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negative stranded can't be read by a translator so it needs to be transcribed into + first. Only then can it be used for protein. + is basically mRNA already.
There's only one double stranded RNA family as far as I know- Reovirus so no encephalitis
Yeah thats the easy part. But the histology is whats hard
I might be mistaken but I also thought Epstein Bar Virus was also implicated in gastric lymphomas?
Yeah but in a chronic case this guy would produce more RBC and not be hypoxic anymore.
How is that NOT posterior to middle concha? bad question
@yotsubato - That would have been if it was the spehnoid sinus (I got it wrong too btw)
Couldnt a psychogenic cause reduce libido?
I love how this cant be straight forward. All the other proteins are either subunits of desmosomes or cytoskeletal components. Because I know molecular biology that well on top of the majority of medicine....FML
Dengue is an arbovirus. The important hints are that she was traveling in endemic (tropical) and that she has **excruciating pain in the joints and muscles**. This is why dengue is aka "break-bone fever"
To expand, SIADH may also result in euvolemic hyponatremia. This is because, as we know, ADH increases absorption of water and therefore initially results in an increased circulating volume. However, this results in increased stretch of the atria and subsequent secretion of ANP. ANP (atrial natriuretic peptide) then results in loss of sodium and water.
Have you mixed Chlamydia in with Mycoplasma?
misread the "accounts for" question as what's the reason for the atypical lymphocytes. So I answered "virus infected B lymphocytes." Anyone else misread it like that?
Shit, I misread that too and I noticed it now. Nerves get the best of us!
why not hep B? i guess another whats the better answer ones... Just rem reading that it was more common with aids pts.. anyone have an idea about this?
Yes, I think CNS lymphoma as an AIDS defining illness wins the day.
My thought was since SHE has AIDS it is most likely from IVDA, which has a high risk of HBV that could go undiagnosed for a long time. at 32, that might not be long enough to have HBV and get HCC (but with no immune system...?)
NBME does trick now and then.. when they zig you zag. then when you think they are going to zag, they zig just to destroy yourself confidence.
The abnormal T-cells are known as Downey type II cells (Sketchy)
I was recognized EBV, then knew EBV infects Bc, and the atypical lymphocytes are Tc. Then I said CD8 are MHC1 for virii, and bingo bango, boom.
^^^ THIS ONE SHOWS DUCT ^^^
If you go back and look at the image you can see that it was highly vascular which is characteristic of granulation tissue. Scar tissue formation will be closer to 1 month, plus you will see lots of fibrosis on histology.
It's a bit misleading, for me, since you do see fibrosis intermixed with the granulation tissue, but granulation tissue was a better answer.
According to FA 2017: 3-14d: Macrophages, then granulation tissue at margins.
2wk to several months: Contracted scar complete. Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus).
i'm getting pretty frustrated with NBME contradictions to FA, and FA omissions of content. this stuff is hard enough to get straight as it is.
I'm confused about the phosphate level in questions like these. Decreased calcitriol would decrease phosphate absorption while PTH decrease lowers phosphate excretion. I'm assuming that the PTH decrease has the greater effect with serum phosphate levels?
PTH = "Phosphate trashing hormone" if PTH is high Phosphate must be low - they are always opposite (unless d/t renal failure then Phosphate will be high - kidneys will be unable to get rid of phosphate)
So low Ca d/t low PTH does not effect 25 H. Vit D ... only 1,25 H Vit D (active Calcitriol)?
Clarification because I was confused: PTH stimulates kidney to produce 1,25-(OH)2 D3 (calcitriol) via 1α-hydroxylase in proximal convoluted tubule. Therefore, without parathyroid glands, low PTH, 25,D is not converted and therefore not down (normal or up). phosphate "trashed" by PTH as eloquently stated above.
that was my reasoning as well. guess not.
Shitty NBME grammar strikes again.
The only thing I can think of is that HIV is a (+)-sense single-stranded RNA virus that relies on an RNA dependent DNA polymerase (reverse transcriptase) to synthesize DNA.
according to [medbullets link](https://step1.medbullets.com/step1-microbiology/104196/rna-viruses_) ns ss RNA must carry RNA dependent RNA polymerase (so that is out).
also, according to medbullets there are very few ds RNA viruses, so "most likely" will be ss. Also, RNA-dependent DNA polymerase = Reverse Transcriptase. Since HIV is a ss ps RNA virus with RT, they've described an HIV cousin. not sure beyond this.
If I'm reading this right, this is just a tricky dicky question. I think CO binds 200x stronger than O2. But if an O2 cycles through binding / unbinding 200 times before a CO gets kicked off, this should still clear the CO from that cell sooner or later. strange to think it is 1. essentially permanently trapped in a cell, and 2. doesn't kill you and can be treated with O2 to resolution within a few hours or a day. They must just be thinking, until that last RBC dies, you've got original CO in a circulating cell. but just a fraction (because you didn't die). not sure how that CO isn't just passed on during recycling, based on this line of thinking.
also remember that in renal failure, 1-alpha-hydroxylase activity is down, so there will be less activation of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is a key mechanism causing hypocalcemia.
why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain
Increased phosphate, since the kidneys aren't working well, leads to the release of fibroblast growth factor 23 from bone, which decreases calcitriol production and decreased calcium absorption. The increase in phosphate and the decrease in calcium lead to secondary hyperparathyroidism.
i think it is critical to remember that constipation is what caused the diverticulosis.
I believe there would be no decrease in O2 saturation because oxygenated blood (high pressure) is shunted into deoxygenated circuit. As long as the lungs can keep up, this should increase venous oxygenation on average.
ty both of you for this, was wondering the same thing
O2 sat won’t change b/c you’re not adding deoxygenated blood to the arterial side. You’re just taking arterial blood and putting it into venous blood. Same reason why L->R cardiac shunts don’t decrease O2 sat (while in contrast, a R->L shunt would).
just realized: the high pressure of the arterial system keeps out low-pressure venous blood in an AV fistula (probably obvious to most ppl but it was a eureka moment for me lol)
But that doesn't make sense. Page 233 of First Aid 2019 edition clearly states that being plasma protein bound creates the lowest volume of distribution, because not being bound to proteins increases the chance it will reach deep into the tissues before it reaches the kidneys. Discrepancy with First Aid?
my reasoning was comparing two drugs, both with Vd of 1, the drug with the lower albumin binding would be cleared faster @kingtime. I don't think you're considering that A and B have equal Vd.