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Welcome to bharatpillai’s page.
Contributor score: 23


Comments ...

 +0  (step2ck_form8#15)

Oh absolutely not. Primary myelofibrosis ALSO presents with splenomegaly, pancytopenia and immature myeloid cells in the periphery. WBC counts for CML are typically >50,000. WTF is this question?


 +0  (step2ck_form6#27)

SPECT is the other name for a PET scan :/


 +1  (step2ck_form6#19)

Aren't Pl effusions due to CHF ALWAYS bilteral??

tinylilron  no more likely to be bilateral but can be unilateral... if unilateral it is more likely to present on the right side. +

 +4  (free120#19)

Subacute combined degeneration never produces exagerated reflexes. It's one of the causes of babinski + with absent ankle reflex.

melchior  From googling it, it seems that B12 deficiency can produce either hyperreflexia or hyporeflexia. This makes sense, because it causes both UMN lesions (causing hyperreflexia), but it also affects the afferent pathways. https://www.hindawi.com/journals/crinm/2013/159649/ +2

 +0  (nbme24#5)

Just adding on- Xray of large muscle groups would help in diagnosis of cysticercosis since cysts are calcified, in trichinella they are not. I think i'm the only one who got this wrong :/

misterdoctor69  Maybe so, but I think that if we get any questions concerning cysticercosis, it would be neurocysticercosis, so you'd do brain imaging instead... Additionally, as per the CDC: muscle cysticercosis is usually nontender?: https://www.cdc.gov/parasites/cysticercosis/gen_info/faqs.html +
brs  I think everyone who has watched House M.D. S1 E1 gets a chance to make it wrong. +

 +0  (nbme24#42)

IRT is measured in routine heel-prick blood taken for biochemical screening of all newborn infants born in the UK. This test is one of a number of completed in newborn screening (the "Guthrie Test"). In Australia it is known 94% of those with eventual diagnosis of CF have a positive IRT on newborn screen. Samples with a raised IRT (defined as highest 1% of values) are then screened for common CF gene mutations. Each centre has a slightly different gene panel; currently 40-50 of the most common genes are sequenced. However, there are more than 2000 known mutations, so gene panel testing does miss occasional CF patients

If gene testing finds one mutation they will then have a sweat test to help confirm the diagnosis. Sweat testing is more likely to be equivocal in infants and typically not attempted in those under 5kg. If sweat test is positive more expansive gene testing is considered. If two mutations are found they are diagnosed with CF.

bharatpillai  i swear to god some asshat who wrote this question immediately followed it up by making a wikipedia post about it to pretend like this is some common knowledge medical students were supposed to have. +

 +0  (nbme24#6)

One way to look at this would be to go back to pathogenesis of fatty streaks. They are most commonly found at the aortic bifurcation, so basically the lower down you go down the abdominal aorta, more turbulent the flow, causing higher potential for atherosclerosis and stenosis of branch vessels. Also, renal artery stenosis is well described which is given off after the celiac trunk so safe to say celiac trunk is spared in any kind of atherosclerotic stenosis.


 +1  (nbme21#24)

am i the only one who chose mesothelioma? didnt that look like a pleural plaque posteriorly to anyone?

brotherimodu  That's what I thought too. +




Subcomments ...

submitted by dr_pepper(-1),

Quick google search reveals that methylphenidate works by inhibiting dopamine and NE reuptake, Am I missing something here? How is this "release of biogenic neurotransmitters"?

bharatpillai  methyl phenydate and amphetamines act by both stimulating release and inhibiting uptake. cocaine and tcas primarily acts by inhibiting uptake think about it this way- meth is purified and made in the lab so it's more effective at increasing NE and DA levels in the synapse. +  
lola915  They block PRESYNAPTIC NE transporters not postsynaptic +  


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ihWle E lcoi is onrlam tgu or,fal ouyr dboy odlwu epfrer it ytsa mtla.nilnaiur

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


IRT is measured in routine heel-prick blood taken for biochemical screening of all newborn infants born in the UK. This test is one of a number of completed in newborn screening (the "Guthrie Test"). In Australia it is known 94% of those with eventual diagnosis of CF have a positive IRT on newborn screen. Samples with a raised IRT (defined as highest 1% of values) are then screened for common CF gene mutations. Each centre has a slightly different gene panel; currently 40-50 of the most common genes are sequenced. However, there are more than 2000 known mutations, so gene panel testing does miss occasional CF patients

If gene testing finds one mutation they will then have a sweat test to help confirm the diagnosis. Sweat testing is more likely to be equivocal in infants and typically not attempted in those under 5kg. If sweat test is positive more expansive gene testing is considered. If two mutations are found they are diagnosed with CF.

bharatpillai  i swear to god some asshat who wrote this question immediately followed it up by making a wikipedia post about it to pretend like this is some common knowledge medical students were supposed to have. +  


submitted by hopsalong(25),
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sThi eositqun sah a tol of wsaern pionsot, dna uoy iaevrr at hlohiNripaesits yb whnitogr uto lla teh htero instpoo by whta si isgimn.s

A, B - irlcaoCt iorsNcse and ypaarlilP rNiesosc tsalom awasyl roucc ni hte tnesigt of scmih.eia uPreylvosi aehtlyh 82 eyar dlo nam ahs no eevedinc of giintscyainlf eedcseard aenlr fuesp.roin

C - teuAc abuuTlr Nisroces si awth oyu sduhol htkin of whti aaitllyeSc D(SNAI) otti.cxiy heeTr ear aymn ethro irhepxctoon gsudr taht csaue ,NAT ubt hnkit fo NTA sa rugd ecndiud nidkey admea.g

D - iiyCtsts - Fnlka pain is eldtear to ndyeik iju,ryn ton dblarde megad.a itytsiCs cdolu be lseisobp ni ensdgniac IT,U utb the teanpit has no ferev dan si laem mc(hu slse noommc ni esl.)am

E - iineGlrmrpotoluehs - Thsi sgte iotn ehtei/rpritonpcnihc y.drmensso ehT esmt ieonnsmt atht he ash obdol in eth irneu cwhhi mya eadl ouy onwd eht tcnprihei a,wahpty but eh dsoe not evha nay of hte eotrh saecotisad msy.ptosm

F - nperhayremopH - thAeron drwo fro alRen lleC .caCnimroa oN itgweh olss ro ohtre acernc eealtdr oymstsmp i(agefut ).tec

G - rstiatilIetn riNeitpsh - Thsi is ntofe a dgru dnceuid UMMNEI aeedtdim rytiphcnoxi.eot ishT si a tepy VI tyeinyesrtihvspi icaernot htta cursco wksee to tsmhno afert eht trsat fo doitncaiem kie(l .)ANDISs ANT si oemr tacdsosiea whti drug reoovdes elhwi tIlnesaitrit is oerm tcdsaeisao wiht mniemu catnroe.i Islitenirta iNhtripse lilw hvea BWC asstc in nr.iue

I - lnysiehiptoPer - dusCae by deciangsn IUT tbu no veerf si .srtenpe

Thsi eavsle erNoshhaiiptisl H)( sa hte cocrtre snar.we 85% fo isirpiNtlhaoshe is iasoetcsad itwh ayoihevpct owleb ssnod.u heT ipan for asherishtoilinp can srpeael nad rim,te and yncoaclaislo the nipa cna eltarv omrf het kenyid alnfk( )inpa to hte trusocm sa het steon omvse ruohhtg eht rert.ue

whoissaad  Great explanation. Always found it hard to differentiate between ATN and AIN due to NSAID use. This made it clear. Thanks! +4  
hyperfukus  yasss +  
dubywow  "occasionally writhes in pain" -- as a guy who has had a kidney stone, writhing in pain definitely hits the mark. Picture yourself knees on the ground, face on the couch, screaming incoherently while the paramedics are there because you can't control your own body movement and don't know if you're dying or whatnot from the canonball sized hole that (may or may not be) in your flank. Then imagine one of the paramedics is your premed study buddy. Never forget writhing and nephrolithiasis and premed study buddies. You will forever get this question correct in the future. +5  
bharatpillai  i swear to god ive done a similar question on the usmlerx qb and they answer was renal papillary necrosis. which is why i got it wrong :( +  
targetmle  i also remember that uw ques which got me this ques wrong. i think in that ques,patient sibling or he himself had sickle cell +  


submitted by qfever(47),
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otamPah 1208 eotdnii egpa teha4r pc 1 - uraCllle urInyj - I.II Rlebisvere map;& rieebsirvelr lcaeulrl ijnyru - ..B1

I had dlyftcifui grtyin to iefgru uto htaw ypdcohir canheg mnaes .hg.toh.u

bharatpillai  i swear i've done the same question before on uworld/ one of the previous NBMEs and the answer to that was intracellular Ca accumulation. +1  
mangotango  @bharatpillai that's also true! Dec ATP >> dec activity of Ca2+ and Na+/K+ pumps >> cellular swelling (earliest morphologic manifestation of reversible cell injury), mitochondrial swelling --- FA, pg 207 Na+/K+ ATPase inhibited >> inc intracellular Na+ >> dec activity of Ca2+/3Na+ exchange pump >> inc intracellular Ca2+ --- this is the same way digoxin works in the heart! +  


submitted by celeste(84),
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sduoSn kile a phothrrpyice .arcs "ryporehpitHc acrss tnncioa imilrpayr ytep III cagleonl nerieotd ealaplrl to het mlirepead arucfes itwh bnnaautd uolneds goaiincnnt slrbyisto,ambfo agrle urecxlleraatl lgeolacn eftnmiasl and eitnfllpu ciiacd uaasc."eiycosclromdph n/hlPb/msi/mgrl.op..wn9/:vi/c2/iht8t7p.cat0e2CswwM3nc

johnthurtjr  I think it may actually be a keloid, not a hypertrophic scar, as it expands beyond the borders of the original incision. +5  
thepacksurvives  I believe this is a keloid; a hypertrophic scar does not extend past the borders of it's original incision, while a keloid does. regardless, the answer to this question is the same :) +  
breis  First AID pg 219 Scar formation: Hypertrophic vs. Keloid +  
charcot_bouchard  They give granulation tissue is a option which is type 3 collagen. so if it was hypertrophic scar it would be ap problem since its only excessive growth of Type 3. while keloid is excessive growth of both 1 and 3 +4  
bharatpillai  I literally ruled put collagen synthesis defect since this is not a collagen synthesis defect at all ( EDS, Scurvy) :/ hate these kind of questions +  


submitted by mbourne(79),
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I tnkhi atth if eyth ahd tnsohgemi elik ittasn" yr"ephta sa na snarwe hocc,ie we lwdou ahve na uamterng ofr ttah as ti olwud eearcdes yaromittl yb hpnelgi pternev NAHREOT erath t.tacak He,verwo I nkhti htat teen-sdparntais yhterpa llwi od a TOL ot vnpteer ciuedis, lwhie -3eagom ftyta dcais taheh(yl as htye rae) 'nulotwd do SA CUHM ot rventpe a taher ka.tatc

ehT niosqeut is alilbsayc k,signa o"Yu can yoln ebrrsceip oen of tshee ot epke sthi ddeu lviae sa olng sa slpesib.o hWihc noe liwl vahe teh tesb ancceh at shcliinacmpgo "h?tat

rTehefo,er eth raswen ldsuho be depteatann-sris rphte.ay

bharatpillai  why antidepressant therapy though? there are not enough features given to suggest MDD. He's 56 years old, not an elderly single male so not at the highest "classical" population at risk of suicide? the question is so ambiguous... Given MI, wouldn't chronic alcoholic intake predispose him to dilated cardiomyopathy? +  
neovanilla  I don't believe it's that he has MDD by the clinical definition. It's more that his QoL has probably changed drastically since the MI and MIs are strongly associated with decreased outlook on life, especially considering how common it is to get a second MI soon after the first. I don't know the stats on suicide post-MI, but helping the patient's depression to make him more pro-active to help himself prevent another MI would be better than "a diet high in omega 3 FAs" (at least, this was my justification, as mbourne was saying) +  
drzed  First sentence of the stem: he has a 6-week history (e.g. >2 weeks) of depression (1), difficulty sleeping (2), fatigue (3), decreased appetite (4), and poor memory/concentration (5) For a diagnosis of MDD, you need a 2 week history of 5 of the SIGECAPS symptoms which he meets (he is only missing suicidal ideation and interest in activities). Thus he meets the diagnostic criteria for a major depressive episode, which means that treatment is indicated with an SSRI. +1  


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taWh asmke tihs iecxkcsao sruiv rove evsr?ouidnA ohBt seacu sicmaityrdo whihc luodw be enes no uyatos?p sI it tjsu meor nmoomc to tge ea?iokcscx

drdoom  the general consensus appears to be that Coxsackie is more common than Adenovirus, but i haven’t come across any papers or textbooks that would agree (they only mention “Coxsackie” and “Adenovirus” as associations with myocarditis) +1  
bharatpillai  there specifically is a question on uworld in which a young woman gets viral myocarditis with sore throat and the answer to that is adenovirus. i think thats why many people (including me) got it wrong :( +  


submitted by usmle11a(76),
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igleeolanl : vrey cmomon in dadavnec gea, OC,DP iseeduomsuprspmn ttnipsea dan " iggon ackb fomr a esnricdee h"lal whhic brolapby had a eimtntoacand AX esmsty bcllay(isa isft yerve neo in het Q)

aodne X : uwodl strnepe iwth vcitniotjcns,ui httoar napi fu l... vsr:iu ton yveoener got het sdieeas S :VR on nlecihdr rptes :mouepn lodwu argtet a elarrg pnoaloiput of yeahtlh eoeplp as we.ll

bharatpillai  why would they say that the only people who didnt get affected by the disease were people on steroids (lupus nephritis and severe asthma) couldnt have been rsv since it causes croup in children. strep pneumo would cause fever and other systemic signs. i went for adenovirus because uworld says most common causes of copd excacerbation are viral infections... +2  
brbwhat  I went for adeno forr the same reason. I guess the MAIN HINT is that this is not a copd exacerbation. Since people without prexesting copd also had pneumonia, also people with copd exacerbation will have different presenting symptoms, here it was told, that we are told that dx was penumonia. People with copd exacerbation wouldn’t be diagnosed with pneumonia if it was an adenovirus infections. +1  
j44n  adenovirus doesnt cause pneumonia its just makes the current COPD sx worse +  
j44n  the SLE and asthmatic patient were both considered slightly immunosupressed or theyre just more likely to get something (SLE pt= your B cells are too busy making Ig's to kill your kidney, and the asthmatic is on corticosteroids that aopotose your t cells) but they're not COPD patients so the pneumonmia wont be as severe, all in all legionella causes really really bad pneumonia in COPD patients and less severe (pontiac fever) in those with mild immunosupression +2  


submitted by hayayah(1077),
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otNiec, eht mest sasy ops"rcreros in the snik"

D3 c)(oeaorcleihlfcl ofrm oeexrups of nisk uartt(ms l)beasa ot nus, siiegnnto fo isfh, ,lmki ltans.p

D2 geaoocr)cl(efril morf onngeiist fo pln,sat gn,fui .syaste

htBo ontcrdvee to 5H2-O D3 otrae(gs o)rfm in lierv dan to eht ceavit ofrm 25-H(O2,)1 D3 (caocl)iitrl in dein.yk

sympathetikey  C is the 3rd letter in the alphabet. Hence, D3 = Cholecalciferol +4  
karljeon  Thanks for the explanation. The question stem made it sound like "what future step will be decreased?" Actual question: "Decreased production of which... is most LIKELY TO OCCUR in this patient?" Maybe NBME needs a grammar Nazi working for them. +8  
bharatpillai  question says "decreased production of which of the following precursors in skin is most likely to occur in this patient? the answer has to be 7-dehydrocholecalciferol! +5  
bharatpillai  7 dehydrocholesterol +2  
brbwhat  Yeah i did the same, but then realised acc to uw flowchart 7dehydrochole.. is converted to cholecalciferol in presence of uv rays. So the decreased precursor would be cholecalciferol since we already have 7 dehydrocholecalciferol not being converted by uvrays Tho the uw chart sites both ergo and chole as dietary sources. +2  
drzed  Wouldn't 7-dehydrocholesterol build up in the skin? Since UV rays convert 7-dehydrocholesterol into cholecalciferol, if you are lacking the conversion, the reactant (7-dehydrocholesterol) should accumulate. +  
brbwhat  They’re asking decreased production of which of the following precursor would occur? 7 dehydrocholestrol builds up, but decreased production of cholecalciferol takes place, which is a precursor in the pathway for vitamin d formation +1  


submitted by hayayah(1077),
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oeict,N het tmse sasy peocrsr"rso ni the knsi"

3D flalohci(oelce)rc romf pueresox fo iskn t(atsrum )blasae to nus, igsnienot of sifh, iklm, .pnsatl

D2 fcoir)ear(olcleg omfr oensignti fo t,pslan fgniu, .ytasse

ohBt trevcedon ot OH2-5 3D rso(eagt fro)m in irelv nad to eht taciev mofr -)2H2O(,51 D3 rollcaitc(i) ni ykni.ed

sympathetikey  C is the 3rd letter in the alphabet. Hence, D3 = Cholecalciferol +4  
karljeon  Thanks for the explanation. The question stem made it sound like "what future step will be decreased?" Actual question: "Decreased production of which... is most LIKELY TO OCCUR in this patient?" Maybe NBME needs a grammar Nazi working for them. +8  
bharatpillai  question says "decreased production of which of the following precursors in skin is most likely to occur in this patient? the answer has to be 7-dehydrocholecalciferol! +5  
bharatpillai  7 dehydrocholesterol +2  
brbwhat  Yeah i did the same, but then realised acc to uw flowchart 7dehydrochole.. is converted to cholecalciferol in presence of uv rays. So the decreased precursor would be cholecalciferol since we already have 7 dehydrocholecalciferol not being converted by uvrays Tho the uw chart sites both ergo and chole as dietary sources. +2  
drzed  Wouldn't 7-dehydrocholesterol build up in the skin? Since UV rays convert 7-dehydrocholesterol into cholecalciferol, if you are lacking the conversion, the reactant (7-dehydrocholesterol) should accumulate. +  
brbwhat  They’re asking decreased production of which of the following precursor would occur? 7 dehydrocholestrol builds up, but decreased production of cholecalciferol takes place, which is a precursor in the pathway for vitamin d formation +1