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 +1  (nbme23#15)

so should we just skip these? cuz there's prob 10 more i couldve gotten write wasting my life on this one


 +0  (nbme22#15)

I think that since they're asking for an explanation of the patient's current SSx which shows that she's in the state of Transient Hyperthyroidism: which is due to C: Release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes


 +1  (nbme22#37)

so the lesion is in the Right MLF right? If so I'm just about to memorize the eye see SAME MiLF lol its the MLF on the same side of the eye keep it simple i hope that's what yall are saying lol


 +2  (nbme22#2)

so I think if you forget actual drugs on the market that we know of and how they work, the question is purposely not asking you that specifically...If you flip it in your head to think what the problem is that leads to inc TG its because of VLDL therefore they said administering a DRUG with which of the following EFFECTS is MOST appropriate--->DECREASING VLDL b/c that's the culprit

Although drugs we know of have the other characteristics, for this guy, we would be looking for the effect of VLDL everything else is a side thing that doesn't directly address his condition


 +0  (nbme21#6)

Also another key is it says normal appearing girl one of the things about the AIS is that they do get secondary sexual characteristics...turner girls don't look normal they'd be short and stubby no boobs fat neck etc


 +0  (nbme21#31)

also in case they ask remember that these are PUFA's(have double bonds) and they are better than Saturated fats(no double bonds)+carbs





Subcomments ...

submitted by docred123(3),

Hey can someone please explain this! I am not sure how to do the math, I keep getting tripped up.

mousie  Equation is Maintenance dose = (concentration at steady state) * (Clearance) if you convert all the units to what it wanted them in (mg/kg/day) you'll get 25.92 like weird-in said above I didn't think to round 0.09 to 0.1 of course so I guessed 2.5 assuming I must have done a conversion wrong and was off by a tenth .... BOO bad Q +4  
hyperfukus  OMG ME TOO!!!!! +  


submitted by wired-in(29),

Maintenance dose formula is (CssCltau)/F where Css is steady-state target plasma conc. of drug, Cl is clearance, tau is dosage interval & F is bioavailability.

Neither dosage interval nor bioavailability is given, so ignoring those & plugging in the numbers (careful to convert units to mg/kg/day): (12 ug/mL * 1 mg/1000 ug) * (0.09 L/hr/kg * 1000 mL/1 L * 24 hr/1 day) = 25.92 mg/kg/day

...which isn't any of the answer choices listed. They must have rounded 0.09 L/hr/kg to 0.1 L/hr/kg, and doing so gives exactly 28.8 mg/kg/day (choice C)

lispectedwumbologist  That's so infuriating I stared at this question for 20 minutes thinking I did something wrong +20  
hyoid  ^^^^^ +2  
seagull  lol..my math never worked either. I also just chose the closest number. also, screw this question author for doing that. +2  
praderwilli  Big mad +4  
ht3  this is why you never waste 7 minutes on a question.... because of shit like this +5  
yotsubato  Why the FUCK did they not just give us a clearance of 0.1 if they're going to fuckin round it anyways... +6  
bigjimbo  JOKES +  
cr  in ur maths, why did u put 24h/1day and not 1day/24h? if the given Cl was 0.09L/hr/kg. I know it just is a math question, but i´d appreciate if someone could explain it. +  
d_holles  LMAO games NBME plays +  
hyperfukus  magic math!!!!! how TF r we supposed to know when they round and when they don't like wtf im so pissed someone please tell me step isn't like this...with such precise decimal answers and a calculator fxn you would assume they wanted an actual answer! +  
jean_young2019  OMG, I've got the 25.92 mg/kg/day, which isn't any of the answer choices listed. So I chose the D 51.8, because 51.8 is double of 25.9......I thought I must have make a mistake during the calculation ...... +  
atbangura  They purposely did that so if you made a mistake with your conversion like I did, you might end up with 2.5 which was one of the answer choices. SMH +  
titanesxvi  I did well, but I thought that my mistake was something to do with the conversion and end up choosing 2.5 because it is similar to 25.92 +  


submitted by welpdedelp(75),

No diet deficiency, the patient had excess carotene due to his diet

sympathetikey  Would never have thought of that. Thanks +2  
medschul  that's messed up dog +3  
hpkrazydesi  Excess carotene in what way? sorry if thats a stupid question +  
davidw  this is directly from Goljan "Dietary β-carotenes and retinol esters are sources of retinol. β-carotenes are converted into retinol. (a) Increased β-carotenes in the diet cause the skin to turn yellow (hypercarotenemia). Sclera remains white, whereas in jaundice the sclera is yellow, which can be used to distinguish the two conditions. (c) Vitamin toxicity does not occur with an increase in serum carotene" +2  
davidw  β-Carotenes are present in dark-green and yellow vegetables. +  
hyperfukus  ohhhh hellllll no +  
dashou19  When I was a little kid, I like to eat oranges, like I could eat 10 oranges at once, and after a few days, I could tell that I turned yellow... +  


submitted by yotsubato(286),

Although acetaminophen (Tylenol) is not considered an NSAID, it too may provoke an aspirin-like sensitivity.

meningitis  For that same reason (not an NSAID) it doesn't reduce inflammation so it cant be used for Gout. +1  
meningitis  And I think Indomethacin is associated with anaphylactic reactions in patients with aspirin-sensitive asthma and aspirin allergies. Can anyone confirm? +  
link981  How many other's like me didn't see "allergic to aspirin"? FML +1  
hyperfukus  OMFG me too i just got so mad and questioned my whole life at least its cuz i can't read not bc i don't understand :((((( +1  


Why is the answer adenylyl cyclase? I looked in FA and I saw that GH uses the JAK2/STAT pathway and that IGF-1 uses the MAP Kinase pathway. Not sure how adenylyl cyclase plays into this.

pug_sheen  I think they are talking about the GHRH receptor on somatotrophs, which works through the cAMP pathway. +  
staygoodpupper  I don’t know how it relates to GH/IGF-1 in particular, but the question said there was a mutation in the alpha subunit of Gs, which activates adenylyl cyclase. +2  
kash1f  I agree the patient does have Acromegaly, but in the question it talked about how the patient had a mutation that prevented the GTPase activity of Gas. So Gs would be overactive --> excess adenylyl cyclase +5  
hyperfukus  ugh i was so excited too bc i thought i remembered jak stat epicfail +  


submitted by hopsalong(3),

This question has a lot of answer options, and you arrive at Nephrolithiasis by throwing out all the other options by what is missing.

A, B - Cortical Necrosis and Papillary Necrosis almost always occur in the setting of ischemia. Previously healthy 28 year old man has no evidence of significantly decreased renal perfusion.

C - Acute Tubular Necrosis is what you should think of with Salicylate (NSAID) toxicity. There are many other nephrotoxic drugs that cause ATN, but think of ATN as drug induced kidney damage.

D - Cystitis - Flank pain is related to kidney injury, not bladder damage. Cystitis could be possible in ascending UTI, but the patient has no fever and is male (much less common in males).

E - Glomerulonephritis - This gets into nephrotic/nephritic syndromes. The stem mentions that he has blood in the urine which may lead you down the nephritic pathway, but he does not have any of the other associated symptoms.

F - Hypernephroma - Another word for Renal Cell Carcinoma. No weight loss or other cancer related symptoms (fatigue etc.)

G - Interstitial Nephritis - This is often a drug induced IMMUNE mediated nephrotoxicity. This is a type IV hypersensitivity reaction that occurs weeks to months after the start of medication (like NSAIDs). ATN is more associated with drug overdose while Interstitial is more associated with immune reaction. Intersitial Nephritis will have WBC casts in urine.

I - Pyelonephritis - Caused by ascending UTI but no fever is present.

This leaves Nephrolithiasis (H) as the correct answer. 85% of Nephrolithiasis is associated with hypoactive bowel sounds. The pain for nephrolithiasis can relapse and remit, and occasionally the pain can travel from the kidney (flank pain) to the scrotum as the stone moves through the ureter.

whoissaad  Great explanation. Always found it hard to differentiate between ATN and AIN due to NSAID use. This made it clear. Thanks! +1  
hyperfukus  yasss +  
dubywow  "occasionally writhes in pain" -- as a guy who has had a kidney stone, writhing in pain definitely hits the mark. Picture yourself knees on the ground, face on the couch, screaming incoherently while the paramedics are there because you can't control your own body movement and don't know if you're dying or whatnot from the canonball sized hole that (may or may not be) in your flank. Then imagine one of the paramedics is your premed study buddy. Never forget writhing and nephrolithiasis and premed study buddies. You will forever get this question correct in the future. +  


This is acute hemolytic transfusion reaction, I believe. Type II HSR so she’s forming antibodies against the ABO groups on the blood cells. Complement is induced by antibodies.

kfratta1  But with hypotension in the stem I thought more of anaphylaxis due to IgA def. Why would a T2 HSR give you hypotension? +1  
2ndmedschool  I think the hemoglobinuria is the key. As I’m looking at it it seems that anaphylaxis would cause hypotension, urticaria, itching, wheezing. ABO incompatibility is the only one that mentions hemoglobinuria. +2  
hyperfukus  abo incompatibility and rh incompatibility with mom blood rxns are gonna TYPE 2 no matter what it looks like +  


submitted by skraniotis(6),

Undialyzed renal failure leads to metabolic acidosis, and as a result bicarb gets depleted as it tries to buffer the accumulation of organic acids.

bubbles  Thanks for the explanation! Do you know why Mg would not be a potential answer? Phosphate also accumulates in those with undialyzed renal failure, so I was thinking that maybe magnesium as a divalent cation would complex with PO3 (in a mechanism similar to Ca). +  
nwinkelmann  From the little bit of research I just did (because I didn't learn anything about dialysis at my medical school), ESRD can be associated with either low or high Mg levels, so the dialysate can cause either increased or decreased Mg levels depending on the patient's serum content, therefore I don't think based on this question, would could determine if removal of dialysis would lead to elevated or decreased magnesium. The end of the first article seems to favor ESRD leading to hypermagnesemia, so if that's the case, then removal of dialysis would cause Mg to increase as well. https://www.karger.com/Article/FullText/452725 and https://www.karger.com/Article/FullText/485212 +1  
hyperfukus  why is it that we aren't learning this stuff and they r just throwing it on step there's barely a blurb in FA about ckd/eskd +  
hyperfukus  does uremia potentially have to do with this? +  
medulla  ESRD and not getting dialysis -> he is uremic -> met acidosis -> dec bic +2  
angelaq11  @medulla this is the best and simplest explanation. I got it wrong and chose Mg, wish I had made that connection. +  


submitted by skraniotis(6),

Undialyzed renal failure leads to metabolic acidosis, and as a result bicarb gets depleted as it tries to buffer the accumulation of organic acids.

bubbles  Thanks for the explanation! Do you know why Mg would not be a potential answer? Phosphate also accumulates in those with undialyzed renal failure, so I was thinking that maybe magnesium as a divalent cation would complex with PO3 (in a mechanism similar to Ca). +  
nwinkelmann  From the little bit of research I just did (because I didn't learn anything about dialysis at my medical school), ESRD can be associated with either low or high Mg levels, so the dialysate can cause either increased or decreased Mg levels depending on the patient's serum content, therefore I don't think based on this question, would could determine if removal of dialysis would lead to elevated or decreased magnesium. The end of the first article seems to favor ESRD leading to hypermagnesemia, so if that's the case, then removal of dialysis would cause Mg to increase as well. https://www.karger.com/Article/FullText/452725 and https://www.karger.com/Article/FullText/485212 +1  
hyperfukus  why is it that we aren't learning this stuff and they r just throwing it on step there's barely a blurb in FA about ckd/eskd +  
hyperfukus  does uremia potentially have to do with this? +  
medulla  ESRD and not getting dialysis -> he is uremic -> met acidosis -> dec bic +2  
angelaq11  @medulla this is the best and simplest explanation. I got it wrong and chose Mg, wish I had made that connection. +  


submitted by bobson150(3),

Is this saying there is vesicoureteral reflux? I could have sworm this same image was on form 20 or 21 and the answer was Wilms tumor

hello  Yes, it was. I think in both vignettes, the picture was basically irrelevant. Or another possible clue -- but definitely not needed to answer the Q. +1  
presidentdrmonstermd  My school uses old "retired" NBME questions for exams and I've also seen this exact same picture multiple times...w/ different scenarios I think. I tried remembering what the questions were but I guess it's mostly irrelevant. +1  
hyperfukus  SAME +  
hyperfukus  I also put wilm's tumor bc it felt really familiar wtf +  


submitted by bobson150(3),

Is this saying there is vesicoureteral reflux? I could have sworm this same image was on form 20 or 21 and the answer was Wilms tumor

hello  Yes, it was. I think in both vignettes, the picture was basically irrelevant. Or another possible clue -- but definitely not needed to answer the Q. +1  
presidentdrmonstermd  My school uses old "retired" NBME questions for exams and I've also seen this exact same picture multiple times...w/ different scenarios I think. I tried remembering what the questions were but I guess it's mostly irrelevant. +1  
hyperfukus  SAME +  
hyperfukus  I also put wilm's tumor bc it felt really familiar wtf +  


submitted by seagull(437),

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 +  
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 +  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +5  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +3  
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?" +  


submitted by meatus(1),

I'm sorry but what am I missing here... I thought the whole point of diuretics is to correct volume overload by diuresis? How would total volume be increased??

niboonsh  the question is asking what would happen to the URINARY ph, bicarb, and volume. dont worry, i misread the question too -_- +5  
link981  Also misread the question, thought about the lab volumes of the BLOOD smh +2  
hyperfukus  yooooo me too!!! this is the second NBME i did this on they purposely don't write urine on the arrow categories to mess u up i swear!!! AHHHHHH +  
medulla  missed this question for the same reason .. still pissed +  


This one was a little tricky. For this one the key is the low radioiodine uptake. This patient has high T4 and low TSH which makes sense in a hyperthyroid patient, perhaps your first thought is that this patient has Grave’s disease. However, in Grave’s your thyroid is being stimulated to make more thyroid hormone from scratch and as such would have an increased radioiodine uptake because the thyroid is bringing in the required (now radiolabeled) iodine. This is why it is not Graves (“release of thyroid hormone from a thyroid stimulated by antibodies”).

So if its not Grave’s what could it be? For this you’d have to know that Hashimoto’s Thyroiditis (also known as Chronic Lymphocytic Thyroiditis and is often referred to as such on board exams to throw you off) has three phases - first they are hyperthyroid, then euthyroid, then the classic hypothyroid that you would expect with low T4 and high TSH. This was the key to this question. The reason for this is that antithyroid peroxidase antibodies in Hashimoto’s cause the thyroid to release all of its stored thyroid hormone making the patient hyperthyroid for a short period of time. After this massive release of thyroid hormone, the antibodies make them unable to make new TH and therefore they become euthyroid for a short period and then hypothyroid which you would expect! Since they can’t make new TH, the thyroid will not take up the radioiodine and therefore there will be low radioiodine uptake. Hence, “release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes.” aka “Lymphocytic (hashimotos) thyroiditis”.

I think “release of thyroid hormone from a lymphomatous thyroid gland” is referring to some kind of thyroid cancer in which case you would expect them to be describing a nodule on radioiodine uptake.

​Summary video here and also a great site in general: https://onlinemeded.org/spa/endocrine/thyroid/acquire

aesalmon  pg 338 of FA lists it under hypothyroidism but it does present as transient hyperthyroidism first +3  
hyperfukus  yep that was the key! Goiter is "HOT" but the remaining answer choices were still kind of bleh D was distracting the hell out of me i spent so long to convince myself to pick C and move on +1  
hello  Pasting nwinkelmann's comment as an addition: Choice "D" is wrong b/c "lymphomatous thyroid gland" = primary thyroid lymphoma (typically NHL, which is very rare) or Hashimoto's thyroid progression. Hashimoto's thyroiditis = lymphocytic infiltrate with germinal B cells and Hurthle cells, which upon continued stimulation, can lead to mutation/malignant transformation to B cell lymphoma. Both of these present with hypothyroidism with low T4 and high TSH (opposite of this patient). +  


submitted by mattnatomy(22),

Most common cause of splenic vein thrombosis is chronic pancreatitis, caused by perivenous inflammation.

Source: https://www.ncbi.nlm.nih.gov/pubmed/14502405

hyperfukus  great link! helps answer other qs too thank you :) +  


submitted by alexb(14),

There is a decent UWorld question explaining how this works. Only reason I remembered it.

hyperfukus  i had notes from forever ago but i totally forgot lol +  


submitted by mattnatomy(22),

I believe this is referring to midgut malrotation. Due to improper positioning of bowel (on the right side). Ladds bands connect the large intestine to the liver.

Can lead to:

  1. Volvulus

  2. Duodenal obstruction

3. SMA Occlusion -- I'm guessing based on the answer to the question

meningitis  Yes, the question clicked for me when I realized the ligament was on the RT side instead of LT so I thought of Volvulus. Image of ligament of treitz: https://media.springernature.com/original/springer-static/image/chp:10.1007/978-3-642-13327-5_17/MediaObjects/978-3-642-13327-5_17_Fig3_HTML.gif +1  
hyperfukus  So Volvulus regardless in baby or adult is gonna cause SMA prob + Duodenal Obstruction: d/t Ladd bands im gonna go back and remember those associations :) +  


Our little friend has a Parvovirus infection, which infects erythroid precursors, causing interruption of erythrocyte production. This is the same way it causes hydrops fetalis in unborn babies and aplastic anemia in sickle cell, etc.

gainsgutsglory  I get Parvo has tropism for RBC precursors, but wouldn’t it take 120 days to manifest? +  
keycompany  RBCs don’t just spill out of the bone marrow every 4 months on the dot. Erythropoesis is a constant process. If you get a parvo virus on “Day 1” then the RBCs that were synthesized 120 days before “Day 1” will need to be replaced. They can’t be because of parvovirus. This leads to symptomatic anemia within 5 days because the RBCs that were synthesized 125-120 days before the infection are not being replaced. +2  
drdoom  @gainsgutsglory @keycompany It seems unlikely that “1 week” of illness can explain such a large drop in Hb. It seems more likely that parvo begins to destroy erythroid precursors LONG BEFORE it manifests clinically as “red cheeks, rash, fever,” etc. Might be overkill to do the math, but back-of-the-envelope: 7 days of 120 day lifespan -> represents ~6 percent of RBC mass. Seems unlikely that failure to replenish 6 percent of total RBC mass would result in the Hb drop observed. +  
yotsubato  He can drop from 11 to 10 hgb easily +1  
ls3076  Apologies if this is completely left-field, but I didn't think this was Parvovirus. Parvo would affect face. Notably, patient has fever and THEN rash, which is more indicative of Roseola. Thoughts?? +2  
hyperfukus  @is2076 check my comment to @hello I thought the same thing for a sec too :) +  
hyperfukus  also i think you guys are thinking of hb in adults in this q it says hb is 10g/dL(N=11-15) so it's not relatively insanely low +  
angelaq11  @Is3076 I completely agree with @hyperfukus and I think that thinking of Roseola isn't crazy, but remember that usually with Roseola you get from 3-5 days of high fever, THEN fever is completely gone accompanied by a rash. This question says that the patient has a history of 4 days of rash and 7 days of fever, but never mentioned that the fever subsided before the appearance of the rash. And Roseola is not supposed to present with anemia. +  


Our little friend has a Parvovirus infection, which infects erythroid precursors, causing interruption of erythrocyte production. This is the same way it causes hydrops fetalis in unborn babies and aplastic anemia in sickle cell, etc.

gainsgutsglory  I get Parvo has tropism for RBC precursors, but wouldn’t it take 120 days to manifest? +  
keycompany  RBCs don’t just spill out of the bone marrow every 4 months on the dot. Erythropoesis is a constant process. If you get a parvo virus on “Day 1” then the RBCs that were synthesized 120 days before “Day 1” will need to be replaced. They can’t be because of parvovirus. This leads to symptomatic anemia within 5 days because the RBCs that were synthesized 125-120 days before the infection are not being replaced. +2  
drdoom  @gainsgutsglory @keycompany It seems unlikely that “1 week” of illness can explain such a large drop in Hb. It seems more likely that parvo begins to destroy erythroid precursors LONG BEFORE it manifests clinically as “red cheeks, rash, fever,” etc. Might be overkill to do the math, but back-of-the-envelope: 7 days of 120 day lifespan -> represents ~6 percent of RBC mass. Seems unlikely that failure to replenish 6 percent of total RBC mass would result in the Hb drop observed. +  
yotsubato  He can drop from 11 to 10 hgb easily +1  
ls3076  Apologies if this is completely left-field, but I didn't think this was Parvovirus. Parvo would affect face. Notably, patient has fever and THEN rash, which is more indicative of Roseola. Thoughts?? +2  
hyperfukus  @is2076 check my comment to @hello I thought the same thing for a sec too :) +  
hyperfukus  also i think you guys are thinking of hb in adults in this q it says hb is 10g/dL(N=11-15) so it's not relatively insanely low +  
angelaq11  @Is3076 I completely agree with @hyperfukus and I think that thinking of Roseola isn't crazy, but remember that usually with Roseola you get from 3-5 days of high fever, THEN fever is completely gone accompanied by a rash. This question says that the patient has a history of 4 days of rash and 7 days of fever, but never mentioned that the fever subsided before the appearance of the rash. And Roseola is not supposed to present with anemia. +  


submitted by hello(67),

Patient has red lacy rash- this fits more with HHV-6 (Roseola virus), not Parvovirus.

HHV-6 causes deformation of erythoblasts, leading to anemia.

hyperfukus  Hey so i just looked in first aid and it says "diffuse Macular Rash for Roseola" and usually you have a super high fever and febrile seizures are almost always mentioned...I found in my notes from uworld that i mustve filled in a long time ago for Parvo: Infects Erythroid precursors + Replicates in BM Face/cheek rash followed by LACY Reticular rash on body...May get Rash from IC deposition...and then again i wrote replicates in erythrocyte progenitors causing reticulocytopenia which makes sense why dec Hb and dec Hct +1  


submitted by enbeemee(5),

what are the other labeled structures? i can discern the parietal and chief cells, but not the others...

hyperfukus  what is A? +  
et-tu-bromocriptine  According to this source, they're mucous neck cells (secrete acidic fluid containing mucin); compare this with mucus produced by surface mucous cells, which is alkaline. http://www.siumed.edu/~dking2/erg/GI082b.htm +1  
hyperfukus  i gosh i see now! thanks so much :) so if it's Pink=Parietal but not granules got it thank you :) +  


Why wasn’t the table enough to determine prevalence in the general population?

sacredazn  For the case control question, it’s taking that principle that you can’t use case control studies to calculate relative risk and applying it to prevalence. Basically with case control studies we start by saying okay, I’m going to find 200 people with sinusitis and 400 without. Then, you go back and look at the number exposed/unexposed and calculate the odds ratio. So you can’t use case controls to calculate prevalence because it all depends on how many cases you picked in the first place. Might make more sense to think about it with a rare cancer like craniopharyngioma or something- let’s say you chose 10 cases and 10 controls and wanted to look at how many people smoked. It wouldn’t make sense to then say the prevalance of craniopharyngioma is 10/20 = 50%. +6  
dr_trazobone69  Thank you, that makes a lot of sense! So we can use relative risk (cohort studies) to calculate prevalence? +  
sacredazn  @trazobone Hmm I think the wording would be key, you could use a prospective cohort to calculate incidence, but you wouldn’t be able to find prevalence of the gen population unless you had more info. I think the concept is that really to calculate prevalence you need a proper ecologic study looking at population-level data. The way it was worded in the question was tricky though lol since when has “cannot be determined from the info given” ever been a right answer. +3  
nwinkelmann  @sacredazn thank you! this was the best explanation to use the rare disease comparison. Made everything make so much sense and hopefully I'll actually just remember it now, instead of learning the factoid and failing to recall it all the time. +1  
hyperfukus  i guess this makes sense but i don't understand why we are asked to calculate it from tables like this then? is there more info in those? +  
hello  @hyperfukus The table was given because that a 22 table is typically what you do see regarding data for case-control studies. If the 22 table wasn't include, then literally everytone would pick Choice "E" as the correct answer b/c you can't calculate something without being provided numbers. The difference in including the data-table is that 1. again, you need to report a 22 table because that is typically what you will see regarding data for a case-control study and 2. by including the 22 table, it actually tests if the test-taker realized that the data in the 2*2 table does not help at all with calculating prevalence-- because case-control studies NEVER report on prevalence. +  


submitted by iviax94(6),

I was between hypokalemia (due to diarrhea) and hypercalcemia/hyperuricemia (since sweat is hypotonic and would cause hyperosmotic volume contraction). I didn’t have a great way to decide between hyperCa/hyperuricemia so I figured they wanted hypoK. Is there a better rationale for why the hyper answers are incorrect?

liverdietrying  I think you over-thought this one a little bit with the hypercalcemia/hyperuricemia. Good fact to commit to memory: you lose bicarb in the stool (hence why diarrhea causes nonanion gap metabolic acidosis), and especially lose potassium with laxative abuse (as mentioned in the question stem). https://www.uptodate.com/contents/acid-base-and-electrolyte-abnormalities-with-diarrhea +1  
w7er  Basically they are asking about electrolyte distrubance that cause collapse mainly due to hypokalemia from laxative abuse because diarreha cause hypokamlemia and also cause incrase in renin angiotensin sytem which will further cause hypokalemia resuling cardiocascular colapse :) +  
hyperfukus  i thought the hyperuricemia thing too but i wasn't smart enough to think they wanted hypokalemia like u :( +  


submitted by d_holles(38),

Goljan stresses the Boards giving the leukemia questions away based on the age given in the question stems.

ALL = 0-14

AML = 15-39; 40-59

CLL = 60+

CML = 40-59

https://forums.studentdoctor.net/threads/goljan-on-leukemias.303605/

impostersyndromel1000  thanks for the reminder, often overlooked are the simple demographic hints. helps you make an educated guess +  
hyperfukus  also a key thing to remember in general is a person who undergoes chemo is a big demographic hint to later developing AML regardless of the clues :) and yes the AGE!!! +  


submitted by gh889(36),

The answer is due to an exception outlined here where niacin is used in pts w/o diabetes who have refractory hypertriglyceridemia at high risk or has a hx of pancreatitis.

I agree that fibrates are first line (and so does that article) but NBME was honing in on a specific exception that niacin can also be used since VLDL and TGs are high in hypertriglyceridemia.

The "clue" they had was "recurrent pancreatitis" which is supposedly a lead towards niacin.

I also put increase HDL....

wutuwantbruv  Correct, you would not want to give fibrates to someone with recurrent pancreatitis since fibrates increase the risk of cholesterol gallstones due to inhibition of cholesterol 7α-hydroxylase. +  
kernicterusthefrog  FYI @gh889 can't follow your link w/o an NYIT username and password, unless there's a more tech-savvy way around that.. I appreciate the info, though. Niacin rx for familial hypertriglyceridemia w/ recurrent pancreatitis. Now I know.. +1  
impostersyndromel1000  Great points, very in depth knowledge taking place here. Also, familial hypertriglyceridemia (per FA 2019 pg 94) has hepatic overproduction of VLDL so picking this would have been the easiest answer (in retrospect) +1  
hyperfukus  @impostersyndrome1000 literally that's the ONE thing i remembered and i went YOLO lol cuz i was staring for a while +  


submitted by dr.xx(45),

CHF patients often display signs and symptoms of increased vasopressin secretion.

hyperfukus  if all else fails i hope i just drill this one statement in my brain and it comes out in the right way on test day thank u!!! +  


submitted by seagull(437),

Why spontaneous? He's engaging in an active sport with an increased risk of Traumatic injury. So we really just assume hes not injured because the stem doesnt directly say he's injured? These questions lead to too many assumptions. (in my opinion)

nc1992  Spontaneous pneumothorax, as a condition, is significantly more likely than a traumatic pneumothorax from just about anything but a car crash (ok maybe if he was in a fight). The car crash or a stabbing is also more probable overall but there's no point in inferring something that isn't provided +  
nwinkelmann  I picked the traumatic injury also. After reading these comments I looked into it further. Traumatic pneumos occur because of blunt or penetrating chest trauma, and I found that the MCC form of blunt trauma (>70%) is motor vehicle acidents that cause significant trauma (i.e. rib fractures) or even blast trauma. Although it didn't say there were no chest wall fractures, at the same time it didn't indicate any rib fractures, which would be most like to cause the traumatic injury pneumo in the patient's case. +1  
drdoom  The stem makes no mention of trauma. +  
hyperfukus  i guess the issue is that you have to assume what they mean by "strongest predisposing risk factor for this patient's condition" I think this is dumb bc the answer is completely different based on what you consider this patient's "CONDITION" to be? either way he has a pneumothorax so if you wan to know what caused that its prob him being active or bumping into someone but if you consider the etiology of the pneumothorax then its the bleb and that is from him being a skinny dude/smoker i went to this b/c he's also only 5/10 that's not tall in my head they could have been nicer and made him 6'1 at least...also i feel like i saw a lot of q's back in the day when i first learned this with a presentation of the person like tripping or something dumb but they already had the bleb and then got the pneumothorax +  


submitted by drdoom(211),

You have to think about this using the concept of CONDITIONAL PROBABILITY. Another way to ask this type of question is like this: “I show you a patient with spontaneous pneumothorax. Which other thing is most likely to be true about that person?” Or you can phrase it these ways:

  • Given a CONDITION (spontaneous pneumo), what other finding is most likely to be the case?
  • Given a pool of people with spontaneous pneumothorax, what other thing is most likely to be true about them?

In other words, of all people who end up with spontaneous pneumo, the most common other thing about them is that they are MALE & THIN.

If I gave you a bucket of spontaneous pneumo patients -- and you reached your hand in there and pulled one out -- what scenario would be more common: In your hand you have a smoker or in your hand you have a thin male? It’s the latter.

someduck3  Is this the best approach to all of the "strongest predisposing risk factor" type questions? +  
drdoom  There is a town of 1,000 men. Nine hundred of them work as lawyers. The other 100 are engineers. Tom is from this town. He rides his bike to work. In his free time, he likes solving math puzzles. He built his own computer. What is Tom's occupation most likely to be? Answer: Tom is most likely to be a lawyer! Don't let assumptions distract you from the overwhelming force of sheer probability! "Given that Tom is from this town, his most likely occupation (from the available data) = lawyer." +2  
drdoom  There is a town of 1,000 spontaneous pneumo patients. Six hundred are tall, thin and male. The other 400 are something else. Two hundred of the 1,000 smoke cigarettes. The other 800 do not. What risk factor is most strongly associated with spontaneous pneumo? (Answer: Not being a smoker! ... because out of 1,000 people, the most common trait is NOT smoking [800 members].) +3  
impostersyndromel1000  this is WILD! thanks guy +3  
belleng  beautiful! also, i think about odds ratio vs. relative risk...odds ratio is retrospective of case-control studies to find risk factor or exposure that correlates with grater ratio of disease. relative risk is an estimation of incidence in the future when looking at different cohort studies. +  
drdoom  @impostersyndrome I love me some probability and statistics. Glad my rant was useful :P +  
hyperfukus  @drdoom i hate it which is why your rant was extremely useful lol i learned a ton thanks dr.doom! +1  
dubywow  I caught he was thin. The only reason I didn't pick Gender and body habitus is because he was not overly tall (5'10"). I talked myself out of it because I thought the body habitus was too "normal" because he was not both thin AND tall. Got to keep telling myself to not think too hard on these. Thanks for the explanation. +  


submitted by chosened(1),

Correct me if I m wrong but I think it's laryngeal papillomatosis. Papillomas can develop anywhere along the respiratory tract, but most often affect the larynx and the vocal cords (laryngeal papillomatosis). Not sure how HY this is but heres More info: https://rarediseases.org/rare-diseases/recurrent-respiratory-papillomatosis/

hyperfukus  yes you are definitely correct i think its a common wtf q that pops up bc there's one on uworld that asks if its true or false vocal cords and i had to hunt my prof down to figure it out... +  
hyperfukus  also i think they love anything that compromises the airway +  
winelover777  Shout out to Pathoma, Respiratory chapter, Larynx section, Laryngeal Papilloma heading. Only reason I got this question right. +  


submitted by chosened(1),

Correct me if I m wrong but I think it's laryngeal papillomatosis. Papillomas can develop anywhere along the respiratory tract, but most often affect the larynx and the vocal cords (laryngeal papillomatosis). Not sure how HY this is but heres More info: https://rarediseases.org/rare-diseases/recurrent-respiratory-papillomatosis/

hyperfukus  yes you are definitely correct i think its a common wtf q that pops up bc there's one on uworld that asks if its true or false vocal cords and i had to hunt my prof down to figure it out... +  
hyperfukus  also i think they love anything that compromises the airway +  
winelover777  Shout out to Pathoma, Respiratory chapter, Larynx section, Laryngeal Papilloma heading. Only reason I got this question right. +  


submitted by bobson150(3),

The wording of this question confused me. This is asking "which of these vessels is the high pressure system" right? So the high pressure superior rectal is causing increased pressure into the inferior rectal?

welpdedelp  Superior rectal comes from the inferior mesenteric vein which comes from the splenic vein --> portal veins Thus, this dude had cirrhosis so it would "back-up" into the superior rectal vein. FA 2018: p360 +5  
nc1992  Superior rectal not superior mesenteric. Took me a minute +  
hyperfukus  ugh am i ever gonna get these right EVER +2  
titanesxvi  why not the inferior mesenteric, since the superior rectal drains there +  
thomasburton  @titanesxvi think it is because question says direct which is why superior rectal +1  
lilyo  thomasburton, so are they asking what vessels do internal hemorrhoids directly drain into? The order is Superior rectal vein--> Inferior mesenteric vein--> portal vein. +  
thomasburton  Yes exactly, so they do eventually reach IMV but not 'directly' +  


submitted by neonem(263),

Sounds like a case of Li-Fraumeni syndrome - since p53 is a tumor suppressor for a bunch of cell types, mutations in this gene (as in LFS) result in a myriad of familial tumor types.

pparalpha  Li-Fraunemi syndrome = SBLA (sarcoma, breast, leukemia, adrenal gland syndrome) and occurs because of an autosomal dominant inherited mutation of p53 APC: linked to FAP (colorectal cancer) RET: linked to papillary thyroid cancer, MEN 2A, MEN 2B RB1: retinoblastoma +3  
privatejoker  The thing that threw me off was that the only connection in her FH to the above SBLA reference was the mention of a paternal cousin with adrenocortical carcinoma. The other two mentioned had brain cancers, which seem completely outside the scope of the above mnemonic. Then again, as mentioned elsewhere, I suppose the best policy on these is just to rule out the absolute wrong answers. I swear, the NBME is lying when they tell us to choose the "best" answer on some of these. What they actually mean in practice is for us to choose the least shitty. +3  
dbg  ^ this guy cracked the code. nbme ur doomed. +1  
cienfuegos  @privatejoker: I feel the pain. Quick FYI: UW includes brain in the associated tumors. +1  
hyperfukus  we can just make her thing SBBLA and hopefully never get this wrong again +  


submitted by seagull(437),

http://www.siumed.edu/~dking2/erg/GI178b.htm

Another histology slide with labels a few seconds ago

enbeemee  what are the other labeled structures? i can discern the parietal and chief cells, but not really the others... +  
hyperfukus  yea wth is A +  


submitted by enbeemee(5),

what are the other labeled structures? i can discern the parietal and chief cells, but not the others...

hyperfukus  what is A? +  
et-tu-bromocriptine  According to this source, they're mucous neck cells (secrete acidic fluid containing mucin); compare this with mucus produced by surface mucous cells, which is alkaline. http://www.siumed.edu/~dking2/erg/GI082b.htm +1  
hyperfukus  i gosh i see now! thanks so much :) so if it's Pink=Parietal but not granules got it thank you :) +  


submitted by nosancuck(38),

Yo dis B got NO INTERNAL FEMALE ORGANS

Why dat!???

We be lookin at someone with an SRY from dere Y chromie! Dey be a Y chromie Homie so they be makin some Testis Determinin Factor which I be sure makes some nice lil ANTI MULLERIAN FACTOR so dey aint got that Female Internal Tract u know what i be sayin

And since wimminz is da DEFAULT they stil be gettin dose pussy lips and breastes

meningitis  The above explanation is correct (disregarding the hard to read and unprofessional dialect) but just in case anyone was wondering: chromatin-negative= Just a quick way of knowing it was a boy. The term applies to the nuclei of cells in normal males as well as those in individuals with certain chromosomal abnormalities +11  
yotsubato  Turner syndrome patients are also chromatin negative as well though.... +3  
sympathetikey  I didn't know a complication post-meningitis was lack of humor. +2  
sympathetikey  Ah, didn't read the last line. Yeah, that is taking it a bit far +1  
niboonsh  yall are haters. this is the first explanation that has ever made sense to me +2  
arkmoses  https://www.youtube.com/watch?v=yuXL-3eoB-o&t=77s Interesting syndrome watching this helped me to put it into real life perspective, interesting points they have no pubic hair/body hair, they apparently also dont smell, and breast size is usually increased... +  
whoissaad  How does chormatin-negative indicate a normal cell? Isn't chormatin just condensed DNA? +1  
cienfuegos  According to this paper most individuals with Turner Syndrome are chromatin negative: "One of the initial laboratory procedures used to confirm or rule out this diagnosis involves a sex chromatin determination from a buccal smear. Cells from the lining of the mouth are stained for the presence or absence of X-chromatin or Barr bodies, which represent a portion of an inactivated X chromosome. The typical Turner’s syndrome patient, who has 45 chromosomes and only one sex chromosome (an X), has no Barr bodies and is, therefore, X-chromatin negative. This abnormal X-chromatin negative finding in the majority of Turner’s syndrome females is similar to the result found in a normal male, who also has only one X chromosome, and differs from the X-chromatin positive condition observed in the normal female, who has two X chromosomes. Occasionally, the patient with features of Turner’s syndrome is found to be X-chromatin positive." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6233891/ +  
hyperfukus  i really hate haters this is awesome! +  


submitted by sympathetikey(316),

The whole "picks at the lesion...causes some bleeding", made me think Psoriasis. Should have gone with Actinic Keratosis based on the patient history (lots of sun exposure).

Actinic Keratosis

Premalignant lesions caused by sun exposure. Small, rough, erythematous or brownish papules or plaques. Risk of squamous cell carcinoma is proportional to degree of epithelial dysplasia.

thisisfine   Same - the bleeding thing pushed me over to psoriasis as well. Oops. +1  
temmy  the distribution of the other lesions, forearm, face, ear, scalp..is not characteristic for psoriasis. +1  
hyperfukus  the scalp and ear are actually very common for psoriasis IRL the key is more of the fact that its in areas with UV exposure...actually UV Therapy is found to be helpful in treating some pts w/Psoriasis. Lastly the appearance and lots of things bleed if they were trying to go for auspitz sign it would have tiny dots of bright red blood with slightly touching it +1  
hyperfukus  oh last thing psoriasis itches! they said no itching +  


submitted by sympathetikey(316),

The whole "picks at the lesion...causes some bleeding", made me think Psoriasis. Should have gone with Actinic Keratosis based on the patient history (lots of sun exposure).

Actinic Keratosis

Premalignant lesions caused by sun exposure. Small, rough, erythematous or brownish papules or plaques. Risk of squamous cell carcinoma is proportional to degree of epithelial dysplasia.

thisisfine   Same - the bleeding thing pushed me over to psoriasis as well. Oops. +1  
temmy  the distribution of the other lesions, forearm, face, ear, scalp..is not characteristic for psoriasis. +1  
hyperfukus  the scalp and ear are actually very common for psoriasis IRL the key is more of the fact that its in areas with UV exposure...actually UV Therapy is found to be helpful in treating some pts w/Psoriasis. Lastly the appearance and lots of things bleed if they were trying to go for auspitz sign it would have tiny dots of bright red blood with slightly touching it +1  
hyperfukus  oh last thing psoriasis itches! they said no itching +  


submitted by mcl(220),

PCOS is associated with abnormal production of sex steroids, including dysfunction of estrogen production and progesterone. Chronically elevated levels of estrogen can cause endometrial hyperplasia.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3917599/

meningitis  Why isnt it endometriosis? Could someone help me out on this? +  
meningitis  Sorry, I was confusing with higher risk for endometrial carcinoma. +  
vi_capsule  Estrogen is responsible for cyclical bleeding and pain associated with endometriosis hence progestin is a treatment modality. But estrogen isnt a risk factor for Endometriosis. Rather theres retrograde flow, metaplatic transformation etc theories are responsible for endometriosis. +  
sympathetikey  Tfw you get so thrown off by a picture that you don't read the question properly. +2  
hyperfukus  @meningitis idk if u still care lol but always go back to endometriosis=ectopic endometrial tissue outside of the uterus so you can rule it out since increased estrogen would cause you to have worsened endometriosis or a thicker one but not directly...you can see the clumps of the follicles in the ovaries if you look super close so that along with the presentation takes you to PCOS and anytime you don't have a baby or stay in the proliferative phase(estrogen phase) you get endometrial proliferation-->hyperplasia--->ultimately carcinoma +  


submitted by haliburton(85),

this is a cervical spinal cord section. the cuneate fasciculus is intact (UE) vibration and proprioception, but the white section is the gracile fasciculus (LE) and is damaged. I think the lateral portion that is uneven is just natural/artifact.

arezpr  thorax section +3  
guillo12  How do you know the gracile fasciculus is damage?!?! +1  
cr  which parte of the image its damage?, the pink? or black? +  
usmile1  the pink park yes +1  
d_holles  If you look at https://en.wikipedia.org/wiki/Gracile_fasciculus#/media/File:Spinal_cord_tracts_-_English.svg you can see that the closer to the center = legs, while further away = arms. +1  
hyperfukus  i still don't see where the damage is lol! FML +  
hyperfukus  i finally figured it out lol that was a slow moment i hope im not this slow on step yikes! +  
angelaq11  @hyperfukus I had the same problem at first, marked it and then came back. If you remember, in the spinal cord the white matter and gray matter are "reversed" compared to the brain. That said, if the butterfly shaped region (ie, the gray matter) is colored (in this case) lilac and the rest (ie, white matter) is blackish, the only thing that is actually abnormal, is the region where the dorsal columns are, because it stains just like the normal gray matter. After that, you have to think about which fasciculus is damaged, the gracilis or the cuneatus. The gracilis is medial while the cuneatus is lateral (picture someone with glued legs and open arms). Hope this helped +1  


submitted by haliburton(85),

this is a cervical spinal cord section. the cuneate fasciculus is intact (UE) vibration and proprioception, but the white section is the gracile fasciculus (LE) and is damaged. I think the lateral portion that is uneven is just natural/artifact.

arezpr  thorax section +3  
guillo12  How do you know the gracile fasciculus is damage?!?! +1  
cr  which parte of the image its damage?, the pink? or black? +  
usmile1  the pink park yes +1  
d_holles  If you look at https://en.wikipedia.org/wiki/Gracile_fasciculus#/media/File:Spinal_cord_tracts_-_English.svg you can see that the closer to the center = legs, while further away = arms. +1  
hyperfukus  i still don't see where the damage is lol! FML +  
hyperfukus  i finally figured it out lol that was a slow moment i hope im not this slow on step yikes! +  
angelaq11  @hyperfukus I had the same problem at first, marked it and then came back. If you remember, in the spinal cord the white matter and gray matter are "reversed" compared to the brain. That said, if the butterfly shaped region (ie, the gray matter) is colored (in this case) lilac and the rest (ie, white matter) is blackish, the only thing that is actually abnormal, is the region where the dorsal columns are, because it stains just like the normal gray matter. After that, you have to think about which fasciculus is damaged, the gracilis or the cuneatus. The gracilis is medial while the cuneatus is lateral (picture someone with glued legs and open arms). Hope this helped +1  


hyperfukus  this link is great! they're still kind of close together :( its so hard to tell for me w/o reference of the others +  
hyperfukus  this link is great! they're still kind of close together :( its so hard to tell for me w/o reference of the others +  


hyperfukus  this link is great! they're still kind of close together :( its so hard to tell for me w/o reference of the others +  
hyperfukus  this link is great! they're still kind of close together :( its so hard to tell for me w/o reference of the others +  


submitted by benzjonez(14),

FA 2018 p. 609. Suspect urethral injury if blood is seen at the urethral meatus. Mechanism of posterior urethral injury = pelvic fracture, which we see in this patient. Urethral catheterization is relatively contraindicated.

hyperfukus  thank you! +  


Hi- I don't have an explanation for this but I am also curious as to why this was the answer.

drdoom  via @hyoscyamine: FA pg.372. Squamous cell carcinoma occurs in the upper 2/3 of esophagus whereas adenocarcinoma occurs in the distal 1/3. Since this was in the mid esophagus, its squamous cell carcinoma. Key feature of squamous cell carcinoma is keratin pearls. +2  
hyperfukus  idk why my dumbass didn't put foci of keratinization and pearls together lmao +  


submitted by haliburton(85),

wikipedia (apologies): The atmosphere is composed of 78% nitrogen and 21% oxygen. Since oxygen is exchanged at the alveoli-capillary membrane, nitrogen is a major component for the alveoli's state of inflation. If a large volume of nitrogen in the lungs is replaced with oxygen, the oxygen may subsequently be absorbed into the blood, reducing the volume of the alveoli, resulting in a form of alveolar collapse known as absorption atelectasis.

I chose cardiogenic edema, but I believe this is incorrect because there is no heart failure risk at this time, so the purpose of the PEEP is certainly not to push out fluid.

bighead478  doesn't there have to be an airway obstruction (mucus, foreign object etc.) in order for this to happen? 100% O2 without any airway obstruction should not cause absorption atelectasis, right? +  
iloveallpotatoes  And Tension Pneumothorax is wrong bc PEEP would furthur exacerbate that. +1  
hyperfukus  @iloveallpotatoes yea i realized that now after getting it wrong :( +  


submitted by enbeemee(5),

i get why it's flagellin, but is the specific reason that LPS is wrong is because it's just not how the vaccine is made? LPS would also elicit an immune reaction, right?

nor16  Lipid A of LPS can be sensed by CD14 of macrophages causing shock, its not a protein, so no immune reaction as in vaccination (humoral, IgG class switch via Th2 and B Cells). +2  
eclipse  actually they do use LPS as adjuvant in vaccines +1  
eclipse  actually they do use LPS as adjuvant in vaccines +1  
hyperfukus  TLRs recognize common motifs called pathogen-associated molecular pattern (PAMP) in bacteria, fungi, viruses, and other pathogens. TLR signaling in the modulation of innate immunity + adaptive immunity against pathogens, TLR agonists: CpG-DNA, flagellin, and lipid became essential candidates of effective+safe vaccine adjuvants. TLR agonists improve the efficacy of vaccine, reducing TCR-based selection thresholds and enhancing the magnitude and quality of memory T-cell response. +  
hyperfukus  some extra info in case they ask another annoying q +  


submitted by enbeemee(5),

i get why it's flagellin, but is the specific reason that LPS is wrong is because it's just not how the vaccine is made? LPS would also elicit an immune reaction, right?

nor16  Lipid A of LPS can be sensed by CD14 of macrophages causing shock, its not a protein, so no immune reaction as in vaccination (humoral, IgG class switch via Th2 and B Cells). +2  
eclipse  actually they do use LPS as adjuvant in vaccines +1  
eclipse  actually they do use LPS as adjuvant in vaccines +1  
hyperfukus  TLRs recognize common motifs called pathogen-associated molecular pattern (PAMP) in bacteria, fungi, viruses, and other pathogens. TLR signaling in the modulation of innate immunity + adaptive immunity against pathogens, TLR agonists: CpG-DNA, flagellin, and lipid became essential candidates of effective+safe vaccine adjuvants. TLR agonists improve the efficacy of vaccine, reducing TCR-based selection thresholds and enhancing the magnitude and quality of memory T-cell response. +  
hyperfukus  some extra info in case they ask another annoying q +  


submitted by usmleuser007(126),

As per FA 1) fatty infiltration 2) cellular ballooning 3) eventual necrosis

hyperfukus  thanks u saved me time in looking that up :) +