom heyolypic)amg

-eunMimadcih acA-loyC odednrghsyaee icidfyeecn ;tg& pairmHany,meemo tytpeohkico gaphoimyycle (seen ni tiooadix-βn sserodd,ri CETXEP enlyudroapoe)ordskyht

Livre idcoutfnyns g;&t riHe,mpymoamean FTsL msedse u,p derlo .tp

lsmarshall  Summary of metabolic issues relating to hyperammonemia +6  
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +3  
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. +9  


submitted by doodimoodi(52),
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Did no one etoicn htat eth ddOs itrao on teh top left is w?rogn mA I isnigms onmt?igseh If ouy elaucctal ,it st'i 6 utsj klei teh opt ighrt n.e...o

mjmejora  thats actually really funny +  
yex  Because I said so, applies here... :-/ +1  
doodimoodi  Cant believe we pay $60 for this crap +33  
aisel1787  best comment doodimoodi) +1  
b1ackcoffee  that fucking threw me off on exam. I was like is there an effect modification by "Not drinking milk". the fuck! +  


submitted by catch-22(67),
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I odwu od a teprsoteeicrv oocthr e.reh I d'ton htkni hsti toqiesun is torcrec nad orpvsedi oot ttleli nritafioomn to tge the ccrrtoe weansr. emiT" te"nffiiec is eht nproeat wodr rehe utb teyh mlspiy 'dnidt oesicnrd atht ritosptvreece rochto ulwod eb a btteer engids here sa nlgo sa eht earlibsav rea dc.doe

sherry  I agree. I was hesitating between the two choices. I still think cohort study is better regarding the "risk". I hope this kind of questions wont pop out on the real thing. +1  
soph  I think key here was they were measuring risk though +  
yex  I also chose cohort, since it is comparing a given exposure. +  
raspberryslushy  I was also thinking retrospective cohort study - just as time efficient, can look at risk, and the Q stem said the cancer was common, and I think of case-control for rare conditions. It's like they forgot a cohort study could be retrospective. +1  
boostcap23  The classic example they always give for why not to do retrospective cohort is because patients who have whatever disease your testing for are more likely to remember all their risk factor exposures than a normal person that doesn't have any disease. Of course in this case I'm sure the people running the study would be the ones who figure out how much arsenic was in the water but this also would be very time consuming to figure out for each individual person in the study. Thus a case-control study where you look at a group of people with >50 arsenic exposure and a group <5 arsenic exposure and simply see who has cancer and who doesn't would be easier and take less time. +  


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nkiS risvoped osnnutilia nad senrtvpe heat ss.lo Tihs 'tpiantes bydo lwli eamctponse for cidenreas erta of etah olss yb egrnsicnia bltoameci raet.

davidw  This is directly from Goljan I) Hypovolemic shock may occur due to loss of plasma from the burn surface (refer to Chapter 5). • Loss of protein from the plasma loss may result in generalized pitting edema. II) Infection of the wound site and sepsis may occur. (a) Sepsis due to Pseudomonas aeruginosa is the most common cause of infection in burn patients. (b) Other pathogens include methicillin-resistant S. aureus and Candida species. (3) Curling ulcers may occur in the proximal duodenum (refer to Chapter 18). (4) Hypermetabolic syndrome may occur if >40% of the body surface is burned. +11  
yex  Can someone explain why is it not increased ECF? +9  
charcot_bouchard  i picked same. Increased ECF but cant remember why. Can you explain WHY it is increased ECF? what was ur reasoning +2  
isotopes  Burns would lead to a decrease in ECF because the protection from fluid loss is absent; it can lead to shock. :) +1  
tinydoc  My reasoning behind picking ↑ ECV was that your losing fluid but not electrolytes with the burn ⇒ the ecv would have increased osmolarity, so the fluid from the ICV would be pushed the the ECV. It made sense to me at the time. I guess technically its wrong because the loss of fluids and the gain of fluids would amount to pretty much the same thing. But the insulation and heat loss thing makes sense I guess. +  
yex  Increased ECF, bc I was thinking about the edema formation.... :-/ +3  
atbangura  I picked increased ECF because burns increase the capillary permeability coefficient, but now that I am going over it I realized that increasing the permeability would only transfer plasma volume to the interstitial volume, which are both a part of the ECF so therefore ECF would not change. SMH +5  
aisel1787  thanks +  
69_nbme_420  Burns (and Diarrhea) cause ISOsmotic volume contraction; Costanzo BRS Physio +  
tiagob  in severe burned patient, also has increased fluid in third spacing or interstitial (leading EDEMA). Different extracellular space is interstitial and vascular +  
peridot  I also wanted to add, another huge job of the skin is to prevent loss of fluid. Burn patients are easily dehydrated because they've lost that barrier. This helped me lean away from increased ECV - despite the edema (from one compartment to another) as others have mentioned above, there is a loss in overall ECV due to evaporation from body. +  


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Did onyane sele go ondw eth: s'seh yhtveisnoep so aymbe eh'sll tge ruatoehwes hndcrfeerisi remsondy ueasecb gtnohin sele is iagnkm sense ot em ta hist ?ino??tp uoter -

runTs out, esevre arlmaai nca cesau aralcrcsaivoud alspcole nda i.osnnheopyt

redvelvet  me too :( +1  
abigail  me three :( +1  
yex  Me four :-/ +1  
link981  Slowly raising my hand as well +1  
tinydoc  Sammmme +1  
bullshitusmle  same here!!!:@ +1  
usmlecharserssss  patient has malaria with obvious picture and clinic, i answered because only thing associated with liver was hypoglycemia +6  
aisel1787  me five( +  
myoclonictonicbionic  I was thinking that she is hypotensive which can cause an infarct of the pituitary (since pituitary is growing during pregnancy) and therefore she'd have secondary adrenal insufficiency. +  
alexxxx30  sammmeeeee +  
snripper  Dumbasses unite lmao +  
usmleaspirant2020  lol saaaaame! +  
usmleaspirant2020  lol saaaaame! +  
anechakfspb  me also :/ sitting there trying to figure it out during the test I thought I was so smart too - like "wow nbme, way to tie in micro and endocrine, not getting me though!" ... i was wrong. +1  


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kSin pveoisdr tniuonlisa nad vsepenrt thea so.ls hTis pset'inat boyd illw pctoaeemns rfo nieardces atre of ehat osls by icensianrg beoimaclt etr.a

davidw  This is directly from Goljan I) Hypovolemic shock may occur due to loss of plasma from the burn surface (refer to Chapter 5). • Loss of protein from the plasma loss may result in generalized pitting edema. II) Infection of the wound site and sepsis may occur. (a) Sepsis due to Pseudomonas aeruginosa is the most common cause of infection in burn patients. (b) Other pathogens include methicillin-resistant S. aureus and Candida species. (3) Curling ulcers may occur in the proximal duodenum (refer to Chapter 18). (4) Hypermetabolic syndrome may occur if >40% of the body surface is burned. +11  
yex  Can someone explain why is it not increased ECF? +9  
charcot_bouchard  i picked same. Increased ECF but cant remember why. Can you explain WHY it is increased ECF? what was ur reasoning +2  
isotopes  Burns would lead to a decrease in ECF because the protection from fluid loss is absent; it can lead to shock. :) +1  
tinydoc  My reasoning behind picking ↑ ECV was that your losing fluid but not electrolytes with the burn ⇒ the ecv would have increased osmolarity, so the fluid from the ICV would be pushed the the ECV. It made sense to me at the time. I guess technically its wrong because the loss of fluids and the gain of fluids would amount to pretty much the same thing. But the insulation and heat loss thing makes sense I guess. +  
yex  Increased ECF, bc I was thinking about the edema formation.... :-/ +3  
atbangura  I picked increased ECF because burns increase the capillary permeability coefficient, but now that I am going over it I realized that increasing the permeability would only transfer plasma volume to the interstitial volume, which are both a part of the ECF so therefore ECF would not change. SMH +5  
aisel1787  thanks +  
69_nbme_420  Burns (and Diarrhea) cause ISOsmotic volume contraction; Costanzo BRS Physio +  
tiagob  in severe burned patient, also has increased fluid in third spacing or interstitial (leading EDEMA). Different extracellular space is interstitial and vascular +  
peridot  I also wanted to add, another huge job of the skin is to prevent loss of fluid. Burn patients are easily dehydrated because they've lost that barrier. This helped me lean away from increased ECV - despite the edema (from one compartment to another) as others have mentioned above, there is a loss in overall ECV due to evaporation from body. +  


yex  There is a Q on UWorld about rotator cuff tendinitis #380186 w/ a similar presentation... I kind of remembered about that, but honestly I do not know how I got it right. +  
yex  Correction: Q id is # 1732 +  


submitted by yotsubato(841),
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Wsa ti usjt me, ro ddi "ega at tsneo ni r"yesa erapap IGHTR aevob teh rmuben of e,tnpasit atrhre anth het .anem cihWh enudsfoc em fro a odgo 3 enmsu.it

fulminant_life  Definitely was the same for me. I was so confused for like 5 mins +13  
d_holles  dude i almost didn't get the question bc of this ... i thought the age of onset was the actual age of onset (36) +6  
mellowpenguins  Are you serious. NBME strikes again with shitty formatting. +6  
yex  OMG!! Now I just realized that. Super confused and also thought onset of age was 36. :-/ +5  
monkey  what is 36 supposed to be? +  
thomasburton  Think the number of people in that group +4  
paulkarr  Yup...was looking at it for a good 3 min before just doing the "fuck it..it's gotta be 99" +3  
arcanumm  Age of Onset is the Title of the table, which I didn't figure out until after exam was over. What terrible formatting. +3  


submitted by usmleuser007(337),
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1. riAtco oslaDciti serruePs 1. ihgH RTP = ighh DP .2 ghiH HR = hhig DP .3 Hgih SV = hgih PD 2. oAirct iSyoltcs eerPusrs .1 hHig itinCalytrtoc = ighh PS 2. Hhgi VS = high SP .3 woL lCaneicpom = ghih P S
yex  https://cvphysiology.com/Microcirculation/M012 This helps somehow, the first part about capillary pressure. +  
usmlelol  that's the exp part:: The average capillary hydrostatic pressure is determined by arterial and venous pressures (PA and PV), and by the ratio of post-to-precapillary resistances (RV/RA). An increase in either arterial or venous pressure will increase capillary pressure; however, a given change in PA is only about one-fifth as effective in changing PC as the same absolute change in PV. Because venous resistance is relatively low, changes in PV are readily transmitted back to the capillary, and conversely, because arterial resistance is relatively high, changes in PA are poorly transmitted downstream to the capillary. +  


submitted by mousie(179),
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Can snmooee apelse ixapenl hist ot me? I o'ndt ntdndsurae why gsnartti the tehor rdgu dowlu nto nocut sa lunsoeicx cetrir?ia

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 whossayin(18),
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teh tqunsoei was yrve olyopr wddreo in my nni,opio ybyanod slee raeg?e

niboonsh  yea it was a dumbass question, whoever is writing these questions is undoubtedly a crazy genius but homeboy (or homegirl...homeperson?) needs a few grammar lessons. +4  
yex  I agree. We know that it is a teratogen, but how does that question directs you to think about teratogenic effects instead of something physiologic? +5  
dr_jan_itor  The questions in the NBMEs by default are reject questions. So highly selective to be awful questsions. I am recieving regular heads up that the stems on the real thing lately are like 10-12 lines long. So these questions are not anywhere near like the test. NBME has f'd us good for this particular round of practice forms. +  


submitted by jotajota94(14),
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esU hte erWnaegbrdy-Hi ioneaqut

  1. aTke hte usqrea otro fo 1/06,10 nad ahtt wlil ivge ouy het refqcenyu fo teh riseevsec eelall = 401/.
  2. lluaCtaec teh efneurcyq of the mnatiodn llelae htwi =+q1,p hichw si =p 9.570.
  3. eTyh era glnetli ouy ot atlelccua het erneuqcyf of teh eiedssa rrcr,isea ichwh si thwi eth aeitonuq p2.q
  4. heyT wnat noyl eth asdesei rceirsra ni wihhc lnotdiee si esrten.p oT eualctcal th,is eus hte q vaule 10)4(/ dna mtiuplyl by 08% in htis dulhso evig ouy 0.20.
  5. nyalFl,i ultcaalec rfo P2 2q =.70(0().509)2 40.0 = 5.12/
yex  Nice! ...and we are supposed to read the stem and do all this in a minute or so? :-/ +14  
charcot_bouchard  Allele frequency 1/40. so carrier freq 1/20. 80% of 1/20 is 1/25 (80/100 x 1/20) +13  
dickass  Ah feck, 2pq got me +  
hello_planet  A handy shortcut for Hardy-Weinberg is that you generally can assume p ~= 1 if q if fairly low. It also tends to be easier to work in fractions if the answer choices are in fractions so you don't have to bounce back and forth between fractions and decimals. So with that, you send up with 2pq = 2 * 1 * 1/50 = 2/50 = 1/25. +1  


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Can meoybods lepsea naxpile hwy teh pKa hsa ot be 6 itesnad fo ?10

masonkingcobra  Since an ionized form is charged (by definition), it will not easily cross a nonpolar lipid membrane. Thus, it is important to recognize the potential of the drug to ionize in order to predict its solubility and the degree to which it can be reabsorbed. The degree of ionization is determined by the drug’s pKa and the pH of its environment. Weak acids and bases are 50% ionized and 50% unionized when the surrounding pH equals the drug’s pKa. At 2 pH units above or below the pKa of the drug, nearly 100% of the drug is ionized or unionized. +3  
masonkingcobra  Basically weak acids are best excreted in alkaline urine, but weak bases are excreted more readily in acid urine. +  
masonkingcobra  In summary, because this is a weak acid at pKa 6, making the urine alkaline will result it its ionization and excretion. Ionized cant move through lipid membranes so can't get reabsorbed and is pissed out. +7  
yex  Following on masonkingcobra explanation: A pKa 4-9 can be either weak acid or base. Weak acid pKa 4-7; strong acid pKa 1-3 Weak base pKa 7-9; strong base pKa above 9 Differents pHs: stomach: 1-2 duodenum: 3-5 early jejunum: 5-7 late jejunum: 7-9 ileum: >9 urine: 4.5-8 Weak acids (pKa) gets absorbed in acidic (pH) environments and cleared in basic. Weak bases gets absorbed in basic environments and cleared in acidic. THIS DOES NOT APPLY TO STRONG BASES OR ACIDS!!!! The best explanation for this is a Biochem lecture from Pass Program and it is available on YouTube, its long but it is for sure worth it!! Look for 19 Biochemistry 1 from Pass Program on YouTube. +1