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 +2  (nbme23#47)

compression of the common peroneal nerve as it wraps around the neck of the fibula causes decreased sensation from the superficial peroneal nerve, responsible for the anterolateral aspect and dorsum of the leg and foot

Deep peroneal nerve is sensory to the webspace between the hallux and 2nd digit

pic

maxillarythirdmolar  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

 +2  (nbme23#34)

Referring to NRTIs and NNRTIs as mainstay of treatment

Mainstay: efavirenz (NNRTI), tenofovir (NRTI), and emtricitabine (NRTI)

ususmle  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
whoissaad  @ususmle NRTIs would still inhibit DNA synthesis since they mess with the reverse transcriptase which is needed to make viral DNA.

 +2  (nbme22#35)

From ShoryukenHadooken on reddit:

What the question is getting at is the sympathetic chain was spared. It was a terrible way of wording it.

Your anterior hypothalamus is responsible for cooling features and is under parasympathetic control. A lesion would cause hyperthermia.

Your posterior hypothalamus is responsible for heating when you're cold and to generate the Fever response and is under sympathetic control. A lesion would cause hypothermia.

In this question it is simply asking a person gets sick, hypothalamus was spared, what happens.

Answer: hypothalamus will still be able to elevate set body temperature to battle infection.

Hint: IF they give a question similar to this but reworded to include a lesion of the sympathetic fibers or of the hypothalamus, you would in turn NOT be able to generate a fever response to infection. The hypothalamus would be entirely under parasympathetic control

This adds more context to the fact the Q states that the sympathetics was spared

oslerweberrendu  So, this says sympathetic also spared and hypothalamus also spared. Then what was wrong with this clinical case??

 +1  (nbme22#26)

according to uptodate thiazides cause a mild hypovolemic state thus your PCT will see more Na and H2O --> by principle that the PCT always reabsorbs 60% of what it sees, it will reabsorb more water and Na.


 +1  (nbme22#24)

Ketorolac is a reversible NSAID given IV, all NSAIDs have a risk of interstitial nephritis, renal ischemia, gastric ulcers, and aplastic anemia.

the best answer is renal failure b/c it is given IV and has less of a chance of causing gastric ulcers


 +1  (nbme22#42)

answer is leading you to finasteride - 5alpha-reductase inhibitor for BPH and male patterned baldness - it blocks the conversion of testosterone into DHT


 +0  (nbme22#9)

The area labeled C is the spot desmosomes between two myocytes and where actin filaments insert on the sarcolemma

LINK


 +3  (nbme22#2)

The answer is due to an exception outlined here where niacin is used in pts w/o diabetes who have refractory hypertriglyceridemia at high risk or has a hx of pancreatitis.

I agree that fibrates are first line (and so does that article) but NBME was honing in on a specific exception that niacin can also be used since VLDL and TGs are high in hypertriglyceridemia.

The "clue" they had was "recurrent pancreatitis" which is supposedly a lead towards niacin.

I also put increase HDL....

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..
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)
hyperfukus  @impostersyndrome1000 literally that's the ONE thing i remembered and i went YOLO lol cuz i was staring for a while

 +0  (nbme22#35)

Could someone please explain which drugs (if any) are at D and E?

usmleuser007  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




Subcomments ...

submitted by gabeb71(15),

The puborectalis muscle, which is one of the muscles that comprise the pelvic floor and plays an important role in both fecal continence and defecation, is tonically contracted and maintains the anorectal angle at rest.

here is a picture: https://www.123rf.com/photo_46940875_stock-vector-the-rectum-and-anus-showing-the-puborectalis-muscle-part-of-the-levator-ani-used-for-the-control-of-.html

gh889  How do you differentiate this from hypertonicity of the internal anal sphincter? +  
gh889  nvm. im dumb lol +  


submitted by gabeb71(15),

The puborectalis muscle, which is one of the muscles that comprise the pelvic floor and plays an important role in both fecal continence and defecation, is tonically contracted and maintains the anorectal angle at rest.

here is a picture: https://www.123rf.com/photo_46940875_stock-vector-the-rectum-and-anus-showing-the-puborectalis-muscle-part-of-the-levator-ani-used-for-the-control-of-.html

gh889  How do you differentiate this from hypertonicity of the internal anal sphincter? +  
gh889  nvm. im dumb lol +  


submitted by docred123(3),

Hi guys can someone please elaborate on these findings. I understand she has lung cancer that's impeding her trachea. But how is this representative of an obstructive disorder? Aren't lung cancers restrictive if anything? Thanks

nlkrueger  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 +  
ferrero  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. +  
mousie  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 ..? +1  
mimi21  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 ) +  
gh889  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. +2  
charcot_bouchard  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. +  


The patient has ATN secondary to renal ischemia. Due to tubular necorsis, the patient will have an elevated FeNa. The patient's urine will also be dilute, but this will be reflected by the low urine osmolality, not the FeNa

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? +1  
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. +  
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. +11  
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! +6  
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  


submitted by sakbarh(4),

She has many cardiovascular risk factors and likely suffered a stroke of the basilar artery causing locked in syndrome. According to FA this can cause a lesion at the pons, medullar, or lower midbrain -- however anatomically the basilar artery runs right on top of the pons so proximity most likely makes it the right answer.

mousie  The Boards and Beyond video of SC strokes was really helpful at explaining this if you are a video kind of person! +  
yotsubato  What pushed me away from pons was "dysarthric speech" which implied she still could speak to some degree.... which made me pick medulla. +1  
mimi21  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 +  
cbrodo  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. +8  
gh889  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 +  


submitted by joha961(14),

Maintenance dose = (Css * CL * t) / F

... where t is elapsed time between doses (not relevant here since it’s continuous infusion) and F is bioavailability (which is 100% or 1.0 here because it’s given IV).

​Contrast with loading dose:

(Css * Vd) / F

... where Vd is volume of distribution.

yotsubato  So do we just have to memorize this... +1  
gh889  yep +1  


submitted by lnsetick(38),

How are you able to tell that the CT slice is not at the level of duodenum?

zelderonmorningstar  I think the small intestine narrows as you go along, so jejunum would most likely intuss into the duodenum. +  
yotsubato  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. +  
gh889  You should also know that the duodenum is almost purely on the right side of the body +5  


submitted by meningitis(165),

Actually, I correct myself: I looked closer and the Genito femoral has an external Spermatic branch and a Lumboinguinal branch. I thought it was the Genitofemoral nerve because the genital branch passes through the deep inguinal ring, enters the inguinal canal, goes to spermatic cord and supplies the cremaster and scrotal skin.

Heres the image: https://upload.wikimedia.org/wikipedia/commons/e/e4/Gray824.png

Correct me if I am wrong please.

gh889  I think you're right, FA2019 pp444 even states that sensory to the scrotum is via the Genitofemoral nerve +2  


submitted by dr.xx(47),

As part of embryonic development, the pancreas forms as two buds from the foregut, an embryonic tube that is a precursor to the gastrointestinal tract. It is therefore of endodermal origin.

https://en.wikipedia.org/wiki/Pancreas#Development

gh889  nice! I reasoned it as that most of the GI system is of endodermal origin +3  


submitted by meningitis(165),

Tanner stages start at TEN years old

Stage I:

  • I is flat, as in flat chest;
  • I is alone, as in no sexual hairs.

Stage II (2): stage II starts at 11 y/o (II look like 11)

  • 2 balls (testicular enlargement)
  • 2 hairs (pubic hairs now appearing)
  • 2 breast buds form

Stage III (3): starts at 13 y/o

  • If you rotate 3, it looks like small breasts (Breast mounds form);
  • If you squiggle the III they look like curly+coarse pubic hair
  • Increased penis length and size can be represented by: II --> III
    (your penis was thin II but now its thicker III)

Stage IV (4): starts at 14 y/o

  • First imagine: The I in IV represents the thigh, and the V in IV looks like the mons pubis between your legs:
    MEANING: you have hair in mons pubis (V) but you have a border detaining the hair from growing into thighs.
  • The V is pointy, as in now the breasts are pointy (raised areola or mound on mound)

Stage V (5): 15 y/o

  • V has no borders detaining hair from growing into thighs (pubic hair + thigh hair)
  • 5 fingers(as in hands) flattening the areolas when grabbing them (areola flatten at this stage and no more "mound on mound")

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +1  
gh889  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? +  
meningitis  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. +  
endochondral1  stage 3 breast mound is for females not males btw +  
endochondral1  see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females +  
angelaq11  this is just too funny, I LOVE it! xD +  


submitted by taway(7),

Just as a note for anybody else who was WTF at how 2(29/30)(30/30) = 1/15...a lot of question banks round 29/30 (or any similarly large fraction) out to 1

gh889  I think you meant 2(29/30)(1/30) just to clarify! +3  
niboonsh  i am confusion +  
arkmoses  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. +3  
garibay92  2pq= 2(29/30)(1/30).... Transform this to 2 1 1 2 1 x x = _ = ____ 1 1 30 30 15 +  
garibay92  Nevermind :/ It didn't come out as planned :( +  
garibay92  /Users/carlosgutierrez/Desktop/IMG_2423.jpg +  


submitted by egghead(0),

This is one of those questions I was never going to get. It's not in FA, I don't think I've seen it in class.

hungrybox  same :( +  
masonkingcobra  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) +  
gh889  FA 2019, pg 551 +3  
meningitis  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. +2  
step1soon  FA 2019 pg 551 +  


submitted by mcl(223),

Methionine is an essential amino acid. All others listed are not.

scalpelofthenorth  Pg 81 Tyrosine is listed as an essential AA. Should be tryptophan for those who got this wrong like me. +  
neonem  But tyrosine can come from phenylalanine, so it's not really essential right? +  
gh889  in FA2019, it is listed as Tryptophan, not Tyrosine. That was corrected. +1  
usmleuser007  Note: Tyrosine is ONLY essential with PKU in children +  
niboonsh  bro FA2018 lists tyrosine as an essential AA. They played us. +1