and we’re back! with BRAND SPANKIN' NEW tangents!
welcome redditors!to snoo-finity ... and beyond!
Welcome to tea-cats-biscuits's page.
Contributor score: 64
School:


Comments ...

 +0  (nbme23#31)

I think I found what the disease was, though I honestly have no idea why they would test this rather than XLA. There’s a condition called Transient Hypogammaglobulinemia of Infancy. It presents w/low immunoglobulin levels post 6 months and can present w/small lymph nodes and tonsils in infancy BUT w/o any other findings of primary immunodeficiency including decreased counts.

Here’s an article about it: https://primaryimmune.org/about-primary-immunodeficiencies/specific-disease-types/transient-hypogammaglobulinemia-of-infancy/

You definitely don’t need to know the disease to get the correct answer since the link of lack of immunoglobulins would clue you into the lack of germinal centers, but I think this is more likely than XLA since every source I read implies that B cell counts are near 0 in the classic presentation (unless I’m missing a reason why leukocyte count w/diff wouldn’t show a significant decrease in lymphocytes due to near-zero B cells). Just wanted to put this here in case other people later came wondering, though I may still be wrong.

keycompany  I think we are all overthinking this question (and it is remarkably simple). I don't think this question is testing us on any of the UFAP immunodeficiency syndromes, per say. What they are really asking is "what would also be absent if there are no immunoglobulins and everything else is normal"? The answer is absent germinal centers b/c that's where Ig is synthesized. I think they put all other aspects of the history in this stem just to help you rule out any of the other answers.

 +5  (nbme24#25)

You know it’s an enveloped virus since it doesn’t hold up to acid or being dried. You know it causes a fever and a cough, while affecting the larynx. Only virus category that fits all that info is the coronavirus (causes SARS) from that list.

zelderonmorningstar  EBV doesn’t cause fever and cough?
zelderonmorningstar  Wow, just checked First Aid and it doesn’t list “cough” as a symptom of EBV.
drdoom  EBV is not a “respiratory virus”; it’s a *B cell virus*. Even though you might associate it with the “upper respiratory tract” (=kissing disease), it doesn’t cause respiratory inflammation since that’s not its trope. B cells are its trope! That’s why EBV is implicated in Burkitt Lymphoma, hairy leukoplakia and other blood cancers. (EBV is also known as “lymphocryptovirus” -- it was originally discovered “hiding” in *lymphocytes* of monkeys.) So, EBV = think B cells.
fulminant_life  EBV does cause pharyngeal and laryngeal inflammation along with fever, malaise, and cough and LAD. The only thing that pointed me away from mono and towards coronavirus was the patients age.
nbmehelp  Can someone explain what not holding up to acid or being dried has to do with being enveloped?
yb_26  @nbmehelp, the envelope consists of phospholipids and glycoproteins => heat, acid, detergents, drying - all of that can dissolve the lipid bilayer membranes => viruses will loss their infectivity (because they need an envelope for two reasons - to protect them against host immune system, and to attach to host cells surface in order to infect them)

 +7  (nbme24#34)

Because you are supine, there’s increased preload going back to your heart (no need to work against gravity, your blood isn’t pooling in your legs as much either). As a result, ANP is secreted due to RA stretch, leading to diuresis and a reduction of blood volume.


 +3  (nbme24#30)

Patient has cardiogenic shock, specifically the LV since it’s an anterior wall MI isn’t pumping. Honestly you don’t need to know what happens to PVR to answer correct since the only choice that has increased SVR and decreased PCWP is the one w/decreased PVR. I’m not absolutely sure if you could figure it out given the values in cardiogenic shock. The equation linking the values is:

PVR = (pulmonary arterial pressure - wedge) ÷ CO


 +8  (nbme24#29)

Partial agonists have weak agonist activity on their own (thus in this case it causes HR to increase, b-adrenergic effect) but when an actual agonist is present (aka when you are exercising, you are producing NE and E that have full b-agonist effects), partial agonist actually have a mild antagonist effect (thus the heart rate decreases).


 +5  (nbme24#42)

Fibronectin is an extracellular matrix glycoprotein, while lamin is an intermediate filament that specifically provides support to the cell nucleus. Don’t confuse lamin with laminin (science hates us clearly); laminin is like fibronectin, an ECM glycoprotein and a major component of the basal lamina of basement membranes.

masonkingcobra  Lamin looks like a "cross" and held up Jesus and the basal lamina is super important just like jesus (you bet there are people who believe this) https://answersingenesis.org/biology/microbiology/laminin-and-the-cross/
dr.xx  blasphemy @masonkingcobra

 +8  (nbme24#24)

The disease here is fructose bisphosphatase deficiency. In it, IV glycerol or fructose doesn’t help because both enter the gluconeogenesis pathway below fructose bisphophatase. Galactose on the other hand enters above it. I don’t think you really need to know this to choose the correct answer since the clinical picture of fasting hypoglycemia that is corrected w/ some sort of sugar that can enter the gluconeogenesis pathway should clue you into the right answer.

neonem  I don't think you could have *totally* ruled out the other answers - I picked glycogen breakdown because it sounded kind of like Von Gierke disease (glucose-6-phosphatase) to me: characterized by fasting hypoglycemia, lactic acidosis, and hepatomegaly since you're not able to get that final step of exporting glucose into the blood. However, I guess in this case you wouldn't see that problem of glycerol/fructose infusion not increasing blood glucose. Nice catch.
vshummy  I think you were super smart to catch Von Gierke! Just to refine your answer b/c I had to look this up after reading your explanation, von gierke has a problem with gluconeogenesis as well as glycogenolysis. So they’d have a problem with glycerol and fructose but also galactose since they all feed into gluconeogenesis before glucose-6-phosphatase. Great thought process!

 +15  (nbme24#28)

Mast cells degranulate, producing histamine which attracts eosinophils. The early stage of an allergic reaction is mast cell mediated, but the late stage (including mucus production) is mediated by eosinophils.

atstillisafraud  Thanks for a good answer. This question made me feel like I was taking T21 pills




Subcomments ...

Can anyone explain how 10cm H20 positive PEEP leads to Peak Inspiratory PA, End Tidal PA, Peak Inspiratory Pip and End Tidal Pip all being positive?

tea-cats-biscuits  In PEEP, bc of how mechanical ventilation works, all the inspiration part of breathing is done by the machine actively pushing air into the lungs. As a result, there is no negative pressures in the system compared to the normal lung which needs the negative inter-pleural pressure to draw air in. +8  
yotsubato  " As a result, there is no negative pressures in the system compared to the normal lung which needs the negative inter-pleural pressure to draw air in. " Thats totally what threw me off. TIL +  


I picked NMDA because it’s stimulatory, but is there any deeper reason for this?

tea-cats-biscuits  The Q is actually asking which of the receptors use Ca+ ions, and of the choices given only NMDA receptors do so. +2  


I thought that the primary sympathetic innervation to the heart was through T1-T4. Why would stimulation of this ganglion not affect skin vessels in the upper limb?

methylased  Stellate ganglion --> sympathetics for sweat to skin in UE + head. Apparently also to increase HR (some cardiologists ablate stellate ganglion for tachy that cant be controlled by beta blockers). +  
tea-cats-biscuits  The stellate ganglion is a sympathetic ganglion, so it wouldn’t increase vasodilation in the skin of the upper extremity. Also in most people, the inferior cervical ganglion is fused with the first thoracic ganglion (T1), forming the stellate ganglion. +1  
sympathetikey  Got this wrong too. I think upper extremity skin vasodilation (which I picked) is probably more due to local metabolites. +  


submitted by hipster_do(2),

I’m going to say it’s X linked agammaglobulinemia rather than SCID, but the difference between these two are tiny but this is why I think it’s the former:

  • Boy (increased risk but both BA and SCID are x linked)
  • Recurrent bacterial infections but don’t mention diarrhea or thrush which is in SCID
  • Timeline is after 6 months, so the mother’s antibodies wore off.

SCID should be immediately because they just don’t have the IL2 receptors. CVID shows up when they’re 20-40 years old. You get absent germinal centers in both. No mention of absent thymic shadow which is in SCID.

placebo079  “Uniformly” low is also a clue; in CVID they are not. +  
tea-cats-biscuits  This makes sense, though what really threw me off was that in Classic Bruton’s Agammaglobulinemia there’s near-zero B counts though (or at least that’s what FA and UTD says, “Absent B cells in peripheral blood” FA 116, 2018). The Q says the leukocyte count was normal though. Wouldn’t the leukocyte count include lymphocytes in the differential? And wouldn’t lymphocytes be low due to the near complete lack of B cells in peripheral circulation if it was BA? +  
partybrockk  @tea-cats-biscuits Bruton’s is a failure of B cells to /MATURE/. So you get normal lymphocyte counts, decreased levels of immunoglobulins, and absent germinal centers. +  
tea-cats-biscuits  @partybrockk That makes sense to me, but I keep getting hung up on how that’s not what either FA or UTD says about the classic lab findings of XLA. UTD specifically says this: “Laboratory findings include hypogammaglobulinemia/agammaglobulinemia, deficient antibody responses to immunizations, and absent or markedly reduced B cells in the blood,” and I previously quoted FA. I suppose it doesn’t really matter, but it’s definitely a bit frustrating unless I’m missing something about how absent B cells in the blood wouldn’t correlate to a decreased lymphocyte count ... +  
temmy  please correct me if i am wrong cos i might be but my logic was there is decreases immunoglobulin uniformly meaning the B cells are uniformly absent and since they develop in the germinal center, the germinal center will be absent. +  


submitted by hipster_do(2),

I’m going to say it’s X linked agammaglobulinemia rather than SCID, but the difference between these two are tiny but this is why I think it’s the former:

  • Boy (increased risk but both BA and SCID are x linked)
  • Recurrent bacterial infections but don’t mention diarrhea or thrush which is in SCID
  • Timeline is after 6 months, so the mother’s antibodies wore off.

SCID should be immediately because they just don’t have the IL2 receptors. CVID shows up when they’re 20-40 years old. You get absent germinal centers in both. No mention of absent thymic shadow which is in SCID.

placebo079  “Uniformly” low is also a clue; in CVID they are not. +  
tea-cats-biscuits  This makes sense, though what really threw me off was that in Classic Bruton’s Agammaglobulinemia there’s near-zero B counts though (or at least that’s what FA and UTD says, “Absent B cells in peripheral blood” FA 116, 2018). The Q says the leukocyte count was normal though. Wouldn’t the leukocyte count include lymphocytes in the differential? And wouldn’t lymphocytes be low due to the near complete lack of B cells in peripheral circulation if it was BA? +  
partybrockk  @tea-cats-biscuits Bruton’s is a failure of B cells to /MATURE/. So you get normal lymphocyte counts, decreased levels of immunoglobulins, and absent germinal centers. +  
tea-cats-biscuits  @partybrockk That makes sense to me, but I keep getting hung up on how that’s not what either FA or UTD says about the classic lab findings of XLA. UTD specifically says this: “Laboratory findings include hypogammaglobulinemia/agammaglobulinemia, deficient antibody responses to immunizations, and absent or markedly reduced B cells in the blood,” and I previously quoted FA. I suppose it doesn’t really matter, but it’s definitely a bit frustrating unless I’m missing something about how absent B cells in the blood wouldn’t correlate to a decreased lymphocyte count ... +  
temmy  please correct me if i am wrong cos i might be but my logic was there is decreases immunoglobulin uniformly meaning the B cells are uniformly absent and since they develop in the germinal center, the germinal center will be absent. +  


Why is the answer decreased blood volume as opposed to decreased plasma sodium concentration?

tea-cats-biscuits  I think it might just be what NBME feels “decreased plasma sodium concentration” means, since through the mechanism that BV is lowered in bedrest, you would definitely have a decreased plasma sodium concentration compared to not-bedrest. However you won’t be presenting with any pathologic signs of hyponatremia because the Na+ would still be maintained in normal limits. Low blood volume is the cause of one of the main pathologic states associated w/bedrest -- cardiac deconditioning and postural hypotension once out of bedrest. Seems like poor wording though. +1  
mnemonia  Remember that changes in sodium concentration over a long period time need to be due to a water dysregulation problem (like SIADH, polydipsia, HF, etc.). Here we just have physiologically increased effective circulating volume, and the body will compensate by diuresing, and since Na+ (and K+) are regulated ions, their plasma levels will not fluctuate. +2  


submitted by colonelred_(44),

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.

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 ... +1  
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. +1  
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 +  
yotsubato  You gotta be preggers to compress your IVC +  
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.... ? +  


submitted by stapes2big(3),

I’m not sure about this one but the way I thought about it was that since the confidence interval included 1, it was not significant. And thus p value must be above 0.05

tea-cats-biscuits  That makes sense! +  
asapdoc  Had the same reasoning +1  
jkan  I get that it's not significant, but why is it 0.05<p<1 and not p>1.0 +3  
jkan  nvm, it's can't be greater than 1 because then it would have a negative% confidence interval which cannot happen (Think if p>0.05 means at least 95% within confidence interval) +3  
charcot_bouchard  p=0.05 means theres 5% chance null hypothesis is true. p=1 means theres 100% chance null hypothesis is true. >1 means >100% chance which isnt possible. +1  
wowo  p is a probability, so can't be greater than 1 +3  


Why is alternative splicing or post-transcriptional modification incorrect?

tea-cats-biscuits  You just have to know that POMC is a pro-protein that must be cleaved; not sure if there’s anything in the stem that would really have given it away. +  
mcl  Dunno if this helps, but it says "this protein" (singular) is the precursor of two different protein products. This must mean that the modification occurs after the protein is made, which means after transcription and splicing has already happened. +2  
ngman  Also I believe mRNA refers to after the splicing already occurs. If the protein products are from the same mRNA then it can't be alternate splicing. +  
medschul  They're cleaved by tissue-specific proteases +  
duat98  I think: Alternative splicing occurs with hnRNA not mRNA. You get mRNA from alternatively splicing the hnRNA. an mRNA can only make 1 type of protein. Since the question says the 2 proteins comes from the same mRNA it cannot be alternative splice or post transcriptional mod. FA 2018 page 43 has a good illustration. +3