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Contributor score: 159

Comments ...

 +8  (nbme23#30)
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ELS is staisodaec thiw cyicenidfe of ylare etpnecmmol s.tieenop(rg ,qC1 4C, )C.2 AF( 1,9 pg. 426)

tinydoc  Am I the only one who has never heard of C1Q? +27
llamastep1  I knew SLE is related to low complement but when it talked about a "mutation" it threw me off. +1

 +3  (nbme23#47)
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nocdAcigr to l,joanG etpahcmlyioy erva si one fo teh tsmo cnmmoo csaseu fo hCiuiraB-dd myr.sonde dgcnArcio ot F,A iaBdru-dhiC is oestsaiacd orem yleerlagn ihwt pehlbrauaygleoc staets, oylaeichyptm eavr, aomtuppsrt s,tetsa nda CH.C

iacHtpe rrochiiss can be eldru uot dsabe on het time urocse of hte sinaptt'e niesttenroap - eh aws efni 2 wseke gao nda eth milboaand iapn rtdetsa na ohru

krewfoo99  Also in cirrhosis, the liver wont be enlarged or tender on palpation +1
almondbreeze  @krewfoo99 Good job. accoring to FA2019 pg.368, congestive liver disease (hepatomegaly, ascites, varices, abdominal pain, liver failiure) seems to be the key in Budd-Chiari SD +2

 +7  (nbme23#20)
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merbemRe on olyihotgs m'ohsiotasH idityitsohr sha wot tisdcitn resuatfe rthleHü eh(lslchwci rae colheniiiops scptialmate clsle atth ilne esllflci)o adn iymdophl gaegtgersa iwht earnmgil sn.ep(gtr.ce 383, FA 9)012 The ctorerc rnwsae esrsebcdi het eatrlt feeurat fo osaHihmt'.os

 +0  (nbme23#39)
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ceilaC rspeu is a aaitnsroopblm nmrsdoey thta tlssuer in steaotrehra nda urltsse ni roin ceiydenicf mn.eiaa sA far as Im' araw,e nnoe of hte ohsert relsut in rnoi cciyidneef m.anaie (I had taBecrali vwrrtooehg sa a oelsc snocde tbu I no'dt ileebev ttash' asitcsaeod thwi orni )inecdeyic.f

yb_26  bacterial overgrowth is associated with iron deficiency, but also with Vit B12-deficiency, so I guess pts will have macrocytic anemia +2
nor16 Vit B12 is key here, moreover, no bloating (IBS and bacterial overgrowth with bloating). bacterial overgrowth is a close one! +1
covid2019  I wrongly chose bacterial overgrowth, but that is wrong because Small Intestine Bacterial Overgrowth (SIBO) must be instigated by something. Commonly, anatomic abnormalities (like surgery causing blind loop syndrome, strictures, or motility disorders that allow the poop to ~fester~). +3

 +7  (nbme23#4)
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ehT itodenfini fo iicDeoiMks-angn cyCtpaai dgcnriaoc to BB+ is ibyatil ot rmdhnpeeco noorniitfam tobua llnseis adn emnrattte opistno nda kame cehicso ni igkpene ithw rnaespol elavsu.

notadoctor  The decision must also remain stable over time, which is the "consistent values" part of the answer. +20

 +2  (nbme23#45)
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v'Ie nbee eihacrngs orf ym scureo rof tish ubt nt'ca emes ot nfid it. ,weroveH eth ywa I oghhutt uobat ti asw atht medea ephsanp via hte pallse.riaci If eehrt si rcsndaeei aenstescri via teh llcpaeripary restnpicsh sa hucm oolbd nt'douwl eb beal to tge otni the caslirlpeai. hTe obldo lwoud nsdaiet get dnsehtu avi oeatsosnasm to eht nies.v hTis lcateri morf scyyvolghcm.poio iplasnxe it a ltetil e:tbetr CV soyPi:hylog sisTeu aemEd adn Genarel leriinPspc of nraariscalTypl Fuild cxahnEeg

 +0  (nbme21#6)
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sThi unisetoq was agniks oabut eht svadree fesfcet fo tonrpo upmp nhtsiiboir iyalpcseel gnvei vriseoup yenikd s.useis sPIP ceersdae srmue gM dan semru Ca sratoiobnp dna acn cseerain the kisr of caerrfut (lcpsiyeale in teh ylel)

yotsubato  PPI therapy *begins* the day she presents. She has not taken PPI before +15
notadoctor  You're right, I missed that! +
naught  MEN 1 is pituitary (monitor cortisol), pancreas, parathyroid (monitor calcium) but is not the ask of this question. +

 +15  (nbme21#36)
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fI uoy ewre ckust neetweb )nomsaihcdgonConrlaata(mr adn ngainh)cE(oeonmrndb bmemrere mononsehdacr aym eedro eht oextrc but nac envre vdutesriadpn/i het .cxreto I hintk hsti was teh tsidntcoini het tquiosne aws ettg.nsi

an_improved_me  Also: Enchondromas are most common in young males (liek 20s) whereas chondrosarcoma are most commin in middle aged men (esp. hips) +

 +31  (nbme21#32)
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saluU seiarlittitn unontpsmeii is het thliaclsoogi idinniofet fo pacdtIoihi ompuarnly fborissi. eW konw hatt hsit ttianpe sah nyuaromlp frsbosii eucebsa eth nieuotqs attess taht reeth si obrfsiu chntkigeni of eth laaevorl Tish tseiquon asw sjtu gtneist ahtt ew ewnk eth etroh nesma ofr ouyrmlaPn osFbr.isi

aneurysmclip  Nbme back at it again +27
pg32  Is it still considered idiopathic pulmonary fibrosis is it appears to have been caused by an atypical pneumonia? +1
zevvyt  Why not Sarcoidosis? Wouldn't Sarcodosis also be a chronic inflamation with fibrous thickening? +2
swagcabana  UIP is a better answer. Sarcoid is a leap in logic, usual interstitial pneumonitis is textbook histological definition of idiopathic pulmonary fibrosis. The biopsy has no mention of noncaseating granulomas and the clinical picture is not consistent with an inflammatory process. You have to focus on the better answers, try not to get caught up in the "why nots?" Calling this sarcoidosis is like someone coming in with prototypical asthma and jumping to eosinophilic granulomatous with polyangiitis. Sure its a possibility but its definitely not likely. +6
mangotango  I picked “diffuse alveolar damage” with Pulmonary Fibrosis in mind but these are actually key words for ARDS :/ +3
zevvyt  thank you swagcabana! Very good explanation and strategy! +

 +9  (nbme22#27)
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ttteMacsia iasesde si more oomnmc htna rriaymp enob r.somtu

lba9587  Might be helpful to consider eg. of a lung tumor. one lesion? you’re leaning lung primary. Multiple lesions in lung? METS. Q stem here included, “numerous lytic lesions along the vertebral column.” Thus, METS. +
jurrutia  Also, pain that is worse at nights and persists regardless of activity. Paget's is typically asymptomatic (although pain is the most common symptom) and would have other findings (deformities, AV shunts, etc.) +
jurrutia  Also, pain that is worse at nights and persists regardless of activity. Paget's is typically asymptomatic (although pain is the most common symptom) and would have other findings (deformities, AV shunts, etc.) +

 +10  (nbme20#29)
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lnsayiAs of eth ltasnei in the esqntiou seohdw a reaeddces numbre of sdisemeno rokis-s.nlcs eessinomD si eadm pu fo ruof inyels e.eduirss Teofherer nmablroa netalis si lykiel siimgns esilny creesasny rof teh iranoftmo fo hsete dnesmisoe knoci.rslss- ikWdpiaei rctilae no mnsDiosee.

dbg  how can i trust you, you aint even a doctor +22
euchromatin69  trust this then U.W 1249 +3
tryntofigritout  UW 1249 was perfect. #loveyourname euchromatin ha +

Subcomments ...

submitted by lsmarshall(415),
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rUea eylcC reroDdiss gt&; tIesoadl eevser oeehyamainmprm g;(t& 0010; e,..i no hteor esvree celmotbia enuricastsdb

hriintOen abrrtyamneasclsa eiecycidnf g;&t s(otm omncmo ruae yccle )ds.i irtoco aia/ariciddicmaeu, emaamhienroymp

rnOgica eAdsmiaci ;gt& eyaneHrm,mpaiom on-pangia isdo,asci tessiok f(rmo micyepahylg)o

idumheniMac- ayo-ACcl ndgrahsedeoye iccfeydein ;&tg emiH,rnemmapayo ttieypkcoho egmahoiylpcy es(en ni tβaio-dxoni oiesrdrs,d CPEETX opnoyrkhetlddu)rayoes

ireLv oftyidnncsu ;gt& mHirenym,eaoapm FsLT mssdee pu, ordle p.t

lsmarshall  Summary of metabolic issues relating to hyperammonemia +7  
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +3  
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria? +2  
charcot_bouchard  if it was mitochondrial disorder no one would escape +3  
wowo  figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB) + also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia +2  
artist90  i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong +4  
artist90  it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things 1-how does acidosis cause Hypoglycemia and Ketosis. 2-why is Ammonia elevated in these pts bc urea cycle will be fine? +  
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld) +1  
yex  According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA. +11  

submitted by sajaqua1(532),
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onteaaGs,ymci esrdpi aigna,taom nda dosanoyigmph sa( wlle as pramal yemte)arh rea lla snsgi fo sexcse senetr.og heT elvri ni ttespian htiw hpaeitc aseised is idreaimp dan so naotcn ecral ogetsner xiS 21 oz bseer liyad 2(7 z,o ro aflh a gnl)aol is oto ,cmhu nda si ndrsiyegot shi vel.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?! +6  
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  

submitted by notadoctor(159),
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Tish oesinqut asw nskgai tboua eth evdsera esfftec of onotpr mupp trihinibos ilealyscpe evign ovireusp yidenk ssi.seu PPsI esraecde surme Mg nad rusem Ca nobrposiat nad can ransciee het isrk of reutafrc leie(pslyca ni het ).relyled

yotsubato  PPI therapy *begins* the day she presents. She has not taken PPI before +15  
notadoctor  You're right, I missed that! +  
naught  MEN 1 is pituitary (monitor cortisol), pancreas, parathyroid (monitor calcium) but is not the ask of this question. +  

submitted by brolycow(27),
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He sah athre lefruia ihwhc esdal ot a dsecerea in ealnr dbloo folw dan lrearenp z.mioaate nI prlneear za,iemota CUrN:B orati is ;g&t= ;20 cinatoitvA fo het SAAR esytsm edu to het rprnelae ietaazom namse ttha eht scep vrga si hgih ta 10.52 dan he si nligohd toon osidmu os urinyar dmious lwli eb owl 2l0;&t,( ENFa ;t%l.1)&

figprincess  did you figure out the the ratio by actually divding out the numbers since the q didn't give it as a ratio? also what resource tells us what prerenal spec gravity should be? +  
brolycow  I just usually remember from class that spec grav 1.001-1.010 is considered dilute urine, and anything 1.025 and above is concentrated. For this question specifically, I think I remember there only being one option that even had the ratio >=20, all of the others were like 15 or less, so just have to rule them out. +7  
benzjonez  Very helpful video for acute kidney injury: +8  
notadoctor  Another explanation that helped me is that inability to concentrate the urine means something is wrong with the kidneys. If you have dilute urine, or the spec gravity is between 1.001-1.010 in someone with low urine output it suggests something is wrong with the concentration mechanisms of the kidney. Because this person had congestive heart failure we were already looking for something that matched up with prerenal azotemia so we can pretty much get rid of all the answer choices that suggest other azotemias. Then finally to get the precise answer I looked at the BUN/Cr ratio which you would expect to be high(>= 20). +  
mikay92  Would fully recommend the OnlineMedEd video on AKI. Goes through the differential, lab results, treatment, etc in a very clear and concise manner. +  
drdoom  repost via @benzjonez -> +  
drdoom  @mikay92 is this the OnlineMedEd video you're referring to? -> +1  
drdoom  aha! there is an updated AKI video but you need an OnlineMedEd (free) account to view it: +  
popofo  I understand that BUN:Cr > 20 if renal perfusion is repaired, but in heart failure wouldn't there be increased secretion of ANP/BNP from the atria that pushes up the sodium excretion? +  

submitted by mousie(216),
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naC eoosenm sepela iplenax htsi ot e?m I 'todn ddarsuntne yhw isntgatr eth oerth gudr uldwo otn nucto sa celnxosui icaiert?r

seagull  This has to do with Intention-to-treat analysis. Essentially, when participants are non-adherent but the data shouldn't be lost. They just undergo another statistical model to account for their changes. Here is a nice video +22  
dr.xx  Where does the question mention "intention-to-treat"? +  
notadoctor  They seem to be pretty obsessed with "intention-to-treat" it's been asked in one way or another in all the new NBMEs that I've done. (Haven't done 24 as yet) +8  
wutuwantbruv  They don't, intention-to-treat is just the best way to go about it @dr.xx +  
smc213  Great for ITT: +4  
yex  I agree with @notadoctor !! +  
ergogenic22  i think if it were per protocol, both groups would be excluded, the ones that were inconsistent, the ones that dropped out, and the ones that switched. But answer choices only allow ITT or exclusion of one group. +  

submitted by notadoctor(159),
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Teh iidetninof of DknasigcnMiio-e tcpyaiCa rcadciogn ot BB+ is alyitbi to eprdmncohe innmarofoit buato sielsnl and teratetnm npsooit dna kmea esihcco ni ipenkeg hitw alsoerpn slaevu.

notadoctor  The decision must also remain stable over time, which is the "consistent values" part of the answer. +20  

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wtih TCP oyu rea ssdpeopu ot oidav cxesveies unshlgti and UV xore.eups heoMtlxesan samek royu iskn emor usseeibcplt ot UV

notadoctor  Wouldn't UV light also be contraindicated in Vitiligo? +5  
sweetmed  Phototherapy with photochemotherapy (PUVA) is a well-known and well-studied modality for the treatment of psoriasis, which involves systemic or topical administration of chemicals known as psoralens and administration of ultraviolet light in increasing dosages after requisite time gap. PUVA is also used in the treatment of widespread vitiligo with moderately good results, though it is being surpassed by ultraviolet B (UVB), which is equally or slightly more efficacious with fewer side effects. +8  
dashou19  Honestly, I didn't even know what Methoxsalen is, just chose the right answer because I know you can not give UV light to people with PCT... +11  
sarahs  what about tcell lymphoma which also has cutaneous lesions? +  

submitted by sklawpirt(30),
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I inthk the eida here is yislpm atht oen husold thnki about hrewe slsceive rea nmicog omrf no etirh yaw to eht lgigo eml.cpox

T"wo spest fraowrd dna eon ptes abc.k" iyelfpclcSa het inusqteo yma eb ngriererf ot a erar aicclfaioanr eidro.drs an saenssewra fo htat aeesisd is otn cesneas.yr ahtW si eescsrany si gsnndnatuired the rogini rmof eewrh esivelsc rae rdtkacfie ot hte oGgli t.purpsaaa

PCIO otrneip is nedeed ot atco evlsces rfom eth RER ot sden ot l.oggi h,suT tiwh a itnaoumt ni atth repinto, the dcepgaka nripoets ttah hlodus bebl ffo dna be tnse ot teh o,iglg teiasnd eumctcalau in the RER nad deaitl i.t uThs the wnsr.ea


hayayah  pg. 47 on FA got the good visuals! +5  
notadoctor  COPII* proteins are needed to coat vesicles from the RER to Golgi. "Two(COPII) steps forward; one(COPI) step back." Anterograde goes RER -> Golgi -> Lysosomes/Secretory Vesicles -> Plasma membrane +23  
titanesxvi  why not small lysosomes? +3  
varunmehru  and I thought large lysosomes due to lack of enzymes to degrade +  
samsam3711  The size of the lysosome is not affected by the presence or absence of protein, but its function is compromised (eg. protein is getting stuck in the RER) +  
fattyacid  I hope this helps to whomever was lost like me Null mutation: A mutation (a change) in a gene that leads to its not being transcribed into RNA and/or translated into a functional protein product. For example, a null mutation in a gene that usually encodes a specific enzyme leads to the production of a nonfunctional enzyme or no enzyme at all. +2  
pingra  I think you made a typo: COPII (RER -> cis-Golgi); COPI (trans-golgi -> cis-golgi and cis-golgi -> RER), clathrin (endocytosis and trans-golgi -> lysosome) +  
kevin  So my thought process was if there is no COP signal then instead of going to Golgi it would be sent astray into cytoplasm, akin to how in I-cell Dx the enzymes get sent out of the cell since there is no trafficking signal (therefore I presumed large lysosome due to eating the aggregated protein). Are we saying without COP or Clathrin that the vesicle will simply stay put where it is? If I can get a reply before my exam (2 weeks) that'd be much appreciated +1  

submitted by mcl(598),
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tatienP aym vahe hdteeairyr aamegnidoe, wcihh si teadssaoic twih nrtc"eeurr atscatk fo isnnte,e ,iesasmv azedllcoi ecbustnuasou emaed ivnnilogv eht ,xmeseeritti le,ntgiaai a,cfe or uk,tnr ro bauluosscm aemed of ppeur yrawia or e"owbs.l Teh cilrate eogs no to ays aeeC-es"1trs rnhibtoii rwkos tyeilrdc on eth mcloemeptn nda cttnoac aplsam cesasacd to ecdreu ydkiairbnn leeesar" chhwi is lsoa pbalbyro odgo to k.wno


notadoctor  Thought this was a trick question as C1 esterase deficiency also results in a decrease in C4. However, the second answer choice was not referring to C4 but to C4 binding protein, which I now know is different. I also didn't realize C1 esterase was technically a complement protein. +4  
youssefa  Based on many sources hereditary angioedema does NOT cause a rash (urticaria) which is a main differentiating point between angioedema and allergy. This mislead me in this question. Any clarification? +22  
ergogenic22  +1 on the above because uptodate states that c1 esterase inhibitor deficiency, both acquired and nonhereditary, are both non-urticarial, non-pruritic, and that is confirmed by the above linked article +2  
sahusema  Question writer probably didn't know the difference between cutaneous urticaria and subcutaneous edema. +3  
almondbreeze  same. got it wrong bc the pt didn't have sx of hereditary angioedema - swollen lips and eyelids +2  
teepot123  fa 19 pg 107 +  
beloved_bet  According to Amboss "Mast cell-mediated angioedema Often associated with urticaria and pruritus Other associated with clinical findings of allergic reactions (see type 1 hypersensitivity reaction) Presents within 30 minutes to 2 hours after exposure and resolves over hours to days" +1  

submitted by oznefu(22),
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hwo od uoy worarn dnwo atht eesetnrottos ndaieesrc enoboihglm cotienrcant?no ustj a daonmr ftca to wokn? i tpu lnileaak ahshaotpesp uecbsea i rgiduef caesrdein seenttsetoor liwl erenacis enbo hotgwr dan rdleu out ofprecp-sttiacies atienng cb tis’ a nmwoa.

hysitron  I guessed this one cause men have a higher hemoglobin than women. +10  
notadoctor  High levels of testosterone will result in amenorrhea. I guessed that since she's not menstruating she will not be losing blood and therefore hemoglobin. Therefore her hemoglobin levels will be higher than expected. +5  
meningitis  It kinda makes sense knowing testosterone causes catabolism so I was in between Alkaline phosphatase and hemoglobin... +1  
enbeemee  isn't testosterone anabolic? +4  
syoung07  ALK phosph is indicative of osteoclast activity. Testosterone keeps male bones strong just like estrogen does for women. Testosterone builds bone (osteoblast activity) therefore we would not see a rise in ALK phos +