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Welcome to tallerthanmymom’s page.
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hTis eatinpt hsa eitipahst ve(leaedt elirv syemez)n deu to etcvia ttiiaesHp C ncnfeii.ot pHe C nda HIV inecnofti rea thob sitodeaasc tiwh nnurvsteioa gudr u.es Wlhei ostm ttpiensa wthi peH A will learc eth uvsir artfe itrhe ucate ,enlliss Hep C saecus hrcinoc nciieotfn ni 0%8 fo iattepsn, ihhwc yam laed ot cosrsihir eorv imte (20~ sr).eya

tallerthanmymom  Wait... I swear we could treat hep C with Sofosbuvir and Ribavirin and that it is curable these days? +1  


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nA sodd arito rgeater anht 1 niiesfgsi rsecesnia dos,d rs,ki ihkoedioll -- whicervhe uyo reeprf ot acll .it fI hte %59 eedifncnoc avrtline eanrg esod otn uelcdni ,1 then eht nefiederfc si liacaltststiy tcnsfiaigni (ogtuhh nto irnsecalyes clanycliil am.infn)uelg

tallerthanmymom  Can someone explain why it is an increase in risk rather than a decrease? Also, relative to what? Do we just assume it is relative to people who do not exercise regularly? +  
banana  Uncertain about this, but I think from my memory of the question that the above explanation should say "relative risk" and not odds ratio. The relative risk is the (number women fractured/total exposed)/(number women fractured/total unexposed):: therefore, >1 means that more women got fractured when they exercised. (FA 2020, 258) +1  
drpee  Same risk: RR = 1 (theoretical). Lower risk: RR < 1. Greater risk: RR > 1 +  
blah  I got confused by the question because I was bringing in my own biases (i.e. doesn't exercising decrease the risk of fractures in this population of women?). If you simply read the question as what does a RR>1 mean? No doubt you'll get the correct answer. +4  


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hleWi E clio si lmoanr utg l,foar oyru doyb wdulo erfper it tsay ut.naimalilrn

tallerthanmymom  Just remember that E.Coli and Bacteriodes Fragilis (sp?) are the 2 main gutys that cause intraperitoneal infections from the gut. +6  
bharatpillai  Why not citrobacter though? +7  
mamed  Common organisms involved in gangrenous and perforated appendicitis include Escherichia coli, Peptostreptococcus, Bacteroides fragilis, and Pseudomonas species (UpToDate) +6  


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heT boorptecsraer rea tcesthr orteeprcs (hte reom ulidf in het lvess,e hte oemr thye .fei)r So a aettnpi ihtw agehcrmirho okhsc lilw see a desacere in het crepteraorbo nrgifi a.ert tavnAtioci of ARSA liwl utsrle in aseercdni surclaav esiarnsetc c(toon)snictiovsra ni eodrr to ntiniama oldob esp.esurr Adn a,acseirilpl uhsc sa steho ni eht nid,yek liwl eb dmeirp rfo sooienptrr dan tno ttiarfonli o(n noe satnw to pee otu gdoo teuidl ruine ewnh rtehey’ hdyda.er)dte iwe,seLki msciesty reipllisaca lilw eepfrr ot lhdo onot aspmal and ont tle it elka tino the imiunertttsi )idh.asr(ptgcn-i

tallerthanmymom  Another thing contributing to the increased SVR is increased SNS tone and decreased PNS tone. When BP is low --> Afferent BR firing decreased ---> Efferent SNS firing increases, and PNS decreases --> the inc in SNS tone stimulates a1 receptors ---> Inc SVR BUT, I don't understand what is causing the increase in the PVR because I always thought that inc SNS tone should be causing vasodilation in the lungs and that is why PCWP is decreased. +6  


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mtlriigFsa is a tnruylaoegc ncyool tlutsgianim rofatc ,SF)(CG wchhi rae rsudg ueds ot srcenaei htwie lbdoo lcel nucto ni siptaten ihwt okaen.peiul unevooLicr icolnif( c)ida dsnuso ilke it duolw osal be grt,ih tbu ’ist ueds to rneepvt obne rroamw ossuensppir ni spntetia kanitg xethmtoeet.ra beDaepirtno kli(e neiiorreo)thytp si edus to ualemtsti red obold lecl diuctn.proo

em_goldman  were we supposed to know that she wasn't taking methotrexate (or did I miss that in the question stem)? +  
tallerthanmymom  I don't think Methotrexate is used to treat small cell lung CA; per first aid (2018) the cancers Methotrexate is used to treat include "Leukemias (ALL), lymphomas, choriocarcinoma, sarcoma". It also has some non-cancer uses in rhuematologic ds, ectopic pregnany and medical abortions. +2  


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The acolheoehbrpnnm ludwo eb no het lactau setuf os tsuj tge ird of D.)( ehT lca"bk e"olh htta eht tsuef is filngtao ni si hte saaetionglt acs so tge rdi fo )(C. Now I ma on atduonlsur epxert btu I nokw atth teh itacmino ivcayt yluevatlen psandex to fseu hitw the rhniooc bethrye inmitnlegai eth ociioncrh victya )B(. In semrt fo eherw het timancoi ycavit si wnhso in hits meig,a I am tno ,urse os myeab osemnoe nac pleh tub tihs velsea teh lkyo asc wcihh pytaclliy pseaarp iwitnh teh oiatenstagl csa rudaon 55. ew.sek

kateinwonderland  At the end of the fourth week, the yolk sac presents the appearance of a small pear-shaped opening (traditionally called the umbilical vesicle), into the digestive tube by a long narrow tube, the vitelline duct. (Wiki) +4  
tallerthanmymom  But why does it look completely detached from the fetus? I eliminated yolk sac first because of this +  
makinallkindzofgainz  If you look reeeeeeeally closely, you'll see some signal between the yolk sac and the baby. Although you can't see the entire connection, they are connected. +4  
thotcandy  Pt is roughly 8 weeks pregnant so and typically by 9th week, Amniotic cavity has expended to fill entire volume of Gestational sac. So the entire black part around the fetus is GS/AC. +2  
euchromatin69  and also by 7 week vitelline duct obliterates between umbillicus and yolk sac +  


submitted by sympathetikey(1350),
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ePr AF .(pg )636: cninorneCg tbrsae .ec.cn.ar

"lcitiionfpaAmpevxe/nsioorres of oespo rgntsroeetrng/ee resoptrce ro r2-cbeB R,E(2H FnaEG )cprteeor is o;comnm RE ,⊝ PR ,⊝ n2HdauRenE / ⊝ omrf rmeo a"sgise.vegr

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 sympathetikey(1350),
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erP FA g.p( 3)66: eCgonrncin aebtrs .ecrna..c

"mtilifpcoAniaoprv/seiserxeon of rgoetoeeerns/tng oeprs reposretc or Brbe2c- H,2ER( FGnE a )retecpor is ;mmcoon RE ⊝, PR ⊝, dH2RnE/neua ⊝ ormf eomr re"aivseggs.

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 mousie(216),
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yM edntisnngurda fi ABg;tCC& hist si banolrma = ucocvtdeni anhrieg slos = eitslorsocos VS useolnSareyrn anrgihe lsso ilwl avhe amlonr BA;gt&CC = loss of hiar cslle

dentist  VS: progressive unilateral hearing loss, doesn't affect Rinne Test, associated with NF2 and actor Mark Ruffalo Otoslcerosis is (usually....) progressive bilateral hearing loss, BC > AC. source +  
tallerthanmymom  If BC > AC in BOTH ears, why does he have hearing loss in only one ear? My logic was that he probably had otosclerosis in both ears and then something extra going on in his right ear that would make it worse than the left. I still don't understand why otosclerosis is the best answer here. +2  
dul071  Finally!!!! Someone who ACTUALLY explains what the fuck bone conduction even is and teaches the whole topic. Here's the link for anyone else who struggled to find someone who takes time to explain this concept https://www.youtube.com/watch?v=cZYJL9Jg-3k +4  
sonofarathorn  ^ Halle-freakin-lujah +  


submitted by sympathetikey(1350),
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eBieelv htsi nseiutoq is irefergrn to sicaVler siiaamisLnehs.

gabeb71  The give away is the Fever, Pancytopenia, and Hepatosplenomegaly after being bitten by an insect and developing the sore. +14  
tallerthanmymom  I got this question directly after the other visceral leishmania question and it made me second guess everything I thought I knew. +7  
qball  Don't forget they like to infect macrophages. +  


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edonnAgrs caues .ncae eernotetTsso si a erttbe anwres anht idenrAtndlsaoo c/b het seTsoneroett is ocsisedaat wtih tb,reypu dloAsiotnadner is emro ctsadeoias hitw eth ealdarn nsd.gal

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