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 +1  (nbme24#44)

Why do you give IV leucovorin with intrathecal methotrexate? Wouldn’t MTX lose its efficacy since leucovorin reverses the effects of MTX?

colonelred_  MTX will still work but yes some purine/pyrimidine synthesis can still occur. You often give leucovorin to decrease adverse effects of MTX.
welpdedelp  ok I have a question, leucovorin is the same as folic acid...so why give one over the other?
lsmarshall  Leucovorin, folinic acid, is a modified version of THF and enter folate metabolism where THF is, after the point where methotrexate takes its effect. I have a pharm. card that says "toxic effects on normal cells may be reduced by administration of folinic acid (a.k.a. leucovorin or citrovorum factor), which is **preferentially taken up by normal cells versus tumor cells**."

 +1  (nbme24#27)

Can someone please explain this? What is the diagnosis here?

welpdedelp  I thought it just as it was, polyneuropathy is supposed to be a burning pain affecting the extremities, he might have acute intermittent porphyria. He was too young and didn't fit ALS due to the rapid onset. No loss of pain in the arms so it couldn't be syringomelia. Wasn't asymmetric so couldn't be polio. Didn't have anything resembling Parkinson.

 +0  (nbme24#4)

Why was the acute hemolytic transfusion reaction due to ABO incompatibility, but not Rh incompatibility?

colonelred_  Rh incompatibility comes more into play with Rh- mother and Rh+ babies.

 +0  (nbme24#21)

Why is it aphthous ulcers if there are no GI symptoms? Why can’t it be herpes zoster?

colonelred_  It’s just canker sores, they come and go. I think in herpes the gingivostomatitis really only happens when you first get infected. After that you just get recurrent cold sores.
hyoid  Herpes zoster is not the same as herpes simplex virus.
bigjimbo  you would see dermatome rash in zoster
kateinwonderland  cf) Just in case someone wanted to know the causative organism of aphthous ulcers :The precise cause of canker sores remains unclear, though researchers suspect that a combination of factors contributes to outbreaks, even in the same person. Unlike cold sores, canker sores are not associated with herpes virus infections.
charcot_bouchard  Herpes Zoster doesnt cause gingivostomatitis. Herpengina can cause vesicular lesion in mouth but happens to children in summer season by entero virus
drdeeznuts1  I'm wondering if this could be a mild case of Behcet syndrome without genital involvement
sherry  It sure can be Behcet or Pemphigus if the q provides us with more info. Canker sores just come and go for years with unclear mechanism. Also herpes zoster is shingles by VZV, not HSV1.

 +0  (nbme24#26)

Why is it not ovarian follicle cells? I thought the female analog of Sertoli and Leydig is theca/granulosa cells.

colonelred_  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen.
brethren_md  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen
sympathetikey  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen
s1q3t3  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen
masonkingcobra  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen
mcl  Wait, but did anyone mention that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen???
mcl  But seriously though, pathology outlines says sertoli-leydig tumor "may be suspected clinically in a young patient presenting with a combination of virilization, elevated testosterone levels and ovarian / pelvic mass on imaging studies." As for follicle cell tumors, granulosa cell tumors usually occur in adults and would cause elevated levels of estrogens. Theca cell tumor would also primarily produce estrogens. Putting the links at the end since idk if they're gonna turn out right lol Link pathology outlines for sertoli leydig granulosa cell tumor theca cell tumor
bigjimbo  LOL
fallenistand  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen.
medpsychosis  So after doing some intense research, UPtoDate, PubMed, an intense literature review on the topic I have come to the final conclusion that...... ...... ...... ...... Wait for it.... ..... ..... Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen.
charcot_bouchard  Hello, i just want to add that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen
giggidy  Hold up, so I'm confused - I read all the posts above but I still am unsure - are sertoli-leydig cells notorious for producing androgen?
subclaviansteele  Hold the phone.....Females can get sertoli leydig cell tumors which are notorious for producing androgen? TIL TL;DR - Females can get sertoli leydig cell tumors = high androgens
cinnapie  I just found a recent study on PubMed saying "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen"
youssefa  Hahahahaha ya'll just bored
water  Bored? you wouldn't think so if you knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen
nbmehelp  I dont get it
redvelvet  how don't you get it that females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen?
drmomo  what if this means..... females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen
sunshinesweetheart  hahahaha this made my day #futurephysicians #lowkeyidiots
sunshinesweetheart  @medstruggle look up placental aromatase deficiency (p. 625 FA 2019), it would have a different presentation

 +2  (nbme24#26)

Can someone explain why does this patient have hypokalemia?

colonelred_  Catecholamines activate the Na/K pump, which will drive K inside.
trazabone  Read online that catachelamines are released following tonic clonic seizures. Besides that, BP of 180/100 could indicate that catecholamines are circulating.
fulminant_life  This mechanism is why giving albuterol for hyperkalemia works
nbmehelp  Why does this guy have increased catecholamines tho
johnson  His SNS activity is seriously increased --> increased catecholamines.
nbmehelp  Why is his SNS activity increased? Is the BP literally the only hint?
youssefa  Alcohol withdrawal creates a hyper- catecholaminergic state + Seizures do that as well.
water  My best guess is that withdrawal puts the body in a state of stress (same for seizures) and with stress you have release of catecholamine which we'll see in the BP and the hypokalemia.

 +0  (nbme24#20)

Why is the answer “granulation tissue”? I thought after 14 days you have a fully formed scar.

colonelred_  If you go back and look at the image you can see that it was highly vascular which is characteristic of granulation tissue. Scar tissue formation will be closer to 1 month, plus you will see lots of fibrosis on histology.
sympathetikey  It's a bit misleading, for me, since you do see fibrosis intermixed with the granulation tissue, but granulation tissue was a better answer.
haliburton  According to FA 2017: 3-14d: Macrophages, then granulation tissue at margins. 2wk to several months: Contracted scar complete. Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus). i'm getting pretty frustrated with NBME contradictions to FA, and FA omissions of content. this stuff is hard enough to get straight as it is.
yotsubato  Thats cause the NBME exam writers read FA, then make questions not fit in with FA
trichotillomaniac  This fits the timeline laid out in Pathoma! 1-3 wks = granulation tissue with plump fibroblasts, collagen, and blood vessels

 +0  (nbme24#48)

Why is duodenal lumen incorrect? I thought pancreatic enzymes (chymotrypsin, carboxypeptidase) would be located here.

colonelred_  Enterokinase actives trypsinogen and is located closer to the intestinal mucosal (“brush border”).
drdoom  Yeah, @colonelred is right. @medstruggle: the duodenal lumen (and the pancreatic /proteases/ you mention) is the site where pancreatic enzymes (“endopeptidases”) cleave large polypeptides into smaller bits. It is at the BRUSH BORDER where the smallest kinds of peptides (dipeptides, tripeptides) are broken down into their amino acids, which finally can be co-transported with Na+ into the intestinal cell. I think about it this way: stomach acid denatures and “opens up” proteins (without any specific cleavage); pancreatic enzymes then cleave denatured polypeptides into smaller bits; brush border enzymes finally break down tiny peptides into absorbable amino acids.
welpdedelp  http://1.bp.blogspot.com/-UDdBiBiEgec/UzM61mV4pTI/AAAAAAAABRA/_qCG05fliGk/s1600/VBN.PNG
drdoom  Nice schematic, @welpdedelp

 +0  (nbme24#40)

Whats the difference between “heterozygous null mutation in B globin gene” and “heterozygous mutation known to cause 50% decrease in B globin gene function of one allele”?

welpdedelp  I interpreted "null" as meaning full deletion while the other heterozygous mutations was only a 50% decrease in the function. One child would inherit 1 null mutation and 1 50% mutation, which would leave them with a 25% functional gene.

 +0  (nbme24#31)

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.
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.




Subcomments ...

submitted by colonelred_(46),

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 ... +2  
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 +1  
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.... ? +1  
urachus  wouldnt low aldosterone cause low plasma sodium? choice B +