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Welcome to theunscrambler’s page.
Contributor score: 4


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 -1  visit this page (nbme24#25)
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Amboss:

Envelope: Lipid bilayer around the capsid that contains viral glycoproteins and host cell proteins. The presence of the lipid bilayer makes nearly all enveloped viruses vulnerable to rapid inactivation by organic solvents (e.g., alcohol), detergents, and dry heat.

Where as non-enveloped viruses are generally resistant to the environment.

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 +1  visit this page (nbme24#40)
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PCV13 for strep pneumo is polysaccharide conjugated to diptheria toxin-like protein (FA20-105). This is needed for a T-cell dependent response which allows for class switching and production of IgG Ab. This is a much more robust immune response. This provides memory and is why the vaccine is given at an early date.

On the contrary, antigens lacking a protein (such as the capsular polysaccharide) such as PPSV23 vaccine are not presented to T-cells, and therefore have a much weaker response + do not class switch.

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 +0  visit this page (nbme24#29)
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Partial agonist: https://link.springer.com/referenceworkentry/10.1007%2F978-3-540-68706-1_548#:~:text=A%20key%20property%20of%20partial,to%20produce%20its%20maximum%20effect.

In the case of exercise, there is increased sympathetic tone (acts as full agonist).

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 +2  visit this page (nbme24#15)
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If anyone was wondering about Ferritin as I was.

Iron level functions as a regulator of ferritin transcription. "when iron levels are low, ferritin synthesis is decreased; conversely, when iron levels are high, ferritin synthesis increases."

If iron is low as it would be in significant blood loss, the body would want to mobilize iron to produce heme and not sequester it. This results in decreased ferritin production and increased transferrin.

https://ashpublications.org/blood/article/99/10/3505/106937/Regulation-of-ferritin-genes-and-protein

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submitted by bwdc(697), visit this page
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Endemic Burkitt lymphoma can happen in Brazil as well as Africa (jaw lesion, puffy face). The photomicrograph is demonstrating tingible body macrophages, a type of macrophage containing many phagocytized, apoptotic cells in various states of degradation.

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weenathon  For anyone else who was wondering why a cancer was undergoing apoptosis (classically we think of cancer EVADING apoptosis), apparently it's due to the myc mutation classic in Burkitt Lymphoma. While myc causes the cell to proliferate, it also induces apoptosis - hence the tingible bodies containing apoptotic cells. (https://www.ncbi.nlm.nih.gov/pubmed/8247541) +4
itsalwayslupus  Also just for people who watch boards and beyond or pathoma (I don't remember which exactly it is from), the "stars" in the "starry night" appearance of Burkitt's (what is being shown here) are lighter because the the cells are dying/gone via apoptosis (supposed to be the "holes" in the "night sky" lol). +6
jbrito718  composed of intermediate-sized lymphoid cells with a “starry sky” appearance due to numerous reactive tingible-body macrophages (phagocytosis of apoptotic tumor cells). There is a characteristic t(8;14) translocation juxtaposing MYC to the immunoglobulin heavy chain locus in most cases. +1


submitted by colonelred_(124), visit this page
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Looked it up and found that because you’re in a supine position for a long time you’re going to have increased venous return which leads to increased CO. This negatively feedsback on RAAS, leading to decreased aldosterone. As a result, you’re going to have increased diuresis which leads to decreased blood and plasma volume.

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medstruggle  Doesn’t supine position compress IVC leading to decreased venous return? (This is the pathophys of supine hypotension syndrome.) There was a UWorld questions about this ... +4
tea-cats-biscuits  @medstruggle *Supine position* decreases blood pooling in the legs and decreases the effect of gravity. *Supine hypotension syndrome*, on the other hand, seems specific to a pregnant female, since the gravid uterus will compress the IVC; in an average pt, there wouldn’t be the same postural compression. +12
welpdedelp  this was the exact same reasoning I used, but I thought the RAAS would inactivate which would lead to less aldosterone and less sodium retention +3
yotsubato  You gotta be preggers to compress your IVC +5
nwinkelmann  Could you also think of it in a purely "rest/digest" vs "fight/fright/flight" response, i.e. you're PNS is active, so your HR and subsequently your CO is less? But the explanation given above does make sense. Also because I think just saying someone is one bed rest leaves a lot up for interpretation, maybe not with this patient because his pelvis is broken, but lots of people on bed rest aren't lying flat.... ? +1
urachus  wouldnt low aldosterone cause low plasma sodium? choice B +5
kpjk  could it be that, while low aldosterone levels decrease plasma sodium levels- there is also decrease in blood volume(plasma),so there wont be a decrease in the "concentration" of sodium +5
almondbreeze  FA 2019 pg 306 on Lt heart failure induced orthopnea - Shortness of breath when supine: increased venous return from redistribution of blood +
almondbreeze  if there was no HF, it would lead to increased CO --> decreased aldosterone +
theunscrambler  @peqmd thanks for sharing that. According to the presentation, the diuresis via ANP occurs (along with sodium), which is followed up by an increased in RAAS --> maintains sodium levels. This cycle can then continue. Slide 13. +
jj375  @urachus - Either BB or Sattar taught me this but I feel like it is often forgotten. "RAAS/Aldosterone affects blood volume, and ADH affects Na level". So Increasing aldosterone will increase blood levels however water follows the sodium so you will not get a change in sodium levels. ADH however does affect Na since aquaporins are bringing in water without affecting sodium levels. +


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