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Welcome to yb_26’s page.
Contributor score: 255


Comments ...

 +0  (step2ck_form6#33)

lithium can cause hypothyroidism by interfering with normal synthesis and release oh thyroid hormone

  • treat with levothyroxine, no need to discontinue lithium

 +10  (nbme24#31)
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yM sepilm anudginrstned si htat st'p eathr ytlitincorcta is eerddecsa edu ot MI tg=&; ahert tna'c pmup a lto fo bodol t;&g= idecsnrea kcaubp folw niot plaruoymn auslucvreat &=;gt isacednre PWPC.

Mero doblo in alpmnryuo racvtuaeusl tg=&; yhte wlil idatle ni rroed to juts pkee lla seteh odblo &tg=; esceeradd plurnmyao urlvaasc eesciastnr

Deraseecd acdciar uttuop t&g=; epharreipl otcsnnotcioasvir ;gt=& dnireesac sicmyets lvasrcua enirtesacs

susyars  The question says “ST elevation in the anterior leads“ so, in some way I was thinking of the most anterior part of the heart which is the right ventricle, and not the left one. +3
makinallkindzofgainz  Anterior STEMI = ST elevations in V3, V4 which is supplied mostly by the LAD. RV is mostly supplied by the RCA, which would show up on an EKG with ischemic changes in II, III, and avF +4
qiss  Btw increased PCWP indicates increased blood in the left atrium, not necessarily increased blood in the pulmonary vasculature see here. +

 +2  (nbme24#8)
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eulrAbotl - eexarls hlbricano ostmoh scmleu rs(oht ciatgn to.g-a)2inβs rFo uatce ta.nbiserexoca naC acuse otremr, rmhiarhyta.

solgabrielamoreno  FA 2019 page 672 +

 +8  (nbme23#14)
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roeM pemsil romf AF 0921: aepn-urieddnicH iycahobpoemtnort is deu ot vpednetelom fo gIG andobtisie siagant ehnbndapu-roi alpettle fcarot 4 )Frdnota(FP 4iA4ip-nPehby- lecpoxm cvitsaaet alpteestl ;&g=t sstbrhmooi dan hyoocoabimnteprt

  • hgihste rsik hiwt iaedatcruontnf henipra

 +12  (nbme23#12)
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  • dibning ot het HCM lcssa II pcoeertr dna rgergtiign eth leresea of scneokyti - patugsrinnees

  • nnibigd ot eth sonculurumera nujotnci adn rpneoevnti of hCA ereslae - tubiunlmo nxtoi

  • bagecolk of a dnibgPGT-ni rptoien tlrseungi ing eht anlucmuotcia fo APMc - psusetirs tnixo

  • lbockaeg fo aescprptyni nbiinitioh fo plnias moort erxseefl - neustat nxtoi

  • tnpienevro of oetpnri hsyesstni yb okgbnicl aotlnnoegi of eth tedlppyoepi hnaic - iirdepahht o,inxt auedsPnsomo agnasuireo tnoxxieo A

thomasburton  Not sure I agree with the second one, M.O.A for botulinum is cleave of SNARE protein preventing pre-synaptic ACH release. Think the second one almost describes something like sux or some other deporalising nicotinic drug. +5
humble_station  You are right but to get the muscle spasms, trismus & seizures it has to inhibit GABA & Glycine release from Renshaw cells Cleaving the snare proteins will cause paralysis +2
texaspoontappa  tetanus->postsynaptic inhibition I believe +6

 -2  (nbme23#7)
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del-Okni oylotliycagns of eceetsdr and eemnbram dbonu esnotirp is a a-aosspirlalntottn envte htta tsake caepl in eth gsliocG-i emoatnrtmpc eatrf tylco-loigysnNa adn igodfln of eht ntpireo


 +8  (nbme23#27)
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  • dcenihlr noeft xhietbi xusael wdokeegln or rivbhaeo ntnourceing ithw rtehi ega.

  • raeusb si wknno to mvitic, lsyluau amel

  • aekp inecendic 92-1 yaers


 +0  (nbme23#28)
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nosWli dsesaie g=t;& icanonF rdynsoem =&t;g bliatemco sisicado (pety II (olxia)rmp ART)


 +6  (nbme23#16)
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obrlaamn etst stuler snaem atth etts etestdc reacnc g&t;=

  • 53 of 05 nem thiw stpratoe recanc veah anlbmaor estt tselur =;&tg n of spt twhi rnecca = 5.0 Tset hossw arencc in 53 nme =g;&t 5=3PT tg;&= ew nac atuccleal FN = 535-0 = 51

  • 02 of 100 men tiuohwt tsreaopt ccnrea hvae ramlnabo test sulesrt g=;&t FP 2=0 tg&=; ew nca cluetlaca TN = 0-18=0002

  • own we acn ulclecaat tiysiccefip = T/+F)N(PNT = 80/100 = 80. i(n % ilwl be %08)

erhe is ym 4/4 ta:ebl [nemn.tm3wt_ptm//2qsce_cstepsc//iii_uub1s.dres:mmuwabmltot//doorfrhlwcotwtns3/oee/]

smc213  Exactly what I did! +
smc213  I googled the meaning of abnormal test results just to make sure. A positive test is one in which the result of the test is abnormal; a negative test is one in which the test's result is normal. +3

 +3  (nbme22#10)
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AF 021,9 egap 29:9 epsyt of riiooeseAcs:tlrrs ortleosasilcirsore and Mberngkeoc issolrse.c

htne no agep :030 rcileAsrsosteho - mfro of eoolcsirasrstrie sceadu yb udulibp fo solhceoterl .uaeplqs


 +5  (nbme21#24)
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[l_etptn/rowi/moue.h2mrp./enme6c/dc_npuraitlw6_tobsmt1nwnes1ffe:t/eso0/tomo4cs9r/xs_diamq/]

rrosy for the in,knap ehpo ttha lilw pelh ooenesm

fadila  median should be: 70 for group X ; 85 for group Y median here is the avarage of Diastolic BP measured betweeen the 50 & 51 patients (since the number of patients in each group in even; Median= (n+1)/2 -> (100+1)/2= 50.5) Group X = (70+70)/2 = 70 Group Y = (80+90)/2 = 85 +1

 +1  (nbme21#24)
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l-1g1r7pSzu8i29-nR.0-deel--jeF410

rorsy ofr the n,aikpn ehpo htat liwl ehlp nsoeemo

yb_26  tried to attach photo, sorry for that( +




Subcomments ...

submitted by lsmarshall(415),
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reaU Clyce osDrisder ;gt& sldeaoIt esvere mereaihnmmaoyp g;t&( 0010; i,..e no ehort reeevs mbtceoila dsutciarnesb

hneOiinrt ancelatrysasbmar cynidfiece ;> (tmso oommnc uera eccly .d)si ctooir iaiuiam/diercdaac, morpyemnieaahm

rinagcO amiisdAce &;gt mHmmnyaeoae,ipr gpon-niaa dasiiosc, oesikst om(rf g)yemhilapcyo

ecmMhau-dnii o-aCyclA osheaygndeedr ineieccfyd t;&g Heiameoyamnp,rm yttopckeohi pylehoimgacy (seen ni oiiβtx-oand derori,dss CTXEPE sukyetayplordho)onrde

vLeir niduocfntsy &g;t aymniHpomaemr,e TsFL sedmes u,p oredl .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 snafull(4),
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aCn deosbmyo ixalpne hyw hsit is ont a nrifoeg ydob la?nomgaur

yb_26  because they mention scattered fragments of foreign material (pt presents 2 months after c-section, sutures are either removed in 1 week or dissolve in few weeks (depends on type of suture material) +  
suckitnbme  I think it IS a foreign body granuloma. The sutures are supposed to be removed or dissolve but sometimes one gets left in. The question says foreign material and sutures are often polarizable. +5  


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You kown ’sti an voeelpend uvsir eicsn it sodten’ hodl pu to adci ro egnbi di.dre uoY knwo ti csseua a erefv dan a chg,uo wheil atfecifng the .xrlany ylOn rivus erygoatc atht sitf lal ttha inof is eht inroucrasov cause(s )ARSS ofrm taht it.ls

zelderonmorningstar  EBV doesn’t cause fever and cough? +1  
zelderonmorningstar  Wow, just checked First Aid and it doesn’t list “cough” as a symptom of EBV. +4  
drdoom  EBV is not a “respiratory virus”; it’s a *B cell virus*. Even though you might associate it with the “upper respiratory tract” (=kissing disease), it doesn’t cause respiratory inflammation since that’s not its trope. B cells are its trope! That’s why EBV is implicated in Burkitt Lymphoma, hairy leukoplakia and other blood cancers. (EBV is also known as “lymphocryptovirus” -- it was originally discovered “hiding” in *lymphocytes* of monkeys.) So, EBV = think B cells. +27  
fulminant_life  EBV does cause pharyngeal and laryngeal inflammation along with fever, malaise, and cough and LAD. The only thing that pointed me away from mono and towards coronavirus was the patients age. +7  
nbmehelp  Can someone explain what not holding up to acid or being dried has to do with being enveloped? +  
yb_26  @nbmehelp, the envelope consists of phospholipids and glycoproteins => heat, acid, detergents, drying - all of that can dissolve the lipid bilayer membranes => viruses will loss their infectivity (because they need an envelope for two reasons - to protect them against host immune system, and to attach to host cells surface in order to infect them) +10  
lowyield  @yb_26 does that mean that non-enveloped viruses hold up better to acid/dryness? +2  
rina  yes enveloped viruses are easier to kill (see post from drsquarepants: https://www.nbmeanswers.com/exam/nbme23/1161). also i think the "when dried" might refer to the fact that coronavirus is spread by respiratory droplets (don't even need to read first aid can just read the news at this point!) +3  


submitted by sympathetikey(1357),
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ttBere ptiruec - /phcw/:tprh-sopea/1nl2d-tsu0o.agu/terlb/Nwt/01ew8/accmavjo.epcnwlt.sB

yb_26  @at0xibolic, I think you won this competition on finding better picture lol thanks +5  
drschmoctor  Those may be better, but this is the BEST. http://bitly.com/98K8eH +10  
brotherimodu  god damnit +1  
jesusisking  Not again (´∀`) +1  


submitted by m-ice(340),
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hsiT woanm ash a lot of ssign ttah ipnot tawrod na tntisiealn icaaisrpt nntci:eifo rentce rvtela ot paPau Nwe ,iunaGe uocgh dna elraaovl rnsef,ilatti ghhi shiooilepn ton,cu nad a tools aemspl thta sah a mwor in t.i tsoM kllyei teh itaeptn ahs a giletoodrnSys ift,nenoic sa hsti is het einltatins tiarpaes ahtt wohss aalvr no ltsoo peasl.m liBcaylas lla sitenltani atirsepsa anc eb aretdet itwh zneedolaB gd,urs chsu sa ozaTebneal.hid izauretPnqal lowdu be eorm iarpeotprpa rof a mrwo or ilrve uklfe otcefi.inn

fulminant_life  just to add to the explanation above," cutaneous larva currens" is a specific finding for strongyloides. Also the picture they used is the exact same one on wikipedia lol +9  
yb_26  they really should add Wikipedia in the list of top-rated review resources with A+ level of recommendation in FA2020))) +10  
usmile1  also a side note: cutaneous larva CURRENS is pathognomonic for strongyloides whereas Cutaneous larva MIGRANS is for ancylostoma braziliense or nectar Americanus +5  
solgabrielamoreno  FA 2019 pg 159 . Bendazoles because worms are bendy. (Treatment for roundworms) Praziquantel is for Cysticercosis (Taenia Solium) and Diphyllobothrium Latum Mefloquine : treats malaria Hydroxycloroquine: treats Malaraia, also RA & Lupus (immunisuppresive & anti-parasite) Dexamethasone: Steroid for inflammation +2  
abhishek021196  FA20 says Ivermectin OR Bendazoles for Strogyloides, so in a future question, if Ivermectin is listed, that could be the right answer for this as well. +2  
jurrutia  When in doubt, pick a bendazole +  
jurrutia  When in doubt, pick a bendazole +  


submitted by neonem(571),
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ihTs ntaietp sace sdsnuo lkei eh has iron diccfyenei ianema (anieam, lwo ritmeotac,h micorcy)ict ofmr a GI bed.el oT tge this iesqunto h,girt you dah ot rbeememr ttha teh wto aorjm rihdeinet IG rcneca ydrsnoesm are FPA (eud to iuotamnt ni ACP eeg,n which si a utmro psueprosrs ee)gn nda chyLn edsrynom AAK aeyiherrdt oooipnns-lpsy rlleooccta mcacnirao P,(HNCC) saecdu yb a ttnmiuao in a unebrm ADN tsmacimh riaerp ,egnes fo wthi MHS2 si a erom ncomom .one

Teh shnicmemsa of tehir iaomacnrc lnotmepdeve aer r;etdfneif in ,FAP surotm arsie mofr a anorlm &-;-tg nmadeao g&-t-; maorccina senqeeuc hlwie ni N,CPCH mrotsu aresi omfr shwat' wnnok sa a arostelictilem yntistialbi aphtaw,y eanldig ot npussaoonet nmoifatro of a amciarcno n(ot edepderc by a eninbg seonli elki na nd.moa.e).a You 'ndtid eend ot ownk sthi to get htis qsoinuet ,grhit but tfinyeldie oogd ot wk.on

medpsychosis  To make it even simpler, if you narrowed it down to FAP vs HNPCC and looked at the image provided in the question, you'd see it's less likely to be FAP due to absence of numerous polyps which would be expected. So HNPCC would be your best choice! +5  
yb_26  I always get Li-Fraumeni and Lynch syndromes confused :/ +1  


submitted by nwinkelmann(293),
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oDes eanoyn vaeh a odgo leinxtpanoa fro yhw dedcesrae llvsee fo bhinini si ?wgrno morF my ns,enuandtridg ibhinin nda vcniiat kwor oeth,ertg in that nhiibin inbsd adn locsbk vcinati danlegi to drdseceea feadckbe no stmahuahplyo adn icvanti erencassi HSF nad nGHR ond.itcr.pou stu,h if uyo eeraecds nibiinh etnh uyo woudl ahve edernsica viitcna hwhic ouwld ldae to dersicean nHRG nda S,HF ?rtghi I fndou eon carteli kgnialt oatub ti ni resgdra ot u,yrbtpe tub it eessm to be a t/oiheptsoynhs omnrdcife ta htsi t.n..ipo si ahtt w?yh uBt .s.li.lt woh do I uerl ti otu on a tts?e

yb_26  I also picked decreased inhibin. may be it was one of the "experimental questions", which are not even counted on the real exam +1  
artist90  Inceased FSH will lead to spermatogenesis and spermiogenesis NOT Increase in Testosterone which is causing increased Height of this pt +6  
artist90  Inhibin B only has negative feeback on FSH not GnRH. see the diagram on the topic of semineferous tubules in FA. Testosterone has a negative feedback on BOTH LH and GnRH +1  
usmile1  Kind of like how nocturnal pulsatile GNRH release occurs during sleep to stimulate growth (FA page327), the same thing happens for puberty. Pg 325 in FA, "pulsatile GnRH leads to puberty and fertility." It doesn't explicitly state during sleep, but pulsatile release of GnRH leading to pulsatile release of LH and FSH will lead to puberty. Puberty starts in the brain, its onset really has nothing to do with decreased inhibin levels which happens in the testes. hope that makes sense! +3  
sars  From what I understand, inhibin is only released by granulosa cells when FSH levels are high. This is a boy. Next off, this question is about puberty, which is due to pulsatile GnRH leading to large amounts of LH and FSH, leading to large amounts of dihydrotestosterone (males) and estradiol (females), and eventually secondary characteristics of puberty. The increased pulse of estrogen and testosterone leads to GH release, which is metabolized into IGF-1 in the liver. This leads to long bone growth from what I understand, which is not much. +  
cassdawg  @sars inhibin B is also released by sertoli cells in males and will feedback to inhibit FSH release, its not just a female thing. Also, there is actually an inhibin B pubertal surge in both females and males that corresponds to maturation of the granulosa and sertoli cells, respectively. Hormones are wack. https://pubmed.ncbi.nlm.nih.gov/15319819/ +  
j44n  I think youre just supposed to see that he's starting puberty and know that the nocturnal pulses are involved +  


submitted by wonderboyg(10),
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isht eps'taint suutre wsa saidrecen ni zies prcmdaoe ot a 12 wkee uetsr.u hse hda egapr leki crsteutusr adn no utfse. hsti duowl cnaeiitd a aiohfddritmy oelm. thsi ttpiaen osal adh on elfta pstar so it wlodu eb a tecmeplo m.loe

cnaoigcdr to m,haatop a iydfdamrhito olme si na n"bralamo ecinocpnot trrcicadaezhe by lensowl nad dsameoute illiv iwth liforreiopatn fo rptssahobl"to

alos in a telcmope eo,ml mtos vlili rae crohdpyi adn thtoblsapsro liwl orflaeeritp defsifuyl nrodua thsee cnroydhi lvi.li

eth esehilkte esmssa of hltoicpybytonrtssosa owlud eiinatcd a ncooiimhaarco.rc

nwinkelmann  Also, ball like masses of proliferating decidua, I think, means ectopic decidua, which can be seen in endometriosis, deciduocervicitis, and in the lymph nodes. Markedly dilated fetal blood vessels can be seen in rare complication of placentomegaly which could potentially lead to IUGR but could also result in a normal neonate. +6  
yb_26  @nwinkelmann no, ball-like masses of proliferating decidua are seen in endometrial papillary syncytial change +15  


submitted by step420(34),
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regtIaln eaenrmbm siepnrto aer oudfn inihtw the malpas eemmrabn nda apns eth hlowe helgtn rocass. The nisdei of hte nebeammr si evyr ocrhhiopydb ude ot eht gonl abncro iahsnc. tsnixeevE hcobpirydho noiarctnetsi tweeneb eht opinetr dsie hncai nda hte dpili taisl lliw lphe ncohar eht etroinp ni teh a.mmnreeb

yb_26  O-linked glycosylation of secreted and membrane bound proteins is a post-translational event that takes place in the cis-Golgi compartment after N-glycosylation and folding of the protein +19  


submitted by sajaqua1(533),
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stroePoir crdo yesndomr ocrcus eud to frnoiinact fo eth prortsieo lhfa fo hte sipaln dor,c orfm oicsnuocl fo eth iportsreo anipls .teyrar Our nttiaep srpentes thiw rcdasedee nonstesia to cnppriik boelw the elelv of eht neeks sa llew as lwiknag wiht a -iaesebwdd ,taig lieylk niangdiict sosl fo o.picptooinperr hTe tentiap is asol eacinm thiw eedrg-heyempstn nh.tleiropsu

egsmeyptneHerd enplrihtsou ear ilpaltyyc suecad by an yniitabil to make uohgen DA,N uescda by a aclk fo sesyecnar sruperocsr nad itmaisnv cgulindin 9B o()eflta dan 2B1 aoacm.l()bin If eth teantpi is talfeo ,idtecinfe ew ees dltaeeev mtehnocesioy fdieiecnc.y fI het tipnate si 2B1 eicn,eidft ew ees lvaeetde ocamtellmynhi cdai dna tsmheoieycon eevl.ls oanrpiymoiheeHysmcet acn irnceesa ohb.rsoistm imorTohsbs in eht peiortors lipasn rtreya nac esuca itprrosoe cdro erdys.mno nI ntd,odaii lack of ivanitm 12B raisimp minley anitmofro nda aslde ot Scubteau idoebnmC ,oirtanenDeeg hchiw fcasetf the cnipioSahmatl tatrc gnnocct(uia rfo deaeedcrs pincpkri snt,s)eniao Cnrlosoitapci atTcr, nda Dslaro en-CluloaMmdi nuiLscmse ratcT nu(intaocgc rof the eceddru toppprinoorc.ie

)A Artenori dcro neosyr-md osls of trmoo anmodc,m sa llew as allretiba olss of ahet dan iapn, hte ettanpi ash tno ltos motro ucofintn, so it notacn eb shit. )B laCrnet rodc osy-mdrne renepsts as a itncbamioon of mootr dna enyssro lso,s ullyasu hwti brdlead dntfons.uicy iThs tneipta esdo tno apydlis otorm sosl ro ddrleab cutoynsfnid. )C dmHcorei ymsoned-r slAo acelld raB,nqdSruewo- tish si opelecmt yrunji ot eetihr hte eltf ro gthir idse fo the lipasn ro.cd tI tespnsre iwth ootrm toduycnfnsi adn frelxe idtnnyscuof yisiatarllelp at teh levle fo het nl;oies slso fo ruepp mootr domncam ewblo eth oisnel riilpetlaslya sitca(ps )sriep;as sosl of adlosr mrodenlau-crci tnssineao ilyeaplrsatil ta nda wlebo the olnie;s nad osls of inpa nad epatreumter ntonaesis lnlalrrcttaoyae 2 ot 3 bearervt ewbol teh .insole )E mSegatnrey nrso-deym a olgncnaeit rlfaeui ot dvloepe tarp fo the anipsl d.cor The ewn osnet of pmyomtss at 28 ersay dol mkaes hist an nklieuly nsodais,.ig

yb_26  amazing, thank you! +  
aisel1787  great explanation +  
rockodude  sensation to pinprick is DCML tract. SCD affects spinocerebellar (not spinothalamic), corticospinal, and DCML. otherwise good explanation. +1  
azibird  Sensation to pinprick is not dorsal column-medial lemniscal tract, it's spinothalamic tract. So this patient has a lesion of the dorsal columns, spinothalamic tract hypersegmented neutrophils, and anemia. What the hell is going on? How is this just posterior cord syndrome? Spinothalamic is not posterior cord. +4  


submitted by sympathetikey(1357),
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Aectu outg netatetrm:

  1. NDISAs
  2. tidsoerS
  3. holieCcnic

,I iekl a b,dymu sidraem noze- fro on-s,e giikhntn ti swa ordstei dcepik atth. oFr anynoe who ears,c zlSnifpronaeuy tctiolipvyeme hiiitbngni urci caid oasportrneib ni eht plramoix uutelb of the i.kdeny

cSoru:e i:tzpi.y/nesikSflrn/eapwhdkptn/.raiieow/ougi

yb_26  even if it would be steroid in the list, if NSAIDs are contraindicated => we give Colchicine, and if pt can't tolerate Colchicine as well => then we use steroids +4  
usmlecharserssss  uptodate - try to avoid steroid therapy in gout , in this case patient has aspirin (NSAID) allergy , so second line is Colchicine , not Allopurinol, which is for chronic management. This case is not RARE and a lot of people sits on Colchicine therapy even if they do not have NSAID problems. Colchicine also First line treatment for Familial Mediterranean Fever, prevent exacerbations. +4  


submitted by joonam(26),
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tuceA ro cnhorci flniaminoamt fo .pahdllbaMdrg relyu ns:gi syinrotriap rstera on RQU nltpiaaop ued ot na.ip aiPn mya retiaad to rgthi uodl(eeh rdus ot tanoiirrit fo crihpen 􏰁ePLr.evn)A fi beil ctdu sbmeceo veondilv e,(g tdihnnagnac.os iecs)ilg

meningitis  To make sure, palpable Gallbladder is more in cholangiocarcinoma and Pancreatic Cancer? And if it were non-tender, could palpable gallbladder mean gallstones? +8  
yb_26  @meningitis, it is a Courvoisier sign of pancreatic adenocarcinoma: jaundice + palpable, nontender gallbladder +2  


submitted by mguan1993(9),
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Fro eestmpcloens ak,se ucdol neeosmo aenlipx het erhot wrgon anwres oiceshc ni arhgp rmf?o I nca asieyl ivsileuaz teh ihgtr eswnar ubt fro smoe ronsea nc'ta pcrtiue eht rtoeh csoiech

yb_26  check UWorld #12299 +7  


submitted by nwinkelmann(293),
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erP iotlscomolpo.hgnayne

uaLieplkkoa = ikrs sfrtoac nuecldi aelm rgeedn, 400-7 syrae dol, ngmsi,ok ehitW atchp or ,aqeulp 5 mm or rmeo, no oral uuscom samrbeenm ttha cannot eb emdevor yb pig,nrasc nto eud to onrtaeh aesseid ttenyi csuh sa hlicne nsplau or cdidiisanas nda tno rsreeedv yb evarlom of trtnsirai dna sionle utsm eb crddoeiens orcrsuaeecpn tunli vnpoer hwor.ieste nnPliareagmt esilon morstrtafnnaio wulod leda ot soininav of teh usmascu.bo

oircM = esaVri lhglsiaoyltioc rfom atn,osscahi kerayritphosse, dissalpya ro iromcaanc ni itus tsa(asceoid whit ymloshypetc dan gochs.mpa)aer sTih arlteci nlsaxpei it cumh rteteb nda has cprtue:si s71pceamt4n.d#veps/oeecmi0e//eoi6vwacac4ertdti/.h-mire86l:. Besda on tish clareti nad teh s,itceupr I'd asy teh hstoi seidl in het osnqueti is at salet eaotmdre maouqssu sayd.iaspl

yraiH kipoLaaukel = hetW,i econutlnf apestch of ufflfy ri(ahy) amu,osc atela,bril agoln llaetra tnu,eog and saacietdso htiw IHV+ ipstneta IAS(D yam pareap iwhint 2 - 3 ares)y tbu luatylac eud to VEB itcinnfeo

tsoHi = Htkoetyiprcaer loar acsomu edu ot gniilp fo toetrkcia aousqsum mhpiieleut, doCywr pety A ualenicrtnar nio,sisculn nBlaool cslle hwit ianaitgrnom fo himontrac nracu(le ig)a;ebnd VEB ptrnese ni lrcae llcse of opissun ray,el blaireav yocslik,otosi eposreimdpus daaiCnd teoinifn,c iowtuth laaomritnymf ensoe.rps

rFom preiscut and( hsti evio:d 6eb/Kh/x.sttopuv/8y:qI1thSuu ptmamitse 21,:)2 ahryi uaikkolelap hsa a hlgilyt iedatsn nadb of cllse l"olbna lcesl" in het utasrtm pnsoimsu hwchi si weher eht VBE .sivle tI olsko muhc dteirnffe hnta eht hsito elsdi hnsow ni hte tequios.n

yb_26  great explanation, thanks for sharing! +  
cathartic_medstu  on point +  


submitted by sympathetikey(1357),
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esyK eerw h:te

ruslo-aicuG

raohasthiu-Pp

Am-ion idacarui

Tsohe douhls be -drbsreeaob yb het TC,P so fi ry'eteh ton, peTy 2 TRA.

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 notadoctor(159),
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laiCce euprs is a alsmoibnpaort mrysndeo that uletrss in rtatosareeh and stlsuer in rnio cieifnedyc eaaim.n As fra as 'mI erwa,a enno fo the sehtor elsrut in oinr cifdyencie ea.anim (I had iBatclrea rowrgetovh as a lsoce descno tbu I 'tdno eelvebi htat's siseadtcoa htwi nroi ccf.)iydneei

yb_26  bacterial overgrowth is associated with iron deficiency, but also with Vit B12-deficiency, so I guess pts will have macrocytic anemia +2  
nor16  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099351/. Vit B12 is key here, moreover, no bloating (IBS and bacterial overgrowth with bloating). bacterial overgrowth is a close one! +1  
covid2019  I wrongly chose bacterial overgrowth, but that is wrong because Small Intestine Bacterial Overgrowth (SIBO) must be instigated by something. Commonly, anatomic abnormalities (like surgery causing blind loop syndrome, strictures, or motility disorders that allow the poop to ~fester~). +3  


submitted by lfsuarez(141),
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20 of teh 010 nem tuwtohi pstaeotr ncecra heva nbalmora stet tlssuer.

ficipeicSyt = PF/PTNF+ = 0200/1 = 0.8 = 08%

seagull  almost. 100/120 = 83% roughly 80% +  
amirmullick3  Not sure what lfsuarez and seagull above mean. Here is my explanation. Specificity = TN/(TN+FP). This test gave 20 false positives out of 100 people, and only 15 true negatives out of 50 men. Specificity also equals 1-FPrate, and here the FP rate seems 20% so 100%-20%=80%. +4  
yb_26  abnormal test result means pt has cancer => TP = 35, FN = 15 (50-35), FP=20, TN =80 (100-20) => specificity = TN/(TN+FP) = 80/100 = 0.8 (in % will be 80%) true negatives are 80 out of 100, not 15 out of 50 +2  
bulgaine  If you replace the values from the question in the table of page 257 of FA 2019, yb_26 explanation is correct. Abnormal test = patient has cancer = test + Question says 35/50 men with prostate cancer (so all 50 have cancer) only 35 have abnormal test results, meaning that TP=35 (disease + test +) and FN= 15 (disease + test - because they do have cancer but the test was not abnormal for them ). 20/100 men without prostate cancer have abnormal test results meaning all 100 DONT have cancer but 20 show that they have cancer when its not true so FP=20 (disease - test +) and TN =80 (disease - test -) +  


submitted by jrod77(28),
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I nikht eyth ghtim eb ncibdegsri o.tin.gan.na ue.rs A2TX si elissrpoebn fro aepttell egagioo,gasrtn ti mya be tgbtiuonrnci ot imb,sroohts uhts smihaeic to eth adcacri eis.stu

sympathetikey  Agreed. I'm pissed though because PGE2 mediates pain, which is why I picked it. +35  
he.sanchez14  If im not mistaken, the question describes unstable angina. Unstable angina is due to thrombosis with incomplete occlusion. So, yes TXA2 is responsible for the thrombus that is causing the symptoms in this patient. I'm also pissed because I also went straight for the PGE2 +5  
vik  hahah, seems like all in same boat like me +  
yb_26  thromboxane A2 is also vasoconstrictor, so my thoughts were about vasospastic angina +4  
youssefa  Went for PGE2 ... shit +  
need_answers  I went for leukotriene B4, what the hell was I doing....SHIT +14  
hopsalong  I picked Leukotrine B4 thinking that the neutrophil infiltration was the source of the pain, seems wrong lol. +  
bballhandler11  Sometimes it helps me to think of it in a general, non med school textbook kind of way. When answering, I narrowed it down to PGE2 and TXA2 as well. Then I asked myself, if someone is experiencing chest pain, would I recommend Aspirin or Advil? That's helped on a few over the counter pharm questions. +7  
ususmle  same here I M PISSED PGE2 +3  
krewfoo99  Maybe PGE2 isint the answer because it mediates pain and fever during episodes of acute inflammation? Thus making TXA2 more likely. +2  
djtallahassee  ditto on the looked at it for 2 seconds and went PGE2 +1  


submitted by yotsubato(1032),
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sihT napteit si rveiopsunesn to nmya ais.nadict Tehy otdn yescpif whcih oesn, utb eht esoiuqnt si acylbslai iaskgn hichw aindcati si hte o.ssnttrge aTht odluw eb ,PsIP whhic biiniht cragist H K ATePsa

yb_26  PPIs are not antacids! +3  


submitted by mousie(217),
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yhw sdoe artttmene of yopdthroiyh (iwth oieoyxthvnerl 'Im ansmsuig) serneaic irsk ofr ty?hpymao I oesch ti ysmpil bc sit a mmoocn easervd cffeet fo naistts tub I otdn' rllyae tdredsanun ohw eantrtig iydhptoyhomsir ta teh msae eitm ldowu ahve nynghait to do hwti ti ??? plhe speae!l

yb_26  They are just asking about side effect of statins, not about treatment of hypothyroidism +5  
mjmejora  Hypothyroidism is just a red herring. +  
ususmle  statins cause both hepatotoxic and mypopathy so I want for hepatotoxic:( I thought usmle expects different stuff +1  
drzed  Statins don't cause 'toxic hepatitis' they just cause a mild asymptomatic rise in LFTs that is reversible with discontinuation of the drug. The more worrisome side effect is of course, myopathy +2  
tyrionwill  statins cause both liver injury and myopathy in a dose related, so kidney failure increases their dose, which leads both liver and muscle risk elevated; Pravastatin is said less liver concerns but the myopathy, so choose myopathy when renal failure. +1  


submitted by armymed88(47),
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A itltel mhta .rpH .ehe si olw ;g-&t- diissoac C 2Op si hgih -g;&-t oipesrrrtya rm Naol senoctpmiona hodslu eb ogyhrul a 1 )ctue(a to rhic4no)c( scaenrei ni rabbic epr ryvee 10 secianre ni O2pC.. tIs wrloe her,e os clyrlae nto dntcsapomee and idinceatd itnoaiadld dpor in icbd-t- r;a&g add no tabem sisaiocd

hello  Hm, what do you mean by "normal compensation?" Are you talking about the bicarb should be increased? Are you saying that a normal compensation would be metabolic alkalosis? Would metabolic alkalosis be an increase in bicarb? +2  
kateinwonderland  How do you know which one has bigger contribution in this situation where there's increased CO2 and decreased HCO-, both indicating acidosis?? +  
yb_26  normal kidney compensation would be an increase in bicarb reabsorption => increased serum bicarb. This pt has low serum bicarb => concurrent metabolic acidosis +  


submitted by armymed88(47),
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Of etshe opsonti ebaalliav, hcnnaSw leslc uowdl eb the olny elcsl pesnter in het PNS. tyocAs ,tesr origclmia adn osgloi aer lla SNC llsce lSi aetlte lsecl aer in eht ulsmec dna verse to aid ni csumle raprie adn reiaeonrgetn

yb_26  Thats myosatellite cells. Satellite cells are also glial cells that form around damaged nerve cells and lie close to neuron bodies in the CNS +16  
drzed  Myosatellite cells are also called satellite cells so it is not clear which definition they were using. +2  


submitted by enbeemee(13),
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uwold na tsocrseetieallcahyen biirhnoti krow as llwe to ieeevrl het most?mpsy tbu tsuj beacesu se'h 7o3y, we're ouespdps to asesum t'si deu to PBH nad veig an 1a hir?noibit

yb_26  acetylcholinesterase inhibitors are used in treatment of urinary retention, not urinary frequency +17  


submitted by d_holles(187),
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shiT oueintsq fcodnseu em bc I tgthouh dailmpreoe ouldc ont corss eth BBB dan reetfeorh dluco otn saeuc arytospreri oeepisdsrn (-oopiudim osgmani at eth atnmbesri ltersus ni /rsyrpSietrCoaN odeei,rspns )1. uBt x@dxr. si rroecct in niotgn htat ↓ RR nda SNC psesreinod ni the tP hdluso acll rof an iumdioo-p aonintasgt rhetra athn obetalhnch (iteimc)hconlomi to ratet sicpo.noaitnt

  1. hul.s.citsi=lqtoa/5dy.na:6tr2iobaarlhgpsapo/e.?9c/e50e7ghrttisaexpss
nwinkelmann  http://medresearch.in/index.php/IJPR/article/view/782/1271 This explains a case in an infant. "Respiratory depression and coma after overdosage have been shown to be reversible by injection of naloxone [6]. Owing to its structural similarity to opioid, loperamide toxicity can be reversed by using Nalaxone which is a specific opioid antagonist acts competitively at opioid receptors. Naloxone hydrochloride is usually given intravenously for a rapid onset of action which occurs within 2 minutes." +3  
yb_26  FA 2019: "Loperamide has poor CNS penetration" - so it still penetrates => can cause respiratory depression +4  
whoissaad  Also maybe because the blood brain barrier in a baby is not developed as well as in an adult. +4  


submitted by hayayah(1077),
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Paenryngc + Hx fo tbosohsimr -;g&t- hitkn naiplphpohoditis yeomsrnd

hTe TP and TTP ear gnlpodroe /dt rrieencneetf fmro the iteiaodsnb to hdpoi.lsipspoh Tonrhbim eimt n.lmroa

adH to ndfi rahrcese ecitsral obuat ti os eakt it mfro eerh and 'ntdo stwae ryuo ..im.et

monoloco  yeah, i’ve never heard of antiphospholipids increasing PT time ... +22  
goldenwakosu  Not sure if that little detail was to throw us off. I think the point of the question was to ID antiphospholipid syndrome based on the clinical criteria (spontaneous abortion + thrombosis) +4  
johnthurtjr  I actually went down a rabbit hole with this one recently - essentially in vitro findings =/= in vivo findings, clot-wise with anti-phospholipid antibodies. +3  
link981  No mention of lupus anticoagulant, anticardiolipin, or anti Beta 2 antibodies. FA mentios prolonged PTT but nothing on PT. What a piece of shit question. But thanks to the dudes above who explained it +8  
yb_26  UWorld mentioned "prolong aPTT (and sometimes PT)" in APS +3  
oslerweberrendu  @yb_26 Can u please tell the QID because the one I have seen it says, "Although patients often have prolonged ptt (because the antiphospholipid interferes with ptt test), pt is normal." QID: 1298 +  
kevin  just to clarify, lupus anticoag is in antiphospholipid and presents with paradoxical increased ptt +/- pt despite increase risk thrombosis +1  


submitted by monoclonal(21),
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r/Z.i/:/aohng2f.pitg.cA3puEtmm

siTh iagem ohsws eth iupmletl vensi iwhhc adirn traesb steu.is seya sla.ivu (to aesy to mssi t,i tbu i )idd

yb_26  this one is the best, thank you! +1  
canyon_run  very nice! +  


submitted by seagull(1566),
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out of oy,crsuiti who aym ppeole enkw i?hst (tndo be ysh to asy uyo idd ro ?dtin)d

My tyvopre ndaoeucti 'dntid gniiarn hist in e.m

johnthurtjr  I did not +3  
nlkrueger  i did not lol +  
ht3  you're definitely not alone lol +  
yotsubato  no idea +  
yotsubato  And its not in FA, so fuck it IMO +1  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +14  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +27  
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +1  
jaxx  Not a clue. This was so random. +  
ls3076  no way +  
hyperfukus  no clue +  
mkreamy  this made me feel a lot better. also, no fucking clue +1  
amirmullick3  My immediate thought after reading this was "why would i know this and how does this make me a better doctor?" +7  
mrglass  Generally speaking Glutamine is often used to aminate things. Think brain nitrogen metabolism. You know that F-6-P isn't an amine, and that Glucosamine is, so Glutamine isn't an unrealistic guess. +4  
djtallahassee  yea, I mature 30k anki cards to see this bs +4  
taediggity  I literally shouted wtf in quiet library at this question. +1  
bend_nbme_over  Lol def didn't know it. Looks like I'm not going to be a competent doctor because I don't know the hexosamine pathway lol +21  
drschmoctor  Is it biochemistry? Then I do not know it. +5  
snoochi95  hell no brother +1  
roro17  I didn’t +  
bodanese  I did not +  
hatethisshit  nope +  
jesusisking  I Ctrl+F'd glucosamine in FA and it's not even there lol +  
batmane  i definitely guessed, for some reason got it down to arginine and glutamine +2  
waterloo  Nope. +  
monique  I did not +  
issamd1221  didnt +  
baja_blast  Narrowed it down to Arginine and Glutamine figuring the Nitrogen would have to come from one of these two but of course I picked the wrong one. Classic. +1  
amy  +1 no idea! +  
mumenrider4ever  Had no idea what glucosamine was +  
feeeeeever  Ahhh yes the classic Glucosamine from fructose 6-phosphate question....Missed this question harder than the Misoprostol missed swing +1  
surfacegomd  no clue +  
schep  no idea. i could only safely eliminate carbamoyl phosphate because that's urea cycle +  
kernicteruscandycorn  NOPE! +  
chediakhigashi  nurp +  
kidokick  just adding in to say, nope. +  
flvent2120  Lol I didn't either. I think this is just critical thinking though. The amine has to come from somewhere. Glutamine/glutamate is known to transfer amines at the least +1  


submitted by link981(160),
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imHsntaei eaucss aietlrore ,dlanisvooati agiunsc a bludpui fo lobod in het c.rsaalliiep The esecdrain bodol in eht laepsiralci iwll eausc the srpsruee rehte ot rsi.e lnttiiaoFr is deteednpn no us,srerep eht eihgrh teh upersesr, eht oemr teh ttiiorn.lfa

emreeRmb loobd :wlfo enisv to ueesnlv ot iplrelcisaa to ilortrsaee ot ietasrre

yb_26  agree in all, except the blood flow - it is right the opposite [https://teachmeanatomy.info/the-basics/ultrastructure/blood-vessels/] +15  
link981  I stand corrected @yb_26. Brainfart moment 🙈 +  
rockodude  lmao including a link to a teachmeanatomy page on basic blood flow +  


unscramble the site ⋅ remove ads ⋅ become a member ($39/month)

whta is hgppinane in sith ?emts neulba to olcdeuc eth daalir raetyr ? aCn osoeemn elpase aixn?ple

lilamk  I chose atherosclerosis because they said “radial artery is non-pulsatile but remains palpable even as the cuff is inflated”--> my reasoning was that normally you can’t feel the artery anymore once you overflate the cuff bc this occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally a hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!) +8  
mnemonia  I think athero is just a subtype of arteriosclerosis. Also my thought process was (like Lila) if something were to not be palpable then it would have to collapse and athero prevents this from happening. +3  
yb_26  FA 2019, page 299: types of Arteriosclerosis: arteriolosclerosis and Mockenberg sclerosis. then on page 300: Atherosclerosis - form of arteriosclerosis caused by buildup of cholesterol plaques. +  


submitted by luckeroo(9),
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why wsa ihst ozmifrligeb dan ont c?inain I swa lckuy nda ueges,ds btu I ugthtoh aincin oecnimdb lduoc lsoa geritgr yymtpoh?a

.ooo.   Gemfibrozil is a CYP450 inhibitor causing an increase drug concentration of statin which would lead to the adverse side effect of myopathy. Not sure about niacin in combination with statin but believe this would be more likely to occur. Hope this helps! +1  
yb_26  yes, it can be seen with niacin and esetemibe as well, according to UWorld. But first choice in such questions is always fibrates. +  
nor16  number one no-go combi is statin+fibrate here +3  


submitted by yb_26(255),
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1d7l21e-zS-1iRl--08r4.p9j-nFeu0eg

rysor fro hte npi,nak ehop ttha wlli hple soemnoe

yb_26  tried to attach photo, sorry for that( +  


submitted by yb_26(255),
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iF81zgSr14Rujep--.2-1eenl079-d0l-

yrosr orf teh kinna,p ehpo thta wlil hepl eonemso

yb_26  tried to attach photo, sorry for that( +  


submitted by hungrybox(1035),
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treoh ners:asw

  • psycan:elor seiacAdots hitw gnghopocyi or mnpoopycphi uilsaonlhcnait.
  • GhpoOny to elspe = ingth temi ilucanshtlaino

  • xayorsplma tanlcronu dynsaep: NHP si a mhclioeyt am.naei No sngsi fo octeylhim aiaenm iar(etamu,h dcn,ueaij edc. bol.o)gnpthai

  • pesel a:eapn seoatAcdsi wtih otbiye,s dlou sro.gnin

doingit21  narrowed down to MDD and restless leg then convinced myself that elderly are at higher risk for MDD than RLS. Is that valid reasoning? +2  
yb_26  Paroxysmal nocturnal dyspnea = breathless awakening from sleep, seen in left heart failure. It is not a paroxysmal nocturnal hemoglobinuria. +12  


submitted by kentuckyfan(43),
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I tge yhw teh midex osevnu xgoyne oiennst .sed r,cdea,eHeorvwe sit'n the scieytms larvcusa isetsncare alos dsere?adce

yb_26  no, decreased CO => peripheral vasoconstriction => SVR will be increased +7  
yssya1992  No SVR will increase due to RAAS and SAN thats why we decrease afterload in HF treatment ( ACEI, ARBs ) +5  
snafull  Wouldn't pulmonary vascular resistance also be decreased here due to pulmonary vasodilation in the setting of an MI? +  
cienfuegos  @snafull: my initial thought is that we would see pulmonary vasoconstriction because of the relatively low oxygen tension (that results from the low cardiac output). +3  


submitted by neonem(571),
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oinhrMpe si a um iopdio iontsag - neo daeevrs eectff fo dpisooi is atms lecl ndgenoluatira atht is Etdne-eenpIdngi. eslaRee fo etiimahns is naik ot an nahpayatlcci tcinoera -t-g&; itiprusr, .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 cr(4),
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why tno C.? ts´I ont esuops that ti vmeoipr eht cyivetefit fo lii?nsnu

yb_26  thiazolidinediones (pioglitazone) increase insulin sensitivity (in muscles and liver) through activation of peroxisome proliferator-activated receptor-gamma (PPAR) I think they are asking about primarily mechanism of action, that's why it is E +  
cienfuegos  UW explanation regarding the genes upregulated 1. GLUT4: insulin responsive on adipocytes/skeletal increases G uptake 2. adiponectin: cytokine secreted by adipocytes increases # of insulin responsive adipocytes and stims FA oxidation 3. PPAR family also plays significant role in pathogenesis of metabolic syndrome +2  
poisonivy  Also, I think the word uptake shouldn't be right when speaking about insulin, it does increase insulin sensitivity and therefore glucose uptake +7  
brotherimodu  @poisonivy That's why I didn't choose C and went with E since it was more specific +