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Comments ...

 +2  (nbme23#42)
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heT petinta had a atolt theyymcetsro os a cucrerrene fo caiercvl acercn si rutilylav ton sbleo.ips Retereaorpotnil ifsorbis loymocnm ertulss fmro odairtani ypeathr to het viep,sl hcwih nca dela ot lrabatlie ensrrhods.phoiy


 +20  (nbme23#28)
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tubbiltertaA iskr = neniicdec ni epxdeso – eniccendi in eepunsxdo

= 001/00,3 soek)sm(r - 00/0033, sroos()knenm
= 300. - 100.
= .002 (os the ltutatabiber rksi si tauob )%2

npipAgyl ti to a noouplptia fo 000,:10

= 20.0 * 10,000
= 020

charcot_bouchard  What if i tell you this is a ques of Attributable risk % in exposed? AR= 0.02 / IR in exposed (30/1000) = 0.6667 30 case in 1000. So 300 case in 10,000 0.6667 x 300 = 200 or in another word 66% cases of 100 lung cancer cases in smokers is actually due to smoking. so in 300 cases of smokers 200 is actually due to smoking +4
charcot_bouchard  This is a mind fuck. Lemme tell u guys if any consolation while doing the ques during test i did it with AR = 0.02; NNH = 1/0.02 = 50. 50 persons smoke to cause 1 cancer. 10K smoke to cause 200 cancer. +3
ls3076  Sorry if this is a stupid question. Why is it incorrect to simply apply the same proportion (30 cancer per 1000 smokers) to 10,000 smokers? +2
krewfoo99  @is3076 Thats exactly what is did. I still dont understand how that is wrong. But i guess they want us to think about it in terms of AR +
hhsuperhigh  @Is3076 and @Krewfoo99, If a person doesn't smoke, the natural risk of getting lung cancer is 30/3000=1%. The smoker's risk is 30/1000=3%. This 3% is not purely contributed by smoking, but mixed with the natural risk. So for calculating the pure contribution made by smoking, you should use 3%-1% which is 2%. And this 2% is the pure contribution of smoking. Not all smokers get lung cancer, the same thing, not all lung cancer among smokers are attributed by smoking. They may get lung cancer anyway despite smoking or not. +12

 -5  (nbme24#7)
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eTh nassiodgi si tsbwyrrrae aohagemnmi, mnlmcooy aephpns ni d,sik etonf eevsoslr no sit now as hyte tge dl.ore

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 +1

 +4  (nbme24#17)
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llarmoNy eht cdranahio ililv irsadn hte FCS mrof eht aonihrubdacs aecps ot eht ounevs myest;s if shit patr mbosece eedvifetc etnh yuo nac aiinmeg lla taht FCS wno inibldgu pu ni eth oanhdusbacir e.acsp

keycompany  Also take into account this patient had surgery that requires penetration into the subarachnoid space (hence through the arachnoid mater). This can lead to scarring of the arachnoid granulations and subsequent communicating hydrocephalus. +16

 +15  (nbme24#42)
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sH’e ensgnitrpe iwht sialcsc nsgis fo itmivna 3B cnicefdeiy in)inc;(a cianin si qiuedrre to rmof the cofotcar DA+N nmcnetiiaio(d inenaed lceuodne.iit)d

bigjimbo  B3 Niacin deficiency = Pellegra = diarrhea, dermatitis, dementia death. = Niacin combines with adenine to become NAD+ https://www.aocd.org/page/Pellagra +11
cbreland  Noted lack of niacin, not making NAD. Did not think about what NAD stands for, instead went down a rabbit hole +11

 +11  (nbme24#42)
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heT nlisaasy nyol swohed a tmnoitua ni eon l.eaell CF si an mlaatosuo eesceivsr sseeida: the idseesa noyl semfstina if rthee are niutastom ni hbto lseaell fo eht RTFC .eneg

If ouy litsl aevh 1 ontcinufal pcoy fo hte FRCT e,eng uyo cna tsill keam teh TFCR eontipr (eht ioclrhde ntlsna/e)thnraerc,orp enech oyru bdoy tnwo’ evah yan ssieu.s

Tihs is snlaagouo ot tmrou pseuosrrsp neges ielk Rb: so lngo sa neo fo eht llelase yuo vahe is ftiunacn,lo ouy can emka unhego of eth oenrpti to km“ae p”u for teh cdteveeif lll.eae fI both egt nocekdk otu )-/(b-R, yuo osle the rctneipoto pdieodvr yb the enge ecubsae onw uoy akem on netrpoi at .lal

heT ylno tginh that dmea sense orf htis ensoqtui asw eht fcat ttha eth theor eleall aws nto lecdunid in eht a.siynlsa

charcot_bouchard  OR another allele has a diff type of mutation because CF is done by like hundreds of diff type of mutation. SO the 70 types that we screened covered one type from one parent but not another that was inherited from other parent. +40
soph  I put D thinking there was a mutation in another protein that interacts with CFTR....thus u dont have CF but some disease with similar phenotype. Is this wrong bc its simply not the case ?? +10
nbmehelp  @charcot_bouchard I think that makes more sense if I understand what you're saying- Probably had a mutation only in 1 of 2 of the same alleles in the analysis but had another mutation in 2 of 2 alleles at a different location not included in the analysis, right? +
fallot4logy  CF is a rare disease , and the possibility to have a mutated gene plus a gene that its not belong to 70 most common cf mutations is extremely rare +4
gubernaculum  @soph i picked D too but now looking back, the panel had 70 of the most common CFTR gene mutations so it is unlikely that they didn't already check a gene that codes for a protein that interacts with CFTR? that's the only way i can rationalize it. its bad writing ultimately +
peridot  I also picked D, but there are over 1700 different mutations for CF and it's too hard to test for them all - the panel in the question tested for the 70 most common. As others mentioned, CF is an autosomal recessive disease, so there must be another mutated allele here for the child to present with the disease. It's more likely, and I imagine not uncommon, that the mutation is not in the panel. As for D, I suppose the best reasoning I can come up for it is that nothing like that exists - what protein interacts with ONE mutated CFTR allele in that it results in the same phenotype as CF, a disorder that requires TWO mutated alleles? I have never heard of such a thing, whereas I have definitely heard of A being the case. +2

 +18  (nbme24#34)
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edoLko ti up dna dnofu tath asbeuec ue’ory in a pineus onpisoit orf a gonl imte eory’u ingog to ehav reasinced unsvoe truenr ihwch alesd to nascrdiee .CO This neaveltiyg fkebeacds no RA,AS nalgeid to edrecadse rd.enteoosla As a us,elrt o’yeru inggo ot vhea ncridaese sieidsur hwhci dlesa to dradecese doobl adn sampal lmve.uo

medstruggle  Doesn’t supine position compress IVC leading to decreased venous return? (This is the pathophys of supine hypotension syndrome.) There was a UWorld questions about this ... +4
tea-cats-biscuits  @medstruggle *Supine position* decreases blood pooling in the legs and decreases the effect of gravity. *Supine hypotension syndrome*, on the other hand, seems specific to a pregnant female, since the gravid uterus will compress the IVC; in an average pt, there wouldn’t be the same postural compression. +8
welpdedelp  this was the exact same reasoning I used, but I thought the RAAS would inactivate which would lead to less aldosterone and less sodium retention +3
yotsubato  You gotta be preggers to compress your IVC +5
nwinkelmann  Could you also think of it in a purely "rest/digest" vs "fight/fright/flight" response, i.e. you're PNS is active, so your HR and subsequently your CO is less? But the explanation given above does make sense. Also because I think just saying someone is one bed rest leaves a lot up for interpretation, maybe not with this patient because his pelvis is broken, but lots of people on bed rest aren't lying flat.... ? +1
urachus  wouldnt low aldosterone cause low plasma sodium? choice B +5
kpjk  could it be that, while low aldosterone levels decrease plasma sodium levels- there is also decrease in blood volume(plasma),so there wont be a decrease in the "concentration" of sodium +4
almondbreeze  FA 2019 pg 306 on Lt heart failure induced orthopnea - Shortness of breath when supine: increased venous return from redistribution of blood +
almondbreeze  if there was no HF, it would lead to increased CO --> decreased aldosterone +
theunscrambler  @peqmd thanks for sharing that. According to the presentation, the diuresis via ANP occurs (along with sodium), which is followed up by an increased in RAAS --> maintains sodium levels. This cycle can then continue. Slide 13. +
jj375  @urachus - Either BB or Sattar taught me this but I feel like it is often forgotten. "RAAS/Aldosterone affects blood volume, and ADH affects Na level". So Increasing aldosterone will increase blood levels however water follows the sodium so you will not get a change in sodium levels. ADH however does affect Na since aquaporins are bringing in water without affecting sodium levels. +




Subcomments ...

submitted by medstruggle(12),
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yWh si ti hohutasp eusrlc fi heter ear on IG msyso?ptm yWh cant’ ti eb epserh ts?rezo

colonelred_  It’s just canker sores, they come and go. I think in herpes the gingivostomatitis really only happens when you first get infected. After that you just get recurrent cold sores. +4  
hyoid  Herpes zoster is not the same as herpes simplex virus. +27  
bigjimbo  you would see dermatome rash in zoster +3  
kateinwonderland  cf) Just in case someone wanted to know the causative organism of aphthous ulcers :The precise cause of canker sores remains unclear, though researchers suspect that a combination of factors contributes to outbreaks, even in the same person. Unlike cold sores, canker sores are not associated with herpes virus infections. +8  
charcot_bouchard  Herpes Zoster doesnt cause gingivostomatitis. Herpengina can cause vesicular lesion in mouth but happens to children in summer season by entero virus +  
drdeeznuts1  I'm wondering if this could be a mild case of Behcet syndrome without genital involvement +  
sherry  It sure can be Behcet or Pemphigus if the q provides us with more info. Canker sores just come and go for years with unclear mechanism. Also herpes zoster is shingles by VZV, not HSV1. +1  
avocadotoast  Most pictures on google show herpangina being present on the hard palate/throat, while aphthous ulcers are commonly on the lower lip. I think his lack of genital lesions are pointing us away from herpangina. +  


submitted by medstruggle(12),
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yhW was eht euatc elomhycti rniftnussoa aotecirn ued to AOB pmiiltinitboyca, utb ont hR cnyoiiaitlpbm?it

colonelred_  Rh incompatibility comes more into play with Rh- mother and Rh+ babies. +1  


submitted by medstruggle(12),
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nCa ooeemsn lnpxiea why esdo iths niaptte veha eioa?halypmk

colonelred_  Catecholamines activate the Na/K pump, which will drive K inside. +11  
trazabone  Read online that catachelamines are released following tonic clonic seizures. Besides that, BP of 180/100 could indicate that catecholamines are circulating. +1  
fulminant_life  This mechanism is why giving albuterol for hyperkalemia works +9  
nbmehelp  Why does this guy have increased catecholamines tho +  
johnson  His SNS activity is seriously increased --> increased catecholamines. +  
nbmehelp  Why is his SNS activity increased? Is the BP literally the only hint? +  
youssefa  Alcohol withdrawal creates a hyper- catecholaminergic state + Seizures do that as well. +5  
water  My best guess is that withdrawal puts the body in a state of stress (same for seizures) and with stress you have release of catecholamine which we'll see in the BP and the hypokalemia. +3  


submitted by medstruggle(12),
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Wyh si eth wnesar itrnu“angalo isut”e?s I guothth fetra 14 adys yuo ehav a ylful mrdefo cr.as

colonelred_  If you go back and look at the image you can see that it was highly vascular which is characteristic of granulation tissue. Scar tissue formation will be closer to 1 month, plus you will see lots of fibrosis on histology. +14  
sympathetikey  It's a bit misleading, for me, since you do see fibrosis intermixed with the granulation tissue, but granulation tissue was a better answer. +2  
haliburton  According to FA 2017: 3-14d: Macrophages, then granulation tissue at margins. 2wk to several months: Contracted scar complete. Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus). i'm getting pretty frustrated with NBME contradictions to FA, and FA omissions of content. this stuff is hard enough to get straight as it is. +1  
yotsubato  Thats cause the NBME exam writers read FA, then make questions not fit in with FA +7  
trichotillomaniac  This fits the timeline laid out in Pathoma! 1-3 wks = granulation tissue with plump fibroblasts, collagen, and blood vessels +10  
alimd  never look at the image in the beginning. They dont want you to success. Most of the time images are made to ditract +1  
garble  UWorld also has a handy chart for post-MI that said granulation tissue at 10-14 days, then collagen and scar tissue at 2-weeks to months /shrug +  


submitted by medstruggle(12),
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Wyh is oddalune lemun eoctrnci?r I tgouhht eatcpcrina zysemne ctpn,yoisy(rhm caebpiysrxpeo)atd ouwld eb dcaleto ehre.

colonelred_  Enterokinase actives trypsinogen and is located closer to the intestinal mucosal (“brush border”). +1  
drdoom  Yeah, @colonelred is right. @medstruggle: the duodenal lumen (and the pancreatic /proteases/ you mention) is the site where pancreatic enzymes (“endopeptidases”) cleave large polypeptides into smaller bits. It is at the BRUSH BORDER where the smallest kinds of peptides (dipeptides, tripeptides) are broken down into their amino acids, which finally can be co-transported with Na+ into the intestinal cell. I think about it this way: stomach acid denatures and “opens up” proteins (without any specific cleavage); pancreatic enzymes then cleave denatured polypeptides into smaller bits; brush border enzymes finally break down tiny peptides into absorbable amino acids. +3  
drdoom  Nice schematic, @welpdedelp +  


submitted by medstruggle(12),
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Why is it nto irvonaa llocefli e?scll I ohuthtg eth mlaefe glanoa fo etorSil dan diygeL si asane/uoahlgcrt ce.lsl

colonelred_  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +11  
brethren_md  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +4  
sympathetikey  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +5  
s1q3t3  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +11  
masonkingcobra  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +3  
mcl  Wait, but did anyone mention that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen??? +38  
mcl  But seriously though, pathology outlines says sertoli-leydig tumor "may be suspected clinically in a young patient presenting with a combination of virilization, elevated testosterone levels and ovarian / pelvic mass on imaging studies." As for follicle cell tumors, granulosa cell tumors usually occur in adults and would cause elevated levels of estrogens. Theca cell tumor would also primarily produce estrogens. Putting the links at the end since idk if they're gonna turn out right lol Link pathology outlines for sertoli leydig granulosa cell tumor theca cell tumor +12  
bigjimbo  LOL +  
fallenistand  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +5  
medpsychosis  So after doing some intense research, UPtoDate, PubMed, an intense literature review on the topic I have come to the final conclusion that...... ...... ...... ...... Wait for it.... ..... ..... Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +9  
charcot_bouchard  Hello, i just want to add that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
giggidy  Hold up, so I'm confused - I read all the posts above but I still am unsure - are sertoli-leydig cells notorious for producing androgen? +4  
subclaviansteele  Hold the phone.....Females can get sertoli leydig cell tumors which are notorious for producing androgen? TIL TL;DR - Females can get sertoli leydig cell tumors = high androgens +  
cinnapie  I just found a recent study on PubMed saying "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" +2  
youssefa  Hahahahaha ya'll just bored +9  
water  Bored? you wouldn't think so if you knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +5  
nbmehelp  I dont get it +  
redvelvet  how don't you get it that females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen? +1  
drmomo  what if this means..... females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen +  
sunshinesweetheart  hahahaha this made my day #futurephysicians #lowkeyidiots +  
sunshinesweetheart  @medstruggle look up placental aromatase deficiency (p. 625 FA 2019), it would have a different presentation +  
deathbystep1  i am sure i would ace STEP 1 if i only knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +2  
noplanb  Wait... I might actually never forget this now lol +3  
drmohandes  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +1  
lilmonkey  Don't forget that females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens! You're welcome! +  
drpatinoire  Now I get it that females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens. Thank you very much.. So why choose Sertoli-Leydig cell tumor again? +  
dr_ligma  The reason is because females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens! This is easy to remember, as you can remember it through the simple mnemonic "FCGSLCTWANFPLOA" which stands for "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen!" +18  
minion7  after receiving a f*king score..... this post made me smile and thanks to the statement-- females can get sertoli-leydig cell tumours, which are notorious for producing lots of androgen! +1  
djtallahassee  My worthless self put adrenal zona fasciculate but now I will never forget that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
medguru2295  Wait..... so can females get Sertoli Leydig cells that produce androgens then?????? +  
peqmd  Going to snapshot this to my anki deck card: "females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of {{c1::androgens}}" +1  
paperbackwriter  Watch me f*ck up the fact that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgens on the real deal. +2  
alexxxx30  just made sure to add to my notes "Females can get sertoli leydig cell tumors, which are notorious for producing lots of androgens" +2  
peridot  I also just wanna add that if you look on in FA on p.696969, you'll see that they'll mention "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" +  
mbate4  According to the literature [lol] females can get sertoli-leydig cell tumors, which are notorious for producing lots of antigens +  
drdoom  the tradition lives on +1  
jamaicabliz  Wait... so for clarification, is it that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen? Or that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen?? HELP +  
abkapoor  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen sorry for bad Englesh +  
faus305  Sertoli-leydig cells are notorious for producing lots of androgens, females can get these. +  
djeffs1  the fact that a bunch of medstudents can get so weird about how females can get sertoli-leydig cell tumors: notorious for producing lots of androgens- just made my week!! I love you guys +  


submitted by medstruggle(12),
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Why od uoy iveg IV urvoneilco with larticneath treexoehtat?m ndl’ouWt MTX leso sti iacfefcy neisc locinevruo esesvrer eth fcsefte fo ?TXM

colonelred_  MTX will still work but yes some purine/pyrimidine synthesis can still occur. You often give leucovorin to decrease adverse effects of MTX. +  
welpdedelp  ok I have a question, leucovorin is the same as folic acid...so why give one over the other? +1  
lsmarshall  Leucovorin, folinic acid, is a modified version of THF and enter folate metabolism where THF is, after the point where methotrexate takes its effect. I have a pharm. card that says "toxic effects on normal cells may be reduced by administration of folinic acid (a.k.a. leucovorin or citrovorum factor), which is **preferentially taken up by normal cells versus tumor cells**." +13  
jj375  @welpdedelp I also struggled with that and chose the wrong one, but then I remembered something from biochem that I think is helpful:I think the good thing about leucovorin is that it doesn't need to be activated by dihydrofolate reductase. Methotrexate is directly blocking Dihydrofolate reductase, so folate can't be activated to help, but leucovorin doesnt need the activation, it is turned into Tetrahydrofolate and rescues the cell! +