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Welcome to smc213’s page.
Contributor score: 117


Comments ...

 +19  (nbme23#28)
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To eb telmoplcye elarc!

Tshi tenapti ash snCiyssoti a arre ausotmoal veirecess oslymlosa rsotgae doriedrs nad msto cmmoon caesu of ncFioan dnmseroy ni lr.cnihed siCtoissyn si timcessy nad edlsa to syeticn clsatyr pidtosse in eclls dna essusit ougttorhhu eth b.dyo

oughAthl nWosisl aiedses nac eald to SF, het carsltsy in het ensacro dose not roreatecl whit sWiosnl eised.as
Mroe inf:o /0hM/iitsnepw/cCanbw4lc.P4:.vomcgt1.61wn/l/mris/t.h8p

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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c,ourM ,zushopRi sidbAai ya Zcgr,urryp(ymg)oeIatlho d,rabo antenpesot hehapy hbcingran at ewid lapnsso.Sierrgsponoega era hneldai rofm il.os hTe gfinu tapenrtee eth ricmbirfo tplae (no biers)ra,r ripfeotlear ni loodb eselvs lasl,w ngsirrsoegp drpyial fmor sseuins nito eth rbina s•et.sui so:rcisyoumMc r,orinhbeelRac rnlatof lboe ases;scb screnuavo niuss bsotiosr.hm idraheatczerC by aanrpasal lgilen,ws ctnrceio stsueis alc(kb nirccoet hesrca on aef)c, agmrorihehc eatsdeux fmro sone dna y,ese meltan leahtg,ry hacedhea, laciaf ipn;a yam eavh lcanira veern vnmev•ol .tine ucOscr in ittiadcokeco ticabide and eepotnncuri ele(i)cukm t eanameTe:pisttntr ebirmntedde of nrcictoe issteu adn npmaceiihort B ro ozsulnoavicea deastrt iialemymdt.e ltFtayai aret si ihgh edu to ridpa hwtrog nda asiv.nion

jboud86  FA 2019 page 153. +




Subcomments ...

submitted by yb_26(191),
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anmblaro etts urlset anems htta etts dectest nacrec &=;tg

  • 35 fo 05 nme wthi soeartpt ncrcea eahv boaalnmr test ltesur t&=;g n fo pst ithw cencra = 05. etTs owssh racenc in 53 nme g;=t& T5P3= t;&=g we cna tlccalaeu FN = 305-5 = 51

  • 02 fo 010 mne twotiuh sapttore nacrce ehav manrablo sett rsltues &t;g= FP 02= &g=t; we cna lualatcce TN = 0012-=080

  • now ew can aultcelac stecyiciifp = NT)(+PF/TN = 0001/8 = 08. i(n % wlil eb )0%8

rehe si my 4/4 belat: [dc/o//3/mseth2_rceiosmuoms:stfaoim_wcemptlbwwertdn.set_emp3uq/nrs.obtt1wl/cu/i/nt]

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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nmblaroa stte teurls namse thta estt tecesdt nracce t&g;=

  • 53 fo 05 mne iwth porsatte cncare avhe abnarolm tset truesl &t=;g n fo tps htwi ccrnae = 05. sTet soshw ecranc in 53 men &g=t; 5P=3T t;g&= ew nca ltcuecala FN = 305-5 = 51

  • 02 of 001 emn hwtuito rtoptsea rcance evha mnlabora tset lrtsues t=;&g FP 2=0 ;t&g= ew nac cetalalcu TN = 180200=-0

  • nwo we acn uealalcct iiepticyfsc = F/NT(PN+T) = /08010 = 08. (ni % lwil be %08)

eehr si ym 4/4 bl:eat [puci2emit./b/telu.ersorotpfru/tcisbmmwtw3_/sntcacomlwown1/nsom__msd/eq3/estdt/:eh]

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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Cna enmoeos speael exnilap isth to m?e I t'ndo naetudndsr why nsatirgt teh rhoet udgr dlwuo otn ucotn sa xilcuones a?teciirr

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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tnPtaie si enrurtc brft,ee-das so ew can ileminate efrousct s(tuerofc si odufn in hnoye dna rsfuit adn eosm uoafrlm, utb ont ni btsrae imk)l. tiePant ash gediunrc stncusaesb tub no gecolsu in eth runi,e so eh stmu osme snuolneco-g as.rug My fentieraidlf orf ecgidrnu ng-ooscnleu srasug ni eth enrui is rriosdesd foecruts ambeimotls or cagesalot ms.moteblai We aveh eiadmentli otcu,esrf so taht elaves us wtih gacakiastelno efeycidicn ro csaiscl sa.aloictagem

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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eTh eyk si eth fere air ni hte lanoamdib ca.viyt lsUecr, laeslpciye doulaedn sl,ercu anc aeetfrpor onit het naobiadlm c.iyavt ihsT anc usace a uoneeepmmntproui rfee( rai drnue hte )dprma.ghai toN a tielsd omtpsym ni shit q,netusoi ubt htis nca aosl aucse rfeedrer anpi ot the udoeslhr by igtaniirrt the penrihc rnev.e FA 0912 pg 347

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 hgtutoh of hits as oqmsusua lcle oranmccia of teh lgnu saugicn seeiandcr TPrPH nda imaaer.epylcch

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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oeDs inebg ctyneelr adsgoiden vs nvgaih CKD fro a ielwh ahencg hsit ea?nsrw eth rcyln"eet dngosea"id tarp hrwte 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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Wtha uspt nltiaern nootarit eorv nai?uoddct siaSurlpsabcu umlsec deos tboh

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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ohrClea = caelF rge/L ailnnasoieor = oaelLgaln upemno = NO psroen to snpreo lnoy yb iohnalinta of actbraei aiantmoencdt ymLert/ wae = tick ieM gnoaccctbii/nloe = nhsgria sariyrrpeto adn rtohta ceerisostn asa(liv ro tp)is. ealnlreG,y ti kstae olsce (orf x,emealp ognuighc ro g)siikns ro gtlnhye contcat ot edpasr tshee itaabrec CCDF(RMS /) = kitc tbei

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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onLmitesu ai na nltaklyagi roesaitnruo odnmuopc duse in tea.omrphhyec lAkltnigya tneags ssrnlocki AND.

pahopedloshiCcmy soilmzebaet ntoi a ohohdperipsam dursm.at Porhdphiasmoe ustmrad fmrso AND sssinclokr hbot twneebe and iwhint ADN dntssar

oelcinhciCh dna Vlansebtiin owkr no cmrultiseobu

erteMhottaxe nda -UF5 both kwro no niprue boesammit.l

Cstyeoin sdabaiorein esrfrienet ihtw het eissntyhs fo .AND stI odme fo notaci is deu ot ist iadpr cnnvseroio otni nyiesoct aiaberosndi ihpsothepra,t hwihc sgeamad DAN nehw hte llce lceyc shodl in teh S ahspe (sesstihny of N.)AD pyiadRl dignvdii lcl,se ihchw ueirerq NDA criponlieat rof iito,sms rae erfeetroh tsom eacdff.te

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(461),
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malsaP bnsermeam aer a pdili iyar,ble llitycpya thwi ppoahehts saehd on ahec fuscera dan ongl nacrob itlsa on teh is.edin ehTse rbncoas rea ,runetla dna nrgdeuo oycpdhhbiro rtannosciiet for na elnyageerltic oareafvbl a.estt

tgrnleIa beanremm torpnise assp hougrht tshi ipidl ,airybel adn so mtsu eb bcalepa fo rnectinaitg boht hwit het rlopa oslvtnse fo rlrinllteucaa adn rlclxtlaeaeru p,esac as lewl as het bicphryohod croe of teh erla.y heT beemsanrrtman proiton efton ahs llelaahiphca- darycnose ico,tmafornno whit oroyiphdchb sieusrde elki gylenci no the dusoite artwods het obcnra ailts hwit aplor inmoa cdai sidurese ucetkd in.

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


submitted by step420(33),
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ngIeltar bernaemm ieptnsro rea nfoud wnhtii eht alamsp nbermaem adn naps hte owleh htgnel rs.saco The sinied fo hte amemenbr is eyrv ichyhpobdor edu ot eht olgn rbanco c.hsain exitEvnse yodbrphicoh nttairnicseo ntbewee het iorpnte isde cahni dna teh ilidp sitla wlli hepl cahonr hte eintrpo in het ebamemn.r

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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ttieIonnn to eTtar syiAnsal

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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ctiSep ksoch is a peyt of iivtesidtbru okchs wcihh si radekm by mesvsai taoadlinvsoi d(/t alimrfomatyn n)orseeps nuiacsg deseeardc ,SVR escrddeae adplreo / PC,WP adn rsneiadce C.O

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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suoSquam ellc amoccinra rha:ietsacrcstci toav,itainc rpiayhlmcecae, eosatcasid ihtw monkgs.i

laSml lcel amy ctulaaly cpdeuro osetndiiba nigtsaa iaenrtppsyc aC ln.ncesha

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


submitted by usmleuser007(326),
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ivaSylar iserecotn 1. tA owl owfl = gHhi itcrnecntnaoo fo mosui;ptas lwo ninrcoasceotnt of ,sdmoiu bi,barc ;mp&a lh2d rioec. ta hhig lwfo = lwo ccoitnetoanrn of sitsuoapm; high cosntoinneatrc of ,duiosm ,ibcabr map;& ohrledci

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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leiaeolngL si oconmm sscaue fo menoipnau mrupisspoede no ihrconc teuviobctsr ayprolunm s.adeeis

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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who do we kwon psakteare eucsa sniphveyysteir sintiepomnu

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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Cesa fo os.iereiatorslcolsr

ratpylpHsiec losciarsorietolrse livsveon gieinntkhc fo veessl lwla by elhyaaisprp of tomosh muclse koinnso(i'-n crpea'na)pea

  • eneqoucsnCe fo aangmtnli rnnteiesyhpo ;1&21t0g8(0/ w/ taecu anr-oedng )madgea
  • uRelsts ni redcedu sveles iablecr twih doernna-g schiemai
  • May alde to iiorbnidf ssrceino of the vessle llwa twhi rhoee;armgh aisllylacsc ucsaes aucte enlar ferluai F)A(R htwi a thctacrisaicer 'l-ittfbnae'e neaapecpar
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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Caes of .rreisaeoirsollocst

elscHyatrpip lloisaorsorrcesite vnovesil tenikicgnh fo lesves wall by hapiplysear fo mhosot eumcls 'oisn(oinnk- pp'er)naacea

  • snouceCeeqn of litgnaanm irnonsptheye 0;2g&8t(11/0 w/ ctuae ndr-eango m)agead
  • setRuls in rdeucde slevse ailrecb whit -gdrnoane chaisime
  • Mya dale to ronidfbii onrscsie fo eth esvles lwla whit rhegerh;mao casalscliyl cusesa etacu raenl eluafir ()AFR htwi a ahiitsarcetccr fae't'nl-ebit aereapanpc
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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ayeiHrarpcb sacesu ecberral nvoiatsi.laod fI oyu ehva reev eesn an rtin-a or taceu tpp-soo gniorlueuscra eintpta, ro lraley yan ipttaen uoatb ot hiatren,e uoy acn ebrrmeem itsh ebscaue eyth wlli be deleatepvnyrthi to pCO2 arnodu 5-302 ot csdreeea IPC iav elecarrb oionrnotsactsvic; ni htsi ,cesa we aveh het tpiseo.po hTe rvceu fo O2Cp sv lceberra oldbo ofwl is eqiut tpsee in eht iholsyocipg neagr nneaigm smlal chgeasn ni vtetiinloan eakm a ngniiasticf eecfrifend in .BFC

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


submitted by hayayah(990),
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Fillmaia deastonmauo ppoosyisl is na smalotoua nonmitda untamiot. duoahssnT of plyosp raesi gtsanirt rtfea pry;ebut pa;iolocnnc wlasay osvnlvei .emuctr ocrPacplyhit tomyleocc or eels 0%01 ssorgper to R.CC

omsoaAtul madtonni deeisass hvea, no vaa,geer 05% caechn fo engib eapssd nwdo ot gfrf.oinps

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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lcpyMamaso oaie enmpdulocn ,gagnntsliui no srpeosen ot il.amxconlii

AF 2:017 iscasCl cueas fo ctyaaipl ”“wgkilna oniueapmn idssuoin(i oes,nt cea,dahhe opvnniurcoedt ohug,c paytch ro sifufed alietrtistin i.tlfetrain) Xa-ry oolks reosw htan ia.pentt gHhi rtiet of odlc sutnalgnigi ,(MI)g hwchi can tauligtegna ro lsey s.CBR wGrno on tnoEa atm regr.aa:etnT scdirea,mlo do,icxyynecl or neliqlurfoounoo iipln(elcni eectiniveff snice samyMcoalp haev no cell al)w.Al CB = ria,Afc isnB,lsden orncChi ictoinfn.e K–D = nhvigetyer nee. allteasNo deiases acn eb qridecua gudrni gaesaps oruhthg nfeitecd ihtrb loa.n aNc clle w.lla Nto seen on Gmra s.atni cirPhopeoml Atlar.eBi ac enarmebm cnsanoti tslsroe fro l.tsiitayb llcmaMoapsy paneinomu si mero onommc ta spnintei l&;t 03 ysear olnuqFerd.t e eobtukasr ni iaitrmyl eisctrru o coMinssdyarmpl.a sapn segt cldo owttuih a tcoa lcle( l.l)aw

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 +  


submitted by hayayah(990),
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nI yeoitcruak el,scl two roajm whaepysatt—h pstotemn-iiuquarobei tyhpawa nad laooslsym oamsoiyeepreltdti—s tnrepio rnaedtigd.ao

eTh ojarm awythpa fo eeeitlcvs pternio ietaodrandg in ectkiruyoa cslel uess uqitbiiun sa a kmerra htat sgaetrt ootclsciy adn nluacer eisrpnto rfo dpira ryiots.solep

hTe eroth mrjoa hwytapa fo eproint daeidrnagot in atuoiyckre elscl lisenovv the apkute fo poiersnt by oelsosysm nad dgieinsto by .aotpeessr

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  


submitted by hayayah(990),
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In autockreyi ,cesll otw ojamr tpash—atwhye ebiioiutanmpqret-osu pawthay and syllmsooa leytapsdsetiooi—emr oetpnri drieto.adnag

eTh major ayptahw fo veltiesce peinrto rtdoaengadi in ytoiuakcer csell sesu uiutibinq sa a kraemr atht etasgrt lyociscot dan rnlucae snetopir for dipar soispore.ylt

eTh ohret amroj hyaptwa of rpienot adgneoitdra in ceiuokaytr sclel vinvolse the uaetpk fo tpseroin yb yomslssoe adn itogiedns yb ospatre.se

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 kthni siht eno hsa ot do ihwt "ltea pigunmd od"-meny-rs ,lliacbasy tahcyrs soodf uscea pceegimhlayry -t&-g; leeears of siunlni -tg;&- loecitmcaehan srgeu g-&;t- heriadr,a c.te

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