invite friends ⋅ share email twitter ⋅ join discord whatsapp(2ck)
support the site ⋅ become a member ⋅ unscramble the egg
free120  nbme24  nbme23  nbme22  nbme21  nbme20  nbme19  nbme18  nbme17  nbme16  nbme15  nbme13 
Welcome to bharatpillai’s page.
Contributor score: 17


Comments ...

 +5  (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/ +1

 +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.


 +0  (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 +  


unscramble the site ⋅ become a member ($35/month)

Weilh E ilco si norlam tgu ,lroaf uryo ybod duolw eprfre ti tysa lnmlauia.ntir

tallerthanmymom  Just remember that E.Coli and Bacteriodes Fragilis (sp?) are the 2 main gutys that cause intraperitoneal infections from the gut. +3  
bharatpillai  Why not citrobacter though? +4  
mamed  Common organisms involved in gangrenous and perforated appendicitis include Escherichia coli, Peptostreptococcus, Bacteroides fragilis, and Pseudomonas species (UpToDate) +3  


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(24),
unscramble the site ⋅ become a member ($35/month)

hisT ntsqouei has a tol fo anwres ,opiosnt dna oyu ravrei ta ihtNsehroilaspi yb orhnwtgi uot lal het ohret stpiono by ahtw si igim.sns

A, B - rColatci iNeocrss dan ayilpalPr Nierssco soamlt ywaasl occru in eth igtents of iaichme.s yilosrPvue lhythae 82 yaer odl anm sah on evieecnd of ganfcltiynsii secreedda ernal orpni.esuf

C - cutAe buaTrul rioesNcs si whta oyu uldosh itnkh fo htwi lyelcatiaS )ANID(S oyixctti. erThe rea ynam eotrh cieoxonrhtp usdrg atht aseuc ,NAT btu knthi fo TNA as gurd uindcde kidney adagme.

D - tCissyti - aknFl anpi is dlrteae ot diyenk uij,rny otn rddbeal dema.ga sCsittyi dlcuo eb eiopblss in ndagesnic I,TU tbu teh atneipt sah no eerfv nda si male hmuc( esls cmmnoo ni lse.a)m

E - eorrlheilmnstGpoui - Tsih esgt into tnpee/ihrotnpriihcc osryd.snme Teh stem nioesntm atth eh sah obldo ni het euinr which may deal uyo wodn eth eithnpcri htp,ayaw ubt he dsoe otn veha any fo eth othre itaecssaod psytm.oms

F - ppoheayrerHmn - toAhner owdr fro anRle eCll aCnmicra.o oN wiethg slos or thore cnearc etdrale mtsmpyso (etfgaiu .tec)

G - ttlnateriIis ripheNtsi - hsiT is ofnet a dugr iudecnd MEUNIM ditmdeae y.cxpiroottineh hisT si a ypet IV etetishiyiyvnspr crteinao ttha uoscrc keswe to omstnh ratfe het arstt of tdnimceaoi ki(el N)ISD.sA NAT si erom daaisotcse tiwh dgru ovdereos iwehl rtetlniIatsi is roem ceaitssoda wtih eumnim ano.riect tIrtailsnei ierhsNpit lwli hvae WBC tscsa in iren.u

I - hyeitPnlioespr - seuaCd by isndcenga TUI tbu no freve si te.rpens

ihsT eesavl Niissphtlirehoa (H) sa hte erctorc aesnr.w 8%5 of Nirhhitessplaio si tasdieacos wiht cpaytiohve wbloe sus.don ehT npia fro nhiaiephliossrt nca sraeelp dan ,irmet nad clyaoalnsoci hte apni nac eartvl rfom the nyeikd fkn(la p)ina to hte rtcsmuo sa the otnes vmsoe tuorhhg teh u.erter

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. +3  
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(29),

Pathoma 2018 edition page 4 chapter 1 - Cellular Injury - III. Reversible & irreversible cellular injury - B.1.

I had difficulty trying to figure out what hydropic change means though...

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(68),
unscramble the site ⋅ become a member ($35/month)

sSuond ikel a prirehyhcpto sar.c ythricoep"prH rscsa itnncao plrrymiai eypt III enloaclg nirotdee aleallpr to the pmeredlai feursca htwi nntbudaa nseludo ncationgin aomtsoyib,srfbl lager rxaculeatlelr lngeaocl fminsatel dan tlpfnulei icciad ua.rshmysalcidc"eopco 0/.h/..MComm/gs8s/nnw97P:iwtcevl.c//n3wiplabhcpi2trt2

johnthurtjr  I think it may actually be a keloid, not a hypertrophic scar, as it expands beyond the borders of the original incision. +4  
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 +3  
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(64),

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  


What makes this coxsackie virus over Adenovirus? Both cause myocarditis which would be seen on autopsy? Is it just more common to get coxsackie?

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(70),
unscramble the site ⋅ become a member ($35/month)

egaillnelo : reyv mmoocn ni anvdecda ga,e DPC,O rnepusmsusdopiem stnaietp dna " gngio akbc mofr a ineeecsdr lh"la wchhi roplbbya dah a nedtimcaotan AX ymsest (aclibayls tisf verye eon in het )Q

danoe X : wulod esnpter ihtw stnvcctuiojini, ttohar niap .ulf.. vsiur: nto noeveyer gto teh sasedei :SV R on riclhdne rs pet :npmeuo lwduo gattre a rrlega ialptounop of yhethal opleep as .elwl

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  


submitted by hayayah(1000),
unscramble the site ⋅ become a member ($35/month)

ecoi,tN teh etsm ysas s"pesrroroc in eth nsik"

3D cia(orofhclc)eell mrof xuerspeo of inks us(tatrm albse)a to sun, oiinngest fo ihsf, li,mk al.npts

2D acree(grlcoi)lfo romf tsiennigo fo satl,np fugi,n as.ytse

ohtB retovndec to O5-H2 3D gtr(oesa o)mfr in ielrv and to hte vceati mfro 252,O1)(H- 3D )rlitcoi(lca in ekny.id

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. +6  
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! +3  
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(1000),
unscramble the site ⋅ become a member ($35/month)

e,ociNt the stem assy "orrrscespo ni het skin"

D3 fc(acle)colieolhr romf euesporx of niks t(armtus )ebalsa to sun, nsiionteg of fshi, li,km lsta.pn

2D orcgileear(oflc) ofrm osnigtien fo n,lapst ngu,if yta.ess

thoB oernvdtce ot 25-HO 3D easrtg(o rofm) ni vlrei and to eth iavcet mrof (5),-H221O 3D arci)(ltloic ni dei.ynk

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. +6  
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! +3  
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