The concept is a convoluted way of asking if you knew how VDJ recombination works, which is that it is actually an example of altering the DNA of the B/T lymphocyte.
Southern blot technique: So when they use a probe against some region, and outputting a size of 1.5 kb or 6 kb, this is telling you the size of the DNA fragment in each cell (doesn’t matter if they say J probe or constant region probe, they’re just saying they’re targeting some nucleotide sequence found in the Ig locus/TCR beta chain locus respectively for B/T cells).
I think the confusing part could be wondering how you know whether you’re partly through rearrangement (answer choices B thru D) or if it hasn’t occurred at all yet (correct answer). Here, the concept is that B cells undergo V(D)J rearrangement in the bone marrow, while T cells do it in the thymus, and it all happens at once. So a plasma cell in the blood like in Multiple Myeloma would have fully undergone recombination, while a T cell in the blood could either be fully educated (and have finished VDJ recombination) or immature (hasn’t started VDJ).
Since the T cell gene was 6 kb and definitely bigger than the 1.5 kb gene, the T cell hasn’t undergone recombination yet.
Did anyone need to read that last sentence like 50 times because the author refuses to use better grammar. Just frustrating.
Which of the following reasons is why this question is bull?
1) Using the word "cyclic" instead of tricyclic for clarity
2) Knowing all of epidemiology of all drugs
3) having to reason out that anticholinergic effects are probably the worst over alpha1 or H1 effects to no certainty.
4) The crippling depression of studying for days-to-weeks on end to probably do average on the test.
This one was a little tricky. For this one the key is the low radioiodine uptake. This patient has high T4 and low TSH which makes sense in a hyperthyroid patient, perhaps your first thought is that this patient has Grave’s disease. However, in Grave’s your thyroid is being stimulated to make more thyroid hormone from scratch and as such would have an increased radioiodine uptake because the thyroid is bringing in the required (now radiolabeled) iodine. This is why it is not Graves (“release of thyroid hormone from a thyroid stimulated by antibodies”).
So if its not Grave’s what could it be? For this you’d have to know that Hashimoto’s Thyroiditis (also known as Chronic Lymphocytic Thyroiditis and is often referred to as such on board exams to throw you off) has three phases - first they are hyperthyroid, then euthyroid, then the classic hypothyroid that you would expect with low T4 and high TSH. This was the key to this question. The reason for this is that antithyroid peroxidase antibodies in Hashimoto’s cause the thyroid to release all of its stored thyroid hormone making the patient hyperthyroid for a short period of time. After this massive release of thyroid hormone, the antibodies make them unable to make new TH and therefore they become euthyroid for a short period and then hypothyroid which you would expect! Since they can’t make new TH, the thyroid will not take up the radioiodine and therefore there will be low radioiodine uptake. Hence, “release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes.” aka “Lymphocytic (hashimotos) thyroiditis”.
I think “release of thyroid hormone from a lymphomatous thyroid gland” is referring to some kind of thyroid cancer in which case you would expect them to be describing a nodule on radioiodine uptake.
Summary video here and also a great site in general: https://onlinemeded.org/spa/endocrine/thyroid/acquire