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 +0  (nbme23#42)

The patient had a total hysterectomy so a recurrence of cervical cancer is virtually not possible. Retroperitoneal fibrosis commonly results from radiation therapy to the pelvis, which can lead to bilateral hydronephrosis.

 +10  (nbme23#28)

Attributable risk = incidence in exposed – incidence in unexposed

= 30/1,000 (smokers) - 30/3,000 (nonsmokers)
= 0.03 - 0.01
= 0.02 (so the attributable risk is about 2%)

Applying it to a population of 10,000:

= 0.02 * 10,000
= 200

charcot_bouchard  What if i tell you this is a ques of Attributable risk % in exposed? AR= 0.02 / IR in exposed (30/1000) = 0.6667 30 case in 1000. So 300 case in 10,000 0.6667 x 300 = 200 or in another word 66% cases of 100 lung cancer cases in smokers is actually due to smoking. so in 300 cases of smokers 200 is actually due to smoking
charcot_bouchard  This is a mind fuck. Lemme tell u guys if any consolation while doing the ques during test i did it with AR = 0.02; NNH = 1/0.02 = 50. 50 persons smoke to cause 1 cancer. 10K smoke to cause 200 cancer.
ls3076  Sorry if this is a stupid question. Why is it incorrect to simply apply the same proportion (30 cancer per 1000 smokers) to 10,000 smokers?

 -1  (nbme24#7)

The diagnosis is strawberry hemangioma, commonly happens in kids, often resolves on its own as they get older.

shaeking  A strawberry hemangioma is normally pink or red (which is why it is named strawberry). The description has a flat purplish lesion which makes me think of a port wine stain on the face. How do you know to think of strawberry hemangioma over port wine based on this question stem?
sheesher  This sounds more like a nevus simplex, which is very similar to a port wine stain, though it regresses over time.
seagull  the age is key here. Newborns have strawberry hemangiomas typically on their face. Sturge-Weber could also be the case but none of the answer choices matched to that description.
vshummy  I would agree with Sturg Webber nevus flammeus but I also noticed First Aid says it's a non-neoplastic birth mark so I should have known not to pick malignant degeneration or local invasion. Also because capillary hemangiomas don't have to be flat but the nevus flammeus is consistently flat. But I'm also reading on Wiki that the nevus flammeus doesn't regress so they must be trying to describe strawberry hemangioma even though I don't agree with their color choice...
nala_ula  Maybe (and I can only hope I'm right and the test makers are not -that much of- sadists) they would have made sure to write "in a cranial nerve 5 (either ophthalmic or maxillary) distribution" if it were Sturge-Weber.

 +4  (nbme24#17)

Normally the arachnoid villi drains the CSF from the subarachnoid space to the venous system; if this part becomes defective then you can imagine all that CSF now building up in the subarachnoid space.

keycompany  Also take into account this patient had surgery that requires penetration into the subarachnoid space (hence through the arachnoid mater). This can lead to scarring of the arachnoid granulations and subsequent communicating hydrocephalus.

 +5  (nbme24#42)

He’s presenting with classic signs of vitamin B3 deficiency (niacin); niacin is required to form the cofactor NAD+ (nicotinamide adenine dinucleotide).

bigjimbo  B3 Niacin deficiency = Pellegra = diarrhea, dermatitis, dementia death. = Niacin combines with adenine to become NAD+ https://www.aocd.org/page/Pellagra

 +6  (nbme24#42)

The analysis only showed a mutation in one allele. CF is an autosomal recessive disease: the disease only manifests if there are mutations in both alleles of the CFTR gene.

If you still have 1 functional copy of the CFTR gene, you can still make the CFTR protein (the chloride channel/transporter), hence your body won’t have any issues.

This is analogous to tumor suppressor genes like Rb: so long as one of the alleles you have is functional, you can make enough of the protein to “make up” for the defective allele. If both get knocked out (Rb-/-), you lose the protection provided by the gene because now you make no protein at all.

The only thing that made sense for this question was the fact that the other allele was not included in the analysis.

charcot_bouchard  OR another allele has a diff type of mutation because CF is done by like hundreds of diff type of mutation. SO the 70 types that we screened covered one type from one parent but not another that was inherited from other parent.
soph  I put D thinking there was a mutation in another protein that interacts with CFTR....thus u dont have CF but some disease with similar phenotype. Is this wrong bc its simply not the case ??
nbmehelp  @charcot_bouchard I think that makes more sense if I understand what you're saying- Probably had a mutation only in 1 of 2 of the same alleles in the analysis but had another mutation in 2 of 2 alleles at a different location not included in the analysis, right?

 +7  (nbme24#34)

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 ...
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.
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.... ?

Subcomments ...

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. +1  
hyoid  Herpes zoster is not the same as herpes simplex virus. +4  
bigjimbo  you would see dermatome rash in zoster +1  
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. +2  
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. +  

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. +1  

Can someone explain why does this patient have hypokalemia?

colonelred_  Catecholamines activate the Na/K pump, which will drive K inside. +5  
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 +3  
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. +1  
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. +  

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. +3  
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 +1  
trichotillomaniac  This fits the timeline laid out in Pathoma! 1-3 wks = granulation tissue with plump fibroblasts, collagen, and blood vessels +  

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 +4  
drdoom  Nice schematic, @welpdedelp +  

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. +2  
brethren_md  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
sympathetikey  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
s1q3t3  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
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??? +8  
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 +5  
bigjimbo  LOL +  
fallenistand  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
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. +2  
charcot_bouchard  Hello, i just want to add that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
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? +  

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**." +2