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Comments ...

 +7  (nbme20#41)

if you look at the answer choices, they are all pain suppressors except for naloxone.

Naloxone is an opoid antagonist so blocking mu receptors would lead to increase in mediators that induce pain.

I don't think you need to know any experimental data, or really anything before the last two sentences. He is given something that reduces pain (opioid agonist), and if you give him naloxone you would be reducing the effect of his opoid agonist.


 +6  (nbme20#24)

As so many posts mentioned this is an ulnar n. problem. cool. But you also have to be able to distinguish between ulnar nerve at the hook of hamate vs ulnar nerve as it courses through the flexor carpi ulnaris.

with the Froment sign you know the deep branches of the ulnar nerve are being effected. This guy is on his bike and rides for 8-10 hours a day - pretty cray. But that's how you know its more likely compression from the handlebars at the hook of the hamate bone and not on the side from his flexor carpi ulnaris.


 +3  (nbme20#46)

I feel like part of this is them seeing if you can recognize those are tubules.

  • So if you say ok these are tubules, chorioamnionitis, endometritis, and PID are probably not right.

  • Glomerulonephritis in my experience so far, they should probably show a glomeruli, not tubules.

Between hematgoneous spread and obstructive uropathy, I feel like I don't have enough info - but sometimes a 50/50 guess is better than playing Battleship.


 +3  (nbme20#44)

The patient has a bruit which is turbulent blood flow due to something obstructing like stenosis causing renovascular HTN.

  • if you measure just aldo, what are you expecting? You heard the bruit, you know there's probably stenosis so does a high aldo tell you the cause? Typically the non-invasive approach to assessing renovascular HTN is checking plasma renin.

  • MR angiography can better explain if the bruit is the reason why the patient has renovascular HTN. We learned in my renal course, gold std is renal arteriography but you can use MRA.


 +3  (nbme20#18)

I had a different thought process to answer this question that might be worth mentioning.

  • urine output increased: pretty simply they are putting tubes in to increase the urine flow into the bag.
  • If you increase urine flow rate you increase K+ secretion. That's why diuretics like thiazides and loops increase K+ secretion. You can sort of think of it as the gradient stays wide for the K+ in the cell to leave into the lumen because as new fluid reaches the principal cell it wouldn't have much K+ allowing for an increased driving force

The aldo reasoning is def true as well, stimulus for aldo is hyperkalemia. Costanzo teaches this well, you can also reference BRS physiology 166-167

sweaterguy  Sounds like a situation similar to the recovery phase of ATN. +

 +3  (nbme20#11)

I interpreted "sequence surrounding first two exons of gene" - to mean they must be talking about introns. Three of the answer choices don't have much to do with introns.

  • missense mutation would have to be in the exon to cause change in amino acid.
  • polyadenylation is at the end of the mRNA
  • inhibition of replication is DNA

that may not be air tight, but helps narrow down. Also knowing some B-thalassemia is due to variants in abnormal splicing helps. (FA 2019 pg 43)


 +0  (nbme20#31)

Golijan had a good point about this in CNS lecture (near the end of the first one). Your CSF has tremendous pressure, and if someone tries to lift a ton of weight without breathing, that's basically like doing a major valsalva. That valsalva reduces preload right...and that pressure backs up - up the jugular vein to the sinuses to the CSF --> rupture intervertebral disc. Apparently that can happen cause the pressure can be so severe. I never thought I'd see a question on it though.


 +0  (nbme20#26)

If you think about it this way, his free T4 is normal and his TSH is normal. Would any other option allow this to happen?

A step further would be, why is his free serum T4 okay but his T3 and T4 dec. His total T4 must be decreased then, which one of those can cause that while keeping free T4 normal.


 +1  (nbme20#42)

when CMV is involved in post transplant patients that typically causes pneumonia. I think that was a question in this NBME too. For EBV post transplant, it would be lymphadenopathy etc. That's what I've taken away so far from nbme. I thought maybe the monomorphous B lymphocytes was hinting more towards EBV too, but I don't see why CMV wouldn't remain latent in a B lymphocyte?

uloveboobs  CMV definitely could remain latent in a B lymphocyte, but also is latent in T cells and macrophages (i.e., all mononuclear cells). I think the key in this question is the phrase "monomorphous population of B cells." EBV remains latent in B cells ONLY, whereas CMV is latent in all mononuclear (not just B) cells. +6
rockodude  ^this is the main point of the question. CMV can cause lymphadenopathy and hepatosplenomegaly as well. Key is the monomorphous phrase. +1

 -1  (nbme22#26)

Just to add thought process. Pt has excessive thirst, and urinating frequently but his Serum osmolality is increased...which means he has to omuch solute in his blood and his ADH is not working.

ADH not working can be due to Central DI or Nephrogenic DI. Central DI is when pt has lack of ADH but in this vignette they say the ADH is increased --> must be nephrogenic.

I don't think you need to know that HCTZ paradoxically works for nephrogenic. I think you can save time and just memorize FA's tx choices for Nephrogenic DI - HCTZ, amiloride, and indomethacin. You could argue it's good to know mechanisms, but I think knowing the drug names and their MOA, you'd be able to figure it out if they went for a 4th order reasoning (there's already enough thinking to do in this question)


 +0  (nbme22#14)

ADA def causes increase of dATP which strongly inhibits ribonucleotide reductase, reducing dNTP needed for DNA synthesis.

This would particularly effect lymphoid proliferation and function that relies heavily on nucleotide biosynthesis. Half of the cases of neonatal onset of SCID are due to ADA def.


 +1  (nbme22#21)
  • Can't be aplastic anemia if the pt is able to produce other cells evident in the labs.
  • Not DIC bc PT and PTT are normal and not increased.
  • If pt has fulminant liver failure I would imagine they would not be able to produce their coag factors so again, not probably it.
  • Vit B12 Def leads to macrocytic anemia and here they were nice enough to give us MCV which is between 80 and 100.

TTP makes sense with what others said. You can also spot some schistocytes in the blood smear.

kevin  yeah I'm pretty sure schistocytes alone could give you ttp as answer +1
kevin  well that and pt/ptt being normal +

 +1  (nbme22#44)

I was between hepatic excretion of bilirubin and Hepatic UDP-gluco.... (Rotor syndrome and gilbert/physiologic neonatal jaundice respectively).

FA 387 (2019) helps where they say

  • high UCB (indirect) --> Crigler Najjar or Gilbert syndrome, or physiologic neonatal jaundice.
  • high CB (direct): think excretion defect for this type of vignette (Rotor Syndrome). Had the question said "with a direct component of 8" I think I would have chosen Hepatic Excretion of bilirubin.

 +1  (nbme22#27)

if you also think, when someone has increased CO2 (as in this patient) they have respiratory ACIDOSIS right...so increased blood pH cannot be the right answer.

Also, compensatory mechanism for respiratory acidosis happens in three ways.

  • ECF: where due to mass action increase of CO2 leads to increase in H+ and HCO3- (but this is minimal - like 3%)
  • ICF: most of the buffering happens here with CO2 going into the cell.
  • Kidney: then over sometime, there will be some renal compensation (not correction) where the kidney will start to let go of H+ and reabsorb new HCO3 to help adjust pH towards normal.

 +3  (nbme22#39)

Dilated Cardiomyopathy can happen in pregnancy (FA 2019 305), but sometimes with less time on your hands it's easy to get overwhelmed with answer choices that all seem relevant. You really have to notice, this person has left heart failure (SOB with lying down) --> lungs (crackles) --> to right side heart (pitting edema). So the answer choice you pick has to explain these symptoms.

  • Amniotic Fluid Embolism is usually related something causing amniotic fluid to get into mother's blood supply. They wrote uncomplicated vaginal delivery, so unlikely to be amniotic fluid embolism.
  • MDD does not fit this vignette - just one week history of fatigue and there are so many other symptoms to worry about first.
  • Pneumonia: 3 day history of non productive cough make it a little less likely, esp with fluid overload. That's not typical in what I've seen for pneumonia questions.
  • Pulmonary embolism - she is tachycardic and has tachypnea but this usually presents acutely and fluid overload in this patient makes it less likely.
  • Pulmonary fibrosis: she has orthopnea which made me think there's gotta be something wrong with the left heart first so probably not this.

 +4  (nbme22#33)

Same type of question was asked in another NBME where I still got it wrong but I believe I understand what they are getting at now.

  • overdose on levothyroxine: that means too much T4, which has the ability to convert to T3 peripherally. So in that case Free Thyroxine AND Free triiodothryonine will be up. (There is no reason for T3 in this scenario to be decreased)

  • overdose on triiodothyronine: Too much T3, which cannot convert back to T4. Recall, T3 is more potent than T4 and will downregulate TRH release from hypothalamus. TSH be decreased but so will T4.

tekkenman101  T4 is more potent than T3, that is why only a fraction of T4 is available to be used and why the body converts most T4 into T3 for later use. +

 +2  (nbme22#33)

45, X / 46, XY is a bit tricky. Not having too much time to think, I almost went for it thinking there is increased risk for gonadoblastoma with 45X/46XY mosaicism - so maybe that's what they are going for? But what I realized after a couple NBME's, if they don't mention something about the body habitus (like here they said male), it's less likely this patient has Turner Syndrome.

We're just medical students, not pathologists. So I think if you just say okay, male so can't be 46 XX or 47 XXX. Then also probably not mosaicism cause of what I mentioned above. You are left with normal 46 XY or 47 XXY - and which is more likely to have fertility issues?


 -3  (nbme24#50)

a little messed up, but "Inability of neurons to perform glycolysis" seems like a tempting answer. But the reality is, the neurons are able to perform glycolysis, they ready to rock but just waiting on insulin. I still chose this as my answer tho.

I guess this is one of those choose the best answer questions. I think FA should add the reasoning behind cerebral edema, being that it's a major cause of death (but I couldn't find it in Robbins either). Having so much glucose in the blood vessels causes water to be drawn out (ICF --> ECF). So that's a intracellular dehydration.


 +2  (nbme24#9)

Reading microfilariae reminds me of three things. all from sketchy.

  1. Loa Loa --> Deer flies --> subcutaneous nodules and larva crossing eye.
  2. Onchocerca volvulus --> black fly --> deposits larva in skin which mature into adults producing microfilariae causing scattered puritiic papules and potentially eye blindness.
  3. W. Bancrofti: this is due to mosquitos and causes elephantiasis. Also has microfiliariae.

Honestly, I was looking for deer fly. But culex mosquito is west nile, reduviid is chagas. I think everyone knows ixodes and body louse is not this.


 +8  (free120#33)

Just to add to explanation. Answer is not congenital adrenal hyperplasia, because pt has normal breast development and normal external genitalia. most common type 21-hydroxylase def would have precocious puberty or clitoral enlargement. Questions says patient has normal appearing external genitalia. 17a-hydroxylase def would lead to ambiguous genitalia in XY and in XX there would be no secondary sexual development because lack of sex steroids. But again, question says pt has normal breast development and external genitalia. In 11B-hydroxylase def, XX would have virilization, again not applicable here.

ectodermal dysplasia would have more characteristics like abnormal teeth, other abnormal findings from ectodermal layer.

a psych disorder could throw you off, maybe patient is not eating enough and is not having a period. But they said normal female body habitus, so I think that seems less likely compared to androgen insensitivity.

Sex chromosome mosaicism made me think of Turner Syndrome. There is a unique body habitus for Turner Syndrome so makes this a wrong answer.


 +8  (free120#9)

You can look at this question strategically.

  1. Southern blot --> so DNA.
  2. they are using an endonuclease to transfer bits, this doesn't really mean anything to you yet.
  3. cDNA is probing for single immunoglobulin-constant region.

That's important, because now you know they are looking at the constant region of immunoglobulin aka Fc of the heavy chain.

So why is this cDNA that encodes Fc, lighting up only once in other tissues, but the same cDNA lights up multiple times in lane 2 (bone marrow)? This is because, at the bone marrow random recombination of light or heavy chain occurs, and our cDNA is present in different random combinations with light chains. That specific cDNA sequence they used didn't change between the tissues or even within the bone marrow, and it will only bind to the one gene sequence. The fact it's lighting up multiple times tells you that the same sequence is present, your question is why so many times.

Also a side note, southern blots are time consuming, so labs use other methods to do the same thing (like PCR), but southern blots are still the best when it comes to checking immunoglobulin and T cell receptor gene rearrangement.





Subcomments ...

submitted by xxabi(261),
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cinnBoergcho iomncaacr = ugln creanc

taTh gnibe di,sa ugnl rainoemdnoccaa aypliclcesif si sastciaeod htwi cphpoeyrithr rhptaroate,yhosto hcihw si a prnisataopclea ydnsrome hicctrreedaaz by iglidta lcbib,ung lagrihar,ta itonj nfoe,sfuis nda issistoepor of laurbtu bones

luke.10  why not systemic scleroderma since i did this question wrong and i chose systemic sclerosis scleroderma , can someone explain that ? +2  
kernicterusthefrog  My best guess answer to that @luke.10 is that: a) there's no mention of any skin involvement (which there would be in order to be scleroderma) b) Scleroderma shows pitting in the nails, not clubbing c) There would be collagen deposition with fibrosis, not hypertrophy of the bone at joints Saying that, I also got this wrong! (but put RA...) so I'm not claiming to "get this" Hope my thought process helps, though! +6  
yotsubato  This is in FA 2019 page 229 +10  
larascon  I agree with @kernicterusthefrog on this one, Bronchogenic carcinoma = lung cancer. Squamous cell carcinoma gives you hypercalcemia (new bone formation; maybe?), commonly found in SMOKERS ... +3  
waterloo  the clubbing is the symptom that takes out alot of the answer choices. It's super tricky. +  
jawnmeechell  Plus the patient has an 84 pack-year smoking history, super high risk for lung cancer +  
veryhungrycaterpillar  FA 2019 pg 229 is all paraneoplastic syndromes. There is no mention of bronchogenic carcinoma in any of them. There is adenocarcinoma, but that is most likely in non smokers, not in someone with 84 pack year of smoking history. Why does he have 5 upvotes for referencing first aid here, what am I missing? +3  
jakeisawake  @veryhungrycaterpillar sounds like bronchogenic carcinoma is a general term for lung cancer. You are right that if a non-smoker gets lung cancer it is most likely adenocarcinoma as non-smokers rarely get small cell. However, smokers can get adenocarcinomas as well. The oncologist that I shadow sees this frequently. Adenocarcinoma of the lung causes hypertrophic osteoarthropathy per 229 in FA2019 +2  
mangotango  @verhungrycaterpillar @jakeisawake Adenocarcinoma is the most common tumor in nonsmokers and in female smokers (like this patient), so adenocarcinoma would still be the most likely cancer for this pt over the others. Pathoma Pg. 96. +3  
fatboyslim  Apparently bronchogenic carcinoma is basically an umbrella term for lung cancer. Source: https://radiopaedia.org/articles/lung-cancer-3 +  
lifeisruff  bronchogenic is another term for adenocarcinoma in situ according to pathoma +  
topgunber  With the exception of mesothelioma- 95% are bronchogenic +  


submitted by imgdoc(135),
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ouY nca scsor uot eht pot hrtee snrewa oecsihc, .BA,C, You owtn be raonbigresb ygnntahi in teh TPC ni fca'nsnio nemy.odsr nLogkio ta aimph,kloeay a,ohiamyerntp dan pooappihhhaemyts won. komialpyHae ta'cn be rtorcec seaceub enev htgouh posamsiut is tlso ti lwli eb deesarobbr at eht trael cihtk sadginenc lopo adn fi that ntsoed aemk ,snsee hte doby wlil djsaut rfo owl uesmr ioassputm but gitvtaacni teh /KH++ pmpu on l.eslc It 'tsni htianypeaorm uaeescb at het lcncogtlie udtc nprlpicai ,elscl itnrbpaeoosr iwll r.occu sihT velase pmaohhtpoiheyaps sa eth rccoter dna oynl rwaesn hic.eoc

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 hayayah(1081),
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dAd no to the roeht emcnomt: F.MSOCKAESICC ne(w Ih Am ngikrdni iarGutepfr ecuij) si teh imonecmn orf eemigenrmrb the P4Y05C nriohIb:tis

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  • C meieniidt
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  • F uozenloalc
  • A utec coolahl besua
  • C hrmocopnaleihl
  • E ynhrmicntyooihytrcmai/rclr
  • S undmloefsai
  • C iiofoanpclrx
  • O roezlpaem
  • M otraizloneed

  • A mrnooidae

  • atruefriGp iecuj
charcot_bouchard  Its not a cytochrome question. IK because i go t it wrong +  
waterloo  both azoles and PPI inhibit cytochrome P450. So one isn't causing the other's lack of effect. +8  
stepwarrior  Nope. Inhibiting CYP450 would enhance the effect of itraconazole, so that can't be the mechanism. +1  


submitted by alexb(47),
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I fdncoesu ledpaslomicsyyt reodsymn iwht rprymai mislsyreoboif bauesce I uhgthto -23 fo tshoe CRsB koeold lkei redaotrp lels.c utsJ liek ehwn yteh owhs an ageim ofr lbuouls phigomiedp dna rseht'e emos dwier nsoecd ipr rgouhht het /balesumamddrelr elray kgmain me tinkh ts'i otn PB evne ouhgth I n'tdo oknw ahwt eels it lwduo .be flm

whoissaad  Made the same mistake +9  
targetusmle  i thought exactly the same!! 2 cells looked like tear drop cells :/ +2  
ilovemypuppies2295  I thought there were tear drop cells too. Seemed like it should be a metaplasia then. Oh well +  
lynn  I did the same, but looking at FA19 pg 423 it says "ineffective hematopoiesis --> defects in cell maturation of nonlymphoid lineage." You can get bilobed neutrophils, or if it progressed to AML you'd see auer rods. Nothing about tear drop cells. Then on pg 406 tear drop cells would be seen in myelofibrosis, and possibly thalassemias +  
waterloo  I thought the same, but I think that would be myelofibrosis, not myelodysplastic. Hb is really high here too. Pretty tricky for them to put that there, easy knee jerk. +1  
jawnmeechell  Interestingly enough, agnogenic myeloid metaplasia is the old name for myelofibrosis, with "agnogenic" being synonymous with "idiopathic." (or did everyone already know this) +  


submitted by hayayah(1081),
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s'eH not gneita on.hgue

eOn fo rcoi'tslos fnoncutsi is to ercneais ioelcsgg,onsnuee yisolpli,s nad .toslopreyis

ankirin  Why wouldn't it be T3? Thyroid hormones also ↑blood sugar and break down lipids +1  
waterloo  @ankirin his symptoms aren't really specific for T3. They don't mention tremors, exopthalmos etc. I think just in physiologic terms, you can bet cortisol is more increased. It's not a great question though imo +  
rockodude  can someone comment on why his appetite is down, per first aid 2019, page 329, cortisol increases appetite. thank you +  
lifeisruff  his daughter isnt there to bring him groceries +  
medstudent22  T3 levels decrease in states of starvation in an attempt to preserve energy. T3 is incredibly metabolically potent - even more so than T4. By decreasing peripheral conversion of T4 to T3 (ie decreasing T3 levels), you are decreasing metabolic activity in "unnecessary tissues", decreasing ATP use, and increasing overall energy availability for necessary tissues (brain). On a side note, rT3 levels may increase but this is not metabolically active and will not be measured as an elevation of T3. Dr. Ryan had a great explanation of this in one of his thyroid videos. https://pubmed.ncbi.nlm.nih.gov/12055988/ +  


submitted by nala_ula(113),
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Teh lohigosty is of ecytospesrh lmsal( hilscepar lselc o/w latencr paol.rl) aeHedirytr ycihspoeorsts is due ot efedtc in nspoeirt itecgnnrait thiw RCB eamemnbr eoenslkt dan mpasla eammenbr nark(nyi, bdan 3, ointpre 4,2. ste)rpinc. Msloty mosaoatlu itomndna nhtirneciae so( ozgeueotsryh uanoittm senic uoy olyn eedn eno tantmu lleela ot gte eth edse)as.i

wuagbe  To add to this: homozygous HS presents with hemolysis even in absence of stressors. this patient is only presenting with pale skin, and there are no schistocytes on the peripheral smear, so it's a heterozygous ankyrin mutation. +8  
pg32  I wanted to pick hereditary spherocytosis but the mean corpuscular concentration was normal and I thought it was supposed to be elevated? Also, why are there so many RBCs that are way bigger than the spherocytes? +6  
nephroguy  I'm assuming that the MCC is normal because the patient is heterozygous for HS. Not sure if this is correct, but that was my thought process +1  
draykid  Are there any papers that explain the difference in expression of homozygous vs heterozygous HS? +20  
waterloo  I don't know if that matters as much, like the phenotype difference of homozygous or heterozygous for this question. Since you only need one allele to show this, play odds. Is he more likely to have AA or Aa. That was my thought process. Also if you see spherocytes you'd be going for ankyrin right, not B-globin bc that should be target cells - regardless of MCHC. +1  
alimd  as I remember AD are always heterzygous. Because homozygous are always lethal. +4  


submitted by castlblack(56),

I have read all the comments, but none explain why hyponatremia is wrong. There is definitely Na+ in stool....thats why sugar+salt is rehydration for peds diarrheal sickness. Low Na+ causes low EVV explaining the low BP, high HR, pallor, and dehydration. Is it correct but just not as correct as C?

waterloo  I Dont know what you mean by low EVV. But here's my thought process. This pt lost lots of water, and when someone takes a laxative causing them to have diarrhea that will lead to metabolic acidosis. A buffering mechanism for the decreased bicarb in the blood is for H+ to leave cells and K+ to go into the cells. So he has to have hypokalemia (low K+ in serum). They gave him IV fluids, so his BP should be headed back to normal. I would think his RAAS will chill out. But it takes time to correct the acidosis, you're kidney won't just immediately stop reabs bicarb so you're body will still be buffering against the acidosis (H+ out of cell, K+ in). +  
waterloo  sorry, I wrote increased bicarb, I meant DECREASED bicarb in the blood. And also should have written "you're kidney won't just immediately START reabs new bicarb" My Bad, wasn't trying to add to confusion. +  
drdoom  i think by `EVV` author meant `ECV` (extracellular volume). @waterloo, appreciate the explanation but think something is off: loss of HCO3- via diarrhea should result in acidemia, which would oppose the presumption of ‌``H+ leaving cell, K+ going in´´. +  
waterloo  hey so sorry, I must have been super tired posting this. Can't believe I made so many mistakes. Read over it again, and it sounds like gibberish. Wish there was a way to delete. My bad. +  
waterloo  I think I tried to explain too hard. Looking at this question again, I think really the only this is when you lose that much volume, you lose bicarb and K+. Nothing really to do with acid-base. My b. +  
drdoom  no worries! +  
castlblack  EVV = effective vascular volume. Thank you for trying to help but I still don't understand. I still agree with my above mechanism as correct. Whether or not it's most correct idk. +  
amy  what about the long steamy bath? He also sweat a lot, and profuse sweating is going to cause hyponatremia? +  


submitted by castlblack(56),

I have read all the comments, but none explain why hyponatremia is wrong. There is definitely Na+ in stool....thats why sugar+salt is rehydration for peds diarrheal sickness. Low Na+ causes low EVV explaining the low BP, high HR, pallor, and dehydration. Is it correct but just not as correct as C?

waterloo  I Dont know what you mean by low EVV. But here's my thought process. This pt lost lots of water, and when someone takes a laxative causing them to have diarrhea that will lead to metabolic acidosis. A buffering mechanism for the decreased bicarb in the blood is for H+ to leave cells and K+ to go into the cells. So he has to have hypokalemia (low K+ in serum). They gave him IV fluids, so his BP should be headed back to normal. I would think his RAAS will chill out. But it takes time to correct the acidosis, you're kidney won't just immediately stop reabs bicarb so you're body will still be buffering against the acidosis (H+ out of cell, K+ in). +  
waterloo  sorry, I wrote increased bicarb, I meant DECREASED bicarb in the blood. And also should have written "you're kidney won't just immediately START reabs new bicarb" My Bad, wasn't trying to add to confusion. +  
drdoom  i think by `EVV` author meant `ECV` (extracellular volume). @waterloo, appreciate the explanation but think something is off: loss of HCO3- via diarrhea should result in acidemia, which would oppose the presumption of ‌``H+ leaving cell, K+ going in´´. +  
waterloo  hey so sorry, I must have been super tired posting this. Can't believe I made so many mistakes. Read over it again, and it sounds like gibberish. Wish there was a way to delete. My bad. +  
waterloo  I think I tried to explain too hard. Looking at this question again, I think really the only this is when you lose that much volume, you lose bicarb and K+. Nothing really to do with acid-base. My b. +  
drdoom  no worries! +  
castlblack  EVV = effective vascular volume. Thank you for trying to help but I still don't understand. I still agree with my above mechanism as correct. Whether or not it's most correct idk. +  
amy  what about the long steamy bath? He also sweat a lot, and profuse sweating is going to cause hyponatremia? +  


submitted by drmohandes(103),
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  • DI,C eiklyun:l PTT/PT mronl;a owt'dlnu jstu ees gum nebidlge
  • :hepsrpiynlmse wludo suace imnaea
  • iron niceyefd:ci ainmea
  • itmnaiv C feic:idnecy ld'nowtu seuac naoyotrhbiepoctm
  • onv nlarbielWd da:eeiss diexm ttoeeunltiapclaalog/ osdrrdei → ouwld acesu edep tnioj endligeb tdsneia fo uascolm mnabmere bignee.ld etnIrdeih auomAslt(o ainnD,mot) odluw ees pystmoms ereb.of PTT anc be o/rnlmihgha.
beto  Bleeding symptoms in von Willebrand disease tend to occur in mucous membranes. deep joint bleeding is rare +4  
castlblack  New onset bleeding? Immediately rule out vWD! +  
waterloo  Vit C def I thought was super tricky. My knee jerk reaction was oh easy bruising, bleeding from gums that's what it has to be. But yeah, I think low platelet is key here. +  
nafilnaf  Platelet count would be normal in vWD because there's nothing wrong with the platelets themselves. +1  


submitted by dr.xx(153),
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heT smto cmonmo and eveesr mrfo of alamousot midntnoa ctylspyoic iydekn seadise (AK)DDP elrsstu omfr muotaitsn in K1PD, eicdognn pcy1ntiolsy- )1.PC(.

4tst8iM..o/Pmarp.9Cis4n:4pwg///.nhl/l/cewvtwnb38micch

yotsubato  Here we thank FA for failing us yet again. Giving us PKD1, but not polycystin. I got the question right but I just guessed it because nothing else made sense. +14  
usmleuser007  Autosomal dominant polycystic kidney disease 1) occurs in patients with mutations in the gene (PKD1) encoding polycystin-1 (PC1). 2) PC1 is a complex polytopic membrane protein expressed in cilia that undergoes autoproteolytic cleavage at a G protein–coupled receptor proteolytic site (GPS). 3) A quarter of PKD1 mutations are missense variants, though it is not clear how these mutations promote disease. 4) GPS cleavage is required for PC1 trafficking to cilia. 5) A common feature among a subset of pathogenic missense mutations is a resulting failure of PC1 to traffic to cilia regardless of GPS cleavage. 6) Missense mutation in the gene encoding polycystin-2 (PC2) that prevented this protein from properly trafficking to cilia.  +2  
waterloo  yotsubo - the book is already so thicc. I think you made a great point tho, nothing else made sense. Sometimes you can't know everything on the test, but you can still play the game. +1  


submitted by hello(317),
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hTeer has ot eb a rteetb lienoatapxn rof why APN is gwnr?o

waterloo  If this pt's ANP/BNP were causing him to become hyponatremic, why does he have fluid overload symptoms (bilateral crackles, JVD, high BP)? There has to be something else overcoming the ANP system. +  


submitted by castlblack(56),

I have read all the comments, but none explain why hyponatremia is wrong. There is definitely Na+ in stool....thats why sugar+salt is rehydration for peds diarrheal sickness. Low Na+ causes low EVV explaining the low BP, high HR, pallor, and dehydration. Is it correct but just not as correct as C?

waterloo  I Dont know what you mean by low EVV. But here's my thought process. This pt lost lots of water, and when someone takes a laxative causing them to have diarrhea that will lead to metabolic acidosis. A buffering mechanism for the decreased bicarb in the blood is for H+ to leave cells and K+ to go into the cells. So he has to have hypokalemia (low K+ in serum). They gave him IV fluids, so his BP should be headed back to normal. I would think his RAAS will chill out. But it takes time to correct the acidosis, you're kidney won't just immediately stop reabs bicarb so you're body will still be buffering against the acidosis (H+ out of cell, K+ in). +  
waterloo  sorry, I wrote increased bicarb, I meant DECREASED bicarb in the blood. And also should have written "you're kidney won't just immediately START reabs new bicarb" My Bad, wasn't trying to add to confusion. +  
drdoom  i think by `EVV` author meant `ECV` (extracellular volume). @waterloo, appreciate the explanation but think something is off: loss of HCO3- via diarrhea should result in acidemia, which would oppose the presumption of ‌``H+ leaving cell, K+ going in´´. +  
waterloo  hey so sorry, I must have been super tired posting this. Can't believe I made so many mistakes. Read over it again, and it sounds like gibberish. Wish there was a way to delete. My bad. +  
waterloo  I think I tried to explain too hard. Looking at this question again, I think really the only this is when you lose that much volume, you lose bicarb and K+. Nothing really to do with acid-base. My b. +  
drdoom  no worries! +  
castlblack  EVV = effective vascular volume. Thank you for trying to help but I still don't understand. I still agree with my above mechanism as correct. Whether or not it's most correct idk. +  
amy  what about the long steamy bath? He also sweat a lot, and profuse sweating is going to cause hyponatremia? +  


submitted by castlblack(56),

I have read all the comments, but none explain why hyponatremia is wrong. There is definitely Na+ in stool....thats why sugar+salt is rehydration for peds diarrheal sickness. Low Na+ causes low EVV explaining the low BP, high HR, pallor, and dehydration. Is it correct but just not as correct as C?

waterloo  I Dont know what you mean by low EVV. But here's my thought process. This pt lost lots of water, and when someone takes a laxative causing them to have diarrhea that will lead to metabolic acidosis. A buffering mechanism for the decreased bicarb in the blood is for H+ to leave cells and K+ to go into the cells. So he has to have hypokalemia (low K+ in serum). They gave him IV fluids, so his BP should be headed back to normal. I would think his RAAS will chill out. But it takes time to correct the acidosis, you're kidney won't just immediately stop reabs bicarb so you're body will still be buffering against the acidosis (H+ out of cell, K+ in). +  
waterloo  sorry, I wrote increased bicarb, I meant DECREASED bicarb in the blood. And also should have written "you're kidney won't just immediately START reabs new bicarb" My Bad, wasn't trying to add to confusion. +  
drdoom  i think by `EVV` author meant `ECV` (extracellular volume). @waterloo, appreciate the explanation but think something is off: loss of HCO3- via diarrhea should result in acidemia, which would oppose the presumption of ‌``H+ leaving cell, K+ going in´´. +  
waterloo  hey so sorry, I must have been super tired posting this. Can't believe I made so many mistakes. Read over it again, and it sounds like gibberish. Wish there was a way to delete. My bad. +  
waterloo  I think I tried to explain too hard. Looking at this question again, I think really the only this is when you lose that much volume, you lose bicarb and K+. Nothing really to do with acid-base. My b. +  
drdoom  no worries! +  
castlblack  EVV = effective vascular volume. Thank you for trying to help but I still don't understand. I still agree with my above mechanism as correct. Whether or not it's most correct idk. +  
amy  what about the long steamy bath? He also sweat a lot, and profuse sweating is going to cause hyponatremia? +  


submitted by hayayah(1081),
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Thsi si a panteit csae of putmsortap tiiydshtoir. anC erias pu ot a aeyr after verieydl nad sah ycmytploihc tt.nleiriaf

almondbreeze  FA 2019 pg 338 +1  
waterloo  Although history seems to point towards that, she has an enlarged thyroid, and in postpartum thyroiditis, thyroid usually normal in size (from FA). regardless either would have lymphocytes infiltrating. +  


submitted by armymed88(47),
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dnoWu leghian rtmlanofa imy rfo pu ilt 3 dsay tcosl,( MsPN, slr tioi)mfPraeevarco 3ydas lti esw-ek garuioalnnt ,stiues enw v,lesses nwe p,ihteemlui aicornctnot r(pirae nad enonreetirg)a el oedmR w1k itl 6-m cpaleer glaecoln III ithw ,I rcsaieen stgnhrte pu( ot 0-706% inirgalo thernstg iplsoseb)

john055  it looks like the patient has new onset erythema which points to infection and I think neutrophils make sense. I myself have marked angiogenesis but I did it offline. Is angiogenesis the right answer ? +1  
almondbreeze  yup +  
almondbreeze  according to FA 2019 pg217, neutrophil is present during inflammatory phase- i.e. only up to 3d after the wound. After that we have the proliferative phase with granulation tiss. and angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction (involved cells: fibroblasts, myofibroblasts, endothelial cells, keratinocytes, mf) +  
mitchell_to_lakers  why not fibrosis? +  
waterloo  mitchell_to_lakers They are asking why is the incision erythematous and slightly warm. When someone is red, Dr. Sattar says that's because blood is going there. Fibrosis isn't a mechanism where someone's tissue will appear red and warm, it's collagen deposition. +4  
juanca10  Very good! +  
srmtn  is not infected, is healing. normally when healing is a little warm and erythematous because of angiogenesis. +1  


submitted by seagull(1583),
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Wihch of teh iwnolfgol aesrnos is why tsih siequnot is lul?b

1) iUsng eht orwd lc"cci"y dstanei of ilccitrcy orf ryctlai

2) nwnKgoi lla of eipyiegmolod fo lal sdugr

)3 ahigvn ot aosnre out taht elicnitoranchgi stceeff era rpbyloba hte sortw evor pahl1a or 1H ceefstf to no ecayntri.t

4) Teh cipnlgirp eedspirosn fo uygtdisn orf aow-dyskeet-s on edn ot apbryblo do agareev on hte e.tst

nlkrueger  yo, re-fucking-tweet +21  
aesalmon  I agree, I picked H1 because such a common complaint for those on TCAs is Sedation, I figure it might be so commonly seen as to be the "most common" reason for noncompliance. I suppose the "hot as a hare...etc" effects would be more severe/annoying, but I didn't think they were more common. +4  
fcambridge  I just like to pretend that there's a reason this question is now in an NBME and no longer being used for the test. Hopefully they realized the idiocy of this question like we all do +1  
link981  Since it said cyclic, I thought of using, discontinuing, then using again. These people who write these questions need take some English writing courses so they can write with CLARITY. Cyclic is not the same as Tricyclic. +5  
waterloo  Incredibly awful question. one thought I did have when deciding between anticholinergic and antihistaminic - nortriptyline and desipramine are secondary amines that have less anti-cholinergic effects (from Sketchy Pharm) so maybe that's what they were getting at? That someone went out and made a new TCA drug that would have less anticholinergic effects. +  
victor_abdullatif  This isn't testing drug epidemiology; it's actually asking "which of these side effects are caused by TCAs and would be the worst to experience?" +  
tekkenman101  "worst to experience" is incredibly subjective lmao. +  


submitted by niboonsh(360),
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tr-iCyCliC entrtpissdeane - atni C lheg,irinoc C tan dnast up a1( b,ck)ol C ridiaxootc rlonpo(g tq yb sinsgem w an hlseannc)

waterloo  that's cool and all but there are so many side affects when it comes to TCAs. H1 antagonism, reduced libido, convulsions. +  


submitted by bking(2),

I understand the edema is from decreased protein- why is Starvation Ketosis wrong? Couldn't his proteins be degraded through this process: Protein--Amino acids-- Acetyl CoA-- Ketones

waterloo  negative nitrogen balance better explains the edema. +  
courtney  I might be totally wrong but I don't think you can technically be in ketosis if you have glucose around and in this case, the patient eats only carbs +1  


submitted by hopsalong(25),
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iThs qnsoietu egts at tewhhre or ont oyu nac rneizoegc suTs'oearsu Sgin ro vketshC'os gSni ni ndik of an unasluu .rneotpeatins laylsBcai ouy etg smucel ttwscihe ni the tgstnei of eiycmaHlcopa. eopmHyxia hruftre aeaxretbecs eth gsni and anc uscea titechsw anrldymo othuurotgh hte y.obd

e'hssoktCv iSgn si aiptnpg on the lafaic erenv fo het ceaf tath isitlilc a acafli cumsel smap.s

suoursT'ase nSgi si nhew uoy tpu a lobdo reesrpus ffcu no a ettapni. isTh secuas slelc ni teh rma to nto vrieeec odbol >-; oN 2O -g&t; No xeatdivio npoptroshihaoyl ;-> casderee ni ATP vbaelliaa t-;g& N+aK/+ pmup ailfs hwutoit TPA &g-t; eecndsraI nilreaarultcl aN+ gt-&; sIdnrecae C+a sbuceea of rdseicnae +a/a+N2C creheaxgn &-;gt esecerdda USEMR a2C+ g;t&- loxeFni of h.dan

ursas'osueT giSn si oemr ssiinveet for a,epiclcoyHam ubt boht rea .sdiaticgon etrOh tsip in hits tsiqenou - ggTniiln rnauod teh humo,t snha,d and eetf can eb ronheta ings fo ccieapyaoH.lm otBh enlirezgeda niil-onotccc ro cfaol romto euezisrs acn cocru iwth eahloccaimyp.

waterloo  Something that could help. Gabapentin is a narrow spectrum anti-epileptic drug used to treat seizures. It blocks voltage gated Calcium channels. It also treats neuropathic pain (which this vignette hints at both). My thinking for this question: the patient is having seizures so must be sodium abnormality. But then they mention the pins and needles and involuntary contractions, and this being the first seizure, it sounded less like a sodium issue and more so Calcium. I think what hopsalong said makes a lot of sense. I think there is a pharm angle this question could have taken as well. +2  


submitted by drzed(221),

Unfortunately, I chose (C) thinking that the down-regulation of receptors would lead to needing higher doses for efficacy (patient is using a patient controlled pump), however tolerance to miosis does not develop, and thus eventually this side effect would occur.

Could anyone point out where my train of thought is incorrect? I suspect that my assumption of the patient increasing their dose is not warranted?

aag  I also chose this, @drzed but looking back, if there was down-regulation of the receptors then she wouldnt have enough receptors to cause altered mental status and respiratory depression, side effects that you do develop tolerance to. How I would have remembered that morphine is metabolized to other active metabolites is beyond me. Happy studying hope this helps. +1  
waterloo  He's also on a controlled analgesic pump. I've been on one before, and basically you can't keep pumping yourself constantly with it. You can hit the button, get a small dose, and then have to wait a bit of time to hit it again. The next time you hit the effect (at least for me) was always the same meaning I wasn't becoming tolerant to it (I was on one for a week). This controlled pump phrase has come up in another exam, which makes me think when they say that they want you to think this isn't someone who's taking alot of meds all the time. I also like aag thought process. +  


submitted by seagull(1583),
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tou fo itu,icryso ohw may lopeep wenk hi?ts todn( be syh to say uoy idd ro i?ntdd)

yM ptveory cdioetaun dn'dti ngianri hsti ni .em

johnthurtjr  I did not +3  
nlkrueger  i did not lol +  
ht3  you're definitely not alone lol +  
yotsubato  no idea +  
yotsubato  And its not in FA, so fuck it IMO +1  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +14  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +27  
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +1  
jaxx  Not a clue. This was so random. +  
ls3076  no way +  
hyperfukus  no clue +  
mkreamy  this made me feel a lot better. also, no fucking clue +1  
amirmullick3  My immediate thought after reading this was "why would i know this and how does this make me a better doctor?" +8  
mrglass  Generally speaking Glutamine is often used to aminate things. Think brain nitrogen metabolism. You know that F-6-P isn't an amine, and that Glucosamine is, so Glutamine isn't an unrealistic guess. +4  
djtallahassee  yea, I mature 30k anki cards to see this bs +4  
taediggity  I literally shouted wtf in quiet library at this question. +1  
bend_nbme_over  Lol def didn't know it. Looks like I'm not going to be a competent doctor because I don't know the hexosamine pathway lol +21  
drschmoctor  Is it biochemistry? Then I do not know it. +5  
snoochi95  hell no brother +1  
roro17  I didn’t +  
bodanese  I did not +  
hatethisshit  nope +  
jesusisking  I Ctrl+F'd glucosamine in FA and it's not even there lol +  
batmane  i definitely guessed, for some reason got it down to arginine and glutamine +2  
waterloo  Nope. +  
monique  I did not +  
issamd1221  didnt +  
baja_blast  Narrowed it down to Arginine and Glutamine figuring the Nitrogen would have to come from one of these two but of course I picked the wrong one. Classic. +1  
amy  +1 no idea! +  
mumenrider4ever  Had no idea what glucosamine was +  
feeeeeever  Ahhh yes the classic Glucosamine from fructose 6-phosphate question....Missed this question harder than the Misoprostol missed swing +1  
surfacegomd  no clue +  
schep  no idea. i could only safely eliminate carbamoyl phosphate because that's urea cycle +  
kernicteruscandycorn  NOPE! +  
chediakhigashi  nurp +  
kidokick  just adding in to say, nope. +  
flvent2120  Lol I didn't either. I think this is just critical thinking though. The amine has to come from somewhere. Glutamine/glutamate is known to transfer amines at the least +1  


submitted by link981(163),
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Per Aiemncra Lnug nsoaicti:oAs mBpranuhoooylcrn saialpdys )B(PD si a rofm of ioccnrh nulg seeidsa ahtt eftacsf sonbrwen ytls(om rmpua)tere dan tnnisaf. tI sesrtul rfom aegdam ot eth nlgus deucas by micnaahecl tiviaonnlte rioarre)t(sp nda gnrmetol- esu fo x.oegyn tMos inafstn recover omfr ,PBD tbu meso mya ehva mtlne-rgo nirabtehg yciftdif.lu + alrPruetemy onrb nftsnai vhae evry ewf niyt air cssa (lleaio)v at i.brth heT ollvaie atth rea senpetr tedn to not eb mtreua gneuho to tnicoufn onr,alm nda het fnitna reesiruq istrpareyro ptpsuro ot hee.brta gohuAthl i,-nvleagfis ehtse renttteasm acn asol euacs glun demgaa

waterloo  per American Lunch Assoc... maaaaan what do I need to be to get this question right, a pulmonologist? +6  


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woH od oyu kown eh ash na cedaciteanrr annuliig haiern nad ont clefa icinpm?oat

sattanki  So as far as I understand, you don’t really get a bulging, defined abdominal mass with fecal impaction. Much more likely to see this with a hernia. +8  
xxabi  Fecal impaction can be palpated in the abdomen, since it'd be accumulating in the rectum and colon, not the groin. Hope that helps! +14  
pseudorosette  a little late but they also mention that the mass had bowel sounds hence it was an incarcerated bowel! :) +6  
waterloo  question said right groin, so idk, didn't think fecal impaction would be that low. + the bowel sounds made me think there is something at the groin that can make bowel sounds? --> Hernia. +1  
thisshouldbefree  think in 3D. mass in right groin. in my head thats very low down below the belt line. i thought if its fecal impaction it would be on the left groin. next they hear bowel sounds over this mass in the right; if it was impaction right there i dont think youll be hearing anything, therefore the bowel loop is over there and is not impacted and thats what they hear. +1