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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.
i understand the link to MEN 1, but why are we checking the calcium level?
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
Couldn't a Pituatary tumor secrete ACTH, causing high cortisol?
Patient has symptoms of a gastrinoma (Zollinger-Ellison Syndrome)- patients present with diarrhea, epigastric pain, duodenal and jejunal ulcers. Associated with MEN1 syndrome.
I don't get why this was downvoted...
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.
i don't understand this at all. i am completely blank...please help
@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.
(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
@henoch280 thank u very much! I got it right by luck but now i do understand :D
I forgot/didn't know this factoid and narrowed it to the correct answer and a wrong answer. Guess which one I chose?
>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?
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.
sweet explanation imgdoc
really~~~ sweet. thankyou :)
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
Myocardial rupture would not happen until 3-14 days. Since this shows signs of <24 hrs, the answer is arrythmia.
@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.
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.
Anyone knows why it's not a cardiogenic shock if it was within 24 hours?
It says "Mottling" which happens in the first day. If it was 3-14 days it would be yellow (p 302 2019). He can be having angina for 3 weeks leading up to an MI.
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).
Flagellum = Protein, (FA19, pg.124)
Right, and that glycolytic enzyme deficiencies lead to hemolytic anemias.
I just thought the typical presentation of pyruvate kinase deficiency would be hemolytic anemia of the newborn.