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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 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.
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.
Right, and that glycolytic enzyme deficiencies lead to hemolytic anemias.