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 image is useful. Note that the stain used makes myelin appear dark.
Vignette is typical for Parkinson's disease. Area D is the substantia nigra.
Nitrogen balance is a measurement of protein metabolism in the body. A negative nitrogen balance indicates muscle loss, as increased amounts of amino acids are being metabolized to produce energy. This increases the amount of nitrogen secreted from the body. Because the amount of nitrogen you are taking in is less than the amount of nitrogen you are secreting, you have a negative nitrogen balance.
This man is malnourished, edematous, cachetic, and has hypoalbuminemia. These clinical findings point to protein malnutrition (Kawashkior Disease), which causes edema due to decreased serum oncotic pressure. Low oncotic pressure in this case is due to protein loss, and hence a negative nitrogen balance.
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
His tidal volume was 500 mL. End-expiratory was +5 cm and end-inspiratory was +25. We were supposed to use the difference in airway pressure, and not the end-inspiratory pleural pressure (+20).
Compliance = ΔV/ΔP = 500 / 20 = 25 mL/cm H2O
I think its the right MLF (area C), not the right abducens nucleus that is lesioned on the cross section. If the abducens nucleus were lesioned she wouldn't have abduction in her left eye. The MLF mediates cross talk between the abducens nucleus on both sides to the MLF on the opposite side (2 abducens nuclei, 2 MLF one on each side). In her case, her right MLF wasn't functioning hence why she was gazing left but her right middle rectus wasn't contacting to mediate leftward gaze.
This picture helps: http://what-when-how.com/wp-content/uploads/2012/04/tmp15F9_thumb.jpg
Calculations for dad. The probability of the father being a carrier is 2/3 since it is known that he doesn’t have the disease. Then the probability of him passing it on to his kid is 1/2, thus:
Calculations for mom. With the Hardy-Weinberg Principle, you can figure out the probability of the mother being a carrier:
q = sqrt(1/40,000) = 1/200
2pq = 2 * 1/200 * 199/200, which is approx 1/100.
For the child to get the allele from mom, two things need to happen: (1) mom must be a carrier [“heterozygote”] and (2) mom must pass the allele to child:
Puting it all together. Now, combine all together:
= (probability of dad being carrier) * (probability of dad passing on disease allele) * (probability of mom being carrier) * (probability of mom passing on disease allele)
2/3 * 1/2 * 1/100 * 1/2
1 in 600
Answer: Increased Central Blood Volume (CBV), Decreased ADH, Increased ANP.
The physiological response to hypothermia is vasoconstriction of peripheral vessels (i.e. the ones in your extremities) in an effort to keep your core body temperature normal, and thus your organs functioning properly. Peripheral Vasoconstriction will increase CBV. Increased CBV will cause an increase in preload, and thus cause an increase in ANP/BNP. ANP/BNP has inhibitory effects on the Renin-Angiotensin-Aldosterone System, resulting in decreased ADH.
1) T-test (tea for two) = looks at the mean values of 2 groups
2) ANOVA (analysis of variance) ~ like t-test but = looks at mean values of 3 or more groups
3) Chi-square = looks at the (%) or proportions between 2 or more groups.
so, just look for how many groups being addressed and what values they are using (% or means)
The description of bilateral lower limb loss of vibration implies DCML damage, and the absent DTRs + Romberg seem to me to be implying that he possibly has tabes dorsalis from syphilis (or something very similar in presentation).
As for the other answers, A is wrong because his motor function is intact, B is wrong because pain and temperature deficits are not mentioned, C is wrong because it implies a specific nerve is entrapped, but he has lost bilateral sensation in his entire lower extremities
D is the trickiest, and I’m not 100% sure, but I would think radiculopathy of the anterior (ventral) roots would cause motor deficits since they carry motor efferents. You might also expect that motor dysfunction to be unilateral, since it would be unlikely to have a problem with the nerve roots on both sides. also the DCML is not located near the anterior roots of the spinal cord, so if the anterior roots were affected you really wouldn’t expect to see vibratory loss.
So basically process of elimination, I do feel like sensory neuropathy is an extremely vague answer though and I wasn’t a fan of the question.
For the peeps who got confused on this question bc of UWorld's weird question on HIV viral load:
acute HIV-1 infection: HIGH viral load, low Ab HIV-2 infection: LOW viral load, low Ab (bc standard HIV assays detect p24, which is not present on HIV-2)
Kinda annoyed I missed an easy immunology concept question :/