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Welcome to paperbackwriter’s page.
Contributor score: 110


Comments ...

 +6  (nbme24#44)

SO suspiciously obvious... NBME has given me trust issues


 +3  (nbme24#26)

I think what threw me off was the fact that it said "most likely" and Sertoli-Leydig cell tumor in a female just seemed like such a rarity that I figured it had to be some cells females typically have.

Keeping this in mind for future questions. If one of the answers actually fits the bill, don't pick one that you're not sure of because the correct one seems unlikely! *bangs head


 +0  (nbme24#49)

Worth noting that not only is there a separate reflex arc for non-psychogenic ejaculation, but that glandular secretion, emission (contraction of everything besides the penis muscles), and ejaculation (contraction of penis muscles i.e. ischiocavernosus and bulbospongiosus) are all under reflex control.

-- All efferents are parasympathetic EXCEPT for emission (sympathetic) and ejaculation (somatic). -- all afferents are pudendal n. except for psychogenic erection which starts with higher centers


 +0  (nbme24#41)

Pg. 157 of 2019 FA picture B depicts Shuffner stippling under Malaria. "Seen with P vivax/ovale"


 +11  (nbme23#11)

S2,3,4 keeps the 3 P's off the floor (Penis, Poo, and Pee)

alexxxx30  love it +1
prolific_pygophilic  A true scholar +3

 -2  (nbme23#41)

INfraspinatus goes OUT (i.e. external rotation) and therefore supraspinatus does opposite (internal rotation).

paperbackwriter  Apologies! Subscapularis does internal rotation. +2

 +1  (nbme23#35)

Obviously you wouldn't allow the husband inside, but after staring at this question for way too long, I reasoned that you wouldn't tell him to leave for 2 reasons:

  1. It might clue him in to the fact that she told you about the abuse, and he will leash out on her if he gets the chance.

  2. If she wants to call the police and press charges it will be better that you know where he is.

123ojm  it's your first point. unless the patient has a foolproof escape plan for when she is discharged, you don't want the husband to know that she told you about the abuse. that will put her in more danger. +

 +2  (nbme23#15)

can we all agree this was far too much math and unit conversion, WHY THE UNIT CONVERSIONS!?! WE ALL CLEARLY PASSED CHEM 101


 +5  (nbme22#18)

According to Goljan, men have boobs three times in their lives: when they're babies, when they're going through puberty, and when they're old. It's physiological/normal.

sars  I agree, babies-estrogen transfer through placenta from mother puberty-testosterone conversion via aromatase to estrogen elderly-increased fat content with androstenedione conversion to estrone read this somewhere and it sticks LOL +

 +3  (nbme22#38)

I think the reason they are being such little turds and calling it dipalmitoyl lecithin instead of DPPC is because there's a thing called the lecithin-sphingomyelin ratio which needs to be high in order to indicate that the fetal lung has matured. Both lecithin (DPPC) and sphingomyelin are present in fetal lungs, but the amount of lecithin shoots way up towards the end of gestation, raising the L:S and indicating lung maturity.

mutteringly  naw they just turd +1

 +7  (nbme22#40)

Half of this test seems to be knowing when the obvious answer is actually right, and when it's a red herring.


 +4  (nbme22#50)

FYI this is nth* question I've seen that wants to see if you know that the CFTR mutation results in a misfolded protein that gets stuck in the rER.

Where n = a very big number

castlblack  I knew that but I thought the chaperone proteins counted as protein regulation :( +1

 +0  (nbme22#27)

I also chose Paget :/ but realized this which I didn't before:

The stages are not uniform across different bones, so you could have some bones that are in the osteoblastic stage, while others are in the lytic stage etc.

orthobullets.com/topic/8040/images/paget's%20bone%20scan.jpg


 -1  (nbme22#1) FA 2019 pg 379 malrotation

something on wrong side --> malrotation --> fibrous bands (ladd) --> duodenal obstruction


 +5  (nbme22#33)

I got so angry at this question. At least this lady had a punching bag


 +5  (nbme22#10)

For those that didn't quite get what the stem was saying, basically Osler's sign is when you're squeezing the blood pressure cuff and keep going higher and higher because the arteries won't collapse as easily (due to natural stiffening of the arteries with age). The lack of collapse upon squeezing is why you can still feel the radial artery in the stem. So even though the pressure inside the arteries might be normal, you're gonna measure it as high (pseudohypertension). Apparently it's a common finding in the elderly.


 +10  (nbme22#46)

As my Bio 101 professor used to say, the answer to everything is either sex or surface area.


 +3  (nbme22#15)

In addition to what everyone else said, they went out of their way to use the word "irregular" TWICE. Maybe simple-minded of me, but as far as I understand benign shtuff is rarely irregular.


 +5  (nbme22#7)

SPOILERS FOR NBME 21 -- DON'T READ AHEAD IF YOU HAVEN'T TAKEN 21

After getting it wrong (because of the NBME 21 Q), I understood it like this:

– Libido is a long term state, meaning your libido could be fine, but anxiety in that MOMENT might cause psychogenic ED

– This guy has some classic SIG E CAPS criteria going on: fatigue (energy loss), sleep disturbances, concentration problems

– It says he hasn't been able to maintain any erection (vs NBME 21 guy that was able to masturbate (his long term sex drive was OK) but had performance anxiety in the moment)

Therefore, lack of sex drive fueled by depression --> low libido, but physiologically nothing wrong with him --> nighttime erections

trump2020  Bless you for including the spoiler warning +2
kernicteruscandycorn  @paperbackwriter: sick name and reference +

 +6  (nbme22#33)

I kind of reasoned through this by thinking that if they said "22 year old man" that means there has to be a Y in there in order for the person to be presumed male. That left options: 45X/46XY, 46XY, and 47XXY. Beyond that I thought that the picture didn't look normal (couldn't make out tubules or individual cells), so it couldn't be 46XY.

I figured 45X/46XY is a mosaic Turner, and I have no idea what a person with that genotype would look like, nor whether they would have testes, but I know that 47XXY would have testes because SRY is on chromosome Y which makes testes determining factor.


 +1  (nbme21#38)

Not sure what the implication was regarding the assisted living facility (I never thought of them as a last resort situation), because it has been shown that social activities are incredibly beneficial in slowing down the progression of dementia. I suppose she is in the early stages of disease and doesn't warrant anything so drastic like moving just yet.


 +2  (nbme21#5)

In addition to the more obvious hint of budding organism, candida has fuzzy edges on blood agar which the others don't.

usmlehulk  @paperbackwriter cryptococcus have a narrow budding. +
lovebug  wow I Didn't know that. THX~! +

 +2  (nbme21#42)

This can be analogized to menopause. Lack of estrogen ––> no negative feedback to anterior pituitary ––> increased levels of FSH and LH


 +0  (nbme21#50)

I had no clue where the damage was either, but with that said:

You feel the grass with your feet ––> gracilus

And the arrangement along the spinal cord is similar to the sensory/motor homunculus of the brain where the feet are on the inside/medial and the arms are on the outside/lateral.

drzed  Only in the dorsal columns; this is reversed if the decussation happens within the spinal cord (e.g. the spinothalamic tract has a somatotropic distribution where the proximal extremities are medial) +




Subcomments ...

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CSN sieobaamsi is most uoonrisloty sdaceu by lraeiNgae ,lrioewf ihcwh I eouancerg oyu ot ieozmmer sa teh bartginea-i“n a”aebmo. nFudo ni esrfawt-rhe bdiseo of rtwae liek podns nad l,aeks it has eehrt omsrf: a ty,cs a itzhtepooor ob(,eami)d nad a eltagbleafil e.i.( has two )lalfglae. fcIitenno si aiv ryoflacto lcle soanx ughrhto hte miirrbocrf ealtp to het ab.rin

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  


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ehT ieeasds ereh is croetsfu ipbsahestpsoha ie.eyidccfn nI i,t VI clelyorg ro strocufe sdnet’o pelh eeaucsb othb eentr eht csgeseoioulenng ahpyawt wolbe fcrtoeus p.otaaibsehshp Gocelasat on teh trhoe dahn eetrsn voeba it. I n’odt nthki ouy lryael nede ot wnko thsi ot ecsoho the corcret wsnear scein teh illccina etcprui fo atsgnfi ymoiphycegal htta si orctrecde w/ oems osrt fo srgau hatt nac teenr teh eioslenoceunsgg hayawpt sodlhu elcu uyo otin eth githr .eswran

neonem  I don't think you could have *totally* ruled out the other answers - I picked glycogen breakdown because it sounded kind of like Von Gierke disease (glucose-6-phosphatase) to me: characterized by fasting hypoglycemia, lactic acidosis, and hepatomegaly since you're not able to get that final step of exporting glucose into the blood. However, I guess in this case you wouldn't see that problem of glycerol/fructose infusion not increasing blood glucose. Nice catch. +25  
vshummy  I think you were super smart to catch Von Gierke! Just to refine your answer b/c I had to look this up after reading your explanation, von gierke has a problem with gluconeogenesis as well as glycogenolysis. So they’d have a problem with glycerol and fructose but also galactose since they all feed into gluconeogenesis before glucose-6-phosphatase. Great thought process! +22  
drmomo  glycerol and fructose both enter the pathway thru DHAP and glyceraldehyde-3-ph. Galactose enters thru Gal-1-ph to glu-1-ph conversion +2  
linwanrun1357  In this cause (fructose bisphosphatase deficiency.,),fructose should help to increase serum glucose, bcz it can become into glucose-6-P by hexokinase. Therefore, this question makes me confused.... +  
krewfoo99  According to uworld, fructose infusion will not increase blood glucose levels in Von Gierkes Disease as well +  
atbangura  I believe Von Gierke is not a plausible answer choice because a galactose infusion would still not see an elevation in glucose levels. Remember, galactose could be converted to galactose 6 phosphate, but in order to complete gluconeogenesis and allow glucose to leave the Liver for an increase of its concentration in the blood, the patient would still need glucose 6 phosphatase which is eliminated in Von Gierke. +1  
lilyo  So what disease is this??? I mean couldnt we have just answered the question based on the fact that the patient responds to galactose being infused and we know that galactose feeds into gluconeogenesis?? I am so confused. +1  
djtallahassee  Its Hereditary Fructose intolerance right? gets sick after fructose and I guess glycerol can jump in via aldolase B on this pathway via page 74 of FA2019. It looked like a fructose thing to me so I just marked out the other ones and moved on. +1  
paperbackwriter  @djtallahassee I was wondering same, but hereditary fructose intolerance also results in inhibition of glycogenolysis :/ confusing question. +  
amt12d  A much simpler way to think about this, without trying to figure out a diagnosis, I looked at the time frame for when the child was presenting. He has eaten poorly for 3 days, by now, his glycogen breakdown is gone. His body would be trying to make glucose, therefore, gluconeogenesis is impaired, not glycogen breakdown. +4  
tyrionwill  if fructose kinase is not available (fructose intolerence), then some fructose may go to F-6-P by hexokinase, then goes to G6P if gluconeogenesis is needed. however this patient's fructose kinase was intact, so no fructose would have go to F6P, so there would be no blood glucose increment after injection of fructose. +  
shayokay  You had to know that fructose and glycerol enter glycolysis at DHAP/G3P, and galactose enters glycolysis at G6P (gal-> gal-1-p -> glu-1-p -> glu-6-p). This means that one of the 3 enzymes between G6P and DHAP/G3P is not functioning properly. Most likely this would be fructose-1,6-bisphosphatase because there does not appear to be anything wrong with glycolysis. "Fructose-1,6-bisphosphatase (FBP1) deficiency is characterized by episodic acute crises of lactic acidosis and ketotic hypoglycemia, manifesting as hyperventilation, apneic spells, seizures, and/or coma. Acute crises are most common in early childhood; nearly half of affected children have hypoglycemia in the neonatal period (especially the first 4 days) resulting from deficient glycogen stores. Factors known to trigger episodes include fever, fasting, decreased oral intake, vomiting, infections, and ingestion of large amounts of fructose." https://www.ncbi.nlm.nih.gov/books/NBK550349/ +1  
shayokay  Also, even though Von Gierke is categorized as a glycogen storage disease it is really a problem with gluconeogenesis not glycogen breakdown. So even if you thought this was VG, you still could have gotten the right answer. In VG, any monosaccharide other than glucose (fructose, galactose, glycerol, etc.) will not raise the plasma glucose level because they all require gluconeogenesis to be converted into glucose and this cannot happen because there is no glucose-6-phosphatase. This is why the treatment for VG is frequent oral glucose in the form of cornstarch and avoidance of fructose and galactose. +  


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saMt ellcs t,adglreuaen induropgc nmahistie chiwh tatrtasc l.soesnoiihp The lreay tgaes of an ecillrag coaertni si astm elcl i,ddateem tub teh elat geast (diiglcunn uucsm oiuct)dprno is tdeieamd yb nisplh.iosoe

atstillisafraud  Thanks for a good answer. This question made me feel like I was taking T21 pills +17  
medguru2295  Thank you- I was really thinking this question had 2 correct answers... of course my dumbass picked Mast cells. +5  
ajss  where do i find this info?? +  
paperbackwriter  @ajss pg 112 of first aid 2019, under type I hypersensitivity. Immediate --> mast cells releasing histamine and tryptase, late--> eosinophils and leukotrienes recruited via chemokines +2  
graciewacie9  Wow, i missed the fact that the question is asking for the RESULT of the reaction, NOT the cause of the reaction. Mast cells cause the initial reaction, eosinophils would be the result of the eosinophils. *facepalm +6  
greentea733  @graciewacie9 SAME UGH +  
lba9587  Pathophys (as far as I understand it)...Mast cell degranulates, thus the phospholipid bilayer et. Al are left behind and needs to be degraded. Who comes in? Our good friend eosinophils, as they contain Major Basic Protein (responsible from breakdown of expired mast cell). Note, you can tie this in to the delayed Leukotriene effects of an allergic rxn, as the bilayer is also broken down by arach. Acid. (See this link to support my credibility https://images.app.goo.gl/3cUF3ZVc7qy8uxAi9) +  
mutteringly  who else looked up what T21 pills were +3  


submitted by nor16(58),
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CMPO is a roopnmreoh dpteiep chan.i

It is slandrteat dan telar ynemsze tuc ihts pepited in eht .ipbesdepstu

otnTariircpsn is gownr i( ahd sith .o.).to /cb its ton eth NAmR htat emkas nritfeefd teppeid o.hensrmo re,rvoeoM tawh I see onw ,is atth sarlninttcoppstoair tiiomdanfcio si orme or ssle s.in.l.cgip so tp.-srttlsaaon fimnootidaic. etnx mtei ew amke ti oectrcr ;-)

medguru2295  This is a perfect explanation. I never knew it was the protein modified (I initially though alternate splicing too) +1  
nerdstewiegriffin  Is this an example of polycistronic mRNA? +  
paperbackwriter  @nerdstewiegriffin possibly (because it says that the original mRNA results in proteins plural, BUT the mechanism for POMC derived hormones specifically is not bc of polycystronic mRNA. Polycystronic means that you get multiple protein products from one mRNA, but in this case we get multiple PROTEIN DERIVATIVES from one PROTEIN, implying that there are some modifications/reactions taking place once we've already made ONE protein which change the protein into multiple diff. products. +1  


submitted by seagull(1539),
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spcmemjwcgkrdMpyi.oei./keoii:laplii_iaeotse/nihts#/gi/FeaGiwy.ltts_oma/sm/BSiderBd:stdsta

I eieelvb tshi si lycalatu eadnsdesimti letyBcamsso deu to the odBar" edBas ndgdiu"B sa snee ni eth iu.eptrc

seagull  However, given the stain and some of the features I now see that this is most likely Crypto. THey like similar. my bad +15  
mjmejora  oh what a catch! I also thought this was Blasto until you explained otherwise +  
drmohandes  Blasto = broad-based budding, the two 'circles' look equal in size. Crypto = narrow-based -unequal- budding. +6  
paperbackwriter  ^ I would disagree a little bit. "Broad based" and "narrow based" refer to how smushed the circles are. So narrow based is when the membrane bit they're sharing is small, and broad based is when they share a lot of membrane. So if just pinching off --> crypto, if they look stuck/have a flat membrane between them --> blasto +2  


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lal hte otehr ,lsevess etehir hvea taaloelclr ppsesuli or ethy uypspl ot ransog twih pmlleuit orusesc fo bodol yupspl

AMI nad MSA hobt ahve ltlrlasoeca hitw haec ohter aiam(nlgr erariset adn mgnaiedner e)steiarr, os caisen teher si tloemnnivev of eon of eth areteris eth doobl uppsly mrfo oehtr cna vetrnep .sechmiai

btu if thob AMS and AIM aer lnvoidev it wuodl tlresu ni emiascih dan smytpoms dbdsreeic ni hte e.tqnisou

paperbackwriter  Spot on! +  


submitted by medstruggle(12),
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Wyh si ti ont avoianr eilfcoll l?scle I ouhghtt the aeemfl glnoaa fo Sroleti nda edgyLi is ualtae/aorhgncs lces.l

colonelred_  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +9  
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 roygbiv(20),
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hyW udocl hits not be taracvruesaxl syhomsl?ei nI AF ti yass aucte molctieyh sutoannirsf rateoinc nac be deu to OAB lipcomaibyinitt ro rsuraactleaxv lisemhyo.s

niboonsh  because extravascular hemolysis is associated w jaundice. Intravascular hemolysis would have hemoglobinuria but that's not an answer +1  
niboonsh  i mean that is the answer lol +  
krewfoo99  According to pathoma: Intrvascular haemolysis will lead to haemoglobin binding to haptoglobin. This complex will travel to the kidneys and be excreted. This will lead to red colored urine and haemosiduria (Note: This can also lead to acute tubular necrosis) Extravascular haemolysis is when macrophages break down the RBC. Then the Haeme is converted to biliverdin then bilirubin and conjugated in liver, and then excreted. +4  
paperbackwriter  If you look under the "clinical presentation" column of the blood transfusion reactions chart (pg114), it says that hemoglobinuria is with intravascular hemolysis and jaundice is with extravascular. Makes sense because with extravascular hemolysis your splenic macrophages are are chewing up the RBCs and sequestering it in the spleen so you don't get "spillover" -- i.e. clean urine. +1  


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llA tuoab hi:titnsg

s.c/bscseu:ntoendojl//aii/sp/n/ate.oeeenmttsshtgtaifoncwher.dcfdhuo

charcot_bouchard  When i faced this ques i did some Kegel. Felt something in my pee pee but not in my b*e. I exclude all option because they are bigger muscle of pelvic floor except EUS & IAS. And also remeber Kegel can be used as a treatment of prem. ejaculation not premature defication. +17  
paperbackwriter  @charcot_bouchard Actually Kegels are used in the treatment of fecal incontinence as well because of effect on EXTERNAL anal sphincter and surrounding muscles which are under voluntary control (you can most definitely feel it if you do a kegel lol). The answer is internal anal sphincter because internal is not under voluntary control (tonically contracted via symp. --> parasymp. relaxes it --> gotta go feeling --> no incontinence because of external sphincter's voluntary contraction). +10  
am4140  @paperbackwriter - Honestly, this depends on how you do the kegel. It is entirely possible to not involve your external anal sphincter at all once you figure out how to isolate your vaginal area. So the internal anal sphincter is under involuntary control so that was especially right, but I was prepared to pick anything with “anal” in it at all. So kegels work for fecal incontinence only if you’re choosing to involve your external anal sphincter, or you don’t know how or are too inexperienced to isolate the muscles around your vagina. I don’t think NBME or USMLE would get this tricky because the external anal sphincter will not always be involved in kegels. +1  


submitted by sympathetikey(1350),
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W'ovlued eebn cnei if eyht ltdo oyu n"2d tteacnolirs pcae"s no fetl or g.htr..imsh

paperbackwriter  It wouldn't have mattered because the murmur is due to increased stroke volume, not anything mechanically wrong with the valves. If they had said A or P then it might have actually caused more confusion (stenosis etc.) +6  
cport12  Also an important side note is that with the addition of the placenta, systemic vascular resistance would actually decrease (another organ added in parallel) which should help point you towards an increase in stroke volume. +1  


INfraspinatus goes OUT (i.e. external rotation) and therefore supraspinatus does opposite (internal rotation).

paperbackwriter  Apologies! Subscapularis does internal rotation. +2  


submitted by step420(34),
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sPneor hsa trma-betELona edysmron x(h fo ulgn cnc,ear and mcleus yvttiaci ttha is tteerb thwi us.e

cirnsapPety C2+a ebdiniasot eptnver hte elreesa of AHc apyrsciyatlplne sebuaec hte sdtbioeani rpvtene the aozpindtoirlea tiinwh eht clel dan rpestnev csyptain essvlse of ChA form nielgva.

thotcandy  ugh, I saw Ca2+ and stopped thinking. +12  
paperbackwriter  @thotcandy Same here :( +1  
sidlersofcattan  they got me too with that Ca++ rip +1  
psay1  FA2019 pg. 463 +  


submitted by mousie(216),
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yWh no ?aswitnge I neam I gte stcEsay is obbrplay the rdgu of eohcci roefbe an lal nhgti caedn yaprt o)l(l but ot'dn nestdnurda ywh heetr udolw be dolc ieisxtmreet dna on ngitewsa enwh si FA it assy ierehaprytmh nad b??rd??aoh

sympathetikey  FA says, "euphoria, disinhibition, hyperactivity, distorted sensory and time perception, bruxism. Lifethreatening effects include hypertension, tachycardia, hyperthermia, hyponatremia, serotonin syndrome." So I think they wanted you to see Sinus Tachy and jump for MDMA. Idk why Ketamine couldn't also potentially be correct though. +11  
amorah  I picked ketamine because it said no diaphoresis. But if you need to find a reason, I guess the half life of ketamine might rule it out. Remember from sketchy, ketamine is used for anaesthesia induction, so probably won't keep the HR and BP high for 8 hrs. In fact, its action is ~10-15 mins-ish iv. +11  
yotsubato  Because the NBME is full of fuckers. The guy is probably dehydrated so he cant sweat anymore? +18  
fulminant_life  you wouldnt see tachycardia with ketamine. It causes cardiovascular depression but honestly i saw " all-night dance party" picked the mdma answer and moved on lol +8  
monkd  Ketamine acts as a sympathomimetic but oh well. NBME hasn't caught on to ketamine as a drug of recreation :) +4  
usmleuser007  Why not LSD? +  
d_holles  @usmleuser007 LSD doesn't cause HTN and ↑ HR. +1  
sbryant6  @fulminant_life FALSE. KETAMINE CAUSES CARDIOVASCULAR STIMULATION. +9  
dashou19  Take a look at why the patient has pale and cold extremities. "Mechanistic clinical studies indicate that the MDMA-induced elevations in body temperature in humans partially depend on the MDMA-induced release of norepinephrine and involve enhanced metabolic heat generation and cutaneous vasoconstriction, resulting in impaired heat dissipation." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5008716/ +3  
drzed  @sbryant6 you're both saying the same thing. Ketamine has a direct negative inotropic effect on the heart, but it is also a sympathomimetic. You are both correct. +  
paperbackwriter  @drzed Can you please site that? As far as I understand ketamine has a sympathomimetic effect on the CV system --> increased chronotropy and BP. I also don't see how they're saying the same thing. One person said "stimulation" and the other said "depression" +  
nutmeg_liver  People tend to drink a lot of water on MDMA. I just guessed the confusion was a result of hyponatremia (too much free water) but no idea if there's any data saying that people tend to become hyponatremic due to water over-consumption on MDMA lol. +1  
cassdawg  "Despite possessing a direct negative cardiac inotropic effect, ketamine causes dose dependent direct stimulation of the CNS that leads to increased sympathetic nervous system outflow. Consequently, ketamine produces cardiovascular effects that resemble sympathetic nervous system stimulation. Ketamine is associated with increases in systemic and pulmonary blood pressures, heart rate, cardiac output, cardiac work, and myocardial oxygen requirements."(https://www.openanesthesia.org/systemic_effects_of_ketamine/) +  
brise  LSD does cause HTN and tachycardia according to uworld! @d_holles +  


submitted by bubbles(69),
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hCniocr renla cffc:isnnueiyi

)1 orpo opspehtah cecnreala t--&;g hhgi eusrm ranignioc horhpospuos

)2 ighh merus hptpeaosh ;g&--t opxmscele iwth dvinelta ctoani aC -t;-g& Ca llasf

)3 aC fasll g-&t;- tisrergg THP asix

)4 dyknie euifrla t--g;& esdceadre tiivtayc of loy-h1srydaxe ta teh edinky -g-;&t lses aioiccltrl

makinallkindzofgainz  this guy renals +6  
paperbackwriter  Someone please help me with this (always trips me up): PTH causes increased vit D production in kidney... are we assuming the increased PTH can't catch up with the kidney failure? Is it the level prior to PTH compensation that they want? D: +  
miriamp3  @paperbackwriter what it works for me ;;;; is find the first abnormality so CKD low calcitriol (no D vit) ---> is gonna increase PTH ---> the kidney are not working (chronic, they don't tell u recently- you can;t revert a CKD so the kidney never going to catch up) --> increase inorganic phosphorus.--> always start with the problem. I also use this for celiac and types of shocks. start with the problem, and trust yourself. +2  
paperbackwriter  @miriamp3 thank you! I will try out your strategy next time!! :) +1  
snripper  I thought renal insufficiency -> inability to reabsorb phosphate at PCT -> decreased phosphate? +2  


submitted by meningitis(537),
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oihrihzohroaldoctdye is DCO orf rhongcepieN bDtiseea isuinpdis uaseebc ti axacdalolipyr sucase na eicrenas in PB by nseianrigc uoismd osriatpnob nad tush taewr nrspboait,o mthaaoP aneplisx tihs y.ienlc

issepmDsnroe si ocrtnriec cuebsae puno inafgts difl(u i)ortirnstce AHD is icnsdreae gnniema AHD is ginbe rleeedas rnlaeCytl but is otn kworing in eht iyneksd ta hte 2V retescrpo fo hte elliehpiat ernla celsl at lelctoigCn tcdu.

On tath ,oent oireidlAm is dseu rof Lhiuitm cuddnie gipecnhreon D.I

hello  Where in Pathoma? I couldn't find it. +1  
almondbreeze  also sketchy says that thiazide s decrease the amount of lithium cleared--> lithium toxicity +1  
paperbackwriter  Agh confused as well because FA2019 (pg 562) says that thiazides are implicated in lithium toxicity D: +  
paperbackwriter  OOPS, please ignore last comment. I just realized that this Q stem never mentioned lithium. And on top of that @meningitis mentioned that amiloride is used if lithium induced. Apologies. +  
jaramaiha  Question is nephrogenic DI. ADH is increased but kidney's aren't reacting, mutated receptors. In which the Tx is HCTZ +  


submitted by meningitis(537),
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yzrotiodrhihehooclda is DOC rfo hnogpcieerN tiabseDe iupisinds csbeaue it xpayadiallocr uesasc an cersinea ni BP yb sainenigcr sumido bsroopnati adn utsh tarwe tobrpai,son amhoPta aspeilxn thsi yni.ecl

sspoemisDner si itcecornr eeuabcs nopu nsigtfa d(uilf itnirect)ors ADH is arnecised ngemnai AHD is iebgn aleseder Catlelyrn ubt si ont nirokgw ni the iedsnyk ta teh V2 otcrepesr of the ipietlahel aelnr llesc at itlegclonC d.uct

nO tath to,ne oildeAmri is dseu ofr itiuLmh cndeudi gopennhicer DI.

hello  Where in Pathoma? I couldn't find it. +1  
almondbreeze  also sketchy says that thiazide s decrease the amount of lithium cleared--> lithium toxicity +1  
paperbackwriter  Agh confused as well because FA2019 (pg 562) says that thiazides are implicated in lithium toxicity D: +  
paperbackwriter  OOPS, please ignore last comment. I just realized that this Q stem never mentioned lithium. And on top of that @meningitis mentioned that amiloride is used if lithium induced. Apologies. +  
jaramaiha  Question is nephrogenic DI. ADH is increased but kidney's aren't reacting, mutated receptors. In which the Tx is HCTZ +  


submitted by zpatel(24),
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Cna onnaye llet teh feetfc fo pinsira on a odlbo bal uaevl e.(i ,niTTibPPT,rF t)cup?dor

paperbackwriter  Aspirin only increases platelet aggregation (blocks COX1/2 --> decreased production of Thromboxane A2 --> decreased aggregation). That's why it only increases bleeding time and has no effect on PT, PTT, and fibrin products. PT and PTT are only affected if something messes the coagulation cascade. +  


I also chose Paget :/ but realized this which I didn't before:

The stages are not uniform across different bones, so you could have some bones that are in the osteoblastic stage, while others are in the lytic stage etc.

orthobullets.com/topic/8040/images/paget's%20bone%20scan.jpg



submitted by keycompany(308),
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olwdtnu’ cnciroh nseoniytpher fo eth elnarL- eytrra cnudei SRAA attiiacovn, nad cnehe abruutl oyhtpyrprhe htiw caocrlit rhpayto?

fcambridge  I had a similar thought regarding mesangial hypercellularity. I missed a UW question on a similar topic. Unilateral renal artery stenosis results in hyperplasia of modified smooth muscle cells (JG cells) due to reduced RBF. The hyperplasia is intended to correct the supposed deficiency via increased production of renin. +  
paperbackwriter  Atrophy of the affected kidney (receiving less blood) and hypertrophy of the opposite kidney. +2  


submitted by sweetmed(143),
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iLPac alrcc:riusi ucsloasm dsolf thta xenedt rfmo sdliat uddnuemo ot ixlapmro elimu A821F0 gp 536

paperbackwriter  not sure why you were downvoted... correct (maybe pg number wrong??) +  


submitted by bubbles(69),
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nhCiroc nelra fficiy:nineucs

1) poro hheoappts laeancrce -g&t-; ihhg mrseu ocrgiainn purphshooos

)2 ighh rumse tpaphhoes -t&g;- emslcoxep whit daltivne onacti aC -;-tg& aC lslfa

)3 Ca lfsla -g;-t& tegsrrig PTH xsai

)4 iydnek eruailf t&g--; ddreesaec tyaiicvt of sar1yxd-oehly ta the kdeyni -g;t&- ssel cialicrlto

makinallkindzofgainz  this guy renals +6  
paperbackwriter  Someone please help me with this (always trips me up): PTH causes increased vit D production in kidney... are we assuming the increased PTH can't catch up with the kidney failure? Is it the level prior to PTH compensation that they want? D: +  
miriamp3  @paperbackwriter what it works for me ;;;; is find the first abnormality so CKD low calcitriol (no D vit) ---> is gonna increase PTH ---> the kidney are not working (chronic, they don't tell u recently- you can;t revert a CKD so the kidney never going to catch up) --> increase inorganic phosphorus.--> always start with the problem. I also use this for celiac and types of shocks. start with the problem, and trust yourself. +2  
paperbackwriter  @miriamp3 thank you! I will try out your strategy next time!! :) +1  
snripper  I thought renal insufficiency -> inability to reabsorb phosphate at PCT -> decreased phosphate? +2  


submitted by hungrybox(1026),
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Dpiscsalty eivn ear a orrrpuces ot .maoenlam yhTe veah ri,elurarg "ps"scdaiylt rodsrbe. mmebreeR eht "B" ni DCBA dsanst rof rrlgruiea os.reBdr Neusv amesn l.moe

Other nws:ares

  • shaantocis siaingcnr - Dnrgnkiae of nkis coetiasdas ihtw pTye II bieeasdt lmestuil

  • aabsl llec aorcacinm fo sikn - rl,aeyR if rvee .ezsmasttaesi Clmymono saectff uppre lip.

  • belu vseun - lBl-ocerudoe pyte fo mcmoon .olme ge.Bnin

  • nedpmiteg bioecrrhse iksarteso - utc"kS on" capaa.eprne lyMots .nnbgie Atcesff edlor plep.eo

  • Noet( - ouy lluasuy ese lnyo en.o fI luimtepl creebosirh taoresske era e,nse it tdcniiesa a IG naiamylgcn - aak leraesté"-LrT isg)n
usmleuser007  correction ~ BCC affects the lower lip more than the upper +1  
sympathetikey  Pathoma says upper lip, good sir +26  
hungrybox  Yeah basal cell carcinoma actually affects the upper lip. Counterintuitive because it's "basal" which seems to go along with the lower lip. Here's another source (this website is fucking gold btw): https://step1.medbullets.com/oncology/121593/basal-cell-carcinoma-of-the-skin +5  
pg32  Can anyone explain how we can rule out C or E purely based on the question stem? If we read into the question that we are looking for something related to melanoma, then I get why we can rule out C and E. However, the question simply asks which lesion appears on both sun-exposed and nonsun-exposed areas of the patient's skin. I would say that C, D and E can all occur in that distribution pattern. +4  
paperbackwriter  @pg32 because it specifies "this patient's skin," and the only ones he is more likely to get than the average person because of his family history are dysplastic nevi +2  
teepot123  fa 19 pg 473 +  
rockodude  just remember BS. basal cell upper, squamous cell lower +  


submitted by usmleuser007(395),
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tJus aerdziel hatt nlare lelc romiaacnc inst' eht rctocre rwasne /bc ti dvandie het unveso aricutcilon adn nto teh eraatrl.i PB amy otn be ectdfaef as m.uch fi CCR rewe the rnswae tnhe ethn eehtr wloud eavh enbe edmae nrsptee adn/or areln TN.H

sympathetikey  Also, just thinking out loud, in the case of RCC, it's the kidney tissue that's dysplastic & moving, so technically the renal artery itself isn't dysplastic, right? +  
paperbackwriter  @usmleuser007 very good point regarding the venous vs arterial circulation that I neglected to consider! +  


submitted by nosancuck(86),
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Yo dawg ew lal otbau TPV ITM aLHL

enhneny,aalilP V,aieln KDpt,TNAyor ,nnihoeerT snu,cIileeo et,nMioheni nieHi,sdit iunceLe eynLsi

meningitis  I don't understand what the question is asking... can someone please explain it to me? Patient doesnt eat protein, shes chubby. What does methionine have to do with this? +2  
charcot_bouchard  Just basically asking which is essential amino acids. +3  
usmleuser007  Essential amino acids (something i came up with) 1. "Three HAL fans will try meth" a. Threonine = Three b. Histidine; Arginine; Lysine = HAL c. Phenylalanine = fans d. Valine; Isoleucine; Leucine = will e. Tryptophan = try f. Methionine = meth +3  
nala_ula  They're saying there is a lack of good quality protein -> slight nutritional deficiency. She may have acquired weight but it's not because of protein. So they're specifically asking what amino acid she might be missing due to her subpar diet. Since essential amino acids are those that the body cannot make itself, out off those listed, methionine is the essential amino acid. It's on page 81 of FA 2019. +11  
nala_ula  correct me if I'm wrong please :) +  
hello  For anyone confused trying to follow @usmleuser007's comment -- slightly modified Essential amino acids mnemonic "Ah, Three fans will try meth" Ah = arginine, histidine Three = Threonine Fans (phans)= Phenylalanine Vil (Will -- German accent pronouncing English word 'will') = valine, isoleucine, leucine, lysine Try = tryptophan Meth = Methionine +1  
pg32  Why does @hello and @usmleuser007 mnemonic contain arginine? That isn't in the PVT TIM HaLL mnemonic for essential amino acids... +  
paperbackwriter  @pg32 arginine is semi-essential. It is essential in preterm infants who cannot synthesize it https://www.sciencedirect.com/science/article/pii/S0955286304000701?via%3Dihub +