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Welcome to peridot’s page.
Contributor score: 67


Comments ...

 +6  (nbme24#20)

Paraxial mesoderm means mesoderm surrounding the axis, aka the neural tube. They eventually form a pair of somites on either side. Somites then differentiate into:

  • sclerotomes -> vertebrae, rib cage, occipital bone (part)
  • myotomes -> skeletal muscle of the back, ribs, limbs
  • syndetomes -> cartilage, tendons
  • dermatomes -> skin of the back

Source

In this case, the patient is lacking spinous processes on top of having spina bifida. Maybe you were thinking spina bifida = neuropore defect, but what does this have to do with sclerotomes? This is what I found:

"Failure of closure of the caudal neuropore during embryogenesis will lead to spina bifida. This condition is always marked by a local lack of osteogenesis, or bone growth. The reason is that the correct differentiation and placement of underlying tissues (the spinal chord and spinal nerves and associated tissues) induce the osteogenesis, even small flaws in the underlying tissues can lead to a problem in the formation of the spine (vertebrae)." Source

So I'm guessing that when the question asks for "cause of the defect" they are talking about the vertebrae, not exactly the cause of spina bifida, which would be failure of neuropores to fuse. If that was an answer choice then def pick that, but the lack of vertebrae is due to lack of sclerotome fusion (because spina bifida could not induce it properly).


 +10  (nbme24#23)

In case anyone else was wondering about the other choices:

A: Acetyl-CoA carboxylase is the first committed step in fatty acid synthesis

B: Homocysteine methyltransferase turns homocysteine into methionine (we can deduce this from knowledge about homocystinuria)

C: Methionine adenosyltransferase makes SAM. SAM has two roles that we know of - one in turning methionine back into homocysteine, and one turning norepinephrine into epinephrine. This could make it a tempting choice but at the time I just saw the word 'methionine' and thought that couldn't have anything to do with cortisol/catecholamines.

D: LOL for methylmalonyl-CoA racemase, wiki says "It is routinely and incorrectly labeled as 'methylmalonyl-CoA racemase'. It is not a racemase because the CoA moiety has 5 other stereocenters." Good job NBME. Anyway, methylmalonyl-CoA epimerase is involved in the same catabolic pathway that we know of through propionic acidemia, so it's involved in breakdown of fatty acids and amino acids.

jurrutia  SAM is also the methyl donor used by DNA methyltransferase (DNa methylation) +

 +3  (nbme21#15)

Here my stab at summarizing all the info. The first diagram on this website is a super helpful as well; This diagram sorta helps too.

Normally, bilirubin from the blood stream is conjugated in the liver to a water-soluble form. This gets mixed with bile to be excreted through the intestines. In the small intestine, it becomes urobilinogen, some of which is excreted by the kidneys, giving pee that good yellow color. Some of the urobilinogen turns into stercobilin and stays in the GI to be excreted in poop, giving poop that good brown color.

In bile duct obstruction, bilirubin gets conjugated to a water-soluble form - then it's stuck. It's unable to be excreted into the intestines, unable to turn into urobilinogen or stercobilin, etc. Conjugated bilirubin builds up in the liver, and eventually gets backed up back into the blood stream where it came from. Since it's water-soluble and floating around in circulation, it eventually gets filtered by the kidneys and ends up in pee. Bilirubin is darker in color, so the pee would be dark. However, the stool would be pale since no stercobilin was made. I believe that symptoms of itchy skin also occurs in these cases as bile salts back up and are deposited in skin.

Hemolysis is not the correct answer because most of the bilirubin is not yet conjugated, so it's not water-soluble and doesn't end up in the kidneys.


 +1  (nbme21#41)

SPOILER ALERT!!

Do not read ahead if you have not taken NBME 22!!!


I'm smh at this question because in NBME 22, they describe a scenario in which loperamide caused CNS effects - particularly ventilatory depression and we were supposed to know that it was loperamide. I guess this question specified "little to no" rather than "none at all" but come ON, I'm annoyed that we have to separate such nitpicky detail when one question emphasizes its lack of CNS effects, then they turn around and test us on an exception of this exact same content. /end rant

This was not very informative at all, I just wanted to consolidate a similar question that I knew I had just seen but it turned into me just being angry I'm sorry.


 +4  (nbme21#8)

I am for some reason learning about this for the first time so I'll write a bit about euthyroid sick syndrome in case it helps someone.

It's a disease of exclusion - the thyroid hormones are whack but the thyroid gland itself seems to be totally fine. Specifically, T3 levels are low, rT3 is high (the activity of different deiodinases are off, so rT3 is made more and degraded less, though it doesn't seem like the rT3 level has any other clinical implications). As the other comments have mentioned, TSH and T4 are typically normal, although they can be decreased as well in severe cases.

Euthyroid sick syndrome is typically due to an underlying critical illness or starvation - the body stops making the hormones as an extreme measure to save energy and resources. The treatment is to treat the underlying illness; thyroid hormone therapy is not recommended as its effectiveness is inconclusive.

In this question stem, the patient has an underlying illness. Her thyroid gland works fine (responds appropriately to TSH). Classic case of euthyroid sick syndrome.

Given that her T4 levels are normal, we can rule out B, D, and E. I'm a dumdum and put C because I had no idea what euthyroid sick syndrome was. But given that her TSH level is also normal, it's not an issue with the hypothalamus or pituitary gland.

(Sources: wiki page and this article)

schep  Thanks! I, too, am hearing about this for the first time +

 +6  (nbme21#34)

Here is my summary of the picture/video that was posted:

There are 3 pathways involved in peeing:

  1. Pelvic n. (aka pelvic splanchnic n.) sends parasympathetic fibers to deltrusor to contract --> squeeze bladder and pee.

  2. Hypogastric n. sends sympathetic fibers to the deltrusor to relax, as well as the internal sphincter to contract --> hold back pee

  3. Pudendal n. sends somatic fibers (under conscious control) to the external sphincter to contract --> hold back pee

In this question, the patient's bladder is filling up so much that it's forced to overflow. That means there is a problem with scenario 1 - damage to pelvic n. so that he can't squeeze his bladder even when it's super full.

peridot  To clarify, this description is meant to go along with @hungrybox's pic link and @eacv's video link +4
lovebug  thanks a lot! +

 +0  (nbme22#22)

While I understand why it's hyperplastic arteriosclerosis and how it classically occurs with HTN, I was wondering why it couldn't be berry aneurysm? Is it because the question is asking which is "most likely", making C the better answer? Thank you.

mannan  Berry Aneurysm is not CAUSED by HTN. It's caused by weakening of the arterial wall (at bifurcations). Hypertensive disease exacerbates them and causes the clinical picture of SAH (worst headache of life) when they rupture. Hope that helps -- Reference: FA CNS pathology, aneurysms. +1
usmleboy  Actually according to Goljan this is incorrect. Berry aneurysms are caused by hypertension. The weakening of the wall (no tunica media) at bifurcations is inherent in human anatomy. Basically you have to have elevated BP to cause the dilation, outside of the inherited connective tissue disorders. Hence why PKD has the berry association. However, these aneurysms present with extremely prolonged HTN, whereas our guy in this Q only has a 1 year history. The key to answering this question is recognizing that this is MALIGNANT hypertension that is relatively acute in onset. Malignant HTN = hyperplastic arteriolosclerosis (onion rings). +1




Subcomments ...

submitted by b1ackcoffee(44),

from @melchior

From the UW ID 666 explanation, although type II pneumocytes normally differentiate into type I pneumocytes after proliferation, they do not differentiate in idiopathic pulmonary fibrosis due to altered cell signals and altered basement membrane, which is why type II pneumocytes are increased.

explanation by @benwhite_dotcom is incorrect

peridot  The UWorld example is talking about idiopathic pulmonary fibrosis, whereas benwhite_dotcom was talking about chronic inflammatory pneumonitis, which presents with increased type II pneumocytes (as indicated by the correct answer). +  
topgunber  either way destruction of basement membrane leads to type II hyperplasia. It may leads to fibrosis because of destruction of the basement membrane (the point of no return for lung parenchyma). Type I pneumoyctes will not rise in number because the destruction in the basement membrane (they are the vast majority of cells covering alveoli) +  


Damn everyone out here looking at the eyes when my dumbass was thinking the girl was missing a nasal bridge or something lol fml

peridot  That is straight up what I wrote: "low nasal bridge???" I was like is this part of some congenital defect +  


submitted by colonelred_(105),
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hTe synsliaa oynl ewhsdo a nuimotat ni oen llel.ae CF is an uotalosma iecrsevse sidase:e hte esiasde ylno nfsiamest if rethe rea itmnaosut in both lleelas of hte TFCR ge.en

fI uyo iltsl eahv 1 ilocfntaun cypo fo hte CFTR gnee, yuo anc tlsil akem teh TCFR pnortei eht( hloeridc ha)rosrprcnttae,/enln ehcne ryou yobd wnt’o aevh nya sises.u

Tsih is uoaalsngo ot ruomt pprsssuroe egnes elik bR: so nglo as neo fo teh llaeles ouy avhe is ,toiclaufnn you nca kmea nghoue of teh iretpon ot “amke u”p rof het vdefieetc a.eelll If bhot etg kckedno tuo ),--(Rb/ oyu osel teh ocioetrnpt eddrvpio yb teh eegn seecuab won ouy eamk on opertin ta .all

eTh lnoy thgni atht aedm sesne for hist iteqonsu wsa het ctaf tath het treho lealle asw ton nieuldcd ni het .salsiayn

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. +38  
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 ?? +9  
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 +3  
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  


submitted by lsmarshall(415),
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CHM lscsa 1 deptipe ngentia cesgniprso ;gt& n"gitAen ietdespp ldedao onot CMH I ni RER feart veiydelr via PAT rsrnoapr(ett sestiacdoa wthi eganint "escgsopri)n - iFrts diA 90.12

Bera yehmtcoypl msodyner eypt 2 SLB( I;I enffcgtai HCM )II si deu ot unamtosti in eensg hatt doce orf cttisroaipnrn crsofta tath ynmralol leegruta eht nreissepox gee(n arntoipnci)rst of the CHM II e.snge Bear chyleyptmo yrodmesn pyte 1 LB(S I; gaciftfne HMC )I, si much emro ,rare dan is socateaids thiw ATP ins.dfeciciee

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


submitted by andro(188),

ATN ( Acute Tubular necrosis ) may be either ischemic or nephrotoxic:

  • Ischemic - tends to affect the Proximal straight segment PST and the TAL ( thick ascending limb)

*Toxic - tends to affect the PCT ( convoluted segment )

peridot  this is on p.591 of FA 2019 for anyone interested +1  


submitted by neonem(568),
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ndsliyosmcioAge ear cthni;ooxrpe ocenhipotxr cumh/sgaerlidcs sueca atecu ltbauru corssnei AT(),N deriaahzcetcr yb edgmaa to teh PCT. TNA euscas hte oinofatrm fo ,nbowr umd,dy ugrranal sctsa ni hte .reiun The ctaf ahtt siht ainptet is a ciagueldiprq gthmi eb sgtenuigsg htta heyt heav a wrole vemolu of itdoiitnrsbu rof the gdru dna( hotreerfe hgeirh oldbo eraoscni.ntonct)

mtkilimanjaro  I would also like to add ATN is nephrotoxic ischemia and the two places in the tubule that are susceptible are the PCT (proximal straight part) and the thick ascending limb. The TAL is not labeled as a choice so that is why it has to be B (and why B is a little further down from the convoluted part) +2  
mtkilimanjaro  Actually aminoglycosides might only affect the PCT idk :( +1  
peridot  on p. 591 of FA 2019, it talks about ATN. The two types are 1. ischemic - affects PCT and thick ascending limb because those two areas use ATP the most (think of all the ion pumps) and 2. nephrotoxic - PCT only (I think of it as that's the first part, so it's most exposed to toxins). Aminoglycosides fall under scenario 2. +2  
cassdawg  If you wanna see nephrotoxic drugs in one place, here's an image with the locations of different nephrotoxic drugs: https://media.springernature.com/lw685/springer-static/image/art%3A10.1038%2Fs41581-018-0003-9/MediaObjects/41581_2018_3_Fig1_HTML.jpg +2  
corndog  Before anyone looks at @cassdawg link, consider taking some Loperamide. +4  


submitted by andro(188),

SIADH is characterized by :

*Excessive free water retention ( less water in urine means specific gravity increases and not decreases as in option E)

*Euvolemic hyponatremia with continued urinary Na+ excretion ( and so urine Na which actually be greater than and not less than 10 mEq/L option D)

*Urine osmolality > serum osmolality ( option C)

Serum potassium does not actually decrease ( counter-intuitively ) because the excess fluid retention suppresses aldosterone secretion . The two main stimuli for potassium loss/secretion in kidneys are - aldosterone - and high urine flow rates. Both of these are decreased in SIADH ( excluding option B )

Serum urea nitrogen and creatinine are diluted , so their concentration decreases

peridot  Great explanation, thank you so much!! +1  


submitted by m-ice(339),
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nI SIAHD, hte cesievexs ADH esusca het nioecctlgl cdtu fo het nykedi to rborabse gheu mnoatsu fo awret htat it losduh lyrmlnoa ret.ecex hTat nemas that het alsmap llwi own haev mhuc orem raetw taireelv ot soutle owl( motalois)ly nda hte nreiu lwli ehav cumh rome alst irletvea to erwat eghir(h os)y.amlltoi

frijoles  So potassium does not become diluted in SIADH? +1  
ruready4this  I feel like I was overthinking this question so much for some reason!! C definitely makes the most sense but I was also wondering what would happen to potassium. Then I was thinking maybe the excess ADH would suppress aldosterone secretion and serum potassium concentration would actually be higher +1  
peridot  @frijoles Aldosterone can adjust the K+ levels: too much water --> less aldosterone --> no excretion of K+, so this helps retain the K+ to a normal level. However, less aldosterone also means --> more excretion of Na+, so the hyponatremia is not corrected. +1  


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aByb eovpeeldd SRD t-;g&- evngu 2O as Rx -g;t&- lacomntisoipc fo 2O peayhr in enneoatd = IRB (FA R29)10 = teonathpiRy of retya mprituI = nrareiarIlcntvu reo raBhgmhe = anrorloycumonpBh saaldipsy

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


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ybBa dovlpeeed SDR ->-; egvnu 2O as xR &-gt-; aiilponcotcms fo 2O eayphr in etnonead = RBI FA( )19 R02 = ypthRnetoai of typirr aemuIt = crualeratvinInr geramheo hBr = roonurpncyaolhBm syadlpias

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


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Baby opevdelde DSR -t;-g& gneuv 2O sa Rx -&t-g; oatmopccsinil fo 2O hraype in eandtneo = RBI A(F )2R01 9 = iaRnpeytoht fo iytetmrIura p = uteaacnrrvlnrIi oeargehmB rh = phmBurncrynaoool dspylsaia

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


submitted by usmleuser007(395),
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freAt soem archsree sthi si why teh herot wasresn rea c:ocerntir

lsBaa nietkocaetyr pa&;m naliam caldiu

  • eIocncrtr bc/ aamlin uldaic is a mtcnopnoe fo het eebamstn eebnmarm hwihc is fodun etwbene eth upimilethe adn rnuiegdyln cetnvinceo sieust e,.(g. dmsiipeer adn dirsme fo het .kni)s
  • tI is a yrhgluo 04 netmeorna iedw nete-lclcotreun zone nebeetw het pmlasa emrbnmea fo hte aasbl elcsl and het t-seed)r(oenecln linmaa dneas fo teh satenmeb rnbmm.aee KI(I)W
  • lbaas teyatioknrec hescttaa ot het neambset emmnerba unigs dsehomememosi

anurlrGa tnyocierkaet pam;& mttrsua orceumn

  • artSmtu umlucid ptsresaea eshet tow arl.eys
  • htree era no meeomsods ttha cectonn ehste tow asyelr
  • aeIgm rfo eeenfcrre

anmaiL licdua &p;am anLmia sndae -- iclkc fro emagi

  • bhto rea ratp of hte netbaesm maebrnme nda nto hte esipmried

eytonecMla ;a&pm lsaab iyektrcteon --- kcilc orf gimea

  • rae tohb cnteeoncd to eetorcha iav -rdihecsEna
  • it si olrpabby eht aedgam to hist ecocntoinn hatt
azibird  The stratum lucidum is only present in the thick skin of the palms, soles, and digits. So the stratum granulosum and corneum do touch in most of the body. I guess they just aren't connected by desmosomes. https://opentextbc.ca/anatomyandphysiology/chapter/5-1-layers-of-the-skin/ +  
peridot  Wow if I'm understanding this correct, lamina lucida (basement membrane) is not the same as stratum lucidum (between stratum corneum and stratum granulosum). That def confused me about this question bc I simultaneously was like wait isn't this in the basement membrane but also recalled the picture in FA with all the layers. Thanks so much for the super detailed explanation of all the answer choices! +1  


submitted by medstruggle(12),
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yWh is ti not ioanavr lclfioel le?cls I hguhtot eht flemea aonlga fo retlSoi nad ediLyg is aau/rgseachotln lc.les

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 temmy(129),
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hatW fo if het eraccn is a elriathlou cancer in teh draebld due to niaitarod htpay.er uwodl it ont asecu irmsail sinsg

charcot_bouchard  Chance of bilateral ureteral ca is very rare. Also preincipal r/f for transitional cell ca is Smoking not radiation +  
peridot  Hi temmy, yes it sounds like it would. There is a similar question from NBME 21 for those who have already taken that one (https://nbmeanswers.com/exam/nbme21/744). In that one, it's cancer in the uterus instead of bladder, but it's the same concept - the cancer can spread from the uterus into the bladder, or compress on the bladder, leading to bilateral hydroureter and hydronephrosis. So basically the takeaway point from that question and this question is that we learned a few things that can lead to bilateral hydronephrosis and hydroureter: 1. bladder cancer 2. uterine cancer 3. surgical and radiation treatment of cancer in that region, leading to bilateral fibrosis of the ureters. +2  
peridot  Whoop just realized that urothelial carcinoma is a possible answer choice here. Well, I'm lost.... :x +  
abcdefbhiximab  Urothelial carcinoma presents as painless hematuria with risk factors (i.e. smoking, aniline dyes) +1  
mutteringly  In addition, the wording says "distal ureteral narrowing" which wouldn't happen with bladder cancer +  


submitted by temmy(129),
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hWta of if het nrceca is a lhoturilea rcecan in teh ebardld ude ot itranaido tehra.yp uldwo ti not aceus irmisla isgns

charcot_bouchard  Chance of bilateral ureteral ca is very rare. Also preincipal r/f for transitional cell ca is Smoking not radiation +  
peridot  Hi temmy, yes it sounds like it would. There is a similar question from NBME 21 for those who have already taken that one (https://nbmeanswers.com/exam/nbme21/744). In that one, it's cancer in the uterus instead of bladder, but it's the same concept - the cancer can spread from the uterus into the bladder, or compress on the bladder, leading to bilateral hydroureter and hydronephrosis. So basically the takeaway point from that question and this question is that we learned a few things that can lead to bilateral hydronephrosis and hydroureter: 1. bladder cancer 2. uterine cancer 3. surgical and radiation treatment of cancer in that region, leading to bilateral fibrosis of the ureters. +2  
peridot  Whoop just realized that urothelial carcinoma is a possible answer choice here. Well, I'm lost.... :x +  
abcdefbhiximab  Urothelial carcinoma presents as painless hematuria with risk factors (i.e. smoking, aniline dyes) +1  
mutteringly  In addition, the wording says "distal ureteral narrowing" which wouldn't happen with bladder cancer +  


submitted by hungrybox(1026),
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opoL rstiicdeu are trsif nlei orf etuac vsetecgion taerh lure.ifa tTha shdlou hlpe oyu rebeermm ahtt eyht rae hte toms etopnt ,druetsiic so hteeyr' entof sued ni the tacue nameettrt fo deam.e

peridot  I think what threw me off was that this lady had such low GFR, figured it couldn't be right. Turns out it's still ok. Furosemide is a miracle drug!! +  


I was duped; did anybody here get it wrong because they thought about the thyroid ima artery arising from the brachiocephalic trunk? No? Just me? Okay.

peridot  Ooh that is tricky tricky. In the question stem they said they already ligated that one ("a branch of the brachiocephalic trunk") and were wondering what else needs to be ligated in addition to that. Therefore the answer is the superior thyroid artery, which is coming from the external carotid. I don't think I knew any of this when I did the question though, cause I had to google all this just now. +1  
anechakfspb  In the stem they said they ligated a branch of the thyrocervical trunk, not the brachiocephalic. According to Wiki, the thyroid ima artery (which does arise from the brachiocephalic trunk) is only present in about 3-10% of the population. Therefore, while technically this answer could be correct, external carotid is "more correct". Source: https://en.wikipedia.org/wiki/Thyroid_ima_artery +1  


submitted by whoissaad(81),
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  • Sine"c sosmpymt can naiercse ni rtvyisee rundig het ign,ht ti lcuod omebce cftiudlfi to alfl peesal or urtner to slepe freat wgkina up"

  • "RSL si eno fo lsevrea idrrssode atht nac escau oxtsneuahi dna eamitdy lse,pneessi ichwh nca gsnylrot ctaffe ood,m oeocantnicnrt, jbo dna lochso mcpferrenoa, dna onsrepla ilasietophrn.s nayM eppelo hitw LSR rrpteo eyth ear nftoe uenabl ot onaertccnet, hvea adpiemir ,remyom or afli ot oismcacphl yaldi k"ssta

  • SL"R crucso in btoh enm dna ,nwome lhhagotu enowm aer emro iylekl to ahve ti tahn .ne"m

  • t"he mmystspo patlyicyl eecbom emor nfteqreu dan ltsa eonglr hwti gea".

creS:uo ecshe-/-gsPigr-la/iEper/ht/.s.ittoStsw-nvaesaywn/ncLtoetCm:troi-rse-uhd.eesnStnDdaesovaeSieR-nrcdFset/igwtdhF

tEgvnierhy ni the mste ispnot rdtasow rsseslte egl .rnemsyod

Pusl I thuhgto uyo edne 59/ of the ISG E ACSP ot osdaengi iseesodnrp.

oeneSom paesel ilexanp :)

peridot  Though everything else fits, in order to diagnose RLS you need to actually have leg symptoms which aren't described here at all. I agree that MDD also requires a bit of a stretch bc not all of the diagnosis requirements are met which is annoying, but at least the core components are there (decreased energy, sleep disturbances, lack of concentration), whereas the core component of RLS isn't there at all. It's like wanting to diagnose someone with a migraine because they have irritability, decreased concentration, and a visual aura but the person never even said their head hurt. It's not a great question and I completely missed MDD as well, but I can kinda see now why it's MDD more so than any of the other choices so it's kind of a "but which is the BEST answer" scenario. +2  


submitted by seagull(1539),
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nngixiaEm tntaepi ofrm a strgiloou siilmpe rBenosk siBa wcihh olwdu kswe hte tpalopinou aenm of rusme aeur gnitnreo away mfro the erut tcearcua n.mae eTh,n rzeilea oieicprns is etdeepndn on ilaasitttcs ""Peowr ichhw is desieranc ebdsa no eht siez of teh oupaplniot of eth yud.st e(cdsaneir pienscroi = ecdaisner sctaiattsli pwer).o hrr,efeeTo an ircnesea in nluiaoppot fo a diaebs rogup ihtw adel ot aarnucycic twih hhgi c.irisepno

forerofore  to add up, the urologist himself doesn't add or remove accuracy (since this is a blood test), what decreases the accuracy is the fact that in order to be sent to a urologist you probably are sick in the first place (selection bias), so your urea nitrogen is likely to be altered. +23  
sharpscontainer  I thought of precision as more of a function of variance. Variance will decrease with a greater sample size. Had a hard time because I was thinking about those 4 darn targets (wouldn't 500 darts look more spread out than 10? but no, the variance will be better) that have been in my textbooks since 7th grade and for the first time I was asked a question about this concept only to discover that I didn't have it down as well as I assumed. +1  
peridot  @sharpscontainer I feel you, I thought the exact same thing. Looked into it a bit and I think it has something to do with the way standard error or standard deviation or something like that is calculated, but I'm still confused and too tired to dig further. Also, wanted to mention that this NBME has a similar question but instead it's about the 95% confidence interval - maybe that'll help you understand the precision thing better since the 95% confidence interval narrows with a larger sample size? So it's kinda tied to precision? +  


submitted by ergogenic22(320),
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hwy is amhlidepiiyper cnyrosdea ot csihgun ryednsom tno a l?yibtpoisis

hello  SIADH = MC paraneoplastic syndrome of small oat cell lung cancer. Also, Cushing syndrome would cause would weight gain, skin hyperpigmentation, and hypokalemia. Not, lyperlipidemia. +1  
charmrooftops  You do get hyperlipidemia in cushing though? https://www.amboss.com/us/knowledge/Cushing_syndrome So still unsure why this is not a possibility. Is it just a "more common" thing for SIADH? +2  
peridot  I was debating the same thing. But yeah I guess the SIADH association is just supposed to be stronger somehow and "more common"? +  


submitted by peridot(67),

Here is my summary of the picture/video that was posted:

There are 3 pathways involved in peeing:

  1. Pelvic n. (aka pelvic splanchnic n.) sends parasympathetic fibers to deltrusor to contract --> squeeze bladder and pee.

  2. Hypogastric n. sends sympathetic fibers to the deltrusor to relax, as well as the internal sphincter to contract --> hold back pee

  3. Pudendal n. sends somatic fibers (under conscious control) to the external sphincter to contract --> hold back pee

In this question, the patient's bladder is filling up so much that it's forced to overflow. That means there is a problem with scenario 1 - damage to pelvic n. so that he can't squeeze his bladder even when it's super full.

peridot  To clarify, this description is meant to go along with @hungrybox's pic link and @eacv's video link +4  
lovebug  thanks a lot! +  


submitted by chandlerbas(97),
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snrbhuoc ttusconrbio tapr s ygeoxn in eaolilv n o ngoitenr bela to trnee acopirt(eshm rai gtierenn dboy %7(8 tgerinno dna 21% ,nxygoe irntnego is so raitmnotp gnnoeitr cb it si a orlypo ordbesab sga nda sthu is ni rgdhaec of kepngie lialoev aty)dnlxo feenig ni teh ilelova is arsbdoeb onti teh bcudodirnel og het vmluoe fo the avoellaieo lvral aoplelcs rp sboionta slaeactiset

bethune  Why is pulmonary hypertension incorrect? +  
samsam3711  PEEP allows the alveoli to remain slightly open with exhalation to prevent atelectasis. Pulmonary Hypertension is going to be related to vascular changes (instead you might see shunting of blood in areas of poor ventilation) +1  
drzed  Pulmonary HTN occurs because of pulmonary vessel vasoconstriction. This can occur d/t multiple factors, but one of the most important ones is hypoxic vasoconstriction that the lungs will undergo (for example, at altitude). In the setting of PEEP, you are ventilating the lungs perfectly; this allows for the pulmonary vessels to open up and not undergo vasoconstriction. Thus, you prevent pulmonary hypertension via hypoxia. +  
peridot  @drzed by your logic, you're arguing for D to be the answer but the correct answer was about preventing atelectasis +  
medstudent  The question is what’s key. The purpose of PEEP is to keep the airway open. The purpose of ventilation with supplemental oxygen can help with preventing pulm HTN. Could be wrong, but that’s what makes sense to me. +  


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no'dt eb a kc?di tno leyarl seur thaw oemr herte is ot .ti hTe etptina otesd'n aveh nya heotr mylafi so htis maonw dushol eb sdniceeodr ifylma

aesalmon  Questions like this usually hinge on asking if you're going to follow the rules or not though, obviously the one asking her to lie and say she was her sister is wrong, but the correct answer is obviously breaking the hospice center's "policy" - presumably if the physician is sending her to hospice then they don't work there so why would the Dr. be able to just tell her its fine? +5  
hungrybox  Yeah, I got this one wrong with the same logic as you, aesalmon. +1  
emmy2k21  I genuinely interpreted this question as though the two women were in a relationship because of the quotes "my close friend". I figured significant others would be allowed to visit simply. Ha seems like I'm the only one who read too far in between the lines! +8  
dr_jan_itor  @emmy2k21 I also thought the quotes implied a lesbian relationship and that the patient was afraid to share this (they grew up at a time when it was heavily stigmatized). So i was thinking, of course you and your "special friend" can stay together. I know this is not just a phase +8  
et-tu-bromocriptine  Anything particularly wrong with A (Don't worry. I'll call you right away...")? It seemed like the most professional yet considerate answer choice. Are we supposed to imply that they're partners based on those quotation marks around "close friend"? Because otherwise it seems like too casual and less professional than A, almost as if it's breaking policy. +5  
lilmonkey  I can swear that I saw this exact same question in UWORLD before. The only reason I got it right this time. +1  
docshrek  @lilmonkey can you please give the QID for the UWorld question? +2  
jakeperalta  Can someone explain to me why following hospital policy is the wrong answer? I'm so lost.And essentially how is this option any different from the last option where he asks her to say its her sister? Both go against hospital policy. Would greatly appreciate some insight yall. +  
jakeperalta  Can someone explain to me why following hospital policy is the wrong answer? I'm so lost.And essentially how is this option any different from the last option where he asks her to say its her sister? Both go against hospital policy. Would greatly appreciate some insight yall. P.s:it struck me as a romantic relationship as well, but it doesn't clear my doubt😓😭 +1  
drschmoctor  @jakeperalta Following the hospital policy is wrong because it would be cruel and unnecessarily rigid to deny a dying woman the comfort of her closest companion. Also, It would be inappropriate to ask the Pt to lie. What's the point of becoming a doctor if you have to follow some BS corporate policy instead of calling the shots and doing right by your patients? +1  
peridot  Ya kinda dumb that usually NBME usually tells us to never break the rules, yet here it's suddenly ok. But here the reason for this exception is that while only "family" is allowed, a lesbian relationship qualifies the "friend" as family (they just were never officially acknowledged as family/married due to stigma or state laws, which society recognizes today is dumb and outdated). It's a stupid technicality that her significant other isn't allowed to visit as a family member, so while we usually never want to break rules, this scenario follows the "spirit" of the rule. Plus it's a really extreme scenario where the woman is dying and just wants to spend her last moments with her loved one and it would be too cruel to deny someone that. There is no lie involved, which kinda leaves open the chance for the situation to be cleared up if worse comes to worst. This is different from E which is a straight up lie. Hope that helped. +  


submitted by zevvyt(30),

Of all the things they can test us on, they're testing our fucking Gadar??

peridot  Don't mean to be an eager beaver but I thought it was pretty cool to get tested on our gaydar! I think that's an important thing to pick up on. As for their answer choices, I'm not always the biggest fan of those since I think there's more than one right way to do something... +1  


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nSik oedvrips ailnsontui adn npeestvr athe s.osl shiT asn'ettpi dybo lwli saotempcen ofr easrendci eatr fo etha lsos by acsnrgieni aociblemt aetr.

davidw  This is directly from Goljan I) Hypovolemic shock may occur due to loss of plasma from the burn surface (refer to Chapter 5). • Loss of protein from the plasma loss may result in generalized pitting edema. II) Infection of the wound site and sepsis may occur. (a) Sepsis due to Pseudomonas aeruginosa is the most common cause of infection in burn patients. (b) Other pathogens include methicillin-resistant S. aureus and Candida species. (3) Curling ulcers may occur in the proximal duodenum (refer to Chapter 18). (4) Hypermetabolic syndrome may occur if >40% of the body surface is burned. +12  
yex  Can someone explain why is it not increased ECF? +23  
charcot_bouchard  i picked same. Increased ECF but cant remember why. Can you explain WHY it is increased ECF? what was ur reasoning +2  
isotopes  Burns would lead to a decrease in ECF because the protection from fluid loss is absent; it can lead to shock. :) +2  
tinydoc  My reasoning behind picking ↑ ECV was that your losing fluid but not electrolytes with the burn ⇒ the ecv would have increased osmolarity, so the fluid from the ICV would be pushed the the ECV. It made sense to me at the time. I guess technically its wrong because the loss of fluids and the gain of fluids would amount to pretty much the same thing. But the insulation and heat loss thing makes sense I guess. +  
yex  Increased ECF, bc I was thinking about the edema formation.... :-/ +3  
atbangura  I picked increased ECF because burns increase the capillary permeability coefficient, but now that I am going over it I realized that increasing the permeability would only transfer plasma volume to the interstitial volume, which are both a part of the ECF so therefore ECF would not change. SMH +5  
aisel1787  thanks +  
69_nbme_420  Burns (and Diarrhea) cause ISOsmotic volume contraction; Costanzo BRS Physio +  
tiagob  in severe burned patient, also has increased fluid in third spacing or interstitial (leading EDEMA). Different extracellular space is interstitial and vascular +  
peridot  I also wanted to add, another huge job of the skin is to prevent loss of fluid. Burn patients are easily dehydrated because they've lost that barrier. This helped me lean away from increased ECV - despite the edema (from one compartment to another) as others have mentioned above, there is a loss in overall ECV due to evaporation from body. +  


submitted by usmle11a(74),
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heT dmeacli usrtqmeeneri ot oitban a tmepir vyra by tt,eas utb aer usyaull iennocfd ot ciiepcfs tysep fo sdlsteiiiiab or otincs.odin shTee as a lnaereg urle lneudic hte use fo nya vasiisste dvieec ushc sa a wehcie,alhr sctcureh, ro ,neca sa lwel as a mnsisgi elg or o.tof oSem tsates aslo cleindu icenrta csaluad,ovrairc i,npa or rryaiepostr tinsonoi.dc Auotb flah of US etssat 2()6 nudicle dliebsnsn sa a uiinafyglq ilatiisydb bnaielng eth rpnoes ot nbtiao a idalibsity gpnarik pmetir fro eus as a rnap,esegs nda 41 saetts edulnci a iddalesb adhn as a fgqlaniyui atibilsi.yd Fruo ssteat cleiudn ,afenseds nda wto ettass ngiVai(ir nad Nwe Yo)rk endcliu natlme elsnsli ro amevenopledtl taiilbiiesds as yquigaifln ledbtsiiiisa

oru ugy sesu a eacn ..os.

btw i tog it gwnor :) acsue i hthotgu ti si up ot hte VDM

usmle11a  also it is the dr who decides the eligibility then sends it to the DMV disability --> Dr --> DMV +4  
peridot  I'm not sure if I'm being here or if the test question changed, but I don't see anywhere in the stem that says that the patient uses a cane? I even ctrl+F the word "cane" lol. I picked referring to PM&R specialist for full assessment cause I figured that another pattern is to always gather more info, but I guess that's not the case here T_T +4  
azibird  It does NOT say he uses a cane. +2  
sonofarathorn  I can also confirm that there was no cane involved. I repeat, NO CANE. +5  


submitted by mousie(216),
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eClahor = ceaFl neseLao oang/liirr = gloLealna mneupo = ON orsenp ot noeprs noly by anathilnoi of biectraa dnatcotaimen /reL mewaty = ictk Me bninaoilt/ecocgic = rashgin otrysairpre adn rotaht srscinteoe (vaalsi or st.)pi leyaner,lG ti astke scole (for mpee,axl nguicgoh ro inig)kss ro lgetnhy noctatc ot seardp teseh raeatbic )FDCCSR M/( = tkci itbe

smc213  Also, when Meningococcal meningitis is treated ... close contacts are also treated prophylactically whereas the others typically are not. There's also a subunit vaccine for n. meningitis due to high infectivity rate especially in crowded establishments. +6  
dentist  So, Cholera is also p2p but Mening is more likely? +1  
usmlecharserssss  in cholera people to water => water to people +  
qball  Remember the fire sprinklers from Sketchy for M. Meningitis. as respiratory droplets are the easiest to transmit from person to person. +  
drschmoctor  but the poop water comes from people so.... +1  
llamastep1  Respiratory dropplets is easier than fecal-oral tho +1  
lowyield  Can also reason that n. meningitidis is common in college students because they live in close quarters which suggests high rate of transmission even amongst immunocompetent individuals +1  
peridot  I can see why fecal-oral can seem like person-to-person transmission. What helped me reason it was that in countries with lots of cases of cholera, the primary reason is lack of water sanitation. Even when you google cholera, you get pictures of people collecting dirty water and how the WHO is aiming to reduce cases of the disease by improving water sources. Therefore it's more of a systemic/environmental problem rather than the fact that one person accidentally touched another person's poopy parts and then transmitted it to their own mouth, making this less of a person-to-person thing, especially when compared to another answer choice such as Meningococcal meningitis. +  
bbr  To add, think of the water in cholera as a reservoir. The bug is going to hang out there between infecting another person. In meningitis it seems we are going from 1 persons saliva to another. Without much of a reservoir inbetween. (might be using the word reservoir incorrectly). +  


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eElpenovs enifebt teh urvsi ni ttha eht rvsui liwl ookl lkei the t,hos ntacfiatilig sfui.no evwe,oHr an lnvdoeeep iursv si arleyelgn ssle tbslea hatn a edkan ohderlsiaca uvsir n(ekda ueivsrs aer yaerllegn r)iahasdoce.l

docred123  So do these patients have h.Flu? What was the giveaway? Thanks +1  
mousie  I chose Enveloped simply bc it said dies when heated, not sure if there where any other clues to narrow this down or make me feel more confident in my choice but I went with it anyway +16  
eclipse  I don't think they expected us to narrow down the answer to a specific virus. Enveloped viruses tend to be less stable (?) than the non-enveloped ones and don't survive as well under harsher environments (outside human's body, heat, etc.) +2  
peridot  To add on, I also have no idea what virus this could be but the question stem does say "A previously unidentified virus is recovered from urine specimens" making me think that it's not something we're supposed to have know about, unless I'm totally understanding it wrong. +1  


submitted by lfsuarez(141),
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Aserwn E

cnnIiogra Ppusrohsoh ; dyartairohP enHmroo ; lltiCaicor

Dsaeeecrd ; ncasIeerd ; escaeeDrd

sihT tneipat si nregfisuf omrf aeclci ,seurp hwhic in stih asce ash udesca mtaiinV D aoiaopmtsnlrb nda refhoerte edeadecrs mures u.alcmic eTh odby wlli rodnesp to teh redesedac ciamulc iva oesrcitne of .HTP Thsi lilw tneh uesac ruossophhop ngtiwas to ocruc in eth xloairmp uolvodentc eub.ltu

kuhnboom  Why does Calcitriol not increase with the increased PTH? Wouldn't the increased PTH stimulate the kidneys to make more activated vitamin D. +1  
batmane  vitamin d malabsorption --> dec calcitriol +4  
peridot  @kuhnboom Yes, while PTH stimulates the kidneys to make more active vitamin D (calcitriol), you need vitamin D precursors to begin with in order to do that. If you have vitamin D malabsorption, then the activated form won't be high even with high levels of PTH. Therefore, calcitriol is decreased. +  
cbreland  Also, Vitamin D causes Ca and Phosphate absorption in the intestines. A lack of activated vitamin D would cause more Ca/Phosp wasting +  


submitted by sweetmed(143),
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coidcrAgn ot hte eNrsus' ahtelH St,udy het srik of pnmuoyrla cnrmeaoacaindo nsseeairc snbiusaalytlt tfrae a glon udtarino fo ctacoob iomsk:ng mkeossr thiw a vopeiusr onimgks tnoaiurd fo –0403 yrsea are oerm ahnt citew sa iklley to vdlpoee ulng anceamdionorac cmpadreo ot eknvsrmsor-ee vre(laiet srik of aimtrxplyeoap )4;.2 a dotniuar of mroe anht 04 sarye eacsenirs ialvrtee srik ot .]58[

isTh rcnaec lysualu si sene pehaelrilryp in het us,ngl sa eopsdpo ot lmasl ecll lgun acecrn nad aqussoum clel nglu encrc,a iwhch ohtb tdne ot eb eorm anlylrtce c0a[],ot[9d1le] otalhguh ti mya slao ruocc sa tncrael l1e0ns]io[s. oFr nnkonuw ,asorsne ti otefn easris ni oianrtel to aplrepehri gnul rssc.a ehT nrertuc ehytro is atht het csar lrbbopya cruderco naeocyrsd ot eth o,tmur hrerat anth gsnicau eth u]0[tr1o.m The norcemnaadcioa sha na seaniredc ecdneinci in msorkes, nad is the omts comonm etpy fo lnug rncaec esne ni -mkrossoenn and w.]1en[0om heT pialhererp cloiaont fo norcmaeoiadanc in the lgnus amy be ued to eth sue fo tierfls ni tgcarestei hcwih rpeenvt the galrer pltcisaer fmro nrgnteei eht afiin.nlgact[riuclo []d21eed11e]n][ eeepDr aotiainlnh fo rtgieetac mkseo rselsut in iprraehple seoslni that aer nfteo the caes ni ndooraeamsnciac fo the .glun lne,yearlG ocmnaeoidcarna rwsgo omer syllwo nad somrf rsaellm essasm than teh ehtro 0t].sb1[espyu roewvHe, it ednts ot etmeaiztass ta na aelry 1e0].a[tgs

peridot  This is super interesting, I was wondering wha the heck the scar had to do with anything! Thank you! +  


other answer choices

black fly - onchocera volvulus (river blindness) tsetse fly - trypanosoma brucei (african sleepling sickness) deer fly - F. tularensis

peridot  Also, deer fly can transmit loa loa (FA 2019 p.159) in addition to F. tularensis +  


submitted by mousie(216),
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A gehmoniama si a tyep of iebgnn noues-na)rco(cn utrom in fn.tinsa ishT almbaron lcsrute fo allms bodol seeslvs repsaap on or nured eht isn,k laitplyyc tnhiiw eno ot teehr ewske traef ihb.rt - sideohoicart.l.nwlwhrpswgaHm amignoe is a VaBaypilc/lr marbhrtik

sympathetikey  Probably a Strawberry Hemangioma since she's a baby +9  
meningitis  Can anyone explain what is option A? +1  
redvelvet  bc, it's a benign "capillary" hemangioma, we can see "thin-walled blood vessels with narrow lumens filled with blood and separated by connective tissue". It sounds similar to "arterioles in a fibrous stroma" but it's capillary. +1  
peridot  @meningitis I believe option A ("arterioles in a fibrous stroma") is describing an angiofibroma. The name angiofibroma already tells you that there is some component of fibrotic tissue involved, whereas in this case of strawberry hemangioma, the name tells you that it's more like pure blood vessels (capillaries in this case). +2  


submitted by meryen13(18),

so I don't think the reason for bilateral hydronephrosis is because it invated the bladder or kidneys. it is probably due to obstruction. there is a cancer in the uterine side of cervix (uterine cervix) that is big and its pushing on the bladder and its obstruction the flow of urine in ureters to bladder, so the urine backs up to the kidney and causes bilateral hydronephrosis and hydronephrosis. the kidney and ureters are full of urine and the cannot empty it to the bladder because this mass in the cervix is pushing on bladder and opening of ureters and squeezing bladder to the pubic bone.

meryen13  i hope thats helpful +  
peridot  Originally this made a lot of sense to me so thank you for contributing, but after looking more into it (on Pathoma p. 140), it specifically says that cervical carcinoma, when advanced, invades through the anterior uterine wall into the bladder and blocks the ureters. This leads to hydronephrosis. Crazy, but I guess true! +4  


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tWhgie loss - inhtk reprcaaytaiHncmn eo - SDIAH ofrm lmals clel unlg caarmnE eced + JVD - VSC ndmesoyr

peridot  I was thinking lung cancer secreting SIADH, resulting in hyponatremia. But because the question asked specifically about the cause of the facial edema, I put hyponatremia (answer choice C). I was wondering how you guys were able to differentiate between C. hyponatremia and E. lung cancer? Thank you! +1  
mannan  The first thing that crossed my mind was SVC syndrome from the cancer obstructing the R brachiocephalic vein preventing venous blood from returning to the heart (and staying in the facial area). Also I assume Hyponatremia would be equivalent to decreased body volume so there wouldn't be edema. FA Renal physiology section has a good chart on what happens during electrolyte imbalances (hypo and hyper) +1  
mannan  @peridot +1  
peridot  I was thinking that hyponatremia would be more loss of osmotic pressure --> edema, but I definitely see the argument for a mass that's simply blocking blood flow. Thank you! +  
jaramaiha  only thing affecting osmotic pressure is albumin, which would be more towards liver cirrhosis. The body will attempt to maintain a Na+ of 140 with various mechanisms, but doesn't contribute to osmotic pressure. +  


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nI hte tegra sorwd of rD att:raS

Pgtlsnaroind"a E2 imdetaes eer"efeeeveeeee

AISsND t;-&g- oblck dsgptioanlnra syn

thisisfine   This is all I heard in my head +7  
temmy  Me it was so weird +  
peridot  I do want to add, that while PGE2 is the right answer, FA19 p.213 says that IL-1 and TNF are involved as well. However, because the question asks about what is going on in the hypothalamus, the answer is PGE2. If the question had been asking about what the macrophages were releasing to influence the hypothalamus, then the answer would have been IL-1 or TNF (FA didn't specify if it was TNF-a though...). +1  
feeeeeever  You know why I'm here +6  


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hyw tno om.o1?useasdiicrtosida rh rattirihs kile . ist3yutso. smne.iyk pleid.mos.2nyv ssiirotse is a itb cnirvolasreot

drzed  Need some pulmonary symptoms to make sarcoid convincing. I know in real life people can present with primary neurosarcoid or something crazy but on exams, it'll be classic presentation. No granulomas, hilar lympadenopathy, or interstitial lung disease = probably not sarcoid +1  
peridot  Just curious but if it had been sarcoidosis, would "systemic release of IL-1 and TNF" be an accurate description for the pathogenesis? +  


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wyh not o1ocreiaia.sm?dioh tsdurs sirtaitrh klie sete.3m toipd.yln.ky .i.voymus2isns srtiessoi is a itb crirtovneolas

seracen  I usually look for the hilar manifestation, when considering sarcoidosis, or the skin manifestations. Personally, I thought Sjogren's when I read this. +1  
peridot  @seracen I can see why you thought Sjogren, but I think Sjogren would have more emphasis on dryness of mucus membranes and eyes (technically the question stem does say "anterior chamber of the eye", but Sjogren is more like the surface of the eye so "anterior chamber" is a weird way to put it - usually that refers more to uveitis). Also, choroid plexus (whether that refers to eye or brain... tbh idk about that yet), but either way, doesn't really fit Sjogren. Kidney involvement is also rather rare with that I believe. +1  


submitted by sacredazn(81),
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eTh enpcotc si a counlvdteo way fo ansgik if yuo nwek owh JVD mnnciebartoio s,krwo chiwh is ahtt it si tlcyaual an aemxepl fo eingtalr hte AND of eht BT/ tlpeyycmo.h

tuoSrhen lobt n:chiqteue So ewhn htey ues a ebrop gianats omse ro,gnei nda ptnouitugt a zeis fo 1.5 kb or 6 kb, sthi is gntilel oyu the size fo het DNA rfntmage ni hcea elcl (stedno’ traetm fi hyte sya J broep or stnnacot egrion peor,b eerty’h usjt ayigsn tr’yhee trentigag osem tnocuedeli uenqesec ndfou ni teh Ig /uTCcRosl ebta aihnc lousc ecetvepsyilr orf TB/ lle.cs)

I inkht the ugoisnfcn trap oucld be wneonridg ohw ouy knwo wretehh r’eouy atlyrp rhtohgu anreterneamrg r(wnase isocche B hurt )D ro if ti nsah’t crucdreo at lal ety o(ctcrer anser)w. ,ereH the penoctc si that B cllse urndeog )JVD( tmrenraeraegn in hte ebon orwram, lehwi T llsce do ti ni teh u,syhmt adn it lal nppseha ta oen.c So a spamal cell ni hte bodlo leki ni uilpMtel yMelamo ouwdl ahve ullyf nregdunoe netoobmacin,ir wheil a T clel ni eht dbloo lcoud riethe eb fully ducetaed (nda ahve dihfeins VJD mb)enocntroiia or mumearti a(hn’st sarttde .VJD)

Scine hte T lcle eegn aws 6 bk dna ldenyifite iggber than het 51. bk nege, eth T lcel a’thsn runegonde taecoinombrni tye.

trichotillomaniac  very nice explanation! +28  
nwinkelmann  This was awesome! Made so much sense and hopefully I will be able to think that critically about questions in the future (because I NEVER would have come up with this on my own, hah). +4  
eacv  OMG! THANK YOU. I DIDNT KNOW ANYTHING about this!! Hope this is not testesd on real examen :p +4  
ajss  wow! this explanation was awesome! thanks! +  
mrglass  Also the T-cell V-D-J segments are not the same as the B-cell V-D-J segments. Therefore a B-cell J segment southern blot would look for whether the B-cell site VDJ segment in a T-cell, which would always non-rearranged. +6  
mynamejeff  Thank you! So is this because multiple myeloma produces excessive monoclonal light chain Ig? Is this the 1.5 kb gene? Whereas, T-cells that have not gone through differentiation yet and their J region includes everything (VDJ) vs. just VJ in the light chain? (FA 2020 pg 104) +  
peridot  This explanation is amazing! However, to fully understand another step of what the question is getting at, please take a look at @highyieldboardswards's and/or @mrglass' explanation as well - a very important addition!! +  


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giehWt slso - kniht arprynHoeiccanaem t - ASDHI fmor samll llec ulng rEadeeccnam + DVJ - SVC dysernom

peridot  I was thinking lung cancer secreting SIADH, resulting in hyponatremia. But because the question asked specifically about the cause of the facial edema, I put hyponatremia (answer choice C). I was wondering how you guys were able to differentiate between C. hyponatremia and E. lung cancer? Thank you! +1  
mannan  The first thing that crossed my mind was SVC syndrome from the cancer obstructing the R brachiocephalic vein preventing venous blood from returning to the heart (and staying in the facial area). Also I assume Hyponatremia would be equivalent to decreased body volume so there wouldn't be edema. FA Renal physiology section has a good chart on what happens during electrolyte imbalances (hypo and hyper) +1  
mannan  @peridot +1  
peridot  I was thinking that hyponatremia would be more loss of osmotic pressure --> edema, but I definitely see the argument for a mass that's simply blocking blood flow. Thank you! +  
jaramaiha  only thing affecting osmotic pressure is albumin, which would be more towards liver cirrhosis. The body will attempt to maintain a Na+ of 140 with various mechanisms, but doesn't contribute to osmotic pressure. +  


submitted by welpdedelp(225),
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So I nikth hatt suies of wstri tseexoinn dr/ona inergf orpd ouldw be erom idlara env.er ow,erHve rteeh saw omer olaimxpr kewseas,n os it olwud eb C7.

-7"8 aly ehtm g",rittsah the pt uocdtn'l l"ay htme iratgs"th os ti dlouw eb C7 roto

welpdedelp  *As an addition, median nerve involvement would have leaned more toward C8 than C7. +5  
meningitis  Do you have anymore useful mnemonics for brachial plexus? +  
henoch280  FA pg 494 for mnemonics +  
winelover777  Doesn't look like there are many in FA 2019. S1/S2 - Buckle my shoe. L3/L4 - Shut the door. C5/C6 - Pick up sticks. +  
drzed  S2-S4 keeps the penis off the floor :) (cremaster reflex) +  
peridot  What's crazy @drzed is that in FA 2019 it says L1-L2 ("testicles move") on p.498 so I wonder if that changed +  


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ncicArgdo ot FA 0219 rciepT xfRele si ddeetami by C,6 esy C6 TON C8, dan C7 nI[ DBLO, ypiimgnl it is reom anpi.mott]r

peridot  This is on p.498 of FA 2019 for anyone curious +  


submitted by hayayah(1074),
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hsTi si a miyrrpa clrtaen ounersv mstyes mmplya.ho Mtos ommynlco coiasastde iwth V;SAHI/ID enepsihtgaso ovvinsel BVE nin.itfcoe

rinoeedCds na nSADidInfige- lsilse.n rbaielVa patnrone:itse cnf,oionsu mmyroe los,s e.zsisure assM ss)enil(o (yam eb irc-egnihnnagn ni soummoincmorpimde aetipn)t no I,MR dnese to eb dgieditusisnh ofmr tsspsooalomxi vai CFS aailssyn or horte bla tts.es xooT yaulusl sha ltmuepli inrg nencgnaih ssion.le

peridot  For those who are curious, this is on p.422 of FA2019 +  


submitted by hayayah(1074),
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yB eag ,75 eth ymuhst is ittell orem nath yatft stseui. trayuenl,Fto teh ytushm scuoerdp lla of ouyr T llces yb the iemt yuo chera b.uyrpet Thye aer elvodgni-l and tsha't hwy oyu acn lsoe ruyo smuthy wiuthot rnmiepmati fo oryu iuemmn .emtsys

sweetmed  Memory T cells live for six months or less in healthy humans (Westera et al., 2013), whereas naive T cells can live for up to nine years +7  
whossayin  so the bone marrow does not take the role of the thymus? +1  
dr_jan_itor  @sweetmed, does that mean that if someone loses their thymus, they would develop imunodeficiencies appx 9 years later as the naive T cells have died off? +8  
hpsbwz  @dr_jan_itor no, because once all of the thymocytes become T-lymphocytes, they are stored in lymphoid organs until they're needed. this is why removal of the thymus in MG does not cause any immune system deficiency. +6  
peridot  @dr_jan_itor From wiki: "Thymic involution results in a decreased output of naïve T lymphocytes – mature T cells that are tolerant to self antigens, responsive to foreign antigens, but have not yet been stimulated by a foreign substance. In adults, naïve T-cells are hypothesized to be primarily maintained through homeostatic proliferation, or cell division of existing naïve T cells. Though homeostatic proliferation helps sustain TCR even with minimal to nearly absent thymic activity, it does not increase the receptor diversity." +3