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Welcome to linwanrun1357’s page.
Contributor score: 9


Comments ...

 -7  (nbme24#25)
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I sjtu ktinh apslm aer ont creeodtpt by het amnleni nda gto htsi hgt.ri

hungrybox  useless +6

 -6  (nbme24#23)
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K*F* this os!qniteu

Kown yaelxct thaw teh sdeaise si wtotuhi nnwoikg hwat hte *ngfk*i ledain"ezegr anibmtosal"orp mae!!ns

tiredofstudying  Hope your day got a little better after this +6

 +0  (nbme24#18)
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e/t/kcecayimlec.l-ausy-voohd5/ip/see-rmpsd:etatmrsmtibc

hTsi kloso rebtet orf teh 3 itresrae


 +0  (nbme24#9)
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:EOTN rilociaMi:arf

risMfroiiiaacl na yarle tegsa ni eth lefi cyecl of aiecntr isrtaicpa mnsdteeoa ni eth maylif erceoa-ihwckdiOi.-cn

linwanrun1357  Only the the black fly is associated with nematodes +




Subcomments ...

submitted by keycompany(296),
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yhW uowld tnoespdioi of bfnodirii optsdesi ie..( fobniiidr otamicr/eilsngnnas N)TH be gwon?r

amorah  Kidney is smaller than normal, suggesting less blood flow to it. Won't see shrunken kidney in the case of HTN. +1  
linwanrun1357  I have done so research showing that it should deposit collagen (see below). Anyway, fuck this question! http://www.pathologyoutlines.com/topic/heartfibromusculardysplasia.html +2  
shapeshifter51  I ruled out selection A since it is involving the interlobar artery. Renal artery stenosis involves the "renal artery" and the stem gives you fibromuscular dysplasia with renal artery stenosis. +3  


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iThs is rasetlioraint-inpn .astmha pnothAnciemea lnyo inbsiiht XOC htwiin het NCS, os eo’dnst uaesc eth koneeiertul ugntihsn tath zaciaechsetrr thta diae.sse

linwanrun1357  why not triptans? +4  
joyceeepan  the girl has tension headache. Triptans is not a drug of choice. NSAID, Acetaminophen, (or TCA for prophylaxis) +3  
vsn001  but question asks which drug she should take to /treat/ her headache? -> I fell into sumatriptan cause I know it didn't have prophylactic indications but more of a treatment. idk, was between the acetaminophen and sumatriptan, and would appreciate if someone can tell me why acetaminophen is the move for this patient. +2  
texasdude4  for HA treatment you want to start off conservative anyway w/ Tylenol / NSAIDs before you move on to triptans. That and triptans are not used for tension HA +  
jurrutia  Triptans are used for migraine headaches by causing trigeminal vasoconstriction. They are not analgesics. +  


submitted by neonem(550),
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hTese ear guot lsctysar. I soppuse the sbte way ot fntdtieiraeef hist esac mofr psoudogeut si htta hte srtslyca ear rasph ;pma& eees-edanlhpd nda ont -drdh.piomeosbha

sympathetikey  Yep. They tried to throw you off with the picture, but the wording in the stem says its a "photomicrograph" -- not exposed to plane polarized light, where you would see the negative birefringence. +17  
linwanrun1357  Why is NBME so mean to us. Do those mean a lot in clinic? +  
suckitnbme  @linwanrun1357 I highly doubt you would be looking at your own joint fluid aspirates instead of sending it to the lab. +3  
nnp  what those yellow white nodules signify? +  
peqmd  In clinic gout is typically a clinical diagnosis. If you can treat w/ NSAIDs instead of aspirate you would do that. You would aspirate if you are considering septic arthritis so you can get culture. I don't think anyone aspirate for heck of it. +  
lowyield  @nnp, the yellow white nodules are tophus which is a sign of chronic gout, characterized histologically by aggregates of uric acid crystals, can show up as skin nodules most commonly on external ear, olecranon bursa or achilles tendon (pg 467 FA 2020) +  


submitted by trazabone(14),
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My getardnnunsid is hatt if pntesar aer aeudelnrt by odobl to hteso e,eaftcfd we usmeas thta tyhe aer otn srcerria n(i eht resecesvi .ca)es frrhTeo,ee fi ew eavh a mlae etfhra eacdfetf thwi dilxnke- erviceses rmerida ot a ,anerrncrio- 'theesr no yaw any of hsi orinfsfpg ulowd eb atee.dfcf

"fI noe nreapt is ton a rrea,rci thne a ichld cna loyn enitrih a essedai elllea rmof eth oerth ae.rntp nI ethse splmbr,oe ew cna msuesa atth yna uiainilddv gaimryrn otin eht ymifla is tno a crrr"e i.arm.d-cnses/oPic.wtrte/nfsctdcuoipit/ttung/n.Cteiss.ws~sn:suuu/ihtipwnc/

linwanrun1357  If we assume that they are not carriers (in the recessive case) Then how came it can be AR?!! +1  
catscan1979  ^exactly what's said above here. I think x-linked recessive is the least likely, but not impossible. +2  


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:NOTE ioa:rMiifcarl

lirMiiifscarao na yelar atsge in hte lief ylcce fo rtncaei iistapacr eamosdetn in teh afmiyl ecia.hcwdc-eok-irOni

linwanrun1357  Only the the black fly is associated with nematodes +  


submitted by brethren_md(87),
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arncOehocc sVuoullv iav mlaefe klcly.fab clBka lie,sf akbcl insk sudn,oel "lkbca gs"iht k(aa esdsinlnB). iutQones mste heer eiscsrdeb eht kacbl slodenu seen ni .carnceOoch

linwanrun1357  There is no black in the stem~~!! +4  
misterdoctor69  nodules can be hypo or hyperpigmented supposedly! +1  


submitted by keycompany(296),
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hisT eitnpat sah a nxhomrtoapeu. nloayeeiHrtpvltin si otn uhoegn ot maeoentspc ofr eth verolla edescaer in nlgu urafces ea.ar

_yeetmasterflex  Could the pneumothorax also cause less ventilation due to decreased lung surface, retaining more CO2 causing respiratory acidosis? That's how I got to the answer at least. +4  
duat98  I think pneumothorax would increase RR because you're probably hypoxic. Also I'm sure when you have a lung collapse on you you'd be scared and that would trigger your sympathetic so your RR will go up either way. +3  
kateinwonderland  Arterial blood gas studies may show respiratory alkalosis caused by a decrease in CO2 as a result of tachypnea but later hypoxemia, hypercapnia, and acidosis. The patient's SaO2 levels may decrease at first, but typically return to normal within 24 hours. (https://journals.lww.com/nursing/Fulltext/2002/11000/Understanding_pneumothorax.52.aspx) +1  
linwanrun1357  How about choice C, --ARDS? +2  
bullshitusmle  there is no bilateral lung opacities as you would see in ARDS +4  
jesusisking  Was thinking some sort of infection b/c of the atelectasis so picked empyema but this makes sense! +  
djeffs1  does it need to be ARDS to cause "diffuse alveolar damage"? +  


submitted by lsmarshall(393),
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"In hte ayrse egnircped psclayhi eptybu,r otbRer .M roayB cdersdoevi ttah teh otorgdonapni lsespu ucorc lony udring lseep, but as euyrtbp rsgerospes tehy nac eb tteceedd irndgu teh .ayd By eth ned of e,byprut hrete is ilttel hadyg-nti ineeeffdcr ni eth tpleumiad and qeyecurnf fo oadipgtoonnr pue.lss

Semo ertistnosivga avhe tubtiradet teh etsno fo yuebrpt to a naeronces of aooslcslitr in eth n1[]8i9][br9[].a90 By iths hnmci,eams eth gditanoopron lsupes htta rcuoc rapmriiyl at htgni utjs oreebf eyrbput esrtenepr ba.t"es - ikWi

linwanrun1357  Who can explain, the 12-y boy with stanner stage 2?? I thought it should be stage 3.... +1  


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eTh ieeasds hree is rfocutes ssetsaihhabppo cfcniyied.e nI ,it IV ygrelolc or reufcost ’tsoend lehp seubeac othb neter hte uilncesgeoogesn tpyaawh bweol rtoscufe ispaeoabphts.h Goatescla no eth teohr dnah nseret vboea t.i I ’dont hiktn uoy lylaer ende to nkow sith ot escooh eht rccrteo renwsa scein het lniiclac perituc fo afgitns iclamhogypye atth is crcortdee /w moes osrt of agurs htta nca nteer het egnnesuiogcosle ypthaaw lohusd cleu uoy tnio hte ihtrg .srnawe

neonem  I don't think you could have *totally* ruled out the other answers - I picked glycogen breakdown because it sounded kind of like Von Gierke disease (glucose-6-phosphatase) to me: characterized by fasting hypoglycemia, lactic acidosis, and hepatomegaly since you're not able to get that final step of exporting glucose into the blood. However, I guess in this case you wouldn't see that problem of glycerol/fructose infusion not increasing blood glucose. Nice catch. +24  
vshummy  I think you were super smart to catch Von Gierke! Just to refine your answer b/c I had to look this up after reading your explanation, von gierke has a problem with gluconeogenesis as well as glycogenolysis. So they’d have a problem with glycerol and fructose but also galactose since they all feed into gluconeogenesis before glucose-6-phosphatase. Great thought process! +22  
drmomo  glycerol and fructose both enter the pathway thru DHAP and glyceraldehyde-3-ph. Galactose enters thru Gal-1-ph to glu-1-ph conversion +2  
linwanrun1357  In this cause (fructose bisphosphatase deficiency.,),fructose should help to increase serum glucose, bcz it can become into glucose-6-P by hexokinase. Therefore, this question makes me confused.... +  
krewfoo99  According to uworld, fructose infusion will not increase blood glucose levels in Von Gierkes Disease as well +  
atbangura  I believe Von Gierke is not a plausible answer choice because a galactose infusion would still not see an elevation in glucose levels. Remember, galactose could be converted to galactose 6 phosphate, but in order to complete gluconeogenesis and allow glucose to leave the Liver for an increase of its concentration in the blood, the patient would still need glucose 6 phosphatase which is eliminated in Von Gierke. +1  
lilyo  So what disease is this??? I mean couldnt we have just answered the question based on the fact that the patient responds to galactose being infused and we know that galactose feeds into gluconeogenesis?? I am so confused. +1  
djtallahassee  Its Hereditary Fructose intolerance right? gets sick after fructose and I guess glycerol can jump in via aldolase B on this pathway via page 74 of FA2019. It looked like a fructose thing to me so I just marked out the other ones and moved on. +1  
paperbackwriter  @djtallahassee I was wondering same, but hereditary fructose intolerance also results in inhibition of glycogenolysis :/ confusing question. +  
amt12d  A much simpler way to think about this, without trying to figure out a diagnosis, I looked at the time frame for when the child was presenting. He has eaten poorly for 3 days, by now, his glycogen breakdown is gone. His body would be trying to make glucose, therefore, gluconeogenesis is impaired, not glycogen breakdown. +2  
tyrionwill  if fructose kinase is not available (fructose intolerence), then some fructose may go to F-6-P by hexokinase, then goes to G6P if gluconeogenesis is needed. however this patient's fructose kinase was intact, so no fructose would have go to F6P, so there would be no blood glucose increment after injection of fructose. +  


submitted by hungrybox(968),
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eTh 2 stncmmeodnam fo hcites itenoq:sus

  1. t'Don rvee ikpc an nawres where oyu dosnu keli a cdki
  2. D'not reve slcount eht hseitc tmmeoitec

deSrev em lwel no ihst q.tieosun

linwanrun1357  If there is a choice about asking what the patient is worried about. Is this right? It does not sound like a dick :) +1  
champagnesupernova3  If this were about a treatment asking why hes worried would be right but hes kind of doing the hospital a favor so I dont think you're supposed to try to convince or pressure him +1  
brasel  also, any patient participating in any research study can withdraw whenever they want. Answer E is wrong because he shouldn't have to go through hoops to quit, he can just drop out at any time. +1  


submitted by nala_ula(100),
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In aticiebd o,eiadiostcks erhte is enidarcse adic ni teh txuaeearllrcl ec.pas gciAdoncr ot AF eethr is a rraanlsllectu sithf ued ot sdreeeadc silunni that eldsa ot rome +H nrneietg teh clle in ehagenxc orf .K+ isTh edlsa to mekahiaepryl ithw lepetdde uatnalllircre etosrs fo K+. Tehre si sloa imcosto erudissi htta edals ot isnecared K+ slso in the eurni nad oatlt boyd K+ ntdp.iolee Teh oinseutq saks hatt is mtso lilyek ot aerseedc twhi nsilnui trayhe:p emrus msopustai naencnciorott lwli sceerdea sa +K is onw dxgenaehc rfo +H neiisd eht l.ecl

cienfuegos  Additional UW fun facts regarding Potassium and DKA: use caution giving insulin and IV fluids to dehydrated hyperglycemic because i forces K in cells causing fast decrease of extracellular Potassium, thus give K supplementation even when serum K elevated +3  
linwanrun1357  Why urine K+ does not decrease? +3  


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’Its ucate ahclolo tsonmiconpu os attyf chegna eorm yeki.ll Caellurl lsingwel tisneidca locohacil iitetphas chiwh uesreqri ocrchni lholaco utnomipocsn e(eS AF 1209 gp .583) At aelst a’htts the gocli I usde to cpik attyf .geanhc

seagull  Seems like fatty change would require more than 1 weekend. I choose swelling since it's reversible and seems like something with a quick onset. +40  
nc1992  I think it's just a bad question. It should be "on weekends" +16  
uslme123  https://webpath.med.utah.edu/LIVEHTML/LIVER145.html +20  
uslme123  So his hepatocytes aren't dying ( ballon degeneration ) vs just damaged/increased FA synthesis due to increased NADH/citrate +  
sympathetikey  @seagull I agree! +  
et-tu-bromocriptine  It's not in pathoma, but I have it written in (so he or Dr. Ryan may have mentioned it) - Alcoholic hepatitis is generally seen in binge drinkers WITH A LONG HISTORY OF CONSUMPTION. +  
linwanrun1357  Do NOT think the answer of this question is right. Cell swelling make more sense! +1  
fkstpashls  some asshole in suspenders and a bowtie definitely wrote this q, as I've seen both acute swelling and fatty change be used to describe one episode of drinking. +12  
msw  short term ingestion of as much as 80gm of alcohol (six beers) over one to several days generally produces mild , reversible hepatic steatosis . from big robin 8th edition page 858. Basically to develop alcoholic hepatitis with cellular swelling etc you have to have sustained long term ingestion of alcohol while steatosis can develop with a single six cap . hope that helps . ps i got it wrong too . +1  
msw  six pack8 +  
mariame  After even moderate intake of alcohol, lipid droplets accumulate in hepatocytes increasing with amount and chronicity of alcohol intake. (...) Fatty change is completely reversible if there is abstention from further intake of alcohol. The swelling is caused by accumulation of fat, water and proteins. Therefore this will occur later. From big Robins 9th pg842. +  


submitted by hayayah(1056),
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hpymL wolf ater si uualysl o.lw It is fcnleunide iailmpryr by het rtea fo hplym oomanfrti. Fro mxep,eal if odolb liaplyacr upersesr si naricseed yb aretlari ivtlosdinaao ro seuvno nrnotitsci,oc the lfow rate fo mylph sanie.scre osA,l eth ofwl trae si teaefcdf by npmsroeiocs fo amslpihtyc by cairttcoonn fo ogbrnihegni teurluaumsc adn by nvtaieeg atrntcricaohi sprsereu bhtar.in)eg(

nrtelitiaIts psurrese (so persruse ni eht ,FEC hhwic ludwo rniaesec fi nveig IV eanis)l adn lyhpm wlof are eisipoyvlt datreel. A samll rcaneies in iinlertaitst ulemvo atryegl ncsreiesa sti u,erssrpe mpnoortig hmlpy lofw htta asct ot etrreso eht ienittartlsi emouvl ot ml.nora

oemr no tihs iptoc: io/g./cn4lk4mnw/v//bohNon:3KB8i5twtbw.hps..s

linwanrun1357  Do not understand the breathing (choice C and D) breath in and out are different? +  
khanhluong  I don't know if it's correct or not but how I approached C & D was that they both cause vasoconstriction in the arterioles (because this is the lung where hypoxia causes vasoconstriction), which decreases hydrostatic pressure through the capillaries and eventually decreases lymph flow. Maybe I completely got this question right for wrong reason, but I felt that it works with all of the answers. For F) I was thinking that it would cause increased capillary oncotic pressure which causes more fluid to go into the capillary than into the lymph vessels... Here's a picture: http://www.lymphedemablog.com/wp-content/uploads/2011/09/Lymphatics.gif +5