Welcome to trichotillomaniac’s page.
Contributor score: 121
Comments ...
nnp
even prolactin causes reduced bone density
+3
jmangels
I was thinking the same thing about the prolactin, but the weight gain made me lean toward ACTH
+5
jurrutia
Prolactinoma reduces bone density due to suppression of estrogen. However, that wouldn't explain weight gain.
+1
burak
I think compressing effect of prolactin macroadenoma may cause decreased level of TSH and by doing so it may lead to hypothyroidism and weight gain. But this is overthinking I guess :(
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freemanpeng
Weight gain saved me.
Prolactinoma is definitely more common pituitary adenoma while ACTH is definitely more common cause of osteoporsis to the point of compression fractrue!
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Subcomments ...
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...?)
+3
yotsubato
God damn this is such BULLSHIT...
+15
sars
My thought process, usually wrong all the time, was that HBV (IVDU) can occur to anyone. Acute hepatitis to Chronic occurs when HBV incorporates its DNA into host and releases mutagenic proteins. This is regardless of immunosuppresion. Primary CNS Lymphoma reappears primarily when you are immunosuppressed (organ transplant, immunodeficiency, HIV/AIDS).
+2
syoung07
Hep C is far more likely to become HCC than hep B
+2
jurrutia
Even if you were thinking skin cancer is more common, that's only true for basal cell and squamous. Melanoma is rare. EBV much more likely in aids patient. Even H pylori was a better answer.
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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!
+7
drdoom
HI LAURI. THANK YOU FOR DEMONSTRATING YOUR PROFICIENCY WITH ALL-CAP COMPOSITION!
+4
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
+1
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.
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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
+2
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
+1
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.
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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
+2
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
+1
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
+2
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).
+5
eacv
OMG! THANK YOU. I DIDNT KNOW ANYTHING about this!! Hope this is not testesd on real examen :p
+5
ajss
wow! this explanation was awesome! thanks!
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mrglass
Also the T-cell V-D-J segments are not the same as the B-cell V-D-J segments. Therefore a B-cell J segment southern blot would look for whether the B-cell site VDJ segment in a T-cell, which would always non-rearranged.
+6
mynamejeff
Thank you!
So is this because multiple myeloma produces excessive monoclonal light chain Ig? Is this the 1.5 kb gene? Whereas, T-cells that have not gone through differentiation yet and their J region includes everything (VDJ) vs. just VJ in the light chain? (FA 2020 pg 104)
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peridot
This explanation is amazing! However, to fully understand another step of what the question is getting at, please take a look at @highyieldboardswards's and/or @mrglass' explanation as well - a very important addition!!
+1
skonys
My logic was wrong but my answer correct. I am suffering from success.
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fhegedus
wow! this is amazing! thank you!
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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
+5
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.
+5
medulla
every time I read about Lupus there is something new!!
+1
aakb
woman of child bearing age + serositis + arthralgias/arthritis >=2
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aakb
kidney issues (main cause of death in sle)
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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
+5
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.
+5
medulla
every time I read about Lupus there is something new!!
+1
aakb
woman of child bearing age + serositis + arthralgias/arthritis >=2
+
aakb
kidney issues (main cause of death in sle)
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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.
+18
kylemax
The abnormal T-cells are known as Downey type II cells (Sketchy)
+4
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.
+6
lilyo
Soooooooo EBV infested B- cells is not considered atypical WTFF??
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med4fun
They are atypical b/c usually you do not see a super high amount of CD8+ in peripheral blood. Now there are a ton to try to stop the infected cells.
+1
aneurysmclip
oh and primary CNS lymphoma caused by EBV has T cells NOT B cells. I just try to remember the peripheral blood has atypical lymphocytes which are CD8+ T cells, and the CNS lymphoma is the opposite, ie; B cells
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mgoyo89
I think there are two questions with this answer!!I was so scared :(
+4
trichotillomaniac
yep ---not IL-2 bc that stimulates Tcells and NK cells- I think I blacked out when I answered this question
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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)
+6
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.
+15
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.
+2
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.
+1
yotsubato
Thats cause the NBME exam writers read FA, then make questions not fit in with FA
+7
trichotillomaniac
This fits the timeline laid out in Pathoma!
1-3 wks = granulation tissue with plump fibroblasts, collagen, and blood vessels
+10
alimd
never look at the image in the beginning. They dont want you to success. Most of the time images are made to ditract
+1
garble
UWorld also has a handy chart for post-MI that said granulation tissue at 10-14 days, then collagen and scar tissue at 2-weeks to months /shrug
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mcl
how do i upvote multiple times
+22
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