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Welcome to charcot_bouchard’s page.
Contributor score: 426


Comments ...

 -8  (nbme23#22)
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ldO eutdetd vhae irotcA nos.isest tAailr onacnttcroi meeocb eteasnisl ofr ihst t.atniep os AS + AIFb is gurnodsea ebsueac hsit recesdu teh VL pdlraeo gcisialfytnni adn shit piettan eolesdpv .HF So AibF ni SA etipnta dnee ot ccertro etymmdiieal

aisel1787  she's not so old! stupid comment +

 +0  (nbme23#28)
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A aesc fo ncinFoa o.ymsrden fI ti wsa iestdaol Tpey 2 ART otnoip B ouldw be hte .arwnes


 -8  (nbme23#1)
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ferAt girtevynhe tsi utjjs an iemepd seq.u lwBoe 55 sv vbeAo 55 ryeas

ls3076  can you elaborate please? +

 +0  (nbme23#44)
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shTi tnpteai has a oabltri ooutbwl rru.fteca ese eth erta ordp n.gsi


 +1  (nbme24#49)
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pApeltrany shreet erlo of eyhmapctits metssy in cncsgehoiyp irenteco adn sit ecmos orfm T21-L1. So fi iaptten hvae ttanisranoc at L5 eyth lose elferx ceortnei tbu lstil riaent hpnoicgyces en.o

BeoAv T9 tacisnnotar ucsea sols of psgoheccyin ieotcern

charcot_bouchard  Below L5* (Not at) +

 +12  (nbme20#23)
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aKp si pH at ihcwh yan rugd is ta sit 05% diezoin t.ates

woN we rae lak euirn i.e icn .pH ehnw pKgp;&Hat it liwl avhe tow diff tpha rfo iaccid gdru &m;ap sbaci ug.rd

iAdicc grud lilw inc sti inlmeotinia ni(c nzidoei f)orm, cisab ugdr lwli be oerm boes ar.dsbo we edne to konw eth drug is icsba aid/c.ic

owN fi u lka einru tis olieiinamnt .cin os ti evha ot eb i.acidc or u nca kwno tis a odis astl fo rdug htwi NSC reorytpp ei. tsmo leki nibtPobalreha Weka( id)ac

os if Kap fo rdgu si ---6at Hp 7 we liwl astrt aeiiminltng

btu fi pKa is 0 ew ndee ot seira Hp fo reinu ta 11 to ttars gtilnat.inaiem atth toipn pevr rgdu pKa)=6( wodlu eb tloytla tuo fo tmsyes.

thsat why A si eht rhtig san Kap( = 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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alypceNsro sha one of eht nlgwoifol 3 htrraccrea - 1. palt.ae 2Cxy cde irnxeo in .cfs3 ERM ncaltey 15;lt& mni

sti ass with (ont dx /mocryiiarniggnop eait(pcpH cl.atnnoialih Sleep lyarisspa

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

 +3  (nbme24#18)
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I gte hyw tis llaeatr btu todn all acnliar neevr xptece 4 risae t?leVrynal TWF yeht add siht roDso efrebo ?tlleara

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 +
doctordave  They all exit the brainstem ventrally, but the nuclei can be located deep within the brainstem +

 +2  (nbme24#11)
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yiloaAdln si ncrealt niap iaz.tontnsesii gigriregTn of apni yb a nno pniaufl uilsi.mt solA nese in a.vFglraim[sb iyo agieapyrlHes : Inc nsoespre to inplfua litmiu]s

tIs a vipsetio ie(. tlyevicA gfe,leni not kacl of fe)engli s.ymtpsmp so B map&; C is ont the s.wa nDer tins wrneas etie.rh as loilianvd crrotpee V1TRP() si loas enfafetr cenovpitcei arisisonmnst eomltua(dd yb si).apanicc navcoiAtti is oons llfdweoo by azit.nosniistdee

A - DI.K fi oblrmep swa ni GDR ehrte lduow eb tlo eorm tosypm.sm

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




Subcomments ...

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This si luoyibosv a cilcinla iratl. fI oyu wokn uyo aer ntggiet a gudr, neht uyo aer ton bnde:ild its’ an ble-opnela rtai.l hTere si no midonornaatzi as trhee si nylo a enlisg tnertmtea .ogpru

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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oemzMier rinsspa’i eiqnuu asabd-cie :csefeft ailtmceob sdoasiic nda oyeprirtsra liasksla.o N,eot isth si ellkyi cutlaa errtpsaoyri as,osalikl ton pilyms arlmon irrtpseroay naticenmsoop rof ielotmacb si.asidco

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(151),
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it.hgr eh tleulyabos utms narmie in hte inwgtia raae os htta eh is ta danh ot cakatt hsi eifw eenvhrew erh exam en.ds og EBN!M

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. +1  
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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heT rpomittna ghtni orf tosm fo het scteih eniuoqsst rea ot kloo rof eht enswra hewer oyu aer igneb hte ssnt/mteoic snoolrefpasi hliwe cnpgesietr the naist’tep nou,taomy ccfnei,enbee -annfolc,inmecee tce. otsM fo teh iceshoc heer reew hetrei csruycaoat ro aibylcals bnige mnae ot het aipte.tn heT trecroc ecchoi is to lhep the tanpite utb oasl vittmaeo ethm ot ucieonnt halypsic reaypht dan to ylon esu het imertp as tlltie as senayes.rc A siirmal sitnuqeo (cwihh I tkinh saw no MBNE 32 -- teyh ear idkn fo ndnbielg )ethoegrt aws the eno eewhr eht niettpa had stte sturels atht cdinitdea he hda ecracn tbu eht dseetinr sida not ot at)uil(nyovlr tlel mih nitlu het itncologso ceam in ealrt ttha day, dna eth tatnpie adkes uoy buaot the srsl.eut ouY otd’n nawt ot the lie to het etiatpn adn sya you dton’ onwk or ahtt he et’dnos aehv ,cearnc but uyo alos nto’d atnw to eb nanretuosbiid to het en’tssderi be)rseo(alna et.urqse

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(1567),
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Tish attnipe is tpnigpir lasb.l Breett od a drgu reencs wihch esesm siou.vob

sympathetikey  When the answer is so obvious that you pick a stupid answer instead of it. DOH +43  
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(1567),
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hisT si a incpa k.ttaac lnrHiittanvoyeep srdop 2OpC nedagil to a rpyitsorrae lsika.slao o2p si tivaerllye ecanffedut ('tndo ksa em o?hw)

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. +23  
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(533),
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ymnGoc,atsiae dispre ,atanoigam and hgyiodpoansm s(a wlle sa plrama )yremehat are lal sings of esecsx roegn.tse hTe rlive ni stainpte tihw cihatep ieesdas si epmiriad dna os coantn rlcae sntreoeg ftfeiynuicsl. ixS 21 oz ebers yliad 2(7 zo, ro lhfa a lnloa)g is oot ,chum nda is rtsieygndo ish evri.l

uslme123  No hepatosplenomegaly, ascites, or edema through me off. We that being said, I shied away from cirrhosis. I thought that he showed signed of depression, so I went with the thyroid. But who's to say he isn't injection anabolic steroids?! +6  
catch-22  The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum. +12  
notadoctor  He likely has hepatitis B/C given his history of intravenous drug use. I believe both can have liver dysfunction but may or may not have ascites, whereas the type of damage we would expect from alcohol that would match this presentation would also show ascites. +  
charcot_bouchard  For Ascities u need to have portal HTN. Thats a must. (unless exudative cause like Malignancy) +2  
paulkarr  For anyone who needs it; the FA photo is kinda burned into my mind for these questions. NBME has some weird infatuation with this clinical presentation.. FA (2019) Pg: 383 "Cirrhosis and Portal HTN". +4  
snripper  @paulkarr the problem was that the FA image was burned into my mind so without no ascites or edema threw me off of cirrhosis. +  
tyrionwill  cirrhosis doesn't present hepatomegaly, instead, the liver could be shrunken. +1  
avocadotoast  Cirrhosis (most likely due to alcoholism in this patient) leads to an increase in sex hormone binding globulin, causing a relative increase in estrogen compared to androgens. Cirrhosis doesn't always have to present with ascites and adema. I agree with @catch-22 that liver disease is a spectrum. This patient does not have ascites because his liver is still able to produce enough albumin to maintain oncotic pressure in the blood. +1  


submitted by sympathetikey(1358),
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ePr FA g(p. 63)6: neorgniCnc satrbe ac..nerc.

"ofltiAmicianpreoeoxiv/nsrpes of erorsneeteost pog/rneg cepsroetr or 2cb-erB 2HRE,( nEGFa r)eetproc is mnmo;oc RE ,⊝ RP ⊝, 2H/uRnae dnE ⊝ mfro mroe rss".eigvage

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(1567),
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Did eaoynn ihnkt tath uzennalif aws igrht? I nddsneautr htat ZersH-ep nac scuae nuoemanip tub yhw si tsih ranwse ttrbee vero ali?eunnzf

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(60),
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hTe rosetproi onlmscu (aucslcuFis asuci/ucleunsusFtac sgiil)arc rcayr intomrionfa to eth ranib irngeadrg enprorop,ciipto nravbt,iio denisvaiimtirc tohcu adn es.persur hyiscaPl maex fsdignni gugesst a oeilsn eher h(te tmapilainhsoc cratt rrisaec ri/iicpnankpp adn te,ueprremta adn seeht rwee ra.lmo)n nceiS the ntaepit sah lnaoabmr ignisndf in het leowr etxrii,tseme nda roanml difisgnn ni eth uperp eemeirxitts, hte asnrew is lFuisuacsc s.rcaiilg iTsh si aseeucb matfniirnoo rmfo doby raeas wbleo teh eelvl fo T6 si arcerdi yb alrsiicg dna fmiorintano rfmo boyd saear bovea eth lvele fo 6T is ircdear by nstucuae.

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(130),
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htWa of if het nrcace si a hrteuolila nercca in het rddebal ude to tonaiarid ayhpr.et luwdo ti otn asecu rmslaii gssni

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(533),
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eTh lignse msot irtpnomat ihgnt tuoab shti rgoss ootpgahly is tath eht sieaesd si uolt.ridlmaun Tsih dicsitnea stteeaasms fomr natdtsi ssti.e

evrLi aessescbs rea asluuy i,glnarsu fleidl whti rcyaem lyeowl u,sp dna yma owsh a fsuibor .luscape sCrshriio neoft ssohw a ewloly locro due to atfyt aceghn sa lelw as reageivneret us,dleon wihch rea nto pntsere ereh. A ocafl rondlua iesrpylahpa is a nsliugra rtmou fo het i,rvel and ihst is mioduar.tlnul eaittisHp B si a ttilel daerhr ot nitisusghdi becueas mofr athw I acn eltl it nac be ulutmrolnaid in eosm sa,cse but shit leivr aosl hsosw neno fo eht ocslssrei omfr crohcin ntfmalmoaiin ttha lduow kleily nmyaapcco Hep B. nlyi,lFa ew ese on krda rtslniacioood ot ncaiietd fnrinoacit.

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! +  
sophia  UW QId: 59 +  


submitted by colonelred_(105),
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tbuaAltebitr ksir = neecidnic ni doeexps – eiccneidn in dpexuesno

= ,00100/3 kms)sr(oe - ,33/0000 onknoe)msr(s
= .003 - 001.
= 0.02 so( hte abraitultteb riks is obaut 2)%

yigAnppl ti to a ultappinoo fo 0001:,0

= 020. * 10000,
= 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. +3  
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. +12  


submitted by colonelred_(105),
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aliberttbuAt srki = ciidnecen ni sxepeod – eendccini ni psduneexo

= /0,00301 sr)(omeks - ,30003/0 nossr)ek(nmo
= .003 - 01.0
= .002 os( eht uttbaritlbea srki is batuo 2%)

plngApyi ti to a pnaioltuop of 00:0,01

= .002 * 0,1000
= 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. +3  
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. +12  


submitted by viz28(-1),
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ehT mmauq-olcnuarso nuoicnjt edtuitsa at the rtanxlee os of eth rvicxe si eon iset hhiwc is higlyh vlrnelueab ot sptieamlaa ro coeaplntsi rmftanroisaton durne aersvde stumenc,cciras cush as ironhcc itnfnocie ro .autarm salu,Uly asmqouus aetsapilam eerhw uuaqomss lsecl plarece het ramolncu cslel of eht ienrvcalocde acan,l is v.eoberds oHevr,we ni less coommn uaotsis,nit tiuapyrllcar arfet atua,rm ublat ltsaiemaap may po,elevd lprnecgia ecidreovnlca ocdtaleiinn cmouanrl htleiaelpi llecs yb tcidl′eia urcml′aon cls,le miarsil to hoset sene in naaflliop t.esub uTlab tapeislama si oltmys ense ni eth ppuer rpta of eht vceecoirdaln aacnl naer the nerlinta ,os utb yma osal be fdonu ni eht ciledenvorca nsdlag ro hte worel vdanoceilrec l.naacbtd/i1/b//th3.bin8j0t/ep0bmc.hipdmni:.i138/jttn

charcot_bouchard  But they are asking in healthy individual. I dont get why they add this ciliated part? +6  
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(1358),
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dMa ta msyelf ofr cinnhgga ym e.srwna

ayFlut icolg maed em rdnweo if nihtitg yrou ehad olwdu csedau cseradnei ICP ,so liek a hicugns leuc,r you luodw gte iecdaersn gasVu erenv yacttiiv and aebym irdarbadyac + nthiyo.soepn But I sesgu eth ARSA mseyst udowl eavh ourcdcatetne tath and sacued vrsanstctoicioon evro 24 rus,oh os cHipvyomloe skohc is yitenfield het sbet ihoe.cc

sAwyla lhdsou og tihw eth ibouosv newasr :)

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(102),
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mmH.m lelW my mdni has olnbw off sabuece awth hti my idnm wsa nydidherota cisen he wsa ni the erse.dt sA oons sa ym dmni rttsead ot nwdrae touab all fo het ehtor tnpsioo atht uocld ekam s..nse.e I utsj dciklce nda em!odv

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


submitted by d_holles(187),
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Eenv oth FA nad cikeScryMhot oed'tsn nemnoit ,it obth naAsmlpaa nad soiEchhrisl era cdairer yb boRni fo dsoIxe.

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 sygu nac oenmeso spaele elbeartao on htees iid.gnfsn I udnrtndsea ehs hsa lung nercac atst'h iepigmdn erh rtheac.a utB ohw si ihst evpeitesneartr fo an eiscottvbur drsreo?id 'nAetr nglu csaecrn ertteiicrvs if ghtniany? haksn T

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 ..? +4  
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. (32),
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I lerlpsoany ohttghu fo hsit utssnoeqi niinhtkg fo it ni tshee .sem.tr Snice hte tenatpi hsa a assm ni the tacahre epak yoeraitrpx dna iyrnatorspi wlfo liwl be ner,ipturtde dna lowdu trerfeheo eb c.ededsrea FC1V olduw sola aevh to deceersa by t.his shTi eteaiildmn lla teh heort icches.o

charcot_bouchard  Are you Me? +3  


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hyW is ti 9%9 dna not 5%9? It esdak fro noste fo esesiad ta sesl naht 9 rysae fo a.ge 'mI llecyra nmssigi mosightne erhe

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? +4  
aakb  I see what you are saying but you have to remember to add the things on the right side to include all the values under 9. So even if you go with the 2 standard deviations for 95%, youd have to add 2.5% that's on the left. which would be 97.5 and you know you would still add more on the left to get to 9 years of age so it would have to be closer to 99% than to 95%. hope that helps +  


submitted by link981(160),
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vrweHeo i,edwr yuo have ot srpcete eth eit'tpasn eiebsfl sa onlg sa yhet tna'er ngpttui eht rnoewnb at ahmr. nI ehtes pyets of suetionsq you aevh to budli npyn-ehasctiitpia ishalnrseoitp sacebue the ptaetni imhtg bceoem fnddofee fi uyo dsigrared rehit ibe.fels oS wilhe het nbronew tosm eilylk hsa gsa nad ton "hte vile ,ee"y chceoi E is het etlsa n"inf"dgeof srnwea htat ssgtsueg t.rtnetmea

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) +4  
jesusisking  I feel it but dang, she lowkey drizzlin salmonella all over that baby +2  


submitted by sympathetikey(1358),
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eysK were te:h

irauGco-sul

ai-ouahpPhsrt

imnAo- ciaadrui

ohTes soduhl eb orsbeebr-da yb het P,TC os fi rehey't ton, ypeT 2 AR.T

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(1358),
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esKy eewr t:he

cuo-urlisGa

-traioPsahpuh

oiAn-m uciriada

oTshe dohslu be er-obedasbr yb teh CP,T so if hye'ter ,nto peTy 2 .RTA

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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Snik pvsrideo lnisoatnui and ntserpev aeht so.ls iThs npst'eita oydb liwl soapenmtce rof dcinasere rtea fo teha sosl by cesnigarin malcbtioe .etra

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? +24  
charcot_bouchard  i picked same. Increased ECF but cant remember why. Can you explain WHY it is increased ECF? what was ur reasoning +2  
isotopes  Burns would lead to a decrease in ECF because the protection from fluid loss is absent; it can lead to shock. :) +2  
tinydoc  My reasoning behind picking ↑ ECV was that your losing fluid but not electrolytes with the burn ⇒ the ecv would have increased osmolarity, so the fluid from the ICV would be pushed the the ECV. It made sense to me at the time. I guess technically its wrong because the loss of fluids and the gain of fluids would amount to pretty much the same thing. But the insulation and heat loss thing makes sense I guess. +  
yex  Increased ECF, bc I was thinking about the edema formation.... :-/ +3  
atbangura  I picked increased ECF because burns increase the capillary permeability coefficient, but now that I am going over it I realized that increasing the permeability would only transfer plasma volume to the interstitial volume, which are both a part of the ECF so therefore ECF would not change. SMH +5  
aisel1787  thanks +  
69_nbme_420  Burns (and Diarrhea) cause ISOsmotic volume contraction; Costanzo BRS Physio +  
tiagob  in severe burned patient, also has increased fluid in third spacing or interstitial (leading EDEMA). Different extracellular space is interstitial and vascular +  
peridot  I also wanted to add, another huge job of the skin is to prevent loss of fluid. Burn patients are easily dehydrated because they've lost that barrier. This helped me lean away from increased ECV - despite the edema (from one compartment to another) as others have mentioned above, there is a loss in overall ECV due to evaporation from body. +  


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hTe omts tamitponr ntsih ot hte uqstnoie ear as ofsl,low ihtw #2 gnieb teh mtso f:pcsiiec

)1 tieatnp roerspt anip hitw aeevdorh timnoo and rotserp eretnrrcu rovedhea oinomt rnidug w.ork hadOeevr mtonoi cna maegad eth uptrpsasniuas leuscm due to intnpmiemeg yb het m.ioaorcn

)2 anPi si swrot thwi tnlnaeir antoiort of hte ohdlresu - htsi is ontseiscnt twhi teh gsiidfnn of the patmc-eyn tets, hcihw endatiisc a tuusnaspsiapr n.juyri

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 +37  
ls3076  why would injury to supraspinatus cause weakness with internal rotation though? +7  
targetusmle  yeah coz of that i picked subscapularis +3  
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(58),
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lla stohe nno thsam gsuy he,re dnot skpi ehest stnu,esioq try to nrargea hte is,nut ehre oud´y ieslya ndif out that uoy sujt vahe ot lpmtiyul! Geiv it a tyr -):

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(47),
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Fcik :ciOrnl= Ciepp eRat fo 2O soamurveepinnroticusot/n 2O trntanccinoeo

OC aemns aiadcrc uoutpt or wlFo fo loodb

charcot_bouchard  This wasnt Fick +1  


submitted by sajaqua1(533),
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Wlotd'un aottl AV dnoal iaotlban seodyrt ot htthriutayociym fo hte pmre?aacke htTa dowul naem tath elbow eth VA done het rhhytm oluwd eb dpedirvo yb a rntirvecual ofi,c dna sthoe slyualu arecte dwei QSR s.cmlexepo

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 +16  
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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pnlpetaAyr etesrh relo of itmpcysthae ytssme ni hisoncgyecp tecrineo nda sti csemo fmro 112L-T. oS fi neiptat have arsotanntic at 5L they sleo reexlf cnoitere ubt tilsl rnteia ceghycipsno eon.

BovAe 9T tsitaanncro aecus sols fo hyseopiccng tcienroe

charcot_bouchard  Below L5* (Not at) +  


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apK is Hp ta wchih yan rudg si ta its 05% zeoinid e.tats

owN we rae akl nrieu e.i nci H.p enwh g;aptHp&K ti liwl veah otw diff thap fro cicadi udrg a;mp& csaib g.rdu

Aidcic dugr wlli inc tsi temanliioni nci( zideoni mr),fo csiba rgud llwi eb roem .db soaebsor we eden ot kown the gdur is abcsi dci/cai.

oNw if u lak nreui ist emanlnoitii n.ci os it vhae ot be cd.iica ro u anc nkow sti a idso last fo grud hitw SNC trrypoep ei. stmo ekil iboathPenrlba aek(W aicd)

so fi aKp fo rgdu si -6t--a pH 7 we wlil trtsa mnaeiitlign

btu fi Kpa si 0 ew eden ot sarei pH of euinr at 11 ot tatsr et.iailnaginmt atht itopn vpre dgur K6a=p)( lwduo eb toylatl otu fo seystm.

ahtts why A si het gitrh sna aKp( = )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(165),
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utoA dmo sesidea rea ualuysl oyhtzegoruse (or so ehyt awnt us to e)sumsa

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(165),
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uoAt dmo seaesid aer usulyal eseotuyogrhz o(r so htey watn su ot suae)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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Kap is Hp ta chwhi ayn udgr si ta tis 5%0 izondie teast.

owN ew are lak erniu .ei nic Hp. hnwe gpK;t&paH ti wlli ahev wto dffi ptha fro ciiadc rgud a&;pm sacbi gu.dr

icAcid ugrd lwil cni sti iialntenimo ic(n iidozne o,frm) bcasi udrg illw be orem rbe.osb aosd ew nede to wkno het drug is ascib /.cidaic

Nwo fi u akl ernui sit anilneioimt nic. os ti eahv ot be cd.aici or u can onwk tis a odsi tlsa fo ugdr hiwt SCN yrteropp .ie stmo eilk narPbibhetola ek(aW iadc)

so fi paK of durg si at---6 Hp 7 we lliw tsart tainmlginie

ubt if paK is 0 we dene to seiar Hp fo uiren ta 11 ot sattr iiinmlantge.at tath topni verp rdug 6K(=)pa duolw be atlltyo tuo fo etsm.ys

attsh hyw A is eht hgrit asn p(Ka = 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(1077),
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ehT ritgh nda tlfe lecrvietn aer endirad by aaretsep pastr fo eth mrfneoa fo nmroo. (eLtf edsi si rdandie by etfl m,rnoo igtrh deis by htigr r.omn)o nA rtootsciubn fo eth ritgh nformea of mrnoo lwli eganerl eht irgth e.vtcilren

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(1077),
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etltLi nifgre = alurn e.ernv

18-CT era the osotr fo eht nlura ,enrve cihhw is a bhcarn fo teh aelmid r.doc heT rlnau reevn si nto udfno ni eht apcalr unenlt te(h edalim eevrn .si)

nUlra .n emadga nca edal ot lsos of srwit xifonel dan dcitun,oad efnolix fo iamlde gifsern, atuncbido nda actunoddi fo gisnref )no(rst,isiee osnacit of lmiade 2 uamicllbr lussc.me osLs fo einotasns orve ailemd 1 21/ fergs,ni ligncduin nyeotahprh nniemee.c

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 +27  
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) +  
topgunber  is this related to RA? Where there is cervical subluxation or am I going nuts +  


submitted by hayayah(1077),
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itststioPra si eetcczhrardia yb yru,dsia feqr,ecnyu yrugne,c low kabc .inpa rmaW, enetrd, elnrdgea ets.taopr

etucA airclbtea torn—tsiptiasi olrde mne smot ncmmoo uartcibme is .E cli.o

ergogenic22  In young men it could be chlamydia but the question stem makes no mention of sexual activity, so it is e. coli +17  
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) +4  
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. +4  
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(1077),
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aCse of .irorlaosoctrelesis

ayepipHltrsc crraitessoreolsilo snvevlio teckgihnin of selvse alwl by yrhiepapsal fo stoomh luemcs so(nknin'-io p)'eenapacra

  • enuqcConees of atianlgnm yirntnoheeps 0t8;01(g21&/ w/ ecuta ned-ronag aeagm)d
  • sutelRs in urdceed sselev ebaricl htwi -dregnnao chsmiiae
  • aMy adle ot ofbidrnii inerscos fo teh sleves awll hwit ogrramhh;ee slalliaycsc casseu cuaet rnlae ueaiflr ()RFA ihtw a hricctrcaeisat inb'e-'lettaf peapcearan
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(1077),
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saCe of srclseirs.iooroalte

ytHlpcpeairs lctsrioasorsrieoel lnieosvv gincnhitek of veesls llaw by pirplashaey fo omhsto lmceus no-sinnko'(i )eraapcnea'p

  • sneecuoCqne of nltgaamin ynhirteopsne /1;(100t2&g8 /w aetcu aon-rdnge )eamgad
  • stRluse in uceeddr ssvlee ibarelc tihw nr-geaond iahecmis
  • yaM adle to fonrbidii necorsis of het seelvs wall twhi gh;areeohrm ylaaslscicl sacsue uctae rlnae lefirua FAR)( tihw a creritsacahcti bnel'a-'itfte apepreacan
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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rblouuacirFms iasrlapepyh iwll sueca epr nearl imza.oeta S. /CBUNr is 2t0g&; ni rep erlna taeoimza tbu in het oiesntuq tsi lveau is icvietndai of rinsitcin elrna ufeal.ir revy cng!fsunoi!

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(50),
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tsoiitsPacs om(meetsis lealdc rsohosiint ro oarrpt siedesa ro rrtapo )verfe si an tieiconnf fo hte lnug enm)uoipna( acdesu yb hte erbutaicm opalaCyhidlmh dalhC(imy)a cpi.saitt

ngsSi dna cposhrt, ymfm uego.sv:e yaluslu httuwoi mcuh hl..ceumpdsheaacr s emh.lhgae etseh acch.s is t.hanepsnsro fo oe tbarehsr. ttaohr.

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! +9  


submitted by strugglebus(165),
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nisLey is edsu in tlansie nad olcaleng crsos n;ligink ti si rocss denkil by slyly adieosx to meak gelncalo sberif

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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srylceNapo hsa one fo eth wflniogol 3 racahtrrec - .1 e .layptxa2C ecd neoixr in c s3f. EMR yancetl 1t5;l& nmi

sti sas hiwt otn( xd tgerp(oiyciHacnaiompp/ grni lti.aalocnnhi Selpe rpasslyai

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


submitted by hayayah(1077),
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hTe tubse era tsretceha utp in fro iruen to wfol noit a g.ab So eruin ouuptt is gniog to a.seernic The nttiape si aslo r.ehmeiyaplkc rsleoAedont spdorsen ot eiehaaryklpm by necgiisnra +K n.oceixret

aeymeariklHp wlli ilmsatuet nladesoetor ieortncse vnee if nneri si resdpssupe ued to sih hsoiynpnte.re lotuAhgh +Na lwli be aobde,rersb tsih lliw be nttierans luds(ho lveroes noce eht mitauopss eelvsl nrmzdali)eo nda icsen ihs urein utoput wlli mtso lkyeil rrentu ot lo,rnam shi olobd spereurs hslodu also en.mlozair

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(1077),
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sihT is na eeaxlpm fo nsSl.ighe sHepre xmpelis and hpeser tzsroe iesursv uacse laoabrnm lecl ivsodiin ni deeimlpar cl,lse nad shit etresca dleluutcemitan iatgn llcse.

A Tnazk aserm wihonsg uiceldatntelum atign sclle si iaetiactrcsrch of aiVrecall tZores ursiV .nesitnfoci V(SH ilwl hvea lsiiram fiingnds).

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(1077),
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Nlpsaeaoi si enw usstei hwtgro ahtt si edtgre,luaun vliseireebr,r dan ao.connlmlo

Cloytlian acn be diremdnete yb heplogh--csposetua6 raeesdyndhgoe ()GP6D mezeyn rismf.oos GD6P si -Xkeidnl.

*roF oemr ofninartimo chkec otu hC. 3 ioaelNpas in aahmtoP

hello  This is great, thank you. +5  
breis  Pathoma ch. 3 pg 23 "Basic Principles" +8  
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! +  
makingstrides  Just to make sure I got this right, because this is neoplastic and its monoclonal, you want to look at the isozymes to determine its clonality? +  


submitted by hayayah(1077),
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ihTs nma si showgni sxs fo an .IM

atlinIi psaeh fo liocmdraay fnricainot elsda to icdelbrdasaonu sicosner ongvivnil lt;& 50% of the ocrldamiya htsiknces ena(oscualddbri orfa)c;nniti KGE hwoss eegstmT-nS pnesreidso.

nutCednoi ro revese eiisacmh g;2t0&( tsmui)en lsaed ot rratslnaum rsoenisc ilvovginn osmt fo het cryalamdio lawl aslur(mrtna )o;firnincta GKE swsho tgSes-nTme tienoea.vl

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(165),
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ocrh=opByonnh miriyx oroaetunppEna =dirtosr lhcrraehcaiotobn usintbcotor nf/soamiser(g yrbnrpsaI tidyo)o osrrdit = angelalyr sosroiscScio ttuunbncu lshasp= test rfo ircpylo neositss

hWen ereht si a dcearrtfu rbi it will uacse a trumaa mtpaohxoern hwhic anc ueasc ria ot ecasep nad mcebeo ppdaert rduen eth nsik aielgdn to ipsruc.te

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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hisT si RYLELTLIA hte maes topoh heyt usde to csirbdee hte eya4d-r-lo oyb wthi ediufsf ciltorac oersicns rmfo NEMB 81. anC ensmeoo xpalnei 'hwsta goign no eher

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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eincS eht pani si ra,ilrcdau a sidc neaiotrinh si msto leyi.lk

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(1077),
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nneigB sortmu are ulyusal rwtiafdletled-neief dan edtea,c-rlmladwe htiw lwo timicto ttiac,ivy on tseatem,ass and on orci.nsse

taaniMnlg tmsrou cnas(r)ce yma owhs opro ein,trfeoaiitndf arcreti wgth,ro llcoa ,nvaisnoi itmaseas,ts nda si.ptaopso High citoimt t.cayivti

Fta rsto:um

  • am:poLi b,neign wlo cittmoi vtatyiic
  • pmarsiL:ocao nmagnat,il cisedrean ticitom tvctyiia
whossayin  why can't it be a rhabdomyosarcoma? +  
charcot_bouchard  Because of histology and gross appearance... very graphic description of fat cell tumor there +6  
dr_cruceta  because the question said irregular vacuolated cells, describing fat cells. Rhabdomyosarcoma comes from skeletal muscle. +4  


submitted by youssefa(131),
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orFm adFi 9021 ewn giferu: F-G1I yalnim ncutsinof as an nliocbaa ehoornm no sumelsc adn eonsb epttyr( uhcm kile uni;ts-lni&g esecsdear musre csuoe)l.g GH csat pyrestaale yb gnimtroop snluiin seeasitncr igsinn(arce emsru s)ogluc.e ofeehr,Tre FI-1G is not eth asewnr. fI HG swa mogna eth aensrsw ti oldwu ehav otg eallyr n.ncfsguoi

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(34),
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hTsi is lmelaruni gs.iaeesn mNlaor asvroei tbu anbtes us.eutr

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 ? +23  
sugaplum  Testosterone would be high if it was androgen insensitivity FA 2019 Pg 625 +14  
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 +2  
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. +5  
rockodude  thank you @dickass +1  
j44n  Also AIS has paradoxically large boobs-> tanner stage 5 and thats not mentioned anywhere +  


submitted by yotsubato(1032),
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csisaipynh" usdloh wslyaa cgeuoenar thhayle aong-adrnmiuir t.aooiu"icmnmcn

soAl uyr'eo oggni to do soem ssroieu hgnsti to uerc stih lsirg' sseedia, egiland up to matoptinu.a uoY tacn ihde hatt morf e.rh

djjix  Non sense ... you can hide the amputation from her +19  
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. +2  


submitted by usmleuser007(397),
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yaSialvr resoteinc 1. tA olw oflw = giHh iecntotanncor of otisa;spum olw oitratsncennco fo o,imusd rb,iacb &pma; lchi.eodr2 ta ghih flow = olw ocnoirtetncna of tui;psoasm hihg tncoitnoscaren fo misu,od brc,bia pa;m& rhclidoe

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(84),
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Sdunso ikel a ichetprpohyr ca.rs hepirr"ctopyH rascs tcnaoni riaiprmyl eytp III cglleano eitredno rlaallep ot teh idpreamle facrsue htwi aduatnbn sulnode ntaoiicnng fomlissbayotrb, aelrg ealexlcarurtl lncgaleo nitfemasl and leultfipn cicadi rp.aioscmadsolyc"chue e.vmnlm/ipibh7i/hMnstnwl.r8o//pcw/P2stcw0c3.g9a:.t/2C

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 +4  
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(259),
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fnel gSwhiotle  p iolce d.gcleh.(,ry rm:dia uageceesise tne→tions i)h Tp sre dcauAcoendtoreidP  T e+→PecaKeNaar+ nAdd/dea ss ppuaCm2+ f d→ iuttfasifncoiviyo  Na da+n etwar tino hte → clle ulgwc ailsnelelrl

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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adcicrgno to udolwr virsshteipiyetny neupsnmoiit is edu ot dtsu nda thta swa aosl na o..o.nt.ip

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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eUs the eyrraH-bgdeiWn qtnueoai

  1. Teak eth aeqrsu roto of 16/,001 dan htta lwil vieg oyu hte fuqyrneec fo hte eivsrseec alleel = 4/01.
  2. eultcCaal het qruefnecy fo het atminndo aellel iwth p,q=+1 ihhwc is =p 7.09.5
  3. ehyT aer tgenill ouy to etaaclucl eth euecryqnf of het seiesda scear,rir which is hwit eht nutaeqio .2qp
  4. Teyh want only het ieassed racsrier in hwchi oedetinl is eenp.rst oT eucaltlca s,thi seu eth q auvel 1)(04/ nad ltymupil by %08 in this hdusol gvei you .200.
  5. lya,iFnl ctaceallu fro q 22P ..0)()052=(970 0.04 = 1/25.
yex  Nice! ...and we are supposed to read the stem and do all this in a minute or so? :-/ +23  
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. +7  
topgunber  hate this whole scramble thing: In one line: 2 * q * 80%. This is for diseased individuals (two q alleles).I = 1/1600 = q^2 The frequency of q = 1/40 Now carriers is 2 p q. P is close to one assuming HW eqm (p+q=1). There's an additional step in this question due to the two different mutations. so 2(q) = 1/20. 80% of these carriers are deletions so multiply 1/20 * 0.8 = 1/25 +  


submitted by hayayah(1077),
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nd-Hepcdurniaie coihyterotbmnapo )H(TI si eht eondtevelmp of GIg enitodsabi iagatns anherpi odbun etllaept torcaf 4 4)PF(. A-i4d-ibnaFPprntheyo xemolcp vtcsietaa eaetpsllt Ž tshrboioms dan amnobry.ooictthep igesthH rkis wiht oidfantruenatc nep.hrai

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(34),
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Ohetr kendiy srpopheiyterH deu to aecrdisne stesrs --> tno yharasippel bc ton esucnocar

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. +43  
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(1077),
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ddA on to eht thore nmtmco:e IACCFOMC.SSKE eh(wn I mA rnnidkig etufpGirar ecjui) si het inecmnmo fro ebrremginme eth 05P4CY rIi:stihonb

  • S umodi vratlpaoe
  • I zdiniaso
  • C mneeidiit
  • K tlconooeaez
  • F lnezcuaolo
  • A tuec loochal uebas
  • C cponelrohalihm
  • E iyhccanmcr/ymroithtrilynor
  • S doluimnesaf
  • C orifcanlpxio
  • O merlepzao
  • M oeeildtzoran

  • A darioeonm

  • aitrpeGurf ujeic
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(1077),
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iefniDtoin fo ujdtantesm dsdirer:o

amtEnoiol ssmtypmo (g,e anetyxi, )issndeproe htta ccour tnwiih 3 shtmon of na iteblefnidai yioolsschapc sseorrst ge(, ioec,vrd sli)ensl agnitsl l&;t 6 mstonh oecn eht srsresot hsa .ddene

If psymtsom eipstsr t;g& 6 mosthn tfera estsorsr edsn, it si .DGA

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. +4  
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. +1  


submitted by strugglebus(165),
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K,O os if I memrebre clcoyretr sthi si eth eon atth sshow eth eenctinirah .pernatt ioionlrahmdtc is olsa speads yb eht ;ermtoh eh,rwoev it cna vhae ivalebar xpeisrtsveyi dna tcoelmpien n,rceenatep hwhci si why mseo eemmrbs wree tno .cefaefdt

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... : ( +21  
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(1077),
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rnoI oovsdree is a eacus fo a hhig onani apg aeiobmctl iscsdoi.a

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. +28  
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 +8  
j44n  they did throw us a bone however I didnt catch it +1  


submitted by neonem(571),
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ceSin sthi eitanpt is a sormnonek,- ti si essl ot eb sallm elcl raicco,mna sqoasmuu cell oirncacma, ro arlge llce ccramnioa of hte n.ugl dsBisee lalsm lcle namicoarc gnbei fmro drrenoicneoenu gr,inio eth noe aomrj ungl rnacce idcdeebsr yb sntse of reldfwiea,netl-tfide g"ul"rrae clels si a codrnciia ourmt. tAnl,olayiddi otsteser rea gstocalioihl euesfatr fo cadcnrioi trsmuo nf(u fc:at rtsoetes aslo in oeprbnaamldes/mosuytasnmoe (ni SC,)N mbslisrt,oeaonat olsrnauag llec ortusm (naivora eac)rn)c

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 +5  
charcot_bouchard  I thought it was Hamartoma & pick chondrocyte! Can lung even have hamartoma? Pardon me it was the laast ques of whole nbme +8  
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. +2  
jj375  Also once it said membrane bound granules inside the cells, I ruled out hamartoma. It seems to be describing the secretory granules inside a carcinoid tumor. Here is a photo! https://www.researchgate.net/figure/b-Higher-magnification-showing-characteristic-membrane-bound-secretory-granules-which_fig2_22540051 +  


submitted by sattanki(71),
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Melcus npia + ribarpeiotl edmea is a lccssia ieentsrptano for ihotcnellra ilaisr.ps eBst dsognaisi rfo ihst si a celmsu bsyp,oi as teh omryw kiels to outhgna intiwh eht lue.smcs

sympathetikey  That's what you get for killing polar bears. +83  
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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Wyh is it otn avnioar efilcllo lscl?e I guohhtt eth lfaeem lanoag fo irSotle and giedyL is acteogr/nasaluh escl.l

colonelred_  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +9  
brethren_md  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +4  
sympathetikey  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +5  
s1q3t3  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +11  
masonkingcobra  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +3  
mcl  Wait, but did anyone mention that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen??? +38  
mcl  But seriously though, pathology outlines says sertoli-leydig tumor "may be suspected clinically in a young patient presenting with a combination of virilization, elevated testosterone levels and ovarian / pelvic mass on imaging studies." As for follicle cell tumors, granulosa cell tumors usually occur in adults and would cause elevated levels of estrogens. Theca cell tumor would also primarily produce estrogens. Putting the links at the end since idk if they're gonna turn out right lol Link pathology outlines for sertoli leydig granulosa cell tumor theca cell tumor +12  
bigjimbo  LOL +  
fallenistand  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +5  
medpsychosis  So after doing some intense research, UPtoDate, PubMed, an intense literature review on the topic I have come to the final conclusion that...... ...... ...... ...... Wait for it.... ..... ..... Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +9  
charcot_bouchard  Hello, i just want to add that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
giggidy  Hold up, so I'm confused - I read all the posts above but I still am unsure - are sertoli-leydig cells notorious for producing androgen? +4  
subclaviansteele  Hold the phone.....Females can get sertoli leydig cell tumors which are notorious for producing androgen? TIL TL;DR - Females can get sertoli leydig cell tumors = high androgens +  
cinnapie  I just found a recent study on PubMed saying "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" +2  
youssefa  Hahahahaha ya'll just bored +9  
water  Bored? you wouldn't think so if you knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +5  
nbmehelp  I dont get it +  
redvelvet  how don't you get it that females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen? +1  
drmomo  what if this means..... females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen +  
sunshinesweetheart  hahahaha this made my day #futurephysicians #lowkeyidiots +  
sunshinesweetheart  @medstruggle look up placental aromatase deficiency (p. 625 FA 2019), it would have a different presentation +  
deathbystep1  i am sure i would ace STEP 1 if i only knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +2  
noplanb  Wait... I might actually never forget this now lol +3  
drmohandes  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +1  
lilmonkey  Don't forget that females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens! You're welcome! +  
drpatinoire  Now I get it that females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens. Thank you very much.. So why choose Sertoli-Leydig cell tumor again? +  
dr_ligma  The reason is because females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens! This is easy to remember, as you can remember it through the simple mnemonic "FCGSLCTWANFPLOA" which stands for "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen!" +18  
minion7  after receiving a f*king score..... this post made me smile and thanks to the statement-- females can get sertoli-leydig cell tumours, which are notorious for producing lots of androgen! +1  
djtallahassee  My worthless self put adrenal zona fasciculate but now I will never forget that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
medguru2295  Wait..... so can females get Sertoli Leydig cells that produce androgens then?????? +  
peqmd  Going to snapshot this to my anki deck card: "females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of {{c1::androgens}}" +1  
paperbackwriter  Watch me f*ck up the fact that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgens on the real deal. +2  
alexxxx30  just made sure to add to my notes "Females can get sertoli leydig cell tumors, which are notorious for producing lots of androgens" +2  
peridot  I also just wanna add that if you look on in FA on p.696969, you'll see that they'll mention "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" +  
mbate4  According to the literature [lol] females can get sertoli-leydig cell tumors, which are notorious for producing lots of antigens +  
drdoom  the tradition lives on +1  
jamaicabliz  Wait... so for clarification, is it that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen? Or that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen?? HELP +  
abkapoor  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen sorry for bad Englesh +  
faus305  Sertoli-leydig cells are notorious for producing lots of androgens, females can get these. +  
djeffs1  the fact that a bunch of medstudents can get so weird about how females can get sertoli-leydig cell tumors: notorious for producing lots of androgens- just made my week!! I love you guys +  


submitted by mousie(218),
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sI 45 uietsmn too nlgo ot be tapycanalcih dna ldowu eth beenacs fo ashr rc,air(utia su)putrir OR ncaip?athclya

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) +8  
hayayah  (also allergy / anaphylactic presents with more skin findings (urticaria, pruritus) +7  
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(571),
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My btse segsu si htta stih tpnteia sha a cpsbiiud caotir evlva and hsa a rmurum ued to sneracdei mvoule veadolor omfr eth cyan.rpeng

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 +6  
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 oauthshp lcesru if hteer aer no GI tsmmp?yso yWh tan’c ti eb sphree zeotrs?

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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All otabu ishttgi:n

necncopnsist.l/itbdhcsadtceismfndeutw/tu.e/ehf/jtreoos:goohs/.n/eaa

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. +17  
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). +10  
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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Teh sanwre is eopxrialfehy cseaebu teh feetfrna car of hte sclume crhtset elxfer sah to go houhgtr eht doalrs rmia and oasrld roto g.ilnaag buDm stei,nuqo I ownk, ubt ’sti eht ylon ewrans htat dmea e.snes If uoy hutr hte DR,G you otn nloy lose trnefafe moiasct ynsrose besf,ir you oasl esol teh nsreoys boseid vdoliven in het orivsau frleseex.

uoY cna aols get ehrfyoialepx ofrm maiagdgn teh eterenff usrnoen atht eirvnnate eht scmuel k(lie a ,MLN) utb as oyu wkon tshee rea ni the arteiorn nroh nda tnerlav ra.im

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? +6  
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 +1  


submitted by leny123(7),
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lreGaen rule - oeCuhrniqlo tseinvesi if orfm eCibnraab ro neatCrl mreAaic tsew of aaamnP naCla, hsit tanepit dramemgiit omrf aondursH so uoy nca tmielaeni qiloocnuher estisaenrc as na warens ciceho (in nditaoid to teh xvleiaaov/v onfi a).vebo

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(415),
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Uare Cycel serdDsoir gt;& doealstI veerse onmirmmeepaayh t(&;g 1000; ,.e.i on treoh vsreee ableoimtc tscrsaneidbu

nrOheniti mearcaatrsalbysn feccidieyn tg&; sot(m nmocom uear yclce d).si toocir irmcd/ieciduiaaaa, rehmyopenimama

Oingrac iismAdace gt;& imHmaae,oremynp naapngo-i oda,issic toisesk fmo(r mgyp)eciylhao

mhudMcaenii- AcyalCo- aeshdeeydrong fncceyeidi t&g; mHm,moniyeapear ocettykohpi coplmhgyaeyi sn(ee in -ooaxidβitn eorrdi,ssd TXCPEE r)adoednyotpekusolhyr

evriL utdyfoscnni &tg; emoapmmnHyre,ai TFsL eesmsd pu, odlre pt.

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


submitted by sattanki(71),
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osDe oneyan vhae any idea no htis on?stqeiu Thhuotg ti swa SAL.

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(1567),
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shTi si teirhe a oetphyrpicr arcs ro ekoi.dl oBth rasie eud ot -erepoviersnsxo fo baetF-T.G

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(340),
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Teh iteatpn sha sslo fo apin nda rerptameteu no het rtigh edsi fo hsi ce.af esSnntiao of the afec is isltl,aairep so hte seisu tmus be on het 'setnitpa gihtr s,ied chihw ew nca cmriofn yb oginkwn hatt sainseton fo teh bdyo si aolattlean,rrc nda eh sha lsot ltfe sddei inpa dna etrrtepumae fo eht bo.dy

iaPn nad repmrtueate snoetinas of teh doyb si tarp of hte paanmsthlocii ,rctat which aswayl runs altllerya uthghro eth etmrnias.b sThi nac eb rnfeoimdc yb erbmgrmeine ttha nstsainoe to eht efac sola runs llrlaeaty rhughot eth eir.satnbm ,oS ew acn cfmoirn itsh si a rghti iesdd lelaart rbsniemat euiss.

heT lsso fo agg flexre adn silrpsyaa of eht oacvl osdcr pymil mtpeniiamr fo lcranai nesver IX nad X, thob of cwhhi eliloazc ot eth ul.dmlae Thre,eefro eth nrweas si ghtri sodelraotrla mdel.ula

duat98  You're a good man. +3  
charcot_bouchard  You must be handsome too +9  


submitted by colonelred_(105),
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hTe ansayisl oynl wdsheo a itanotum in one l.elela FC is an slumaaoot iceversse eesas:di hte aediess loyn fsnmesati if eetrh aer tutmnasio in otbh lelasel fo het TFRC gn.ee

fI uoy lltsi ehav 1 lfcntonaiu oypc fo eht RTFC ne,eg uoy acn itlsl amke the TRFC noetrpi (teh iocedrhl ror)scnheaeat/ntrpnl, neceh ryou ydob wn’to have yna .ssiesu

Thsi si ulsooagan to mruto upsorprses esegn klei bR: so goln sa eon fo het ellales yuo vhea is culnioant,f yuo cna mkae neuhog of the nroitpe ot mek“a u”p ofr hte fcveieedt lelael. fI bhto egt ekonkdc tuo )-R-/,(b yuo oesl teh ctotpnoire pdiodevr yb eth eneg sbaeeuc own you eamk no neioprt ta .lal

hTe oyln tignh taht dmae neses rfo stih inestquo was teh ctfa taht the rothe elleal aws otn ilcdedun ni teh ain.aslys

charcot_bouchard  OR another allele has a diff type of mutation because CF is done by like hundreds of diff type of mutation. SO the 70 types that we screened covered one type from one parent but not another that was inherited from other parent. +38  
soph  I put D thinking there was a mutation in another protein that interacts with CFTR....thus u dont have CF but some disease with similar phenotype. Is this wrong bc its simply not the case ?? +9  
nbmehelp  @charcot_bouchard I think that makes more sense if I understand what you're saying- Probably had a mutation only in 1 of 2 of the same alleles in the analysis but had another mutation in 2 of 2 alleles at a different location not included in the analysis, right? +  
fallot4logy  CF is a rare disease , and the possibility to have a mutated gene plus a gene that its not belong to 70 most common cf mutations is extremely rare +4  
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(259),
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tMos mconmo eaucs of utcea ttssipaorit in rdeol enm is .E ,loCi and enht oaPsmos.uedn

charcot_bouchard  Grandpa is monogamous. Sexual history was just to throw u off +13  


submitted by rocmed(-1),
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:sgoleDemin otepComnn fo ee,somosdms hhwci cocnten tsroyekeniact ni hte amttusr iusponms - AF 28,01 .46,p7 peuPmisgh lusaVrig

By hist I nac loyn asemus ahtt yteh anem tath lsigenmoed neotnccs teonretyciaks ot HCEA THOE,R hecen ywh het rteho oipsnot ngicnconet stteyiakrcneo to ohret ercrtustus rae rtocriecn

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(1032),
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oCol natrohe soqietnu kneta fmor teh stil fo tigshn otn ni 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. +22  
yotsubato  But not in this context +5  


submitted by stapes2big(12),
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Im’ otn sreu tauob thsi eon ubt the wya I uhtogth otaub it wsa taht cesni eth fciecnoden rnaetvil dledcnui 1, ti saw nto nagifitncsi. ndA suht p lauev tmus eb beaov 0.50

tea-cats-biscuits  That makes sense! +  
asapdoc  Had the same reasoning +21  
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(58),
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yAn iaed why ochiprlmyreeha 'inst an ?renaws eTh ihrdeara dluow csaue an oarlnm nanio gpa rpiomhche(ly)rec beamtloci soicsdi.a

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 +26  
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(26),
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tebs ywa to ohcaappr ti si to ska cihhw one ahs a paolrt oatlciruinc nad a symtseic cralctiouni ( uYo OTDN eend ot kwon eht ueepcrdro ot nawres hsti nuisoqet.

xl:empea atcn be ropurise icterasgip dan efrnoiir tiepcgsrai escebau oseht ear obth mctyssie lao s cant be pieursro lceatr frn(ieior cstnrieeem hc)nbra nad esroipur setrnmeeic uesceab theos rea ohtb olrpat emysst

hewn oyu warnor it don,w nhet tis a 550/0 .sgseu

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 +7  


submitted by nosancuck(87),
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Yo wadg ew lal atbou TPV ITM aLHL

ainahenleylPn, Vanl,ie tpoKDNTyAr, nTrenie,ho sul,ioneceI ieonntehM,i snd,eHitii ieLcneu yLeins

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. +11  
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 +