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Actinic keratosis is FA2020 p482 if anyone needs it!
Sweet name @osler_weber_rendu #represent #cureHHT
Point 4) above helps you RULE OUT MUSCLE BREAKDOWN. It will cause initial hyperkalemia. Hypokalemia, if at all happens weeks later in ATN.
Thanks for explaining why it's not muscle breakdown. Was stuck on that one.
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
@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.
but ATRA is letting transcription of an abnormal protein ( that is 15:17 translocation)
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
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?
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.
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.
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!
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
for anyone who wants to see it: FA 2019 pg591
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?
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
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.
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..
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)
@impostersyndrome1000 literally that's the ONE thing i remembered and i went YOLO lol cuz i was staring for a while
@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
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.
@mtkilimanjaro I believe it was in BnB. Dr.Ryan mentioned that there hasn't been enough evidence that raising HDL would be beneficial as far as lipid control goes. Better studies were done on statins hence why they are usually first line Tx.
Meckel diverticulum itself occurs in 2% of the population.
Also it would present much sooner rather than in a 28 year old man.
Meckels is an incidental finding in 98% patients. (only 2% symptomatic)
It is a well known lead point for intussusception
Exactly. Three months can fall under chronic rejection as well.
FA pg 119 states "interstitial fibrosis".
Chronic rejection is predominantly Bcell mediated (plasma cells).
chornic rejection > 6 month
acute < 6 month
also there are no B cells in the site of fibrosis. humoral response due to antibody themself,not by direct B cells response
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.
@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.
the question is asking what would happen to the URINARY ph, bicarb, and volume. dont worry, i misread the question too -_-
Also misread the question, thought about the lab volumes of the BLOOD smh
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
missed this question for the same reason .. still pissed
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.
Am I the only one who thought portal of entry cant be through a nerve and just ignored all the nerves?
@osler_weber_rendu I thought the same... I knew it was through cribriform plate, but not that was actually through the nerve
@osler_weber_rendu yeah same here, otherwise would have been a much simpler question
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.
this is such an AWFUL disease, I worked in a hospital in south carolina where it happens A LOT and there's nothing at all you can do for them. When your cells go to phagocytose it it has an outer layer it sheds off like how a lizzard will sacrifice its tail when attacked by a predator.
How does telling an "embarrassed kid" that he will have big tits for 12-18 months help?!
my exact thought, telling him that it will last for somewhere around a year and a half doesnt seem so reassuring
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.
"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!"
What is the gynecomastia is from a prolactinoma?
@therealslimshady the gynecomastia is from the sudden surge of testosterone during puberty being converted into estrogen => more breast tissue.
My breasts are not rubbery nodules, thank you very much!