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Welcome to bharatpillai’s page.
Contributor score: 22


Comments ...

 +0  (step2ck_form6#27)

SPECT is the other name for a PET scan :/


 +0  (step2ck_form6#19)

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


 +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 +

 +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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Wheli E iolc si mlnaor tug fal,or oyur doby dwulo perefr it tsay .llnnauitrami

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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isTh iouqents has a lot fo raesnw ino,opts and ouy arveri ta aoiNhietlshipsr by hwriognt otu lla het retho piootsn yb wtah si .imsnigs

,A B - laorCcit srsiceNo dna Pairallpy rossNeic almsot awlysa occur in eht nsetgit of iahmies.c youvPirsel hyealht 28 yrea dol amn hsa no eeecivdn fo fltnisyiiangc cedeaedsr rlaen ifronsp.eu

C - Aucte Talruub eicNsosr is hwat uoy dsulho ktihn of wthi iatyaceSll NSA()DI toyt.xici rehTe ear yanm otreh rtocxneohip rdusg htat seacu ,ATN but tiknh fo TNA as urgd ndicedu nykdei mdg.aea

D - iiytsCst - lnaFk anip is rdetlae to deykni ,jniruy otn leraddb agae.md iisCtsty luocd be esplsbio in nadnicgse UIT, tbu het tniatpe hsa no vefer dan si mlea u(mch less momnoc in l)m.aes

E - iiGlmherusprtonole - Tsih egts inot phneinrtipo/rhtecci mssrn.deyo ehT tmes nnmeoits that he ahs loobd ni the eurni hhwic mya ldea ouy wdno teh cniepihtr hyt,aapw tub eh eosd tno vahe ayn fo het rthoe scadisaoet mstoypm.s

F - pHnoerheamrpy - rneAhto drwo for neRla lCel Coaimnacr. oN whgtie lsso ro rhote ceanrc ealerdt mtosmpsy uta(geif .etc)

G - Irtltsnitaei psireNiht - siTh si otfne a grud dueindc IMUMEN ddmieate yx.eitpctrohnoi sihT is a eytp IV tsiiypiyeternhsv oicanter ttah ocusrc ekwes ot smtnho tafer the sratt of ndoiaimtce i(kle s.DIA)NS NAT si meor iceosdtaas wthi gudr drovseeo ewlih strnIatielit si more aeotdcaiss hitw mniume eio.atcrn atisnltierI sirtNieph lwli haev WBC tcsas in iru.ne

I - ylohpteirsienP - sauedC by cnaidsnge TUI btu no evref si r.tepens

hTsi aeevsl riNphlaisteoihs H() sa eht tecrcro a.rnesw 85% of eisraihltNiosph is csotsidaae wtih yavoteciph bowle dss.uon heT pina fro lnritpsasieohhi acn rselpea dna t,eirm and ciocanlolysa teh ainp acn rlaetv morf hte ynkied kafn(l i)nap to teh rsmutco as het eonst ovsem rtuhohg eth .reuert

whoissaad  Great explanation. Always found it hard to differentiate between ATN and AIN due to NSAID use. This made it clear. Thanks! +3  
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. +4  
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(45),
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mtaoahP 0812 onteiid paeg c4aepr th 1 - llraleuC nuyrIj - II.I sbleierveR mp;a& erlebiirsrev cleullar rjuniy - .1B.

I dah iicuyftldf rynigt ot ruegfi uot twha iyorcdhp heganc msena ugothh...

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(82),
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Sdunso ielk a crthoeirpyph rsc.a itohHyprpcre" scasr nciaotn rlyamriip ptey III nlogecal etedorin perlaall ot the maeelidrp ucsrfea wtih ndnbuata eounlds tnoinignca s,obbitflmaoyrs lgare llteraraclxeu clnalego asifnteml dna fnietullp dciica eslccdpoumsy".aichaor ciei.bC8/wapvg/w2.Mn.m/9cs/0pm.iPnl/nt7tt2ho:3hcrsw/l

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(78),

I think that if they had something like "statin therapy" as an answer choice, we would have an argument for that as it would decrease mortality by helping prevent ANOTHER heart attack. However, I think that anti-depressant therapy will do a LOT to prevent suicide, while omega-3 fatty acids (healthy as they are) wouldn't do AS MUCH to prevent a heart attack.

The question is basically asking, "You can only prescribe one of these to keep this dude alive as long as possible. Which one will have the best chance at accomplishing that?"

Therefore, the answer should be anti-depressant therapy.

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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ahtW aesmk sith csocekxai rivus over ued?iAvorns oBth cesau osiiractdym ciwhh doulw eb nese no osyp?tau Is ti utjs oemr omncmo to etg aesc?ckoix

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(74),
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inallgeole : ervy ocmomn ni andvaedc ag,e OCDP, ompusrneissmudep teianstp adn " noigg cakb ormf a ieescnedr lal"h iwhch rpboably dha a oacnetitnmda AX messty iayla(lscb isft rveey eon ni eht )Q

ndeoa X : duwol etpsner twhi svo,itntjucnici rthtao pina ...f lu uirsv: tno onevyree got het asedeis S:R V no lnicdhre rsept enu:omp olduw gartet a erlarg plputonoai fo elthhay poelep as elw.l

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(1074),
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ei,oNct eht tmes asys ocs"orrprse in hte knis"

3D rllf(eheccc)oaoil mrof ueosxrep fo nisk s(mttuar s)ablea to nsu, tioiesnng fo ,fihs lim,k alnt.ps

2D looe)era(lcrfgci fmro sigtoeinn of l,atpsn inufg, t.yeass

thBo crdnteove ot -5O2H D3 seo(tgar o)rmf ni vlrie adn to eht ctveia mfro 1O(2-,25H) D3 to)crcllia(i ni .yeidkn

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(1074),
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,Notice hte tsme assy oscspreo"rr in het sink"

3D loecar)flhlco(iec frmo uosxepre of kins tutsmr(a bsleaa) to uns, toiignnse of ish,f klim, tlp.nsa

D2 oicacf)e(rrlegol fmro ngtieiosn of s,atnpl u,gnif .yetass

hBot nverodtce ot 2O-H5 3D oas(rteg mrof) in rielv dna ot hte vectai ofrm O,1H-52)2( 3D tiar)oll(cic ni dn.eyki

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