to snoo-finity ... and beyond!
Welcome to gh889's page.
Contributor score: 41
You might be able to damage the superficial peroneal nerve with damage to the lateral malleolus but the description in the stem has deficits in the end targets of both the deep and superficial peroneal nerves
I guess he is asking about integrate,,,,, where his should be integrated into host dna to get replicated .. triple therapy includes. 2drugs NRTIs and other one is integrate
@ususmle NRTIs would still inhibit DNA synthesis since they mess with the reverse transcriptase which is needed to make viral DNA.
So, this says sympathetic also spared and hypothalamus also spared. Then what was wrong with this clinical case??
i think the sympathetic system is actually impaired b/c it's cut before it can "outflow"...at least it's the only way this makes sense
I agree. I think the question stem is saying the sympathetics were lesioned. Not that they were spared.
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
1) label D (VLDL -->ILD --> LDL) = anything that increased LPL = Fibrates which use PPAR-alpha (Rx) are good at reducing [VLDL]; therefore, less VLDL means more ILD.
2) VLDL --> fatty acid oxidation = using fats (TAGs) for energy production
Here PPAR-gamma plays a role= which are Thiazolidinediones (also called glitazones) are a class of medicines that may be used for the treatment of type 2 diabetes. They are also good at reducing serum TAGs
Note VLDL are very rich in TAGs
How do you differentiate this from hypertonicity of the internal anal sphincter?
nvm. im dumb lol
How do you differentiate this from hypertonicity of the internal anal sphincter?
nvm. im dumb lol
I agree that it's confusing but I looked at it as a physical *obstruction* since it's impinging on the airway.... but yeah idk this is weird
Doesn't the trachea have cartilage rings so it wouldn't collapse which makes it seem less like a typical obstructive disorder? I'm really not sure why FVC would change because I don't see how total lung capacity or residual volume would change because those are static conditions where there is no airflow at all. I understand FEV1, peak expiratory flow, peak inspiratory flow etc.
Agree this is a really tough Q but I also think I really over thought it... I eliminated all with a normal Ratio bc something obstructing would obviously produce an obstructive pattern although I don't know why FVC would be decreased. I wasn't sure about both peak expiratory and inspiration flow being decreased can someone help me with this or tell me I'm totally overthinking again.. are they both decreased simply bc theres an obstruction ..?
Yea I got confused on this question. But I guess they wanted us to look at it as a obstructive disease . If this were the case all of those function tests would dec. ( See FA )
Because the obstruction is above the alveolar regions there is a decrease in air flow, not lung volumes, which would make this an obstructive pathology.
FVC here dec same way it dec in Obstructive lung disease. Read the concept of Equal pressure point of BnB. There he says in bronchitis we have onstructive pattern because inflammed airways gen more resistance. so EPP comes early. I guess here due to tracheal narrowing pressure inc downstream. which collapses smaller airway. result in air trapping.
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?
The Boards and Beyond video of SC strokes was really helpful at explaining this if you are a video kind of person!
What pushed me away from pons was "dysarthric speech" which implied she still could speak to some degree.... which made me pick medulla.
I think FA may be misleading. Primarily it will effect the Pons because that is where the majority of the Basilar Artery is located. and I guess it could effect the other locations? but everywhere I have looked Locked-in syndrome is an issue with the Pons. But someone please continue to clarify, cause I was a bit tripped up at first with this question
Although FA says it can be pons, medulla, or lower midbrain, "locked-in" syndrome generally arises from BL pons lesions. Another way you can rule out medulla and midbrain in this question is the ocular movement findings. Since the patient has impaired horizontal gaze BL, you can conclude that the Abducens nuclei are involved on both sides. The abducens nuclei are located in the pons.
USMLE secrets also states that it is most commonly in the pons
Bates states that locked-in syndrome preserves consciousness but these patients have limited speaking ability
So do we just have to memorize this...
I think the small intestine narrows as you go along, so jejunum would most likely intuss into the duodenum.
Duodenum is fixed to the retroperitoneal wall, and also has lots of named vessels attached to it, along with the pancreaticobiliary duct and ampulla. It cant really intussuscept.
You should also know that the duodenum is almost purely on the right side of the body
I think you're right, FA2019 pp444 even states that sensory to the scrotum is via the Genitofemoral nerve
nice! I reasoned it as that most of the GI system is of endodermal origin
Sorry about the format, it came out wrong but I hope his helps.
looks good to me!
According to FA2019, stage 2 ends at 11, stage 3 starts 11.5-13, and stage 4 starts at 13-15, where did you get your info from?
You can change it to ENDS at 11, ENDS at 13, ENDS at 14... I simply have it as a range just like you stated in a couple of them. The importance is in how the kid presents because he/she will have some things mature but others not, the age will vary in questions.
stage 3 breast mound is for females not males btw
see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females
this is just too funny, I LOVE it! xD
I think you meant 2(29/30)(1/30) just to clarify!
i am confusion
You have to use the hardy weinberg formula (1=p^2+2qp+q^2)and p + q = 1 they basically tell you that q^2=1/900 which makes q=1/30 now you can figure out (p=1-q) so p=1-(1/30), p=29/30 then to figure out carrier you solve for 2qp, 2(29/30)(1/30)=1/15 I got it wrong cuz I forgot how to figure out p but hopefully wont happen on the real deal.
2pq= 2(29/30)(1/30).... Transform this to 2 1 1 2 1
x x = _ = ____
1 1 30 30 15
Nevermind :/ It didn't come out as planned :(
How do we know this disease is autosomal recessive? I assumed it was just because they love these carrier frequency questions with AR diseases, but how do we know it's AR?
My issue was the stem said no skin damage (I would think pulling out your hair damages your scalp)
[Turns out it does not](http://onlinelibrary.wiley.com/doi/full/10.1111/j.1529-8019.2008.00165.x)
FA 2019, pg 551
Compulsively pulling out one’s own hair. Causes significant distress and persists despite attempts to
stop. Presents with areas of thinning hair or baldness on any area of the body, most commonly the
scalp. Incidence highest in childhood but spans all ages. Treatment: psychotherapy is first line;
medications (eg, clomipramine) may be considered.
Pg 81 Tyrosine is listed as an essential AA. Should be tryptophan for those who got this wrong like me.
But tyrosine can come from phenylalanine, so it's not really essential right?
in FA2019, it is listed as Tryptophan, not Tyrosine. That was corrected.
Note: Tyrosine is ONLY essential with PKU in children
bro FA2018 lists tyrosine as an essential AA. They played us.