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Welcome to tyrionwill’s page.
Contributor score: 15


Comments ...

 +1  (nbme24#9)

probably only 2 parasites are related to nodules: 1. trichinella spiralis: muscle mass, muscle ache, systemic symptoms 2. onchocerca volvulus: skin nodules, without significant systemic signs until blindness

tyrionwill  probably cannot find any abnormality on the skin surface or no obvious mass found along body. only biopsy from the painful muscle can detect the larve of trichinella spiralis. however, skin change due to onchocerca is popular to be easily found when doing PE +

 +0  (nbme24#30)

we can make things simple like this way: if we want to know whether X1,or X2 correlates Y, we just separately test X1 and Y, and X2 and Y accordingly. When test X1 with Y, we require no X2 exposure; When test X2 with Y, we require no X1 exposure;

We test cookie with diarrhea, when milk was not drunk (top right): positive We test milk with diarrhea, when no cookie was eaten (lower right): negative

conclusion: only cookie correlates to the diarrhea





Subcomments ...

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iftrs uhlsod nowk that tish si teh ufunds ro oydb of eth ctsa,gri so ti ldhuso eb the ailrteap lcle n;maeiod ten h tkhni hte umusc si hte perttiovce oen , A twuitho isehtae.t nhet the rtohe on eht uerpp gaadlrlun yelra lusdho eb teh paelrta lcl,e wihch is B. shteor ikel C is so sllam i,n hte depere ranlgulda alrey nad liapcsbialh oglniok ambey is eth fecih ellc . neht eeerdp cudlo eb het sauousmcb .raley UW ID214 ify.

zme331  ???? +  
tyrionwill  how would I know where is superficial and where is the deep layer? +  


submitted by cassdawg(930),

This boy has cystic fibrosis, which is caused by a defect in the CFTR gene which codes for an ATP gate chloride channel. The most common mutation leads to a misfolded protein (defect in protein structure) that results in the protein being retained in the RER and not transported to the cell membrane. (FA2020 p60)

tyrionwill  CFTR is not a receptor which binds ligand to make a change of second messagers inside. CFTR is a protein channel allowing ions in and/or out. so choice B is wrong. +1  


submitted by cassdawg(930),

This woman has gout which is associated with hypertension and diabetes and attacks can be precipitated by diuresis (such as with furosemide). Negatively biorefringent crystals (uric acid crystals) are also characteristic of gout. Gout is associated with kidney stones (nephrolithiasis). [FA2020 p467]

frijoles  I don't see where it says that gout is associated with kidney stones. Gout is more commonly caused by underexcretion than overproduction, yes? And this patient has renal insufficiency, yes? So if anything, they have LESS uric acid in the urine and are LESS likely to have stones. It's the reason they have gout to begin with (because it's out of the urine and into the blood). This answer would make sense if the gout was due to overproduction but there is no evidence of that here. This isn't a very good question imo. Please lmk if I'm missing something here. +2  
jt263619  uric acid stones... +2  
tyrionwill  hyperuricemia may cause kidney stone if urine turns to be acidic or condensed. so I think this question is asking a general possible complication. +  
i_hate_it_here  I think that what they were trying to ask was what could also occur due to the predisposing factor that led to gout. The patient was on a loop diuretic which can lead to hypovolemia. Kidney stones and gout occur more frequently when the substrates are able to concentrate in low volume. +1  
kard  furosemide and acetazolamid---> Nephrolithiasis! +  


submitted by 123ojm(7),

Specifically didn't choose coronavirus due to the evidence that COVID-19 is spread fecal-orally. How does it get through the GI tract if it's inactivated by pH < 6? Can someone explain why my thinking is wrong?

hello  ...COVID-19 is transmitted via respiratory droplets. +3  
123ojm  Right but some research has come out saying it's also spread fecal-orally. So I'm wondering what I'm missing in this question. +  
tyrionwill  Don't trust US CDC in this pandemic. They always downplayed the truth. Cronavirus does spread mainly by droplets, when they drop, they contaminate the surface, then fecal-oral could be a second pathway. Wearing mask, social distancing are both to prevent a droplet. +  
boostcap23  I thought covid used to be low yield when this test was made and they didn't mention helical so I didn't pick it smh I'm an idiot. +1  


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ehT idessea reeh si csuretof tihspoapasbseh e.indiyccfe nI ,it IV lrgocley ro focsrteu ’stdeno pelh eubesca both enetr the goncseogeneiusl twaaphy ebolw cufosrte pot.aiahsepshb oeaalcGst on eth hoter hdan nertes eovba i.t I ont’d hnkit yuo llyaer ende ot okwn hsti ot eocosh het rectorc aewrns siecn hte nalcicil uireptc of faisgnt capelmyigohy taht si occeerdtr w/ esmo orst fo rugas ahtt anc eetrn het gescgnoeonilesu awtpyah lhdous luec ouy itno het gtrhi wsarn.e

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 usmle11a(73),
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usyg GV udlow ewrnso thiw oaaceglst sfnnouii, mmrerebeb hety otnd vhae a6sGeP whihc samen htye natc ctnreov agnyhnit to cogelus

tyrionwill  Yes, VG makes the liver into muscle, where all sugars (except glucose) can only be burned to lactate+glycerol(from glycolysis), ATP (from TCA metabolism, to give uric acid), and fat deposit (from glycerol+pyruvate going to FA+TG) to worsen the situation. Sugar cannot be made into glucose in liver for other tissues. +  


submitted by lsmarshall(393),
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MHC scasl 1 pdipeet antnige onecrisgsp t&g; eg"nAint eppiedts deolda oton MCH I in ERR fatre vedyirel vai PTA oratp(srnret ocdasesait whti ientgna in")pegosrsc - iFrts iAd .0129

Bare eycptyhlom nmsoryed etyp 2 LSB( I;I fnefcgiat MCH II) si edu ot ntaiuotsm ni nseeg ttah cdeo ofr srtcatnroipin rftsaco hatt ryalolnm aetgeulr hte srxenepsio n(gee pitsicro)ntrna of hte MHC II esgne. Bera yeoclythpm oryednms ptey 1 SB(L ;I giftnecaf HCM )I, is hmuc reom earr, dna si soetasiacd tihw TPA .ceidescnifei

tyrionwill  in the question, it says absence of MHC-I presenting cells. I guess the meaning is lack of MHC-I. IF TAP is missing or dysfunction (bare lym syn type-1), MHC-I should be there, however Ag cannot be loaded to the MHC-I. Can anyone help me to understand more. +  
peridot  @tyrionwill From wiki: "The TAP proteins are involved in pumping degraded cytosolic peptides across the endoplasmic reticulum membrane so they can bind HLA class I. Once the peptide:HLA class I complex forms, it is transported to the membrane of the cell. However, a defect in the TAP proteins prevents pumping of peptides into the endoplasmic reticulum so no peptide:HLA class I complexes form, and therefore, no HLA class I is expressed on the membrane. Just like BLS II, the defect isn't in the MHC protein, but rather another accessory protein." +  
j44n  i hate this question because MHCI is on all nucleated cells. So this person is literally a bag of RBC's +1  
soccerfan23  @j44n Not quite. It's true that MHC I is on all nucleated cells. Because of the TAP mutation, these cells don't express MHC I on their membranes. But these cells still exist. That is what is meant when the vignette says "flow cytometry shows absence of class I MHC-expressing cells. +  


submitted by famylife(86),
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oT elur otu IAHDS ey:pt u"Serm psoasimut toctreniaonnc lgeynarel rasemin ehcang.udn tMnmoeve of aitmoupss ofmr hte aauerrclllnit caeps ot hte xlarereclluta sacep esprvtne uililoantd .hopleykmaai As dnrhegyo oisn vmoe lllraailuceryt,n ehyt aer hadnecxge rof tsmuisoap ni redro ot nitiamna cyn".trertulaeoleit

emrdrnpewyeo-ssfhei6iasme8amoeh-/oe2-3n-tar--f-0iwsot/tewunms-4aenpippdseoaoo-csdtoo:sr/smlsce-t/.w-i5ii.arrm6vophdtph3eeafcnseciturasw8/tl--dnrcu

usmile1  Does anyone know if SIADH is associated with hypertension? I don't think it is due to the body's response of downregulating aldosterone, but if someone could verify that I would appreciate it. +  
sunshinesweetheart  @usmile1 pg 579 FA 2019 = BP can be normal or high in SIADH +  
usmlecrasherss  in SIADH GOLJAN says you have diluteonal hypokalemia +  
tyrionwill  SIADH -> excessive ADH -> water retention -> atrium excretes more ANP, ventricule excretes more BNP -> water is excreted more. So that is why not too much plasma volume increment, resulting mostly normal BP. +  


submitted by aneurysmclip(134),

pretty straightforward question but another thing you couldd do is figure out his lymphocyte count 5%x2000 = 100 which would line up with a low Cd4 count however you divide it

tyrionwill  Yes agree! Lymphocyte count is so low, which suggest HIV. +  


submitted by ameanolacid(24),
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sisloecoresrAht si eth TOMS mmocno scuae of nreal rarety .w.sssi.otniteh ufcumarrilbso asyldpasi egibn teh CDOENS ostm nmoomc cueas ene(v ghuoth it si enitgmpt to ohceso hsti notiop cgsnrnoiedi eht aeis'nttp )mdohcgr.iaep

xxabi  Is there a situation where you would pick fibromuscular dysplasia over atherosclerosis if given both options? Thanks for your help! +5  
baconpies  Atherosclerosis affects PROXIMAL 1/3 of renal artery Fibromuscular dysplasia affects DISTAL 2/3 of renal artery +45  
gonyyong  Why is there ↓ size in both kidneys? This threw me off +3  
kateinwonderland  @gonyyong : Maybe because narrowed renal a. d/t atherosclerosis led to renal hypoperfusion and decrease in size? +1  
drdre  Fibromuscular dysplasia occurs in young females according to Sattar Pg 67, 2018. +10  
davidw  Normally you will see Fibromuscular dysplasia in a young female 18-35 with high or resistant hypertension. She is older has a history type II DM predispose you to vascular disease and normal to moderate elevation in BP +9  
suckitnbme  @gonyyong there's bilateral renal artery stenosis. The decrease in size of both kidneys should be from atrophy due to lack of renal blood flow. +3  
tyrionwill  1 year ago, she did not present any physical or Lab abnormalities. This means she must not suffer fibromuscular dysplasia, otherwise she must have presented renal abnormalities for a long long time, or even before DM-2. +2  
rockodude  a little surprised that atherosclerosis leading to bilateral renal artery stenosis and shrunken kidneys could happen that quickly after everything was A okay the year prior +  


submitted by brethren_md(87),
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Meak a upnntet qsaure ihwt a csrso of B B+ adn B 0B; +B eetsnrsper %05 inuftcno eilwh B0 essneperrt 0% )(lunl tf.conniu So ni tsih ec,sa teh subdnah wloud have a B B0 eoyetpng wiehl eht feiw sah a B B+ e.oetypng

sCros fo thsee owt lliw utlsre in eth ngooflliw ptnges;yoe ,BB 0,BB +BB, 0BB+ B B = 0%10 n,futoinc B+B = %57 nu,tonfci BB0 = 50% ofinctu,n +BB0 = 5%2 ncunfito

So het nswrea lliw be 1 in 4 haev a %25 ufonitnc igvne teh enept.ogys

tyrionwill  how about the choice of D: 1 in 4 have 50% function, which is true. shall 50% function needs transfusion? +  
tyrionwill  In FA, it defines beta thalassemia into minor (HbA2 >3.5%) and major (both HbF and HbA2 go further up), and the major needs transfusion frequently. How can we take this classification based upon quantitive way like in this question? how much percentage of function left does not need a frequent transfusion? +  
azibird  D says one in TWO, not one in FOUR. +2  
hemehero  Is there a way to know that B+B0 will = 25% function. I was stuck between 25% function and 10% function, but couldn't figure out how to reason between the two of them. +  
neil_simmons  The question says the mother has a mutation known to cause 50% decrease in beta-globin gene function of one allele. So if one allele is working at 50% (B+) and the other allele is working at 0% (B0), then that would mean that particular set of alleles would function at 25%. +  


submitted by brethren_md(87),
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eakM a nuptetn aserqu hitw a srosc of B +B dan B B;0 B+ ersserpnte 50% ntcnifou elhiw 0B pnserreset 0% u(l)nl u.ninocft So ni ihts cse,a eht ndhuasb odwlu ahve a B 0B epoytgen elhiw hte ifew sha a B +B .otnypgee

osrCs fo etseh wto lliw erlstu ni eth lfgloinwo nytes;epog BB, B,B0 ,B+B B+0B B B = 001% ouif,nnct B+B = 57% onin,utfc 0BB = %05 nuiotfn,c +0BB = 2%5 nfuoicnt

oS het wrsnae wlli eb 1 ni 4 have a %52 tnociufn gvine teh et.oynpsge

tyrionwill  how about the choice of D: 1 in 4 have 50% function, which is true. shall 50% function needs transfusion? +  
tyrionwill  In FA, it defines beta thalassemia into minor (HbA2 >3.5%) and major (both HbF and HbA2 go further up), and the major needs transfusion frequently. How can we take this classification based upon quantitive way like in this question? how much percentage of function left does not need a frequent transfusion? +  
azibird  D says one in TWO, not one in FOUR. +2  
hemehero  Is there a way to know that B+B0 will = 25% function. I was stuck between 25% function and 10% function, but couldn't figure out how to reason between the two of them. +  
neil_simmons  The question says the mother has a mutation known to cause 50% decrease in beta-globin gene function of one allele. So if one allele is working at 50% (B+) and the other allele is working at 0% (B0), then that would mean that particular set of alleles would function at 25%. +  


submitted by tyrionwill(15),

probably only 2 parasites are related to nodules: 1. trichinella spiralis: muscle mass, muscle ache, systemic symptoms 2. onchocerca volvulus: skin nodules, without significant systemic signs until blindness

tyrionwill  probably cannot find any abnormality on the skin surface or no obvious mass found along body. only biopsy from the painful muscle can detect the larve of trichinella spiralis. however, skin change due to onchocerca is popular to be easily found when doing PE +  


submitted by yotsubato(964),
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dnKi of tkricy ustioqe.n heT oosnyeizpht rea unleoqchori ei.nstsart tBu eth espeisc amy ton eb.

P. Fcuraamipl is ntrtaisse nad loosk liek a naanb,a tub you ndot wnko if eth lraaami in het BRC si cluarafpim ro .nto

tyrionwill  whether resistant or sensitive, depends on the region, not on the species falci coming from Hatii could be sensitive +  


submitted by nutcraker(4),
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ksoLo ilek easbT dsiorals typeuplhnyaoro ot ,em 19 oy/ tiwh osls of irctpoo,popien prasa.sihse.a.t

tyrionwill  also probably B12 deficiency: lost vibration sensory, weakness of extremities, and possible ataxia if more information is collected... Syphilis will not impair muscle strength. +  


submitted by hhsuperhigh(32),
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eTh eidt si rbrdpces,ie so no dnee to rrfee to atidnciie onrm.eya tI si a easc of teh ptitnae a-onnplcemiocn fo tdei. Btu why n'tac evaids the arntpse to stpo r?eibkgicn

therealslimshady  I remember Boards and Beyond said that you never want to pick any statements that sound "scolding", plus it couldn't be much help to just say "stop arguing", it's better to find out information on what's causing the arguing so that you can stop it entirely, which choice B will allow you to do. +  
tyrionwill  stress is the thing to worse the condition of DM, and will be better after being seen, comforted, and accepted. +  


Rituximab

Mechanism = Monoclonal antibody against CD20, which is found on most B-cell neoplasms.

Use = B-cell Non-Hodgkin lymphoma, CLL, ITP, rheumatoid arthritis, TTP, AIHA, MS.

Adv effects = Increased risk of progressive multifocal leukoencephalopathy in patients with JC virus.

tyrionwill  low IgG in response to infection/vaccination leads to broad bacteria and virus infection or reactivation. bacteria: strep pneumonia, Hib virus: JC, HBV, CMV... +  


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DMMA is het olyn hgcelnauoiln ttah hsa pmsatciythe ytcativi sa ti si iddeevr fomr esmentmhhaihpetma ( kolo ta tsi me)an ... htat pnsxilae greevnih.yt

tyrionwill  Yes, good point to remember. In the category of FA stimulants, 2 agents has sympathetic activity: 1)MDMA; 2)PCP +  
jackie_chan  Basically how I solved it, all the other drugs are downers +  
jackie_chan  Even tho ketamine has sympathomemetic effects, they would be widly tripping, they dont call it falling into a K-hole for nothing. +  


submitted by yotsubato(964),
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rhiCn"eld ieixthb eorbhvia outnreigcnn htiw erhti aeg adn etomevnpel"d in eaxlsu uba.es

tyrionwill  mostly the age difference exceeds 4 years trigger so called "incongruent with their age". age incongruence plus signs of being forced, like this case which the 4-year-old boy was found crying, lead to suspicious more on sex abuse than sex play. +2  


Bortezomib, carfilzomib

Mechanism = Proteasome inhibitors, induce arrest at G2-M phase and apoptosis.

Use = Multiple myeloma, mantle cell lymphoma.

Adv Effects = Peripheral neuropathy, herpes zoster reactivation

tyrionwill  under Bortezomib, the proteasome cannot digest viral Ag and presents it to the membrane-bonded MHC-I. Therefore CD8-Tc cannot recognize the host cells containing relapsed VZV. That is probably why shingles is one of the popular side effect of Bortezomib. +  


submitted by krewfoo99(88),
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So yblialsca tahw ihst is gnisay atth NAD lilw be mdtranitste ot the gnopery ton .ASoN R DAN lwli ritpceela ni het G2 shaep dna trsefnar fo DNA atieamrl to ngoyrpe lwli uocrc ni eht M a.heps heT NAR aym be dtuaetm nda kmagni veeictefd rutcd,spo ubt htsi lwli nto mttanrsi nito the ge,rynpo uths not fftinegac eipsces sravuliv bsdea on NAR umat.tnios

bk2458  makes sense!! +  
almondbreeze  good work +1  
tyrionwill  the question asks the reason of no impact on its survival. if a protein translated from a wrong mRNA loses its function, how can we say the bacteria will still survive well? if there is always fatal error happened during mRNA transcription, and always leading to fatal dysfunctional protein, how can the bacteria and its progeny still survive? so the point will be whether the fatal errors will always happen during transcription? I dont know... +  
tyrionwill  actually FA and NBME seem to have made a wrong statement that RNA polymerase has no proofreading function. RNA polymerase has more fidelity to DNA than DNA polymerase by 2 ways: 1) highly selection of correct nucleotide, and 2) proofreading. (Jasmin F Sydow and Patrick Cramer, RNA polymerase fidelity and transcriptional proofreading: https://pure.mpg.de/rest/items/item_1940413/component/file_1940417/content) however, if survival of the species refers only to the reproduction of progeny, mRNA mutation has nothing with the progeny. +1  


submitted by krewfoo99(88),
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So iasalclyb htwa ihst si syangi that AND iwll be mdtnatretsi ot teh pynrgoe tno N AoS.R DNA lilw pitcrelae in eht 2G phesa nad searntrf fo DAN eratmila to nogprye ilwl cocur in het M hsae.p Teh RAN amy eb metatdu adn gnmkia eftveidec rstdcoup, tbu isht liwl not ntmratsi iotn teh neypgro, thsu not nfacftgie scieesp saivvrlu bdaes on ARN namttiu.so

bk2458  makes sense!! +  
almondbreeze  good work +1  
tyrionwill  the question asks the reason of no impact on its survival. if a protein translated from a wrong mRNA loses its function, how can we say the bacteria will still survive well? if there is always fatal error happened during mRNA transcription, and always leading to fatal dysfunctional protein, how can the bacteria and its progeny still survive? so the point will be whether the fatal errors will always happen during transcription? I dont know... +  
tyrionwill  actually FA and NBME seem to have made a wrong statement that RNA polymerase has no proofreading function. RNA polymerase has more fidelity to DNA than DNA polymerase by 2 ways: 1) highly selection of correct nucleotide, and 2) proofreading. (Jasmin F Sydow and Patrick Cramer, RNA polymerase fidelity and transcriptional proofreading: https://pure.mpg.de/rest/items/item_1940413/component/file_1940417/content) however, if survival of the species refers only to the reproduction of progeny, mRNA mutation has nothing with the progeny. +1  


submitted by nor16(57),
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in ß aaesiTlsham teher si HbA2 ncarsiee nad HAb ar,seesdec veen in , +ß mrlaon rpioehcoseltrse sluer hsti t.ou aesm fro -))CA

tyrionwill  Yes! The key point is the normal electrophoresis. Hemoglobin will not show any abnormalities until least one single allele of Hb fully develops mutation. alpha chain of Hb is contributed by two points within one single allele, while beta chain of Hb is made of only one point in one single allele, therefore: -- in alpha thalassemia Hb electrophoresis will be normal if only one point gets mutation, i.e., aa/a- which we call it the "minima type". If two points get mutation, i.e., cis aa/--, or trans a-/a-, the "minor type", the Hb electrophoresis will be either abnormal(Hb Barts 3-8%) or still normal. overall, we assume the parent both are the minima type, so their children have 50% chance to be the minor type, 25% to be fully normal, and 25% to be the trans minor. -- However in beta thalassemia, the mutation of one allele will lead to whole allele changed, so we just need the mutation once to generate an abnormal Hb electrophoresis result. +1  


submitted by sajaqua1(518),
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acysa,imGteon pidsre ,iotamgnaa nda pymidhasnoog s(a well sa amralp mre)htyea aer lal gniss fo scsexe .eogrtsne The leirv in pantetis thiw hapeitc asseide si rimipeda dan so toncna lcear enserotg sfft.lniueyci xiS 12 oz sebre adily 72( zo, ro hlaf a alnlgo) is oot hmc,u dan is yrdsnoiteg shi l.iver

uslme123  No hepatosplenomegaly, ascites, or edema through me off. We that being said, I shied away from cirrhosis. I thought that he showed signed of depression, so I went with the thyroid. But who's to say he isn't injection anabolic steroids?! +5  
catch-22  The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum. +12  
notadoctor  He likely has hepatitis B/C given his history of intravenous drug use. I believe both can have liver dysfunction but may or may not have ascites, whereas the type of damage we would expect from alcohol that would match this presentation would also show ascites. +  
charcot_bouchard  For Ascities u need to have portal HTN. Thats a must. (unless exudative cause like Malignancy) +2  
paulkarr  For anyone who needs it; the FA photo is kinda burned into my mind for these questions. NBME has some weird infatuation with this clinical presentation.. FA (2019) Pg: 383 "Cirrhosis and Portal HTN". +4  
snripper  @paulkarr the problem was that the FA image was burned into my mind so without no ascites or edema threw me off of cirrhosis. +  
tyrionwill  cirrhosis doesn't present hepatomegaly, instead, the liver could be shrunken. +1  
avocadotoast  Cirrhosis (most likely due to alcoholism in this patient) leads to an increase in sex hormone binding globulin, causing a relative increase in estrogen compared to androgens. Cirrhosis doesn't always have to present with ascites and adema. I agree with @catch-22 that liver disease is a spectrum. This patient does not have ascites because his liver is still able to produce enough albumin to maintain oncotic pressure in the blood. +1  


submitted by sajaqua1(518),
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cseBaeu teh baybs' rtoemh has pyTe 1 basteeiD esitulm,l it is aluiplbes ahtt heyt had eletadev blodo olcgesu vllees irgund ro sortlyh refeob h.brti uInslin sdeo nto ossrc het aa,ectpln but soulegc eos,d so udnrgi rithb het nnoeaet olwdu heav bene ylmecyiehrcp.g siTh dwlou leda ot eht aetnolna aeparsnc sginaelre isuli,nn iidgnvr ulgecso toin slcle nda utnnigr wond ueneleiggso;oncs thsi is yhw het ybab is mccyhgipeloy grhit nwo.

)B sderDceae gyonclge tncctioenr-noa I 'dotn wonk eth onlegcgy cornntiecaont adopcrme to an ultda teint,pa btu a erdeesca in cggenlyo nietacnrctono doulw diinctea geesc/lnolyocgug lsaee,re hiwch olduw nto be a olchgmyyciep .teast C) dcrDeseae nggycoel aehsnsyt iatctyi-v redseadce engyolcg syhsneat yitvtaic diianects ngeeyr olis,amtabc nda oldwu aled to rhgeih msure csogule ls.leve )D rDsedeeac uemrs snlniiu ncct-onorienat esdaedrec rusem snlinui ouwdl edla to igrehh lseelv fo luseogc in suemr. )E eIacdnsre umers ulikilisnn-e wthrgo tac-rof FGI does not idbn raynel as ellw ot usilinn rescotper as usninil ,sdoe adn so lwdou veha ot eb ni lxmeertey hhgi tntrnconoiasec ot aevh isth tc.feef FGI is aeociadsts hiwt isaotmc trhwog nda mceusl emle.otvpned

yotsubato  His glycogen concentration is high, since he's been hyperglycemic with lots of insulin until birth. +3  
alexb  Also explains why he's 12 pounds. +3  
krewfoo99  Also, think of it like this: Insulin causes hypoglycemia, thus this baby must have increased insulin. It is also an anaobolic hormone which is clear by the babys weight. Insulin increases glycogen synthase activity, and causes an increase in concentrations of glycogen. Decrease in insulin would do exactly the opposite +1  
tyrionwill  fetus of a mom with DM will develop pancreatic beta cell hyperplasia, which leads to insulinemia trying to reduce the blood glucose. after birth, the excessive blood glucose will be automatically withdrawn while the insulin at that moment is still high, which leads to hypoglycemia. +2  


submitted by uslme123(57),
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shTi tqusnoie semka no nesse to .em eSh sah an eexmerylt wlo nneipgo usepserr ety has gsisn of sneiacerd tlnacraniira esrpr.eus diD ethy anme to utp 32 cm ??0???2?H???

uslme123  Standard lab values are incorrect, way to go NBME. +3  
wutuwantbruv  I think they mean to put mm Hg. Normal CSF pressure is about 100-180 mm H20 which equates to about 8-15 mm Hg. +3  
alexb  I lost a bit of time wondering about that ugh lol +1  
mjmejora  I thought there must be an obstruction in the ventricles somewhere preventing csf from getting to the spine. so pressure is low in spinal tap but in the head it must be really high. +2  
donttrustmyanswers  Does anyone have clarification on this question? +  
llamastep1  Pseudo tumor cerebri can have normal ICP. Who knew +  
tyrionwill  Hi, mjmejora, MRI did not see anything abnormality, couldn't this mean that there was no obstruction in the ventricles? +1  


submitted by usmleuser007(370),
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MVN otg .it

tJus I:YeFt h IC wsa detsat to eb orfm 11106-1 ihtw 9%5 nda eamn fo 3,.1o1 S on erhite ehert rea wto DS no ireeht dises of 113 the( )mane thta gvie the .%59

=1-13116 3 wtnhii 2DS vbaeo hte nmae 0-1 31=11 3 inihtw S2D lwboe het mena

3 iiedvdd yb the 2 SD = 51. rep SD.

ot etg rmfo 9%5 to %99 you hvea to aiporconter one mreo DS 3( S)D on treeih eidss fo hte mean 3(11)

oerrThe;fe ta 99% IC =-1115.0 081. 5 IC 61+.5=11 571.1

Rnuod htsee up dan uoy egt -181108

tyrionwill  95%CI = M ± Z(SE) instead of SD 116-113 = 3 within 2SE, not 2SD SE = SD/extract the square root of n = SD/2 and SD = 2SE +  
tyrionwill  Sorry I made a mistake, neglect the abobe +  
tyrionwill  if you use Mean ± 2SD = 95%CI to know SD, then use Mean ± 3SD to only know 99.7%CI, a bit larger than 99%CI +  


submitted by usmleuser007(370),
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VMN got ti.

suJt h :FYtIe CI aws astdte ot eb omfr 1061-11 ihwt 9%5 nda maen fo ,11 oS.3 no eihetr teehr rea otw SD on rehiet iessd of 311 th(e en)ma hatt give the %95.

1111-=36 3 nhiwit SD2 obeva hte eanm 113110-= 3 hntiwi DS2 eblwo het amne

3 eiddivd yb the 2 SD = 5.1 erp S.D

ot get ofrm 59% to 99% yuo hvea ot neortpicora eon emro DS 3( SD) no erehit edssi fo eht aemn ()113

Tr;ehefeor at %99 CI 10=-.511 01 5.8 CI 5161+1.= 1175.

unoRd teehs up dan ouy egt 08-1811

tyrionwill  95%CI = M ± Z(SE) instead of SD 116-113 = 3 within 2SE, not 2SD SE = SD/extract the square root of n = SD/2 and SD = 2SE +  
tyrionwill  Sorry I made a mistake, neglect the abobe +  
tyrionwill  if you use Mean ± 2SD = 95%CI to know SD, then use Mean ± 3SD to only know 99.7%CI, a bit larger than 99%CI +  


submitted by usmleuser007(370),
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MVN otg ti.

Jtus FYt:ehI CI was edtats ot be mfor 01111-6 with 9%5 dan nema of ,31.o S1 no eeirth rtehe rae two DS no rheiet ssedi of 311 ht(e ne)ma atth eigv hte 95%.

613-1=11 3 hniwti S2D ovbea het eman 111= 1-03 3 ithinw DS2 owbel eth eman

3 vieddid by the 2 SD = .51 erp S.D

to teg rmof %59 ot %99 uyo veah to nerrotpiaoc eno eomr SD (3 DS) no riteeh dessi fo teh neam 1)1(3

oer;efreTh at %99 IC 115.1-=0 8 0.15 IC 1+6=1.15 .1517

uRnod stehe pu adn uoy get 1-81810

tyrionwill  95%CI = M ± Z(SE) instead of SD 116-113 = 3 within 2SE, not 2SD SE = SD/extract the square root of n = SD/2 and SD = 2SE +  
tyrionwill  Sorry I made a mistake, neglect the abobe +  
tyrionwill  if you use Mean ± 2SD = 95%CI to know SD, then use Mean ± 3SD to only know 99.7%CI, a bit larger than 99%CI +  


submitted by mousie(209),
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hyw seod rtenmetta fo tirdpoyyohh (wtih hvteeooxlryin I'm gsnsim)au eaiecrsn rkis rfo ohy?ymtap I ohesc ti ympsil cb sti a cmnmoo sdveaer effcet of atisnts but I tnod' yerall dasentdnur ohw enatrtig dmyishphtooryi at hte msae miet ldwuo hvae nthiyagn to od hitw it ??? eplh l!asepe

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


submitted by hungrybox(963),

Fucking NBME test writers lmao

Me: "Wait... isn't the answer 25.9? How come I don't see it here."

NBME: "Oh yeah, we rounded it."

Me: "To 30? I don't see that here, either..."

NBME: "No, to 28.8"

tyrionwill  When I got 25.9 and found nothing exactly matched, I guessed that the maintenance dose might be a bit more due to the bioavailability. So this antibiotic probably was not an I.V. formula, but an oral one, with a roughly 90% BA. +2  
eradionova  Well then it could have been equally likely that it had a 50% BA and the answer would be 51.8 exactly. I almost considered picking that but in the end stuck with the one that was closest to my answer lol +2