Official: "Wow, that's a great Board Q" (Awesome Medical knowledge) thread

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virilep

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I figured it's about time we just start one thread that we can talk about questions or topics that seem pretty good or have seen sometime throughout our preparation. Even people that have taken the test, if you'd like to chime in with something you saw on the wards or anytime (after the big day)

If you have an answer, keep it to yourself (or you can PM it). We can post our answer by just replying to the thread to keep it active. If we're late, send a PM.

I'll start.


female patient presents with Christmas disease. What other abnormalities can be seen? (thought this was kind of cool)

:luck: everyone.

ps. laryngeal lesions are not cool. :laugh:

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Saw a patient with empty sella syndrome (i.e. no pituitary).

Sodium was 185.

She was fine...
 
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How do alpha and beta cells in the pancreas communicate with one another to coordinate hormone production?

(I thought it was just a somatostatin thing shutting down all of them, but that's not the whole story....)
I'm sure there's a lot more to the story that I don't know, but insulin has regulatory effects on alpha cells, and glucagon on beta cells.
 
This thread should be retitled:

Official: "Wow, that's a great Board Q&A" (Awesome Medical knowledge) thread


I'm curious to know about the pancreas question as well...
 
Posting the answer to the pancreas question in white to avoid spoiling for those who don't want to know yet. Highlight below if you want to see it.

It turns out that the endocrine pancreatic cells are connected by gap junctions. I was going, gap junctions in the endocrine pancreas??? Yes, if we are to believe Linda Costanzo; it's on page 255 of her BRS Physio: "Gap junctions link beta cells to each other, alpha cells to each other, and beta cells to alpha cells for rapid communication." Even Wikipedia knew this, though they didn't get it totally right: "Islets can influence each other through paracrine and autocrine communication, and beta-cells are coupled electrically to beta cells (but not to other cell types)." I can't imagine this info ever being the slightest bit useful, but it's kind of cool anyway. :)
 
I hear that both signaling mechanisms and CD4 count/related HIV disease are both high yield for those pesky practice questions.
 
My favorite piece of "could be on the boards but you will never see it in your medical career" medical trivia --

What enzyme contains Selenium, and what is the consequence of Selenium deficiency?

Glutathione Peroxidase / Congestive Cardiomyopathy ("Keshan Disease")

(If this were to ever appear on the boards, the patient would likely be from Inner Mongolia or thereabouts)
 
That was on our path practical and a written section exam.
 
I figured it's about time we just start one thread that we can talk about questions or topics that seem pretty good or have seen sometime throughout our preparation. Even people that have taken the test, if you'd like to chime in with something you saw on the wards or anytime (after the big day)

If you have an answer, keep it to yourself (or you can PM it). We can post our answer by just replying to the thread to keep it active. If we're late, send a PM.

I'll start.


female patient presents with Christmas disease. What other abnormalities can be seen? (thought this was kind of cool)

:luck: everyone.

ps. laryngeal lesions are not cool. :laugh:
Since Christmas Disease - AKA Hemophilia B - is an X-linked recessive diease, and the patient is a girl, we can suspect that she only has one X chromosome. So she's has Turner's Syndrome. From that, I'm sure you can figure out what else she could have. Just never thought about it this way. There are case reports about this happening and I'm assuming it can happen to any of the X-linked Recessive diseases. Hope is helps someone. Back to the grind. Test in 4 days.
 
Since Christmas Disease - AKA Hemophilia B - is an X-linked recessive diease, and the patient is a girl, we can suspect that she only has one X chromosome. So she's has Turner's Syndrome. From that, I'm sure you can figure out what else she could have. Just never thought about it this way. There are case reports about this happening and I'm assuming it can happen to any of the X-linked Recessive diseases. Hope is helps someone. Back to the grind. Test in 4 days.

Are males with this disease sterile or do they die at an early age? I'm just confused...why can't BOTH of her X chromosomes be defective - as in, one from ma and one from pa?

Or am I completely off?

POST#500
 
Are males with this disease sterile or do they die at an early age? I'm just confused...why can't BOTH of her X chromosomes be defective - as in, one from ma and one from pa?

Or am I completely off?

POST#500

I think the prevalence for turner's is much higher than that of Hemophilia B so if a patient is female with a very rare X-linked recessive disease she's more likely to have Turner's/1 allele than 2 alleles.

It does beg the question though about the effect of each deficiency on one another with respect to fetal viability i.e. a turner's/HemoB child would have to not be lost during pregnancy and would have a much higher rate of spontaneous abortion than a homozygous recessive HemoB female, possibly compensating for some of the allele frequency advantage the turner's/HemoB combo.

Probably overthinking this one though.
 
The other thing you should consider for a girl w/ symptomatic hemophilia is that she's a mosaic. In other words, she could have had uneven lyonization of her Xs during embryogenesis and come out unlucky with more of the normal copies inactivated. My understanding is that even a lot of Turner's patients are mixed 46 XX/45 XO; I get the impression that mosaics are probably more common than total 45 XO karyotype. Mosaicism could help explain RC's question too.
 
If a person has this condition, they would be immune to rabies? (not a vaccine...)
 
:confused:

Kartagener's is the only thing that comes to mind that might be remotely plausible.
 
heh, that almost makes me feel smart. almost.
 
heh, that almost makes me feel smart. almost.
Hahaha, I was just starting to ask for an explanation about the mechanism, and then I thought--dynein, retrograde transport, nerves, virus can't get to CNS. Um, yeah. Little bit of a delayed synaptic connection there. :laugh:

Ok, here's another one that should be pretty easy to figure out if you think about it: you know how you can use anti-cardiolipin antibodies to test nonspecifically for treponemes? Why would cardiolipin be cross-reactive with a treponeme antigen? A hint that should make the answer pretty obvious is provided in white below if anyone wants it. (On a side note, I read that cardiolipin is the only antigenic human glycerol-containing phospholipid.)

Look up where it's located in the cell.
 
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