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Welcome to osler_weber_rendu’s page.
Contributor score: 55

Comments ...

 +4  (nbme17#21)

What you can see is

1.Hyperkeratosis (thickened stratum corneum) 2.Parakeratosis (you can see the nuclei very clearly in the stratum corneum) 3.Dysplasia (notice keratinocytes hyperchromatic and large nuclei go up almost all the way to the top. This isnt so in normal skin)

all this fits actinic keratosis

cassdawg  Actinic keratosis is FA2020 p482 if anyone needs it! +4
baja_blast  FA2019 p. 472 +1

 +0  (free120#15)

Monoclonal Antibodies are always last resort! I just use this as a general rule

Subcomments ...

submitted by rolubui(10),

1) Alcohol withdrawal --> seizure

2) Seizure --> increased release of catecholamines (, also BP of 180/100 indicates high levels of catecholamines

3) Major hormones that shift K+ intracellularly are insulin & beta-2-adrenergic agonists (e.g. epinephrine (

4) Also they are asking why serum K+ is low, NOT why urine K+ is high

osler_weber_rendu  Point 4) above helps you RULE OUT MUSCLE BREAKDOWN. It will cause initial hyperkalemia. Hypokalemia, if at all happens weeks later in ATN. +2  
hungrybox  Thanks for explaining why it's not muscle breakdown. Was stuck on that one. +  

submitted by sympathetikey(980),
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sHtoeni cttayieolna owlasl rfo nolexaiatr fo hte ADN os atth iptontrcisnra nac peroe.dc All santr citrnoie icad asuecs eht tuoesnrlcgay in ALPM ot uhrfert tauer,m wchhi urseeqri DAN riicnpnatotrs / tia.ltnsnoar

osler_weber_rendu  The questions asks for response to ATRA. Should that not be decreased transcription to treat the cancer? Which makes methyl transferase (aka methylation) the more likely answer +1  
pg32  @osler, no @sympathetikey is correct. ATRA's mechanism in treating APML is to encourage the cells to mature. Maturation would require gene transcription, meaning histone acetylases would be used. +  
nnp  but ATRA is letting transcription of an abnormal protein ( that is 15:17 translocation) +2  
lowyield  i believe the mechanism of APML is that the compound protein is ineffective at allowing for maturation of the blasts. giving ATRA allows the blasts to circumnavigate this step, relieving the backup +3  

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hTe tapntie sah ANT ecaoyndrs to nlera ceims.iah eDu ot atrulbu oenssicr, hte taipetn illw evah na eatdvele e.aNF hTe stanpet'i nurie llwi sola eb ,tidlue ubt hsti ilwl be eeeftldcr by the wlo reuni loyism,alto ont eth NFae

mousie  Hypotension can also cause pre renal azotemia with a FENa <1%.... How do you know this is ischemic ATN and not hypotension induced Prerenal Azotemia? +7  
sympathetikey  I had the same thought as you @mousie, but I think "azotemia" and low urine output push it more towards ATN (looking back; I got it wrong too). Plus, the initially MVC / muscle damage probably caused some tubule injury by itself. +2  
ajo  This might help clarify why the pt. has ATN rather than pre renal azotemia. The question did mention, though subtly, that the bleeding was controlled. That most likely indicates that his hypovolemia has been corrected. Developing azotemia 24 hrs after correction of hypovolemia is more suggestive of ATN (since he doesn't have hypovolemia anymore). I hope that helps and feel free to correct me, if I am wrong. +25  
ajo  In addition to my earlier comment, I just noticed the question also explicitly mentioned that he was fully volume restored. Which is consistent with my earlier assumption! +13  
gh889  Although initially, hypotension causes prerenal azotemia, the volume correction pushes you away from prerenal azotemia. but they want you to remember that in hypovolemia, the kidneys are also becoming ischemic, and so development of azotemia 24 hours later is more indicative of intrarenal azotemia due to ATN +  
sugaplum  for anyone who wants to see it: FA 2019 pg591 +1  
divya  i'm confused about one thing. if the tubules aren't working like they should, the bun:cr ratio falls right? doesn't that essentially mean azotemia reduces too? +  
osler_weber_rendu  Lets all take a moment to admire how shit this question is "Bp 90/60.""Repeated episodes of hypotension in the OR" and still the answer is ATN +4  
donttrustmyanswers  @osler_wever_rendu ATN can be caused by ischemia. +1  

The receptor in question is a G protein receptor on the pituitary mass. This would be the GHRH receptor. The GH receptor will be present downstream so that GH released from the pituitary can bind to it (these are JAK/STAT receptors). GHRH receptors are G¬s receptors. These receptors are bound at the alpha-subunit to GDP in the inactive state. When GHRH binds they activated when GTP attaches to the alpha-subunit instead. And thereby promotoes adenyl cyclase activity. GTPase is responsible to cleave this GTP from the alpha subunit to switch of the receptoe. Therefor a lack of GTPase activity will render he Gs receptor in a prolonged on state  Increased activity of Adenyl Cyclase.

osler_weber_rendu  Brilliant explanation +  

submitted by gh889(89),
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The neaswr is ued ot na enietxcpo etnouidl reeh eerhw nanici is uesd ni tps /wo tebsiead ohw vhae efratyrocr erlpdaiereymtigrciyh at high kris or sah a xh fo istcri.aepatn

I garee htat fsteirba are srfti enli (adn so odes atth cleait)r but NEMB asw gohinn in on a ciifpsce poexteinc ahtt nancii cna aosl be ueds enics DLLV nad GsT ear hihg in r.eriieatyhgmeiycdlrp

ehT l""ceu tyhe ahd was et"urrecnr irisn"tptaeac cihhw si olsepyspud a dlea waostrd .ninica

I aosl ptu arineces D..L.H.

wutuwantbruv  Correct, you would not want to give fibrates to someone with recurrent pancreatitis since fibrates increase the risk of cholesterol gallstones due to inhibition of cholesterol 7α-hydroxylase. +  
kernicterusthefrog  FYI @gh889 can't follow your link w/o an NYIT username and password, unless there's a more tech-savvy way around that.. I appreciate the info, though. Niacin rx for familial hypertriglyceridemia w/ recurrent pancreatitis. Now I know.. +2  
impostersyndromel1000  Great points, very in depth knowledge taking place here. Also, familial hypertriglyceridemia (per FA 2019 pg 94) has hepatic overproduction of VLDL so picking this would have been the easiest answer (in retrospect) +1  
hyperfukus  @impostersyndrome1000 literally that's the ONE thing i remembered and i went YOLO lol cuz i was staring for a while +  
osler_weber_rendu  @gh889 I agree niacin is the answer, but even niacin causes increase in HDL. As if getting to the drug wasnt tough enough, NBME puts two of its actions in the options! What a shit question +1  
mtkilimanjaro  I forget where I saw (maybe UWorld), but I always thought increasing HDL is never really a primary form of lipid control. You want to lower the bad cholesterol etc. since increasing good cholesterol wont change LDL VLDL etc. +  

submitted by usmleuser007(326),
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tIuitcensnpouss is ellyeagrn aesucd by a ckaolbeg ni eth IG acrtt esduac by a ro,tmu ,pploy tuiiecd,uvrml ro sjut iomyibtmil at atpr of the

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hpsbwz  Meckel diverticulum itself occurs in 2% of the population. Also it would present much sooner rather than in a 28 year old man. +  
osler_weber_rendu  Meckels is an incidental finding in 98% patients. (only 2% symptomatic) It is a well known lead point for intussusception +1  

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Can ynoane pnleaix hwy iFurbso srcsa wthi lmspaa eclsl si nto the ccretro ?asrnew

osler_weber_rendu  Exactly. Three months can fall under chronic rejection as well. FA pg 119 states "interstitial fibrosis". Chronic rejection is predominantly Bcell mediated (plasma cells). +  
beto  chornic rejection > 6 month acute < 6 month +2  
beto  also there are no B cells in the site of fibrosis. humoral response due to antibody themself,not by direct B cells response +2  

submitted by usmleuser007(326),
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In asecs fo hldic ro uatld aseub

1) fi teerh is lerac deencvei shcu as fi a ldhic etsast tath ptseran pihsnu by iti,htng dchli is hinwgos rfea fo parnte ---- llca hlcdi pcrotonite igtrh aayw ( don't eend to wiat dan a)sk

)2 esam ightn eogs for hte dluat ubt llca teh autdl ntoctrioep secsrvie

osler_weber_rendu  Does anyone not remember Dr Daugherty's lessons which said domestic violence on adults is NOT necessary to report? Instead help them find an escape route in case of an emergency and encourage them to report it themselves. +  
makinallkindzofgainz  @osler_weber_rendu: Domestic violence is not the same thing as dependent adult abuse, such as a special needs adult or an elderly adult (basically anyone who depends on others for care). What you said applies IF the adult is living independently and fully capable to make their own decisions. +6  

submitted by meatus(1),
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'mI orrys utb hwat ma I iinsgsm .ee.r.h I tohthug eth wehlo otnpi fo urciisetd is to otcercr mlvoue drvoeaol yb seis?uidr How lodwu ttoal elomvu be n?ca?deersi

niboonsh  the question is asking what would happen to the URINARY ph, bicarb, and volume. dont worry, i misread the question too -_- +12  
link981  Also misread the question, thought about the lab volumes of the BLOOD smh +5  
hyperfukus  yooooo me too!!! this is the second NBME i did this on they purposely don't write urine on the arrow categories to mess u up i swear!!! AHHHHHH +2  
medulla  missed this question for the same reason .. still pissed +2  
osler_weber_rendu  I DID NOT READ "URINARY" OH NOOOOOO. Im so dumb. +2  

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mullerplouis  To add to this it causes Meningoencephalitis. Look out for confusion and brain signs mixed with signs of meningitis. Only a handful of organisms that cause both. +2  
osler_weber_rendu  Am I the only one who thought portal of entry cant be through a nerve and just ignored all the nerves? +18  
luciana  @osler_weber_rendu I thought the same... I knew it was through cribriform plate, but not that was actually through the nerve +6  
paperbackwriter  @osler_weber_rendu yeah same here, otherwise would have been a much simpler question +  
melchior  In line with the thinking above, SketchyMicro teaches it as if it just passes through the cribriform plate, ignoring the nerves. Wikipedia says that it actually enters the nerves, then passes through the plate. +2  

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pRiesoinhlta hitw efomrr etntspia rea lrneyegla ednwofr o,n tbu yeetr’h ycelapisle pmalteiorbc fi teh tiptaen saw a ctrhspacyii enitat,p sa hte orewp eamalbnci fo eth niotpeatcitine-rprat onetripihsla and noifnaoimrt eth prdiroev si pvyri to euecbsa of iethr aitpetn reca evtloneinvm repueldc a thlayeh lcanebad plrthseianoi fo sequa.l

osler_weber_rendu  But what if she hot? +2  

submitted by gonyyong(83),
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eTh kdi sha atoiymscaegn due to peurtyb (sceesx rtoeestoetsn → hotTsignee r)s geso aawy aulnaylrt elypnrtap(a in 21 to 18 s)mhtno

I tkhni uoy tnd'o aevh to do bdloo stste escbeua eh sah noalmr xselua vnpeeotemdl orf ihs ega dna rehet era no roteh ?ssngi

osler_weber_rendu  How does telling an "embarrassed kid" that he will have big tits for 12-18 months help?! +20  
howdywhat  my exact thought, telling him that it will last for somewhere around a year and a half doesnt seem so reassuring +1  
suckitnbme  I thought it was reassuring in that the kid is being told this isn't permanent as well as that this isn't something serious. It's important to inform him about the prognosis. +6  
thotcandy  "don't worry your gynecomastia isn't permanent, but the mental scars from the bullying you will receive in HS definitely will be :) good luck!" +2  
therealslimshady  What is the gynecomastia is from a prolactinoma? +  
misterdoctor69  @therealslimshady the gynecomastia is from the sudden surge of testosterone during puberty being converted into estrogen => more breast tissue. +1