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Welcome to atstillisafraud’s page.
Contributor score: 156

Comments ...

 +8  (nbme24#28)
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emryiDtsa ( so,al sasoeididanyikd dna tioninetn omertr) is raaletl cuelbe.erml E).(

iaaxtA si a lobepmr whit hte eancrlt mreeelbclu ()D ro at aslte stath the best I uocdl emoc up htw.i

ronald-dumsfeld  I actually think D is pointing at the Flocculonodular lobe. See here: So a lesion at D would present with Nystagmus +3
urachus  flocculonodular is medial (central). but yes it'll have nystagmus and truncal ataxia +

 +47  (nbme24#35)
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Tnkha ouy NBME orf teh hgih uatylqi u.spertic tI seamk ethse xmsae rsetss free nda

sympathetikey  Feels bad man. +3
zoggybiscuits  Those Sclera sure look blue. wow. +11
yotsubato  the same girl shows up on so many NBME exams its not even funny. Its just like that poor kidney that's cut in half that shows up in all kidney questions. +9
aneurysmclip  I turned my brightness up and down 2 times to make sure it wasn't my brightness messing with the sclera. I'm declaring it, NBME stands for "Naturally Bad at Making Exams" . +4
peqmd  $60 a pop and no competitors...That's what happen when there's a monopoly. +3
peqmd  Actually they used their best software to generate images. You might have heard it before, it's called MS Paint. Quite legendary. +3
feochromocytoma  It feels like they cranked up the contrast and saturation on a normal eye to make it look "blue"... +4

 +54  (nbme24#42)
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I liek isht suqoitne eacsbue ti mniesrd me ttah ieeaxmsrn nthik cejtosb acn teixs in 2

 +4  (nbme22#11)
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i-inPkcNamen sasDeie erestpsn iwth atlenm aireatdrnto, ipdli ladne (oamf cells) in ebno rmoraw dan crrhye dre stpo no m.aacul oN sionygieaepmsnhl russtel ni dulpibu fo gohipnlsyinem hwhic ibldsu up ni osmgacher.ap

meningitis  "Pick your **Big** **Foamie** **Zeibra** nose with your Sphinger" Choose options with the letter I. SpIngomyelin, Sphingomyelinase, bIgorgans (hepatomegaly etc), zeIbra bodies, Foam cells +1

 +5  (nbme22#38)
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mPreei ahs no stacanufrt

egntiiosnAn II - etrnaedeg in pahileooymv

plmtiyoliDa cilhteni aak daililpiheohcndpoilahptytomyls lgnu ntsuaraftc

pyitiohnhslodatsolPi obip-hshp5e,4ast aka IP2P Gq rrceepto aawytph

rhhlpdeePyiastonis -dlvioevn in tciiinrns patsiosop hwen xepdose on rcretuxlaella ruefascs

oplnSniieghmy - oesspmoc neyilm and sola ahs esrlo ni lgansi u,dtnnrcsotai oioppasts. :cLtieinh gnlSnoeyimhip itrao t;&g2 idisncate rumeta flaet g.nslu

endochondral1  how are we supposed to know that dipalmitoyl lecithin is the same thing as dipalmitorylphosphatidylcholine +5
qfever  FA 2019 page 647 Pulmonary surfactant is a complex mix of lecithins, the most important of which is dipalmitoylphosphatidylcholine (DPPC). Also: Screening tests for fetal lung maturity: lecithin- sphingomyelin (L/S) ratio in amniotic fluid (≥ 2 is healthy; < 1.5 predictive of NRDS) +9

 -8  (nbme22#48)
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esntioQu is naskig tbuoa tlnaedpscuae gromnsais figincnet GCD apstti.en El.ioc is saol cse.taleundpa Cna enyaon pnadxe on i?tsh

keycompany  Step pneumonia is the most common pathogenic organism in CGD, and the most common cause of pneumonia, otitis media, meningits, and sepsis. While CGD are at an increased risk of encapsulated E. coli infections, however, they are at MOST risk for S. pneumo. This is kind of just a memorization fact that you need to know about S. pneumo. +
keycompany  Sorry english is clearly not my shit, but you get the point +
biliarytree220  CGD is susceptible against catalase-positive organisms (FA 109), of which S. aureus is the one to look out for. It's not about encapsulated organisms, like I had it confused in my head. +6
.ooo.   You are completely right about E.Coli being encapsulated and is also a CAT+ organism and patients with CGD would have an increased risk of infection for both S. Aureus and E. Coli. How you narrow down the two is the most common infections are S. Aureus and Aspergillus (FA 109 like mentioned above) and also using the pneumonic "Cats Need PLACESS to Belch their Hairballs" (FA 128) Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E.Coli, Staphylococci, Serratia, B cepacia, H pylori +6

 -1  (nbme22#25)
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ismaitneH cseusa liyaarplc trelarrioa dolntiai (raedeces stsnc(esiderarence)ia srersuep in hte rplyaclai abueecs senrfetfe imnear eht mase iez)s siemiatHn aslo assieercn alrcpyila ibpl.iyeermta

 -4  (nbme22#23)
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muoiugAbs tnoeqsui utb in seuaecb ti si arely ohk,sc ereth is ont uhenog miet to etaicavt teh ASRA to neearcsi ieynkd n.oifersup

makinallkindzofgainz  This is not an ambiguous question. It makes perfect sense. +3
khaleb  In early shock you have increased SVR due to vasoconstriction. This would cause increased flow to the kidney. I could be wrong but I think what makes that answer incorrect is NOT that RAAS hasn't been activated yet. It is what is causing vasoconstriction via Angiotensin II. What is possibly wrong about that answer is that it says via sympathetic stimulation. I do think it is a little vague between those two answers though. Because you can get sympathetic activation of the RAAS system causing vasoconstriction and blood shunted to vital organs such as the kidneys. Bottom line is you can't argue with weak pulse during hypovolemic shock.... so an obvious right answer. You could make a case for the increased blood flow to the kidney though. +

 +5  (nbme22#31)
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ghtiWe osls - kihtn omeyHacnerai pctrna - DISAH ormf lmlsa cell nugl aEedcramenc + DVJ - CVS nomsdrye

peridot  I was thinking lung cancer secreting SIADH, resulting in hyponatremia. But because the question asked specifically about the cause of the facial edema, I put hyponatremia (answer choice C). I was wondering how you guys were able to differentiate between C. hyponatremia and E. lung cancer? Thank you! +1
mannan  The first thing that crossed my mind was SVC syndrome from the cancer obstructing the R brachiocephalic vein preventing venous blood from returning to the heart (and staying in the facial area). Also I assume Hyponatremia would be equivalent to decreased body volume so there wouldn't be edema. FA Renal physiology section has a good chart on what happens during electrolyte imbalances (hypo and hyper) +1
mannan  @peridot +1
peridot  I was thinking that hyponatremia would be more loss of osmotic pressure --> edema, but I definitely see the argument for a mass that's simply blocking blood flow. Thank you! +

 +11  (nbme22#15)
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ngitlyaAkl natesg eerletaiohhrm(mc)n (het hteor gsudr dlseti aer cbtemrilouu )isihtoibnr nisereac het srik fo A.LM

keycompany  Additionally, AML is the only answer choice that has multiple blast forms (myeloblasts, promyelocytes, etc.). ALL is characterized by a single blast form (lymphoblasts). +25
seagull  CML has blasts too but they tend to favor mature forms. +4
kash1f  You see numerous blast forms == AML, which is characterized by >20% blasts +4
keycompany  The answer choices are all of lymphoid origin except for AML and Hodgkin Disease. We know Hodgkin Disease is a lymphoma (not leukemia) and would present with lymphadenoapthy. So the answer must be AML #testtakingstrategies +12
impostersyndromel1000  @atstillisafraud thanks for mentioning the merchlorethamine increasing risk for AML, i was trying to make a connection with the drugs but couldnt. Had to lean on the test taking skills just like key company +1
sweetmed  Procarbazine is alkylating as well. +
pg32  @keycompany how did you know the phrase "multiple blast forms" meant literally different types of blasts and not just many blast cells were seen? +3
castlblack  this link says CLL has 'large lymphocytic variety' under the picture of the peripheral smear. I am not arguing against you, just researching here +

Subcomments ...

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tsaM lcsle dlaarget,eun dcugiprno ieitanhsm ihhcw atrsttca oo.pnsihesli The relay etags of an gcrlaile tanoicer si smta lelc itedd,ame ubt eth aetl satge nd(icgniul cumsu d)pctoronui si edadetmi by .lsonpihiseo

atstillisafraud  Thanks for a good answer. This question made me feel like I was taking T21 pills +15  
medguru2295  Thank you- I was really thinking this question had 2 correct answers... of course my dumbass picked Mast cells. +3  
ajss  where do i find this info?? +  
paperbackwriter  @ajss pg 112 of first aid 2019, under type I hypersensitivity. Immediate --> mast cells releasing histamine and tryptase, late--> eosinophils and leukotrienes recruited via chemokines +2  
graciewacie9  Wow, i missed the fact that the question is asking for the RESULT of the reaction, NOT the cause of the reaction. Mast cells cause the initial reaction, eosinophils would be the result of the eosinophils. *facepalm +2  
greentea733  @graciewacie9 SAME UGH +  
lba9587  Pathophys (as far as I understand it)...Mast cell degranulates, thus the phospholipid bilayer et. Al are left behind and needs to be degraded. Who comes in? Our good friend eosinophils, as they contain Major Basic Protein (responsible from breakdown of expired mast cell). Note, you can tie this in to the delayed Leukotriene effects of an allergic rxn, as the bilayer is also broken down by arach. Acid. (See this link to support my credibility +  

submitted by beeip(118),
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tyInilbia to vtleaee eth aelatp segtgssu daemag of het asguv ernev.

.F N(C )X

atstillisafraud  I guess F is the vagus nerve. Thanks to NBME I am also training to become a mind reader. +25  
seagull  Thanks to the NBME I have crippling depression +32  
drdoom  bonus cadaver diagram via @mcl +2