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Welcome to temmy’s page.
Contributor score: 130


Comments ...

 +2  (nbme23#43)
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docnAgcir to Dr S.tr.taa mceridaocnnaoA is eth tmso ncommo eusac of ugnl earcnc in eflmae non oserk.ms

drzed  Correction: he says it is the most common in NONSMOKERS and FEMALE SMOKERS. +7

 +0  (nbme23#42)
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htaW of if het cacner is a erullahiot nreacc in the dbedalr ude ot aidnitrao at.ypher duolw it ont scaeu siirlma isngs

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 +

 +11  (nbme23#27)
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Dr attSar atslk butao eaierscn ylapilrca ibrepmyteial in eht yosrplalptcai unvlese adn atolsiidnova in eth orasreitle sa insaoct fo .snmitehia hatT swa atwh i tutgohh of nweh i asenwder hte oeqisnus.t


 +4  (nbme21#8)
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I ereag hitw awth ash been iads tub aols tneo tath the eintpta acedll ehr tnriitnse to help her radssed teh cicontfl eewetbn teh two yihpsnacsi hhiwc ahs enottg erh ri.rweod atTh is rhe sde.eir dnA rfom wath i eahv adrte,ehg wrhee lsie,obsp eth ttpeasni wesihs udhlos be e.tm

mambaforstep  true... i totally missed the part "pt CALLS HER PRIMARY CARE INTERNIST TO HELP ADDRESS THIS CONFLICT BTW THE 2 PHYSICIANS" smh +1

 +4  (nbme21#1)
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hytelHa peeopl ohw teg iksc ihwt spvuoirrav amy eahv a aisccnbulil lsnleis ihwt lgitharaas as the olyn oy.mtmsp Btu kilcse lelc itastnep dan aestntip ihwt aceedesrs phioesmaostei illw el[dpevo noeb mwrrao ulrafei scauebe eht vsrui affect the toetheacmioip mets lecls lnidgae to aatilscp cisrse nda iyalbiitn rof eht oneb aromrw to yleautedaq ompesatenc enhce teh wol eoctectluiry rvaptioo.u rucnsv ls.dcuepeasas.p ehksce ni d ksi ydhrosp itelsaf in ufst,e iactalsp csries ni kleisc ellc nad iaharsratlg ni orhte tns.aetip

henoch280  thanks. very helpful +

 -4  (nbme21#10)
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peasel phel ccaiogrnd ot ntrwsei nqiuotae hte iteatnp ahs a lnrmoa noian pga

ergogenic22  winter's formula is to look at the compensation to see if it is appropriate. PCO2 = 1.5[HCO3-] + 8 +/- 2 In this case, 1.5* 10 (Pt's bicarb) +8 +/-2 = 21 to 25 Pt's PO2 is 23, so compensation is appropriate. If PCO2 was below 21, it would be concomitant respiratory alkalosis +5
ergogenic22  in other words, winter's formula is not necessary for this question +2
the_sacramento_kings  lol unless you want to make sure its not A. +1
hello  @ergogenic22 Someone might use Winter's formula to rule out choice A. +
maxillarythirdmolar  respiratory depression of alcohol should rule out "A" +
baja_blast  Isn't the low pCO2 enough to rule out A? +1

 +3  (nbme21#27)
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Adn ernve pick an onopit atht sakem uyo uonds aiitclrc


 +5  (nbme21#27)
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hnwe ni do,but ickp na enpo dened .osqitneu Tehy ivge eth iaetntp na typotnpriou ot ssslpeer hsemtevex twih rgtnoppmi mrfo eht tdoocr


 +5  (nbme21#40)
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lmtAso afield ihts tinuoqes tbu i petk graneih rD aSttra geicrnasm tsgrnialadonp 2E EEEEEEEVEFR


 +1  (nbme21#23)
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FIN gaamm itluestsma acheompgars ot pcordeu rgsamlonau


 +5  (nbme21#43)
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ohw i eremerbm it rof lal oemroagfl dnsamur .N..yFbI tiidnnaMemmag aa by TNF ahalp

ammaG sromf ahapl aitnanism sisuas(tn ).ti htTa si ywh malinixfbi nda (rctaaepnet NTF ahpal sioitrh)inb iwll akber nwod het oagmanrlu if se.du


 +1  (nbme21#42)
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ebsbai fo tibdeaci msmo den pu nebig gregib nad atth amy ldea to drolesuh tdayiocs

sahusema  If one of the answer choices was, "that baby gon be big lol" I would have gotten it right +19

 +0  (nbme21#48)
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i nhikt the qentiusos is niytrg to hwos het recmpoanit of tuiyn aognm fmiyla bermesm hwen eethr is a ptniate hwo is ovdle by btoh ifew dna id.sk ehT yutd of het doroct si to eeusnr the iyflam is nietud ni stourpp of the anpetti the and ni ceas heret si lilst ncflitco grnagider hatw ot d,o you ues teh ychhareir ewreh wief emosc t.irsf i tge ti swa a dbum ubt tshi aws my ogic l

 +3  (nbme21#16)
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ypeT 2 psomtencyeu eodcurp mets lselc dna ufsr.atncat

 +2  (nbme20#43)
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i hknit it si nto greonadn stnnysiivieit ebceaus eht otsseerttoen eellsv rea naolr.m yThe houdsl be ghih ni A.SI





Subcomments ...

submitted by dr.xx(151),
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r.tgih he baleoyslut stmu ainemr ni eht tnigiaw eaar os thta he si at ahnd ot kcatta sih iefw hwenevre rhe axme n.sed go ENBM!

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. +4  
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 cbrodo(61),
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The peooirtrs ucnslom si(cluascuF tculiuaFsensccasu/u gra)iscil rcyar nmoatrfinoi ot the rnabi dgegairrn octiprripopoen, b,ioarvtin vtidcensiamiri ctouh nda seserupr. caihslPy eaxm nngsiidf stsgeug a esoinl here the( anhmltaoscpii rttca rsecari pnik/niiapcrp dna etrmreeaup,t nda heest rewe )rl.naom eSnci teh ntptaei hsa rblaonma ngiinfds ni the ewolr triemixtse,e and mnalro fsgnndii ni eht rpuep sxeteeiirt,m eht rsaenw si Faucsciusl rlica.gis hiTs si eusbaec nmrinitoafo fomr odby aaesr lebow het ellev of 6T is iadcrer by rsgilcia and imoonfiratn fmro yodb rseaa bevoa the vleel of T6 is dacrier by cantusue.

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 hipster_do(6),
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m’I giogn to ysa ’sti X kledni gaabiiuaoegmlmlamn ratehr ahtn ISDC, tbu the nfedcfeeri ebetnew shtee wto rae nyit tub tsih si ywh I htkni ist’ eth fre:mor

  • Byo creen(iasd iskr utb obth BA nda DCIS aer x kld)ein
  • ncreurtRe abtliaerc iitsnncfoe tbu notd’ inenotm hiadrare ro uthhsr cwhhi is in DISC
  • iemTinle si treaf 6 sthmon, os the sreom’th dieiabonts woer o.ff

IDSC duohls eb iaelmdimtye abueesc tyhe jtsu ont’d aehv eht 2LI cseor.ertp VDIC wsosh pu ehnw rhtey’e 4020- ysare .dlo uYo gte natsbe aermglni esretnc in hto.b oN inntmoe of bnetas imhcty wsdaho hhicw is in I.SCD

placebo079  “Uniformly” low is also a clue; in CVID they are not. +4  
tea-cats-biscuits  This makes sense, though what really threw me off was that in Classic Bruton’s Agammaglobulinemia there’s near-zero B counts though (or at least that’s what FA and UTD says, “Absent B cells in peripheral blood” FA 116, 2018). The Q says the leukocyte count was normal though. Wouldn’t the leukocyte count include lymphocytes in the differential? And wouldn’t lymphocytes be low due to the near complete lack of B cells in peripheral circulation if it was BA? +2  
partybrockk  @tea-cats-biscuits Bruton’s is a failure of B cells to /MATURE/. So you get normal lymphocyte counts, decreased levels of immunoglobulins, and absent germinal centers. +5  
tea-cats-biscuits  @partybrockk That makes sense to me, but I keep getting hung up on how that’s not what either FA or UTD says about the classic lab findings of XLA. UTD specifically says this: “Laboratory findings include hypogammaglobulinemia/agammaglobulinemia, deficient antibody responses to immunizations, and absent or markedly reduced B cells in the blood,” and I previously quoted FA. I suppose it doesn’t really matter, but it’s definitely a bit frustrating unless I’m missing something about how absent B cells in the blood wouldn’t correlate to a decreased lymphocyte count ... +3  
temmy  please correct me if i am wrong cos i might be but my logic was there is decreases immunoglobulin uniformly meaning the B cells are uniformly absent and since they develop in the germinal center, the germinal center will be absent. +2  
almondbreeze  Picked 'decreased # of CD4 lymphocytes'.. ->Both CD4 and CD8 T lymphocytes were affected; the decrease was most pronounced for naïve T cells. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809006/) +  


submitted by dubchak7(1),
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heTy ggtsesu itolosrpMso to erottcuacn NIDSs.A.. hWy ont s?PIP

hayayah  PPI's don't have many side effects! If the question didn't involve the diarrhea side effect the answer would have been to give her a PPI. +1  
tsarcoidosis  I guess one takeaway is that PPIs don't directly cause diarrhea, but they do increase the risk for C-diff, which causes diarrhea. +14  
usmleuser007  PPI side-effects: + increased risk for C. diff + Increased risk for resp infections + can cause hypomagnesia + decrease absorption of (Ca2+, Mg2+, & iron) + increased risk of osteoporotic hip fractures (d/t low serum calcium) +1  
temmy  The patient got severe gastric burning and discomfort as an effect of the drug. My logic was since the patient was taking an NSAID it had to be a COX 1 inhibitor that destroys the protective barrier of the GI mucosa due to inhibition of prostaglandin so we needed to treat with a drug that will regenerate prostaglandin and prostaglandin is a vasodilation which might be the reason for the diarrhea. +  


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dgrAosnne uscea .enca soeTetsoertn is a betetr srenwa atnh diordntnaolAse c/b eth seeetoTstrno si ascdoeista hitw ytbpr,eu ldeAinradnstoo is emor ecsaatoisd ihwt eth lnraead ndls.ag

meningitis  I chose Testosterone but I almost chose GnRH because it is surged when starting puberty and therefore increases everything downstream. +10  
temmy  When answering the question, i thought to myself that if GnRH is correct, LH will be too cos GnRH stimulates the Leydig cells via LH to release testosterone. That left testosterone as the best answer because it had the most direct effect. +10  
goaiable  GnRH and LH are increased in a pulsatile fashion at the onset of puberty, so idk if that constitutes as the "rapid increase" that this question is asking for. Tripped me up also. +  
tallerthanmymom  I originally eliminated testosterone and chose androstanediol because women can have Acne Vulgaris too, and Testosterone should not be rising to the same degree. Do I not understand how puberty works? +1  
drzed  Women can still make testosterone though; and androstAnediOL is not the same as androstEnediONE +3  


submitted by drdre(24),
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geaP 650 FA 2109 ssecrideb asead.hech

Csulert

  • alrntilaeU
  • 51 imns ot 3 srhuo
  • ibPritolear aipn ithw itlrnaciamo dna herhiarnro
  • x:T ntuaStaprim

ir ieMang

  • lUaalirnte
  • 4 to 72 uhros
  • Plutnaigs apin thwi aunes,a oio,bphahotp phhnapo,oobi mya aehv rau"a"
  • CN V, ninsemge ro olbdo seevsl raitoiritn
  • x:T NSSDA,I t,nsaptri iteoniohageryddmr

i sTnoen

  • leaaitrlB
  • 4 ot 6 urosh
  • aBn-kleid pani
  • x:T gnscisa,ale A,SNDSI oaaenehnptimc

drdre  yay formatting fail +  
drdoom  @drdre, next time try hitting enter twice ("start a new paragraph") before beginning a list. +  
temmy  cluster mostly seen in men +1  


submitted by neonem(571),
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ihsT is a eacs fo aucte .gotu uoisdmoMno tuaer crasltsy aer keatn up by iuohrtel,nps elagidn to an cauet imlanfmrytao i.ocetran -lclesT aern't rleayl vdieolnv ni toug mre(o iedmahruto irirhsa)t.t

hungrybox  Great explanation! So frustrating that I got this wrong, should have been easy. +3  
temmy  the way i thought about it was how did the neutrophils get there? the answer is via increased vascular permeability +16  
nor16  they, unfortunately, did not ask " how did neutrophils get there" but " whats the cause of the swelling " not to confuse with " what causes the swelling " +1  
divya  absolutely right temmy. that's how i thought about it too. +  


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tI aids ti saw aftal ot samel ni ote,ru and teh seuoniqt kadse touab viel onrb rfis.ofgpn ineSc hte eamsl tra’ne eibng born in eth trsfi cpale, I idsa %05 faemles adn %0 msal.e

hungrybox  fuck i got baited +32  
jcrll  "live-born offspring" ← baited +23  
sympathetikey  Same :/ +  
arkmoses  smh +  
niboonsh  why is it 50% females tho? +2  
imgdoc  felt like an idiot after i figured out why i got this wrong. +2  
temmy  oh shit! +  
suckitnbme  This isn't exactly right as males can still be born as evidenced by individuals III 6,9,11. This basically an x-linked recessive disease. A carrier mother can still pass her normal X chromosome to a son (50% chance). It's just that the other 50% chance of passing an affected X chromosome results in death of the fetus in utero. Thus all males actually born will not be affected. +2  
makinallkindzofgainz  @suckitnbme, Correct, but if you're a live-born male, you 100% for sure do NOT have the disease, so the chance of a live-born male "being affected" is 0. +3  
spow  @suckitnbme it's not X-linked recessive, otherwise every single son would be affected and therefore have died in utero. It's X-linked dominant +3  
qball  Jail-baited +  
srmtn  correct @spow affected females= X linked Dominant +  


submitted by sympathetikey(1368),
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Teh eolwh ip"csk at the aui.e.sonslecs. smoe geb,delin" mdea me tnhki oPssr.isia ulhodS ahve eong ihwt cAiinct sKreaosit adbes on hte nitptae ihystor tos(l of usn .uexrsepo)

iticAcn erisstoaK

anglntirmPae olniess deaucs yb snu oee.uxsrp Slm,la ou,ghr thmurteayeos or bohwisrn sulpape ulaerpos.q sRki of usqauosm lcel comacinar is poltranpioor ot eedger fo palhietile ilasay.sdp

thisisfine   Same - the bleeding thing pushed me over to psoriasis as well. Oops. +5  
temmy  the distribution of the other lesions, forearm, face, ear, scalp..is not characteristic for psoriasis. +6  
hyperfukus  the scalp and ear are actually very common for psoriasis IRL the key is more of the fact that its in areas with UV exposure...actually UV Therapy is found to be helpful in treating some pts w/Psoriasis. Lastly the appearance and lots of things bleed if they were trying to go for auspitz sign it would have tiny dots of bright red blood with slightly touching it +4  
hyperfukus  oh last thing psoriasis itches! they said no itching +4  
drzed  Those locations may be common IRL, but on step 1, if they want you to think psoriasis, the illness script is going to be someone in their 30s (autoimmune age) with symmetric cutaneous plaques that have a silvery scale on the extensor surfaces. In this case, the age and non-classic description (location, type of lesion) made me steer away from psoriasis. +1  


submitted by neonem(571),
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rojMa kris fcator rfo iatcor idnisesoct si tnorneypi,esh dan ni tsih acse tmghi be ude to aonciec se,u whchi aucses kmrade otihneypnre.s ssiDocneits esuac a eart ni eht tauicn nimati -- odolb anc lfow abraskwdc tnio hte eridpucrima nad casue pan.motdea hsTi stfaimnse as srcacelk ni eth ulng edu ot oopr eltf reacivtrnlu coufnint l(cfloingst/dliaii bromple due ot pcio)eo.nmssr

forerofore  there is another clue, the man has diminished pulses in just one arm, which means that the left subclavian artery must be involved somehow, and an aortic dissection would be the best answer explaining this. +9  
temmy  please why is there where a diastolic mumur? +1  
whoissaad  @temmy Aortic dissection especially near the root of aorta can lead to dilatation of the aortic valves, which can lead to Aortic regurgitation (diastoic murmur at left sternal border) +8  
garibay92  Does anyone know why is this patient's tepmerature elevated? +1  
ratadecalle  @garibay92, not important for this question I think but cocaine can cause malignant hyperthermia +1  
almondbreeze  judging by his heart murmur, he probably has marfan syndrome. that's the only place where FA talks about dissecting aneurysm +  
almondbreeze  he's only 28 - another clue for marfan? +  
turtlepenlight  did anyone else think it was weird his only sx was SOB? I always think of radiating pain as being a good clue for dissection +2  
cmun777  @almondbreeze his heart murmur is at the LSB (aortic regurg) and not consistent with MVP plus no other sx/indication of Marfan. I think the only association of RF you should think about in this question is the cocaine use and consequent HTN. +1  
ibestalkinyo  @turtlepenlight I agree. I chose another answer because I was like, there's no way this guy doesn't hurt if he's got a dissection. +1  


submitted by aishu007(3),
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anc yeaonn aiexnpl why lctfaonsceeiorsaecuc si teh aerwsn he?re

priapism  Best I can guess is that both S. aureus and E. faecalis can cause UTI, but S. aureus is described as having clusters where as the other Gm+ cocci are in chains +6  
nala_ula  My doubt here in this question is the fact that Enterococcus faecalis is a normal gut microorganism that causes these different symptoms of sickness after genitoruinary or gastrointestinal procedures... but in this question there is no mention of any procedures. +  
fez_karim  its says chains, so not staph. only other is entero +  
temmy  according to first aid, staph aureus is not one of the high yield bugs for UTIs +1  
temmy  uti bugs are E.Coli Staph saprophyticus Klebsiella pneumonia Serratia Marcescens Enterococcus Proteus mirabilis Pseudomonad aeruginosa +  
privatejoker  Where in FA 2019 does it list that C.coccus is specifically in chains? +  
privatejoker  E.Coccus* i mean +  
divya  @privatejoker FA 2018 Pg 134 table +  
jennybones  @privatejoker Enterococcus is Group-D STREP. Streps are arranged in chains. +2  
santal  FA 2019 Page 639, too. +  
backwardsprogress  Enteroccocus is also a pretty common cause of chronic prostatitis, which was the give away in the prompt if you didnt know the characteristics of entero: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3715713/ +  


submitted by aishu007(3),
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nac noaeyn pxenlia yhw isnsueecefaooccacrtl si het arwnes ree?h

priapism  Best I can guess is that both S. aureus and E. faecalis can cause UTI, but S. aureus is described as having clusters where as the other Gm+ cocci are in chains +6  
nala_ula  My doubt here in this question is the fact that Enterococcus faecalis is a normal gut microorganism that causes these different symptoms of sickness after genitoruinary or gastrointestinal procedures... but in this question there is no mention of any procedures. +  
fez_karim  its says chains, so not staph. only other is entero +  
temmy  according to first aid, staph aureus is not one of the high yield bugs for UTIs +1  
temmy  uti bugs are E.Coli Staph saprophyticus Klebsiella pneumonia Serratia Marcescens Enterococcus Proteus mirabilis Pseudomonad aeruginosa +  
privatejoker  Where in FA 2019 does it list that C.coccus is specifically in chains? +  
privatejoker  E.Coccus* i mean +  
divya  @privatejoker FA 2018 Pg 134 table +  
jennybones  @privatejoker Enterococcus is Group-D STREP. Streps are arranged in chains. +2  
santal  FA 2019 Page 639, too. +  
backwardsprogress  Enteroccocus is also a pretty common cause of chronic prostatitis, which was the give away in the prompt if you didnt know the characteristics of entero: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3715713/ +  


submitted by mcl(599),
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Nto esru if ihst is eth thrgi ayw ot ikhtn buato ,it ubt if TP nda PTT rae hbot lo,gndroep tshi toms kleiyl esnma teerh is a rpoebml wthi the oommcn ywhatap aak( ratcof X.)

temmy  exactly...i just thought the problem has to be where they meet or somewhere similar to both..hence the common pathway 12(PTT Heparin) 7 (PT, Warfarin) 11 9 10 5 2 1 In my head, both sides are looking for the perfect 10 +  


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In eth treag roswd fo Dr t:Satar

ot"rdsaiagPnln 2E demiesta eeer"eeefeeeeev

IsSNAD -g&-;t lbkco optngalnasdir nys

thisisfine   This is all I heard in my head +7  
temmy  Me it was so weird +  
peridot  I do want to add, that while PGE2 is the right answer, FA19 p.213 says that IL-1 and TNF are involved as well. However, because the question asks about what is going on in the hypothalamus, the answer is PGE2. If the question had been asking about what the macrophages were releasing to influence the hypothalamus, then the answer would have been IL-1 or TNF (FA didn't specify if it was TNF-a though...). +1  
feeeeeever  You know why I'm here +7  


submitted by yotsubato(1032),
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Why is hsi iobdiL ?aonlmr tsI' tyotlal xeetpced ttha he yam heva decedur odlbii fater ihs wfie ided 2 yaers ago ormf oesm birrleoh oeldpngor lnsles.i

nala_ula  perhaps it's more to do with the fact that he can get erections when masturbating, outside of nocturnal erections which are not mediated by sexual desire. So his libido must be intact since he has sexual desire evident in being able to masturbate. +  
nala_ula  At least, that's the way I saw it. +  
home_run_ball  "Testosterone concentration is within the reference range" and the fact that he has no difficulty masturbating = normal libido. Low testosterone would contribute to low libido And if he had low libido he would have difficulty masturbating +  
thisisfine   The way I made the decision about normal vs. decreased libido is also that he presented to his doctor due to difficulty maintaining an erection while trying to have sex - meaning he has the libido to try to have sex. Does that make sense? +1  
btl_nyc  It also says there are no signs of depression, which would cause the low libido after his wife died. +  
temmy  two years is a enough time to mourn...just saying +  
temmy  thisisfine, it makes absolute sense. That is the same way i saw it +  
dr_jan_itor  He misses his wife man, isn't ready for other women. Psychogenic ED. physically hes fine (can crank his meat) +  


submitted by yotsubato(1032),
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hWy is shi bidioL alrno?m tsI' yolttla dexeptec taht he yma vaeh eddrceu ibdilo arfte ihs wfei died 2 sryea oag rfom meso hobrelri pgnrdooel ie.nslls

nala_ula  perhaps it's more to do with the fact that he can get erections when masturbating, outside of nocturnal erections which are not mediated by sexual desire. So his libido must be intact since he has sexual desire evident in being able to masturbate. +  
nala_ula  At least, that's the way I saw it. +  
home_run_ball  "Testosterone concentration is within the reference range" and the fact that he has no difficulty masturbating = normal libido. Low testosterone would contribute to low libido And if he had low libido he would have difficulty masturbating +  
thisisfine   The way I made the decision about normal vs. decreased libido is also that he presented to his doctor due to difficulty maintaining an erection while trying to have sex - meaning he has the libido to try to have sex. Does that make sense? +1  
btl_nyc  It also says there are no signs of depression, which would cause the low libido after his wife died. +  
temmy  two years is a enough time to mourn...just saying +  
temmy  thisisfine, it makes absolute sense. That is the same way i saw it +  
dr_jan_itor  He misses his wife man, isn't ready for other women. Psychogenic ED. physically hes fine (can crank his meat) +  


submitted by didelphus(58),
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nyA aide yhw rehmpochylarei tnsi' an ?sranwe eTh eardhria uldow csuea na mnrola anoin agp hmr)eyiloecch(pr bceimoatl scd.soiia

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 haliburton(214),
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iThs is rwtae xiona.ointcti wp5inw7t.u.om/n77:hsi9h//mdplbgtw8./vn1ebc.

thisisfine   Agreed! It's along the lines of those marathon runners who collapse questions. Nothing but water for 24 hours = getting rid of too much sodium. +1  
temmy  are we just going to ignore the diarrhea for 3 days? what is its significance +4  
kard  Temmy, We aint Ignoring the Diarrhea, Actually the most likely electrolytes to get lost with it is sodium> chloride> potassium> bicarbonate... Plus the Water intoxication -> HYPONATREMIA +1  
bronchophony  why not hypoglycemia? +1  
saulgoodman  Because glucose is not an electrolyte, it does not conduct electricity in solution. The question is asking "Which of the following electrolyte abnormalities". +4  


submitted by usmleuser007(397),
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ujst a cu.n.hh.. mOlazeoper si ywlsaa teh rtghi sweanr

nala_ula  Famotidine is an H2 blocker which really only stops acid secretion via the stimulation of H+/K+ ATPase by histamine, but it still has vagus and gastrin stimulation. If you use Omeprazole, you get irreversible inhibition of the pump itself which stops the secretion of acid even if there is histamine, gastrin, vagus stimulation. +6  
temmy  what about the healing of her mucosa. Is that not the action of prostaglandin?. That threw me off cos according to FA, misoprostol increases secretion of the gastric mucosa +5  
cry2mucheveryday  same doubt..marked miso +2  
sahusema  I guess because misoprostol is more associated with treatment of NSAID related ulcers and PPIs are 1st line DOC for GERD? +1  
makinallkindzofgainz  @temmy, I think that Omeprazole is a better answer because although Misoprostol would promote healing of her esophageal mucosa, it wouldn't do anything to relieve the symptoms of GERD (due to acidic contents in the esophagus) +  


submitted by yo(86),
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sTih durorcec htiiwn 6 hsour adn csuade esom lormnayup edema nda orarysretpi reidssst erfta a snfitrounas sdecau by teh srodo'n aektcuy-otleni ebaintsdio ujts eotsngirdy eht cpetrienis lsorpenithu dan yraoitpsrre hltadenoiel cslel.

lhiwe yanaras/pclahgleliix anc eucsa rsiyreaptro arrtes dna okhsc it ash a ohmwtsae etriffdne ircutep, no igweh,zen nesicisth ro ewvrteha dna oacidgnrc to ftris idA it sphnpea iinwht suenmti to 32- srhou ihwch is ta selta doeulb ahtw e'rew ingese rehe. losa weebra of IAg tdefiienc epoepl ni itsh ie.chco

,EP eh I don't iknth ti ceafsft a2oP thta feton mhcu aorcdnicg ot htis spure drepu hghi deyli er.rsoeuc btu huh heay 'tdoesn lefe PE ankdi iqu sento/d0i0noa.p/u/:e19sdhel#w0a3rctoi-kermic1p2cm.cpcetetes/m

,menonpai tighr tefra lal the noufnisi subsensi and no ninotme fo evref ro tinnay?hg ah.N

og to egpa 141 of tsrif .adi mI' ytrept seru we dnee ot nkwo oru snannrpotuisitanl/f rpca uesbcae ti jstu kesep imncgo up in dowurl but sthi hwloe exam is a sahroopc.t

vrieoFg me if I dmea a i/tmskaernwog btauo ahgiy,nnt I lysmot got oinf fmor sfrit a.id zlp octrecr fi hetre si a eitmkas, dgoo u.ckl

hungrybox  we gonna make it bro +7  
hungrybox  or sis +8  
nala_ula  I did the same, basically went through each one and the time of onset between each. Good luck on your tests!! +  
temmy  i don't think pulmonary embolism will cause bilateral lung infiltrate +6  
athenathefirst  I hope you guys made it. Your post 9 months ago +1  


submitted by hungrybox(1044),
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tnHtsnogi'un aesside

  • nopitinictaa: hse sah a mrsaili redrodis sa her fehatr but iedd riaerel

Rmbeemer T"HNU 4 an i,lanma put ti ni a GCe.A" utininHgnt egen unofd no eomorhmoCs 4. CGA si eth tdieriecontlu tr:aeep

  • ar,oehC aaedcut eulsnuc
  • aaAxit
  • oolmyG in)sop(deser
sbryant6  Side note: atrophy of the caudate nucleus leads to a widened anterior horn of the lateral ventricle. I've seen it worded both ways in UWorld. +22  
sbryant6  Side note: atrophy of the caudate nucleus leads to a widened anterior horn of the lateral ventricle. I've seen it worded both ways in UWorld. +  
foulari112  How would you differentiate this from Frontotemporal lobe dementia +  
temmy  Foulari 112..the ageof the patient and the anticipation cos her dad had it too. Also in frontotemporal pick, you will see personality changes where they act completely different vs huntington where they are aggressive and depressed. +1  
castlblack  CAG = Caudate loses ACh and GABA (from FA) also points you to caudate +  


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VA luFsitsa ro-ture dlobo rfom het iltearar messty to eth esvuno tyes,sm apb-ygnssi the eisoltrreA = reacnseI LP &g-t--; SEANICER R.V All in all = Icrasnee C.O

gcroncdAi to dW,Ulro eht oatislreer are a jraom rucose fo tirsnseace ... so spaiyngsb eht sitloraree ulsrtse ni a edceesar ni toaTl Ppierhlear tcenaessiR ... niuscag na arsencei in hte rate nda muoevl of boldo nirengtur ot eth h.eart I ma yptetr rsue trhee si reom to eth yohgsyolip dniehb hts,i but I oeph hsit iaxndpeel a l.eittl

big92  "Immediately following creation, arteriovenous fistula (AVF) is associated with an increase in cardiac output (CO), achieved predominantly through a reduction in systemic vascular resistance, increased myocardial contractility, and an increase in stroke volume (SV) and heart rate. Over the following week, circulating blood volume increases in conjunction with increases in atrial and brain natriuretic peptides. These alterations are associated with early increases in left ventricular (LV) filling pressure with the potential for resultant impact on atrial and ventricular chamber dimensions and function." (PMID: 25258554) There's also another study by Epstein from the 1950s looking at the effects of AVF's effect on CO in men (PMID: 13052718). Apparently, the increase in resting CO is a big problem because it can lead to high-output cardiac failure (LVH). +28  
hungrybox  Jesus big92 you went in on the research lmao u must be MSTP +6  
temmy  big92 you are right. that is why pagets disease pagets have high output cardiac failure because of the av shunts. +4  
kevin  what is "increase PL" +3  


submitted by hungrybox(1044),
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esmo rnwog arew:sns

ekas*m ssnee cb/ lsemltayosb are rcssorpeur to ueagylon,srtc hwchi use MPO ot fight off eoncnisift

temmy  Hungrybox aka life saver +1  
hello  Thank you!!! +  
bbr  ....uh yeah im pretty sure we just call em "Auer Rods" now. Appreciate the answer tho! +7  


submitted by hungrybox(1044),
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ohetr wsse:rna

bitihnoiin fo H2 os:pretecr f(ro DE)RG pnevter iagsrtc cdia troinesce ediitcmine,(

tnbniiiioh fo pthsdssoioseaehepr )EP:(D

  • eetynihohlpl ma(htsa) tibihsin cAPM PDE
  • sn-flai d(kci lipl)s fro DE ibnhiti PMcG EDP

β2 gotsis:an rfo( )saatmh eucsa ihnrodiontlacob

  • ealulbrto oht(rs iatgnc - A ofr utAe)c
  • smlo,eltare oorrfeomlt gnlo( ctagni - iasxp)hpolyr

kid( tyyelmhcop erebnmam tizotban)aisil

hungrybox  H2 blockers are the -tidines +2  
yotsubato  > dickpills lol +17  
temmy  hungrybox, you are a life saver +1  
cienfuegos  Via FA: take H2 before you dine, think "table for 2" to remember H2 +2  


submitted by moo(-1),
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if hte sulng eewr eclar to aluuntcastio dna eht idk eenv dais he odt'ens tnwa ot be no hte eamt yrmaneo ywh otcnu'ld it be mr?ieiggnlan

amarousis  malingering would be a conscious faking of symptoms to avoid being on the team. he wouldn't have the mid-systolic click and he would probably complain of his symptoms all the time and not just limited to during exertion. +1  
temmy  malingering is also doing it for some external gain. which was not indicated in the stem +1  
garibay92  Also, patients with asthma are usually asymptomatic at the time of physical exam unless they are examined precisely during the attack. +  


submitted by cantaloupe5(77),
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cesrcoPs fo lieatnoniim orf shit on.e woT you acn lateienmi idetmmliaey ujst romf ikoglno ta hte aecmcolhibi awtahpy atcrh. The orthe otw dqurriee nolgedkew that eiumennla is mroe itpercevot ntha nieaplhomne h(sit is ywh aeedrshd nrbu more asily.e) aucBsee pnmloneaihe is sesl ottrip,eevc etreh wldou be more tno essl ORS from shlgn.uti

temmy  i don't understand this at all. i am completely blank...please help +3  
henoch280  @temmy. This question tests our knowledge on albinism which is normally a tyrosinase deficiency disease but the vignette states that the boy's albinism is caused by a genetic mutation in the TYRP1 gene which is shown in the biochemical pathway. A gene that helps in the synthesis of Eumelanin. Now you have to understand that all precursors before that gene is the pathway would still be available if not increased which make 2 of the options in the question wrong. you also have to understand this: (Eu)melanin = (normo)melanin i.e normal melanin which is protective to the skin, decreases reactive oxygen species and gives the dark pigments to the iris, choroid, skin, hair e.t.c. while (feo)melanin = (fake)melanin i.e pheomelanin, the one present in our patient here which is less protective again the uv rays, cannot pigment and cannot decrease ROS generated in the skin. i hope this helps +26  
eacv  @henoch280 thank u very much! I got it right by luck but now i do understand :D +  


submitted by neonem(571),
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orihpMen is a um pooidi igtaosn - one veaersd ctfefe of dipoios si tsam llce aeogrinanultd htta si inpnee-dtdIenEg. aeleRse of iiemhtsan is knia to an aiapchctnayl iacotren t-g-;& iustrpri, .tce

sympathetikey  Never had heard of that one. Just a good guess. Thanks! +  
yb_26  IgE-independent mast cell degranulation can also be caused by radiocontrast agents, some antibiotics (vancomycin) +7  
temmy  it was a u world question +  
mambaforstep  FA 2019 pg 400 +  
mannywillsee  i'm in FA 2019 and pg 400 is blood groups and hemolytic diseases of the newborn. I found this info in page 535 +  
mannywillsee  i'm in FA 2019 and pg 400 is blood groups and hemolytic diseases of the newborn. I found this info in page 535 +1  
mambaforstep  under mast cells "IgE-independent mast cell degran"! FA 2019 pg 400 +  
mumenrider4ever  Uworld QID 11852 talks about this Also FA 2020 pg. 408 (under mast cells) +  


submitted by moneysacs(2),
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Wyh is odse a PAD afert rhbti lsture ni ehhrgi" athn nomlra fetl rnetiuarlcv adicrac o"ptutu evro airedscen "rigth racuivntrle ?PO"2 eosD het lupm retrya &t;-g- atrao nshtu omeecb edreersv taefr b,rhti os hgirhe oxeyng raaot oodbl udlwo fwlo abck onti eth hgrit iece?vtlnr I get thta oerm dlboo ldouw eb eppudm to hte tlfe ltcrnv,eei erisntulg ni RLV/VHH, ubt tndo' ndusdterna eht 2O ibt.

usmleuser007  1) higher than normal CO b/c blood is shunted from aorta to pulmonary arteries. This blood is added to the volume that was pumped into the pulmonary arteries by the RV. Now when the oxygenated blood returns to the LA & LV, the O2 content would be greater d/t higher blood volume. Also for that same reason more blood is returning to the LV (d/t LV volume plus fraction of RV volume). This increased the CO. Right--> Left shunts have late cyanosis b/c the RV is pushing against the excess pressure generated by the LV. This leads to Eisenmenger Syndrome as RV enlarges and pushes against the pressure from the LV in the PDA. Thus shifting Left to right to right to Left and thus the late cyanosis +2  
temmy  The anatomy is aorta-pulmonary artery-pulmonary veins-left atrium-left ventricle Notice that the blood did not come across the right heart at all and because of the LEFT TO RIGHT shunt of the PDA, we add more volume to the LEFT side. Hence the increased left ventricular output +2  


submitted by ihavenolife(68),
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dIk fi it pshel ubt I tog ti nigsu het oHt neT-oB AKstE eomcninm

otH -t;&g LI 1 Fvee(r)

T ecll iutmitolans t&;-g LI 2

enBo amorrw timialonstu t;g&- IL 3

gIE &t-g; IL 4

IgA -;t&g LI 5

aKeut epahs noetrip -;> LI 6

temmy  cyclosporine inhibits transcription of IL2 +14  
mysticsoul  FA2018 Pg 120 +3  
teepot123  same page also for 2019 edition^ +  


submitted by hayayah(1079),
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oDwn rmnodSey :asLb

  • cin. ulcnha uecntanylcrs
  • .cni hGC
  • .icn iibnnih
  • rededsaec APF
  • ddscaeeer AAPPP
celeste  I remember this as Down Syndrome has high HI (hCg and inhibit) +18  
temmy  Thanks celeste. I'll remember Hi +1  


submitted by asdfghjkl(3),
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nonAey onkw ywh IF1-G ulnotwd' be inedrseac as wle?l HRGH is eslttduiam in ieympohgyclc stets.a

nala_ula  Honestly, it's something that has confused me for a while. Why is it that GH secretion is stimulated by hypoglycemia? I mean, it's literally called growth hormone (for growth!), and hypoglycemia, which is basically a "starvation" state, will stimulate this hormone? +  
shaeking  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3529368/ This might help answer your question. I basically didn't pick IGF-1 because it would increase the uptake of glucose leading to a worsen hypoglycemic state. Didn't have a true reason otherwise. +  
temmy  IGF-1 is regulated by insulin. so it will be decreased because insulin levels are also low. +2  
nala_ula  thank you @shaeking! +  
nwinkelmann  I found this and it also explains to a more genetic/cellular level. Essentially, it says that starvation induces some factors that cause GH resistance and IGF1 suppression. +1  
nwinkelmann  Sorry forgot the link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2575072/ +