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 +0  (nbme24#10)

i get why it's hyporeflexia, but why not fibrillations? it's also an LMN sign

et-tu-bromocriptine  Imagine a simple reflex arc: you have an afferent neuron, some interneuron shenanigans, and an efferent neuron (aka LMN neuron). If you damage the LMN, you will get hyporeflexia (due to damaged reflex arc) and fibrillations (because your LMN won't be able to effectively contract muscle on command). However, if you damage the afferent part of the arc, you will still get a damaged reflex arc (hyporeflexia), but your motor neuron will still be able to do its stimulating effectively, so your muscles won't show weak contractions when stimulated by a higher pathway. Kinda confusing but I hope I made it a tad simpler!
eli_medina9  https://imgur.com/1z4OF4l Gonna piggy back off your comment and just post this kaplan image

 +3  (nbme21#3)

i get why it's flagellin, but is the specific reason that LPS is wrong is because it's just not how the vaccine is made? LPS would also elicit an immune reaction, right?

nor16  Lipid A of LPS can be sensed by CD14 of macrophages causing shock, its not a protein, so no immune reaction as in vaccination (humoral, IgG class switch via Th2 and B Cells).
eclipse  actually they do use LPS as adjuvant in vaccines
eclipse  actually they do use LPS as adjuvant in vaccines
hyperfukus  TLRs recognize common motifs called pathogen-associated molecular pattern (PAMP) in bacteria, fungi, viruses, and other pathogens. TLR signaling in the modulation of innate immunity + adaptive immunity against pathogens, TLR agonists: CpG-DNA, flagellin, and lipid became essential candidates of effective+safe vaccine adjuvants. TLR agonists improve the efficacy of vaccine, reducing TCR-based selection thresholds and enhancing the magnitude and quality of memory T-cell response.
hyperfukus  some extra info in case they ask another annoying q

 +0  (nbme21#36)

what are the other labeled structures? i can discern the parietal and chief cells, but not the others...

hyperfukus  what is A?
et-tu-bromocriptine  According to this source, they're mucous neck cells (secrete acidic fluid containing mucin); compare this with mucus produced by surface mucous cells, which is alkaline. http://www.siumed.edu/~dking2/erg/GI082b.htm
hyperfukus  i gosh i see now! thanks so much :) so if it's Pink=Parietal but not granules got it thank you :)

 +1  (nbme22#45)

sketchy says that kaposi's has infiltrating lymphocytes, so why would large aggregates of atypical lymphocytes be incorrect?

titanesxvi  Bcz I think vascular is the key thing here, whereas atypical lynphocytes would be more of EBV

 +0  (nbme22#8)

would an acetylcholinesterase inhibitor work as well to relieve the symptoms? but just because he's 73yo, we're supposed to assume it's due to BPH and give an a1 inhibitor?

yb_26  acetylcholinesterase inhibitors are used in treatment of urinary retention, not urinary frequency

Subcomments ...

submitted by seagull(413),


Another histology slide with labels a few seconds ago

enbeemee  what are the other labeled structures? i can discern the parietal and chief cells, but not really the others... +  
hyperfukus  yea wth is A +  

submitted by oznefu(7),

how do you narrow down that testosterone increased hemoglobin concentration? just a random fact to know? i put alkaline phosphatase because i figured increased testosterone will increase bone growth and ruled out prostate-specific antigen bc it’s a woman.

hysitron  I guessed this one cause men have a higher hemoglobin than women. +1  
notadoctor  High levels of testosterone will result in amenorrhea. I guessed that since she's not menstruating she will not be losing blood and therefore hemoglobin. Therefore her hemoglobin levels will be higher than expected. +3  
meningitis  It kinda makes sense knowing testosterone causes catabolism so I was in between Alkaline phosphatase and hemoglobin... +1  
enbeemee  isn't testosterone anabolic? +