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Welcome to j44n’s page.
Contributor score: 56


Comments ...

 +0  (nbme20#49)

I hated everything about these answer choices


 +1  (nbme17#0)

Dr. Sattar for the win, this is a reperfusion injury. The cells dont have ATP so they cant run reduction reactions when they get 02 again. Its like being bankrupt they cant "pay" for thing like glutathione system etc so they get a build up of free radicals and free radicals cause lipid peroxidation


 +0  (nbme17#49)

this was kind of a garbage question because she's still having normal periods, she hasnt hit menopause yet but shes close. What sells it it the BMI of 27 which is techncially overweight (normal BMI ends at 25) so the elevated fat is causing her to have hyperplasia from all the estrone coming from her fat. So during her proliferative phase the added estrogen from her fat is causing it to be overdone


 +1  (nbme17#50)

you cant blame anyone for your being late. You have to deflect and stay broad because it creates a distrust in the medical system all the other ones place blame else where or make you look like the encounter isnt a priority

thegout  idk why this wasnt as obvious to me, i picked the apology followed by this wont be long. I thought if i apologise and bring up her being late, it might just trigger her further if she really is late. +1
whoopthereitis  I put that answer too, I think that by saying "but this won't take long" can be considered as you promising the patient something that you can't guarantee. And also like you are going to rush the experience afterward because of your mistake or tardiness whatever. +

 +1  (nbme17#29)

the semantics of this question made me want to put my fist through my laptop screen


 +0  (nbme17#40)

this lady has eithe OCD or an anxiety disorder both first line for tx is an SSRI-> she washes her hands 30x a day and wakes the poor baby up 14 times a night. She's got multiple repetitive behaviors that aren't productive to solving the perceived problem


 +0  (nbme20#17)

Possible causes of galactorrhea include: Medications, such as certain sedatives, antidepressants, antipsychotics and high blood pressure drugs. Opioid use. Herbal supplements, such as fennel, anise or fenugreek seed

^ from the mayo clinic.... emphasis on the HTN drugs


 +1  (nbme19#0)

the way I approached this was that it didnt increase the amount of substrate to reach vmax so it couldnt have been any kind of comp inhib, also the efficacy is the same so it couldnt be an allosteric inhib


 +0  (nbme19#39)

I picked the adrenal glands because cortisol has a permissive effect on blood pressure and gluconeo


 +1  (nbme24#18)

I hate these so much these questions give me MCAT PTSD


 +0  (nbme24#35)

Just another piss poor government institution cutting corners. If you've done NBME 18 and seen the cell diagram figure it is the literal pinnacle

drdoom  the NBME is a private, for-profit corporation. individual U.S. states use its products (i.e., the certification it gives you when you pass their exams) to determine your eligibility to practice in their state. but they are not a government entity. +

 +0  (nbme24#4)

For as much money as the NBME scams off of us they really do give you the most HEINOUS figures... if you've done NBME 18 there's a cell diagram that looks like the test writers toddler drew.


 +0  (nbme24#30)

AT-II is the main stimulator of aldosterone release. This is kind of bull shit because that was the answer to one of the other NBME questions in ACTH cushing's disease "wHaT pArT oF tHe GlAnD iSn'T eNlArGed?"


 +0  (nbme24#50)

this is how I looked at it extra cellular osmoles> intracellular so it will pull the h20 out.... then the high osmotic pull of the sugar overwhelming the SGL2 transporter in the kidney will pull the h20 out of the body dehydrating the extracellular compartment

j44n  also the brain/CNS/neurons have the highest affinity GLUT transporters.... thats why giving glucagon brings someone out of hypoglycemia when theyre passed out. The glucagon increases the blood sugar and it goes straight to the brain restoring concious +

 +0  (nbme24#19)

The only reason I got this right is because I did a study for a practice on surgery cancelation rates and when we did lit review I read a paper that in middle eastern countries in areas where they are very very conservative muslim a lot of surgeries get canceled because their husbands dictate all of their care or can't be there to see their wives during the surgery. I think they're just wanting you to see the cultural difference and be aware of it. Which unless you haven read that one specific paper is like trying to see something with the sun in your eyes. Not defending the NBME but this question was garbage and almost as much bull shit as the platelet question


 +0  (nbme24#5)

I got thrown off because there's an arrow point to the three unaffected daughters (with an affected father) so I thought XLR because they'd be carriers. And there was no generation skipping so that made me think AR





Subcomments ...

submitted by claptain(21),
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I 'tdno neaddstnru tish uiotsenq. hTey tquaee arracttreusi-s ot aenm fcatfdee yb het ee.llla We kwno reh erthom is a aerrirc ecsabeu ehs ash tdelvaee .KC hTat emsan eth pttiane ash a 0%5 ecchna to eb a airrerc esnic sesh' mef.lae oRnmad tiXvnnc-oiatia etsodn' tatrem wnhe iltagnk buoat rcrraie atstus ecesuba htbo eallles ahve a nahecc ot etg ssaedp o.n odmnaR X viataitcionn si nyol mainotprt fro mnendigirte hweerht esh llwi pedoelv tm.pysmos

I sgeus htsi is hwy eht tusniqeo aws orwhnt uto? esUsnl mI' sgsimni no.smeihtg

claptain  Nvm, this question played me. I realize that E is the only possible choice. Both A and B would be 25% chances, not 50% chances, and you cannot assume whether she is or is not a carrier without genetic analysis (choices C and D). That leaves only E. +5  
beansbeansbeans  Wait I agree with your first comment, can you explain what made you change your mind and understand this? +  
yerpderp  They are referring to x inactivation in the daughter which would mean she could be a carrier but we cant tell. +1  
cbreland  so her mom is a carrier because she doesn't have complete symptoms like the brother and uncle?? I guess I thought it was all of nothing with duchenne +  
cbreland  Damn, her mom is 50. Duchenne patients don't live that long... nvm dumb on my part, should have made the connection +  
j44n  her mom cant have the full blown disease because its an XLR disease. I think we had to narrow this down by process of elimination +  


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CNS misaboasie si smot unroliotsyo sudace by regNeaial or,welif hchwi I renguaoec uyo ot imeromez sa het aagnnieri-b“t abe.oa”m unodF ni rrshwfaete- ioedbs of arwet kiel dpnos nda e,slak it ash erhte :orfsm a y,tcs a tpoetrzoiho odbe(a),mi adn a tgalebilfale e.(.i has otw gllalf.)ea cnneIioft si vai raoytoclf llec saonx orhthgu teh ircrfrimob petla to eth brnia.

mullerplouis  To add to this it causes Meningoencephalitis. Look out for confusion and brain signs mixed with signs of meningitis. Only a handful of organisms that cause both. +3  
osler_weber_rendu  Am I the only one who thought portal of entry cant be through a nerve and just ignored all the nerves? +37  
luciana  @osler_weber_rendu I thought the same... I knew it was through cribriform plate, but not that was actually through the nerve +10  
paperbackwriter  @osler_weber_rendu yeah same here, otherwise would have been a much simpler question +  
melchior  In line with the thinking above, SketchyMicro teaches it as if it just passes through the cribriform plate, ignoring the nerves. Wikipedia says that it actually enters the nerves, then passes through the plate. +5  
j44n  this is such an AWFUL disease, I worked in a hospital in south carolina where it happens A LOT and there's nothing at all you can do for them. When your cells go to phagocytose it it has an outer layer it sheds off like how a lizzard will sacrifice its tail when attacked by a predator. +1  


submitted by dixie96(2),

trichuris trichiura can present with rectal prolapse in kids which perhaps accounts for why this boy thought he defacated in his pants

mes1717  will also see presence of worm on stoop O&P +  
madden875  this is ascaris, NOT trichuris +3  
j44n  i agree trichiura only get to 50mm +  


submitted by hayayah(1074),
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noIr voeoersd is a ucaes fo a ihgh nioan apg boitaemcl di.osacsi

meningitis  I found this to add a little bit more explanation as to how it causes the acidosis if anyone needs it. 1. Mitochondrial toxicity - decreases aerobic respiration and shunts to lactic acid production 2. Cardio toxicity (Secondary to Mitochondrial toxicity) leads to cardiogenic shock (hypoperfusion), which causes lactic acidosis 3. Hepatotoxicity - Decreases lactate metabolism, causing lactic acidosis 4. When in trivalent form (Fe+3), it can react with 3 molecules of H2O --> FeOH3 + 3H+ This will then deplete Bicarb buffering system resulting in non-gap acidosis. Source: https://forums.studentdoctor.net/threads/iron-poisoning-anion-gap-or-non-anion-gap-acidosis.958285/ +17  
sympathetikey  None of the other choices were even metabolic acidosis. They threw us a bone with this one. +28  
imnotarobotbut  Don't changes in bicarb take a few days? How did his bicarb drop down to 8 in 12 hours? +2  
charcot_bouchard  its met acidsis. not compensation +8  
j44n  they did throw us a bone however I didnt catch it +1  


submitted by lamhtu(118),
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lnasuuU ahtt het eatnpti si a ognuy gli,r COTD is LXR anriin.eceth

eacv  yes !!!!! that make me doubt and choose the wrong one -.- +  
ally123  FA p. 83 +1  
j44n  could have turners and we just dont know it yet or skewed x inactivation.... but thats really really really going down the rabbit hole tbh im glad I didn't notice that when i answered this +1  


submitted by imgdoc(135),
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uYo cna rcoss tou the pot eethr enwrsa ioh,secc B.C,A, uoY nwto be ersoabbrign ahngntiy ni eth TPC in c'fanoisn ds.yonrem knioLog at amkoepylah,i aopthnreia,my and eomaoathsppphyhi won. epHkaaolmiy ca'tn eb coetcrr bsceuae nvee ohuhtg upiatmsos is tlso it liwl eb breeodrsab at eht elrat chkit sgaendinc ploo dna if htat tnedso kaem sesne, eth obdy liwl jtsaud orf wol muesr amspiouts utb vaatgcntii het K++/H mpup on e.llcs It sin't tpaemyraoihn auscebe at hte ingollectc cdtu parplcnii sce,ll tnpaeobirros lwli rocu.c Tsih easlve iahtoahspoyheppm sa hte ectrocr nda nloy ewrnsa .hicoce

imgdoc  by* +2  
larascon  Excellent explanation, thank you ! +1  
waterloo  It's worth mentioning, that 25% of Na is reabs in the thicc ascending limb. 67% of filtered Na is reabsorbed in the PCT, whereas 85% of phosphate reabsorbed in the PCT. So pt more likely to show Hypophos. +  
coconut  UWorld QID:7626 says lab results in people with Fanconi syndrome will show hypokalemia +  
j44n  coconut i thought that too but then i remebred fanconi is associated with hypophosphatemic rickets/ VIT D resistant rickets and this little dude is going to be growing because he's 5 and thats gonna increase the demand for phosphate in his body +  


submitted by neonem(568),
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Oistbucretv ohaurpty saeusc a oaslenptr ieazmato t--;g& hnwe leopdg,nro uaurblt mdgeaa eessun. sihT aldse to na tceua rbaulut ossnicre, chearidaecrtz yb intrccoe lgpsu in eth arbluut tsyems sa eesn in hte mieag

meningitis  Does anyone know the relevance of the stem saying: "during this time she also has been crying frequently"? +43  
usmleuser007  Think the postrenal azotemia is d/t her pregnancy. With the increasing in size fetus, the pelvic cavity is being compressed and thus there is pressure on the ureters. This leading to the presentation. As per above --- the crying maybe just d/t her pain and emotional stress caused by worrying about possible complications regarding her fetus. +4  
maxillarythirdmolar  My gut tells me it must be some sort of transient change in placental size with hormonal changes. It's reminiscent of what you might expect for breast changes during the menstrual cycle, imo +  
j44n  or maybe the fetus is literally crushing her ureters into the wall of her pelvis and shes got an infected kidney +1  


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I inthk tihs noe sah to od with tela" ipungdm -rsedo"nmy- yla,labcsi chatrys odfos acues eipgmelacyrhy --t;g& realees of siinlnu g-;-&t celhmentioaac urseg --&t;g ardhi,aer t.ec

merpaperple  It's not necessarily late dumping syndrome, this is the dietary guideline for early dumping syndrome too. Based on UpToDate and ScienceDirect this is how it works: Absent or dysfunctional pyloric sphincter -> food is rapidly emptied from the stomach into the small bowel -> hypertonic solution forms in the jejunum -> rapid fluid shifts from the plasma into the bowel -> hypotension and SNS response (eg. colicky abdominal pain, diarrhea, nausea, tachycardia) Simple carbohydrates are more hypertonic, I think. https://www.sciencedirect.com/topics/medicine-and-dentistry/dumping-syndrome +2  
j44n  starches are complex carbs= more than 2-3 sugar molecules, if they have dumping syndrome they have decreased gastric transit time= more undigested carbs are delivered to the intestines and that gives you more carbs for bacteria to break down (flatulence and osmotic diarrhea) +  


submitted by xxabi(257),
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I wsa duern hte mosnpersii tath hsit was an rcaito o,nisetdcis ude to ers"vee hcset npi"a sa lwel sa the false mueln ni eht aar.ot ndA THN is eth 1# risk artfco orf tcioar cn.stidoies enmSooe crcrtoe me if im' r,nowg tbu I nihkt shti is aorcti tiscodneis ehartr naht criaot yrusen.am

chefcurry  I believe so, FA 2018 pg 299 +3  
ergogenic22  It is dissection "extra lumen in the media of the proximal aorta" = "a longitudinal intimal (tunica intima) tear with dissection of blood through the media of the aortic wall" ... answer is still hypertension +2  
breis  FA 2019: 301 +  
pg32  First Aid says that aortic dissection causes widening of the mediastinum and is due to an intimal tear, so I thought it wasn't an aortic dissection. Can anyone help me understand why First Aid was wrong in this case? Thanks! +3  
nephroguy  @pg32 The question stems states that there is no widening of the Aorta, not the mediastinum. Widening of the mediastinum is seen in dissection while widening of the aorta is seen in aneurysm. Also the intimal tear creates a false lumen between the intima and media. Hope that helps! +10  
j44n  https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.118.312436 pictures worth a 1,000 character limit +  


submitted by suku008(9),
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tI’s a nocmmo dsaesei taht cmtspia bbaise nda lrcei.hdn RGED sandst fro grsota hgeasoleap exurfl adieess. Dr. iairVne aseoW,rryeoai a iepridtca gtooniarogeeslrtts on eth aeimldc fsaft of soaiGnlo h’rCsienld oHatspil of tseoStuwh oF,rilad assy nnftasi aer orpne ot ganivh fxluer nltiu etrih gut emurats ta autbo 12 ot 18 .mhotns But DEGR is rome atnh tsju e.xfurl Wt“ha stih piesmli is nisaudidvil woh eahv smopeblr htiw rtgaso nttonesc ttha omev up ot eth goaehpsus ro tnio teh uot.mh

suku008  https://www.youtube.com/watch?v=DFcySw14rIo +2  
j44n  if youve ever had GERD like me you know exactly what they're talking about. You legit bring up food you ate hours before +  


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icraburuFmosl ehyrisppaal wlli cuase erp renal .iamoteaz S. BUCr/N si 0gt2;& in erp nrela amioeatz tbu in teh oquestni tis lueav is vcidtieain fo srnitnici lrnae rl.afeiu yrve sgnocfin!u!

charcot_bouchard  Not really, Hypotension cause pre renal azotemia. Here long standing HTN resulting in end organ damage so intrinsic renal failure +2  
cry2mucheveryday  ugh! i just noticed there's a fairly long h/o of poorly controlled HTN which makes this question simpler now. Thanks!! +  
j44n  arterioles are in the kidney.... ya know like afferent/efferent ARTERIOLE @ the glom. if this was in the renal artery he'd have pre renal azotemia +  


submitted by studentdo(9),
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ehT oamjr otoinm fo asosP marjo si onieflx of hi.p hisT etatpin is edlh ni "dgiri en,"nesxiot chene he edos tno want to lef.x saosP is eth lnoy cmelus on shti tlis thta etnconsc het urlbams to oewrl xyeritemt l"dhos sih rhtig werol etemri"xty

myoclonictonicbionic  The qstem said "lower extremity in rigid extension" which made it sound like extension at the knee joint rather than at the hip. Confusing wording +2  
j44n  if you lay on your back and kick your leg straight up this is lower extremity extension, hes doing that to prevent any weight being placed on his psoas, I know because ive had psoas problems before and you will do ANYTHING to keep your hip from flexing (like doing a sit up or pulling your knees toward your chest) getting in and out of a car was a nightmare +  


submitted by hayayah(1074),
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mriaMueycbcto miavu xlpceom sncoifeitn aer a mmnooc tpocpsuiontri fnieonitc ni nettipas hiwt neaacdvd DIAS D(C4 tcuon 5lt&;0).

realfakedreams  @hayayah you were being lazy.. smh.. Homie started anti-retroviral therapy. HIV infects CD4 T-Cells through either CCR5 or more commonly CXCR4. Because of anti-retrovirals start working, HIV isnt able to infect anymore CD4 T cells. Thus CD4 t lymphocytes levels start to rise and are able to active B cells. +13  
myf1991  Why can't it be monocyte? macrophage eat MAC and interact with CD4 +1  
weenathon  @myf1991 I also incorrectly chose monocytes, but if you look at the question carefully, it is specifically asking what cell is required for the lymph nodes to enlarge, not which cell is handling the mycobacterium avium infection. Since CD4 cells stimulate B cells to proliferate in lymph node follicles, which would make them bigger, CD4+ T cells is the answer. +3  
j44n  macrophages dont enlarge nodes in fact they make them smaller, tingle body macs eat all the bad B cells in a node so improved mac fxn would decrease the node size +  
mpel14  To add to @namira, an infectious disease doc described this concept in an HIV lecture where he said that prior to the Tx with antiretroviral therapy, the pt has such low CD4 count that their immune system cannot form a response to the infection, and after their immune system is given a slight boost with the drugs, their immune system can finally "see" the infection -> mount response -> causes S/S +  


submitted by hayayah(1074),
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ihsT is vertacie yyahlpetciom erv,a hciwh si eud ot hhgi lttuadie ro unlg sde.iaes aSO2 si ,wlo nad PEO is cdeai.esrn

neAroht ayw to acophapr teh osqntuie is lonokig at eth lbodo ms.are I'st tyrtpe rnmola o(n ,tkyseromaegcay on ieesrnacd emunrb of tltals,eep no rod,s tohginn ,buel .ce)t A dobol sraem fomr a DOPC tpenita will be .ralmon stJu na eaencrdis meubrn of sRCB edu ot hte carisdnee OPE ngaedil ot inecesrad gH.b

mbourne  You shouldn't call it reactive polycythemia "vera", as polycythemia vera is a seperate disease with entirely different etiology. This is Reactive Polycythemia, or as another poster said, appropriate absolute polycythemia secondary to chronic hypoxia. +16  
j44n  i jumped on myelodysplastic thinking it was PV due to the jak w mutation but you technically get elevated everything in that mutation so it would be more than just RBC's +  
beetbox  I also thought it was PV. How can we tell reactive polycythemia from actual PV, if PV does not show other kinds of blood cell counts raised but just an isolate of RBC rise? +  


submitted by strugglebus(165),
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I oehcs ihts oleyls asecbue ti aws so ndam icipcefs

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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I cohes itsh sloyle baceeus it asw so ndma pciifecs

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 step420(34),
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ihsT si elulnmria .eegiasns raNlmo rvoaise tub aentbs esu.tur

endochondral   why not androgen insensitivity? +  
shaeking  I was wondering the same thing because doesn't androgen insensitivity also have normal female secondary characteristics. Was it the levels of hormones because she doesn't have abnormally high testosterone? +2  
swb  Androgen insensitivity has the same presentation and symptoms. What's the clue that it is mullerian agenesis instead ? +23  
sugaplum  Testosterone would be high if it was androgen insensitivity FA 2019 Pg 625 +14  
charcot_bouchard  Testo would be high in AIS. in AIS pubic hair, axillary hair doesnt devlop because of androgen insensitivity. both have normal breast dev and primary amenorrhea +2  
dickass  This is not androgen insensitivity because she has perfectly normal Estradiol, which means she has perfectly normal ovaries. She also has regular female levels of testosterone. +5  
rockodude  thank you @dickass +1  
j44n  Also AIS has paradoxically large boobs-> tanner stage 5 and thats not mentioned anywhere +  


submitted by usmle11a(74),
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nilegollea : evyr mcmoon ni aavcdden g,ae CD,OP smisremepospunud tpitsean dna " ginog ackb mrof a rdseieecn "ahll hwcih aroypblb hda a toctemdnania AX ytsems a(yallcibs fsit veery noe in het )Q

eadon X : dlwou esenrpt wtih vtcouiinict,jns hattor pnai u...f l :uisrv ont oneyever gto eht iesdaes R:SV no hrdelinc tspr e e:moupn dwolu erattg a rlreag tanplipouo fo teahhly poepel sa ellw.

bharatpillai  why would they say that the only people who didnt get affected by the disease were people on steroids (lupus nephritis and severe asthma) couldnt have been rsv since it causes croup in children. strep pneumo would cause fever and other systemic signs. i went for adenovirus because uworld says most common causes of copd excacerbation are viral infections... +2  
brbwhat  I went for adeno forr the same reason. I guess the MAIN HINT is that this is not a copd exacerbation. Since people without prexesting copd also had pneumonia, also people with copd exacerbation will have different presenting symptoms, here it was told, that we are told that dx was penumonia. People with copd exacerbation wouldn’t be diagnosed with pneumonia if it was an adenovirus infections. +1  
j44n  adenovirus doesnt cause pneumonia its just makes the current COPD sx worse +  
j44n  the SLE and asthmatic patient were both considered slightly immunosupressed or theyre just more likely to get something (SLE pt= your B cells are too busy making Ig's to kill your kidney, and the asthmatic is on corticosteroids that aopotose your t cells) but they're not COPD patients so the pneumonmia wont be as severe, all in all legionella causes really really bad pneumonia in COPD patients and less severe (pontiac fever) in those with mild immunosupression +2  


submitted by usmle11a(74),
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gelielonla : yerv moonmc in adevcand e,ag DPCO, rmmpinosdesuespu piaetsnt nda " gogin ackb fomr a sedeircen h"lla hwhci aylrpbbo dah a tnnetadcamio AX symtes ysall(baci tfsi yever noe in eht )Q

onead X : dlouw senprte whti snonc,ttviuiicj hratto npia f..ul. rs:viu not eoynvere ogt teh easidse R:S V on cdrniehl prtse pnoe:um olwdu eagttr a arelrg laoptpionu fo yehhtla opplee sa llew.

bharatpillai  why would they say that the only people who didnt get affected by the disease were people on steroids (lupus nephritis and severe asthma) couldnt have been rsv since it causes croup in children. strep pneumo would cause fever and other systemic signs. i went for adenovirus because uworld says most common causes of copd excacerbation are viral infections... +2  
brbwhat  I went for adeno forr the same reason. I guess the MAIN HINT is that this is not a copd exacerbation. Since people without prexesting copd also had pneumonia, also people with copd exacerbation will have different presenting symptoms, here it was told, that we are told that dx was penumonia. People with copd exacerbation wouldn’t be diagnosed with pneumonia if it was an adenovirus infections. +1  
j44n  adenovirus doesnt cause pneumonia its just makes the current COPD sx worse +  
j44n  the SLE and asthmatic patient were both considered slightly immunosupressed or theyre just more likely to get something (SLE pt= your B cells are too busy making Ig's to kill your kidney, and the asthmatic is on corticosteroids that aopotose your t cells) but they're not COPD patients so the pneumonmia wont be as severe, all in all legionella causes really really bad pneumonia in COPD patients and less severe (pontiac fever) in those with mild immunosupression +2  


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Tish is YLLILRTEA the eams ptoho tyeh sued ot cbedseir het -l-4edaryo yob wthi iefdusf liaccort rcesoisn ofrm BNME 18. anC enosemo napilxe wth'as niggo no hree

lancestephenson  *Tubular atrophy, not cortical necrosis lol +  
charcot_bouchard  Can u fuckers talk about spoilers +1  
adong  same photo because the end gross pathology is the same. whether it's due to cancer or whatever the 4 year old boy had (some sort of obstruction IIRC) it ends with atrophy of the kidneys +  
j44n  they used the same kidney on NBME 17 for posterior urethral valves lol +  
j44n  this is probably the most famous kidney in medicine +  


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iThs is RLTAELILY het seam phoot htye ueds to dscibere the d-a4orl-ye yob hitw fdifesu iorcaltc nceisosr omfr MBNE 8.1 nCa meoeons peilanx hw'tas going on erhe

lancestephenson  *Tubular atrophy, not cortical necrosis lol +  
charcot_bouchard  Can u fuckers talk about spoilers +1  
adong  same photo because the end gross pathology is the same. whether it's due to cancer or whatever the 4 year old boy had (some sort of obstruction IIRC) it ends with atrophy of the kidneys +  
j44n  they used the same kidney on NBME 17 for posterior urethral valves lol +  
j44n  this is probably the most famous kidney in medicine +  


submitted by sympathetikey(1350),
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uttinosaM in TL-TM1 nlltoyoahMid(ric edcenod NARt enuecli )1

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  • hnditriloocaM yhcnytmelapaopeho
  • citcaL dssaoiic
  • Sekerkt-loi pseeiosd )ASEM(L

EASLM is a rera odcinhrilmato odirdsre owknn to ateffc yman pstar of the dbo,y seylcapile teh eunorvs etsmys nda the arnb.i Smomptsy of LEMAS iceul:dn

  • uerentcRr veeres haadeeshc
  • sMucel waknsees y(hto)pamy
  • giaerHn lsso
  • kte-kiSrole epessido twih a sosl fo sncs,scnosuieo ur,sziese and horet brsopelm igfanfcet the urosnve smteys.

uScro:e pLnis-T:itwa/rpTwkikeeod1./ig/h.tM/i

j44n  i just saw that every tissue that was affected had a high 02/aTP requirement and mixed with the lactic acid that meant she wasnt using her electron transport chain so i picked the only answer that had mitochondria in it +3  
topgunber  The disease is MELAS. Mitochondrial encoded tRNA leucine 1 is the mutation. Apparently associated with high tone deafness. It is apparent its mitochondrial with maternal transmission, though unfortunately the etiology is utter memorization / process of elimination. Maybe next time the stragy will focus more on mitochondiral diseases and see that this choice is the only mitochondiral answer choice. Mitochondrial Encephalomyopathy Lactic Acidosis Stroke like symptoms."MELAS is a rare mitochondrial disorder known to affect many parts of the body, especially the nervous system and the brain. Symptoms of MELAS include recurrent severe headaches, muscle weakness (myopathy), hearing loss, stroke-like episodes with a loss of consciousness, seizures, and other problems affecting the nervous system.[5]" Source :Wiki +  


submitted by step420(34),
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tehOr kidyen orpepHeitshry edu ot enaiscerd stsers ;tg&-- ont iyelahsappr bc ont csaorencu

masonkingcobra  Above answer is incorrect because hyperplasia can be either physiological or pathological. Prolonged hyperplasia can set the seed for cancerous growth however. Robbins: Stated another way, in pure hypertrophy there are no new cells, just bigger cells containing increased amounts of structural proteins and organelles. Hyperplasia is an adaptive response in cells capable of replication, whereas hypertrophy occurs when cells have a limited capacity to divide. Hypertrophy and hyperplasia also can occur together, and obviously both result in an enlarged (hypertrophic) organ. +43  
johnthurtjr  FTR Pathoma Ch 1 Dr. Sattar mentions hyperplasia is generally the pathway to cancer, with some exceptions like the prostate and BPH. +4  
sympathetikey  Tubular hypertrophy is the natural compensation post renal transplant. Just one of those things you have to know, unfortunately. +2  
charcot_bouchard  Isnt Kidney a labile a tissue & thus should undergo both. This ques is dipshit +  
brbwhat  Dr Sattar says, kidney is a stable tissue, at least pct is as seen in ATN. But I read, basically kidneys are mostly formed whatever number of nephrons have to be formed by birth, after that they can only undergo hyperplasia aka increase in size/or regenerate if need be in case of atn. We cant have more number of nephrons. +1  
mambaforstep  @brbwhat , do you mean kidneys can only undergo hyperTROPHY? +2  
j44n  .... you're not making more cells..... so it cant be hyperplasia +  


submitted by kstebbins(10),

I was thrown off because Pathoma/Dr. Sattar and pixorize say it is critical to start steroids ASAP to avoid permanent damage to the ophthalmic artery and blindness in patients suspected of having Giant Cell (Temporal) Arteritis.

This means not waiting for diagnostic confirmation.

However a 99% sensitivity does not equate to a 99% certainty of GCA/TA. So additional testing is the best answer choice even though her elevated ESR gives us strong suspicion of GCA/TA.

nsinghey  exactly, the reason why its not steroids is because that answer choice says the diagnosis of TA has been established with 99% certainty which is NOT true +1  
j44n  this question threw me because you tx this on clinical suspicion alone. So i was torn between the right answer and the fact that if you repeated ESR again and its positive you youd the give steroids +2  


submitted by bingcentipede(243),

https://imgur.com/RQGrWLw

G represents the primary somatosensory area of the parietal lobe. The stem describes a 69 (nice) year old woman with sensory issues on the left side. She presents w/ a Babinski sign on the left, decreased somatic sensation in the left foot, agraphesthesia (when you "draw" a number on someone's skin and they can't interpret it) on the plantar surfaces of the toes, decreased position sense in the toes. The question says there is an edematous area in the cerebral cortex of the right hemisphere.

I had trouble with this, but I think it's describing somatosensory because of the sensory problems. Don't understand the UMN lesion (Babinski). Here's what Wikipedia says: "Lesions affecting the primary somatosensory cortex produce characteristic symptoms including: agraphesthesia, astereognosia, hemihypesthesia, and loss of vibration, proprioception and fine touch (because the third-order neuron of the medial-lemniscal pathway cannot synapse in the cortex). It can also produce hemineglect, if it affects the non-dominant hemisphere. Destruction of brodmann area 3, 1, and 2 results in contralateral hemihypesthesia and astereognosis."

mittelschmerz  The Babinski tripped me up too, here's what I found: "Sixty percent of the CST fibers originate from the primary motor cortex, premotor areas, and supplementary motor areas. The remainder originates from primary sensory areas, the parietal cortex, and the operculum. Damage anywhere along the CST can result in the presence of a Babinski sign." from https://www.ncbi.nlm.nih.gov/books/NBK519009/ +10  
yourmomsbartholincyst  I think this question is more simply about the topographical arrangement of the homunculus (which I once again somehow managed to flip backwards during the exam). Lower extremity is topographically mapped to more medial portions of the somatosensory cortex, hence letter G and why ACA strokes tend to affect the LE more. Homunculus, our favorite hunk, FA2020 pg 502 +10  
j44n  youre occluding the MCA blow flow from the MCA flows front to back so if you occlude the section that provides blood flow to the precentral gyrus you will also occlude the section that supplies the sensory portion http://what-when-how.com/neuroscience/blood-supply-of-the-central-nervous-system-gross-anatomy-of-the-brain-part-1/ +  
j44n  excuse me i miss spoke its the ACA because its her legs, look at figure 4-2 in the link on my previous comment +  
j44n  so if you have motor and sensory the infarct is in the portion that belongs to the motor portion, if you have sensory only youve occluded the artery more distally +  
jy1544  I thought G was indicating the primary motor cortex in the frontal lobe from a medial view (anterior to the central sulcus), hence the weakness - and the sensory disturbances were due to edema affecting the adjacent somatosensory cortex https://web.duke.edu/brain/siteParts/images/fig1-5_2018.jpg +2  


submitted by bingcentipede(243),

https://imgur.com/RQGrWLw

G represents the primary somatosensory area of the parietal lobe. The stem describes a 69 (nice) year old woman with sensory issues on the left side. She presents w/ a Babinski sign on the left, decreased somatic sensation in the left foot, agraphesthesia (when you "draw" a number on someone's skin and they can't interpret it) on the plantar surfaces of the toes, decreased position sense in the toes. The question says there is an edematous area in the cerebral cortex of the right hemisphere.

I had trouble with this, but I think it's describing somatosensory because of the sensory problems. Don't understand the UMN lesion (Babinski). Here's what Wikipedia says: "Lesions affecting the primary somatosensory cortex produce characteristic symptoms including: agraphesthesia, astereognosia, hemihypesthesia, and loss of vibration, proprioception and fine touch (because the third-order neuron of the medial-lemniscal pathway cannot synapse in the cortex). It can also produce hemineglect, if it affects the non-dominant hemisphere. Destruction of brodmann area 3, 1, and 2 results in contralateral hemihypesthesia and astereognosis."

mittelschmerz  The Babinski tripped me up too, here's what I found: "Sixty percent of the CST fibers originate from the primary motor cortex, premotor areas, and supplementary motor areas. The remainder originates from primary sensory areas, the parietal cortex, and the operculum. Damage anywhere along the CST can result in the presence of a Babinski sign." from https://www.ncbi.nlm.nih.gov/books/NBK519009/ +10  
yourmomsbartholincyst  I think this question is more simply about the topographical arrangement of the homunculus (which I once again somehow managed to flip backwards during the exam). Lower extremity is topographically mapped to more medial portions of the somatosensory cortex, hence letter G and why ACA strokes tend to affect the LE more. Homunculus, our favorite hunk, FA2020 pg 502 +10  
j44n  youre occluding the MCA blow flow from the MCA flows front to back so if you occlude the section that provides blood flow to the precentral gyrus you will also occlude the section that supplies the sensory portion http://what-when-how.com/neuroscience/blood-supply-of-the-central-nervous-system-gross-anatomy-of-the-brain-part-1/ +  
j44n  excuse me i miss spoke its the ACA because its her legs, look at figure 4-2 in the link on my previous comment +  
j44n  so if you have motor and sensory the infarct is in the portion that belongs to the motor portion, if you have sensory only youve occluded the artery more distally +  
jy1544  I thought G was indicating the primary motor cortex in the frontal lobe from a medial view (anterior to the central sulcus), hence the weakness - and the sensory disturbances were due to edema affecting the adjacent somatosensory cortex https://web.duke.edu/brain/siteParts/images/fig1-5_2018.jpg +2  


Pre-central gyrus= motor deficit (muscle weakness) UMN lesions (cerebrum) will cause increased reflexes (I think of Babinski present as hyperreflexia) IDK if it's like seizures, but I know seizures can start out as primary motor and expand to involve the sensory cortex as well. Maybe it was expansion of the edematous area

j44n  i agree you cant have UMN signs unless the precentral gyrus is infarcted +  


submitted by bingcentipede(243),

https://imgur.com/RQGrWLw

G represents the primary somatosensory area of the parietal lobe. The stem describes a 69 (nice) year old woman with sensory issues on the left side. She presents w/ a Babinski sign on the left, decreased somatic sensation in the left foot, agraphesthesia (when you "draw" a number on someone's skin and they can't interpret it) on the plantar surfaces of the toes, decreased position sense in the toes. The question says there is an edematous area in the cerebral cortex of the right hemisphere.

I had trouble with this, but I think it's describing somatosensory because of the sensory problems. Don't understand the UMN lesion (Babinski). Here's what Wikipedia says: "Lesions affecting the primary somatosensory cortex produce characteristic symptoms including: agraphesthesia, astereognosia, hemihypesthesia, and loss of vibration, proprioception and fine touch (because the third-order neuron of the medial-lemniscal pathway cannot synapse in the cortex). It can also produce hemineglect, if it affects the non-dominant hemisphere. Destruction of brodmann area 3, 1, and 2 results in contralateral hemihypesthesia and astereognosis."

mittelschmerz  The Babinski tripped me up too, here's what I found: "Sixty percent of the CST fibers originate from the primary motor cortex, premotor areas, and supplementary motor areas. The remainder originates from primary sensory areas, the parietal cortex, and the operculum. Damage anywhere along the CST can result in the presence of a Babinski sign." from https://www.ncbi.nlm.nih.gov/books/NBK519009/ +10  
yourmomsbartholincyst  I think this question is more simply about the topographical arrangement of the homunculus (which I once again somehow managed to flip backwards during the exam). Lower extremity is topographically mapped to more medial portions of the somatosensory cortex, hence letter G and why ACA strokes tend to affect the LE more. Homunculus, our favorite hunk, FA2020 pg 502 +10  
j44n  youre occluding the MCA blow flow from the MCA flows front to back so if you occlude the section that provides blood flow to the precentral gyrus you will also occlude the section that supplies the sensory portion http://what-when-how.com/neuroscience/blood-supply-of-the-central-nervous-system-gross-anatomy-of-the-brain-part-1/ +  
j44n  excuse me i miss spoke its the ACA because its her legs, look at figure 4-2 in the link on my previous comment +  
j44n  so if you have motor and sensory the infarct is in the portion that belongs to the motor portion, if you have sensory only youve occluded the artery more distally +  
jy1544  I thought G was indicating the primary motor cortex in the frontal lobe from a medial view (anterior to the central sulcus), hence the weakness - and the sensory disturbances were due to edema affecting the adjacent somatosensory cortex https://web.duke.edu/brain/siteParts/images/fig1-5_2018.jpg +2  


submitted by andro(188),

There are two types of infarcts : Pale infarcts - occurs in organs with a single end arterial blood supply
Red infarct ( also known as hemorrhagic ) - occurs in venous occlusion and tissues with multiple blood supplies ( eg liver , lung , intestine , testes )

Our patient clearly has a red infarct of the small intestine due to " mesenteric venous occlusion " .

The cause may very well be thrombosis secondary to a Polycthemia caused by his hepatocellular carcinoma( which secrete Erythropoietin) . Regardless of the cause however , we just had to recognise that this is a red infarct , and these are due to venous occlusion

j44n  also with HCC you get loss of ATIII production and predisposes to thrombi +  


submitted by cassdawg(1101),

Wegener granulomatosis, also called granulomatosis with polyangiitis, is a vasculitide that commonly presents with the triad of focal necrotizing vasculitis, necrotizing granulomas in the lung and upper airway, and necrotizing crescentic glomerulonephritis (FA2020 p 314 and 596)

Wegener is associated with chronic sinusitis, hemoptysis, and PR3-ANCA (antineutrophil cytoplasmic antibody, formerly called c-ANCA).

None of the other answers are associated with ANCA except Churg-strauss syndrome. Churg-strauss syndrome (also called eosinophilic guanulomatosis with polyangiitis) is associated with MPO-ANCA (formerly called p-ANCA). However, Churg-strauss does not have lower respiratory involvement, hemoptysis, or patchy lung opacities on CXR.

j44n  All ANCA's are against proteins in the cytoplasm, they were intentionally vague and wanted you to ddx this off of clinical pres +1  
jurrutia  Churg-Strauss can affect the lungs, but not the upper airway. +1  


submitted by cassdawg(1101),

This is basically a question of terminology. (FA2020 p219)

Invasive means it has penetrated the basement membrane but "microinvasive" would assume it has not invaded surrounding tissues as it has not metastasized.

dhkahat  am i crazy here? This questions seems odd to me. Because full thickness of the epithelium had to have been covered by neoplastic cells first right? idk maybe i got confused by the wording what "lead to this diagnosis" +  
j44n  what they're talking about with that one is a carcinoma insitu-> IE its neoplastic but it has yet to invade +1  


submitted by cassdawg(1101),

Hormone sensitive lipase (HSL) is the enzyme which degrades triglycerides stored within adipocytes (FA2020 p93). Thus, it makes sense that it is activated in times of fasting and suppressed in the fed state.

Insulin would inhibit HSL, as insulin is a fed state enzyme secreted by the pancreas and would want to trigger storage of triglycerides.

In contrast glucagon is secreted in response to hypoglycemia by the pancreas and will trigger fasted state activation. In terms of the fed/fast state I always think of glucagon and epinephrine kind of like a superhero and their side kick, because they usually work together in the fasting state on similar targets to ensure the body has enough energy (this helps me remember that epinephrine and glucagon are fasting state hormones). Here though is epinephrine's big action away from glucagon, where glucagon has minimal effect and epinephrine has the big action of activating HSL! Glucagon has a minor role and other catecholamines and ACTH can also serve to activate HSL as well.

Another example of the synergistic work of glucagon and epinephrine is in glycogen breakdown (FA2020 p85). Both will trigger cAMP increase and protein kinase A activation which will phosphorylate glycogen phosphporylase and activate it (FAST PHOSPHORYLATE! Hormone sensitive lipase is actually phsophorylated to activate it as well).

FUN FACT: Hormone sensitive lipase actually got its name because it was sensitive to epinephrine!

flapjacks  In Type 1 DM, the glucagon response to hypoglycemia is not functional and these individuals are reliant on the epinephrine-stimulated hepatic glycogenolysis. I recall this by remembering you can administer glucagon to these patients if they're having a hypoglycemic episode. They can respond to it, but they aren't releasing it. +1  
passplease  How did you eliminate thyroxine? As it also plays a role in lipolysis. I was thrown off my the low blood pressure and therefore did not select epinephrine. Why would they still have a low blood pressure? +  
jackie_chan  ^ they have low blood pressure because DKA causes a lot of dehydration (vomiting, diuresis due to osmotically active glucose in urine) so low BP Thyroxine I eliminated because remember that thyroxine is unique in that it functions similar to a steroid hormone and acts in the nucleus to upregulate expression of many genes. I figured hormone-sensitive lipase needs to be activated, not stimulated to upregulate expression, so I thought about EPI and beta-3 stimulation. fuckPeter +  
schep  I figured since he has low BP/dehydrated, his body would try to maintain cardiac output by increasing sympathetic tone (releasing epinephrine). In hypovolemic shock, systemic vascular resistance is up because of this compensation. +  
j44n  also thyroxine works like a steroid hormone meaning it takes a while to cause its effect +  
flvent2120  That'd be cool if it were called "epinephrine sensitive lipase" +  


submitted by bingcentipede(243),

The patient is clearly showing that he understands the procedure (information) and that he's willing to go through with the procedure (voluntariness).

The 2nd choice should be capacity because competence is the legally declared one (from a court). Honestly bad ? because of this.

But, family agreement (which technically wasn't achieved yet) and cost are not necessary factors for informed consent.

According to FA '19 p. 264, you need: disclosure, understanding, capacity, and voluntariness.

j44n  tf are you downvoting this for? +2  


submitted by bingcentipede(243),

Flipping a coin = randomization. You're also testing a new drug, which is the point of a randomized clinical trial.

j44n  it also cant be case series because they have a control group +1  


submitted by flapjacks(56),

My reasoning for this question:

  • In both situations, you see a cyclical increase in pain before receiving the injection. This could be seen if the effect was wearing off; however, if you notice, there is a decrease in pain before the injection is even given. I believe this implies that something inherent about the injection is providing pain relief.
  • Furthermore, both curves follow the same path with an eventual decrease in pain, regardless of intervention.
  • Maybe an additional point - I am not questioning their pain, but fibromyalgia typically shows no abnormal lab results in addition to typically coexisting with some form of mental pathology. I don't think placebo being demonstrated is far off.
j44n  I agree that was my though process, except i didnt notice the decrease before the injection, good eye! also the other answers didnt really apply regression toward the mean is the phenomenon that arises if a random variable is extreme on its first or first few measurements but closer to the mean or average on further measurements and there was no way for us to know about confounding or their selection procedures so from that we couldn't really know about the types of errors they made +  


submitted by cassdawg(1101),

The question stem is referring to a conjugate vaccine. This is because conjugate vaccines convert T-independent antigens (polysaccharides) into T-dependent antigens by conjugating them with a protein. [FA2020 p127]

Remember that in order for a T-cell to be able to respond to an antigen via MHC, it MUST be a protein. Thus, T-dependent (dependent on T-cells) responses are to proteins. T-dependent responses are overall better because then B-cells can then undergo affinity maturation and class switching through interaction with T-cells. So, by conjugating bacterial polysaccharides to proteins, the immune response will be a more robust T-dependent reaction and will yield better protection. [FA2020 p103]

Conjugate vaccines exist for encapsulated bacteria (as the capsules are polysaccharide and would need to be conjugated to protein to improve response). These are Neisseria meningitidis, Haemophilus influenzae, and Streptococcus pneumoniae

You can remember these encapsulated organisms and their conjugate vaccine because they are THE SAME organisms that you become susceptible to when you have a splenectomy and which necessitate vaccination.

drippinranch  I appreciate this explanation so much. Thank you. +5  
j44n  cassdawg you are a beast +2  


submitted by breis(50),
unscramble the site ⋅ remove ads ⋅ become a member ($39/month)

CGH eiositncjn odnw rlugaete eht riyuttipa sreelea fo nHG.R

rhwoeve GHC ahalp utunsbi nac ettmailus sllec cduifnnlee by ,HL ,HFS STH.

cassdawg  (FA2020 p633) - Basically HCG acts like FSH which stimulates estradiol production by the sertoli cells (see http://www.ansci.wisc.edu/jjp1/equine/male_endo/estrpath.html). There is no feedback inhibition since it is injected so there are elevated levels of estradiol causing gynecomastia. +12  
j44n  also FSH upregs aromatase so you increase test (LH) and increase aromatase (FSH) that then converts that test to estradiol +  


submitted by cassdawg(1101),

She has Mycoplasma pneumoniae which causes walking (atypical, interstitial) pneumonia and increase in cold agglutinins (IgM)

FA2020 p150

If you are a sketchy person (which I am not), I am pretty sure Mycoplasma is depicted in the cold, or as a guy on skis in drug ones, which can help you remember cold agglutinins. Also Mycoplasma -> IgM (the letter M).

Also (for immuno nerds or rationalizers), IgM is the first antibody to be produced so it would make sense that you would have IgM this early in the infection which can cause cold agglutination (she has only been sick for a few days). IgG causes warm agglutination, which is typically seen in more chronic processes like SLE and CLL (FA2020 p423). No idea if that is the actual mechanism but it is how I keep them straight in my mind and makes sense.

flapjacks  As a "sketchy person" and not a "rationalizer", I can confirm the Mycoplasma has red blood cell "pucks" agglutinized with IgM snowflakes +17  
j44n  Just to add, she has interstitial infiltrates so its an atypical pneumonia, no other kind of atypical pneumonia would cause them to have agglutination. I'm not a rationalizer I'm a massive over thinker +1  
sexymexican888  Yeah, im a sketchy person too! Side note, for autoimmune hemolytic anemia I remember it this way: IgM -> Me Cold, go INSIDE (cold agglutination, intravascular hemolysis) IgG -> Go outside its HOT (warm agglutination, extravascular hemolysis) +1  


submitted by bingcentipede(243),

A premature infant does not have mature surfactant levels until week 35. Being born at 28 weeks, his type II pneumocytes are not fully mature yet/haven't produced enough yet.

Type I and II pneumocytes line the basement membrane. Type I (C) are squamous, and type II (D) are cuboidal.

E: alveolar macrophage B: RBCs A: capillary endothelial cell?

jj375  Here is a labeled diagram that may help! A) Capillary endothelium B) RBCs C) Type I pneumocyte D) Type II pneumocyte E) I kinda think these are alveolar macrophages https://ib.bioninja.com.au/_Media/lung-tissue-diagram_med.jpeg +4  
j44n  did anyone else think D was trying to show a lamellar body that ID's a type II pneumoyte +  
j44n  my bad i meant B**** +  
i_hate_it_here  I sure did +  
prostar  Lamellar bodies are not visible in this magnification. They are viewed in Electron microscopy. +1  


submitted by bingcentipede(243),

A premature infant does not have mature surfactant levels until week 35. Being born at 28 weeks, his type II pneumocytes are not fully mature yet/haven't produced enough yet.

Type I and II pneumocytes line the basement membrane. Type I (C) are squamous, and type II (D) are cuboidal.

E: alveolar macrophage B: RBCs A: capillary endothelial cell?

jj375  Here is a labeled diagram that may help! A) Capillary endothelium B) RBCs C) Type I pneumocyte D) Type II pneumocyte E) I kinda think these are alveolar macrophages https://ib.bioninja.com.au/_Media/lung-tissue-diagram_med.jpeg +4  
j44n  did anyone else think D was trying to show a lamellar body that ID's a type II pneumoyte +  
j44n  my bad i meant B**** +  
i_hate_it_here  I sure did +  
prostar  Lamellar bodies are not visible in this magnification. They are viewed in Electron microscopy. +1  


Figure from this paper shows the course of the inferior alveolar n.

https://www.ncbi.nlm.nih.gov/books/NBK546712/

Inferior alveolar n. is also sometimes called the inferior dental n. b/c it supplies sensation to the lower teeth.

j44n  why couldnt it be the maxillary artery? doesnt that run through the jaw as well +  
hiroshimi  @j44n: Maxillary artery give a branch called inferior alveolar artery that travels with the inferior alveolar nerve. The maxillary artery itself will travel up and give branches other including the middle meningeal artery around the temporal. So saying maxillary is too broad I think. +  
sexymexican888  This shit is so fucking annoying LMAO its so fucking shitty how they ask questions on shit you can find or FA +  


submitted by tinyhorse(7),

Frankly pretty floored that anybody thought that this question contained enough information for someone to confidently answer it.

The question has you assume that both parents are heterozygotes at the locus. Why? I assume I'm missing some esoteric fact about P450 allele frequencies.

flapjacks  I got lucky guessing the same % chance that siblings share HLA markers +2  
baja_blast  I agree with OP seriously no idea how anyone could have gotten this right without totally guessing it. Am I missing something here?? +1  
snow_6  Personally I got this question wrong, partially due to me panicking in this question. Looked through it later and understood the following: - the pt. is homozygous i.e. AA; meaning each parent is heterozygous for the allele - if her sister is to have the same alleles, she is also homozygous i.e. AA - do the punnet square for Aa (mom) and Aa (dad) to get a homozygous allele of AA for only 25% of the time - based on the assumption that parents are heterozygous because question doesn't state any other extra information Only if i could've thought like this during the actual exam +  
sschulz2013  However, if one parent is homozygous and the other is heterozygous, then it works out that the sister will have the same allele 50% of the time, not 25%. So still not sure about the above answer. Don't think assuming the parents are both heterozygotes is something we should have to do. There is probably more to it than just that. +1  
j44n  the probability for being the same gene as a sibling thats homozygous is always 25% this has been on just about every practice NBME +  


submitted by cassdawg(1101),

The description cooresponds to rhabdomyolysis which is excessive breakdown of skeletal muscle tissue that can lead to excessive release of myoglobin into the blood which causes myoglobinuria and kidney damage. Rhabdomyolysis can be precipitated by overexertion (such as a triathalon) and commonly presents with weakness and muscle tenderness and may also present with shortness of breath due to fluid buildup in the lungs.

Rhabdomyolysis will present with elevations in creatinine kinase as well as myoglobin, but it is the elevated myoglobin which causes the symptoms and acute kidney injury as seen in this patient. Creatinine kinase elevation causes no toxic effects, even though it occurs, as reported here.

Here is another article about rhabdomyolysis as it is not covered in depth in First Aid.

j44n  I went with my gut on this just base on the physical exam. But they did have elevated Hemoglobin in the urine as well and I know Dr. Golijan said you cant get that after a marathon. Does anyone know why hemoglobin is wrong? +  
prostar  hemoglobin is due to the breakdown of RBCs, not muscles. +  
srmtn  During the dipstick test on a urine sample to evaluate for the presence of blood, the reagent on the test strip detects the presence of pigment in the urine sample. This pigment can be hemoglobin or myoglobin +  


submitted by celeste(82),
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iWelh hte tmeiefil rsik ni eht anelreg upotilpaon is tsuj ebwlo 1,% ti is %6.5 in ersr-geditfe svilterea of netsipta and ti rsies ot moer than %40 in zgomocntyio wnsit of ecfeftad pe.olep inyzganAl lsascic sueitds fo eht eegnscit of sznioharehpci dnoe sa eryal as ni 3s,091 chFsier douensccl ttha a orcodcnaecn rtae fro iscyphsso of aoubt 50% in nmyizcoogot swnti smees ot eb a ecratslii ,siettmea wihch is tsgfinylainci ighhre thna that ni zdgitoyic wtisn of aubot %01–19 (nni.2mf.i/ehn9/laPo#./g4t6cM35c/vimlCrcbs6per3)

imnotarobotbut  How is one supposed to know this before having read this article? +33  
imgdoc  This question falls under the either you know it or you dont category. It isnt in FA or Uworld +  
jaxx  So why would these A-holes put it on there as if prepping for this exam isn't stressful enough :-| +7  
doodimoodi  Lol just why seriously +2  
champagnesupernova3  This was mentioned in the Kaplan behavioral videos +  
usmlecrasher  and there's so much unnecessarily BS instead of real questions +1  
j44n  I'm just glad we're seeing this garbage now instead of having an aneurysm in the prometric center +2  


submitted by sympathetikey(1350),
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saeC ieSres

A prgou ro rseeis fo easc trsoepr ivgonnvil tnesatip how eewr nivge imsalir matntr.eet optresR fo esac sieres lsuuayl ntcoina talddeie ioroatnimfn uotba teh luvdaiindi taspne.it ihTs ldnsiceu arcemogidph rnifnoamtoi o(fr peem,xal e,ga ,egnrde ehcnit gir)ion and iantiofmonr on sigindosa, ent,atretm roenseps to teetmtnar, adn -foupllwo eratf ttemnare.t

nI tish ste,uoiqn ti oskol keli htey d'itnd ylrale osfuc on eht rnattemet prat fo ti ubt shoter,iew kmesa nsees

sympathetikey  Source: https://www.cancer.gov/publications/dictionaries/cancer-terms/def/case-series +2  
ngman  I think another factor is that in case series studies there is no control group vs case-control, cohort...ect +19  
leaf_house  "There is often confusion in designating studies as 'cohort studies' when only one group of subjects is examined. Yet, unless a second comparative group serving as a control is present, these studies are defined as case-series." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998589/ +  
fataldose  explanation of one of the wrong options - correlational study A correlational study is a type of research design where a researcher seeks to understand what kind of relationships naturally occurring variables have with one another. In simple terms, correlational research seeks to figure out if two or more variables are related and, if so, in what way. (source - https://study.com/academy/lesson/what-is-a-correlational-study-definition-examples.html ) +  
j44n  you dont need a control group in a cross sectional one so how do you differentiate that +  


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aerItzooalcn eqresiur teh aiiccd renoiennmvt of the soahtcm ot be abrs.dbeo rpelaoemOz ntihbiis the KH/++ pump of hte a,hscotm treybeh drsngcieae the yiadcti of hte .octsahm So enhw hte tepinat tesak zmOroleape dan eoazlrncIaot ert,teohg ratnaIocezlo ot'wn eb redsabob iton eht b.ody 'Tthas yhw ti hsa on t.eecff

st'I encedmoemdr to take niameocstdi at taels 2 housr riopr ot giknat an dtaniac.

necrotizingfasciitis  Just adding support to the above explanation: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3671798/ +3  
pakimd  do all azoles or just itraconazole only requires an acidic environment to be absorbed? +2  
chandlerbas  just itraconazole and posaconazole +5  
lilyo  @chandlerbas, where did you find this information? I was looking over this on FA but they do not mention it and I would like a bit more information. Thanks! +5  
chandlerbas  haha no stress! the article above submitted by @necrotizingfasciitis does a descent job explaining it, however its not good enough, I looked into a bit more on uptodate but wasn't fruitful in my endeavours. goodluck! +  
haozhier  How are we supposed to know this!! It is not in UWORLD or FA right? +9  
kevin  Someone said it on here, since there was no CYP inducer of the answer choices, the only way to even think about an answer to this question was to just go with a less acidic environment from the PPI affecting absorption. It was simply the only reasonable answer choice, I don't think there's any way we were expected to know of this exact interaction prior +1  
aoa05  Golan pharm book states the exact same thing. Cannot be given to patients with acholrhydria. +  


submitted by hayayah(1074),
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ofinDntiie of tjntsdaemu isrreo:dd

tEiloamon tsmsmyop ,eg( ytneiax, sio)rpsdene htat ccrou nhtiiw 3 hsnmto fo na iniibaeltefd sochoapilsyc rstesrso eg,( ev,cdori eisnsll) tnaigls < 6 nshmto ocne hte erssorts hsa dde.ne

fI mmspoyts ssietpr t;g& 6 nhstom ferta tssersro se,dn it si A.GD

hello  Yep, and I think what we are supposed to take from this Q is: The only info. we have for this patient is that he ended chemo 2 months ago and has been calling the doctor a lot -- this is supposed to mean he has been calling a lot since ending chemo 2 months ago. His frequent calls starting after ending chemo and within 3 months of the stressor fits with the above-stated definition of "adjustment disorder" with anxiety. I stressor in this case could possibly be either the actual illness or the ending of chemo/treatment. It probably does not matter much in this case. +4  
charcot_bouchard  I think doing uw done me wrong here. Adjustment disorder isnt diagnosed when symptom match another disorder --- it was like never a right answer. But ofc its right answer in nbme +5  
maxillarythirdmolar  Just to add to that, the tingling in his fingers may seem like a distraction/it probably is. Likely has some relation to his Chemo. +3  
j44n  shit I thought this poor guy had OCD with all the repetitive behaviors. +1  


submitted by strugglebus(165),
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rNeewho ehav I neeb ebal ot dnif ywh eth hlle siht si a .nghti

yotsubato  Its not in FA, Sketchy, or Pathoma, or U world. I knew it wasnt cancer because its bilateral. And Diabetes made no sense to me. So I just threw down Drug effect and walked away. +6  
breis  same^^^ +  
feliperamirez  The only possible explanation I think is that she was under a K sparing diuretic, such as spironolactone (which would lead to gynecomastia). +  
chandlerbas  you had me at its not in sketchy ;) +2  
j44n  i thought HTN induced empty sella would cause this because they got type II diabeetus. So if you need a pro zebra hunter holler at me. +  


submitted by hungrybox(1026),

I got confused with aquaporins so I picked E :(

But aquaporins are in the collecting duct, NOT the proximal tubule

j44n  there are AQP's in the PCT but they're not that abundant. Look at it this way, AQP's are by definition a transporter and therefore they can be saturated. The PCT is the king of all resorption and a big reason for that is paracellular transport, which can't be saturated. This also makes sense as to why we can treat nephrogenic DI witha thiazide, it causes INCREASED resorb at the PCT which can over power the rest of the nephron. The PCT does everything and the rest of the nephron gets the left overs +1  


submitted by beastaran1(1),

Believe this one is tubulointerstitial fibrosis of the kidney:

medullary cystic disease is characterized by autosomal dominant inheritance pattern progressive and slow impairment in renal function that ultimately results in end-stage renal disease no or minimal proteinuria with a bland urine sediment medullary cysts on renal ultrasound in most cases medullary cysts are not present can see shrunken kidneys on ultrasound

makepoopinggreatagain  Tubular atrophy (hint: dilated ureter/calyx in image) ↓ Posterior urethral valves is the 1 cause of bladder obstruction in males ...Diagnosed by hydronephrosis and thick walled bladder +  
nbmeanswersownersucks  this can't be posterior urethral valve because then both kidneys would be effected. +8  
j44n  I agree its the medullary cystic kindey disease-> FA19-592 talks about it +  


submitted by motherhen(41),

Are these gottron's papules from dermatomyositis? Pareaneoplastic syndrome from adenocarcinoma, esp ovarian?

j44n  it is not. The pt has a history of being immunocompromised. Also, gottron's are over the hands and dermatomysitis can present with a rash over the eyelid as well! There is also no history muscle weakness at the proximal muscles (shoudler/ hip area) and no mention of an elevated creatine kinase! - hope this helps :) +1  


submitted by nwinkelmann(292),
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oDes nenyoa vahe a oogd lpaetxoanin fro hwy sdrdeaece llesve of iinnihb is n?rwog orFm my nedsungntdrai, iinihbn and tivaicn kwro tehot,erg ni hatt inibinh sinbd nad bcklso ntivaic iegndal ot edaersdce fkecaedb on omahpthauysl dna icvntia ensraseci FHS adn RGnH dtunro..cpio ,htus fi yuo ceasdree inbnhii hnet uyo uldwo eahv eidenarsc vcniati hwcih uldwo dael ot edaersnic RHGn adn S,FH rthig? I fdoun neo itarlec liktgan tuabo ti ni rrsdgae to ,uyerbtp but it smese ot be a epsotihhnoyt/s ndmeiorfc ta isht .tnoi.p. is hatt w?yh utB l.s.li.t woh do I eulr it tuo on a ?tste

yb_26  I also picked decreased inhibin. may be it was one of the "experimental questions", which are not even counted on the real exam +1  
artist90  Inceased FSH will lead to spermatogenesis and spermiogenesis NOT Increase in Testosterone which is causing increased Height of this pt +6  
artist90  Inhibin B only has negative feeback on FSH not GnRH. see the diagram on the topic of semineferous tubules in FA. Testosterone has a negative feedback on BOTH LH and GnRH +1  
usmile1  Kind of like how nocturnal pulsatile GNRH release occurs during sleep to stimulate growth (FA page327), the same thing happens for puberty. Pg 325 in FA, "pulsatile GnRH leads to puberty and fertility." It doesn't explicitly state during sleep, but pulsatile release of GnRH leading to pulsatile release of LH and FSH will lead to puberty. Puberty starts in the brain, its onset really has nothing to do with decreased inhibin levels which happens in the testes. hope that makes sense! +3  
sars  From what I understand, inhibin is only released by granulosa cells when FSH levels are high. This is a boy. Next off, this question is about puberty, which is due to pulsatile GnRH leading to large amounts of LH and FSH, leading to large amounts of dihydrotestosterone (males) and estradiol (females), and eventually secondary characteristics of puberty. The increased pulse of estrogen and testosterone leads to GH release, which is metabolized into IGF-1 in the liver. This leads to long bone growth from what I understand, which is not much. +  
cassdawg  @sars inhibin B is also released by sertoli cells in males and will feedback to inhibit FSH release, its not just a female thing. Also, there is actually an inhibin B pubertal surge in both females and males that corresponds to maturation of the granulosa and sertoli cells, respectively. Hormones are wack. https://pubmed.ncbi.nlm.nih.gov/15319819/ +  
j44n  I think youre just supposed to see that he's starting puberty and know that the nocturnal pulses are involved +  


submitted by madojo(176),
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g/.rmtswoeccssck./pcdmtiy:wtc/hoeaotllphatdaw/u

VAORCSOIURN ETCHKSY

isovitep esnes NAR us,irv cnsnuro w cknoagni ro iarewng breo - lieeacndlaseacl htpu isurv - ipalnsirg rad,o lcaileh s engesrezniet nad ionlbwg nigk - mmcoon cdol wthi nbooichlr eert no ikgn ipnoigtn to SARS dna lmdide esta rtepiyroars rdeomsyn t(eauc bn)srhoicit

hTis visur isarletcpe in het osmcplayt shtta why nigK si odsutei ish acetls eulsun)(c

j44n  I'm so glad i dont have to take step one once they discover all this shit about the new corona strain. +  


submitted by cassdawg(1101),

My dumb ass thought ketonemia was like anemia of ketones or something and thus meant low ketones so I almost put fatty acid oxidation (hypoketotic hypoglycemia). FYI ketonemia is high ketones.

Defects in fatty acid oxidation would also be corrected with the sugar additions so even if you suck at medical vocab you could rule it out.

j44n  if it was glycolysis they wouldnt be able to metabolize the galactose either, a defect in glycogen breakdown/glycogenolysis would't effect the immediate metabolism of a monosacharide it would effect the long term storage of it. I don't think we were supposed to know what disease this is I think we were just supposed to think about the metabolism of the three sugars in question. Hexokinase only converts fructose when it is extremely overloaded with fructose(it has a low affinity for it... they'll never say that so lets say "high Km"). Glycogen synthesis happens over time and he had poor feeding for 3 days so his glycogen would already be gone and he would be immediately symptomatic the second his blood glucose dropped +  


submitted by lsmarshall(415),
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vyaebrnotnSip si eth tagret of itsnpmeatsano ns(tuate );xitno smucle ampsss are tatiaerhsc.ccir Olny eroth ewsnar you might sndrcieo si cncsesaletyileAetrho neisc he si a reafmr nad szwubrdoz nfteo aryrc su ot eht mprdoesi n.a.dl. but mysoptsm of a lcncoghriei rtoms aer b.tnaes

vshummy  Synaptobrevin is a SNARE protein. Why they couldn’t just give us SNARE I’ll never know. +45  
yotsubato  Cause they're dicks, and they watched sketchy to make sure our buzzwords were removed from the exam +46  
yotsubato  Oh and they read FA and did UW to make sure its not in there either +37  
soph  This toxin binds to the presynaptic membrane of the neuromuscular junction and is internalized and transported retroaxonally to the spinal cord. Enzymatically, tetanus toxin is a zinc metalloprotease that cleaves the protein synaptobrevin, an integral neurovesicle protein involved in membrane fusion. Without membrane fusion, the release of inhibitory neurotransmitters glycine and GABA is blocked. -rx questions! +6  
qfever  So out of curiosity I checked out B) N-Acetylneuraminic acid It's sialic acid typical NBME +2  
alexxxx30  shocked they haven't started calling a "farmworker" a "drudge" <-- word I pulled from thesaurus. +3  
snripper  "You shouldn't memorize buzzwords. You gotta learn how to think." Lemme pick another random ass word that doesn't have anything to do with critical thinking skills and use it instead. +5  
mw126  Just as an FYI, there are multiple "SNARE" Proteins. Syntaxin, SNAP 25, Synaptobrevin (VAMP). From google it looks like Tetanospasmin cleaves Synaptobrevin (VAMP). Botulism toxin has multiple serotypes that target any of the SNARE proteins. +2  
wrongcareer69  Here's one fact I won't forget: Step 1 testwriters are incels +2  
baja_blast  FML +  
j44n  its not an ACH-E inhib because he doesnt have dumbell signs +  
flvent2120  I'm not even mad I got this wrong +  


submitted by sympathetikey(1350),
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sA per ohtaa,mP

suV"alarc riyetmlepabi cucors ta het pcoa-trpsllyia eevlun"

iTsh si yw,h nwhe you vhae d,meae ouy odluw heva gaps in eht sev.nuel

j44n  that was my exact reasoning +2  


submitted by lsmarshall(415),
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CHM alcss 1 pdeptie nntiega sesrgcnpio tg&; enAtnig" piteepds ldedoa ntoo MCH I in RER trfae elrvdyie aiv TAP traprosr(ten ocaaesidts twih itaenng en"scsrigpo) - Ftisr iAd 10.92

erBa tocmlypeyh rymeodsn pyte 2 (SBL I;I feafinctg CMH )II si edu to onumisatt ni sngee ttah eodc orf rnioatcistnrp srftoca atth lryanmol eeutglar het ispsenxoer en(ge trpsio)ancnrit of eht HCM II eg.sen eraB ploychytem rdyomnes teyp 1 B(LS ;I gaifentcf MHC I), si hcum emor are,r dna si taoadsisce htiw TPA ceicsfn.ideie

tyrionwill  in the question, it says absence of MHC-I presenting cells. I guess the meaning is lack of MHC-I. IF TAP is missing or dysfunction (bare lym syn type-1), MHC-I should be there, however Ag cannot be loaded to the MHC-I. Can anyone help me to understand more. +  
peridot  @tyrionwill From wiki: "The TAP proteins are involved in pumping degraded cytosolic peptides across the endoplasmic reticulum membrane so they can bind HLA class I. Once the peptide:HLA class I complex forms, it is transported to the membrane of the cell. However, a defect in the TAP proteins prevents pumping of peptides into the endoplasmic reticulum so no peptide:HLA class I complexes form, and therefore, no HLA class I is expressed on the membrane. Just like BLS II, the defect isn't in the MHC protein, but rather another accessory protein." +  
j44n  i hate this question because MHCI is on all nucleated cells. So this person is literally a bag of RBC's +1  
soccerfan23  @j44n Not quite. It's true that MHC I is on all nucleated cells. Because of the TAP mutation, these cells don't express MHC I on their membranes. But these cells still exist. That is what is meant when the vignette says "flow cytometry shows absence of class I MHC-expressing cells. +  


submitted by seagull(1539),
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ta IBM 51 ton noyl ash she erevn hda a pdroie tbu seh vnree adh a l.ema

sympathetikey  You're on fire man lol +1  
monkey  How the fuck is it not related to anorexia nervosa is beyond me. +4  
avarkey  the blind vaginal pouch points away from it being anorexia related +3  
j44n  Its actually a man, there's no DHT to to dev the external genitals. +1  
am4140  @monkey - with real anorexia, she wouldn’t necessarily have boobs either. If she’s got boobs she has the nutrition to develop boobs. That was my thought. +  
freckles  the patient is actually what ever gender they want to identify as. If this was a 5 alpha reductase deficiency the patient would have experienced masculinization of external genitalia during puberty when testosterone levels increase significantly. The pt most likely has Androgen Insensitivity Syndrome. +1  


submitted by suckitnbme(176),

Tfw NBME said there's no repeats on 23 and 24 and then you get a repeat.

j44n  The NBME is full of shit... they also say there's "no trick questions" +1  


submitted by j44n(56),

this is how I looked at it extra cellular osmoles> intracellular so it will pull the h20 out.... then the high osmotic pull of the sugar overwhelming the SGL2 transporter in the kidney will pull the h20 out of the body dehydrating the extracellular compartment

j44n  also the brain/CNS/neurons have the highest affinity GLUT transporters.... thats why giving glucagon brings someone out of hypoglycemia when theyre passed out. The glucagon increases the blood sugar and it goes straight to the brain restoring concious +  


Mixed up cytoscopy with culposcopy so I put HPV. Insert upsidedownsmileyface.jpg

j44n  if it makes you feel better I miss ID'd the PCT not once but twice on this exam +1  


submitted by enbeemee(13),
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i teg yhw s'ti ri,poeyafxhle tub hwy ont lt?sinbailrfoi sit' loas an NLM gnsi

et-tu-bromocriptine  Imagine a simple reflex arc: you have an afferent neuron, some interneuron shenanigans, and an efferent neuron (aka LMN neuron). If you damage the LMN, you will get hyporeflexia (due to damaged reflex arc) and fibrillations (because your LMN won't be able to effectively contract muscle on command). However, if you damage the afferent part of the arc, you will still get a damaged reflex arc (hyporeflexia), but your motor neuron will still be able to do its stimulating effectively, so your muscles won't show weak contractions when stimulated by a higher pathway. Kinda confusing but I hope I made it a tad simpler! +14  
eli_medina9  https://imgur.com/1z4OF4l Gonna piggy back off your comment and just post this kaplan image +10  
hungrybox  Very helpful image, thanks bro +  
j44n  its not a efferent motor neuron its the sensory/afferent branch +  


submitted by sympathetikey(1350),
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yevroenE who otg thsi itoenqsu girth is a c.po ⌐ل༽■■༼͟

dr_ligma  Fkn narcs +2  
j44n  whippet_gang +  


submitted by sweetmed(143),
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srcilTuaet noorsti tsomly nepasph in oygnu ,ysbo ryrale in sdat.ul oAls teh niap tedsrta ta the ak,fnls hhwic si not owh niroost npia asstr.t

j44n  I actually had testicular torsion and my pain started in my appendix area and by the time I got to the hospital it localized to my testicle +3  


submitted by colonelred_(105),
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hTe iagndsois si bersraytrw anaioehmmg, ocnlmmyo snapphe in ids,k noetf eesolvrs no tsi own sa ehyt teg elor.d

shaeking  A strawberry hemangioma is normally pink or red (which is why it is named strawberry). The description has a flat purplish lesion which makes me think of a port wine stain on the face. How do you know to think of strawberry hemangioma over port wine based on this question stem? +3  
seagull  the age is key here. Newborns have strawberry hemangiomas typically on their face. Sturge-Weber could also be the case but none of the answer choices matched to that description. +1  
vshummy  I would agree with Sturg Webber nevus flammeus but I also noticed First Aid says it's a non-neoplastic birth mark so I should have known not to pick malignant degeneration or local invasion. Also because capillary hemangiomas don't have to be flat but the nevus flammeus is consistently flat. But I'm also reading on Wiki that the nevus flammeus doesn't regress so they must be trying to describe strawberry hemangioma even though I don't agree with their color choice... +  
nala_ula  Maybe (and I can only hope I'm right and the test makers are not -that much of- sadists) they would have made sure to write "in a cranial nerve 5 (either ophthalmic or maxillary) distribution" if it were Sturge-Weber. +1  
j44n  this is literally on every NBME along with the 10,000 ways to not get a boner +  


I get these VERY often. I seem to get them only after eating something that can damage the mucosa in my mouth such as hard chips (Tostitos, very jagged very pain). These are NOT cold sores (HSV). This is simply a aphthous ulcer; they can be stress induced (studying for hard test). they are very painful and do reoccur. there are no associated sx with them.

j44n  they're also caused by stress. I got 3 in my mouth the day after Prometric canceled my test for the 3rd time! +8  


submitted by jucapami(11),
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rx-ay rsosdponrce ot a tnsioen nuomoeatxphr = inemnimt sitrroepayr ferailu if dutar.etne gRiht ugnl si lyufl cld,paoles iiesgrnacn hi-cnicttraaor esrursp,e pgniimra 2O nachxeeg (deu to amss cfefet atodwr tlfe gnu,l nda oalcdelsp hrtig ,e)on hcnee cctnmuiglaau OC2 in( ,oodl)b iucgnidn pyrrteiroas sodsiiac.

j44n  how is it a tension if there is not tracheal deviation? +2  
djeffs1  I can see that its resp. Acidosis, but wouldn't the most risky potential complication be diffuse alveolar damage (If you arent able to reinflate sometime? +  


submitted by centeno(2),

I thought that the cognitive impairment could be the manifestation of neurosyphilis. In addition, the doctor should talk directly to the patient to check for sexual abuse.

j44n  The maximum MMSE score is 30 points. A score of 20 to 24 suggests mild dementia, 13 to 20 suggests moderate dementia, and less than 12 indicates severe dementia. On average, the MMSE score of a person with Alzheimer's declines about two to four points each year. she only has mild dementia. I had to look this up she could still retain her capacity +1  


submitted by lamhtu(118),
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elePtlat deehanrec dan teelalpt ioganragtge era eenrdtfif hgtsin and itsh erfncredei ETMARST A OL.T ucFk yu,o BM.NE hTees cdfeesfrnei seoplspdyu aermtt no mseo tsqsoiune adn tno no sertho. ehWre is eht cenoscts?iyn lleoH?

hungrybox  Agreed. This is so fucking stupid. +  
hungrybox  "Aspirin inhibits platelet aggregation and produces a mild bleeding defect by inhibiting cyclooxygenase, a platelet enzyme that is required for TXA2 synthesis." literally straight from Big Robbins +1  
susyars  Im gonna upvote this bc i love to be right +6  
regularstudent  It's always a horrible, horrible feeling to pick the wrong answer that you know they think is right. Amazing job NBME... +4  
j44n  yeah i thought adherence was the GP1B receptor that's already on the platelet +1  
j44n  im also glad we're getting exposed to this horse shit now and now when I'm in a testing center about to put my fist through a screen. +1  
jurrutia  GPiib/iiia receptor is not inhibited by aspirin. Aspirin prevents the upregulation of GPiib/iiia which is not the same as inhibiting the receptor itself. +  


submitted by susyars(32),

Im gonna fight this one because AGGREGATION is mediated by expression of Gp IIb/IIIa.

If your platelet increases TXA2 that means is gonna upregulate AGGREGATION by which receptor? ... Duh

Once Im done with this test and become a Pathologist Im gonna send you a copy of my journal and research on platelet aggregation mediated by TXA2 and Gp IIb/IIIa and also im gonna go over every single WTF NBME question and prove them so wrong

Maybe i should change my username before submitting this

corgilobacter  Dr. Tio Goljan Jr. In the house everyone. CLAPS +  
susyars  Tio Goljan would be so proud of me +  
j44n  I agree TXA2 up-regulates the GP2b3A receptor that mediates aggregation. +  


submitted by lamhtu(118),
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elltaetP ndaeecerh nda peteltla ianeagtggor aer rfditefen tihnsg and iths eidcrefren TSAETMR A TLO. kFcu ,yuo M.NBE Tseeh sdnirefcfee dypseplosu tmtear on oems nieussqot adn ont no s.rhoet ehrWe is the ?ycioectnssn lHe?lo

hungrybox  Agreed. This is so fucking stupid. +  
hungrybox  "Aspirin inhibits platelet aggregation and produces a mild bleeding defect by inhibiting cyclooxygenase, a platelet enzyme that is required for TXA2 synthesis." literally straight from Big Robbins +1  
susyars  Im gonna upvote this bc i love to be right +6  
regularstudent  It's always a horrible, horrible feeling to pick the wrong answer that you know they think is right. Amazing job NBME... +4  
j44n  yeah i thought adherence was the GP1B receptor that's already on the platelet +1  
j44n  im also glad we're getting exposed to this horse shit now and now when I'm in a testing center about to put my fist through a screen. +1  
jurrutia  GPiib/iiia receptor is not inhibited by aspirin. Aspirin prevents the upregulation of GPiib/iiia which is not the same as inhibiting the receptor itself. +  


submitted by gonyyong(107),
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'Wasnt eusr oabut ,rhoste tbu ymagmmoaphr fro aeregln oolupinatp int's rmeeemddnoc ultin 04

_yeetmasterflex  Also wouldn't mammography be secondary prevention since you'd look for asymptomatic disease already present? +22  
suckitnbme  USPSTF recommends starting screening at age 50. 40 by patient choice if there's risk factors. +2  
j44n  @_yeetmasterflex thats a good point i didnt think about that +  


submitted by snoodle(23),

just wanted to add that questions that ask small details like this make me want to carve my eyeballs out

j44n  This is the shit that keeps me up at night +2  


submitted by krewfoo99(93),
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gnuL lmeovu lilw edaecesr ni teoybsi vtaitpohnioeyln redsom.ny eEnv tuhgho stih tnapeti is boe,se he ash lal het inclcila utaerefs of lspee neapa

j44n  also the lung volume would't have an "episodic" decrease. It would be constant due to the weight on their chest. +  


submitted by medstruggle(12),
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shaWt hte fecednifer wenetbe zgr“hyoeeotsu llun toamtniu in B ilbgno ”nege adn hyutoszrgoe“e atunmoit nwonk ot uceas 5%0 deeecasr ni B gbniol nege ftnincuo fo eno ”?leelal

welpdedelp  I interpreted "null" as meaning full deletion while the other heterozygous mutations was only a 50% decrease in the function. One child would inherit 1 null mutation and 1 50% mutation, which would leave them with a 25% functional gene. +15  
j44n  A thal is the deletion, B thal is mutations on promoters or splice sites. +  


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aByb odevelpde SDR -;tg&- ugven O2 as xR gt-;-& ioocplncsmtia of O2 yerpah ni nedatnoe = IBR (AF 29) 01R = toenRtyhiap fo yitmerrptauI = erItavcinlnraru rmegrehoaB h = Bmnloupoorynrach lidaysaps

peridot  RDS (respiratory distress syndrome) and O2 therapy complications are described on p.647 in FA 2019! +1  
peridot  This is due to free radicles, which is also briefly touched upon on p. 210 of FA 2019 +  
peridot  radicals* +1  
j44n  also I saw on one of the other NBME's that retinopathy is more likely than the intraventricular hemorrhage. I did some reading and found that the eyes adapt to local changes faster. So when you give them 100%02 their eyes get used to the elevation in 02 so when you take them off of it they upregulate a ton of VEGF to try to normalize back to the level they were used to on the 100% +2  


submitted by medstruggle(12),
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Can noeeoms eelpsa pxneial ?thsi htWa si teh siaosndgi ereh?

welpdedelp  I thought it just as it was, polyneuropathy is supposed to be a burning pain affecting the extremities, he might have acute intermittent porphyria. He was too young and didn't fit ALS due to the rapid onset. No loss of pain in the arms so it couldn't be syringomelia. Wasn't asymmetric so couldn't be polio. Didn't have anything resembling Parkinson. +5  
j44n  I got tripped up on this too. I think what youre supposed to see is multiple areas of nerve damage on the motor tracts and proprioception is a senory component, so instead of saying they feel burning, they cant tell where their limbs are in 3D space. If they said burning you wouldn't have to know all the other 4 possible answer choices to get to this one. +  


submitted by susyars(32),

From a girls perspective, is really hard to understand this penis/erection physiology questions

john055  hahaha. thats hilarious lol +  
thisshouldbefree  from a males perspective it is really hard to understand the mensural cycle +8  
j44n  I'm a man.... and i still miss every boner question +1  


submitted by sattanki(71),
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erheT ear owt mcmiasensh fo itengalgru laenr odbol ,wlfo eth egyinomc scahinmme adn tebuumlougloralr- akbc.fdee sThi sqtnoieu akss erulpy otabu eht meogcnyi mna,csmeih iwhhc si weehr eth ntfferae ortilerae orcsotln bolod wlfo bedsa yrulep fof odobl epeursrs ienngert hte edykn,i wihhc si ywh eadcsreed ffearten rtiaolrrae siesrnaect is eht etbs eawrns (eth eiaerotrl is iadgnitl in eensrosp to het eredeadsc odlob oflw ni tptmtae to tiainnma olramn oobdl wolf ot eht eid)n.ky

nwinkelmann  Man... I took this WAY TOO FAR, lol. I totally didn't recognize the clue of GFR and RPF as staying the same to tell me it was talking about normal, physiologic autoregulation. Silly mistake! +5  
j44n  I agree. All I saw was a stenosed artery and ATII constriction +