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 +0  (nbme22#22)

While I understand why it's hyperplastic arteriosclerosis and how it classically occurs with HTN, I was wondering why it couldn't be berry aneurysm? Is it because the question is asking which is "most likely", making C the better answer? Thank you.

mannan  Berry Aneurysm is not CAUSED by HTN. It's caused by weakening of the arterial wall (at bifurcations). Hypertensive disease exacerbates them and causes the clinical picture of SAH (worst headache of life) when they rupture. Hope that helps -- Reference: FA CNS pathology, aneurysms.




Subcomments ...

submitted by meryen13(2),

so I don't think the reason for bilateral hydronephrosis is because it invated the bladder or kidneys. it is probably due to obstruction. there is a cancer in the uterine side of cervix (uterine cervix) that is big and its pushing on the bladder and its obstruction the flow of urine in ureters to bladder, so the urine backs up to the kidney and causes bilateral hydronephrosis and hydronephrosis. the kidney and ureters are full of urine and the cannot empty it to the bladder because this mass in the cervix is pushing on bladder and opening of ureters and squeezing bladder to the pubic bone.

meryen13  i hope thats helpful +  
peridot  Originally this made a lot of sense to me so thank you for contributing, but after looking more into it (on Pathoma p. 140), it specifically says that cervical carcinoma, when advanced, invades through the anterior uterine wall into the bladder and blocks the ureters. This leads to hydronephrosis. Crazy, but I guess true! +  


Weight loss - think cancer Hyponatremia - SIADH from small cell lung cancer Edema + JVD - SVC syndrome

peridot  I was thinking lung cancer secreting SIADH, resulting in hyponatremia. But because the question asked specifically about the cause of the facial edema, I put hyponatremia (answer choice C). I was wondering how you guys were able to differentiate between C. hyponatremia and E. lung cancer? Thank you! +  
mannan  The first thing that crossed my mind was SVC syndrome from the cancer obstructing the R brachiocephalic vein preventing venous blood from returning to the heart (and staying in the facial area). Also I assume Hyponatremia would be equivalent to decreased body volume so there wouldn't be edema. FA Renal physiology section has a good chart on what happens during electrolyte imbalances (hypo and hyper) +1  
mannan  @peridot +1  
peridot  I was thinking that hyponatremia would be more loss of osmotic pressure --> edema, but I definitely see the argument for a mass that's simply blocking blood flow. Thank you! +  


In the great words of Dr Sattar:

"Prostaglandin E2 mediates feeeeeeeeeever"

NSAIDs --> block prostaglandin syn

thisisfine   This is all I heard in my head +6  
temmy  Me it was so weird +  
peridot  I do want to add, that while PGE2 is the right answer, FA19 p.213 says that IL-1 and TNF are involved as well. However, because the question asks about what is going on in the hypothalamus, the answer is PGE2. If the question had been asking about what the macrophages were releasing to influence the hypothalamus, then the answer would have been IL-1 or TNF (FA didn't specify if it was TNF-a though...). +  


why not sarcoidosis? 1.rheumatoid arthritis like symptoms 2.uveitis 3.kidneys ...only serositis is a bit controversial

drzed  Need some pulmonary symptoms to make sarcoid convincing. I know in real life people can present with primary neurosarcoid or something crazy but on exams, it'll be classic presentation. No granulomas, hilar lympadenopathy, or interstitial lung disease = probably not sarcoid +1  
peridot  Just curious but if it had been sarcoidosis, would "systemic release of IL-1 and TNF" be an accurate description for the pathogenesis? +  


why not sarcoidosis? 1.rheumatoid arthritis like symptoms 2.uveitis 3.kidneys ...only serositis is a bit controversial

seracen  I usually look for the hilar manifestation, when considering sarcoidosis, or the skin manifestations. Personally, I thought Sjogren's when I read this. +1  
peridot  @seracen I can see why you thought Sjogren, but I think Sjogren would have more emphasis on dryness of mucus membranes and eyes (technically the question stem does say "anterior chamber of the eye", but Sjogren is more like the surface of the eye so "anterior chamber" is a weird way to put it - usually that refers more to uveitis). Also, choroid plexus (whether that refers to eye or brain... tbh idk about that yet), but either way, doesn't really fit Sjogren. Kidney involvement is also rather rare with that I believe. +  


submitted by sacredazn(59),

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! +7  
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). +4  
eacv  OMG! THANK YOU. I DIDNT KNOW ANYTHING about this!! Hope this is not testesd on real examen :p +3  
ribosome01  I would like to meet you personally and say thank you I wish I had a teacher like you +  
ajss  wow! this explanation was awesome! thanks! +  
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. +4  
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) +  
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!! +  


Weight loss - think cancer Hyponatremia - SIADH from small cell lung cancer Edema + JVD - SVC syndrome

peridot  I was thinking lung cancer secreting SIADH, resulting in hyponatremia. But because the question asked specifically about the cause of the facial edema, I put hyponatremia (answer choice C). I was wondering how you guys were able to differentiate between C. hyponatremia and E. lung cancer? Thank you! +  
mannan  The first thing that crossed my mind was SVC syndrome from the cancer obstructing the R brachiocephalic vein preventing venous blood from returning to the heart (and staying in the facial area). Also I assume Hyponatremia would be equivalent to decreased body volume so there wouldn't be edema. FA Renal physiology section has a good chart on what happens during electrolyte imbalances (hypo and hyper) +1  
mannan  @peridot +1  
peridot  I was thinking that hyponatremia would be more loss of osmotic pressure --> edema, but I definitely see the argument for a mass that's simply blocking blood flow. Thank you! +  


submitted by welpdedelp(157),

So I think that issue of wrist extension and/or finger drop would be more radial nerve. However, there was more proximal weakness, so it would be C7.

"7-8 lay them straight", the pt couldn't "lay them straight" so it would be C7 root

welpdedelp  *As an addition, median nerve involvement would have leaned more toward C8 than C7. +1  
meningitis  Do you have anymore useful mnemonics for brachial plexus? +  
henoch280  FA pg 494 for mnemonics +  
winelover777  Doesn't look like there are many in FA 2019. S1/S2 - Buckle my shoe. L3/L4 - Shut the door. C5/C6 - Pick up sticks. +  
drzed  S2-S4 keeps the penis off the floor :) (cremaster reflex) +  
peridot  What's crazy @drzed is that in FA 2019 it says L1-L2 ("testicles move") on p.498 so I wonder if that changed +  


According to FA 2019 Tricep Reflex is mediated by C6, yes C6 NOT C8, and C7 [In BOLD, implying it is more important].

peridot  This is on p.498 of FA 2019 for anyone curious +  


submitted by hayayah(884),

This is a primary central nervous system lymphoma. Most commonly associated with HIV/AIDS; pathogenesis involves EBV infection.

Considered an AIDS-defining illness. Variable presentation: confusion, memory loss, seizures. Mass lesion(s) (may be ring-enhancing in immunocompromised patient) on MRI, needs to be distinguished from toxoplasmosis via CSF analysis or other lab tests. Toxo usually has multiple ring enhancing lesions.

peridot  For those who are curious, this is on p.422 of FA2019 +  


submitted by hayayah(884),

By age 75, the thymus is little more than fatty tissue. Fortunately, the thymus produces all of your T cells by the time you reach puberty. They are long-lived and that's why you can lose your thymus without impairment of your immune system.

sweetmed  Memory T cells live for six months or less in healthy humans (Westera et al., 2013), whereas naive T cells can live for up to nine years +4  
whossayin  so the bone marrow does not take the role of the thymus? +1  
dr_jan_itor  @sweetmed, does that mean that if someone loses their thymus, they would develop imunodeficiencies appx 9 years later as the naive T cells have died off? +5  
hpsbwz  @dr_jan_itor no, because once all of the thymocytes become T-lymphocytes, they are stored in lymphoid organs until they're needed. this is why removal of the thymus in MG does not cause any immune system deficiency. +3  
peridot  @dr_jan_itor From wiki: "Thymic involution results in a decreased output of naïve T lymphocytes – mature T cells that are tolerant to self antigens, responsive to foreign antigens, but have not yet been stimulated by a foreign substance. In adults, naïve T-cells are hypothesized to be primarily maintained through homeostatic proliferation, or cell division of existing naïve T cells. Though homeostatic proliferation helps sustain TCR even with minimal to nearly absent thymic activity, it does not increase the receptor diversity." +2  


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