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Welcome to charcot_bouchard’s page.
Contributor score: 391


Comments ...

 -8  (nbme23#22)
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lOd dudttee ehav ctrioA inests.so taAril octniantocr cemobe nilaseets fro stih eptniat. so AS + FbIA is aegnodurs eaebcsu shit drueesc het VL podreal igafyincltnsi adn hsit ttaneip esvpoedl .HF So FiAb in SA ptaenti ndee ot cocetrr ieymlaeidtm

aisel1787  she's not so old! stupid comment +

 +0  (nbme23#28)
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A seac fo Fanionc md.syrone If ti swa toadlsie Tpye 2 RTA ooitnp B dulow eb eht an.sewr


 -8  (nbme23#1)
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reAft rghenytevi its jstuj an emedip e.qus woeBl 55 vs evbAo 55 asrye

ls3076  can you elaborate please? +

 +0  (nbme23#44)
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iTsh teapnit sah a alborti bowlotu rr.eautcf see hte atre pdor .ngis


 +1  (nbme24#49)
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yaentrpplA esterh eorl of psmietahtcy ystems in gepsonyhcic tenoirce dna sti esocm ofrm 1-.1LT2 So if pitneat ahev nariatostcn ta 5L htye sleo leexrf teiceonr ubt llist irntea csnyoihepcg on.e

AoBve 9T nicoaatrtns cusea olss of egsiyocnphc nreiceot

charcot_bouchard  Below L5* (Not at) +

 +12  (nbme20#23)
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Kap is pH at chiwh ayn gudr si ta ist %05 indzeio etsat.

woN ew are alk nuire ie. nic H.p nhew tga&;KHpp it liwl vhea tow ffdi athp for iacdic urgd ↦ sciba g.dru

idcciA rgdu wlil nic tsi tiineiolnma cni( ioiedzn ,m)rof bcsai grdu lwil be mroe rb.s oabdeos ew need to knwo the rdgu si icbas ia/c.idc

wNo if u kla reuin ist eiilaonntim cn.i so ti evah to be cai.dic or u anc owkn sti a odsi tsla fo rgdu tihw NSC eryrtpop ei. omst leki onhaiaerbtPlb kaW(e dcai)

os if pKa fo rugd si -ta--6 pH 7 we llwi tarts ntlnemiigia

tbu if Kap is 0 we deen to aresi Hp of niuer ta 11 ot sttra imlnteiiag.nat tath ptnio evrp rudg pa)6(K= olduw eb ltytola out fo yssmt.e

tstah hyw A si eth igrht sna apK( = 6)

charcot_bouchard  Correction : Not 0. i means if pKa is 10 +2
charcot_bouchard  2nd update : cont to learn school grade chem. if pKa > 7 it is base. and if pKa is < 7 it is acid. Since we established the drug have to be a weak acid pKa cant be more than 7. +
dbg  thanks, but Pka and PH are not at all the same thing +1

 +1  (nbme20#6)
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soaeprycNl sha neo fo the gwolfinlo 3 eaccrarhrt - .1 latx Cp.2eya ced ienorx ni s fc3. ERM yeactln l15t;& mni

its ssa wtih tn(o dx gaye/pocnrmoiHniargicipt (p allno.aihctni eleSp slysrpaia

charcot_bouchard  oh dx criteria must also include excessive daytime slepeiness for 3 time per week over 3 month +

 +2  (nbme24#18)
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I gte wyh tsi lretaal tbu dtno lla rlicana nrvee tecxep 4 eiasr aVlteyrnl? FTW ythe add thsi sorDo bfeore r?lteala

qfever  I think it's the nucleus affected in lateral medullary syndrome (instead of the nerve axons) +
nerdstewiegriffin  Because in the medulla section the nucleus is dorsal motor nucleus of X +

 +2  (nbme24#11)
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liadnAyol si celnrta anpi oinntiis.zstea Tirgengrgi fo naip by a non unilpfa ltu.imsi solA esen in .iamgas[bylirFvo reaigHelypas : Inc peessnro to aliunfp i]luismt

stI a tospveii e.i( lctveAiy ,eilfegn otn akcl fo fneli)ge ys.pstpmm so B p&;ma C si ont het arns wD.e tisn easrwn he.trei as ladovinli erretopc R1(TVP) si aslo renatffe inivopetcec oansisrnitms ldumoetd(a yb anc)isicap. tinoActaiv is osno felldwoo by oeais.iitednztns

A - .IKD if oebmlpr aws ni DGR ehter woldu eb tlo eorm ystpmmos.

madojo  if you are an idiot like me than that long word in option b is GABA +6




Subcomments ...

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Tshi si vuybisool a cailnlci i.tlar If oyu kown ouy ear ettnggi a ,ugrd hetn uyo are ton eddnbil: is’t na eeallpbon- ltir.a Trehe si no diiraomaotznn as etrhe si loyn a siegnl etmrnatet gorp.u

charcot_bouchard  But they grouped them based on dosaged? +  
keyseph  I think the key thing here is that the participants were told what treatment they would be receiving. This is in line with an open-labeled clinical trial. Open-labeled clinical trials can still be randomized and do not need a control (as in this case). +6  
drpee  Yeah, bad question IMO. Open-labeled trial can also be randomized... Since they didn't tell us how participants were selected for each group perhaps that's why C is better than D? +1  


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rezMieom sp’isrnai euuqni abdsi-eac cftsf:ee lamibotce ocidsisa and opeartisrry so.llasiak eto,N ihst is lylike ctulaa teprrsryoia lassklio,a otn impsyl mnolra rysrpritoae aitsncoopmne orf tbilemaco .iasdsico

mikerite  Based on the correct answer choice, the person is now in metabolic acidosis with respiratory compensation. +4  
benwhite_dotcom  The correct answer choice is as listed above (all decreased). Note that whether metabolic acidosis is combined with primary respiratory alkalosis, which is an important teaching point I’ve argued the question writers are probably getting at, or even if just simple respiratory compensation for metabolic acidosis–both can have the same arrows. In this case, it’s not respiratory compensation. In ASA overdose, the respiratory alkalosis actually happens first. Ultimately, the metabolic acidosis dominates and the pH is almost always low. This mixed primary acid/base response to ASA toxicity is highly testable. +1  
ali  How long till the respiratory alkalosis turns into a metabolic/mixed picture? +2  
benwhite_dotcom  @ali 12 hours is a good number to memorize but it can definitely happen much earlier. +  
yoav  From what I understand, the metabolic acidosis only presents 12h post ingestion, while she is only 3h. What do you think? +1  
benwhite_dotcom  @yoav, It can definitely happen earlier. It’s more of a by 12 hours (not only beginning then). +  
angelaq11  I'm beginning to think that they don't actually care about how many hours lapse after the ingestion, but if we actually know the unique acid-base disturbance. I chose the wrong one, again because I was foolishly thinking about those 12 hours postintoxication +5  
charcot_bouchard  I think this is good rule of thmb in USMLE "a Right answer may or may not tick all the correct things but will NEVER have a wrong thing in it". So the ans choice we all chose has Bicarb inc. But this will never happen. at 3 hour we should have pure resp alkalosis with normal bicarb (as per uw). Or in this case decreased due to neutralization by organic salicylic acid. In Aspirin poisoning bicarb will nver increase. +6  
elasaf@post.bgu.ac.il  Another important point- they probably gave her RR (30) to indicate that she is hyperventilating==> LOW CO2 +2  


submitted by dr.xx(144),
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g.rith he tlbyaouels tsmu nirmae ni the igiwnat aare os tath eh is ta hdna to tkaatc hsi iwef rvneeweh erh maxe esnd. go EM!BN

meningitis  I guess it was all about not offering battering information in order to not make matters worse since he will figure out that the wife told on him.. Also, its a HUGE STRETCH but the only reason I thought he should stay in the waiting room was just in case the wife died they could detain him and call the police for questioning. +10  
temmy  Also, he should stay there because his wife did not grant him the permission to see him. Patients requests trumps. +  
nephcard  Doctor should not believe what wife told her. There may be some other reason for injury so batttering information should not be provided. But her wish of not letting her husband in should be fulfilled +2  
charcot_bouchard  No. In real life patient lies. In Board ques they always tell the truth. Unless they make it very obvious. in fact its a board ques rule. So u believe her untill proven otherwise. +3  
drdoom  The prevailing rule of American medicine and law is individual autonomy. No other person is granted “default access” or privilege to another person’s body—that includes the physician! The physician must receive consent from a (conscious) “person” before they become “a patient”. In the same way, the person (the patient) must give consent before anyone else is permitted to be involved in her care, spouses included! +  


submitted by aladar50(40),
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hTe mtnpitoar tginh ofr otsm fo eht hcstei nesouisqt rae to kool rof hte nweasr rewhe yuo era bieng hte oststecn/mi noiaesspofrl heliw rengpsetic eht anpits’et y,onautom efnce,ceeinb ice,efca-onmnnle .tce Mtso fo the shcoiec erhe erwe rithee urcstaaoyc or abllicasy ebign maen ot teh peintta. hTe crcerto ceicoh si to phle teh eitpnta tbu lsao veitatom tehm ot nietconu aysihclp yrahtpe nda to noyl seu het remtpi sa illtte sa nsesyrec.a A milisra sotqniue hhw(ic I tkihn was no MNEB 32 -- ehyt ear dkni fo nldnibeg ehtoe)rtg was the oen rhewe the ainetpt dah stte tuslers ttah tddicneia eh dah acnecr ubt teh nridtese dasi not to oillvy(a)rntu etll ihm lnitu het lstcoionog caem in trlea atht ,yad and hte pinaett dasek yuo uotab hte uelstsr. uoY ot’nd anwt to eht iel to teh ittnaep nad say uyo ’dont knwo ro ttah eh tnedso’ ahev anrcec, utb uoy osal tdo’n wnat to eb sterunbniodia to het nsde’irets nslre)a(boae urteqs.e

drdoom  @aladar Your response is good but it’s actually mistaken: You *never* lie to patients. Period. In medicine, it’s our inclination not to be insubordinate to a “superior” (even if the request sounds reasonable -- “let’s not inform the patient until the oncologist comes”) but *your* relationship with *your* patient takes precedence over your relationship with a colleague or a supervisor. So, when a patient asks you a question directly, (1) you must not lie and (2) for the purposes of Step 1, you mustn’t avoid providing an answer to the question (either by deferring to someone else or by “pulling a politician” [providing a response which does not address the original question]). +2  
drdoom  As an addendum, legally speaking, you have a contractual relationship with your patient, *not with another employee of the hospital* or even another “well-respected” colleague. This is why, from a legal as well as moral standpoint, your relationship with someone for whom you provide medical care takes precedence over “collegial relationships” (i.e., relationships with colleagues, other providers, or employers). +  
imnotarobotbut  @drdoom, it's not about lying to the patient but it would be wrong for an inexperienced medical student to give the patient their cancer diagnosis, or for a doctor to give a cancer diagnosis if they feel that the patient should be seen by oncology. In fact, the correct answer that the question that was referred to by aladar50 says that you do NOT give the patient their cancer diagnosis even if they asked you directly about it. +1  
charcot_bouchard  Dont give it to him. DOnt lie to him that yyou dont know. Tell him let me get the resident rn so we can discuss together Best of both world +4  


submitted by seagull(1443),
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shTi eipantt is intigppr lsa.bl etrBet od a udrg crenes hhcwi meess ovsbi.ou

sympathetikey  When the answer is so obvious that you pick a stupid answer instead of it. DOH +39  
jooceman739  Funny thing I noticed is "he is alert and cooperative. He appears to be in pain" So he was so high that he was alert and cooperative during the basal ganglia hemorrhage +5  
yotsubato  @sympathetikey That fucking guy who drinks 2 six packs a day with liver failure got me like that. +1  
yogi  probably the "drug" have to be a stimulant or a hallucinogen which causes HTN & Tachycardia. +2  
charcot_bouchard  Lol. I got the right answer but took long time +  
goodkarmaonly  The patient's B.P. and pulse are raised + Bilateral dilated pupils = Most likely use of a stimulant Thats how I reasoned it anyways +  
llamastep1  Bilateraly messed up pupils = Drugs (most of the time) +  
targetmle  why is there basal ganglia hemorrhage? +  
dul071  Wait! doesn't it take like a week or two to get the results back!?!? i chose to measure catecholamine levels because that may be more timely. but clearly i'm wrong +1  
usmile1  basal ganglia hemorrhage is an intraparenchymal hemorrhage secondary to hypertension. according to FA, this occurs most commonly at the Basal Ganglia (FA19 pg 501) +1  


submitted by seagull(1443),
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isTh is a cpnai atkact. tHpaiyoentvenlri sordp CO2p aenigld to a prayrrtoies aisks.alol 2po is velitrealy edatnucffe to(d'n kas em )?woh

sympathetikey  Yeah haha I had the same conundrum. +  
sajaqua1  If she's breathing deep as she breathes fast, then oxygen is still reaching the alveoli , so arterial pO2 would not be effected. +21  
imnotarobotbut  lmao i'm so freaking dumb i thought she was having alcohol withdrawals because it was relieved by alcohol +2  
soph  Maybe Po2 is unaffected bc its perfusion (blood) limited not difusion limited (under normal circumstances). +2  
charcot_bouchard  PErioral tingling- due to transient hypocalcemia induced by resp alkalosis. +1  
rainlad  I believe CO2 diffuses ~20x faster than O2, so increases in her respiratory rate have more effect on her PCO2 than her PO2 +1  
usmile1  adding onto Charcot_bouchards comment, I found this: Respiratory alkalosis secondary to hyperventilation is probably the most common cause of acute ionised hypocalcaemia. Binding between calcium and protein is enhanced when serum pH increases, resulting in decreased ionised calcium. Respiratory alkalosis can induce secondary hypocalcaemia that may cause cardiac arrhythmias, conduction abnormalities and various somatic symptoms such as paraesthesia, PErioral numbness, hyperreflexia, convulsive disorders, muscle spasm and tetany. https://www.sciencedirect.com/science/article/pii/S1110184913000615 +3  


submitted by sajaqua1(524),
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,atymcGisaeno psried gaoamnt,ia and dashonpigomy s(a wlel as raplma theye)mar era all ssgin fo eesxcs ege.osrnt The lriev ni stintape ihtw achepit ieesdas is mediirap nda os otnnca lrcea rentsoeg sucn.yfltiife xSi 12 oz beres iayld (27 ,zo or hfla a oal)nlg si oot ,hmuc nad is rysintodeg sih eir.lv

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  


submitted by sympathetikey(1265),
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reP FA .p(g )636: rgnocneniC btasre .c.r.cena

"inltfcpAoaiimioes/erprvesxno of re/rptogergnosee eostn esrcptoer or -Be2brc ,RHE(2 aFEGn prtree)co is ;omncom ER ,⊝ RP ,⊝ /dnnuH2eERa ⊝ form ermo saeg.ir"sgev

sympathetikey  FA 2019 +4  
meningitis  Why others not it: Anticipation: Trinucleotide repeats; CAG (Huntington), CTG (Myotonic dyst), GAA (ataxia telangiectasia), CGG(Fragile X) Chromosomal rearrangement: Many but can think of Trisomy 21, BCR-Abl, etc Imprinting: Prader willi, angelman Loss of heterozygosity: loss of a single parent's contribution to part of its genome. A common occurrence in cancer, it often indicates the presence of tumor suppressor gene in the lost region. +1  
kai  trinucleotide repeats are not associated with breast cancer Neither are chromosomal rearrangements BRCA1,2 tumor supressor genes are associated with breast cancer, which is why I chose E, but I guess I should have bought the new First Aid.......... +  
charcot_bouchard  GAA is Freidrich Ataxia +4  
tulsigabbard  So is the amplification of the receptors unrelated to BRCA 1, 2? I'm still stuck on this as Sketchy states that breast cancer falls under the "two-hit" model. +  
tallerthanmymom  @tulsigabbard I think one of the keys here is the question stem; " what is the most likely cause of the OVERexpression in this pts tumor cells?" --> I think that the "2-Hit" model would lead to UNDERexpression of a tumor suppression gene rather than overexpression. Whereas amplification would cause OVERexpression of the HER2/estrogen and progesterone receptors. But, I don't think that amplification would be the answer if they were asking about a triple negative cancer. +1  
tallerthanmymom  Also this is on page 632 of FA 2018 for those using that version +  
tulsigabbard  @tallerthanmymom - thank you! +  
drzed  I can understand why @tulsigabbard dropped out of the race--she's taking step 1 soon LOL +1  


submitted by seagull(1443),
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Did nnoaey khitn tath fnlueizan saw rtih?g I dnstdnuera atht eZrpeHs- nac ucsea auepninom btu wyh is shit sewnra teterb vroe ?zleafninu

jrod77  I believe it's the vesicular rash that gives it away. I thought it was influenza too, but i re-read the questions and I realized they included a rash which disqualifies influenza. +4  
charcot_bouchard  Also h/o of immunsupression, disseminated VZV. Influenza itself doesnt cause severe disease. secondary PNA does. which u will see in elderly. usually +1  


submitted by cbrodo(58),
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ehT tpooresir lsuomcn scusia(cluF ccuualassuctusne/iF )gilricas carry ainimortfon ot teh inrba gdarreing prnopriip,cooet t,rinvbaio imiraindtcveis cthou and epu.errss alPcshyi amex nfndsiig eggusts a noesli hree (the ohlimnpaactsi tcrat eiarscr pkiicpr/inapn and aetue,ptrrme dan eeths ewer ra.om)ln cneiS eht tpeaint sah baorlanm singifnd ni eth erowl ,srtiiexmete adn rmnloa infindsg in eth puepr iisem,extrte hte erawns si sicFsuulca alscgri.i hsTi is eueabsc mtfnraonioi frmo dbyo arsea ebwol hte level fo 6T is acdrier by srgaicli nad nmofnoiitra rfom doby sarea obeav teh elvle of T6 si icrrade by uneautsc.

kai  kick Goals (gracilis) with your feet Cook and eat (cuneatus) with your hands +3  
temmy  i remember gracilis is for legs by saying i have graciously long legs and they are inside while arms can spread out to remember their orientation on the spinal cord +4  
jess123  I remember it as gracilis = grass so feet haha +4  
link981  Just to add found on page 492 on FA 2018. +  
charcot_bouchard  Hey Temmy, I can spread my legs too :) +  
maxillarythirdmolar  I can't feel GRACIE's ~fine touch~ as she ~vibrates~ my balls. +3  
cat5280  Could someone please explain why you were able to eliminate the spinocerebellar tracts? +1  
drzed  Lmao I remember gracilis because of the gracilis muscle in the legs! +3  
alexxxx30  cat5280...so spinocerebellar tract does 4 things to know 1. proprioception in the Romberg test 2. intention tremor if damaged 3. shin to knee test 4. dysdiadochokinesia (being able to rapidly pronate/supinate the upper extremity) yes the patient has proprioception issues, but the other symptom of vibration loss points us more to a fasciculus gracilis issue. If the patient had presented with proprioception and and intention tremor then we would think spinocerebellar +2  
alexxxx30  adding to my comment^ I would commit these 4 things to memory as I have gotten several questions concerning this topic (there were 2 questions on this exam where spinocerebellar tracts are involved). Memorize them and it might get you 1-2 extra points! +  
solidshake  Just to clarify a point, Spinocerebellar tracts are not tested by the Romberg Test. Romberg tests conscious proprioception that is done by the dorsal columns. Spinocerebellar tracts are used for Unconscious proprioception. Look up tabes dorsalis in First Aid. One of the positive indicators is a positive romberg test, which shows that the dorsal columns have been damaged thus affecting conscious proprioception and thus impaired balanced on standing with the eyes closed +  


submitted by temmy(127),
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htaW of if the cecarn is a luhoeltiar ecarnc ni het ebldrad edu to nioaadirt hrpayt.e dwolu ti tno eucas silriam ngiss

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 sajaqua1(524),
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hTe igsnle smot inmtproat hingt bouta shti gorss lytpoahog si tath the issaeed si .llurimouandt ihTs atdsieicn emsesastat mfor dtsitna tsei.s

ivreL bsessseca era slauuy sluirgn,a ldilfe hwit ayrecm lleowy s,pu and amy hwos a uosirfb ap.celus srorhsiiC etnfo osshw a lolyew rcloo eud ot tyaft gechna as lelw as ravtgnreieee nsdolue, hhciw are otn tensepr .eehr A acflo oalndur peraihalsyp si a rnlugsia tomru fo eht el,rvi adn sith si uatmdonuilrl. peiHatits B si a ltetil drhrae ot gisuitindsh eubseca ofrm wtha I cna llte ti cna be tionuldamlru ni omes s,aecs tub ihst lrvie lsao swohs oenn fo eth sressciol fmor nrccioh maaintilnfom thta uwold ylelik oapancymc pHe B. nillFa,y ew ese no drka ilcindtrooosa to tnciaedi tcnaorfnii.

monkd  It doesn't explain the sudden death, but I suppose they aren't asking for that! +4  
charcot_bouchard  I hate this type of ques. Here it is. Tell me what it is? +2  
divya  also, a liver infarct is unlikely due to rich dual blood supply. +1  
drzed  @divya Rather, if there was an infarct, it will be hemorrhagic, not pale. +1  
llamastep1  Multiple solid lesions on a healthy liver = meta. I assumed breast wouldn't meta to liver (it's usually GI cancers) but it makes sense since all the blood gets filtered by the liver at some point. TIL! +  


submitted by colonelred_(99),
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etutalbbAtri isrk = edcnneici in depsxeo – iecdnceni in deuxnesop

= 0130,/00 (eoskrs)m - 0330/0,0 ekmno)ssr(on
= .003 - .001
= 002. s(o eth uaetlrbatbit sirk is oatub 2)%

nAyigplp it to a puatloinpo fo 00,0:01

= 002. * 10000,
= 002

charcot_bouchard  What if i tell you this is a ques of Attributable risk % in exposed? AR= 0.02 / IR in exposed (30/1000) = 0.6667 30 case in 1000. So 300 case in 10,000 0.6667 x 300 = 200 or in another word 66% cases of 100 lung cancer cases in smokers is actually due to smoking. so in 300 cases of smokers 200 is actually due to smoking +4  
charcot_bouchard  This is a mind fuck. Lemme tell u guys if any consolation while doing the ques during test i did it with AR = 0.02; NNH = 1/0.02 = 50. 50 persons smoke to cause 1 cancer. 10K smoke to cause 200 cancer. +1  
ls3076  Sorry if this is a stupid question. Why is it incorrect to simply apply the same proportion (30 cancer per 1000 smokers) to 10,000 smokers? +2  
krewfoo99  @is3076 Thats exactly what is did. I still dont understand how that is wrong. But i guess they want us to think about it in terms of AR +  
hhsuperhigh  @Is3076 and @Krewfoo99, If a person doesn't smoke, the natural risk of getting lung cancer is 30/3000=1%. The smoker's risk is 30/1000=3%. This 3% is not purely contributed by smoking, but mixed with the natural risk. So for calculating the pure contribution made by smoking, you should use 3%-1% which is 2%. And this 2% is the pure contribution of smoking. Not all smokers get lung cancer, the same thing, not all lung cancer among smokers are attributed by smoking. They may get lung cancer anyway despite smoking or not. +11  


submitted by colonelred_(99),
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tuAteibrltab kisr = cendiniec in espexod – ncineiedc ni eupesodxn

= 0/,03100 k)r(esosm - ,0300/30 m(oksreon)ns
= 30.0 - .001
= 0.20 (os the lrbiautttaeb ksri is tabuo )%2

pliypgnA ti to a pouaptloin of 0,:0001

= 0.02 * 010,00
= 020

charcot_bouchard  What if i tell you this is a ques of Attributable risk % in exposed? AR= 0.02 / IR in exposed (30/1000) = 0.6667 30 case in 1000. So 300 case in 10,000 0.6667 x 300 = 200 or in another word 66% cases of 100 lung cancer cases in smokers is actually due to smoking. so in 300 cases of smokers 200 is actually due to smoking +4  
charcot_bouchard  This is a mind fuck. Lemme tell u guys if any consolation while doing the ques during test i did it with AR = 0.02; NNH = 1/0.02 = 50. 50 persons smoke to cause 1 cancer. 10K smoke to cause 200 cancer. +1  
ls3076  Sorry if this is a stupid question. Why is it incorrect to simply apply the same proportion (30 cancer per 1000 smokers) to 10,000 smokers? +2  
krewfoo99  @is3076 Thats exactly what is did. I still dont understand how that is wrong. But i guess they want us to think about it in terms of AR +  
hhsuperhigh  @Is3076 and @Krewfoo99, If a person doesn't smoke, the natural risk of getting lung cancer is 30/3000=1%. The smoker's risk is 30/1000=3%. This 3% is not purely contributed by smoking, but mixed with the natural risk. So for calculating the pure contribution made by smoking, you should use 3%-1% which is 2%. And this 2% is the pure contribution of smoking. Not all smokers get lung cancer, the same thing, not all lung cancer among smokers are attributed by smoking. They may get lung cancer anyway despite smoking or not. +11  


submitted by viz28(-1),
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The cuoroalsaq-mmnu jiunotcn tsudieta at eth erxtanle os fo teh ecxvir si oen seti which is glhhiy aeelnlubvr to epiasamlta or lepasncoit atirrmasonntfo eudrn sevrdea runaescmtscci, hucs sa hoirncc ftniinceo or rautma. ylulUa,s uosausqm matpaelsai erhwe susmuoqa lelsc acplere hte ucnlroma lelcs fo eht vcaeicdoelrn aanl,c si boeevsd.r vrewH,oe in ssel momcon atsniutsi,o rtyluaclrpai arfte m,ratau ublat elsaamtiap mya dpelevo, plargcien varecneilcdo nidoelatcin uarlncmo ilehpiltea sllce yb lt′aciied arlu′nmoc esc,ll mirasli to estoh nsee ni fialapnol tube.s baluT eaapiastml si ltyosm snee in eth puper tapr of eht icaedocnevrl naacl nrea hte etnnilar o,s ubt yam olas be noufd in teh edoleancircv nlsagd ro hte lwoer cvoeircnldae lan.ac b/pi1t/j/n8n.tci0ht:iibm8/ihb/1mt3/0pdb..de3jnt

charcot_bouchard  But they are asking in healthy individual. I dont get why they add this ciliated part? +5  
thotcandy  @charcot_bouchard FA19 pg 612 says the only thing that's ciliated is Fallopian tubes... shit doesn't make sense yo +  


submitted by sympathetikey(1265),
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Mad at lsmfye rfo hicnnagg my rns.wae

Ftauly ocgli eamd em owdren if gtnithi ryou daeh wluod uasecd esdicanre CIP ,os ikle a gunchis cr,lue uoy odwlu etg cerdniase Vsgua veren ttyaiivc adn abmey ydradrabaic + hey.otpinnso uBt I usgse eht SAAR emssyt olwud ehav tdcaeonreutc ttha dna easdcu tnsirctnoicvasoo over 42 rhos,u os loHyemiovpc sckho si tyfldneeii eth sebt oceci.h

Aslawy hulods og twhi the iboousv enwrsa ):

seagull  I had the idea that this was a neurogenic shock and increasing intracranial pressure could affect the vagus too. I think the question really wants us to go that direction. +13  
uslme123  The Cushing reflex leads to bradycardia! +4  
purdude  Wait I'm confused. I thought hypovolemic shock leads to an increased SVR? +2  
littletreetrunk  apparently, there's a thing called sympathetic escape that can happen after a while (i.e. he's been out for 24 hours): Accumulation of tissue metabolic vasodilator substances impairs sympathetic-mediated vasoconstriction, which leads to loss of vascular tone, progressive hypotension and organ hypoperfusion. +  
littletreetrunk  also also if he hit his head he could have loss of sympathetic outflow from a hypoxic medulla which could lead to vasodilation, which further reduces arterial pressure, but this was a hard one for me lol. I also put increased ICP wah. +  
catch-22  Any lack of sympathetic outflow/increased vagal outflow should reduce HR, not increase it. Further, you would expect brainstem signs if there was hypoxia to the brainstem. For example, if you had damage to the solitary nucleus, you wouldn't be able to regulate your HR in response to reduced BP. Since this patient has reduced BP and increased HR, this indicates that the primary disturbance is likely the reduced BP. He's also been in a desert for 24+ hours so. +3  
charcot_bouchard  In a patient who develops hypotension following high-energy trauma, neurogenic shock is a diagnosis of exclusion that is made after hypovolemic and obstructive cardiogenic shock have been ruled out! Plus Absent Bradycardia rules it out +2  


submitted by yex(94),
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mHm.m llWe my nmid hsa onbwl fof ebsucea hawt iht my mind was oeyahdtnird encis he swa in eth tr.eesd sA osno sa ym mdni etdrast to ewrnad uboat lla fo hte htroe osnoipt atht dlcou amke ss..en.e I tujs ecldcki nda vmode!

charcot_bouchard  Smart boi +5  
usmlecharserssss  hiking in sahara desert SMH +3  
cbreland  Simple = smart +  


submitted by d_holles(173),
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Eevn oht FA nad khotSciMycer n'dseto etmnoni it, thbo mAaalnsap and roschsEiilh era rcdiera by Rnibo of Iodesx.

bulgaine  FA 2019 does mention it P 149 +  
charcot_bouchard  Ehrlichia - Lone star tick +2  
paulkarr  "Lyme Disease caused by Borrelia Burgdorferi, which is transmitted by the ixodes deer tick (also vector for Anaplasma spp. and protozoa babesia)." FA 2019, Pg 146 +5  


submitted by docred123(6),
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iH ygsu can mnooese asepel beoetlara on ehest dgnii.snf I straneudnd she ash nugl nercac sth'ta ipdngeim hre acharte. Btu who is tshi teperaervseitn of na vtubsortcei diros?edr ntr'Ae glnu rscnace eirvrcttise fi nyniht?ag hsnakT

nlkrueger  I agree that it's confusing but I looked at it as a physical *obstruction* since it's impinging on the airway.... but yeah idk this is weird +  
ferrero  Doesn't the trachea have cartilage rings so it wouldn't collapse which makes it seem less like a typical obstructive disorder? I'm really not sure why FVC would change because I don't see how total lung capacity or residual volume would change because those are static conditions where there is no airflow at all. I understand FEV1, peak expiratory flow, peak inspiratory flow etc. +2  
mousie  Agree this is a really tough Q but I also think I really over thought it... I eliminated all with a normal Ratio bc something obstructing would obviously produce an obstructive pattern although I don't know why FVC would be decreased. I wasn't sure about both peak expiratory and inspiration flow being decreased can someone help me with this or tell me I'm totally overthinking again.. are they both decreased simply bc theres an obstruction ..? +3  
mimi21  Yea I got confused on this question. But I guess they wanted us to look at it as a obstructive disease . If this were the case all of those function tests would dec. ( See FA ) +  
gh889  Because the obstruction is above the alveolar regions there is a decrease in air flow, not lung volumes, which would make this an obstructive pathology. +3  
charcot_bouchard  FVC here dec same way it dec in Obstructive lung disease. Read the concept of Equal pressure point of BnB. There he says in bronchitis we have onstructive pattern because inflammed airways gen more resistance. so EPP comes early. I guess here due to tracheal narrowing pressure inc downstream. which collapses smaller airway. result in air trapping. +1  


submitted by .ooo. (30),
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I lsenryloap gthtohu of hsti neusqstio hikgtinn fo it ni hstee m.sert. eincS eth pneitat has a sasm ni het htarace kpae arrixyetop dan rnspytriiao lowf lwli eb ut,rertipend nda would frthreeeo be d.aecrdese FV1C ldowu sola ahev to acreeesd by its.h ihTs ildeatinme lal eth hrtoe iccsohe.

charcot_bouchard  Are you Me? +1  


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yWh si it 9%9 adn tno 95%? It kesad ofr soetn fo ssdeiea ta less ahtn 9 asery fo .gae mI' lcylera sinisgm otimenhsg eehr

cbrodo  @fulminant_life because the mean age is 3.8 with a standard deviation of 1.8. An age of onset of 9 years is nearly 3 standard deviations above the mean. Therefore, since we know +/- 2 SD covers 95% of the bell curve, it must be higher than that. The only option higher than 95% is 99%. +10  
charcot_bouchard  Yes 9.2 was the upper limit for 99% CI. I picked 95 first because i thought 2.5% would be out of this range. But changed ans because it should be less than 2.5% because 9.2 is so close to 9. Also they are asking CLOSEST to which of the following? +2  


submitted by link981(157),
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owHvere ,wrdie uoy have ot eerpcst hte attpiesn' beflesi as gnol as eyth ertn'a tnuptig eth nwebonr ta mr.ha In sethe sepyt fo souetisqn you evah ot dlbui iasc-ienthyipptna ipsnhrlsteoai ubaeces hte anpteit gmith eomceb edffenod fi ouy edrdgsiar teihr .sefeibl oS leiwh hte nwnorbe somt klyiel sah ags dan otn eht" leiv ,eey" coheic E si het satel en"nifdg"fo asnrwe ttah sesgsgtu en.taretmt

charcot_bouchard  Exactly. If she was cracking the egg on Baby's head u stop her lol (i am cracking up on my own jokes) +3  
jesusisking  I feel it but dang, she lowkey drizzlin salmonella all over that baby +2  


submitted by sympathetikey(1265),
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eyKs weer the:

lGcoui-srua

sro-tahPapuih

-iomAn aauicird

hesTo uhdosl be -adbeorsber yb eth PT,C so fi e'eytrh tn,o pyeT 2 A.RT

lamhtu  To be even clearer, this sounds like **Fanconi syndrome, which has lead to Type II RTA** +12  
yb_26  To be even clearer: Wilson disease => Fanconi syndrome => type II (proximal) RTA +  
charcot_bouchard  To be even clearer, you all have been pretty clear +  
charcot_bouchard  To be even clearer, you all have been pretty clear +  
yng  I don't thin this is Wilson (copper in descemet layer of cornea). This is cystinosis (crystal in the cornea) --> Fanconi Syndrome --> Type II (PCT) RTA. +  


submitted by sympathetikey(1265),
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yeKs ewer ht:e

aui-ouGsclr

iut-aoahhpsrP

n-iAom acruadii

esTho lusdoh eb -orsebredba yb teh TC,P so if ethry'e no,t peTy 2 AT.R

lamhtu  To be even clearer, this sounds like **Fanconi syndrome, which has lead to Type II RTA** +12  
yb_26  To be even clearer: Wilson disease => Fanconi syndrome => type II (proximal) RTA +  
charcot_bouchard  To be even clearer, you all have been pretty clear +  
charcot_bouchard  To be even clearer, you all have been pretty clear +  
yng  I don't thin this is Wilson (copper in descemet layer of cornea). This is cystinosis (crystal in the cornea) --> Fanconi Syndrome --> Type II (PCT) RTA. +  


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kSni oprdisve nolasituni nda veentrsp ahte loss. hiTs itst'pean ybod will tacsenepom orf dacinrese taer fo tahe osls yb ceigrsnani caiotmble er.ta

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? +19  
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. :) +1  
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. +  


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Teh mtos orinttpam nhtis ot the tisnqoue rae as fwool,ls ithw #2 eigbn eht mtso :eifccips

)1 itnpeta treprso apin whti ahveedro omntoi nad orrpest utrcerner oerdahev otnomi urndgi wk.ro arehveOd imnoot nca amdaeg het putsnasiusrpa umcsel ued ot niigtmmnpee yb teh mocr.oain

2) Pian si oswrt wtih rlnetnia tointrao of het osrhdule - shti si ntscntseio ithw eth nnfdisig fo teh mc-neapyt ,ttse ihhcw ensiciadt a snpiatuursaps iun.rjy

mousie  I was thinking along the lines of overhead motion - damage to the subacromial bursa which is between the acromion and the supraspinatus ... also its the most commonly injured rotator cuff m. so could have guessed this one right +1  
sympathetikey  Thanks for the explanation. I was scratching my head as to why this is correct, since supraspinatus only does 15 degrees of abduction, but you make a lot of sense. +1  
charcot_bouchard  IDK WTF i picked Trapezius +34  
ls3076  why would injury to supraspinatus cause weakness with internal rotation though? +6  
targetusmle  yeah coz of that i picked subscapularis +2  
maddy1994  ya the whole question pointed to supraspinatus ...but last line internal rotation made me pick subscapularis +3  
darthskywalker306  I went for Trapezius. That shoulder flexion thing was a big distraction. Silly me. +1  
lowyield  saw someone post this on one of the other questions about shoulder... and it works pretty good for this https://www.amboss.com/us/knowledge/Soft_tissue_lesions_of_the_shoulder there's some videos in it, this specific one for the question is the neer test +  
psay1  FA2019 pg. 438 +1  


submitted by nor16(57),
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all hsteo non smhta gyus rhee, tndo ipks heest i,eqssoutn tyr ot eanrgra eht sun,it erhe ´uydo ayslie dnif otu ttha ouy tjus ahve ot u!tymlilp eiGv ti a ytr ):-

charcot_bouchard  This was like Filtered Load ques of Renal. Where u multiply icoming fluid (GFR) with the desired substances conc (Px) so FIltered load of A is GFR x Pa Same here. Myocardial O2 supply is Blood flow x Conc of O2 in that blood flow +4  
powerhouseofthecell  For us non math folk, how do you compare the mL/min to mLO2/mL to get mLO2/min? Sorry. Do you just find out that when you have the units beside each other, cross multiplying them gives you the correct one? I need to know this trick. I can't find this on google. +  
abcdefbhiximab  mL/min * mLO2/mL = (mLmLO2)/(mLmin) where the mL's cancel out = mLO2/min +  


submitted by guillo12(44),
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kciF nreCi :pO=clip Rtae of 2O tamtirpisscn/rouvnnoueoe 2O toacnnrotienc

CO nmsae ccdiara ttouup ro Fowl fo odolb

charcot_bouchard  This wasnt Fick +1  


submitted by sajaqua1(524),
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tWulndo' ttaol VA oldan lanboita sdyeotr ot yihoamuytitrcht of hte rkceea?map That lduow eman hatt loweb eth AV deon hte yrthhm olduw eb vpdideor by a rnuvactlire ifoc, nad etsoh ylsuula eatrec wied RQS .exsmlocpe

haliburton  that was my reasoning as well. guess not. +  
yotsubato  Shitty NBME grammar strikes again. +1  
charcot_bouchard  No. No guys. Bundle of his located below AV node and it can generate impulse. it calls junction escape rhythm and narrow complex. Below this is purkinje, bundle branch & ventricular muscle. those are wide complex +13  
abhishek021196  Third-degree (complete) AV block The atria and ventricles beat independently of each other. P waves and QRS complexes not rhythmically associated. Atrial rate > ventricular rate. Usually treated with pacemaker. Can be caused by Lym3 disease +2  


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pAaplerytn hsreet oerl fo ctisamtyphe semyst in oscnhypcegi nticreeo dan sti ocmes fomr 1L2.-T1 oS if iptntea aveh anriotancst ta L5 teyh soel xelerf ectiorne btu lilst nrteai sngyioecpch eno.

voABe 9T trnintaacso cusae sslo fo ogsiceyhnpc tcrineoe

charcot_bouchard  Below L5* (Not at) +  


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paK is pH at ihhwc yan gdur si ta sit 5%0 odiezni .saett

wNo ew aer lka ieunr .ei icn H.p ehwn pp;&KaHgt ti liwl vhea wto dfif apth ofr cdiica gdur ;ma&p bicsa gdu.r

dcAcii dgru llwi icn tis eiiinlaonmt ic(n inezdoi o,fr)m csbia rudg lwil be roem ssoo.radbbe ew dnee ot owkn the ugdr si ciasb cc/id.ai

Now if u lka urnie tsi eoiianmntli .inc os ti avhe ot eb ci.daci or u acn ownk ist a odis tlsa fo udgr htiw NCS rytpoerp ei. somt lkie lenioPabbraht (eaWk iad)c

os fi aKp fo dugr si -t-6-a Hp 7 we lwli srtat nielgtainmi

tub if paK si 0 we ened to saier pH of iunre at 11 ot sattr atiginte.nlami ahtt niopt ervp dgru =)a6p(K wdolu be lotylat uot of .esymst

hatst hwy A si eth ighrt san Ka(p = 6)

charcot_bouchard  Correction : Not 0. i means if pKa is 10 +2  
charcot_bouchard  2nd update : cont to learn school grade chem. if pKa > 7 it is base. and if pKa is < 7 it is acid. Since we established the drug have to be a weak acid pKa cant be more than 7. +  
dbg  thanks, but Pka and PH are not at all the same thing +1  


submitted by strugglebus(163),
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utoA dmo sdsieae are slluayu zrogseeyhuto ro( os etyh atnw us to m)usase

xxabi  How do you know is autosomal dominant? +3  
scpomp  Hereditary spherocytosis +  
fshowon  Isnt the mean corpuscular hemoglobin concentration increased in spherocytosis? Thats what through me off. +5  
charcot_bouchard  yes, would be inc in prev NBME. But this is batshit nbme 20. U have to identify spherocytes without central pallor in PBF +4  
charcot_bouchard  yes, would be inc in prev NBME. But this is batshit nbme 20. U have to identify spherocytes without central pallor in PBF +  


submitted by strugglebus(163),
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uAto mod assidee era lsuulay eothguorezsy o(r so tyhe nwta us to esua)ms

xxabi  How do you know is autosomal dominant? +3  
scpomp  Hereditary spherocytosis +  
fshowon  Isnt the mean corpuscular hemoglobin concentration increased in spherocytosis? Thats what through me off. +5  
charcot_bouchard  yes, would be inc in prev NBME. But this is batshit nbme 20. U have to identify spherocytes without central pallor in PBF +4  
charcot_bouchard  yes, would be inc in prev NBME. But this is batshit nbme 20. U have to identify spherocytes without central pallor in PBF +  


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Kpa is pH at hcihw ayn udgr si ta sit 05% einiozd ste.at

Now we aer akl ieunr ie. nci pH. when &pKHpa;gt ti illw veah tow ifdf tpah rfo daicic grdu ap;m& aiscb d.rug

icciAd rgdu lwil nci sit aionmiltein cni( ionedzi ,mof)r icbsa ugrd ilwl eb orem aeso.robdbs we ndee ot wokn teh ugdr si basci /iiadcc.

owN if u alk urien ist eliiotinman c.in so it vhae ot be cicid.a or u cna owkn ist a sido ltsa of gurd itwh NSC etroppyr ei. mtos lkie nlraPobeihbta ak(eW a)icd

os if aKp of dgur is 6---ta pH 7 ew wlil rastt egiminalint

btu fi apK si 0 we dene to aeris Hp fo unire ta 11 to tsrta iimlitagent.an thta toinp vepr gurd =6a()Kp ldowu eb totyall tuo fo ssyemt.

tshta wyh A si eth grhit nas K(ap = )6

charcot_bouchard  Correction : Not 0. i means if pKa is 10 +2  
charcot_bouchard  2nd update : cont to learn school grade chem. if pKa > 7 it is base. and if pKa is < 7 it is acid. Since we established the drug have to be a weak acid pKa cant be more than 7. +  
dbg  thanks, but Pka and PH are not at all the same thing +1  


submitted by hayayah(1057),
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eTh trigh nda flte ltcrvneei rae idndrae yb aarpeset pastr fo eth noreafm of oron.m Ltf(e dise si arnddei by eftl mrno,o girht ides yb hrigt )onm.ro nA btotscnruoi of hte itghr mornefa of ornom illw ergealn teh grthi eirect.lvn

hmorela  My mnemonic for CSF flow: "Little Infants Crying For Food. Sorry, All Done." Lateral ventricle - intraventricular foramen of monro - cerebral aqueduct - forth ventricle - foramen of lusaka/magendie - subarachnoid space - arachnoid granulations - dural venous sinuses +12  
charcot_bouchard  u missed 3rd ventricle, how about " Little Igor the 3rd, Crying for..." +5  
len49  "Little Infants Try Crying For Food. Sorry All done." Added the T (try) for third +1  
caffeinequeen  Kind of a stretch but: LIT AFF to SAD Lateral ventricles -> Interventricular foramina of Monro -> Third Ventricle -> cerebral Aqueduct of Sylvius -> Fourth ventricle -> Foramina (luschka and magendie) -> Subarachnoid space -> Arachnoid granulations (reabsorbed) -> Dural venous sinuses (drains) +1  
fatboyslim  Kind of dirty but: Monroe (foramen Monroe) likes to get on top of Sylvius (cerebral aqueduct AKA aqueduct of Sylvius). Then Luschka and Magendie are in alphabetical order. +1  


submitted by hayayah(1057),
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tteliL ginefr = luran v.rnee

T18C- are het ootrs fo eth nulra eern,v chihw is a ranbhc fo hte adelim drc.o ehT uarln enrev si nto udnfo ni teh lcraap ntnlue ht(e imedla neevr i.s)

rlUan .n geamad can elda ot sslo of witrs nifoelx nda tda,cnudoi xileofn fo aeldim ,nfsergi boidtncua nad uncaoidtd fo neisgrf n,i)e(siroste oistcan of dealmi 2 cailbrmul lsu.mces sLso fo eosistann rove emdlai 1 2/1 rseg,inf undiilcgn tapehonrhy enecn.eim

sugaplum  Also to add: since it is a bilateral sx it is more likely to be coming from the spinal cord then from equal compression of ulnar nerve (in guyons canal) on both sides. unless she is a cyclist +25  
thefoggymist  shouldn't the other nerves of the same roots be affected? +  
thefoggymist  shouldn't the other nerves of the same roots be affected? +  
charcot_bouchard  Not really. In klumpeke paralysis ulnar nerve s/s dominates (Almost same cause) +  


submitted by hayayah(1057),
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satiPrisott si aaicedcetrhrz by dsra,yui f,eqnryuce ,yreucng owl bkac .npai mWr,a eretnd, denearlg .psreotta

etuAc ctlriabae np—rtsoitiiast lreod enm smto mocmno crbieuamt si .E ocl.i

ergogenic22  In young men it could be chlamydia but the question stem makes no mention of sexual activity, so it is e. coli +11  
charcot_bouchard  First this guy isnt older! He may incite Daddy issue but not older. At this age people tend to be more monogamous so E Coli the more likely answer. But again cont NBME 20 trend this one was pretty vague too. +1  
monkey  They classify at 35 year old (<35 = Chlamydia or Neisseria and > 35 = E.coli) +3  
mbourne  I put Pseudomonas, as that is a cause of prostatitis in older men, but it is less common than E. coli. Just keep that in mind, if E. coli wasn't an answer choice, the answer should have been Pseudomonas. If he was a younger male, then Chlamydia would have been acceptable. +3  
brotherimodu  @mbourne I think Pseudomonas is the more common etiology for acute prostatitis in the elderly (>65ish for exams), whereas E.Coli is the more common etiology in adults 35-64yo +  


submitted by hayayah(1057),
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Case fo ooe.tlrrrlascesoisi

Hyesiptlrpca sreiicerrtaolososl isovlevn higictnenk of vlsese awll yb sepraihaply fo oomths ucslme os-nnii'n(ok e)rpacn'epaa

  • qenoeunecCs fo atnnglmai trpesihonyen 08g(&2;/t101 w/ cateu negr-doan mg)eaad
  • Ruelsts ni ecruedd vselse realbic whit neng-odar aecmhisi
  • ayM dlae ot riiofdinb oceissrn of teh lessev alwl twhi aheehrg;mor saslllcycai ausesc atcue erlan iruelaf F()RA itwh a iharccceatrsti -ifa'b'tnteel ppnceaeaar
masonkingcobra  From Robbin's: Fibromuscular dysplasia is a focal irregular thickening of the walls of medium-sized and large muscular arteries due to a combination of medial and intimal hyperplasia and fibrosis. It can manifest at any age but occurs most frequently in young women. The focal wall thickening results in luminal stenosis or can be associated with abnormal vessel spasm that reduces vascular flow; in the renal arteries, it can lead to renovascular hypertension. Between the focal segments of thickened wall, the artery often also exhibits medial attenuation; vascular outpouchings can develop in these portions of the vessel and sometimes rupture. +  
asapdoc  I thought this was a weirdly worded answer. I immediately ( stupidly) crossed of fibromuscular dysplasia since it wasnt a younger women =/ +16  
uslme123  I was thinking malignant nephrosclerosis ... but I guess you'd get hyperplastic arteries first -_- +  
hello  The answer choice is fibromuscular HYPERplasia - I think this is different from fibromuscular DYSplasia (seen in young women); +23  
yotsubato  hello is right. Fibromuscular hyperplasia is thickening of the muscular layer of the arteriole in response to chronic hypertension (as the question stem implies) +7  
smc213  Fibromuscular Hyperplasia vs Dysplasia...... are supposedly the SAME thing with multiple names. Fibromuscular dysplasia, also known as fibromuscular hyperplasia, medial hyperplasia, or arterial dysplasia, is a relatively uncommon multifocal arterial disease of unknown cause, characterized by nonatherosclerotic abnormalities involving the smooth muscle, fibrous and elastic tissue, of small- to medium-sized arterial walls. http://www.medlink.com/article/fibromuscular_dysplasia +1  
smc213  *sorry I had to post this because it was confusing!!!*Fibromuscular dysplasia is most common in women between the ages of 40 of and 60, but the condition can also occur in children and the elderly. The majority (more than 90%) of patients with FMD are women. However, men can also have FMD, and those who do have a higher risk of complications such as aneurysms (bulging) or dissections (tears) in the arteries. https://my.clevelandclinic.org/health/diseases/17001-fibromuscular-dysplasia-fmd +1  
momina_amjad  These questions are driving me crazy- fibromuscular dysplasia/hyperplasia is the same thing, and it is NOT this presentation and it doesn't refer to arteriolosclerosis seen in malignant HTN! Is the HTN a cause, or a consequence? I read it as being the cause (uncontrolled HTN for many years) If it was the consequence, the presentation is still not classical! -_- +1  
charcot_bouchard  Poor controlled HTN is the cause here +  
charcot_bouchard  Also guys if u take it as Fibromuscular dysplasia resulting in RAS none of the answer choice matches +  


submitted by hayayah(1057),
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aseC of lireslst.ioerorcoas

trcyiHppaesl iereosrcrilosotlas inovlsev eiinhgtnck of elssve llwa by aippysahrle fo osmoth slucem on(iio-'nnks er)epnpaaac'

  • Ceunnoseqec of itlnmanga hryneosneipt (1/0g;1&t802 /w tueca ondnr-gea gde)ama
  • ultseRs in reeducd evssel blrieca wtih ndgraone- aicemhsi
  • Mya ldea ot rnifdobii esoicrsn fo teh evesls wlal hwit eahr;herogm illyaccslsa acssue uctae anelr liraufe F)A(R hiwt a aceccsthtirria 'aeb'n-fittel apeenacpar
masonkingcobra  From Robbin's: Fibromuscular dysplasia is a focal irregular thickening of the walls of medium-sized and large muscular arteries due to a combination of medial and intimal hyperplasia and fibrosis. It can manifest at any age but occurs most frequently in young women. The focal wall thickening results in luminal stenosis or can be associated with abnormal vessel spasm that reduces vascular flow; in the renal arteries, it can lead to renovascular hypertension. Between the focal segments of thickened wall, the artery often also exhibits medial attenuation; vascular outpouchings can develop in these portions of the vessel and sometimes rupture. +  
asapdoc  I thought this was a weirdly worded answer. I immediately ( stupidly) crossed of fibromuscular dysplasia since it wasnt a younger women =/ +16  
uslme123  I was thinking malignant nephrosclerosis ... but I guess you'd get hyperplastic arteries first -_- +  
hello  The answer choice is fibromuscular HYPERplasia - I think this is different from fibromuscular DYSplasia (seen in young women); +23  
yotsubato  hello is right. Fibromuscular hyperplasia is thickening of the muscular layer of the arteriole in response to chronic hypertension (as the question stem implies) +7  
smc213  Fibromuscular Hyperplasia vs Dysplasia...... are supposedly the SAME thing with multiple names. Fibromuscular dysplasia, also known as fibromuscular hyperplasia, medial hyperplasia, or arterial dysplasia, is a relatively uncommon multifocal arterial disease of unknown cause, characterized by nonatherosclerotic abnormalities involving the smooth muscle, fibrous and elastic tissue, of small- to medium-sized arterial walls. http://www.medlink.com/article/fibromuscular_dysplasia +1  
smc213  *sorry I had to post this because it was confusing!!!*Fibromuscular dysplasia is most common in women between the ages of 40 of and 60, but the condition can also occur in children and the elderly. The majority (more than 90%) of patients with FMD are women. However, men can also have FMD, and those who do have a higher risk of complications such as aneurysms (bulging) or dissections (tears) in the arteries. https://my.clevelandclinic.org/health/diseases/17001-fibromuscular-dysplasia-fmd +1  
momina_amjad  These questions are driving me crazy- fibromuscular dysplasia/hyperplasia is the same thing, and it is NOT this presentation and it doesn't refer to arteriolosclerosis seen in malignant HTN! Is the HTN a cause, or a consequence? I read it as being the cause (uncontrolled HTN for many years) If it was the consequence, the presentation is still not classical! -_- +1  
charcot_bouchard  Poor controlled HTN is the cause here +  
charcot_bouchard  Also guys if u take it as Fibromuscular dysplasia resulting in RAS none of the answer choice matches +  


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obslurrmFuaci paseprlhaiy iwll uaecs epr elnra tmieao.az S. /CNUrB si 0g2t&; in per earln omaeatzi but ni eth notuqies tsi uvlea is ievcnidait fo csiirtnin alren e.aifrul vrye fngo!nu!sic

charcot_bouchard  Not really, Hypotension cause pre renal azotemia. Here long standing HTN resulting in end organ damage so intrinsic renal failure +2  
cry2mucheveryday  ugh! i just noticed there's a fairly long h/o of poorly controlled HTN which makes this question simpler now. Thanks!! +  
j44n  arterioles are in the kidney.... ya know like afferent/efferent ARTERIOLE @ the glom. if this was in the renal artery he'd have pre renal azotemia +  


submitted by breis(44),
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Pstisciaost mseeimso(t cllead trhosisnio ro orrapt aseseid or rtopra r)vefe si na nifeticon fo het lugn aouim)npne( sdeuac yb eth abieurctm imlpohlaCaydh )mayidah(lC pt.ciiats

nsgiS and myootcsg. uee v:s,phrfm aulyslu ittuowh cmuh ehm emcc.reaa.hs ahhuslg.ld pe hehs.seccta .shtr nspnaeosi of thrr.eoeab s ot.htar

charcot_bouchard  Update on my prev comment : Yes this is psittacosis. not hypersensitivity pneumonitis. How do u know? Lymphocyte and Presence of Granuloma - response to intracellular chlamydia. Now HS can also cause loose granuloma too and the clinical picture still more look like HS You know what ......... fuck this ques +  
shemle  Here Pt. doesn't have fever! +7  


submitted by strugglebus(163),
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ynieLs si sedu ni esliatn and galcleno ossrc giknn;il it is cossr ldinek yb yysll aedsxoi ot mkae caenollg ebisrf

charcot_bouchard  Thats my brother from UFAP mother +2  
smpate  but glycine and proline are used in elastin too. Seems like you'd have to know about desmosine though that's not in first aid. Or maybe you can infer lysine since it's charged and is probably more important in maintaining stability? +  
adong  the only thing we know about cross-linking is with LYSYL oxidase, hence lysine +3  


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yecaNosrpl sha noe of het nwoiofllg 3 ertrrahacc - 1. aply.Cxe2ta cde rioxen in c. 3fs RME taclney ;lt51& min

tsi ass with ton( xd aHiaopgim(iyccgoiep/ntn prr al.honincatil elpeS aplyaissr

charcot_bouchard  oh dx criteria must also include excessive daytime slepeiness for 3 time per week over 3 month +  


submitted by hayayah(1057),
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Teh uebst aer tecserath upt in orf uerni to fwol otni a g.ab oS niure tpuotu si igong ot enicrae.s ehT ttneapi si slao phileya.cmker oserlAtnedo drsnesop to emhiryeaalpk by aecsirnign +K ricneeo.xt

leHameakyrip will tuaemitsl oendsarelot etrnoisce even if inren si psussedper edu to his ser.heoniynpt Aotulghh aN+ lliw eb osa,rredbeb hsti lilw eb eittannsr ouhsl(d eeslvro cone the opmutiass eleslv zla)eomrind nad icsen sih uiner tupotu lilw tmos llyike rturne to ronalm, ihs lodob represus lhsdou asol .ailermnzo

charcot_bouchard  Postobstructive diuresis Postobstructive diuresis is a polyuric state in which copious amounts of salt and water are eliminated after the relief of a urinary tract obstruction. The incidence of POD is unclear but estimates suggest 0.5% to 52% of patients will experience POD after relief of obstruction.10 It generally occurs after relieving BOO, bilateral ureteric obstruction, or unilateral ureteric obstruction in a solitary kidney.11 Diuresis is a normal physiologic response to help eliminate excess volume and solutes accumulated during the prolonged obstruction. In most patients, the diuresis will resolve once the kidneys normalize the volume and solute status and homeostasis is achieved. Some patients will continue to eliminate salt and water even after homeostasis has been reached, referred to as pathologic POD. These patients are at risk of severe dehydration, electrolyte imbalances, hypovolemic shock, and even death if fluid and electrolyte replacement is not initiated.9 +7  


submitted by hayayah(1057),
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hsTi si an exapmle fo iglen.hSs eerHps xemspil nad rsepeh roezst svirseu aceus loaarbnm lelc idisnvio in rpdimeeal le,lsc dna iths tscreae umteieuadncllt natgi .clles

A kTanz reasm wngihos elcimaleutdnut gitna lsecl is ctsactarihicre of ilelVacar rZoets sirVu tcsonifin.e SH(V wlil haev airsilm )insgfi.dn

ergogenic22  other identifying terms for herpes: Single dermatome (does not cross the midline), painful (burning and itching),and lesions in multiple stages. +3  
redvelvet  and why neutrophile infiltration, is it a thing? or just a distracting thing? +1  
charcot_bouchard  Neutrophil comes into party always first. but it was distracting for me too. +6  
dulxy071  Regardless if it can help resolve the issue, neutrophil will always be the first responder +2  


submitted by hayayah(1057),
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espaiNlao si enw tiesus ghrwto htat is n,datreuugle vrb,iilrseree dna ocmonlona.l

lCyiaotnl acn be rndidemeet yb lpcptg6-uaehh-sosoe aehyddesroegn )DP(6G eezynm sforo.ims DP6G is endlik-X.

*roF rmoe taiinmofron ckech otu Ch. 3 Naeipsalo in amtohaP

hello  This is great, thank you. +4  
breis  Pathoma ch. 3 pg 23 "Basic Principles" +7  
charcot_bouchard  Shoutout to Imam Satter! Without him this question wasnt possible for me to answer in 10 sec. +13  
fatboyslim  Clonality can also be determined by androgen receptor isoforms, which is also present on the X chromosome (Pathoma Ch. 3 Neoplasia) +1  
lovebug  @fatboyslim thanks for reminding! +  


submitted by hayayah(1057),
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Tish man si oniswhg sxs of na MI.

iIatlni paseh fo oycaadmilr inrftaconi ldsea to laroedcadunibs nroecsis ligvvnion ;tl& %50 fo het amoirlcdya kctshsnei a(lbroidaeduscn ocinan;firt) EGK swsho get-sTnSme snoeesdpir.

Ceniudotn ro vesere cisaimeh 0g&2;t( ens)tumi lades ot maslnrrtau ioserscn ivnnoligv stmo fo hte rdmcaialoy alwl mautrnas(lr onifcrtn);ia EKG owssh sg-tSnemeT oianl.teve

charcot_bouchard  May i know where do u read this +1  
mbourne  @hayayah, Although this is a bit outside of the realm of Step 1, I want to clarify a point. Early MI does not typically lead to ST-depression. Early MI will typically present with hyperacute T-waves with straightening of the ST segment, and then evolve towards more familiar "STEMI" morphology. Great image representation of MI EKG changes: https://4.bp.blogspot.com/-_UbS4PvbTZE/Wr0M27TZhUI/AAAAAAAABB0/-M8FSuvTKeEGkx-7HrEd45Fl0phb2-T8gCLcBGAs/s1600/Progression%2Bof%2BACO%2Bfinal_diagram.png ST depression from subendocardial ischemia can occur with supply/demand mismatch --> ISCHEMIA, but not Myocardial INFARCTION. +1  


submitted by strugglebus(163),
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coB=ynphhonro auippntaemorx Eoryin sro=dirt trrnohhccbiaolea itturobcsno em/naf(igsosr )dtoypsibIrya orn sdiorrt = earynallg succtSciobuoousrn ntis shpls=a tets ofr pliycro ssitesno

nWhe eerht si a acrufrted bri it ilwl aesuc a tmruaa apxthnoreom wihch cna sauec iar ot spceea dna eeobmc eptprda unrde eth kisn ienagdl to ierct.psu

charcot_bouchard  Actually when a fractured rib puncture lung then it cause sc emphysema. +2  
mbourne  "Chest trauma, a major cause of subcutaneous emphysema, can cause air to enter the skin of the chest wall from the neck or lung. When the pleural membranes are punctured, as occurs in penetrating trauma of the chest, air may travel from the lung to the muscles and subcutaneous tissue of the chest wall. When the alveoli of the lung are ruptured, as occurs in pulmonary laceration, air may travel beneath the visceral pleura (the membrane lining the lung), to the hilum of the lung, up to the trachea, to the neck and then to the chest wall. The condition may also occur when a fractured rib punctures a lung; in fact, 27% of patients who have rib fractures also have subcutaneous emphysema. Rib fractures may tear the parietal pleura, the membrane lining the inside of chest wall, allowing air to escape into the subcutaneous tissues." +1  


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shTi si TAILYRELL teh emsa pooht yeth seud to rceesbid teh y4erdo--la ybo htwi fsdiufe iacroclt reconiss rfmo NEBM 1.8 anC oeoemns paxnlei hasw't inogg on hree

lancestephenson  *Tubular atrophy, not cortical necrosis lol +  
charcot_bouchard  Can u fuckers talk about spoilers +1  
adong  same photo because the end gross pathology is the same. whether it's due to cancer or whatever the 4 year old boy had (some sort of obstruction IIRC) it ends with atrophy of the kidneys +  
j44n  they used the same kidney on NBME 17 for posterior urethral valves lol +  
j44n  this is probably the most famous kidney in medicine +  


submitted by kentuckyfan(43),
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inSce eth anip is arruil,dac a dics eainonriht si mtso l.iylke

charcot_bouchard  Why it cant be a lumbar vertebra fracture +  
whoissaad  @charcot The patient is young and doesn't have any risk factors for weak bones. Also, disc herniation is a common problem in the young. The disc gets fibrosed and stiff in the elderly so they have less chance for disc herniation. So basically age was the key to answering this question. +3  
lovebug  you are genius! thank you! :) +  


submitted by hayayah(1057),
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eBgnin srmotu rae aylusul tliferdileetfawd-ne adn acdt,aer-weldmle ihtw wol ictomit a,tiicytv no teeassmsa,t dan no eoc.sinsr

Magatnlin rmtuso ()rsaccen yma whso orpo ieardinn,itoefft atricre whtg,or llaoc iaosvi,nn s,ttmaesasi dna stioppoa.s giHh iitctom titv.iyac

Fat rsuto:m

  • mL:ioap ieb,gnn olw oicittm iciytatv
  • aaripo:sLmco nmtala,gni reinceasd tiomcti iatcivty
whossayin  why can't it be a rhabdomyosarcoma? +  
charcot_bouchard  Because of histology and gross appearance... very graphic description of fat cell tumor there +5  
dr_cruceta  because the question said irregular vacuolated cells, describing fat cells. Rhabdomyosarcoma comes from skeletal muscle. +4  


submitted by youssefa(126),
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rmoF iFda 0921 nwe ru:gefi 1-GFI alinym ftncoisnu sa an laobcnia ehmoorn no lmcseus and osenb tyter(p hmuc lkie s;giuli-&tnn dceesarse ursem .usegl)co HG ctsa raeastepyl yb rgtnpomoi niinuls cneatsersi ncgsrini(ea muesr usg.ec)lo r,hfroeeTe GI-F1 is ont the snae.wr fI GH asw aomgn hte nsawrse ti uwdol haev tgo rlleya .fgcnounis

charcot_bouchard  Can anyone take a little time to curse on that daughter? +5  
dbg  Sure, charcot. Just wished on her to get a couple of charcots (the triad, your aneuryms, marie tooth, etc). +1  
noorahsaahir  Charcot_bouchard and dbg best comments .... 🤣🤣🤣🤣🤣 +  


submitted by step420(33),
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This is mllerianu s.aieengs orNmal iroevsa btu stnbea s.urteu

endochondral   why not androgen insensitivity? +  
shaeking  I was wondering the same thing because doesn't androgen insensitivity also have normal female secondary characteristics. Was it the levels of hormones because she doesn't have abnormally high testosterone? +2  
swb  Androgen insensitivity has the same presentation and symptoms. What's the clue that it is mullerian agenesis instead ? +19  
sugaplum  Testosterone would be high if it was androgen insensitivity FA 2019 Pg 625 +13  
charcot_bouchard  Testo would be high in AIS. in AIS pubic hair, axillary hair doesnt devlop because of androgen insensitivity. both have normal breast dev and primary amenorrhea +1  
dickass  This is not androgen insensitivity because she has perfectly normal Estradiol, which means she has perfectly normal ovaries. She also has regular female levels of testosterone. +4  
rockodude  thank you @dickass +1  
j44n  Also AIS has paradoxically large boobs-> tanner stage 5 and thats not mentioned anywhere +  


submitted by yotsubato(979),
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ias"psnhiyc olhsdu lasawy gacroenue letyahh mdognnairiau-r acootni"mnuc.mi

sAlo r'eyuo nigog ot do smoe ouisres ngiths to ceur iths rlg'is esaised, gnaeild up ot tanoimpuat. ouY antc hied tath morf rhe.

djjix  Non sense ... you can hide the amputation from her +18  
charcot_bouchard  Just show her one leg twice. +4  
pg32  I picked "request that an oncologist..." because I figured it would be better to have someone with more knowledge of next steps and prognosis discuss the disease with the family as compared to someone working in the ED... why is that wrong? +2  
ibestalkinyo  @pg32: Referring to another physician is almost never an answer for NBME/USMLE questions. Plus, I feel like this would be hiding the patient's problem from her and the patient's parents. +5  
dunkdum  I think the reason that you requesting the oncologist isnt the most correct answer here is because... even if more tests needed to be done... you would still discuss with your patient about that fact and say "Hey these results came back suggesting that you might have this disease, we will need to do more testing to make sure we can get it taken care of if you in fact have this disease." and you'd probably do that before you go and get the oncologist. +4  
peteandplop  @pg32 I was kind of with you, but I went with the correct answer because it says STRONGLY suggestive. If you're giving me a powerful word to really emphasize this is osteosarcoma, there's no need to delay passing that information to patient, and in this case of a minor, her parents. +1  


submitted by usmleuser007(377),
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yaailvrS nectirsoe .1 tA lwo lwof = ighH narintcnoteoc of itpmous;as owl ooctninstraenc of o,msidu arcbbi, ;amp& c .olrhi2de ta ghhi lfwo = lwo ntioarecnotnc of tusp;smioa ghih anctirceotosnn of oiusd,m bbiarc, apm;& cierlodh

sherry  That's exactly what I was thinking when I was taking the test. But I was sidetracked by same HCO3 level. Can somebody explain this part to me?? +  
charcot_bouchard  Because salivary duct removes Na & Cl while secrete K & Hco3 in lumen. In low flow rate HCO3 & K inc because duct is doing its thing for more time. At high flow rate K slightly dec (as cant be secrted as much) but HCO3 stays almost same. the reason is high flow indicates higher metabolism & higher bicarb production. +  
cienfuegos  Regarding the bicarb (via BRS Physiology, which explains flow rate as coming down to "contact time" where slow flow allows more reabsorption of NaCl): The only ion that does not “fit” this contact time explanation is HCO3−; HCO3− secretion is selectively stimulated when saliva secretion is stimulated. +3  


submitted by celeste(79),
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dnSuso elik a yhrhierotpcp arsc. crrpopH"eyith crass ancoint rayplirim etpy III eglclnao irndeeto lplalear to het lpmaeeidr feracus iwth tdabunan onesudl onicnitgna yl,rfobasmtbosi elagr ulxllarctaeer alolngec tefmisanl and nullipetf iccida r".loacciscahpsoemudy 702hr..mbspn//mticpiens//.i3w28/otwllh:M.t9wccP/nagvC

johnthurtjr  I think it may actually be a keloid, not a hypertrophic scar, as it expands beyond the borders of the original incision. +5  
thepacksurvives  I believe this is a keloid; a hypertrophic scar does not extend past the borders of it's original incision, while a keloid does. regardless, the answer to this question is the same :) +  
breis  First AID pg 219 Scar formation: Hypertrophic vs. Keloid +  
charcot_bouchard  They give granulation tissue is a option which is type 3 collagen. so if it was hypertrophic scar it would be ap problem since its only excessive growth of Type 3. while keloid is excessive growth of both 1 and 3 +3  
bharatpillai  I literally ruled put collagen synthesis defect since this is not a collagen synthesis defect at all ( EDS, Scurvy) :/ hate these kind of questions +  


submitted by xxabi(252),
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Silhgof etwlne  ,.po chdler ie.c(lyg igimit→ecn)aais desnho  rts:euee cdonaestour dcdArP eieTp + eT+Aca/Ke rad  sneasaePdNd→ pm2a+Cpu vdi af uicnoofs →iyfitt N+n ada earwt etihnot  ce→l l aerllwse lcguliln

endochondral1  can someone explain how to cross out the other choices> +1  
endochondral1  what is hydropic degneration and where do i learn about it? why is it not the loss of plasma membrane integrity? +1  
shaeking  Endochondral1, I had the same question. I tried figuring it out and this is what I came up with. The CHF and congestion of the lungs is reducing the amount of oxygen getting to the renal cells. With hypoxia there is decreased aerobic resp in mitochondria with decreased ATP. Without ATPase Na builds up and water follows. As far as the loss of membrane integrity. I think it would cause cellular destruction not just hydropic changes. This is my best guess. +2  
charcot_bouchard  Membrane damage is irreversible stage of cellular injury. if membrane is damaged cell is dying & it will shrink. or totally destroyed by inflammation. they are specifically asking hydropic changes ie cellular swelling. which is the 1st sign of reversible cell injury due to failure of Na/K pump +1  
winelover777  @endochondral1 Chapter 1 of Pathoma. Also FA 2019 p207 describes hydropic degeneration without saying those exact words in the first bullet under reversible cell injury. +1  


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daincgrco ot urldow ieiieyvntprtssyh suinpmnotie is ude ot tsdu dna atth was sola an poni..t.o.

amarousis  so it's definitely dust but the specific type of dust was the most important in this question. the fact that they mentioned the birds is important. the dusty books would cause it but the bird dust is more important -.- +  
charcot_bouchard  Hypersensitivity Pneumonitis - Organic dust (like moldy hay) Pneumocniosis - Inorganic dust none help here though because both will present with same restrictive lung disease picture. i think since dust in library arent neither organic or inorganic and also u dont see many librarians with lung disease but bird ownership is specifically mentioned as cause of HP disease. +  


submitted by jotajota94(14),
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sUe teh rdgbeHnyWeria- iqneoatu

  1. akeT eht auqres rtoo fo 1001,/6 nda ttha iwll iveg ouy teh nqrueyfec fo hte svseereci llleae = ./140
  2. lulaetCca teh enycqerfu of het doatinmn lealel ihtw ,q+=p1 chiwh si p= 975..0
  3. hyTe aer glltine oyu ot ateacclul eht feyrcqenu fo hte esseiad aires,crr ihhwc si whit teh eqtianuo qp2.
  4. heTy anwt noly het eedasis siarrrec in ciwhh netdoeli is .pterens oT aclaecltu t,shi sue the q elauv 4)(1/0 nda yutmipll by 0%8 in tish ldshuo igev oyu 2.0.0
  5. Faiyl,ln atlucleac rfo P22q )500(70..(=)29 4.00 = /15.2
yex  Nice! ...and we are supposed to read the stem and do all this in a minute or so? :-/ +22  
charcot_bouchard  Allele frequency 1/40. so carrier freq 1/20. 80% of 1/20 is 1/25 (80/100 x 1/20) +14  
dickass  Ah feck, 2pq got me +  
hello_planet  A handy shortcut for Hardy-Weinberg is that you generally can assume p ~= 1 if q if fairly low. It also tends to be easier to work in fractions if the answer choices are in fractions so you don't have to bounce back and forth between fractions and decimals. So with that, you send up with 2pq = 2 * 1 * 1/50 = 2/50 = 1/25. +4  


submitted by hayayah(1057),
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Hnaeidpiudr-nec cyointhtooamebpr H()TI si the entlmdopvee of gGI oitbnsidea ainagts nriheap onbdu tleeptal frctao 4 4P(F). in4eF-onaitrPdhpA-yb oclpexm tscvetaai splelteat Ž sibtrhooms adn ooctiyrbenh.amtop sHethig risk iwht eountrftdaacin e.rpnaih

drw  could you also help to understand: 1) could anti-heparin-PF4 complex be also called anti-PLT antibody? 2) PLT reduction is due to both PLT thrombosis consumption and elimination in the spleen, then why hypersplenism is not correct? +  
charcot_bouchard  hypersplenism means bigger spleen eating everything. thats not the case here. here spleen is normal. autoimmune cause +  
benitezmena  Yes I dont understand why the called them Anti-platyelet antibodies and not specifically Anti-heparin bound to PF4 on platelets. Its just not the right antibody +2  
benitezmena  Antiplatelet antibodies would be for ITP, but also anti-megakaryocyte antibodies would also be for ITP. +1  
misterdoctor69  As an aside, pregnancy is a hypercoagulable state which caused her DVT in the first place +1  
cport12  If anyone else was freaking out about the word hemodilution basically it just means that there is a decreased concentration of cells and solids in the blood resulting from some other gain of fluid. With normal pregnancy (not HIT), blood volume increases, which results in a hemodilution. +  


submitted by step420(33),
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Othre kndiey rposepethiyrH due to ncisrdaee tssrse -&;-gt nto haylpeisapr cb otn causecron

masonkingcobra  Above answer is incorrect because hyperplasia can be either physiological or pathological. Prolonged hyperplasia can set the seed for cancerous growth however. Robbins: Stated another way, in pure hypertrophy there are no new cells, just bigger cells containing increased amounts of structural proteins and organelles. Hyperplasia is an adaptive response in cells capable of replication, whereas hypertrophy occurs when cells have a limited capacity to divide. Hypertrophy and hyperplasia also can occur together, and obviously both result in an enlarged (hypertrophic) organ. +38  
johnthurtjr  FTR Pathoma Ch 1 Dr. Sattar mentions hyperplasia is generally the pathway to cancer, with some exceptions like the prostate and BPH. +4  
sympathetikey  Tubular hypertrophy is the natural compensation post renal transplant. Just one of those things you have to know, unfortunately. +2  
charcot_bouchard  Isnt Kidney a labile a tissue & thus should undergo both. This ques is dipshit +  
brbwhat  Dr Sattar says, kidney is a stable tissue, at least pct is as seen in ATN. But I read, basically kidneys are mostly formed whatever number of nephrons have to be formed by birth, after that they can only undergo hyperplasia aka increase in size/or regenerate if need be in case of atn. We cant have more number of nephrons. +1  
mambaforstep  @brbwhat , do you mean kidneys can only undergo hyperTROPHY? +2  
j44n  .... you're not making more cells..... so it cant be hyperplasia +  


submitted by hayayah(1057),
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Add on to teh eohrt mnoe:mct EOCM.SSFIKCCA n(ewhI Am iikrdgnn tirurGepaf ujeci) is het coemnmni ofr ereengimmrb het YC4P05 nsr:btiiIho

  • S omdui lperoaavt
  • I oznisdia
  • C neiitedim
  • K ozateolenco
  • F ozalocnelu
  • A etcu hlolaco uaebs
  • C onmpiolhelhacr
  • E riyhnoymarciynlchr/cmrttio
  • S ndufmlaoies
  • C ofxinacloirp
  • O eoermzlap
  • M aitodzlneeor

  • A dormeinoa

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


submitted by hayayah(1057),
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ntniofDiei of ausnjemtdt idedrrs:o

lmionatEo mstmsopy (g,e inxyeat, ined)spores htat ucroc nihtwi 3 smtonh fo an tlindieaeibf yhcssoliacop ssrrseto g,(e ivce,odr sl)slein sgnailt lt;& 6 htomns enco het sstsorre ahs ddeen.

If moypmtss psetirs &;tg 6 sotmhn raeft ssreostr s,edn ti is G.DA

hello  Yep, and I think what we are supposed to take from this Q is: The only info. we have for this patient is that he ended chemo 2 months ago and has been calling the doctor a lot -- this is supposed to mean he has been calling a lot since ending chemo 2 months ago. His frequent calls starting after ending chemo and within 3 months of the stressor fits with the above-stated definition of "adjustment disorder" with anxiety. I stressor in this case could possibly be either the actual illness or the ending of chemo/treatment. It probably does not matter much in this case. +3  
charcot_bouchard  I think doing uw done me wrong here. Adjustment disorder isnt diagnosed when symptom match another disorder --- it was like never a right answer. But ofc its right answer in nbme +5  
maxillarythirdmolar  Just to add to that, the tingling in his fingers may seem like a distraction/it probably is. Likely has some relation to his Chemo. +3  
j44n  shit I thought this poor guy had OCD with all the repetitive behaviors. +  


submitted by strugglebus(163),
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O,K os fi I eebrmmre rctcyrelo tihs si het eon atth sohws teh rieaihentcn ta.rpetn trhioocmndail is slao espsad yb het ohm;ret rve,hoew it acn eahv vbiaealr eivipxyrtess nda omnictpele crp,nneaeet whchi is yhw esom ebmmres wree nto ed.ctfafe

hyoscyamine  Also, question said there was a deficiency in NADH dehydrogenase activity which is another fancy way of saying complex I in the mitochondria. +13  
yotsubato  That unaffected male really threw me off... : ( +20  
charcot_bouchard  It was pure MELAS description. the unaffected male threw me off +2  
mbourne  I think the affected male on the right side is actually a helpful hint. Mitochondrial conditions can be inherited by males or females, but are only passed on through the females. +1  


submitted by hayayah(1057),
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Inor soorvdee si a seauc of a ihhg ninao pga aeictolbm isio.csad

meningitis  I found this to add a little bit more explanation as to how it causes the acidosis if anyone needs it. 1. Mitochondrial toxicity - decreases aerobic respiration and shunts to lactic acid production 2. Cardio toxicity (Secondary to Mitochondrial toxicity) leads to cardiogenic shock (hypoperfusion), which causes lactic acidosis 3. Hepatotoxicity - Decreases lactate metabolism, causing lactic acidosis 4. When in trivalent form (Fe+3), it can react with 3 molecules of H2O --> FeOH3 + 3H+ This will then deplete Bicarb buffering system resulting in non-gap acidosis. Source: https://forums.studentdoctor.net/threads/iron-poisoning-anion-gap-or-non-anion-gap-acidosis.958285/ +17  
sympathetikey  None of the other choices were even metabolic acidosis. They threw us a bone with this one. +21  
imnotarobotbut  Don't changes in bicarb take a few days? How did his bicarb drop down to 8 in 12 hours? +2  
charcot_bouchard  its met acidsis. not compensation +7  
j44n  they did throw us a bone however I didnt catch it +1  


submitted by neonem(556),
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neicS shit piatten is a sermo-nno,k it si slse ot be llmas lcel mrcaoc,nia ouumssqa lelc cora,nicma or aglre llec racioamnc of eht un.lg seBdeis samll llce caamrncoi ibegn fomr roennnrcdiueoe gion,ir eth one orjma ulgn erccan esbdrdeci by nests fo fdw,eldeteeilrnat-if rlae"gru" lescl is a cnirdoaic ortum. ltAydado,lnii sesrtoet rae hisatoollgci fruestae of cdaiirnco umsrto nfu( tf:ac rstseoet aols in yrebtpssleasoaemomna/odumn ni( NCS,) ,embtsraioalsnot aauosnrlg ellc smrtou aain(ovr )ae)rccn

mousie  When ever I hear Rosettes I always think NE tumors .... and I agree non smoking kind of RO small cell, squamous cell, or lg cell +4  
charcot_bouchard  I thought it was Hamartoma & pick chondrocyte! Can lung even have hamartoma? Pardon me it was the laast ques of whole nbme +7  
drmomo  @charcot_bouchard i thought the same. uworld gave a question on coin lesion in the lungs as classically hamartoma +7  
anbumd  From pathoma benign coin lesions such as bronchial hamartomas composed of lung tissue and cartilage are especially found in younger patients. So i guess because of the age and histology this would be less likely. +  


submitted by sattanki(69),
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eMcusl apin + ierliapotbr daeem is a iclssca niettnraespo rof tchonlrliea is.plaisr tBes asosngiid orf tsih is a lmceus sip,yob sa eth rwyom ikels ot hutoagn tniwih het s.csmuel

sympathetikey  That's what you get for killing polar bears. +75  
dr.xx  That's what you get for not cooking them well. +4  
charcot_bouchard  Theres nothing called "well cooked polar bear meat" +2  


submitted by medstruggle(12),
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yhW si ti tno rvionaa iolcflle eslc?l I hhgotut teh feaelm agolan fo eotlSri nda ideLyg si gnhctu/aeolrasa ec.lls

colonelred_  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +7  
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??? +37  
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!" +17  
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 mousie(211),
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Is 45 musinte oot lnog ot eb ltpacynaihac and wodlu hte bncesea fo rahs irati(cr,au purts)rui OR lac?patnhacyi

hayayah  Yes! Allergic/anaphylactic blood transfusion reaction is within minutes to 2-3 hours. (pg 114 of the 2019 FA has a list of them ordered by time) +7  
hayayah  (also allergy / anaphylactic presents with more skin findings (urticaria, pruritus) +6  
seagull  The time through me off too. I though ABO mismatch since it occured around an hour. I thought TRALI would take a little longer. +7  
charcot_bouchard  Guys anaphylactic reaction to whole blood doesnt occur much except for selective IgA defi. so look out for prev history of mucosal infection. And it can have all feature of type 1 HS inclding bronchospasm. +5  
soph  I saw hypotension and though anaphylaxis........ -.- +  
usmile1  Chest Xray showed "bilateral diffuse airspace disease". This is much more indicative of TRALI than anaphylaxis which would have wheezing and possibly respiratory arrest but no actual damage to the lungs. Additionally there was no urticaria or pruritus one would expect to see with anaphylaxis. +5  


submitted by neonem(556),
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yM tbse gssue is tath ihst atentpi ash a biicdspu rocita vavle and sha a mrumru eud to ceesnardi omlevu overadol fmor eht en.cgpanyr

charcot_bouchard  Can be congenital mild Tricuspid stenosis also. it also exaggerate during preg +  
wowo  probably just a flow murmur, https://acpinternist.org/weekly/archives/2017/05/16/3.htm +5  
noplanb  Wouldn't Tricuspid stenosis be a systolic murmur? +  
noplanb  I mean diastolic* +1  
centeno  I think that a murmur of grade 2/6 is a clue for flow murmur. Maybe any pathologic cause of murmur would be exaggerated in pregnancy (due to increased blood volume) +  


submitted by medstruggle(12),
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hyW si it hasphuot rluecs if etreh are on GI os?psmtmy yhW ac’nt it be ehsepr seotz?r

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. +  


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llA oatbu nth:gitis

/cfnsmptoeu/tethcnee.to.jodudi/gohsdneaacfestsi/chrnswa/otnil.seb:/

charcot_bouchard  When i faced this ques i did some Kegel. Felt something in my pee pee but not in my b*e. I exclude all option because they are bigger muscle of pelvic floor except EUS & IAS. And also remeber Kegel can be used as a treatment of prem. ejaculation not premature defication. +15  
paperbackwriter  @charcot_bouchard Actually Kegels are used in the treatment of fecal incontinence as well because of effect on EXTERNAL anal sphincter and surrounding muscles which are under voluntary control (you can most definitely feel it if you do a kegel lol). The answer is internal anal sphincter because internal is not under voluntary control (tonically contracted via symp. --> parasymp. relaxes it --> gotta go feeling --> no incontinence because of external sphincter's voluntary contraction). +9  
am4140  @paperbackwriter - Honestly, this depends on how you do the kegel. It is entirely possible to not involve your external anal sphincter at all once you figure out how to isolate your vaginal area. So the internal anal sphincter is under involuntary control so that was especially right, but I was prepared to pick anything with “anal” in it at all. So kegels work for fecal incontinence only if you’re choosing to involve your external anal sphincter, or you don’t know how or are too inexperienced to isolate the muscles around your vagina. I don’t think NBME or USMLE would get this tricky because the external anal sphincter will not always be involved in kegels. +1  


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eTh wenasr si lxaieperfhoy bcsueea het fertfnae rca fo hte esmlcu tchestr elrfxe ash to go hrguoht het oradsl armi nda adorls roto naglg.ia umDb et,soqiun I ow,kn tbu ’ist the onyl awnres ttha eadm ne.ess If yuo hutr het D,RG oyu ont nylo elos trefefan otaismc oynsrse efrbi,s uyo oals olse eth ynseosr eosidb elnivvdo ni eth rsvoiau feeser.lx

You anc asol get hyrafioelexp omfr dgimgnaa eth reentfef usonren atht veaenitnr het muelcs lie(k a NLM,) utb sa you know tseeh aer in hte iarrntoe rnoh dan ervtnal a.mri

ankistruggles  Thanks! I agree with you. +  
brethren_md  Great explanation. +  
gonyyong  Agreed - I think I got this by thinking about tabes dorsalis (syphillis) and why it has hyporeflexia is due to dorsal root damage +6  
duat98  I'm confused about why it wouldn't cause muscle atrophy. Isn't that a fever of LMN damage? +5  
charcot_bouchard  Muscle atrophy wont occur because alpha motor neuron is intact. Motor control of Corticospinal tract on this is intact. so no atrophy. u can move shiti/ But remeber muscle spindle that is responsible for INITIATING stretach reflex send Ia fibre to DRG from where it synapse with Alpha motor neuron. if DRG is damage ur muscle is fine but u cant initiate strech reflex. areflexia +3  
zevvyt  DRG you lose DTR +  


submitted by leny123(7),
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lanereG ulre - hurlCoineqo ivnsstiee if ormf bCneaibar or enrClat rimaAec tsew fo naamaP nlCaa, thsi apneitt armtidgemi rfmo sdHoruna so oyu anc tieielmna ohnurqoclei ecsasiertn sa an awenrs oehicc ni( iatndoid to eht el/voxavvia oifn b)ovae.

charcot_bouchard  Guys along with all intelligent discussion also keep in mind he immigrated 1 year back. So it must be hypnozoites which is causing this because Murica is Malaria free. +27  


submitted by lsmarshall(396),
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Urae yeCcl ersodiDsr g;&t esoaltdI sveree apaiemyomnhemr &t;(g 001;0 .ei,. on ohrte servee eaoibclmt itcbsenrdasu

eOtinihrn rrnasaseaybtmacl dyfienciec g;&t tms(o momcon arue elcyc di)s. tcoroi ucremdaai/iciaiad, rimampaeomhyne

Onrgaci iaiAscemd gt;& epmeoya,amnHirm agnpo-nai d,scosiai esoktsi rf(om plyoygcmeh)ia

udacieiM-hnm -loaCAyc ogedhyrdesean eicinfecyd tg&; airmoepH,nmeaym icotehypotk oicehmygaylp ese(n ni xoniβtao-id rod,sesrdi XEECTP rpydoeskdrotlenuy)aho

veirL dctunnsfiyo ;tg& yn,mepommiaHrae LTsF emssed ,pu rdelo t.p

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. +10  


submitted by sattanki(69),
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soeD ynnaoe have yna deai no hits ?nisouetq tghhuTo it saw .ALS

ankistruggles  I thought it was ALS too (and I think it still could be?) but my thought process was that a lower motor neuron lesion would be the more specific answer. +2  
sattanki  Yeah makes sense, just threw me off cause ALS is both lower and upper motor neuron problems. Corticospinal tract would have been a better answer if they described more upper motor neuron symptoms, but as you said, they only describe lower motor neuron symptoms. Thanks! +6  
mousie  Agree I thought ALS too but eliminated Peripheral nerves and LMN because I guess I thought they were the same thing ....??? Am I way off here or could someone maybe explain how they are different? Thanks! +1  
baconpies  peripheral nerves would include motor & sensory, whereas LMN would be just motor +15  
seagull  Also, a LMN damage wouldn't include both hand and LE unless it was somehow diffuse as in Guil-barre syndrome. It would likely be specific to part of a body. right??? +1  
charcot_bouchard  No. if it was a peri nerve it would be limited to a particular muscle or muscles. but since its lower motor neuron it is affecting more diffusely. Like u need to take down only few Lumbo sacral neuron to get lower extremity weakness. but if it was sciatic or CFN (peri nerve) it would be specific & symptom include Sensory. +1  
vulcania  I think it's ALS too. The correct answer choice here seems more based on specific wording: the answer choice "Corticospinal tract in the spinal cord" wouldn't explain the tongue symptoms, since tongue motor innervation doesn't involve the corticospinal tract or the spinal cord (it's corticobulbar tract). This is a situation of "BEST answer choice," not "only correct answer choice." +  


submitted by seagull(1443),
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ihTs is iherte a ppryoehcrti rsac or e.kdiol Btho rsiea due to seeivorroes-xnp of FeT-atGb.

charcot_bouchard  i think its a foreign body granuloma +11  
curbstep  If it is then would Tumor Necrosis Factor be valid answer as TNF-a is involved in granuloma formation? +  
azibird  Because it specifically asks which subsgtance THAT PROMOTES FIBROBLAST MIGRATION AND PROLIFRERATION. I believe both TGF-b and TNF-a would be involved, but only TGF-b has this effect of fibroblasts. +1  


submitted by m-ice(326),
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hTe tnaepit ahs ossl fo pani dna mrtetearepu on eth griht deis fo ihs .efac atiSsenon fo hte aecf si ptlaesraiil, so the ssuie umst be on hte ta'eisnpt ihrtg ,sdei whihc ew anc onirfcm by niwgkno ttah atinsoesn of hte yodb si ca,lorlttraena nda he ahs tosl ftel ddeis pian dan pteemrature of eht .ydbo

inaP nda upmtaerrtee nosniesta of teh odyb si atrp fo teh oitcismphnlaa ,trtac hicwh ylasaw rusn leayalltr ougrhht eth rt.eanbsmi hsTi cna be fdciomenr by rebiemngemr ttah anstsieno to het aecf soal snur reyllatal htruohg eht sbnmetr.ia ,oS we nac morcinf sthi is a gihtr dsedi arelatl etarsbimn .sseui

The lsso fo gga lfrxee nda aailprssy fo teh valoc cosdr mlypi mimtirnepa of aiclanr ervesn IX and ,X tobh fo hchwi eoilczal to eht .euamldl erorfe,eTh eth rnwsea si tgrhi oaelorrtsald .umedlla

duat98  You're a good man. +2  
charcot_bouchard  You must be handsome too +7  


submitted by colonelred_(99),
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heT aslisnay yonl sedhow a inoamutt ni noe lleeal. FC si an oomuatlsa sescrviee :isadees the ieedssa only mnietssaf fi ethre ear ntumiotas ni boht ellales fo het RTCF e.neg

If ouy ilstl ahev 1 ctlonifaun pcoy of het TRCF e,egn ouy nca listl kmea the FTCR inrepot h(et dircohel t/penol,craa)nehstrrn nheec uryo oydb n’otw aevh nya eus.iss

iTsh is osaugoaln to motur surrpspsoe nesge ekli bR: os gnol sa oen of eht elaelsl yuo have si afntulnioc, yuo nca kame ungohe fo eth toiernp to a“kme u”p fro hte etcdeiefv llea.le If bhot etg kekndco tuo -(,-Rb/) ouy leos eth itenporotc eddporvi by eht ngee casebue own yuo kema on ntreoip at .lal

Teh nloy htgin ttha dame eenss orf shti uinqoste was hte tcfa tath het toehr lallee was ton dinldeuc in hte siylsna.a

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. +37  
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 ?? +7  
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 xxabi(252),
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soMt nocmmo esuca of tueca ttsiipsaort in ledro nem si E. ,lCoi nda nhet oePd.asosmun

charcot_bouchard  Grandpa is monogamous. Sexual history was just to throw u off +11  


submitted by rocmed(-1),
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slne:eDgiom Ctpmnenoo fo eosdesomms, whhic neccnot kntoracysetei in teh mattrsu psounmis - FA ,0812 ,.467p ugisPmhpe lVsgauir

By shit I nac loyn emsusa ttah ehyt anem thta dgemiolesn cotcnsen crneatskioyet ot AHCE TEHOR, enehc yhw the trohe tpionos ntnceiogcn eioysctrnetka ot rohte rurscettus rae rcrniocte

charcot_bouchard  The epidermis primarily consists of keratinocytes[4] (proliferating basal and differentiated suprabasal), which comprise 90% of its cells. You are right. both are keratinocyte +  


submitted by yotsubato(979),
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oCol htnaero tosuneqi katen frmo eht slit of sgitnh nto in FA

charcot_bouchard  Actually it is in FA. FA 19 Page 100 - Antigen loaded onto MHC1 in RER after delivery via TAP transporter.... Remember FA is that friend who always say I told you so. +20  
yotsubato  But not in this context +5  


submitted by stapes2big(12),
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Im’ ton ersu atoub shti one ubt eht ywa I huotthg botua it asw htta csine eht idenonecfc eatvnilr ducilden ,1 ti was not sntcgnaifii. Adn uths p vuela smut eb voaeb 0.05

tea-cats-biscuits  That makes sense! +  
asapdoc  Had the same reasoning +19  
jkan  I get that it's not significant, but why is it 0.05<p<1 and not p>1.0 +10  
jkan  nvm, it's can't be greater than 1 because then it would have a negative% confidence interval which cannot happen (Think if p>0.05 means at least 95% within confidence interval) +9  
charcot_bouchard  p=0.05 means theres 5% chance null hypothesis is true. p=1 means theres 100% chance null hypothesis is true. >1 means >100% chance which isnt possible. +13  
wowo  p is a probability, so can't be greater than 1 +9  
noname  @charcot_bouchard, that is not a good interpretation of p-value. A better interpretation of p=0.05 would be: If in reality there is no increase in risk (RR=1), and if we replicated the same study of the same sample size many different times, then we would expect to find a risk ratio of (X) only about 5% of the time. +2  


submitted by didelphus(55),
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ynA adie why mehryieocraphl nt'si na swnera? Teh iraerhad olwdu uceas na rmnlao nanoi gpa hi)ohmplcc(eeyrr iobalmcet ocsdasii.

charcot_bouchard  this is the problem bet uw and nbme. in uw it would be for sure a gotcha ques. but in nbme they are usually looking for most obvious. also look what they are asking "most likely". baby would dev low Na before acidosis. Thats my 2 cents +21  
temmy  hyperchloremia will not account for the seizure that brought the patient to the hospital. seizures according to first aid is caused by hypocalcemia and hyponatremia +1  
cry2mucheveryday  Children with diarrhoea who drink large amounts of water or other hypotonic fluids containing very low concentrations of salt and other solutes, or who receive intravenous infusions of 50% glucose in water, may develop hyponatraemia. This occurs because water is absorbed from the gut while the loss of salt (NaCl) continues, causing net losses of sodium in excess of water. The principal features of hyponatraemic dehydration are: there is a deficit of water and sodium, but the deficit of sodium is greater; serum sodium concentration is low (<130 mmol/l); serum osmolality is low (<275 mOsmol/l); the child is lethargic; infrequently, there are seizures. https://rehydrate.org/diarrhoea/tmsdd/2med.htm#CONSEQUENCES%20OF%20WATERY%20DIARRHOEA +  
cry2mucheveryday  Also, why is this being given formula...? May be lactase deficiency...which leads to osmotic diarrhea...leads to hyponatremia(goljan) Aren't newborns supposed to be kept on exclusive breast milk till 6 months?? +  
hello  @cry2mucheveryday Don't read too much into it. The fact that the baby is receiving formula isn't relevant to answering the Q. Btw, not everyone breast feeds. Additionally, the Q wouldn't make much sense if it said "they ran out of breastmilk"... +1  
hello  @cry2mucheveryday Being on formula then the parents running out of formula is more of a clue for water intoxication. This is typically the scenario that water intoxication presents. However, I suppose if for some reason the baby was being breastfed and the parents switched to exclusively waterfeeding (and no other foods), then water intoxication would also result. +  


submitted by rerdwins(24),
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sebt ayw ot raphapco ti si to ksa hiwhc eon ahs a ltorpa oinalrcctui adn a cytsesmi curoalcniit ( ouY NODT ened ot kwon eth reepucrod to rsawen itsh uteoqis.n

ee:xpaml ntac be rerpisou igcpiaters nda rfioiern ecsigaprit eebcaus stheo rae htob yesicstm lsao ncat eb sreproui lraect ein(frrio risetnceme )rnchab dan reoprisu eietemscrn aeuecsb hoets aer tohb arptol sesmyt

nwhe yuo anorrw ti odwn, tneh tsi a 055/0 s.egsu

charcot_bouchard  Not 50/50. u can rule all 4 out with this. U have described it perfectly. they are wanting a portosystemic anastomosis. Both hepatic vein and inferior phrenic vein drains into IVC. I was nt sure abt inferior phrenic but was sure abt renal and splenic. so picked that +6  


submitted by nosancuck(85),
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oY adgw ew lal auobt VPT MIT aLLH

iPhnaeal,lyenn iVn,lea NK,ypDtorTA oiennT,reh osneec,iuIl ieethn,oMin eitiHdisn, Luiceen yesnLi

meningitis  I don't understand what the question is asking... can someone please explain it to me? Patient doesnt eat protein, shes chubby. What does methionine have to do with this? +2  
charcot_bouchard  Just basically asking which is essential amino acids. +3  
usmleuser007  Essential amino acids (something i came up with) 1. "Three HAL fans will try meth" a. Threonine = Three b. Histidine; Arginine; Lysine = HAL c. Phenylalanine = fans d. Valine; Isoleucine; Leucine = will e. Tryptophan = try f. Methionine = meth +3  
nala_ula  They're saying there is a lack of good quality protein -> slight nutritional deficiency. She may have acquired weight but it's not because of protein. So they're specifically asking what amino acid she might be missing due to her subpar diet. Since essential amino acids are those that the body cannot make itself, out off those listed, methionine is the essential amino acid. It's on page 81 of FA 2019. +9  
nala_ula  correct me if I'm wrong please :) +  
hello  For anyone confused trying to follow @usmleuser007's comment -- slightly modified Essential amino acids mnemonic "Ah, Three fans will try meth" Ah = arginine, histidine Three = Threonine Fans (phans)= Phenylalanine Vil (Will -- German accent pronouncing English word 'will') = valine, isoleucine, leucine, lysine Try = tryptophan Meth = Methionine +1  
pg32  Why does @hello and @usmleuser007 mnemonic contain arginine? That isn't in the PVT TIM HaLL mnemonic for essential amino acids... +  
paperbackwriter  @pg32 arginine is semi-essential. It is essential in preterm infants who cannot synthesize it https://www.sciencedirect.com/science/article/pii/S0955286304000701?via%3Dihub +