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 +1  (nbme18#30)

its best to think about pituitary adenomas as one of three big options, prolactin secreting, ACTH secreting, or GH secreting. The only pituitary tumor that causes osteoporosis and therefore the compression fractures seen in the questions could be a ACTH secreting pituitary adenoma (note: macroadenoma just means that the tumor is >10mm in size). increased ACTH leads to increased cortisol and therefore decreased osteoblastic activity (bone formation) = osteoporosis


 +1  (nbme22#25)

basically glucose stimulates Beta cells to exocytose insulin. Any process involving exocytosis involves fusion of an intracellular vesicle with the plasma membrane.


 +0  (nbme22#25)

basically glucose stimulates Beta cells to exocytos insulin. An process involving exocytosis involves fusion od an intracellular vesicle with the plasma membrane.


 +0  (nbme22#23)

antibodies form against the presynaptive Ca2+ channels at the NMJ-most commonly seen in patients with small cell lung cancer


 +0  (nbme22#23)

antibodies form against the presynaptive Ca2+ channels at the NMJ-most commonly seen in patients with small cell lung cancer


 +1  (nbme24#44)

cipro is a fluoroquinolone. the MOA of fluoroquinolones is to inhibit prokaryotic topoisomers II (DNA Gyrase) occasionally Gram (-) organisms like e-coli develop resistance by mutating their DNA gyrase so drugs like cipro cannot inhibit





Subcomments ...

submitted by lsmarshall(181),

I thought this was a trick question since skin cancers are the most common type of cancers overall. But actually among HIV patients, HIV-related cancers are much more common than non-HIV-related cancers (even skin cancers). EBV-induced primary CNS lymphoma is the only option that is AIDs-defining illness/cancer.

medskool123  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? +1  
haliburton  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...?) +1  
yotsubato  God damn this is such BULLSHIT... +5  
trichotillomaniac  Why you gotta do me dirty like this NBME +  


submitted by lauri(0),

I CANNOT VIEW THE ENTIRE QUESTION. IS THIS NORMAL?

trichotillomaniac  Hi Lauri, this is normal. We can't post the whole question due to copy right laws but you can almost always find the question you are looking for and the answer to by going to the form and then Ctrl + find -ing the age of the patient and other key words or the answer! +1  
drdoom  HI LAURI. THANK YOU FOR DEMONSTRATING YOUR PROFICIENCY WITH ALL-CAP COMPOSITION! +  


submitted by bubbles(25),

Just as clarification, capillary hydrostatic pressure would decrease because of systemic vasoconstriction in response to aortic rupture/systemic hypotension?

lolmedlol  i believe you get peripheral vasoconstriction and central vasodilation in the first stages of shock, which would cause stasis in the capillary beds, which would mean decreased capillary hydrostatic pressure, despite interstital hydrostatic pressure going down as well. https://www.sciencedirect.com/topics/medicine-and-dentistry/vasoconstriction and amboss shock description +  
trichotillomaniac  ^ this type of question is really hard for me to conceptualize. the link above walks you through it step by step with pictures. Theres not much of an explanation in FA. +  
trichotillomaniac  Overall is has to do with osmotic vs hydrostatic pressure. osmotic pressure stays the same and hydrostatic decreases. Hydrostatic pressure is the pressure pushing fluid out of the capillary and in the setting of blood loss this would decrease in efforts to keep as much fluid in the intravascular compartment as possible +  


submitted by bubbles(25),

Just as clarification, capillary hydrostatic pressure would decrease because of systemic vasoconstriction in response to aortic rupture/systemic hypotension?

lolmedlol  i believe you get peripheral vasoconstriction and central vasodilation in the first stages of shock, which would cause stasis in the capillary beds, which would mean decreased capillary hydrostatic pressure, despite interstital hydrostatic pressure going down as well. https://www.sciencedirect.com/topics/medicine-and-dentistry/vasoconstriction and amboss shock description +  
trichotillomaniac  ^ this type of question is really hard for me to conceptualize. the link above walks you through it step by step with pictures. Theres not much of an explanation in FA. +  
trichotillomaniac  Overall is has to do with osmotic vs hydrostatic pressure. osmotic pressure stays the same and hydrostatic decreases. Hydrostatic pressure is the pressure pushing fluid out of the capillary and in the setting of blood loss this would decrease in efforts to keep as much fluid in the intravascular compartment as possible +  


submitted by bubbles(25),

Just as clarification, capillary hydrostatic pressure would decrease because of systemic vasoconstriction in response to aortic rupture/systemic hypotension?

lolmedlol  i believe you get peripheral vasoconstriction and central vasodilation in the first stages of shock, which would cause stasis in the capillary beds, which would mean decreased capillary hydrostatic pressure, despite interstital hydrostatic pressure going down as well. https://www.sciencedirect.com/topics/medicine-and-dentistry/vasoconstriction and amboss shock description +  
trichotillomaniac  ^ this type of question is really hard for me to conceptualize. the link above walks you through it step by step with pictures. Theres not much of an explanation in FA. +  
trichotillomaniac  Overall is has to do with osmotic vs hydrostatic pressure. osmotic pressure stays the same and hydrostatic decreases. Hydrostatic pressure is the pressure pushing fluid out of the capillary and in the setting of blood loss this would decrease in efforts to keep as much fluid in the intravascular compartment as possible +  


submitted by sacredazn(18),

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.

trichotillomaniac  very nice explanation! +3  
nwinkelmann  This was awesome! Made so much sense and hopefully I will be able to think that critically about questions in the future (because I NEVER would have come up with this on my own, hah). +1  


submitted by airhead5(1),

Does anyone know the disease they are talking about? I was thinking lupus which makes sense with the answer, but i can’t find anything on anterior chamber of eye and choroid plexus.

liverdietrying  It's lupus, all the symptoms listed are classic especially the serositis. Anterior chamber of the eye = uveitis. Choroid plexus = cerebritis. For a great overview, check out this (free) video: https://onlinemeded.org/spa/rheumatology/lupus/acquire +1  
in_a_pass_life  I think this was reactive arthritis, not lupus. Choroid plexus not just in the brain, also in eye (can’t see, can’t pee, can’t climb a tree). Mechanism of reactive arthritis is immune complex deposition, per UWorld, which was correct answer. +2  
trichotillomaniac  The inside of the eye is divided into two chambers: the anterior chamber and the posterior chamber. Both chambers contain fluid, and when there’s inflammation in the eye, a specialist can often see inflammatory cells in the fluid. https://www.hss.edu/conditions_eye-problems-lupus.asp +  
trichotillomaniac  I agree that this is Lupus after doing some more research! +  
nwinkelmann  I find this article describing the SLE ocular manifestations, including uveitis and cerebritis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4908056/ Also this talks about the lupus cerebritis (choroid plexus inflammation): https://en.wikipedia.org/wiki/Cerebritis +  
medulla  every time I read about Lupus there is something new!! +  


submitted by airhead5(1),

Does anyone know the disease they are talking about? I was thinking lupus which makes sense with the answer, but i can’t find anything on anterior chamber of eye and choroid plexus.

liverdietrying  It's lupus, all the symptoms listed are classic especially the serositis. Anterior chamber of the eye = uveitis. Choroid plexus = cerebritis. For a great overview, check out this (free) video: https://onlinemeded.org/spa/rheumatology/lupus/acquire +1  
in_a_pass_life  I think this was reactive arthritis, not lupus. Choroid plexus not just in the brain, also in eye (can’t see, can’t pee, can’t climb a tree). Mechanism of reactive arthritis is immune complex deposition, per UWorld, which was correct answer. +2  
trichotillomaniac  The inside of the eye is divided into two chambers: the anterior chamber and the posterior chamber. Both chambers contain fluid, and when there’s inflammation in the eye, a specialist can often see inflammatory cells in the fluid. https://www.hss.edu/conditions_eye-problems-lupus.asp +  
trichotillomaniac  I agree that this is Lupus after doing some more research! +  
nwinkelmann  I find this article describing the SLE ocular manifestations, including uveitis and cerebritis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4908056/ Also this talks about the lupus cerebritis (choroid plexus inflammation): https://en.wikipedia.org/wiki/Cerebritis +  
medulla  every time I read about Lupus there is something new!! +  


submitted by m-ice(116),

This girl has Mono caused by Epstein-Barr Virus. The symptoms are relatively vague, but lymphadenopathy like this would be common for Mono. The CBC shows elevated lymphocytes, implying this is not a bacterial illness, so viral is likely. Combined with the lymphadenopathy, this makes us worry about Mono. The Mono-Spot test for EBV is what the question is referring to when describing the sheep erythrocytes agglutinating. From there, this question requires that you know that in EBV infection, EBV infects B cells, but does not cause them to become abnormal. Instead, CD8 cells, which are actively trying to kill the B cells, become abnormal.

medskool123  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. +5  
kylemax  The abnormal T-cells are known as Downey type II cells (Sketchy) +2  
haliburton  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. +  
trichotillomaniac  congrats you played yourself +2  


I could be wrong.. but the normal ANC (absolute neutrophil count) ranges from (1,500 to 8,000/mm3) this patient is way below the normal ANC range, thus a GMCSF could help boost neutrophils which are granulocytes!

mgoyo89  I think there are two questions with this answer!!I was so scared :( +1  
trichotillomaniac  yep ---not IL-2 bc that stimulates Tcells and NK cells- I think I blacked out when I answered this question +  


submitted by famylife(33),

Not a full answer but it's a start (in the context of an obstruction): "Obstruction of urine flow results in an increase in hydrostatic pressures proximal to the site of obstruction. It is this buildup of pressure that leads to the accompanying pain, the distention of the collecting system in the kidney, and elevated intratubular pressures that initiate tubular dysfunction. In the first days of obstruction, the dilatation of the poorly compliant collecting system may be minimal. As the increased hydrostatic pressure is expressed in the urinary space of the glomeruli, further filtration decreases or stops completely." (Harrison's, 20e, Chapter 313)

trichotillomaniac  the key here is the term hydronephrotic kidney. anytime there is that, there is a post renal obstruction of some sort. The fact that he has progressive renal failure just contributes to the idea that his kidneys have seen damage before and are not able to withstand the pressure from the back up as well. I got tripped up on this. The important thing to note is that Hydronephrosis and dilation = back up = increased in volume pressure (hydrostatic) +1  


Why is the answer “granulation tissue”? I thought after 14 days you have a fully formed scar.

colonelred_  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. +3  
sympathetikey  It's a bit misleading, for me, since you do see fibrosis intermixed with the granulation tissue, but granulation tissue was a better answer. +  
haliburton  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. +  
yotsubato  Thats cause the NBME exam writers read FA, then make questions not fit in with FA +1  
trichotillomaniac  This fits the timeline laid out in Pathoma! 1-3 wks = granulation tissue with plump fibroblasts, collagen, and blood vessels +  


submitted by seagull(349),

The semantics of this question made me vomit blood.

One day a patient will look me in the eyes and ask, "Where are tripetides broken down?" I will smile at them and say, "the intestinal mucosa and not the duodenum." They'll smile back and I'll walk away and think of this moment as I jump from the window.

sympathetikey  Too real. +2  
mcl  how do i upvote multiple times +4  
trichotillomaniac  I made an account solely so I could upvote this. +2  
dragon3  ty for the chuckle +1  
cinnapie  @trichotillomaniac Same +2