invite friends ⋅ share via emailtwitter
support the site ⋅ become a member ⋅ unscramble the egg
free120  nbme24  nbme23  nbme22  nbme21  nbme20  nbme19  nbme18  nbme17  nbme16  nbme15  nbme13 
Welcome to avocadotoast’s page.
Contributor score: 5


Comments ...

 +1  (nbme23#4)

This child has spina bifida. Failure to close the neural tube can lead bladder and bowel dysfunction in the fetus --> oligohydramnios --> compression of the fetus, clubfeet, etc. Axis specification and zone of polarizing activity is implying a defect in the sonic hedgehog gene that would lead to holoprosencephaly Closure of the rostral neuropore would cause anencephaly. Defective development of the apical ectodermal ridge would cause distal limb malformations. Without the neuropore, the neural plate and nervous system wouldnt form. Defect in scheduled apoptosis can present with webbed fingers, etc.


 +2  (nbme23#36)

Boards and Beyond has a good flow chart for ambiguous genitalia. If the patient is XX - do they have mullerian structures? If yes, it's CAH (increased androgens). If they patient is XY - do they have mullerian structures? If yes, gonadal dysgenesis (no MIH). If no, then it could be due to abnormal androgen receptors, CAH, or low DHT.





Subcomments ...

submitted by radshopeful(17),
unscramble the site ⋅ become a member ($42/month)

cinocrh deniyk saeised tg;--& ederacdse OPE -&;g-t escreeadd or ontmiehrtcichac iknedy asdiese g-t&;- esradceed OP-4 nexireotc ;&tg-- aerdnisec rcH oThPcin edykni edsesai t;g-&- eaeecsddr 512, dhidvrDyoti llt(iacor)ic -t;-&g cansredei HTP

jotajota94  she is also volume overloaded. more fluid leads to a decrease in Hematocrit. +4  
h0odtime  I thought PTH increases 1-alpha-hydroxylase which increases levels of 1 ,25? +1  
batmane  it's supposed to in the setting of proper kidney fxn +2  
h0odtime  Whoops +1  
avocadotoast  The decrease in GFR leads to decreased delivery of 25 dihydro vit D to the PCT and the decrease in functional renal mass limits production of 1a-hydroxylase. The increase in PO4 also stimulates FGF-23 from bone, which inhibits PO4 reabsorption and 1a-hydroxylase. +  


submitted by tinydoc(196),
unscramble the site ⋅ become a member ($42/month)

shTi qisonteu is evyr saek,yn ubt ni escesne shti si ahwst gpnaeih.pn

hTe nadecacilt aoelvmr fo eth THP gsdlna dunigr cdyeyrtmoihot ⇒ ↓ TPH

PHT al:noryn-m-il oben: ↑ lovarme of ⁺²aC nad paehoPht rmfo nbone-- i eykdns:i ↑ Ca⁺² btoreionprsa and ↓ PO₄³⁻ a obn-trsor↑pe-i rionecvsno fo 52, vymatHdyrxiino D ot ,251 ditvHoyanrmiyx D tio(llciarC - ceviat m)rfo via ↑ iitycvat of 1-a slryaedHoxy nidcfieyce

fTereeroh a ↓ THP oluwd aled t:o

⇒ ↑ ₄³⁻OP ⇒ ↓ a²⁺C ⇒ ↓ 215, ayirmvxHdtnyio D

eTh enuotqsi is asyken uchm( lkei hte sert fo thsi ae)mx bseeuac oeosmne who ints ingucfos lelyar rdha or ni a rush mgith icpk teh iponto C ewreh papethho si ↑ adn PTH is ↓ BUT ↓ 52 yxnrtyhdivaiom D

hisT is rwngo sa olyn 125, mdtxohyirayniv D udlwo be rdede,aesc eht nersonvocis orebef this ear ndoe by eht ikns hins()lugt dna vlr.ei

I raelly siwh yhte lwudo spto kaimng eht soqniseut coigsnufn PRUYLE orf hte aske fo gkanim emth suo.fgcnin tnIs ti egonuh hatt we vaeh ot owkn tihs rdliuiucso noaumt fo toio,afrinnm iohwutt ihvang mhet iennitlltanoy magink it rhread by tignpino yuo ot 1 naersw iochec utb gaihnngc a muneit eldtai ot kame ouy awnser n.ogwr rO sgnui a nmrdoa ssa luctreeonman orf a dsiseea ot diavo aikmng it oot eipmsl S(PNG = eralei"tvfprio NG)"

tinydoc  I literally got this wrong because I had the font zoomed in and assumed the 1 was on the line above like on uworld when it tries to squish the whole title in the same space x_X +1  
hungrybox  Holy fuck they got me. They boomed me. The fucking NBME boomed me. +2  
graciewacie9  Amen to the PSGN question. They got me on that one. lol +  
msw  the psgn question is pinting to rapidly proliferating glomerulonephritis b/c the pt has developed acute renal failure within days of the insult +  
msw  *pointing +  
snoodle  HOLY GOD MY BRAIN FILLED IN THE 1. i had to read this explanation 4 times to finally see 25-hydroxyvitamin D and not 1,25. F U NBME +1  
avocadotoast  this bs is prob why the question isnt on step 1 anymore +  


unscramble the site ⋅ become a member ($42/month)

hyW is ti spahouht lcures if rtehe are no IG s?sotmpym Why tn’ac it eb seperh ?tsezor

colonelred_  It’s just canker sores, they come and go. I think in herpes the gingivostomatitis really only happens when you first get infected. After that you just get recurrent cold sores. +3  
hyoid  Herpes zoster is not the same as herpes simplex virus. +21  
bigjimbo  you would see dermatome rash in zoster +2  
kateinwonderland  cf) Just in case someone wanted to know the causative organism of aphthous ulcers :The precise cause of canker sores remains unclear, though researchers suspect that a combination of factors contributes to outbreaks, even in the same person. Unlike cold sores, canker sores are not associated with herpes virus infections. +6  
charcot_bouchard  Herpes Zoster doesnt cause gingivostomatitis. Herpengina can cause vesicular lesion in mouth but happens to children in summer season by entero virus +  
drdeeznuts1  I'm wondering if this could be a mild case of Behcet syndrome without genital involvement +  
sherry  It sure can be Behcet or Pemphigus if the q provides us with more info. Canker sores just come and go for years with unclear mechanism. Also herpes zoster is shingles by VZV, not HSV1. +1  
avocadotoast  Most pictures on google show herpangina being present on the hard palate/throat, while aphthous ulcers are commonly on the lower lip. I think his lack of genital lesions are pointing us away from herpangina. +  


submitted by drmomo(15),
unscramble the site ⋅ become a member ($42/month)

yhw ac'tn ti eb ecuxl sq?uotoim beyma eiewurrcha boifrntca a?fisiaslri

sunshinesweetheart  diff presentation - that's elephentiasis +2  
sunshinesweetheart  plus filariasis isn't the same as microfilariae +  
avocadotoast  @sunshinesweetheart wucheria bancrofti shows microfilariae on blood smear. Filariasis in the name is referring to the microfilariae +  


submitted by diabetes(16),

U(UtI) ==> sepsis ==>ARDS==>INCREASE alveolar capillary permeability ==> hypoxemia ==> hyperventilation ==>hypocapnia

avocadotoast  This is correct. The patient doesn't have pneumonia, but sepsis from her UTI. Sepsis is a known cause of ARDS. ARDS can be due to extra-pulmonary tissue damage that leads to the release of inflammatory mediators, alveolar damage, pulmonary edema, and hyaline membrane formation. The hyaline membranes impair gas exchange and lead to hypoxia. +  


submitted by drmohandes(75),

Our patient has a metabolic alkalosis with (partial) compensatory respiratory acidosis.

_

Metabolic alkalosis → H+ loss or HCO3- gain:

  • vomiting: lose H+ (and lose K+/Cl-)
  • loop diuretics: lose H+ (and K+)

_

Metabolic acidosis, possible causes in this context:

  • diarrhea/laxatives → lose HCO3- (and K+) ; Cl- compensatory increase (normal anion gap)
  • acetazolamide → lose HCO3- (and K+) ; H+ also decreases but not enough to overcome the alkalosis caused by HCO3- loss
  • spironolactone
snripper  This makes sense, thanks! +  
dysdiadochokinesia  I was able to break it down to diuretic or alcohol use and chose alcohol use under the assumption that the patient's serum Cl- levels were low (90; N = 95-105) since Cl- is also lost with vomiting. Im assuming that it was wrong for me to make the association between alcohol use and vomiting. +  
avocadotoast  @dysdiadochokinesia I think we can rule out alcohol use by looking at our patient's history and demographic. A 16yo girl who is dieting and constantly studying probably isnt getting turnt because 1) alcohol has empty calories (defeats the point of dieting), 2) why would you try to study when you're drunk, 3) where will this 16yo in social isolation get alcohol +  


submitted by meningitis(417),
unscramble the site ⋅ become a member ($42/month)

I sloa hguohtt the saem as @usbbbl,e btu own iyntgr to "ifjst"uy shit krycti BMEN ieqn:otus I kniht tshi orevvles no teh cfat thta the aipntet sha a HGHI oodbl suersepr igmenna ew lduhos ufsco no an wsaner ahtt nilxpaes hobt rdicanese PB nda vaioloeHmyp ie:(. ieeracdsn DAH chwih anstotvricssoc adn olas osabsbr ewfeetr-a,r othb of chiwh ceesrnai PB nad uscea .oyvmio)plaeh

eyaMb fi siht tiepnta rewe moetcpeddnesa with LOW ,BP noe ucdlo nhkit rmeo otaub PNA.

I istll kthin sith ueqtsino si OOT yiktc.r

meningitis  Sorry, hyponatremia* right? +  
mantarayray  I think that it's not ANP because ANP will cause a loss of Na but water will follow (they usually go together), whereas ADH will cause absorption of only water and will cause hyponatremia except only thought this post getting the question wrong :") +3  
mantarayray  Oops sorry the formatting is confusing: I think that it's not ANP because ANP will cause a loss of Na but water will follow (they usually go together), whereas ADH will cause absorption of only water and will cause hyponatremia. +2  
pg32  @mantaray pretty sure you are right and that is the only way to get this question correct. Remembering that Na concentration really is a measure of water balance is key. If the pt is hyponatremic, that just means they have too much water in the blood, which is caused by ADH. If the patient was hypoVOLEMIC, that might mean they are losing too much Na. This is illustrated by pts with SIADH. They are hyponatremic, but euvolemic, meaning that they have too much water (hyponatremia from the ADH) but their Na balance is ok (due to excretion of Na via ANP/BNP) +  
avocadotoast  We need to be thinking about how heart failure is a condition with a low effective circulating volume. Our patient had an MI and now his heart cant keep up with the volume (low CO), leading to congestion. When congestion occurs, water is pushed into the interstitial spaces and isn't circulating in the arterial system. For that reason, the body ramps up the RAAS and ADH despite an actual increase in body water. This is a non-osmotic release of ADH. At this point plasma sodium levels are determined by relative intake and losses and hyponatremia is common in these patients because of that. Also, ANP and BNP don't hold a candle to the RAAS. +  


submitted by seagull(1133),
unscramble the site ⋅ become a member ($42/month)

mI soal dnonvceci libcokgn L-I2 si aols a mn?tetrate yHW is al-FapThN het retbet rnasew ?eehr

amorah  FA P120-122. Immunosuppressants for RA are calcineurin inhibitor (cyclosporine and tacrolimus), 6MP, and TNFa inhibitors (adalimumab,infliximab, etanercept). It is important to distinguish that calcineurin inhibitors block t cell activation by preventing IL-2 transcription, not necessarily block IL-2 action. Sirolimus(rapamycin) blocks IL-2 action but it is used for kidney transplant rejection prophylaxis specifically. +12  
sbryant6  Spot on. This image explains how Sirolimus blocks the effects of IL-2: https://image.slidesharecdn.com/11-150813013011-lva1-app6892/95/11immunosuppressants-30-638.jpg?cb=1439429471 +  
krewfoo99  in addition to the above responses, IL 1 antagonists (Anakinra) can be used to treat RA. Anakinra is a recombinant human IL 1 receptor anatagonist but less effective than other treatment modalities. +  
snripper  Prednisone is a glucocorticoid (which inhibits IL-2 synthesis) is already being used with no effect. So TNF-alpha is the next option. +  
avocadotoast  DMARDs: methotrextate, sulfasalazine, hydroxychloroquine, leflunomide, TNF inhibitors, Anti- IL6 (Tocilizumab), JAK inhibitor (Tofacitinib), Rituximab. You can use cyclosporine and tacrolimus to treat RA, but those aren't first line treatments. DMARDs are used the long term treatment of RA and methotrexate is often started first, and the other drugs are prescribed if methotrexate does not sufficiently control symptoms. None of the other choices listed are a part of DMARD therapy. +  


submitted by nwinkelmann(260),
unscramble the site ⋅ become a member ($42/month)

Can oomesen xepnlai hwo ot urle uot teh hrote wranse reoc?hisc

warbyparker1  you can r/o SMA because as kidneys ascend they get stuck low in the INFERIOR MA (L3 level). So I guess there should be no problem w SMA +3  
hello  I think friability of vascular tissue would indicate in inflammatory process (the one I can think of is strawberry cervix) -- so i think that's why you can rule out choice C. +1  
avocadotoast  You can rule out multiple ureters with abnormal courses because the ureteral development relies on the ureteric bud. There will multiple ureters if the ureteric bud divides before it comes in contact with the metanephric blastema. Horseshoe kidneys are simply due to fusion of the lower poles and don't involve the embryonic tissues, so those two processes are not likely related. +  


submitted by adong(84),

uworld says somewhere that testosterone increases hematocrit, increases LDL, and decreases HDL

passplease  Estrogen increases HDL. Testosterone is converted into estrogen. Why doesnt testosterone increase HDL. Why is my logic wrong? +  
avocadotoast  The woman in this vignette has an increased androgen:estrogen ratio, so the effects of testosterone on lipid levels will be greater than those of estrogen on lipid levels. Boards and beyond also states that testosterone causes an increase LDL, decreased HDL, and increase in hematocrit, which is why males with primary hypogonadism can present with anemia and the use of anabolic steroids can present with erythrocytosis. +  


submitted by yotsubato(822),
unscramble the site ⋅ become a member ($42/month)

oS for indaCad ew acn seu

Aesloz e(cal)flunooz nh(iiibt 0P45YC n)heytoetiamld

ohtpcAinmer B (oepr timnorofa in nafugl llec )eanbermm

upfgsnaoinC pnt(reve glsinoknrcis fo btea snglcua in llce )lawl

ro tNsniya rof arlo or hoplseagae cssae pr(eo iotofmnr)a

Tish qetusnoi is asiygn tath hes si tkaign an LAOR rugd to trate adacdni vaisii.gnt

nmocerAptih is VI

npgufnCosia si osla VI

so wr'ee felt thwi ezaosl

zsAelo ibinhti syessnhit fo rsltoeroge by nigntibihi CYP 045 tath crtonevs teroalonsl to oo.gtlerrse

qball  Nystatin does treat vaginal candidiasis but is TOPICAL. +  
thotcandy  Nystatin is NOT for esophageal candidiasis, Swish and spit, not swallow. +2  
staghorn  Me - picks Metronidazole -_- +  
alexxxx30  @thotcandy...actually you can swish and swallow nystatin for esophageal infections (per Sketchy micro candida sketch) +2  
turtlepenlight  I have seen that on the wards so I hope it works! +  
fexx  and my smartass picks amphp B +1  
avocadotoast  Please no one give a poor girl with a yeast infection amphoterrible +1  


submitted by sajaqua1(464),
unscramble the site ⋅ become a member ($42/month)

snetiyGaaco,m espird anoai,matg and spiygomdhnao (sa ewll as maprla yrmeeaht) rea lal gsnsi of scexes ogr.neset The leirv in senttiap tiwh etphaci sesedia is iemradpi dna os oncant carle sgroneet sliffiyt.ncue xiS 21 zo sreeb aiydl (72 ,oz ro ahfl a na)ogll is oot umhc, dna is eytnrgiods shi evl.ri

uslme123  No hepatosplenomegaly, ascites, or edema through me off. We that being said, I shied away from cirrhosis. I thought that he showed signed of depression, so I went with the thyroid. But who's to say he isn't injection anabolic steroids?! +4  
catch-22  The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum. +11  
notadoctor  He likely has hepatitis B/C given his history of intravenous drug use. I believe both can have liver dysfunction but may or may not have ascites, whereas the type of damage we would expect from alcohol that would match this presentation would also show ascites. +  
charcot_bouchard  For Ascities u need to have portal HTN. Thats a must. (unless exudative cause like Malignancy) +2  
paulkarr  For anyone who needs it; the FA photo is kinda burned into my mind for these questions. NBME has some weird infatuation with this clinical presentation.. FA (2019) Pg: 383 "Cirrhosis and Portal HTN". +3  
snripper  @paulkarr the problem was that the FA image was burned into my mind so without no ascites or edema threw me off of cirrhosis. +  
tyrionwill  cirrhosis doesn't present hepatomegaly, instead, the liver could be shrunken. +1  
avocadotoast  Cirrhosis (most likely due to alcoholism in this patient) leads to an increase in sex hormone binding globulin, causing a relative increase in estrogen compared to androgens. Cirrhosis doesn't always have to present with ascites and adema. I agree with @catch-22 that liver disease is a spectrum. This patient does not have ascites because his liver is still able to produce enough albumin to maintain oncotic pressure in the blood. +1  


unscramble the site ⋅ become a member ($42/month)

owH si hits eht nrwaes fi ether is no ilfmya yrsihot fo uetrrnecr ?rcfruetas I utohthg egossetioesn cetfmepira asw lotsumaoa omatn?ind

seagull  Exactly!! it's an autosomal dominate disease! +7  
emcee  Autosomal dominant diseases are variably expressive. Still, I think this was a badly written question (should have given us some family history). +  
wutuwantbruv  Also, FA says that fractures may occur during the birthing process, which is what I believe they were going for. I don't believe these findings would be seen at birth with any of the other choices. +  
d_holles  Yeah I thought I outsmarted NBME by selecting Rickets bc it said no family history ... guess I got played lol. +9  
jean_young2019  Could it be a sporadic cases? Spontaneous Mutation This is a change in a gene that occurs without an obvious cause, in a family where there is no history of the particular gene mutation. OI is inherited as an autosomal dominant trait. Approximately 35% of cases have no family history and are called "sporadic" cases. In sporadic cases, OI is believed to result from a spontaneous new mutation. http://www.oif.org/site/PageServer?pagename=Glossary +6  
avocadotoast  Amboss says the severe subtypes (types II, III) of OI are usually due to a new (sporadic) mutation in COL1A1 or COL1A2, while patients with the mild forms (types I, IV) typically have a parent with the condition. +