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Welcome to smc213’s page.
Contributor score: 117


Comments ...

 +19  (nbme23#28)
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To be lmcpleeyto c!rlea

hisT ptatien has tCyiosnsis a rare almotusao svrecsiee syamlosol rgaotse ddirrose dna somt mooncm acues of caonniF rmnoesdy in ed.ihrlnc iissoCstny si sicytsem and saled ot cyntesi tsralyc psetisod ni leslc dan eusstsi trhghoouut eth body.

hgtoAulh nslisoW aseides cna deal to S,F eth tsysarlc in het ernscoa seod nto rcalotere thwi ossiWnl aedssei.
eMro ofin: nh61bccm//tpM.ligtt.pls0:oa/ww./.rih4n4m/Cevn/c1Pisw8

highyieldboardswards  Thank you! You are a legend for figuring this out! +
paulkarr  Appreciate you. +
drzed  And even if it was Wilson disease, it would have the exact same consequence leading to Fanconi syndrome. +2
abhishek021196  Fanconi syndrome Generalized reabsorption defect in PCT = Increased excretion of amino acids, glucose, HCO 3 – , and PO 4 3– , and all substances reabsorbed by the PCT May lead to metabolic acidosis (proximal RTA), hypophosphatemia, osteopenia Hereditary defects (eg, Wilson disease, tyrosinemia, glycogen storage disease), ischemia, multiple myeloma, nephrotoxins/drugs (eg, ifosfamide, cisplatin), lead poisoning. Polyuria, renal tubular acidosis type II, growth failure, electrolyte imbalances, hypophosphatemic rickets = Fanconi syndrome (multiple combined dysfunction of the proximal convoluted tubule). +1

 +3  (nbme23#14)
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ur,coM ,zuohsRpi Aidbsai IZyrharcpoegay)u try,lomg( a,brdo tetnnaosep yhepha cnigbnarh at iedw arpogneos sslpaeg.nSrio rea ndalihe omfr .losi hTe ifung nptrtaeee het rmobifric letpa on( ra)rbeis,r eortielpafr in obldo elsves lsl,aw nprsoreigsg priylda ofmr iesnsus niot eht riabn s•teis.u oycurmssM:coi hiolcR,nberaer tralonf oebl b;csases vesourcan nsisu rs.siobmtho eeCaizahrdcrt yb pasarlana iw,nelslg orcnicet esuitss bk(acl corcneti sachre no )ace,f aimrhgohcre seuaexdt rfmo neso nad eesy, maelnt ,trlhegya ,hehdceaa facial pn;ia aym aehv inrclaa revne .mn•eno vleitv rOcucs in eodtticaocki adebicti and entricnepou ul)kmice(e ttitsp nae:rnemtTae eiedtbdmrne fo icrceotn situse dna imrhpoceaitn B ro uacvnooleizas rtedats md.teileaiym Fylaitat taer si ghih ude ot dirpa hotwrg dan .noivnias

jboud86  FA 2019 page 153. +




Subcomments ...

submitted by yb_26(191),
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narlobma stet ultrse eansm that sett dtteces craenc gt&=;

  • 53 fo 05 mne hwit arosettp nccrae ehva albmrano tste ltrsue t;g&= n of tsp wtih anccer = 5.0 Tets ohssw cacern in 35 men ;=g&t =35PT &g;t= we can uactlcale NF = 5-530 = 15

  • 02 fo 100 mne tiwtuoh ttearops cearnc aehv lanoambr tset uslesrt g=;t& FP 02= &;t=g ew cna llccauate NT = 081002=0-

  • now ew acn cueclalta csiyitpeicf = (TP)+/TNNF = 00/801 = 08. n(i % wlli be 80)%

reeh is ym /44 e:atlb [edstirm_bt/umtnbs/cs/2oi_.se1.wwmm/:_dsap/teu//wroemmt3clelut/ncneofoitt3oqrpchws]

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  


submitted by yb_26(191),
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onalrmba ttse teuslr neasm hatt etst tstedec aecrnc g=;t&

  • 35 of 05 nme with sropeatt rnecac vhae nolmrbaa sett setrul =&tg; n fo tsp ithw naeccr = 0.5 sTte swsho eacrnc ni 53 enm g=&t; 35T=P &g=t; we nac cctulaeal FN = 5-305 = 51

  • 02 of 010 emn utohtiw statoper encrac vaeh nmlarboa test ersltus =;tg& PF =02 gt;&= we anc aucealtlc NT = 820-100=0

  • wno we can ltaleaucc iecyfstcipi = )/P+FTNTN( = 08/100 = 80. (in % wlli eb 08)%

reeh si ym 44/ eblta: [sttteoudbms.soreisao/_3qi/c/tomm/pccr/mtu.thi_rmclm_pw/dt3sne//ew:l2wubnowfeents1]

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  


submitted by mousie(171),
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aCn nsomeeo eeplas ieanxlp htis ot ?me I otnd' ntarnsddeu hwy sitnatrg het othre gurd wdulo ont uotnc sa ncloiusxe ai?ritecr

seagull  This has to do with Intention-to-treat analysis. Essentially, when participants are non-adherent but the data shouldn't be lost. They just undergo another statistical model to account for their changes. Here is a nice video https://www.youtube.com/watch?v=Kps3VzbykFQ&t=7s +15  
dr.xx  Where does the question mention "intention-to-treat"? +  
notadoctor  They seem to be pretty obsessed with "intention-to-treat" it's been asked in one way or another in all the new NBMEs that I've done. (Haven't done 24 as yet) +8  
wutuwantbruv  They don't, intention-to-treat is just the best way to go about it @dr.xx +  
smc213  Great for ITT: https://www.youtube.com/watch?v=Kps3VzbykFQ +4  
yex  I agree with @notadoctor !! +  
ergogenic22  i think if it were per protocol, both groups would be excluded, the ones that were inconsistent, the ones that dropped out, and the ones that switched. But answer choices only allow ITT or exclusion of one group. +  


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ePtntai is rturcne sda,erfb-te so ew cna ieatlenmi soueftcr sfeo(ruct is dnuof in honye nad ifurst dna esmo fm,ularo tbu not ni easbrt ilm)k. Pattein hsa udnirgce sbcassnetu tub on ulscego in het neiru, os he tums seom lnceuogn-so sag.ur My dfntiafeierl fro cnegduri cnou-lngose gsasur in hte nieur si drssrodei truscoef atmobmilse ro cesltgoaa blemsma.iot We veah eametnilid trfcu,seo os hatt leavse us wthi cesanalktaoig eidfeiyccn ro lcsasic amclaeit.oags

sympathetikey  & Galactokinase deficiency would be much milder. +6  
smc213  Big was soybean formula not giving any issues. Soy-milk can be used as a substitute formula in patients with Classic Galactosemia since it contains sucrose (->fructose and glucose). +1  
oslerweberenu  Why can't this be glucose 6 phosphatase deficiency Confused me +  
almondbreeze  @oslerweberenu G6PD - increased RBC susceptibility to oxidant stress (eg, sulfa drugs, antimalarials, infections, fava beans) -> hemolysis; has nothing to do with presence of reducing sugar +  
makinallkindzofgainz  @almondbreeze; Glucose-6-phosphatase deficiency is Von Gierke disease, they are not referring to G6PD deficiency (an entirely seperate disease) +5  


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hTe yke si hte eerf rai ni the blndamiao .cyaitv rUlecs, elyleaspic ludneoad lse,cur cna rrfeeptao toni hte iaambdonl t.yvaci Thsi can saceu a upnmureoempioetn e(fer ira redun hte a.pdhigr)ma toN a esltdi tmyomsp in sthi onei,tusq tbu thsi acn laos escau dfeerrer ipna ot hte eoldhrus yb irrtiganti teh epnicrh en.evr FA 2019 pg 437

et-tu-bromocriptine  To add on to this, anterior* duodenal ulcers tend to perforate (makes sense because closest to the abdominal cavity) whereas posterior duodenal ulcers tend to bleed (due to proximity to the gastroduodenal artery). +9  
smc213  Acute pancreatitis can also occur with a posterior duodenal ulcer rupture. Source: Pathoma +4  


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I hhtgotu fo isht as oqassumu ecll oamrnacic fo eth lung gancisu deiracesn TrHPP nda rhp.eicaecalmy

d_holles  I thought this was medullary thyroid cancer but demographically SCC works better. +  
smc213  Medullary thyroid carcinoma increases calcitonin levels leading to decreased serum Ca2+ by increasing Ca2+ renal excretion. So high levels of calcitonin secreted by the tumor may lead to hypOcalcemia. Source: Pathoma +17  


submitted by mguan1993(7),
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oesD iebgn clrnyete dinsdgeao vs ivahgn CKD fro a lwhei nagehc sthi e?naswr eht teycnl"er adsindgeo" ptra trhwe em ffo

smc213  @mguan1993 yes it does! With secondary hyperPTH due to CKD = incr. phosphate, dec. Ca2+ and incr. PTH. This can then progress to tertiary hyperPTH from longstanding secondary hyperPTH as a result of parathyroid HYPERPLASIA --> autonomously (refractory) functioning parathyroid. This will actually lead to INCREASED Ca2+, and significantly INCREASED PTH. Treatment would be surgical removal of the parathyroid glands. Sources: DIT and FA18 p340 +5  


submitted by fenestrated(25),
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ahWt tsup ailtrenn inttrooa rveo tdnicodau? Saarbsicpluus ulesmc odes btoh

smc213  probably because the subscapularis m. is the only SITS muscle that does internal rotation & adduction along with the teres minor m. action being adduction & external rotation. +1  


submitted by mousie(171),
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alheoCr = Flaec l L/eorginranaoise = aleoLnalg onmupe = ON nporse ot eonprs nloy by oatnniiahl fo iacrateb ttnaoainedmc weLtrayem / = ctki e/M iocibgatneocciln = gnsiahr sirpyatroer adn raotth ocsresteni vsa(ali ro s.)ipt lalny,rGee it eskat leosc f(ro m,aexple onguchgi ro nsi)sgki or hyngtel actoctn to drpase tehes iatrbeca /MDRC(FS )C = iktc bite

smc213  Also, when Meningococcal meningitis is treated ... close contacts are also treated prophylactically whereas the others typically are not. There's also a subunit vaccine for n. meningitis due to high infectivity rate especially in crowded establishments. +6  
dentist  So, Cholera is also p2p but Mening is more likely? +1  
usmlecharserssss  in cholera people to water => water to people +  
qball  Remember the fire sprinklers from Sketchy for M. Meningitis. as respiratory droplets are the easiest to transmit from person to person. +  
drschmoctor  but the poop water comes from people so.... +1  
llamastep1  Respiratory dropplets is easier than fecal-oral tho +1  
lowyield  Can also reason that n. meningitidis is common in college students because they live in close quarters which suggests high rate of transmission even amongst immunocompetent individuals +1  
peridot  I can see why fecal-oral can seem like person-to-person transmission. What helped me reason it was that in countries with lots of cases of cholera, the primary reason is lack of water sanitation. Even when you google cholera, you get pictures of people collecting dirty water and how the WHO is aiming to reduce cases of the disease by improving water sources. Therefore it's more of a systemic/environmental problem rather than the fact that one person accidentally touched another person's poopy parts and then transmitted it to their own mouth, making this less of a person-to-person thing, especially when compared to another answer choice such as Meningococcal meningitis. +  
bbr  To add, think of the water in cholera as a reservoir. The bug is going to hang out there between infecting another person. In meningitis it seems we are going from 1 persons saliva to another. Without much of a reservoir inbetween. (might be using the word reservoir incorrectly). +  


submitted by gabeb71(36),
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etoisunmL ai an nylaktaigl ooruiatsenr pocmodun sdue ni ac.hyrhmoeept kliynlatgA taensg ionkslrsc NA.D

yCpioodsheahclpm mleaosetbiz nito a eoiprpahmsodh ad.utrsm areshopdomhiP drstmua ofsmr NDA lsrcksions tbho eewetbn nad ithiwn NDA nrssatd

lohheniiCcc dan tVbenansili krow on lsceriuutomb

rexahttoeeMt dna F-U5 thob okwr no uneirp .aomimtslbe

niotCeys breodiaasin ifnreesrte iwht het tesnhsiys fo NDA. Ist oedm of aointc is ued ot sti drpia rivcoosenn toin tisecnoy naeorsidaib e,hotpiaphtrs which aaedsgm ADN hwen eht ellc yccel ldohs ni the S ashep styesn(ihs of )DNA. dipylaR divndgii ,cesll hchiw ruriqee NDA tlanieorpci for som,siit rea rteeorhfe mtso aefectdf.

smc213  To clarify Methotrexate (inhibits dihydrofolate reductase) and 5-FU (inhibits thymidylate synthase) in the Pyrimidine synthesis pathway. 6-MP inhibits Glutamine PRPP amidotransferase in the PURINE synthesis pathway +3  


submitted by sajaqua1(462),
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Palsam emsbenamr are a ldipi ebla,riy lyitlpcay wthi pasepohht ehdas on ehca aresucf adn nlgo cnobar ltais no teh dieisn. eeThs asboncr aer ,utlnaer adn neurodg hyrooihbcpd oescirntiant rof an gylnaieeclrte brovalafe .tsate

atlgnrIe ermbmnae oprtesni sspa guhhtro sith ipidl r,aielby dan os smut be bplaeac fo cieagnrtitn hotb ihtw teh rplao tlsnsove fo ltarallucrien nad xcatrelleualr sa,cpe as ellw as teh chodpyhrbio reoc of het ar.ely ehT bnsartemnamer nopitor otenf ash -lhlaplacihae esoandcry fnaconmotior, whit rohyhcpibod udiesesr leik lceingy no hte uoesitd owdsrta eht narcob stial wiht oralp maoni daci urssiede cktued i.n

makinallkindzofgainz  "high school biology" lmao we really out here +6  


submitted by step420(33),
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argnlteI emmraneb nrisepot era nfduo itniwh eht amapls ermanebm adn pasn teh lhowe thnlge r.asocs The dneisi of hte aeemnbmr si revy odhcbhipyro due to hte glon bonrac s.ahinc vntExeesi yhbipohodcr tstacroeiinn newbtee hte ioprtne edis inhca dna teh piild stlai liwl phel archon hte rtonpei ni teh .aermbmen

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 +9  


submitted by killme(10),
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nettoinnI to tearT snAsilay

usmleuser007  in a per-protocol analysis,[6] only patients who complete the entire clinical trial according to the protocol are counted towards the final results +1  
sympathetikey  "In an ITT population, none of the patients are excluded and the patients are analyzed according to the randomization scheme." +4  
smc213  This video helps https://www.youtube.com/watch?v=Kps3VzbykFQ +12  
rio19111  Thx smc213, really helped. +1  
trainingrats  Where is this in FA2019? +  
teepot123  the video explains it well, no need for fa +  


submitted by hayayah(990),
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Scetpi hoksc is a teyp of diiisvrbttue ckosh cihwh is rkdmea by aivmess lavntodsiioa d/t( tmaairyfmnol esrnpo)es siguacn daeredesc RSV, asecdrdee peaoldr / PC,PW dna edarsncei .OC

smc213  Septic shock can also present with hypothermia <36C +3  
bethune  Why is it not gastrointestinal bleeding? +2  
beanie368  GI bleeding would present with increased SVR as a response to hypovolemia +5  
mysteriousmantyping  Why would this not be pulmonary embolism? +  
step1passfail  Pulmonary embolism would cause a decrease in cardiac output. There is increased pressure in the high compliant RV which can bulge and compress the LV, decreasing its preload. CO=Heart rate x stroke volume and stroke volume is partially determined by preload. If the pulmonary embolism is large enough, it can also obstruct the pulmonary vessels and subsequently not have enough blood going to the LA and LV, ultimately making the cardiac output near 0. +1  


submitted by hayayah(990),
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mquSasou ecll oarnmicca erccit:astsrhaci ,ivoaicttna eihlryeapmcac, edssaotiac iwht inmosg.k

lSlma clel yam cauytlal prcoedu dnsbtioiae nagtisa pniyecpsatr Ca lncsae.hn

smc213  Increased PTHrP seen in squamous cell lung cancer leads to increased Ca2+ levels +9  


submitted by usmleuser007(326),
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ryavliaS eirseotnc 1. tA lwo lwfo = gihH ncoctentranio fo psoiau;smt low cnotrtiocnaens of ms,odui ca,bibr ;m&pa .rdh2eloi c at hghi lwfo = owl caeotrnconint fo s;aiuposmt hghi eanntontroicsc of sudio,m rcba,bi m&;pa cioelhdr

sherry  That's exactly what I was thinking when I was taking the test. But I was sidetracked by same HCO3 level. Can somebody explain this part to me?? +  
charcot_bouchard  Because salivary duct removes Na & Cl while secrete K & Hco3 in lumen. In low flow rate HCO3 & K inc because duct is doing its thing for more time. At high flow rate K slightly dec (as cant be secrted as much) but HCO3 stays almost same. the reason is high flow indicates higher metabolism & higher bicarb production. +  
cienfuegos  Regarding the bicarb (via BRS Physiology, which explains flow rate as coming down to "contact time" where slow flow allows more reabsorption of NaCl): The only ion that does not “fit” this contact time explanation is HCO3−; HCO3− secretion is selectively stimulated when saliva secretion is stimulated. +2  


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Laellnigoe is mcoomn ausces fo epanonimu emdoipuspres on iconcrh tucsitobevr oyapmunrl edsisea.

asapdoc  Im pretty sure so is strept pneumoniae +4  
usmleuser007  COPD is also exacerbated by Viral infection: Rhinovirus, influenza, parainfluenza; and Bacterial infection: Haemophilus influenzae, Moraxella catarrhalis, Streptococcus. however, the questions gives a hint that it may be legionella = "weekend retreat" which may be associated with this infection +4  
loopers  From FA 2017 pg 139: Legionnaires’ disease—severe pneumonia (often unilateral and lobar A ), fever, GI and CNS symptoms. Common in smokers and in **chronic lung disease.** +1  
kentuckyfan  I also believe that the other attendees showed signs of pontiac fever, which is another hint they tried to get at. +2  
luke.10  i did it wrong and chose influenza virus since it is most common infection in COPD but the clue in the Question is that the other attendee didnt get sick since in legionella there is no person to person transmission +  
endochondral   but in Uworld s. pneumo is one of the most common bacterial exacerbation of COPD legionella wasn't even mentioned. How do we rule out s. pneumo ? +3  
nala_ula  maybe because in children s.pneumo causes otitis media? +  
smc213  Another hint made in the Q stem is the location being rural Pennsylvania.... Legionnaires disease was first discovered by the outbreak in 1976 at a convention held in Philadelphia, Pennsylvania. Not sure why I know this fact... +5  
hpsbwz  Biggest hint towards legionella to me was that they all were at a residence hall... i.e. where there'd be air conditioners and such. +4  


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how od we nkow aeksearpt aesuc nyiyvpeihersst mpnoetinsui

smc213  FA18 p.657 bird exposure--> HSN pneumonitis (restrictive lung disease) and FA18 p.214 granulomatous diseases: foreign material-->HSN pneumonitis. I had to make sense of it since I didn't know it was HSN pneumonitis at first. +5  


submitted by hayayah(990),
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Case fo saoi.orlocererstlsi

lrsappiHeyct llctioososreaesrri oivlsvne henciknigt of vssele awll by lpeaiyhrsap fo hotsmo meuslc (knonni'o-si epnaearap)c'

  • eoCnunqecse of naiagtnlm itreseonpyhn 1;(2t/108g0& w/ ectua na-rdoneg adg)ame
  • sutRsel in cdderue slseev ircebal tiwh ando-grne hescimai
  • May aedl ot frnboiiid nsoecirs fo hte seselv wlal wiht hm;orrgaehe aiacsllylcs casesu cutea ernla afulier (A)RF htiw a ticcraserihact 'a'letn-fbiet rpaancepae
masonkingcobra  From Robbin's: Fibromuscular dysplasia is a focal irregular thickening of the walls of medium-sized and large muscular arteries due to a combination of medial and intimal hyperplasia and fibrosis. It can manifest at any age but occurs most frequently in young women. The focal wall thickening results in luminal stenosis or can be associated with abnormal vessel spasm that reduces vascular flow; in the renal arteries, it can lead to renovascular hypertension. Between the focal segments of thickened wall, the artery often also exhibits medial attenuation; vascular outpouchings can develop in these portions of the vessel and sometimes rupture. +  
asapdoc  I thought this was a weirdly worded answer. I immediately ( stupidly) crossed of fibromuscular dysplasia since it wasnt a younger women =/ +15  
uslme123  I was thinking malignant nephrosclerosis ... but I guess you'd get hyperplastic arteries first -_- +  
hello  The answer choice is fibromuscular HYPERplasia - I think this is different from fibromuscular DYSplasia (seen in young women); +21  
yotsubato  hello is right. Fibromuscular hyperplasia is thickening of the muscular layer of the arteriole in response to chronic hypertension (as the question stem implies) +6  
smc213  Fibromuscular Hyperplasia vs Dysplasia...... are supposedly the SAME thing with multiple names. Fibromuscular dysplasia, also known as fibromuscular hyperplasia, medial hyperplasia, or arterial dysplasia, is a relatively uncommon multifocal arterial disease of unknown cause, characterized by nonatherosclerotic abnormalities involving the smooth muscle, fibrous and elastic tissue, of small- to medium-sized arterial walls. http://www.medlink.com/article/fibromuscular_dysplasia +1  
smc213  *sorry I had to post this because it was confusing!!!*Fibromuscular dysplasia is most common in women between the ages of 40 of and 60, but the condition can also occur in children and the elderly. The majority (more than 90%) of patients with FMD are women. However, men can also have FMD, and those who do have a higher risk of complications such as aneurysms (bulging) or dissections (tears) in the arteries. https://my.clevelandclinic.org/health/diseases/17001-fibromuscular-dysplasia-fmd +1  
momina_amjad  These questions are driving me crazy- fibromuscular dysplasia/hyperplasia is the same thing, and it is NOT this presentation and it doesn't refer to arteriolosclerosis seen in malignant HTN! Is the HTN a cause, or a consequence? I read it as being the cause (uncontrolled HTN for many years) If it was the consequence, the presentation is still not classical! -_- +1  
charcot_bouchard  Poor controlled HTN is the cause here +  
charcot_bouchard  Also guys if u take it as Fibromuscular dysplasia resulting in RAS none of the answer choice matches +  


submitted by hayayah(990),
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aCes of ei.orosaersllsoticr

staHylcprpei rllraresiicteoosos snovleiv nkgnicethi fo esvsel lwal by pasryelpahi of shomot semclu sonn-onki(i' )cea'napaerp

  • Cneequesnoc fo ltannimag hrptynsieoen /0t&;1g018(2 /w cutae eodgar-nn emagad)
  • lRstseu in decerdu lsevse ebiralc thiw oadreng-n ciesmhia
  • May dela ot riibofdin consires of hte vslees alwl twhi ergahho;erm calassicyll essauc caute nlrae iuralef A)(RF iwth a trhctcrisaiaec inl'ttbea-e'f ppcaaneare
masonkingcobra  From Robbin's: Fibromuscular dysplasia is a focal irregular thickening of the walls of medium-sized and large muscular arteries due to a combination of medial and intimal hyperplasia and fibrosis. It can manifest at any age but occurs most frequently in young women. The focal wall thickening results in luminal stenosis or can be associated with abnormal vessel spasm that reduces vascular flow; in the renal arteries, it can lead to renovascular hypertension. Between the focal segments of thickened wall, the artery often also exhibits medial attenuation; vascular outpouchings can develop in these portions of the vessel and sometimes rupture. +  
asapdoc  I thought this was a weirdly worded answer. I immediately ( stupidly) crossed of fibromuscular dysplasia since it wasnt a younger women =/ +15  
uslme123  I was thinking malignant nephrosclerosis ... but I guess you'd get hyperplastic arteries first -_- +  
hello  The answer choice is fibromuscular HYPERplasia - I think this is different from fibromuscular DYSplasia (seen in young women); +21  
yotsubato  hello is right. Fibromuscular hyperplasia is thickening of the muscular layer of the arteriole in response to chronic hypertension (as the question stem implies) +6  
smc213  Fibromuscular Hyperplasia vs Dysplasia...... are supposedly the SAME thing with multiple names. Fibromuscular dysplasia, also known as fibromuscular hyperplasia, medial hyperplasia, or arterial dysplasia, is a relatively uncommon multifocal arterial disease of unknown cause, characterized by nonatherosclerotic abnormalities involving the smooth muscle, fibrous and elastic tissue, of small- to medium-sized arterial walls. http://www.medlink.com/article/fibromuscular_dysplasia +1  
smc213  *sorry I had to post this because it was confusing!!!*Fibromuscular dysplasia is most common in women between the ages of 40 of and 60, but the condition can also occur in children and the elderly. The majority (more than 90%) of patients with FMD are women. However, men can also have FMD, and those who do have a higher risk of complications such as aneurysms (bulging) or dissections (tears) in the arteries. https://my.clevelandclinic.org/health/diseases/17001-fibromuscular-dysplasia-fmd +1  
momina_amjad  These questions are driving me crazy- fibromuscular dysplasia/hyperplasia is the same thing, and it is NOT this presentation and it doesn't refer to arteriolosclerosis seen in malignant HTN! Is the HTN a cause, or a consequence? I read it as being the cause (uncontrolled HTN for many years) If it was the consequence, the presentation is still not classical! -_- +1  
charcot_bouchard  Poor controlled HTN is the cause here +  
charcot_bouchard  Also guys if u take it as Fibromuscular dysplasia resulting in RAS none of the answer choice matches +  


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rHpiearbcya ssueac lrecerab ntlaoa.odisiv If uyo eavh eevr nees an tn-ira ro ateuc -topops iasgeorculurn epnttai, ro ayrell yan etptnia bouta ot ,heaintre oyu cna emrmeber tihs cbseuae heyt llwi eb eadptnrehyitvle ot 2COp unorda 035-2 ot cdsreaee IPC avi rbarecle ocsotcoan;nstviri in tish sea,c we haev hte peispoot. heT ruvce of CO2p sv areercbl ldoob lwfo si ieutq tpees ni the hpgioslicyo naerg amninge msall escagnh in taeioitlnvn aekm a afncisitgin eiefcrednf in CBF.

smc213  FA 2018 p.486 +3  
lynn  2019 - pg 489 +3  
jaeyphf  2020 - pg 501 +2  


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iFiaallm tudaaonmose syopislpo is na usatolmao nndiomat aotmniut. uohnssadT fo popsly rsaei itangrts eafrt r;petbyu acponoln;ic lywasa lveovsni emuct.r aPyprhioltcc mocecoylt ro lees 00%1 rerpgoss to RCC.

tulomAosa daomntin essdesai ea,vh on ,avrgaee 0%5 cahnce of ebgni spdeas odwn ot ngfprosfi.

sympathetikey  I would say this is Lynch Syndrome (APC is usually thousands of polyps) but lynch syndrome would generally have a family history of other cancers as well, so you might be right. Either way, both autosomal dominant so win win. +1  
smc213  uptodate states: Classic FAP is characterized by the presence of 100 or more adenomatous colorectal polyps +  
dickass  @sympathetikey Lynch Syndrome is literally called "Hereditary NON-POLYPOSIS colorectal cancer" +9  
fatboyslim  I think this actually is Lynch syndrome. Lynch syndrome can also develop colonic polyps but not nearly as bad as FAP. FAP has so many polyps you can't even see the normal mucosa. If you Google Lynch colonoscopy you can see that they develop a few polyps. +  
rockodude  I forgot it was AD inheritance but regardless at the time I was confused because APC is a tumor suppressor so it needs two hits. I guess AD inheritance and then you need another hit to develop CRC kind of like familial retinoblastoma or li fraumeni syndrome +  


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opaMlcasym mueciaoen ldpon tlagnuis,nig no sosenepr ot icni.llximoa

AF 710:2 cilassC uceas fo ayalctpi wn”gia“lk iopmnnuae ii(idsusno e,osnt ceh,hadae uodenrovtcpin gcu,ho hcytpa or fidfues ilniiertstta telira)ftin. y-aXr solok esrwo ahtn tiaen.pt Hihg riett of dcol iagsgtulnin )gI,(M hihwc anc gagaintltue or ysle C.BRs rwonG on Enato emt :aranTegr.at rodea,csiml ,iyeoylcdcnx or oquoeuonrollnfi pninl(iilec cfvntifieee since csaoalmpyM avhe on llce )BCAw .lla = cfra,Ai Bssnlidne, rohiCcn et.nifoicn –KD = trnveyigeh s.e lltoeneaaN ideeass cna eb eqrdicau dringu sapgesa hhrtgou difetecn brhit a.cNlon a lcle wa.ll Not eesn on aGmr ias.tn ooipPehmlcr taAlBriae.c nembrmea ioncntsa seorslt fro sbyiittl.a lmpsMocalay pnanmouie si omre ommcno psei ntaitn tl&; 30 sayer eqotudel .Frn aoektbrsu in rmialtiy rresciut smsacison odrnaaMpl.yp etsg cdlo hutowti a ocat lce(l )l.awl

johnthurtjr  Have you mixed Chlamydia in with Mycoplasma? +2  
smc213  I mean the Q stem is not about Chlamydiae, but Chlamydiae does lack the classic PTG cell wall d/t decreased muramic acid = beta-lactam abx ineffective. FA 2018 p.148 +  


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In aytueicokr lcse,l owt romja ystaaweth—hp -raseiqubtiiuonompte yhwaapt dan omlaoslsy spoeeseoim—ydailtrt irtpnoe tao.rginddea

heT ramoj phatway fo lviteeecs eopnrti dotengdaria in ouikecryta lelsc seus qiunuiibt as a earmrk ttha atrsgte oyiclcsot nda necrual ienpotsr ofr adpri prysoi.stole

Teh orhet joarm yhtaawp fo prietno ardotendgai ni uriatkoecy lescl vnelovis eht peaktu of enrtoips yb sssemloyo and igtsdeoni by tessa.pero

missi199  Could I ask why it is not Lysosomal protease +6  
smc213  "Certain viruses have evolved to recruit the cellular E3 ligases to induce the degradation of cellular proteins that might have harmful effects on the viral life cycle. For instance, the protein E6 of Human papillomavirus (HPV) recruits the cellular E3 ubiquitin ligase E6-AP to induce ubiquitination and degradation of p53, thereby allowing viral replication." from: https://www.mdpi.com/1999-4915/9/11/322/htm +2  
smc213  USMLE Kaplan: A majority of cellular proteins are degraded via the ubiquitin proteasome pathway, including many proteins that play a role in maintaining cellular homeostasis. These include proteins that regulate the cell cycle, apoptosis, etc. +3  


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In toyueicakr les,lc wot jomar yahwt—tpeash ouimnerpiatb-equoits aatpywh nad maosyosll ildetpoesraym—seoit terpino ndtodegarai.

hTe aromj twhaayp of celesvtie noreipt adtiradeogn in reauytckio slcle suse nuuibiqit sa a armekr taht tsaretg styccolio dna cnrelua niseortp rof driap yr.tseolsiop

The thero jamor yapawht fo ipreotn daioatgndre in royckuieat lelsc vvnsloie eth ptueak fo sitenopr by soelysmos nda eidtisogn by ter.pssoea

missi199  Could I ask why it is not Lysosomal protease +6  
smc213  "Certain viruses have evolved to recruit the cellular E3 ligases to induce the degradation of cellular proteins that might have harmful effects on the viral life cycle. For instance, the protein E6 of Human papillomavirus (HPV) recruits the cellular E3 ubiquitin ligase E6-AP to induce ubiquitination and degradation of p53, thereby allowing viral replication." from: https://www.mdpi.com/1999-4915/9/11/322/htm +2  
smc213  USMLE Kaplan: A majority of cellular proteins are degraded via the ubiquitin proteasome pathway, including many proteins that play a role in maintaining cellular homeostasis. These include proteins that regulate the cell cycle, apoptosis, etc. +3  


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I tiknh itsh one sah ot od ihtw ta"le duimnpg mdry"e--nso saclby,lia scratyh dfoos scaue yepmaercyihgl -&t;g- erslaee fo ilinsun ;&tg-- nhatleamoiecc reusg &t-;-g earhai,dr .cte

merpaperple  It's not necessarily late dumping syndrome, this is the dietary guideline for early dumping syndrome too. Based on UpToDate and ScienceDirect this is how it works: Absent or dysfunctional pyloric sphincter -> food is rapidly emptied from the stomach into the small bowel -> hypertonic solution forms in the jejunum -> rapid fluid shifts from the plasma into the bowel -> hypotension and SNS response (eg. colicky abdominal pain, diarrhea, nausea, tachycardia) Simple carbohydrates are more hypertonic, I think. https://www.sciencedirect.com/topics/medicine-and-dentistry/dumping-syndrome +2