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Comments ...

 +0  (nbme22#10)

Wouldn't telling the patient about the referral do more harm than good?

  1. Pt considers it a bribe and leaves
  2. Ruins study due to placbo effects
  3. Puts doc/hospital at risk for potential legal hassle.

I guess maybe I read it as a study when it really is just a referral but its not that much of a leap to think that this "experimental"" treatment is part of a study

drzed  I think this more of an ethical question (not a legal, or study design problem). Ethically, between the choices of being transparent with your patient, or not, the choice would be to disclose. Disclosing and offering to share would come across as a bribe, so that is less favorable than simply being transparent and putting the patient in charge of their decision.




Subcomments ...

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. +4  
brethren_md  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +3  
sympathetikey  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +4  
s1q3t3  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +3  
masonkingcobra  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +2  
mcl  Wait, but did anyone mention that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen??? +24  
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 +9  
bigjimbo  LOL +  
fallenistand  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +4  
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. +6  
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? +3  
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" +1  
youssefa  Hahahahaha ya'll just bored +2  
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 +3  
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? +1  
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 +  
deathbystep1  i am sure i would ace STEP 1 if i only knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
noplanb  Wait... I might actually never forget this now lol +1  
drmohandes  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +1  
lilmonkey  Don't forget that females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens! You're welcome! +  
drpatinoire  Now I get it that females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens. Thank you very much.. So why choose Sertoli-Leydig cell tumor again? +  
dr_ligma  The reason is because females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens! This is easy to remember, as you can remember it through the simple mnemonic "FCGSLCTWANFPLOA" which stands for "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen!" +9  
minion7  after receiving a f*king score..... this post made me smile and thanks to the statement-- females can get sertoli-leydig cell tumours, which are notorious for producing lots of androgen! +1  
djtallahassee  My worthless self put adrenal zona fasciculate but now I will never forget that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
medguru2295  Wait..... so can females get Sertoli Leydig cells that produce androgens then?????? +  
peqmd  Going to snapshot this to my anki deck card: "females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of {{c1::androgens}}" +  
paperbackwriter  Watch me f*ck up the fact that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgens on the real deal. +  
alexxxx30  just made sure to add to my notes "Females can get sertoli leydig cell tumors, which are notorious for producing lots of androgens" +  


submitted by cocoxaurus(48),

The presentation here seems to fit that of mesenteric vascular occlusion- postprandial pain that lasts 1 hour, food aversion, weight loss. The patient also has risk factors associated with mesenteric vascular occlusion- older than 60 years old, Hyperlipidemia, Hypertension, PMHx.

"The mesenteric circulation consists of three primary vessels that supply blood to the small and large bowel: the celiac artery, superior mesenteric artery (SMA), and inferior mesenteric artery (IMA). Blood flow through these arteries increases within an hour after eating due to an increase in metabolic demand of the intestinal mucosa.Chronic occlusion of a single vessel allows collateral blood flow to compensate, thus symptoms do not typically present until at least two primary vessels are occluded." https://www.ncbi.nlm.nih.gov/books/NBK430748/

Collaterals between SMA and IMA near the splenic flexure (Meandering Mesenteric artery). There is also collateral between Celiac Artery and SMA (Pancreaticoduodenal arcade).

Lastly, I know that there is a 3-cm ectatic aorta found on CT, but an aortic aneurysm would not produce these symptoms. Even if you thought that the symptoms were due to the AAA, you could still get to the correct answer if you use fahmed14's reasoning.

honey-crusted lesion  Great explanation! There's also a slide about this in the 100 Anatomy Concepts pdf but doesn't go into as much detail as this explanation. Thanks! +  
djtallahassee  Good explanation but I think an AAA would be more likely superior mesenteric and hepatic. the SMA and IMA are more than 3 cm apart (L1 to L4ish), Triple A affecting both would be very large. I blew this question because I saw 3cm and jumped to AAA, didnt even see it was a sclerosis thing. Put the two closest arteries and moved on +  


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. +15  
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! +17  
drmomo  glycerol and fructose both enter the pathway thru DHAP and glyceraldehyde-3-ph. Galactose enters thru Gal-1-ph to glu-1-ph conversion +2  
linwanrun1357  In this cause (fructose bisphosphatase deficiency.,),fructose should help to increase serum glucose, bcz it can become into glucose-6-P by hexokinase. Therefore, this question makes me confused.... +  
krewfoo99  According to uworld, fructose infusion will not increase blood glucose levels in Von Gierkes Disease as well +  
atbangura  I believe Von Gierke is not a plausible answer choice because a galactose infusion would still not see an elevation in glucose levels. Remember, galactose could be converted to galactose 6 phosphate, but in order to complete gluconeogenesis and allow glucose to leave the Liver for an increase of its concentration in the blood, the patient would still need glucose 6 phosphatase which is eliminated in Von Gierke. +1  
lilyo  So what disease is this??? I mean couldnt we have just answered the question based on the fact that the patient responds to galactose being infused and we know that galactose feeds into gluconeogenesis?? I am so confused. +1  
djtallahassee  Its Hereditary Fructose intolerance right? gets sick after fructose and I guess glycerol can jump in via aldolase B on this pathway via page 74 of FA2019. It looked like a fructose thing to me so I just marked out the other ones and moved on. +  
paperbackwriter  @djtallahassee I was wondering same, but hereditary fructose intolerance also results in inhibition of glycogenolysis :/ confusing question. +  
mdrahimi7  See linwanrun1357 because very few amount of fructose metabolize by hexokinase and most of them goes through aldolase b so they need fructose b is phosphatase +  
mdrahimi7  See @linwanrun1357 because very few amount of fructose metabolize by hexokinase and most of them goes through aldolase b so they need fructose bis phosphatase. +  


submitted by jrod77(21),

I think they might be describing angina...not sure. TXA2 is responsible for platelet aggregation,so it may be contributing to thrombosis, thus ischemia to the cardiac tissue.

sympathetikey  Agreed. I'm pissed though because PGE2 mediates pain, which is why I picked it. +17  
he.sanchez14  If im not mistaken, the question describes unstable angina. Unstable angina is due to thrombosis with incomplete occlusion. So, yes TXA2 is responsible for the thrombus that is causing the symptoms in this patient. I'm also pissed because I also went straight for the PGE2 +2  
vik  hahah, seems like all in same boat like me +  
yb_26  thromboxane A2 is also vasoconstrictor, so my thoughts were about vasospastic angina +1  
shriya goyal  same I went for pgE2 ... I M PISSED +1  
shriya goyal  same I went for pgE2 ... I M PISSED +  
youssefa  Went for PGE2 ... shit +  
need_answers  I went for leukotriene B4, what the hell was I doing....SHIT +3  
hopsalong  I picked Leukotrine B4 thinking that the neutrophil infiltration was the source of the pain, seems wrong lol. +  
bballhandler11  Sometimes it helps me to think of it in a general, non med school textbook kind of way. When answering, I narrowed it down to PGE2 and TXA2 as well. Then I asked myself, if someone is experiencing chest pain, would I recommend Aspirin or Advil? That's helped on a few over the counter pharm questions. +4  
ususmle  same here I M PISSED PGE2 +1  
krewfoo99  Maybe PGE2 isint the answer because it mediates pain and fever during episodes of acute inflammation? Thus making TXA2 more likely. +1  
djtallahassee  ditto on the looked at it for 2 seconds and went PGE2 +  


submitted by welpdedelp(154),

The pt had asthma (SOB, wakes up at night out of breath, has allergies). It asked for the precursor of leukotrienes, which is arachidonic acid. The prob gave him Montelukast or inhaled glucocorticoids.

ls3076  wtf is up with the phrasing of this question +19  
djtallahassee  Must have been Montelukast right? Since GCs do more of a downregulation thing than a true receptor blocking. Maybe I am not reading that last sentence correct though. +  
alexxxx30  @Is3076 haha agreed!! +  


submitted by sam1(12),

What about the additional flow through the circumflex?

maddy1994  exactly man i got 4.5 and i thought he asked ventricle and left circumflex should be there so i put 5 ...glad someone thought like me.i was just cursing myself for over thinking. +6  
djtallahassee  Yea put 5 here too. they are essentially saying the myocardial oxygen supply to the left ventricle comes from the LAD. Not sure if true or not but figured that the LCX would at least contribute 20% of the blood +  
justherefortheyield  100% agree. This is definitely a better answer. I assumed the # would be beyond 5 but that it was closest to the right value. +  


submitted by nwinkelmann(218),

So this question was something I really struggled with. I didn't recognize that the presentation was of MERRF as someone stated below, and I know you don't need to know that to answer the question, but it would have been helpful. My biggest frustration was the wording of the biopsy results "abnormal accumulations of mitochondria." This annoyed me because the definition of ragged red fibers (which I'm assuming was their intention) is "accumulations of abnormal mitochondria." Those are two very different statements in my mind, lol. The first, to me, just means there's too much mitochondria, but the second means there's too much AND they aren't functioning properly. It's also just the fact of remembering all of the terms for ETC at the time of reading the question (i.e. I didn't think about the fact that ETC is also called cellular respiraton or just respiration).

I also didn't really understand fully what VO2max is = "VO2 max, also known as maximal oxygen uptake, is the measurement of the maximum amount of oxygen a person can utilize during intense exercise... and is based on the premise that the more oxygen consumed during exercise, the more the body will generate adenosine triphosphate (ATP) energy in cells... VO2 max is reached when your oxygen consumption remains at a steady state despite an increase in the workload. It is at this plateau that the [muscle] moves from aerobic metabolism to anaerobic metabolism" https://www.verywellfit.com/what-is-vo2-max-3120097.

Based purely on this definition, where VO2max = essentially the time at which aerobic switches to anaerobic respiration, my interpretation of too much mitochondria vs too much and bad mitochrondria didn't matter, because even when the mitochondria are functioning properly, they reach a point and switch to anaerobic, thus if there was too much normal mitochondria, this would occur faster because there would be more overall cellular respiration occuring, meaning the body would switch to anaerobic and utilize glycolisis to lactate for energy, stop utilizing the mitochondria, and thus VO2max would decrease.

HOWEVER.... because this is a MERRF question, the order of events is a little different, despite the outcome being the same (at least that's how I understand it). So, I think the key to any mitochondrial disorder is remembering that the mutations are almost certainly going to affect an encoded protein and thus a deficiency of that protein. One article that I found said that the tRNA mutations (as in MERRF) cause: "disrupt mitochondrial protein synthesis, decreasing the activity of Complex I and to a lesser extent Complex IV... which decreases respiration and lowers proton pumping, dramatically decreasing the membrane potential and proton electrochemical potential gradient across the mitochondrial inner membrane. The proton electrochemical potential gradient is the driving force for ATP synthesis and decreasing it substantially lowers the maximal rate of ATP synthesis." https://febs.onlinelibrary.wiley.com/doi/full/10.1046/j.1432-1327.1999.00066.x

Based on my understanding of oxidative phosphorylation, O2 consumption (i.e. taking the electron from complex IV and putting it on 1/2 O2 to create H2O and H+ drives the proton gradient which drives ATP production. Thus: deficient respiratory oxidation (i.e. mtDNA mutations of the ETC enzymes) leads to lowered O2 consumption (so lowered VO2 max) which then leads to lowered ATP production, and thus defective mitochondria. Then, lowered mitochondrial function leads to decreased aerobic respiration shunting ATP production to anaerobic respiration, driven by glycolysis, and thus increasing lactate levels.

Hope this helps! This took me WAY TOO LONG to figure out, lol, but hopefully I never freaking forget it, lol.

Also, if you want any more reading, I finally found an article that actually fully explains the biochemical and pathophysiology of mitochondrial myopathies: https://academic.oup.com/brain/article/126/2/413/332457

Sorry it's so long!

djtallahassee  lol yea. I thought they were trying to say there was an abnormally large amount of mitochondria present which made me get the opposite answer :/ +1  
alexxxx30  no I so agree. The grammar was completely wrong (clearly whoever wrote the question needs to work on english). This was very frustrating to me because I recognized that it was ragged red fibers, but then the wording made me doubt my own knowledge (thinking how could the test writer mess that up?). abnormal accumulations either means too much or too little. accumulations of abnormal mito means thee mitochondria is faulty. Correct grammar is putting the adjective right next to the word it is describing. So this was definitely wrong and I share your sentiment. This really frustrated me! +1  


submitted by adong(51),

literally know every single name they can possibly call this

djtallahassee  literally a new name every nbme +4  


submitted by seagull(839),

out of curiosity, how may people knew this? (dont be shy to say you did or didnt?)

My poverty education didn't ingrain this in me.

johnthurtjr  I did not +1  
nlkrueger  i did not lol +  
ht3  you're definitely not alone lol +  
yotsubato  no idea +  
yotsubato  And its not in FA, so fuck it IMO +1  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +10  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +14  
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +  
jaxx  Not a clue. This was so random. +  
wolvarien  I did not +  
ls3076  no way +  
hyperfukus  no clue +  
mkreamy  this made me feel a lot better. also, no fucking clue +1  
amirmullick3  My immediate thought after reading this was "why would i know this and how does this make me a better doctor?" +5  
mrglass  Generally speaking Glutamine is often used to aminate things. Think brain nitrogen metabolism. You know that F-6-P isn't an amine, and that Glucosamine is, so Glutamine isn't an unrealistic guess. +2  
djtallahassee  yea, I mature 30k anki cards to see this bs +3  
taediggity  I literally shouted wtf in quiet library at this question. +1  
bend_nbme_over  Lol def didn't know it. Looks like I'm not going to be a competent doctor because I don't know the hexosamine pathway lol +1  
drschmoctor  Is it biochemistry? Then I do not know it. +2  
snoochi95  hell no brother +  
roro17  I didn’t +  
bodanese  I did not +  
hatethisshit  nope +  
jesusisking  I Ctrl+F'd glucosamine in FA and it's not even there lol +  
batmane  i definitely guessed, for some reason got it down to arginine and glutamine +1  
waterloo  Nope. +  
monique  I did not +  
issamd1221  didnt +  
baja_blast  Narrowed it down to Arginine and Glutamine figuring the Nitrogen would have to come from one of these two but of course I picked the wrong one. Classic. +  
amy  +1 no idea! +  


submitted by d_holles(104),

Can portal HTN contribute to hepatic encephalopathy?

djtallahassee  Sorry for the late add. Portal system does contribute to hepatic enceph ESPECIALLY when there is a TIPS or shunt that bypasses the liver. However before, it won't directly contribute to more NH3+ +1  


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