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Welcome to avocadotoast’s page.
Contributor score: 12


Comments ...

 +2  (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.


 +3  (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 anu(4),
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thwa utboa het reseicna in mpyaourln aacrlvus iearsestnc ? sodent CWPP lalf ni ihrhcmgaoer ckhos

ibestalkinyo  I think this may have something to do with hypoxic vasoconstriction? +  
medguru2295  PCWP falls because there is less blood going into the Lungs and therefore, less blood coming out (decreased preload). However RESISTANCE is a measure of how difficult it is for blood to flow. That essentially means constriction. As stated above, it is likely hypoxic vasoconstriction as well as just global sympathetic attempt to maintain BP. If it said pressure in pulmonary arteries, it would likely be decreased as the vasoconstriction cannot full compensate the blood loss! +1  
medguru2295  PCWP falls because there is less blood going into the Lungs and therefore, less blood coming out (decreased preload). However RESISTANCE is a measure of how difficult it is for blood to flow. That essentially means constriction. As stated above, it is likely hypoxic vasoconstriction as well as just global sympathetic attempt to maintain BP. If it said pressure in pulmonary arteries, it would likely be decreased as the vasoconstriction cannot full compensate the blood loss! +  
sharpscontainer  Actually I don't think this is due to hypoxic vasoconstriction. The alveolar oxygen content of the lungs remains high, so there's still a good amount of oxygen getting into the pulmonary vessels, even if less of it can bind to Hb. I think instead it's that there's tons of sympathetic stimulation from hypovolemia, so alpha 1 in the pulmonary blood vessels is activated (which is separate from beta 2 bronchodilation which is a smooth muscle thing). https://www.ncbi.nlm.nih.gov/pubmed/10378571 +6  
avocadotoast  PVR = (PAP - PCWP) / CO. There is a decrease in cardiac output in hypovolemic shock. Given its inverse relationship with pulmonary vascular resistance, we should choose an increase in PVR for this question. +1  


submitted by radshopeful(17),
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icrhnoc kinyde sieesad tg-&-; rcdeeasde EPO ;g-&t- eecddesar enohoricitcrchta m eknyid sdeasei -&g;-t adedcrese -4PO txeenrcio t;&-g- raecndsie ncTPHcoirh knyied sseaeid ;gt-&- ecadsrede 5,21 iodvdiytDhr r)ialc(tcilo -;-> ireeadscn HTP

jotajota94  she is also volume overloaded. more fluid leads to a decrease in Hematocrit. +5  
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. +1  


submitted by tinydoc(223),
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sTih etqinosu si yrve ays,kne utb in sseeenc tsih si htaws neipgnhp.a

Teh liadtenacc omvlrae of eth PHT ngdasl gindru ietyrmthoocyd ⇒ ↓ HTP

TPH rln-ynmia-l:o be:no ↑ rlvoema fo a²C⁺ adn phhaoPte ormf ne-bn-oi yesdki:n ↑ ⁺a²C rtaioobernps nda ↓ ⁻³OP₄ p↑s-i-eor obntra vonoernsic fo ,52 rydxiHamyonitv D ot 25,1 nyvHrmxtioadiy D tcaolrCl(ii - cievta form) avi ↑ yatiictv fo a-1 aerosyxyHld icneifecyd

foTrreehe a ↓ HTP uowld dael ot:

⇒ ↑ P₄⁻³O ⇒ ↓ C⁺²a ⇒ ↓ 21,5 aovxHrnyyimdti D

The qiteousn is yeasnk (mhcu klei het etrs of shti )xmae ceeabus nosmeeo hwo snit goniufcs aleylr rahd ro in a srhu gihmt ipkc teh tioopn C ehewr taphepho is ↑ and HTP si ↓ UTB ↓ 25 ahtvmdyxirinyo D

Thsi si ngrow sa noyl 125, ahotyxyirmivdn D dluwo be seaeded,rc teh ivorcnoessn obrefe hsit ear edno by eht snik ltu()shgni and rivl.e

I yalerl ishw thye dolwu tops nmkgia eth uqtsiosne ufincgsno PUEYLR rof eth kaes fo gkanim mteh gncfisn.uo Itns ti hogneu ahtt ew ehav ot wokn hsti drisucoiul mntuao fo oatfmnrioin, owhttiu agvhin hmte ynnoetilnital anmkig it rardeh by oinigpnt you to 1 aenrsw coiche btu ggninhca a emunit tdilea to amek uoy aswnre .gornw Or using a nmodar sas atenucnelmor rfo a sdiease to vdoia mkgnai it oot lmeisp (PSNG = piieorervtf"al ")GN

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 +  
zevvyt  so since conversion of 25 --> 1-25 is disrupted , would 25 be high? I know its not an answer choice, just wondering +  


submitted by medstruggle(12),
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yWh si ti htohpsau ulcrse if tereh are no GI smmpt?yos yhW nact’ it be eprshe ?ezrsot

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


submitted by drmomo(18),
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wyh a'cnt it eb celux soim?tuqo eyabm eceaihwurr ritnfcoba fsai?iilsra

sunshinesweetheart  diff presentation - that's elephentiasis +3  
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 +1  


submitted by diabetes(25),
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()UtUI t=;g=& espsis AN;=ES=SCDIgt;=gREtRA&&= rlloavae ylaracpli ertpbimeliay ==t&;g yempihaox &;t=g= rleapyhivnnoitet =y;p&oatanhcigp=

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. +1  


submitted by drmohandes(84),
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uOr antptie ash a eimlcboat kailasosl with iltar)a(p oceymnprasot eitaroyrpsr ocisaisd.

_

Mtibcaeol aklaiosls → H+ loss ro 3O-CH i:nag

  • g:ionvtim oels H+ na(d sleo +Kl)C-/
  • opol rduicetsi: osel +H ad(n +K)

_

ecoMtbali iocsisd,a lbsespoi cussea ni htis xctn:eot

  • lsaiavdaaeri/ertxh → seol 3-COH nd(a K)+ ; Cl- ymsaeotorncp enisecra mr(oanl nonia gap)
  • omelectdzaaai → soel -OHC3 nda( K)+ ; H+ aosl eeesdscar tbu tno uhgneo to rvoeocme eth ialasksol cuaesd by H-C3O slso
  • atnelicoronspo
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(502),
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I lsoa utohthg eth smae as bbu,lb@se tbu now rginyt to "ufs"jity itsh tkicry ENBM notuiqe:s I iknth sith veeovslr on eth ctaf htat het titaepn ahs a IHHG obdol ersurpse nameign ew dushlo cosfu on an nwreas ttah lpsnexia tobh rdseaicne PB adn oiveHlayomp .e:(i sriacened HDA hcihw ocrtvsatnsicso dan asol osabsbr atweferr-,e obth of whihc eirnaces PB nda uasec olyap.vimh)oe

ybMae if this etitnap rwee noeetmdespcda tihw WLO B,P eno lucod itkhn ermo oatbu AN.P

I itlls tinhk shti osnqetui is OTO ri.kytc

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 :") +4  
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(1404),
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Im asol ccnvnieod cboknigl 2L-I si olas a nteematt?r WyH is -hpNaalTF the ebtetr wseanr ?here

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. +16  
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 +1  
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(284),
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anC semnooe aipelxn who to erul otu eth hoert enwras oicr?cesh

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(94),

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(968),
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oS fro Caddian ew anc seu

leozAs leuoozcl(na)f hniti(bi CYP405 ttmnd)hiolayee

thrcipemAno B (oerp omitfnoar in glafun ecll mab)rneme

uinasofngCp e(pervnt gikrocnssiln fo ebta anlgucs ni lelc )wall

or iyanstN ofr laor ro lsheaepoag scsae (pore n)atoimfor

ishT esounitq is gysnia hatt seh is gkatni an ORAL gurd ot aetrt dancdia ita.igsivn

ieAcrpmonth is VI

Caipsonngfu is oals VI

os 'eewr tfel ihwt ozesal

lzAeso bihtini yseitsnsh of tseroeolrg yb hgtinnbiii PCY 504 that envorsct ltnoorsale ot tleoesrr.go

qball  Nystatin does treat vaginal candidiasis but is TOPICAL. +1  
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) +3  
turtlepenlight  I have seen that on the wards so I hope it works! +  
fexx  and my smartass picks amphp B +2  
avocadotoast  Please no one give a poor girl with a yeast infection amphoterrible +2  


submitted by sajaqua1(519),
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iotGacsna,yme erpsdi toagaainm, adn yshgdiomonap (sa well sa apmarl eryeth)am era lla isngs fo xseces otnegse.r eTh levri in tpaitsen whti eihptac seeidas is dpmeiiar nad so noatnc lrace soertgne tci.enuyflfis ixS 21 zo sreeb dialy 2(7 o,z ro falh a nola)lg is oto ch,um and si ondyigtrse sih erv.li

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?! +5  
catch-22  The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum. +12  
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". +4  
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  


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owH is iths teh ranswe fi reteh si on ifalym shrotiy fo urreecrtn ?aeuftrrcs I ougthht eesootnegiss tameicerpf saw oluastaom m?tidanno

seagull  Exactly!! it's an autosomal dominate disease! +10  
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. +