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(nbme21#25)

She’s intaking 450 mOsm per day so she needs to excrete 450 mOsm per day to maintain equilibrium. You can’t just excrete mOsm’s by themselves -- they have to be dissolved in some amount of water.

Let’s say you excrete 450 mOsm with 500 mL of water -- that means your kidneys are concentrating urine to:

`450 mOsm ÷ 500 mL = 900 mOsm/L`

But the maximum this lady’s kidneys can concentrate urine to is 450 mOsm/L, so she has to excrete more water to get it that dilute. That amount of water is 1 L, because 450 mOsm/1 L = 450 mOsm/L.

Now there’s nothing stopping her from excreting the 450 mOsms in an even more dilute urine -- for example if she drank an extra L of water one day, the kidneys could get rid of that extra L with the same amount of 450 mOsm by diluting the urine to `450 mOsm ÷ 2 L = 225 mOsm/L`. But the question asks for the minimum amount of water -- which is 1 L by the kidneys (+ 1 L from the other stuff for a total of 2 L).

(nbme21#6)

Recurrent kidney stones should include hyperparathyroidism on your differential, couple that with gastrinoma and you’re looking at MEN 1. Lipomas are also associated with MEN 1.

sympathetikey  Yeah, I probably should have went with that. Just got thrown off, since I know that usually the serum calcium levels for someone with Calcium kidney stones is normal.
snoochi95  i understand the link to MEN 1, but why are we checking the calcium level?
cmun777  I feel like it's important to get a baseline of where the calcium is at for two reasons: 1. if the patient does indeed have MEN 1 it would be good to know if she has high calcium levels and possible Parathyroid etiology 2. You're putting the patient on a PPI which are known to decrease calcium levels and increase risk of osteoporosis for both these possible factors/concerns it would be good to see where calcium is currently at

(nbme21#31)

Hypo/hyperthyroidism is diagnosed with TSH w/ reflex to T4 (this just tells the lab if TSH is normal don’t check T4 but if TSH is abnormal, check T4 too). TSH wasn’t an option so T4 is the best answer.

hello  I don't get why this was downvoted...
maxillarythirdmolar  To take it a step further, Goljan mentions that there are a myriad of things circulating in the body, often in a 1:2 ratio of free:bound, so in states like this you could acutally see disruption of this ratio as the body maintains its level of free hormone but further increases its level of bound hormone. Goljan also mentions that you'd see the opposite effect in the presence of steroids and nephrotic syndromes. So you could see decreased total T4 but normal free T4 because the bound amounts go down.

(nbme21#15)

Proccess of elimination for this one. Two you can eliminate immediately just from looking at the biochemical pathway chart. The other two required knowledge that eumelanin is more protective than pheomelanin (this is why redheads burn more easily). Because pheomelanin is less protective, there would be more not less ROS from sunlight.

henoch280  @temmy. This question tests our knowledge on albinism which is normally a tyrosinase deficiency disease but the vignette states that the boy's albinism is caused by a genetic mutation in the TYRP1 gene which is shown in the biochemical pathway. A gene that helps in the synthesis of Eumelanin. Now you have to understand that all precursors before that gene is the pathway would still be available if not increased which make 2 of the options in the question wrong. you also have to understand this: (Eu)melanin = (normo)melanin i.e normal melanin which is protective to the skin, decreases reactive oxygen species and gives the dark pigments to the iris, choroid, skin, hair e.t.c. while (feo)melanin = (fake)melanin i.e pheomelanin, the one present in our patient here which is less protective again the uv rays, cannot pigment and cannot decrease ROS generated in the skin. i hope this helps
eacv  @henoch280 thank u very much! I got it right by luck but now i do understand :D

(nbme21#45)

This one was tricky but I think you could’ve done this one without knowledge of NMDA receptors. Stem told you that glutamate activates both non-NMDA and NMDA receptors but it activated only non-NMDA receptors in the early phase. That means NMDA receptors activate after non-NMDA receptors. That means something was delaying NMDA receptor activating and the only answer that made sense as the Mg inhibiting NMDA at resting potential. Once the cell is depolarized by non-NMDA receptors, NMDA receptors can be activated.

hungrybox  I forgot/didn't know this factoid and narrowed it to the correct answer and a wrong answer. Guess which one I chose?
yotsubato  >That means something was delaying NMDA receptor activating and the only answer that made sense as the Mg inhibiting NMDA at resting potential. What makes the fasting gating kinetics choice incorrect then?
imgdoc  NMDA receptors are both voltage gated and ligand gated channels. Glutamate and aspartate are endogenous ligands for this receptor. Binding of one of the ligands is required to open the channel thus it exhibits characteristics of a ligand channel. If Em (membrane potential) is more negative than -70 mV, binding of the ligand does NOT open the channel (Mg2+ block on the NMDA receptor). IF Em is less negative than -70 mV binding of the ligand opens the channel (even though no Mg2+ block at this Em, channel will not open without ligand binding. Out of the answer choices only NMDA receptors blocked by Mg2+ makes sense. Hope this helps.
divya  sweet explanation imgdoc

(nbme21#11)

Histology showed coagulative necrosis (preserved architecture of myocardial fibers) with neutrophil infiltration which hinted that the MI was within 24 hours. Most likely cause of death within first 24 hours of MI is arrhythmia. Myocardial rupture would also be visible on gross appearance of the heart, which they described in the stem.

bighead478  in FA it shows softening of the myocardium to happen at 3-14 days. Do you think this was overly misleading people (like me) into choosing myocardial rupture? I understand the histo features are consistent with < 24 hours, but the stem should also match this in every detail
sbryant6  Myocardial rupture would not happen until 3-14 days. Since this shows signs of <24 hrs, the answer is arrythmia.
hello  @bighead478 You have to look at the whole picture. Histo shows preserved architecture, which indicates coagulative necrosis -- coagulative necrosis is a histo finding only in the first 24h. The most common causes of MI-related sudden death are: arrythmia > cardiogenic shock (heart pump problem) > rupture.
jcmed  I chose the rupture as well due to the timeline. Somebody gave me this advice the other day, NBME classically will give you an entire vignette leading you somewhere, and the what it asks will be something completely different; or in this case will give you a photo of something and will ask about the photo. They do what they want.

(nbme21#3)

Capsular polysaccharide vaccines are often conjugated to proteins to improve immunogenicity. Flagellin is the only answer choice that's a protein.

mambaforstep  both MHC 1 and 2 are present antigens that are PROTEINS (FA 2019 pg 100). so in order to elicit a T cell response, you need a protein (CANT BE A POLYSACC). that is why vaccines for polysaccaride antigens are often conjugated to PROTEINs--> so that we can elicit a T-cell response (FA 2019 pg 127).

(nbme21#45)

For this one you just had to know the glycolysis pathway. Stem told you 2,3-BPG is elevated, which is upstream of pyruvate kinase.

neonem  Right, and that glycolytic enzyme deficiencies lead to hemolytic anemias.
toxoplasmabartonella  I just thought the typical presentation of pyruvate kinase deficiency would be hemolytic anemia of the newborn.