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Welcome to kevin’s page.
Contributor score: 17


Comments ...

 +0  (nbme19#42)

Tubocurarine competitively antagonizes nAchR. Phrenic nerve was still functioning, so the problem was at the neuromuscular junction. Of the answer choices, the only pure NMJ blocker was this

solidshake  Just to show why the other answers are wrong: Lidocaine - Blocks Na channels, Morphine Sulfate - mu opioid receptor blocker, Pentobarbitol - increased duration of GABA-A channel thus increased Cl thus decreased nerve firing, Potassium Chloride - replenish K, Tetrodotoxin - Blocks Na channels. Question shows Phrenic nerve trying to make the diaphram move with Ach release but fails because Tubocurarine is a competitive antagonist of Ach at the NMJ. +2

 +3  (nbme20#34)

Empathize, then open ended question. Doesn't matter how dumb it is, if it ticks that box it's right


 +0  (nbme21#46)

Li Fraumeni, Tp53 mutation. SBBLA cancers

  • sarcoma

  • brain

  • breast

  • lung

  • adrenal

kevin  leukemia not lung, sorry +

 +0  (nbme21#14)

Asplenic, think SHiN (Strep pneumo, Haemophilus, Neisseria). Do not bother with any other encapsulated organisms


 +0  (nbme21#28)

statin + fibrate = myopathy. possibly most HY pharm principle tested


 +0  (nbme21#44)

Double Flip — If R. Lower quadrantanopia --> L. Upper (Parietal) lesion.

Just remember Double Flip


 +2  (nbme22#11)

Just to clarify all the comments.

  • (B) Rectus innervation would not be as deep as the spermatic cord (thoracoabdominal/intercostal nerves)

  • (A) & (D) are both pudendal nerve, I think it's reasonable to exclude both as an answer choice as such

  • (C) Process of elimination. Sure, we can nitpick if it's genitofemoral or ilioinguinal but I think that's all we're being tested on here





Subcomments ...

submitted by azibird(158),

How can we differentiate RSV from the common cold? Is it the bilateral, diffuse wheezes and expiratory rhonchi? Along with the intercostal retractions, signifying significant respiratory problems?

nbmeanswersownersucks  I was initially thinking it was rhinovirus too but in retrospect I think the wheezes etc make RSV more likely +2  
kevin  The key demographic for RSV is infants (<2yo), so based on age alone RSV is what they're going for imo. +3  
lpp06  Signs of respiratory distress = bronchiolitis over rhinovirus +1  


submitted by cassdawg(938),

Penicillin can cause a direct Coombs + autoimmune hemolytic anemia

The Direct Coomb's test involves anti-Ig antibody (Coombs reagent) added to patient’s RBCs. RBCs agglutinate if the RBCs are already coated with antibodies (indicating that the body is making antibodies that bind the RBCs). RBCs tagged with antibodies are destroyed in the spleen. Penicillin is thought to act as a hapten binding with proteins on the RBCs and triggering an antibody response against the penicillin-RBC complex [FA2020 p423]

cbreland  To add, LDH would be increased with many types of hemolytic anemia. Not be the best answer, not as specific +  
kevin  Penicillins and cephalosporins act as haptens, alpha-methyldopa causes direct Abs against self Ag on RBC. - Dr. Sattar +2  


submitted by anjum(15),

7-dehydrocholesterol is a form of pre-vitamin D3 synthesized in the skin from UBV. It is converted to Cholecalciferol, which is the inactive form of Vitamin D3 that is actually in first aid.

kevin  Cholecalciferol is synthesized from 7-dehydrocholesterol by UV, but yes, correct +  
i_hate_it_here  Didn't know the products of it were considered hormones my bad i guess +  


submitted by johnthurtjr(139),
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ilhWe I nca get on ordba with Auetnjdtms ,sDridero I 'todn ese how tihs waresn si nya etbetr than Siatocm Stymmpo oDdsr.rei oFmr A:F

Vaytrie fo ybidol otmisnlpac sngilta tmhons ot yesar atadoiessc whit v,eesxecis issetnetrp uhgttsho and ieanxty touab ptmsy.oms yMa pocpre-aa whit .lliesns

SDS goblsne ni a guopr of edrossrid chetacrraediz yb ihpscayl ptmsmosy uginsca igfntnsacii ristssed nda etranmmi.ip

savdaddy  I think part of it stems from the fact that this patients symptoms are occurring within the time-frame for adjustment disorder while SSD seems to have a longer timeline. Aside from that I find it difficult to see why SSD wasn't a possible answer. +4  
chillqd  To add to that, I inferred that the obsession with checking temp and with the tingling sensation were signs provided to him by the physicians of recurrence. He is anxious over his cancer recurring, and they are more specific than a variety of body complaints +1  
hello  In somatic symptom disorder, the motivation is unconscious. I think for the patient in this Q-stem, his motivation is conscious -- he wants to make sure that recurrence of cancer is not going "undetected". +13  
cienfuegos  I also had issues differentiating these two and ultimately went with SSD, but upon further review it seems that a key differentiating feature was the timeline. His somatic symptoms would have had to have been present for at least 6 months per the DSM criteria https://www.ncbi.nlm.nih.gov/books/NBK519704/table/ch3.t31/ +3  
almondbreeze  @chillqd Same! Why not OCD? He's fearful that something bad might happen (=cancer relapse; obsession) and calling his doc (=compulsion) +  
kevin  great reasoning @hello, this was confusing me but that makes perfect sense +  


submitted by rockodude(16),

why couldn't this be platelet dysfunction, option E, like a qualitative platelet disorder even though the quanitative amount of platelets are normal

kevin  She's in her 90s, she would've likely presented with a platelet disorder decades ago. Given the vignette a normal aging process was most likely +1  


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Icolnzoaetra rqsureei het icdaci neerointmvn fo eht mschato to be sod.rbbea rzeemlopaO nbihiits teh HK+/+ upmp fo het ,oshtmca rbehtey cndegrasie hte icaiytd of het atcho.sm So newh het eintpat satek polzaeeOrm nda rtlneoaacIoz rot,eethg neolIoaacztr 'tnow be adoesrbb toin hte d.yob tThsa' hyw ti ash on teefc.f

sIt' comeedmdern to teka iisnaotedmc at stael 2 oshur rriop ot kgitan an cianta.d

necrotizingfasciitis  Just adding support to the above explanation: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3671798/ +3  
pakimd  do all azoles or just itraconazole only requires an acidic environment to be absorbed? +2  
chandlerbas  just itraconazole and posaconazole +5  
lilyo  @chandlerbas, where did you find this information? I was looking over this on FA but they do not mention it and I would like a bit more information. Thanks! +5  
chandlerbas  haha no stress! the article above submitted by @necrotizingfasciitis does a descent job explaining it, however its not good enough, I looked into a bit more on uptodate but wasn't fruitful in my endeavours. goodluck! +  
haozhier  How are we supposed to know this!! It is not in UWORLD or FA right? +7  
kevin  Someone said it on here, since there was no CYP inducer of the answer choices, the only way to even think about an answer to this question was to just go with a less acidic environment from the PPI affecting absorption. It was simply the only reasonable answer choice, I don't think there's any way we were expected to know of this exact interaction prior +  
aoa05  Golan pharm book states the exact same thing. Cannot be given to patients with acholrhydria. +  


submitted by hayayah(1057),
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Its' tlsoainniatr llce acarmnic,o wchih mgnksio is a oomcnm skri fctroa fro; ti anc lnvievo eht leanr svsceiye/.acllp hTe hsoti aeimg hsosw het lpiayalrp antuer fo eht umotr ehr(ewov ti can slao eb laft ro unadlro dccagorin ot a.)atoPmh

Asol kwonn as ehlluaiotr aiarcnm.co sMto oomnmc rmtou of nyiarur atcrt mestsy acn( roccu ni larne yclacse, nerla lp,evsi es,urret and )bddlae.r naC eb stueggsed by psainsel maeiauhrt (on )cts.as

usmlecrasher  i'm sorry guys it's bladder cancer blocking urine flow => reflux ureteral widening => reflux nephropathy. +6  
hello_planet  FA 2019 pg 588 +2  
kevin  Is the idea since that since the histology shows transitional cell cancer the most likely is smoking and that's the answer? The fact that this was unilateral really threw me off. Is it common to have unilateral carcinoma of the ureter (if that's what this case was, of the ureter) rather than bilateral? +  
lovebug  I Choose F) vinyl chloride <- only liver angiosarcoma. :( about many Carcinogen FA2019, 226pg. +  


submitted by hellohello(8),

Schistosoma mansoni and haematobium can be ID'd by their unique spines. S. mansoni has a lateral spine as seen on the path while S. haematobium has a terminal spine (S. japonicum has no spine).

See following for path comparisons (mansoni L, haematobium M, japonicum R)

https://www.yourgenome.org/sites/default/files/images/photos/Schistosome%20eggs.jpg

fatboyslim  Schistosoma haemaTobium: spine is on the Tip ("T" for Tip and haemaTobium) and Schistosoma manSoni has a spine on the Side ("S" for manSoni and Side) +2  
kevin  nice +  
thegooddoctor  Excellent explanation! +3  


submitted by laminin(14),
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cTneycierlast hvea a hgih ytafinfi to ofmr asceleht hiwt npeotyvall aletlicm ctnisao such sa F+e,++ +F+,e ,+l+A+ Mg++ and a+C+. nMay fo hsete riteacel-mcttaylne oclpxseme rea irhete onsluileb or ihsewetor rlyopo sbleaarbob fomr teh stot-neiasgnriatl trcta. iMlk adn other daryi rtdp,souc tdaisnac cnagiitonn aloplevnty iosnac,t as lewl as aruvois irno astls gnditese nlytuosileumsa whit clenrceytita rvsteiv,diae thgmi ieefetrnr iwht heirt rsoinaptob by 50 to 09% or nvee mre.o :osc rue :tb.tsinp4omw9.89hm.hide6/5/vncg/pwnu/w.lb

almondbreeze  FA 2019 pg. 192: Do not take tetracyclines with milk (Ca2+), antacids (eg. Ca2+ or Mg2+), or iron-containing preparations b/c divalent cations inhibit drugs' absorption in the gut +1  
fatboyslim  This is also why tetracyclines are teratogenic and should not be given to children because tetracyclines chelate with the calcium in the teeth and cause tooth discoloration and inhibit bone growth in the fetus/growing child (Source: SketchyPharm) +  
kevin  just remember fluoroquinolones also are prone to chelation. you know it's gonna pop up on the real one +  


submitted by hayayah(1057),
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In dorre fro a dgru to be lrcedea yb teh ydien,k it stmu tifrs be ieldrfte ni hte uog.ilrmel grDus hiwt a hgih DV hvea emro of teh rdug in the essuti htat rae not allbvaeia ot eteidlfr by eth .nediky ugsrD with ighh tnieopr dignnib to'nw be dlfeirte teh.rei oS yuo want a urgd hitw wol dV dan olw dingnbi if oyu twan it learecd iva het siknyde and ir.eun

zevvyt  But a low VD corresponds to high Plasma Binding Concentration(FA 233, 2019). That's my main confusion with this question. +2  
kevin  If it's high plasma binding, then it's low Vd. But, low VD doesn't necessarily require high plasma binding. Low Vd can simply be due to it being a large polar molecule +  


submitted by neonem(552),
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siTh teiantp lkylei has osem mfor of prpue otomr erunon nsoeil or diasees - MNU iosnesl aer rcaeacdztihre yb awsenkes, dnaeiercs edpe dnonet sr,eleexf nda stispca assipr.e olnaBcfe is a -ABGAB tnagios ipicfsec ot eth naslip d,orc euds to trate lecmus pca,iiytsst atdyiosn, nda SM. G-AABB is a ni-Grtpeo pdeuocl ecoeprrt uplceod to ,Gi os nsgoiam of thsi cretoerp euscas rpithaaeiorznolyp of het nosunre dan dedercsea esalere of eiyrxcttao .tetalamug

kevin  stimulates K+ efflux (hyperpolarization) and inhibits Ca2+ influx (no vesicle release) +1  
lovebug  FA 2019, 538page !! +  


submitted by fatboyslim(38),

I chose Aspirin. So aspirin is a non-reversible inhibitor of COX-1 and 2 which should decrease TXA2 levels, and according to FA 2020 page 485, TXA2 causes platelet aggregation and increases vascular tone...I'm guessing the overall combined effect of COX 1 & 2 inhibition will cause a net effect of either vasoconstriction or no change to vascular tone?

spaceboy98  Me too. i thought aspirin blocking off the TXA2 production would allow for vasodialation. +1  
kevin  This was a UWorld question. I originally thought the same, it's just cilostazol does the vasodilation and inhibition of platelet activation most directly +  


submitted by neovanilla(35),

The crux of the question is asking, if the patient feels decreased pain (which is driven by opioid molecules; that's why opioids are administered as painkillers), then how do you stop the inhibition? An opioid antagonist (naloxone is the only one that is an antagonist)

neovanilla  wrong answers: b-endorphin - an endorphin and ACTH hormone (similar to ACTH, POMC) that can bind to the µ-opioid receptor Enkephalin - a neurotransmitter involved in the indirect basal ganglia pathway (along with GABA); it can also bind to delta-opioid receptors Morphine - an opioid agonist (used for pain relief) Oxycodone - Another opioid agonist (~same potency as morphine) +3  
kevin  enkephalin, endorphin, dynorphin are the bodies endogenous opioids +  


submitted by apop(6),
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hseeT oeitslpanxna narte ra.egt tI desnot yralle avhe ucmh ot od wiht AASR icvnaoiat.t It sha lsaomt evyietrnhg ot do ihwt a mnpenoenoh alceld teh inlakael .eitd In crhoinc ,titvnmoig you lwdou xpetce C-l to eb wlo adn =K to eb lwo ilsim(ra ot bal rstlsue in oeoenms hwti emilubla.) To antecsoepm rof het olw lC,- het actomhs hsa an aitrrtpnoe cwhih xsgnhecea C-l ofr -3H.OC foThrere,e -lC iwll eb sepdlhneier ni eth ,hstmcoa ewhil OCH3- lwil nsaiecre ni eht ,bdolo iausngc an ssaki.lalo In lotickala teta,ss teh +K+H/ itrenpaort wlil enibg ot cteiaa,tv nigsifth +K ITNO cslel eamlka(yop)ih adn iesnacrgni H.p RSAA bporbyla lysap a orel ni kamnig het akepalmihoy wesro ubt hte klelaina dtie is emro titpraonm .eher

spaceboy98  Isnt alkaline tide related to an increase in pH after meals? Your logic is on point but I'm not sure whether we can apply that concept here. +1  
cp87  If you're already losing chloride through vomiting, why would you push chloride out into the stomach, which would further decrease serum chloride? +  
cp87  You can get contraction alkalosis from vomiting (decreased skin turgor). Therefore, the RAAS system would be activated. +  
kevin  concept can be applied here because we need to replete the Cl- in order to create HCl; the stomach doesn't care if Cl- is low in serum, only that Cl- is low in the parietal cells and so will pump out HCO3- in its expense +  


Is there any drug which would cause enhancement of cell membrane permeability to chloride? It seems like the MOA of ETEC & V. cholerae adenylate cyclase toxins and somewhat that of Ivacaftor used in cystic fibrosis.

kevin  For the purposes of STEP 1 I don't think there is an antibiotic that would do that. If you wanted to really stretch the definition of enhanced cell permeability you could go with a polymixin which is essentially a detergent for bacterial membranes and can be used rarely for pseudomonas and other bacteria +  


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'Im suer si't ledtear ot eth cativagtin eeffct of oortislC on shrm,eenioearfahseenlalyN-hpnnemtlyatt- nonivgertc EN to Epi. dSuons ielk a srtiicgenys tgihn ot .me F()3.A8

kevin  It's permissive because without cortisol Epi wouldn't be able to attain its full effect +  


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mI ton yarlel suer ubt I tihkn eth ipton is thta ithw teh olcprapti ncdliuraedoi snac treeh is a eydal ni icnftoun fo eht ikdy.ne atWh tyeh ednwta us ot embremer ereh is ttha wenh oyu give a " A "iplr ot a anptiet htwi Rlaen yrtear hertsseslocaoir the anelr nutnoicf erwonss cesbaeu etreh si tcnirtosionc fo teh eftrefne raolreiet

AF 8102 - 675

kevin  efferent dilates with an ACE-I due to loss of angiotensin mediated vasoconstriction +  


Decreased sensations over the thumb and anterior forearm indicates a lesion of the c6 dermatome, which is confirmed by the physician's suspicions of c5/6 nerve damage. The MOST SPECIFIC way of confirming this would be to test for deltoid muscle action (abduction of shoulder) since it's innervated by musculocutaneous nerve (c5/c6). Even though other nerves (like radial) also shares roots with c5/c6, testing those nerve functions will not be as specific.

kevin  Axillary controls deltoid not musculocutaneous but otherwise yes +  


submitted by neolidone(0),
  • ACEI prevent the conversion from Angiotensin I to Angiotensin II. It leads to a dilation of the efferent artery which is constricted under ATII's effect.

  • The point of this question is to realize which structure is the efferent artery. In the picture, the label C is Juxtaglomerula cells, the adherent part of the label E is Macula densa of DCT. Those structures are in close contact with the afferent artery to sense sodium and perfusion pressure, so the F is the efferent artery.

kevin  Just look at the arrows; the last one will be efferent since it flows from afferent to efferent +1  


submitted by sklawpirt(28),
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I kihtn het deia reeh is plmsiy atht one odulsh htnik btuao ewher cvleseis are cngimo omrf on tireh yaw to eth ligog expol.mc

T"ow esstp wrraodf dan eno tspe ab.k"c pilyaSclcfe the euistqno aym eb ergnirfer ot a erar aaciornlifac ddi.sorer na earsseawns of that esaesdi is ont csseenary. htWa is ycrsseane si tdnnnsderiuga hte orgnii rmfo ewhre evlissce ear crfketdai to eht lGigo auapsa.prt

COPI opniert is ednede to toac lceevss rmof het ERR to dnes ot io.lgg sThu, htiw a uintamot ni taht pneo,tri the peagkcad isorenpt htta odsulh blbe fof dna be tesn to hte oli,gg adsinet muaaluetcc in eht RRE nda ealdit it. hTus teh ews.nra

63pas(20f-dwctw:20o9hm20h0)2ll/./9/Sp141p.ftw.d/c-j7g/e

hayayah  pg. 47 on FA got the good visuals! +5  
notadoctor  COPII* proteins are needed to coat vesicles from the RER to Golgi. "Two(COPII) steps forward; one(COPI) step back." Anterograde goes RER -> Golgi -> Lysosomes/Secretory Vesicles -> Plasma membrane +22  
titanesxvi  why not small lysosomes? +3  
varunmehru  and I thought large lysosomes due to lack of enzymes to degrade +  
samsam3711  The size of the lysosome is not affected by the presence or absence of protein, but its function is compromised (eg. protein is getting stuck in the RER) +  
fattyacid  I hope this helps to whomever was lost like me Null mutation: A mutation (a change) in a gene that leads to its not being transcribed into RNA and/or translated into a functional protein product. For example, a null mutation in a gene that usually encodes a specific enzyme leads to the production of a nonfunctional enzyme or no enzyme at all. +2  
pingra  I think you made a typo: COPII (RER -> cis-Golgi); COPI (trans-golgi -> cis-golgi and cis-golgi -> RER), clathrin (endocytosis and trans-golgi -> lysosome) +  
kevin  So my thought process was if there is no COP signal then instead of going to Golgi it would be sent astray into cytoplasm, akin to how in I-cell Dx the enzymes get sent out of the cell since there is no trafficking signal (therefore I presumed large lysosome due to eating the aggregated protein). Are we saying without COP or Clathrin that the vesicle will simply stay put where it is? If I can get a reply before my exam (2 weeks) that'd be much appreciated +  


submitted by kevin(17),

Li Fraumeni, Tp53 mutation. SBBLA cancers

  • sarcoma

  • brain

  • breast

  • lung

  • adrenal

kevin  leukemia not lung, sorry +  


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VA aiFutssl ur-eort olbod fmor teh eralatir semtsy to het vuenso syem,st bspis-yagn teh lAroeirste = aIeersnc PL t-g;&-- RESCAINE VR. lAl ni lla = eneacIrs CO.

iAdcocrgn ot Ud,lWor eht reeatsilro ear a oarmj orescu fo itersnasce ... so iyspbnasg teh relieaorst eusrtsl ni a deresaec in tlaTo lrahpriePe aecsnstiRe ... iaugsnc na esciraen ni hte erat adn vuolem fo bolod riurtnnge ot eth eraht. I am ptyret resu reeht si roem to hte yosglhyiop nbhdei s,hit btu I hpeo itsh eadpxilen a l.tetli

big92  "Immediately following creation, arteriovenous fistula (AVF) is associated with an increase in cardiac output (CO), achieved predominantly through a reduction in systemic vascular resistance, increased myocardial contractility, and an increase in stroke volume (SV) and heart rate. Over the following week, circulating blood volume increases in conjunction with increases in atrial and brain natriuretic peptides. These alterations are associated with early increases in left ventricular (LV) filling pressure with the potential for resultant impact on atrial and ventricular chamber dimensions and function." (PMID: 25258554) There's also another study by Epstein from the 1950s looking at the effects of AVF's effect on CO in men (PMID: 13052718). Apparently, the increase in resting CO is a big problem because it can lead to high-output cardiac failure (LVH). +23  
hungrybox  Jesus big92 you went in on the research lmao u must be MSTP +6  
temmy  big92 you are right. that is why pagets disease pagets have high output cardiac failure because of the av shunts. +4  
kevin  what is "increase PL" +2  


submitted by nerdy nik(10),
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TVD that ntew ot eth inarb. fI it wdulo aveh gone to hte nrloauymp rytrae seh luwod vahe a ,PE btu it seocrds hte arait llwa avi a npaett orfnaem eloav dna etwn ilycetrd to hte b.rian

cienfuegos  Some more UW info: incomplete fusion in up to 25% of adults: remain functionally closed until RA > LA pressure (e.g. valsalva), esp. concerning if hypercoagulable (e.g. OCP) -evaluate cryptogenic stroke with buble study: inj agitated nl saline and look for bubbles in left heart +2  
athenathefirst  Are you very sure of this answer? because she is an adult and not a baby anymore so it can't be a patent foramen ovale. +  
teepot123  has not closed basically +  
kevin  cienfuegos is spot on with his explanation @athenathefirst +  


submitted by tinydoc(223),
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xPt rpaapes ot eahv uMlsec itycpatiss sa a urlste of SM. iiapcysStt si rtdaete thiw a selmuc enxratla lkei eoafBnlc hiwch is a ABAG gaots.ni nlteacoaBh is a hlinmiCmtnooiec chwhi nca eb duse to tater rUiarny ndcfyoitsnu ni lltMpeiu csioe.sslr tub eth uQniseto sask htaw ulwod elph raett eht pticiatss.y

athenathefirst  Why not mecamylamine? +  
athenathefirst  Is it because it's MS? So for sure need a GABA agonist +  
kevin  Never heard of mecamylamine, just know UW and FA say Baclofen, GABA-B agonist for spasticity. It's not solely because it's MS, it's just the drug they want us to know for specifically spasticity +  


submitted by adong(95),

Cecum is intraperitoneal even though it's part of the ascending colon

azibird  How were we supposed to know this? Thanks for the clarification. I picked cecum because FA says Crohn is usually the terminal ileum and colon, so I figured cecum would be the most likely vs the descending colon. +10  
kevin  Yeah that's what I thought at first too. Figuring it was a tricky question, I went with descending colon because 1) ascending and descending are retroperitoneal, so we know the latter is for sure right, and 2) cecum has it's own name (ie it's different than the ascending colon), so it probably isn't retroperitoneal in that regard. You can remember ascending and descending are retroperitoneal by remembering the greater omentum wraps around the transverse colon and from anatomy lab that there's a mesoappendix, mesocecum, etc (peritoneal) +  


submitted by nmb29(0),
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I ithgm be kinveigonthr ti t,ub H bond frtanmoio fo 'asa amkes the rsdaoneyc rturteucs fo hte ptoinre anocge(ll in htsi )sec.a Teh yGl ot alA ubstttuosnii seod lsutre in elss H nodb ianorof,mt utb of vniuldiadi saa' otn eneewbt lleconag oleemlcus thta( gihtm be rmeo ofr ruryaqtena euts)rrtuc

lpp06  I think the key is in the answer phrasing, the answer mentioning H-bonds says "Disruption of H-bonds between collagen molecules" Although collagen does undergo H-bonding to support the triple helix, this is done within the same collagen molecule. Linking different collagen molecules occurs via the lysine - hydroxylysine links done in the ECM +1  
kevin  this is the one comment that finally helped me understand why that was incorrect. thank you +  


submitted by taediggity(30),

So this patient is essentially in hypovolemic shock because he's hemorrhaging blood from the aorta.

A) You'd have increased ADH to conserve volume B) You'd have increased BUN:Cr ratio b/c due to a decrease in blood flow C) Increased TPR naturally due to less pressure on barorecptors D) Decreased Capillary hydrostatic pressure b/c they have decreased volume E) Decreased Carotid sinus firing rate b/c less pressure F) The Answer: RAAS is activated -

drzed  (B) You get an increased BUN:Cr ratio because increased urea absorption at the proximal tubule (conservation of water), but you lose the same amount of Cr since none of it is reabsorbed; thus the ratio increases. +5  
kevin  I may be wrong but I think more of the urea (BUN) would be absorbed in medullary collecting duct in this situation due to ADH; think I saw a question on this in uworld, could pop up +  


submitted by waterloo(71),
  • Can't be aplastic anemia if the pt is able to produce other cells evident in the labs.
  • Not DIC bc PT and PTT are normal and not increased.
  • If pt has fulminant liver failure I would imagine they would not be able to produce their coag factors so again, not probably it.
  • Vit B12 Def leads to macrocytic anemia and here they were nice enough to give us MCV which is between 80 and 100.

TTP makes sense with what others said. You can also spot some schistocytes in the blood smear.

kevin  yeah I'm pretty sure schistocytes alone could give you ttp as answer +  
kevin  well that and pt/ptt being normal +  


submitted by waterloo(71),
  • Can't be aplastic anemia if the pt is able to produce other cells evident in the labs.
  • Not DIC bc PT and PTT are normal and not increased.
  • If pt has fulminant liver failure I would imagine they would not be able to produce their coag factors so again, not probably it.
  • Vit B12 Def leads to macrocytic anemia and here they were nice enough to give us MCV which is between 80 and 100.

TTP makes sense with what others said. You can also spot some schistocytes in the blood smear.

kevin  yeah I'm pretty sure schistocytes alone could give you ttp as answer +  
kevin  well that and pt/ptt being normal +  


submitted by meningitis(507),
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kevin  just for people who are taking exam this year, ewing is now understood to be mesenchymal stem cell neoplasm (uworld) +1  


submitted by someduck3(58),
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Fta seoblul smtinaiv rae EA,,K,D. oS tboh D ;&mpa E odcul be ecaeddser in hsti p.t utB yuo eahv to wkno atth tmniiaV E ifyedeccin is soaetadcsi iwht dyiantmeileno pm&a; has nebe itaadescos hwti tesoiprro noclmu eynmlioatidn.e oAsl Vit E acn be nvgie htiw lihmeezrA spttinae sa ti eslhp wthi eref iaa.csld.r?

aesalmon  I actually thought that the posterior column findings were likely due to B12 deficiency - "subactue combined degeneration", due to malabsorption, as we see in this pt (. Turns out vitamin E can also cause symptoms which look like subacute combined degeneration: https://www.ncbi.nlm.nih.gov/pubmed/9012278, as does Copper (TIL): https://www.ncbi.nlm.nih.gov/pubmed/15249607 +3  
jooceman739  Vitamin E deficiency causes posterior column findings and hemolytic anemia :) +5  
nwinkelmann  The way I think about it is that essentially, vitamin E is an anti-oxidant. Vitamin E deficiency = LOTS of oxidation, i.e. free radicals, which are toxic to most cells in the body (particularly myelination and RBCs). That's why it can be used with Alzheimer's patients. +3  
makinallkindzofgainz  Vitamin E presents like B12 deficiency but without megaloblastic anemia +  
kevin  B12 would also affect lateral corticospinal tracts, vit E doesn't to my knowledge (b12 deficiency would also present with hyperreflexia but E deficiency just romberg sign, loss of proprioception and touch, ataxia) +  


submitted by hayayah(1057),
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encngPrya + Hx fo osmrobhtis -g-&;t inhtk tplosadiiihphpon erdymson

Teh TP nad PTT rea rgldpoone dt/ fnrrineectee omfr the nedsotiaib ot hsi.plpshoiopd oimrnbTh time .naolmr

adH to infd rshcraee reatlics otuba it os keat ti rmof reeh dna otnd' aetws ryuo .ti..me

monoloco  yeah, i’ve never heard of antiphospholipids increasing PT time ... +20  
goldenwakosu  Not sure if that little detail was to throw us off. I think the point of the question was to ID antiphospholipid syndrome based on the clinical criteria (spontaneous abortion + thrombosis) +4  
johnthurtjr  I actually went down a rabbit hole with this one recently - essentially in vitro findings =/= in vivo findings, clot-wise with anti-phospholipid antibodies. +3  
link981  No mention of lupus anticoagulant, anticardiolipin, or anti Beta 2 antibodies. FA mentios prolonged PTT but nothing on PT. What a piece of shit question. But thanks to the dudes above who explained it +8  
yb_26  UWorld mentioned "prolong aPTT (and sometimes PT)" in APS +3  
oslerweberrendu  @yb_26 Can u please tell the QID because the one I have seen it says, "Although patients often have prolonged ptt (because the antiphospholipid interferes with ptt test), pt is normal." QID: 1298 +  
kevin  just to clarify, lupus anticoag is in antiphospholipid and presents with paradoxical increased ptt +/- pt despite increase risk thrombosis +1  


submitted by hello(302),
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kevin  saturday night palsy is radial nerve; only hint for axillary was arm abduction +  
anechakfspb  The crutches would affect the radial nerve (FA p440). +1