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 +2  (nbme22#21)

NBME's love to test on the pentad of TTP, which can be remembered by the mnemonic FAT RN (fever, anemia, thrombocytopenia, renal involvement, neuro symptoms). This pt has fever, confusion (neuro sx), decreased urine production (renal involvement), anemia and thrombocytopenia. Boom. TTP.


 +0  (nbme22#23)

How did anyone get this as T cruzi? That was literally the first answer I ruled out. She has swelling of the eye, but that is the only sx that fits. Chagas presents 10-20 years after initial infection, not two weeks later. It also doesn't present with recurrent fever, muscle aches and joint pain. I mostly ruled it out because of the time course.


 +0  (nbme21#27)

The only way to get this question correct is to break the rules of the hospice center because you assumed there was a romantic relationship between the women. Couldn't be more straightforward.


 +1  (nbme21#12)

NBME/Uworld love to test renal artery stenosis in the setting of hypertensive urgency/emergency. Just because this has been done so many times, you can basically get the right answer from the first half of the question. Pt with end organ issues (headache, confusion) and really high BP (I know it isn't 180/120, but it is really high). So this guy basically has hypertensive emergency. I'm already thinking it's renal artery stenosis. Next sentence? A bruit over the left abdomen. Bingo. Renal artery stenosis, most often caused by atherosclerosis in older men (as compared to fibromuscular dysplasia in younger women).


 +0  (nbme20#48)

Can anyone explain why the lipase concentration is so high if there is an issue with LPL in hyperchylomicronemia?

garima  due to pancreatitis
neovanilla  ELI5?
suckitnbme  @neovanilla Type 1-hyperchylomicronemia has increased risk of pancreatitis

 +3  (nbme24#30)

The fact that the odds ratio in the top left is incorrect makes this question very difficult. It makes it appear as if the cookies are causative but the milk had some protective factor. So obnoxious.

drpatinoire  God I thought totally the same way as you did. I stared at this question for at least 5min and asked myself what's wrong with my statistics.




Subcomments ...

basically polycystic kidneys won't work properly, they've hinted at this with the s.creat of 4mg/dl. thus the kidney won't do what its supposed to do. REMEMBER to check whether they are asking SERUM changes or URINE changes

Kidneys normal function - reabsorb HCO3- , its not doing that now > decreased HCO3

PTH - would cause increased Calcium reabsorption in kidneys, but kidneys aren't able to reabsorb calcium > PTH responds to low calcium levels and levels increase

PO4 ties into PTH as well, PTH acts be DECREASING PO4 reabsorption. Since kidneys aren't working ie: not responding to PTH > there would be increase in PO4

pg32  Sometimes these questions are made more difficult by trying to decipher the order in which these changes happen (first cause). In my mind, whenever I see a question on renal insufficiency, I know that phosphate in the serum will increase. In response, Ca will decrease and in response to that, PTH will increase. Lastly and unrelated, HCO3 will decrease because the kidneys aren't absorbing HCO3 as they usually do. +  


submitted by sugaplum(128),

FA 2019 Pg 373
chronic gastritis mucosal inflammation leading to atrophy

pg32  I would also add that I think they are specifically trying to get us to think of pernicious anemia here, where parietal cells are destroyed/lose their fxn. In that case, ECL cells may hypertrophy to encourage acid secretion because the parietal cells are not responding to their usual signals. All the other answer choices are quite clearly incorrect, and Zollinger-Ellison is a gastrinoma, which causes hypertrophy of the gastric mucosa so that is also wrong. +2  


submitted by tinydoc(135),

I picked E) inhibition of TNF-a because I thought 2 years of diarrhea sounds like IBD (specifically crohns Disease without bloody diarrhea vs uc which must have bloody diarrha). I still don't see any reason why I wouldnt guess that.

tinydoc  Nevermind just saw the "typically relieved with defecation" which is a pretty big indicator of IBS. +  
pg32  I still agree with you though. This sounds like a case of IBD and I picked E to try and tone down inflammation. Giving someone an opiate for intermittent diarrhea seems kind of dumb... +  
pg32  Just googled, "Indications for loperamide" and this is what came up: Imodium® (loperamide hydrochloride) is indicated for the control and symptomatic relief of acute nonspecific diarrhea and of chronic diarrhea associated with inflammatory bowel disease. +  


submitted by tinydoc(135),

I picked E) inhibition of TNF-a because I thought 2 years of diarrhea sounds like IBD (specifically crohns Disease without bloody diarrhea vs uc which must have bloody diarrha). I still don't see any reason why I wouldnt guess that.

tinydoc  Nevermind just saw the "typically relieved with defecation" which is a pretty big indicator of IBS. +  
pg32  I still agree with you though. This sounds like a case of IBD and I picked E to try and tone down inflammation. Giving someone an opiate for intermittent diarrhea seems kind of dumb... +  
pg32  Just googled, "Indications for loperamide" and this is what came up: Imodium® (loperamide hydrochloride) is indicated for the control and symptomatic relief of acute nonspecific diarrhea and of chronic diarrhea associated with inflammatory bowel disease. +  


submitted by lamhtu(57),

Stem should maybe say some lesions are lytic and some are sclerotic. Breast mets to bone is mixed type according to FA? If you go off the mets being purely lytic, one could think thyroid carcinoma is the correct primary tumor.

lae  thats also what I thought +1  
pg32  Yeah I didn't pick breast for the same reason. Then I didn't pick thyroid because I doubt serologic studies would be normal in thyroid cancer (if you check T3/T4 and TSH). So I went with avascular necrosis -_- +  
lynn  in the FA index, the only things listed under lytic bone lesions are adult T cell lymphoma, langerhan histiocytosis, and multiple myeloma. Obviously there's more than that but those might be the main ones we need to know. You could also say that a giant cell tumor is also technically lytic, considering they describe it as "osteoclastoma." Idk. I thyroid but looking at FA, none of the thyroid carcinomas describe metastatic lytic lesions. Medullary carcinoma might be the one to confuse you, but it secretes calcitonin which inhibits osteoclasts, so it shouldn't cause resorp or lytic lesions. Right?? +  


So the vitamin deficiency the girl is having is vitamin D. why? because of her diet how? bone fractures + demographics result? diet --> gut fiercely affects intestinal calcium absorption in the gut.

the distractor was the bone fractures and poor wound healing which wanted you to pick collagen synthesis.. which I did twice -_-.. but I think in this case of a question; when it seems too simple; explain to yourself why the other answers don't make sense.

I think I keep choosing A not realizing that vitamin C deficiency would present with lot more signs and symptoms like easy bruising and bleeding gums.

pg32  I think it's also important to realize that their veganism is the giveaway. Vitamin C is in fruits and vegetables and wouldn't be lacking in her diet. Vitamin D3 is mostly found in milk supplemented with Vitamin D, though it can be found in smaller amounts in plants as well. +  
pg32  Additionally, if you want to get reeeeally picky about collagen synthesis as an answer choice (cuz I was debating picking that one as well), a vitamin C deficiency causes an issue with collagen cross-linking rather than "synthesis." I know it is nit-picky, but the question says the vitamin deficiency DIRECTLY affects the process. +  


So the vitamin deficiency the girl is having is vitamin D. why? because of her diet how? bone fractures + demographics result? diet --> gut fiercely affects intestinal calcium absorption in the gut.

the distractor was the bone fractures and poor wound healing which wanted you to pick collagen synthesis.. which I did twice -_-.. but I think in this case of a question; when it seems too simple; explain to yourself why the other answers don't make sense.

I think I keep choosing A not realizing that vitamin C deficiency would present with lot more signs and symptoms like easy bruising and bleeding gums.

pg32  I think it's also important to realize that their veganism is the giveaway. Vitamin C is in fruits and vegetables and wouldn't be lacking in her diet. Vitamin D3 is mostly found in milk supplemented with Vitamin D, though it can be found in smaller amounts in plants as well. +  
pg32  Additionally, if you want to get reeeeally picky about collagen synthesis as an answer choice (cuz I was debating picking that one as well), a vitamin C deficiency causes an issue with collagen cross-linking rather than "synthesis." I know it is nit-picky, but the question says the vitamin deficiency DIRECTLY affects the process. +  


submitted by sympathetikey(644),

Histone acetylation allows for relaxation of the DNA so that transcription can proceed. All trans retinoic acid causes the granulocytes in APML to further mature, which requires DNA transcription / translation.

osler_weber_rendu  The questions asks for response to ATRA. Should that not be decreased transcription to treat the cancer? Which makes methyl transferase (aka methylation) the more likely answer +  
pg32  @osler, no @sympathetikey is correct. ATRA's mechanism in treating APML is to encourage the cells to mature. Maturation would require gene transcription, meaning histone acetylases would be used. +  
nnp  but ATRA is letting transcription of an abnormal protein ( that is 15:17 translocation) +  


Mild jaundice with increased unconjugated in an older fellow is decreased UDP-glucuronyltransferase activity. Particularly in context of stress (appendectomy)

pg32  Went with hepatitis because of his recent surgery. Seen problems like this before where recent surgery means they were given inhaled anesthetic that can cause hepatotoxicity/hepatitis. That, along with the elevated AST/ALT and unconjugated bilirubinemia (signifying liver losing its ability to conjugate bilirubin due to inflammation) made me pick hepatitis. Why is that wrong? +  
suckitnbme  @pg32 AST/ALT are only slightly elevated. The patient also is not particularly symptomatic. He's really not that sick. Hepatoxicity is also most associated with halothane which is no longer used in the US. It would be a different story if the patient had surgery done in a different country (as is common in Uworld questions on this) +  


The scenario described is heart failure 2/2 mitral valve regurgitation. If we want to prove the regurg, we can confirm and grade it using an echo.

pg32  Why isn't catheterization also correct? Via catheterization we would be able to see elevated PCWP, which is a measure of left atrial pressure. +2  


submitted by welpdedelp(146),

It was scabies, which is transmitted person-operon.

welpdedelp  **person-person lol +4  
suckitnbme  NBME loves their scabies +5  
dentist  did you get scabies from "burrows" and "night itching" +  
pg32  My question is where do you get scabies originally? I knew it was transmitted person-to-person, but thought it has to originate somewhere (a pet possibly?) so I went with pets. The internet only seems to say that you get scabies from another person with scabies, so the question remains: where do people contract scabies from? +  


submitted by meningitis(273),

I also thought the same as @bubbles, but now trying to "justify" this tricky NBME question: I think this revolves on the fact that the patient has a HIGH blood pressure meaning we should focus on an answer that explains both increased BP and Hypovolemia (i.e: increased ADH which vasoconstricts and also absorbs free-water, both of which increase BP and cause hypovolemia).

Maybe if this patient were decompensated with LOW BP, one could think more about ANP.

I still think this question is TOO tricky.

meningitis  Sorry, hyponatremia* right? +  
mantarayray  I think that it's not ANP because ANP will cause a loss of Na but water will follow (they usually go together), whereas ADH will cause absorption of only water and will cause hyponatremia except only thought this post getting the question wrong :") +2  
mantarayray  Oops sorry the formatting is confusing: I think that it's not ANP because ANP will cause a loss of Na but water will follow (they usually go together), whereas ADH will cause absorption of only water and will cause hyponatremia. +2  
pg32  @mantaray pretty sure you are right and that is the only way to get this question correct. Remembering that Na concentration really is a measure of water balance is key. If the pt is hyponatremic, that just means they have too much water in the blood, which is caused by ADH. If the patient was hypoVOLEMIC, that might mean they are losing too much Na. This is illustrated by pts with SIADH. They are hyponatremic, but euvolemic, meaning that they have too much water (hyponatremia from the ADH) but their Na balance is ok (due to excretion of Na via ANP/BNP) +  
mdrahimi7  Also read my answser mdrahimi7. I think it seems logical... +  


submitted by bobson150(4),

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 +10  
nc1992  Superior rectal not superior mesenteric. Took me a minute +  
hyperfukus  ugh am i ever gonna get these right EVER +5  
titanesxvi  why not the inferior mesenteric, since the superior rectal drains there +2  
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' +  
pg32  Also worded poorly because the varicosities are connections between the superior rectal and the middle/inferior rectal veins of the systemic circulation. So the blood could be in both the superior rectal vein and the middle/inferior rectal vein as that is what a varicosity is. +  
snripper  You just gotta know indirect vs. direct hemorrhoids. In this case, it's an indirect hemorrhoid (superior rectal vein) because of the rectal bleeding. +  
jesusisking  @titanesxvi DrDoom explained it pretty well below: "Defining tributary: https://i.imgur.com/2zDxPbW.png Nice images make the term easier to recall. Smaller streams "pay tribute" to larger rivers (by flowing into them)" +  


Alkylating agents (merchlorethamine) (the other drugs listed are microtubule inhibitors) increase the risk of AML.

keycompany  Additionally, AML is the only answer choice that has multiple blast forms (myeloblasts, promyelocytes, etc.). ALL is characterized by a single blast form (lymphoblasts). +16  
seagull  CML has blasts too but they tend to favor mature forms. +4  
kash1f  You see numerous blast forms == AML, which is characterized by >20% blasts +3  
keycompany  The answer choices are all of lymphoid origin except for AML and Hodgkin Disease. We know Hodgkin Disease is a lymphoma (not leukemia) and would present with lymphadenoapthy. So the answer must be AML #testtakingstrategies +9  
impostersyndromel1000  @atstillisafraud thanks for mentioning the merchlorethamine increasing risk for AML, i was trying to make a connection with the drugs but couldnt. Had to lean on the test taking skills just like key company +  
sweetmed  Procarbazine is alkylating as well. +  
pg32  @keycompany how did you know the phrase "multiple blast forms" meant literally different types of blasts and not just many blast cells were seen? +2  


submitted by keycompany(184),

Alteration of the thermostatic set point is a hypothalamic process mediated by prostaglandins and is independent of the sympathetic nervous system.

B, C, D, and E all require sympathetic nerves to ellicit a response.

pg32  Can anyone explain the mechanism behind shivering and the sympathetic nervous system? +1  


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 +4  
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 +2  
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). +  
taediggity  I absolutely love your @liverdietrying, however the pathogenesis of postpartum thyroiditis is similar to Hashimoto's, so I think this person has postpartum thyroiditis and your explanation of transient thyrotoxicosis is spot on, which would also occur in postpartum thyroiditis +3  
pg32  I agree with @taediggity. Also note that women eventually recover from postpartum thyroiditis and typically become euthyroid again, which doesn't happen with Hashimoto's. +  
vulcania  In FA (2019 p. 338) it says that thyroid is usually normal size in postpartum thyroiditis, but the patient in this question had a thyroid "twice the normal size." I guess at the end of the day it doesn't matter which diagnosis is right for this question cause they both seem to lead to the same correct answer :) +1  


submitted by mattnatomy(31),

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 +2  
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 :) +  
pg32  Yeah, recall that the midgut rotates AROUND THE SMA in development. If you can recognize that the ligament of Treitz is on the wrong side (right) then you know you have a malrotation issue. Then you recall the midgut rotates around the SMA and you pick that answer out of pure association recall and get it right. Nice. +1  


submitted by hello(149),

Why isn't this a cohort study?

drdoom  This is a cohort study! (Since it involves splitting people into "groups"; group = cohort.) But the stem asks what "best describes" the design. So, yes, it's a cohort study but a more precise ("more specific") description is Open-label. In other words, "Open-label clinical trial" is a type of cohort study, and, in this case, "Open-label" is a more precise description of what is described in the stem. +3  
drdoom  For a more technical explanation of "Cohort studies", see the definition from the National Library of Medicine: https://meshb.nlm.nih.gov/record/ui?ui=D015331 +  
angelaq11  It is a cohort, just as @drdoom said, but it isn't an "Observational" one. +1  
pg32  It's actually not a cohort study, imo. In a cohort you find people with an exposure and see if they develop some outcome. In this experiment, people were RANDOMLY ASSIGNED to the different exposures. That doesn't happen in cohorts. +1  
pg32  It may be a cohort in that these people are in groups, but for the purposes of Step 1, I don't think we will deal with typical "Cohort" studies in which participants are randomly assigned. +  


submitted by hello(149),

Why isn't this a cohort study?

drdoom  This is a cohort study! (Since it involves splitting people into "groups"; group = cohort.) But the stem asks what "best describes" the design. So, yes, it's a cohort study but a more precise ("more specific") description is Open-label. In other words, "Open-label clinical trial" is a type of cohort study, and, in this case, "Open-label" is a more precise description of what is described in the stem. +3  
drdoom  For a more technical explanation of "Cohort studies", see the definition from the National Library of Medicine: https://meshb.nlm.nih.gov/record/ui?ui=D015331 +  
angelaq11  It is a cohort, just as @drdoom said, but it isn't an "Observational" one. +1  
pg32  It's actually not a cohort study, imo. In a cohort you find people with an exposure and see if they develop some outcome. In this experiment, people were RANDOMLY ASSIGNED to the different exposures. That doesn't happen in cohorts. +1  
pg32  It may be a cohort in that these people are in groups, but for the purposes of Step 1, I don't think we will deal with typical "Cohort" studies in which participants are randomly assigned. +  


submitted by seagull(736),

If you don't know what Dicumarol does like any normal human. The focus on what aspirin doesn't do, namely it's doesn't affect PT time and most pills don't increase clotting (especially with aspirin). This is how I logic to the right answer.

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT? +3  
ls3076  Why isn't "Decreased platelet count" correct? Aspirin does not decrease the platelet count, only inactivates platelets. +1  
drmohandes  Because dicumarol does not decrease platelet count either. +  
krewfoo99  @usmleuser007 Because the answer choice says decrease in PTT. If you take a heparin like drug then the PTT will increase. Drugs wont increase PTT (that would be procoagulant) +2  
pg32  I think usmleuser007 and is3076 were working form the perspective of not knowing what dicumerol was. If you were unsure what dicumarol was, there really wasn't a way to get this correct, contrary to @seagull's comment. You can't really rule out any of these as possible options because aspirin doesn't do any of them. +  
snripper  yeah, it wouldn't work. We'll need to know with Dicumarol is. +2  


submitted by k_tron_3000(21),

Just a random factoid (as far as I know), in patients with pancreatitis the most likely vessel for thrombosis is the splenic vein due to close “anatomic ties” with the pancreas. This would also cause gastro-splenic varices, explaining the vomiting of blood.

meningitis  Also explains the splenomegaly. If you have thrombosed splenic vein, the blood will pool in the spleen, can also cause expansion of red pulp of spleen. +5  
pg32  I picked splenic vein because of this ^^ association. However, why is the patient vomiting blood if there isn't a backup of blood into the left gastric/esophageal veinous system? +1  
savethewhales  The splenic vein drains the fundus of the stomach. So, splenic vein thrombosis can cause gastric fundal varices, which explains his bloody vomit. +2  


submitted by armymed88(31),

Glucose is co-transported into enterocytes of SI via sodium

toxoplasmabartonella  That makes that glucose needs to be given with sodium. But, what about bicarb? Isn't the patient losing lots of bicarb from diarrhea? +2  
pg32  Had the same debate. I knew glucose/sodium was the textbook answer for rehydration but also was wondering if we just ignore the bicarb loss in diarrhea...? +2  
makinallkindzofgainz  @pg32 - Sure, they are losing bicarb in the diarrhea, and yes this can effect pH, but it doesn't matter that much. You're not going to replace the bicarb for simple diarrhea in a stable, but hydrated previously healthy 12 year old. You're gonna give him some oral rehydration with a glucose/sodium-containing beverage. Don't overthink the question :) +  
makinallkindzofgainz  *dehydrated +  


submitted by iviax94(6),

There have been a couple of questions about this topic on the newer exams. I’ve been answering by equating libido to testosterone levels and nocturnal erections to health of vasculature (atherosclerosis or not). Is this correct?

liverdietrying  When you’re thinking of libido, don’t just equate it to testosterone -- make sure you’re always considering depression! Depression following stroke is common, especially with residual physical disability, so this would decrease his libido. Nocturnal erections equate to “does it actually work?” not just the vasculature but the neural input as well. For example, during prostatectomy damage to the pelvic plexus (nerves) can lead to impotence. There’s nothing to suggest that he has vascular or neurologic erectile dysfunction here, which is why his nocturnal erections are intact. +11  
_pusheen_  @liverdietrying Was it premature to assume he has trouble with erections because of neural damage from the stroke? I put low libido, low nocturnal erections. Is it because the stroke resulted in hemiparesis and not autonomic dysfunction or something like that? +3  
liverdietrying  @pusheen Correct, you won’t classically get impotence after a hemiplegic stroke. His inability to achieve an erection is much more likely to be 2/2 psychosocial effects than organic disease. If this vignette instead said that this had gotten a prostatectomy with resulting damage to the pelvic nerves that allow for erection, then it’d be a more safe choice to put no nocturnal erections. +3  
fast44  Is there a video or somewhere that explains these sexual dysfunctions? This seems to be a topic that keeps repeating on the new exams. +1  
forerofore  well, i though that because he had a stroke he would be likely to have atherosclerosis, which would keep libido high and reduce nocturnal erections, i kinda ignored the whole "he´s depressed" part of the vignette despite understanding the mechanism well. but from a clinical depression point of view, if his arteries are intact, and he is depressed, then libido would be low, and erections present at night. +4  
pg32  I can't remember exactly but I swear the question on NBME 21 the guy's wife had died as well...? Or they had gotten divorced? Either way, he had some psychological baggage as well, but his libido was still normal, and the explanation was that his testosterone would be fine regardless of his depressed mood. So I went with that logic here and missed this question. I don't understand how I am supposed to gauge someone's libido based on vague hints at their mood, especially when in one exam mood does not decrease libido and in the other it does. +  
drzed  @pg32 bro spoilers +1  


submitted by mguan1993(3),

can someone explain why the answer is not adrenal gland? I feel ike if adrenal gland was the issue there would also be decreased concentrations of FSH, LH, and estrogen right?

mguan1993  ^nvm had a brain fart and go adrenal gland mixed up with anterior pituitary lmao +2  
nor16  ovaries are #1 estrogen producer no estrogen no lubricant = dyspareunia no estrogen and no fsh/lh --> there must be a "higher" problem, up there in the brain +3  
pg32  I agree that hypothalamus is the most logical answer, but if she had overactivation of the adrenal gland (cortisol secreting tumor), that could also inhibit GnRH and cause these same symptoms. +  
drzed  @pg32 the physical examination would not be normal with either a ACTH or cortisol secreting tumor. +  


submitted by d_holles(83),

This video explains the pediatric neurocutaneous disorders well.

https://www.youtube.com/watch?v=Lom7tnK8HCk

Basically the key here is hypopigmented macules. NF1 has cafe au liate spots (hyperpigmented macules) while TSC has ash leaf spots (hypopigmented macules). This is a decode the buzzword style question. I felt like I didn't really understand these orders until I watched the above video.

pg32  I figured this out for a few reasons. The hypopigmented patches are ashleaf spots and the raised, flesh-colored lesion on the back is a Shagreen patch (only seen in TSC). Multiple brain lesions = hamartomas. Additionally, NF1 has 100% penetrance, though it also has variable expressivity, meaning if it were NF1 we would probably see some family history of similar symptoms. +2  


submitted by bubbles(47),

Can someone could explain to me how this is unequivocally tuberous sclerosis despite NF-1 and Sturge-Weber also presenting with skin lesions, hypopigmented macules, and seizures?

And considering the negative family history, I would have assumed that a sporadic mutation (like SW) would be more likely...

cocoxaurus  This question was tricky! Tuberous sclerosis= Hypopigmented= Ash leaf spot (The skin lesion in NF is Hyperpigmented- Cafe au lait and in Sturge Weber it's a port wine stain (also not hypopigmented). I'm assuming that the SINGLE raised flesh colored lesion is a Hamartoma (The angiofibromas in NF1 are typically multiple). Although both Tuberous Sclerosis and Sturge Weber are both associated with seizures, I used all the other stuff to narrow it down to the correct answer. Also, don't forget that there is Incomplete penetrance and variable expressivity in Tuberous Sclerosis. So I think the lack of family history of "seizure or major medical illness" was there to throw us off. +16  
bubbles  Thank you! :) I thought I really knew my congenital disorders, so I was a little annoyed when they trotted this question out +1  
pg32  @cocoxaurus I believe the single raised flesh-colored lesion is actually a Shagreen patch, which helps you arrive at TSC as the diagnosis. +1  


Lifting head while prone: 1 month Social smile: 2 months Cooing: 2 months

pg32  Where do you guys learn that cooing starts at 2 months? It isn't in first aid or boards and beyond so this was an annoying question for me +  
drschmoctor  @pg32 From being a parent! Otherwise little chance I'd remember all these milestones. +1  
drzed  I'll get right on that @drshmoctor :). If only I could have a kid to memorize all these damn developmental milestones. That would make life easier haha. +2  
snripper  Yeah, I don't see cooing anywhere. +  


Can someone correct my reasoning here:

I was thinking positive airway pressure will increase alveolar ventilation and decrease hypoxia induced pulmonary vasoconstriction. Thus, RV after load would decrease => more preload to LV and more cardiac output. Then wouldn't BP decrease?

Any help is appreciated. Thanks.

pg32  I just thought of it as follows: he has high BP due to pulmonary vasoconstriction as well as widespread sympathetic activation (as if he is being partially strangled all the time, because he basically is). Increasing oxygenation will relax his pulmonary vasculature and decrease sympathetic stimulation throughout the body, leading to a drop in blood pressure. +1  


submitted by tinydoc(135),

Type 1 Familial Dyslipidemia (pg. 94 FA 19 )

increased TG ---> pancreatitis Eruptice / pruritis Xanthomas and HSM

Can be caused by Lipoprotien lipase or Apoprotien CII deficiency

they said that LPL is fine so its APO CII

Heparin seperates LPL from Herparin Sulfate Moeity on Vasc Endothelium allowing us to test its function in the lab.

I got it wrong too - Stupid Rote memorization recall Question.

masonkingcobra  I think you need to know that ApoCII activates LPL not necessarily know the disease +5  
yotsubato  Knowing the disease makes it easier to remember the details though +1  
pg32  Mnemonic for these 4 types of dyslipidemias and their causes: 1 = LP meaning LPL is deficient (or anything associated with activating LPL, like C-II) 2 = LD meaning LDLR is deficient (or anything involved in interacting with LDLR, like B-100) 3 = E meaning ApoE is defective and 4 for more (VLDL) ("more" just meaning more letters in the cause (VLDL oversecretion)) +1  


euthyroid sick syndrome is sometimes called "low T3 syndrome." Also you know that the patient is euthyroid because her T4 and TSH are within the reference range. She is sick.

yotsubato  This is not in FA btw. +6  
niboonsh  https://www.ncbi.nlm.nih.gov/books/NBK482219/ probably caused by her recurrent pneumonia +2  
eacv  I though in this one as a sick sinus syndrome hahaha in UW. +  
pg32  Pretty sure boards and beyond teaches this wrong. Dr. Ryan says that in euthyroid sick syndrome T3, T4 and TSH will be low, but rT3 will be elevated. +  
pathogen7  In reality, TSH and T4 levels can be highly variable based on the stage of Euthyroid sick syndrome. One thing that happens for sure, I believe, is that T3 is down and rT3 is up. +  


submitted by tinydoc(135),

Hyperparathyroidism causing bone lesions is via Osteoblasts increasing RANK -L expression to bind to RANK on Osteoclasts and stimulating them ---> inc Bone Resorption

pg32  Picked D despite understanding the above ^^ because IL-1 is also known as osteoclast acitivating factor... +2  
plzhelp123  ^ I did the same, but it appears that IL-1 activates osteoclasts in multiple myeloma. Which makes sense as that is a neoplasm of immune cells which can produce interleukins. +  


submitted by readit(9),

Addition to Hungrybox's explanation:

Why it's not 47,XXY:

This would be referring to Klinefelter's, which is characterized by small, poorly functioning testicles.

However, question states "morphologic studies of a biopsy specimen of the testes show no abnormalities"

readit  More specifically, in Klinefelter's, you would see "hyaline seminiferous tubules/sertoli cells" on histology +2  
pg32  Thanks! Where did you get the histologic description from? +  


submitted by taway(16),

Just as a note for anybody else who was WTF at how 2(29/30)(30/30) = 1/15...a lot of question banks round 29/30 (or any similarly large fraction) out to 1

gh889  I think you meant 2(29/30)(1/30) just to clarify! +3  
niboonsh  i am confusion +  
arkmoses  You have to use the hardy weinberg formula (1=p^2+2qp+q^2)and p + q = 1 they basically tell you that q^2=1/900 which makes q=1/30 now you can figure out (p=1-q) so p=1-(1/30), p=29/30 then to figure out carrier you solve for 2qp, 2(29/30)(1/30)=1/15 I got it wrong cuz I forgot how to figure out p but hopefully wont happen on the real deal. +3  
garibay92  2pq= 2(29/30)(1/30).... Transform this to 2 1 1 2 1 x x = _ = ____ 1 1 30 30 15 +  
garibay92  Nevermind :/ It didn't come out as planned :( +  
garibay92  /Users/carlosgutierrez/Desktop/IMG_2423.jpg +  
pg32  How do we know this disease is autosomal recessive? I assumed it was just because they love these carrier frequency questions with AR diseases, but how do we know it's AR? +  
turtlepenlight  Sounds like Gaucher (ish?) if i'm remembering correctly +2  


The patient suffered from Immune Thrombocytopenia. autoantibodies against the glycoproteins GP2B/3A.

On labs, you’ll see: increase in megakaryocytes; on the question stem they’re described as “rare but large.” Megakaryocytes are not suppressed.

ergogenic22  isolated thrombocytopenia (low platelets) should be highly suggestive of ITP https://www.aafp.org/afp/2012/0315/p612.html +1  
pg32  I agree that in ITP you will see an increase in megakaryocytes, but where did you see that in the stem? Platelets being, "rare but large" doesn't mean megakaryocytes, does it? Also... can anyone explain why she was anxious but alert and had petechiae distal to the blood pressure cuff? +  


submitted by liltr(15),

I choose MVP too, but this patient’s main symptom is cough only during exercise. This is more indicative of exercised associated asthma. You could see shortness of breath in MVP during exercise, but choosing MVP leaves the cough unaccounted for.

.ooo.   I agree! Also, At the end of the stem, the question is which of the following best explain the patients symptoms? Not physical exam findings. Since this patient is coming in with a chief complaint of SOB while playing sports exercise induced asthma is the best choice. Hopefully that helps. +10  
uslme123  I mean... couldn't increased BP during exercise worsen his MVP and give him SOB? +  
uslme123  (by causing slight regurg) +1  
yotsubato  "Lungs are clear to auscultation" +6  
sahusema  But wouldn't choosing exercise-induced asthma leave the murmur unaccounted for? +  
cienfuegos  I incorrectly chose malingering and am wondering if the fact that he presented (although it doesn't state who brought him in/confirmed his symptoms while exercising) makes this less likely despite the fact that he clearly states "I don't want to play anymore" which could be interpreted as a secondary gain? Also, regarding the MVP, I'm wondering if the fact that these are usually benign should have factored into our decision to rule it out? Thoughts? +1  
cienfuegos  Just noticed that he has FHx, game changer. +1  
kimcharito  clear lungs, they try to say no cardiogenic Pulm. edema, means is not due to MVP shortness of breath while doing sports and no shortness at rest makes me to think more asthma induced by exercise) +  
pg32  Isn't exercise induced asthma usually found in people running outside, especially in cold weather? I feel like that is how it is always presented in NBME questions, so this threw me off. Not to mention the MVP. +  


submitted by yo(36),

I just knew that sperm need fructose, not sure what disease process this is though. He was pretty normal so 5a reducatase doesn't present like that. I wasn't sure if there was any odd use of the other answers. here is a link. Feel free to expand.

https://www.labce.com/spg27422_question.aspx

Fructose makes up 99% of the reducing sugar present in semen. This sugar is produced in the seminal vesicles. Diminished levels of fructose have been shown to parallel androgen deficiency and the testosterone level. Following testosterone therapy, the level of fructose increases. Although the fructose test is not part of a routine semen analysis, it is useful in cases of azoospermia (absence of sperm in semen). In azoospermia secondary to the absence of vesicles or if there is an obstruction, no fructose is present. In testicular azoospermia, fructose is present. When azoospermia and low semen volume exists, the fructose test should also be done, on a postejaculate urine sample to check for retrograde ejaculation. This occurs when the ejaculate goes into the bladder instead of out the urethra. The procedure for determining the amount of fructose in semen involves heating semen in a strong acid in the presence of resorcinol. Fructose gives a red color (Selivonoff reaction) and may be read in a photometer. The normal average is 315mg/dL fructose.

sam.l  Thank you for the explanation. I'm still confused about this answer. I was in between Zinc and fructose. Zinc deficiency also presents with anosmia (pg 71 First Aid 2019). Fructose is used for the movement. His hormones are normal. +1  
d_holles  Apparently diabetes, occlusion, and inflammation can result in ↓ fructose in sperm. Mauss et al, Fert Stert 25, 1974 https://www.fertstert.org/article/S0015-0282(16)40391-2/pdf +1  
cienfuegos  Thanks all for the info, quick note on the Zinc reply above @Sam.I: anosmia = lost sense of smell. +  
sam1  Great find yo! I believe this question was alluding to cystic fibrosis and the congenital absence of the vas deferens. Here is a link to a NEJM article about it below: https://www.nejm.org/doi/full/10.1056/NEJM196807112790203 +  
burak  zinc deficiency cause hypogonadism. there is no hypogonadism, sperms are damaged? +  
fatboyslim  @Sam1 but cystic fibrosis will show abnormal physical findings (clubbing, pulmonary crackles etc). The question says physical exam shows no abnormalities. +  
pg32  Confused as to how we can rule out zinc... From medicalnewstoday.com: "Zinc also plays a role in healthy sperm production. According to a 2018 review article in the Journal of Reproduction and Infertility, zinc deficiency may contribute to poor semen quality and infertility." +  


submitted by hungrybox(445),

Dysplastic nevi are a precursor to melanoma. They have irregular, "dysplastic" borders. Remember the "B" in ABCD stands for irregular Borders. Nevus means mole.

Other answers:

  • acanthosis nigricans - Darkening of skin associated with Type II diabetes mellitus

  • basal cell carcinoma of skin - Rarely, if ever metastasizes. Commonly affects upper lip.

  • blue nevus - Blue-colored type of common mole. Benign.

  • pigmented seborrheic keratosis - "Stuck on" appearance. Mostly benign. Affects older people.

  • (Note - you usually see only one. If multiple seborrheic keratoses are seen, it indicates a GI malignancy - aka "Leser-Trélat sign)
usmleuser007  correction ~ BCC affects the lower lip more than the upper +  
sympathetikey  Pathoma says upper lip, good sir +13  
hungrybox  Yeah basal cell carcinoma actually affects the upper lip. Counterintuitive because it's "basal" which seems to go along with the lower lip. Here's another source (this website is fucking gold btw): https://step1.medbullets.com/oncology/121593/basal-cell-carcinoma-of-the-skin +3  
pg32  Can anyone explain how we can rule out C or E purely based on the question stem? If we read into the question that we are looking for something related to melanoma, then I get why we can rule out C and E. However, the question simply asks which lesion appears on both sun-exposed and nonsun-exposed areas of the patient's skin. I would say that C, D and E can all occur in that distribution pattern. +  
paperbackwriter  @pg32 because it specifies "this patient's skin," and the only ones he is more likely to get than the average person because of his family history are dysplastic nevi +  


submitted by hayayah(620),

the majority of carbon dioxide molecules are carried as part of the bicarbonate buffer system. In this system, carbon dioxide diffuses into the RBCs. Carbonic anhydrase (CA) within RBCs quickly converts the carbon dioxide into carbonic acid (H2CO3). Carbonic acid is an unstable intermediate molecule that immediately dissociates into bicarbonate ions (HCO3-) and hydrogen (H+) ions.

The newly synthesized bicarbonate ion is transported out of the RBC into the plasma in exchange for a chloride ion (Cl−); this is called the chloride shift. When the blood reaches the lungs, the bicarbonate ion is transported back into the RBC in exchange for the chloride ion. The H+ ion dissociates from the hemoglobin and binds to the bicarbonate ion. This produces the carbonic acid intermediate, which is converted back into carbon dioxide through the enzymatic action of CA. The carbon dioxide produced is expelled through the lungs during exhalation.

hungrybox  Amazing explanation. Thank you!! +  
namira  in case anyone wants to visualize things... https://o.quizlet.com/V6hf-2fgWeaWYu1u23fryQ.png +3  
ergogenic22  CO2 is carried in the blood is bound to hemoglobin, known as carbaminohemoglobin (HbCO2) (5%), dissolved CO2 (5%), bicarb is 90% +3  
pg32  Nice explanation, but can anyone clarify how we know from the question that we are measuring HCO3 rather than dissolved CO2? +1  
qball  @pg32 This question is asking about what accounts for the LARGER amount of co2 and the HCO3 buffer is about 85% of this transport and dissolved C02 is about 5-7%. https://courses.lumenlearning.com/wm-biology2/chapter/transport-of-carbon-dioxide-in-the-blood/ +  


submitted by nosancuck(59),

This b has Sarcoidosis so her granulomas be activatin dat VitD

sbryant6  Your mom activates my VitD. +6  
pg32  Anyone know why there is hepatosplenomegaly? +  


submitted by celeste(49),

The constellation of symptoms sounds like tuberous sclerosis. Cardiac rhabdomyoma is a rare benign tumor that is frequently associated with tuberous sclerosis.

tinydoc  Cardiac Tumors in adults -- usually myxoma Cardiac tumors in kids -- usually Rhabdomyoma ( ass. w/ Tuberous Sclerosis. ) --> its in the first aid rapid Review +5  
tinydoc  Cardiac Tumors in adults -- usually myxoma Cardiac tumors in kids -- usually Rhabdomyoma ( ass. w/ Tuberous Sclerosis. ) --> its in the first aid rapid Review +2  
arlenieeweenie  He also has seizures and pink-yellow papules, which I think they're trying to describe one of the characteristic ash-leaf or shagreen patches (doesn't sound like either of them to me lol) but that all points to tuberous sclerosis +  
pg32  @arlenieeweenie I think they are actually trying to describe angiofibromas that appear on the face in tuberous sclerosis, though I still think their description is pretty bad haha +1  


submitted by nosancuck(59),

Yo dawg we all about PVT TIM HaLL

Phenylalanine, Valine, TryptoDANK, Threonine, Isoleucine, Methionine, Histidine, Leucine Lysine

meningitis  I don't understand what the question is asking... can someone please explain it to me? Patient doesnt eat protein, shes chubby. What does methionine have to do with this? +2  
charcot_bouchard  Just basically asking which is essential amino acids. +2  
usmleuser007  Essential amino acids (something i came up with) 1. "Three HAL fans will try meth" a. Threonine = Three b. Histidine; Arginine; Lysine = HAL c. Phenylalanine = fans d. Valine; Isoleucine; Leucine = will e. Tryptophan = try f. Methionine = meth +3  
nala_ula  They're saying there is a lack of good quality protein -> slight nutritional deficiency. She may have acquired weight but it's not because of protein. So they're specifically asking what amino acid she might be missing due to her subpar diet. Since essential amino acids are those that the body cannot make itself, out off those listed, methionine is the essential amino acid. It's on page 81 of FA 2019. +8  
nala_ula  correct me if I'm wrong please :) +  
hello  For anyone confused trying to follow @usmleuser007's comment -- slightly modified Essential amino acids mnemonic "Ah, Three fans will try meth" Ah = arginine, histidine Three = Threonine Fans (phans)= Phenylalanine Vil (Will -- German accent pronouncing English word 'will') = valine, isoleucine, leucine, lysine Try = tryptophan Meth = Methionine +1  
pg32  Why does @hello and @usmleuser007 mnemonic contain arginine? That isn't in the PVT TIM HaLL mnemonic for essential amino acids... +  
paperbackwriter  @pg32 arginine is semi-essential. It is essential in preterm infants who cannot synthesize it https://www.sciencedirect.com/science/article/pii/S0955286304000701?via%3Dihub +  


submitted by notadoctor(107),

Usual interstitial pneumonitis is the histological definition of Idiopathic pulmonary fibrosis. We know that this patient has pulmonary fibrosis because the question states that there is fibrous thickening of the alveolar septa. This question was just testing that we knew the other names for Pulmonary Fibrosis.

aneurysmclip  Nbme back at it again +10  
pg32  Is it still considered idiopathic pulmonary fibrosis is it appears to have been caused by an atypical pneumonia? +  


submitted by hungrybox(445),

Hydrochlorothiazide is a thiazide diuretic => thiazide diuretics are associated with hypokalemia.

What other diuretics are associated with hypokalemia? Loop diuretics.

Why?

Inhibition of Na+ reabsorption occurs in both loop diuretics (inhibit NKCC cotransporter) and thiazide diuretics (inhibit NaCl cortransporter). All of this increased Na+ increases Aldosterone activity.

Relevant to this problem, Aldosterone upregulates expression of the Na+/K+ ATP antiporter (reabsorb Na+ into body, expel K+ into lumen). This results in hypokalemia in the body.

Hang on, there's more high yield info!

Aldosterone does one other important thing - activation of a H+ channel that expels H+ into the lumen.

So, given that this patient has hypokalemia, you know there is upregulation of Aldosterone. Do you think her pH would be high, or low? Exactly, it would be high because inc. Aldosterone => inc. H+ expelled into the lumen => metabolic akalosis.

Now you understand why both loop diuretics and thiazide diuretics can cause what's called "hypokalemic metabolic alkalosis."

hungrybox  jesus this answer was probably too long i'm sorry +1  
meningitis  I disagree. It's the complete thought process needed for many Thiazide/Loop question that can be thrown. Thanks. +8  
amirmullick3  This is what NBME should be providing with each question's correct answer! Thanks hungrybox! +  
amirmullick3  @hungrybox did you mean "All of this DECREASED Na increases aldosterone activity."? +1  
pg32  Anyone care to explain why she feels she has, "lost [her] pep"? Is that due to the hypokalemia? Or hypercalcemia caused by the thiazides? +  
cmun777  @madojo @pg32 I assumed between her hypokalemia (which can cause weakness/fatigue) and possible contraction alkalosis those were the most likely causes for the "lost her pep" comment. I think if they wanted to indicate hypercalcemia to differentiate if loop diuretics were also in the answer choices they would certainly give more context for hypercalcemia sx +  


submitted by nuts4med(5),

I was thinking Chron’s because of the narrowing of the lumen and the picture seemed like there was creeping fat. Now that I think about it though, the LLQ and constipation should have led towards diverticulitis pretty quickly.

suckitnbme  Also agree the narrowing of the lumen plus the pic is pointing towards Crohn's. The acute systemic sx of fever and chills is what made me go with diverticulitis (along with the hx of increasing constipation). +1  
pg32  Why does the question say there is NARROWING OF THE LUMEN? Does that happen in diverticulitis? I went with Chron's at the last second against my better judgment because Chron's can cause strictures/narrowing of the lumen. +1  


submitted by hayayah(620),

Secondary hyperparathyroidism (usually d/t chronic renal failure).

Lab findings include ↑ PTH (response to low calcium), ↓ serum calcium (renal failure), ↑ serum phosphate (renal failure), and ↑ alkaline phosphatase (PTH activating osteoBlasts).

haliburton  also remember that in renal failure, 1-alpha-hydroxylase activity is down, so there will be less activation of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is a key mechanism causing hypocalcemia. +1  
cr  why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain +  
nala_ula  Increased phosphate, since the kidneys aren't working well, leads to the release of fibroblast growth factor 23 from bone, which decreases calcitriol production and decreased calcium absorption. The increase in phosphate and the decrease in calcium lead to secondary hyperparathyroidism. +1  
privatejoker  Probably a dumb question but how do we definitively know that the ALP is elevated if they give us no reference range in the lab values or Q stem? Everything stated above definitely makes sense from a physiological standpoint, I was just curious. +1  
fatboyslim  @cr the question asked "the patient's BONE PAIN is most likely caused by which of the following?" Increased levels of 25-hydroxycholecalciferol might exist in that patient, but it wouldn't cause bone pain. PTH causes bone pain because of bone resorption +  
suckitnbme  @privatejoker ALP is included in the standard lab values +  
makinallkindzofgainz  @privatejoker ALP is listed under "Phosphatase (alkaline), serum" in the lab values +  
pg32  Why does AlkPhos increase in renal osteodystrophy? The PTH would be trying to stimulate bone resorption (increase osteoCLAST activity), not bone formation (osteoBLAST activity). +  
drzed  @pg32 the only way to stimulate an osteoclast in this case (e.g. via PTH) is by stimulating osteoblasts first (thru RANKL/RANK interaction), thus ALP increases. +1  


submitted by monoloco(86),

This is a hypoplasia of the pleuroperitoneal membrane. The guts herniate into the thorax, usually on the left side, and result in hypoplasia of the lungs (because they're horribly compressed).

johnthurtjr  Usually on the left because the liver prevents herniation through the right hemidiaphragm +5  
asdfghjkl  aka congenital diaphragmatic hernia +2  
pg32  What's weird to me is that if you usually see air in the intestines on x-ray when they are in the abdomen, why is there no air in the thorax in CDH? The intestines should still have air in them, right? Also, what is filling the abdomen that causes it to appear grayed-out in CDH? +  
drzed  @pg32 You can actually see a gastric bubble if you squint hard enough. Look at where the NG tube is placed; there is a radiolucency to the patient's right of the NG tube which is most likely the stomach. It probably then is radioopaque distally due to the pyloric sphincter, and air having a tendency to rise. +  


submitted by yotsubato(543),

"physicians should always encourage healthy minor-guardian communication."

Also you're going to do some serious things to cure this girl's disease, leading up to amputation. You cant hide that from her.

djjix  Non sense ... you can hide the amputation from her +9  
charcot_bouchard  Just show her one leg twice. +4  
pg32  I picked "request that an oncologist..." because I figured it would be better to have someone with more knowledge of next steps and prognosis discuss the disease with the family as compared to someone working in the ED... why is that wrong? +1  
ibestalkinyo  @pg32: Referring to another physician is almost never an answer for NBME/USMLE questions. Plus, I feel like this would be hiding the patient's problem from her and the patient's parents. +1  
dunkdum  I think the reason that you requesting the oncologist isnt the most correct answer here is because... even if more tests needed to be done... you would still discuss with your patient about that fact and say "Hey these results came back suggesting that you might have this disease, we will need to do more testing to make sure we can get it taken care of if you in fact have this disease." and you'd probably do that before you go and get the oncologist. +  


submitted by hayayah(620),

A big thing here too is noticing that the ALP is decreased. Osteoblast activity is measured by bone ALP. I think that was the main focus here and not that you necessarily need to know the CBFA1 gene mutation.

sympathetikey  Exactly. That's the only way I got to the answer. +  
pakimd  isnt increased alk phos consistent with increased osteoblastic activity? +  
champagnesupernova3  A defect with chondrocytes would cause an short limbs like in achondroplasia so those are ruled out +  
pg32  Exactly. Can also be helpful if you remember that the clavicles are formed by intramembranous ossification rather than endochondral; that allows you to rule out the chondroblast/cyte answer choices. +  


submitted by usmile1(34),

If you look at Uworld question ID 12299 it has a wonderful explanation for this. If they share the same epitopes, it will have a downward slope. If they share none of the same epitopes, the line will be horizontal across the graph (indicating no change as the amount of Y added increases)

eacv  omg YES!! thanks Uworld I got it correct! exactly this qx asked the exact opposite thing! Hahaha I loved it !! +4  
pg32  Even after reading the UWorld explanation, I am still not sure how the answer that reads, "Protein Y expresses all of the epitopes expressed by protein X, but protein X does not..." is incorrect. Based on the graph, I don't see a way we can rule out that answer choice and it sounds more likely than both X and Y having the EXACT SAME epitopes. Can anyone explain? What would the graph look like if the quoted answer choice was correct? +1  
69_nbme_420  If you make up an example with numbers, it really helps! “Protein Y expresses all of the epitopes expressed by X, but protein X does not express all of epitopes expressed by Protein Y.” If we say protein Y has epitopes 1, 2, and 3. Then Protein X has epitopes 1 and 3. Then we can clearly see the relationship the AMOUNT of Y added relative to X bound would NOT be linear. Stated another way – we need an exponentially more amount of Y to COMPLETELY unbind X and therefore there would not be a one to one depiction in the graph Similar logic applies for the answer choice that states "protein X expresses all of the epitopes expressed by protein Y, but protein Y does not express all of the epitopes expressed by protein X. E.g. If protein Y has epitopes 1 and 2. And protein X has epitopes 1, 2, and 3. Here again, we have satisfied the answer choices condition, and no matter how much we increase protein Y, protein X will still have epitope 3 bound in this case. +1  
69_nbme_420  Just to clarify for the first scenario: We have 3 epitopes on Y, and 2 epitopes on X. That means, assuming the epitopes are all present in equal amounts, if I add 300 grams of protein Y to the solution - only 200 grams will bind protein X. AND ONLY 200 grams of protein X can be unbound. Hope the numbers help! +  


submitted by xxabi(146),

I was under the impression that this was an aortic dissection, due to "severe chest pain" as well as the false lumen in the aorta. And HTN is the #1 risk factor for aortic dissection. Someone correct me if i'm wrong, but I think this is aortic dissection rather than aortic aneurysm.

chefcurry  I believe so, FA 2018 pg 299 +2  
ergogenic22  It is dissection "extra lumen in the media of the proximal aorta" = "a longitudinal intimal (tunica intima) tear with dissection of blood through the media of the aortic wall" ... answer is still hypertension +1  
breis  FA 2019: 301 +  
pg32  First Aid says that aortic dissection causes widening of the mediastinum and is due to an intimal tear, so I thought it wasn't an aortic dissection. Can anyone help me understand why First Aid was wrong in this case? Thanks! +3  
nephroguy  @pg32 The question stems states that there is no widening of the Aorta, not the mediastinum. Widening of the mediastinum is seen in dissection while widening of the aorta is seen in aneurysm. Also the intimal tear creates a false lumen between the intima and media. Hope that helps! +3  


submitted by nala_ula(54),

The histology is of spherocytes (small spherical cells w/o central pallor). Hereditary spherocytosis is due to defect in proteins interacting with RBC membrane skeleton and plasma membrane (ankyrin, band 3, protein 4.2, spectrin). Mostly autosomal dominant inheritance (so heterozygous mutation since you only need one mutant allele to get the disease).

wuagbe  To add to this: homozygous HS presents with hemolysis even in absence of stressors. this patient is only presenting with pale skin, and there are no schistocytes on the peripheral smear, so it's a heterozygous ankyrin mutation. +1  
pg32  I wanted to pick hereditary spherocytosis but the mean corpuscular concentration was normal and I thought it was supposed to be elevated? Also, why are there so many RBCs that are way bigger than the spherocytes? +2  
nephroguy  I'm assuming that the MCC is normal because the patient is heterozygous for HS. Not sure if this is correct, but that was my thought process +  


submitted by drdoom(375),

This is an interesting one. I like to remember it this way: in people with narcolepsy, all the “right kinds” of sleep are happening at all the “wrong times” of day. During the day, when a power nap would typically throw you immediately into REM, this kid is only entering Stage 1 or 2 (lightest sleep = slightest noises jar him back to reality). At night, when he should peacefully drift into Stage 1, 2, and so on, he instead completely zonks out. Classic narcolepsy.

From UpToDate: “Narcolepsy can be conceptualized as a disorder of sleep-wake control in which elements of sleep intrude into wakefulness and elements of wakefulness intrude into sleep.”

chextra  Isn't REM a rather light sleep stage? Brain waves during REM are very similar to awake states. I think you even wake up briefly in the middle of REM sleep. I don't think FA gave me a great understanding of narcolepsy, but I see it as going from awake to REM (light) for any kind of sleep, daytime or night time. +  
sammyj98  I'm definitely not ace on this subject, but I think the brain waves present in REM are similar to wakefulness because of the dreaming component. I think of it as though the brain has to go through a process of hypnotizing the body into a state of relaxation, and then properly paralyzing it, and then it can simulate wakefulness (dreaming) to go through with it's defragging of the hard drive. So REM is actually the deepest sleep because the body is fully paralyzed. Please someone correct me, this is probably an inacurrate perspective. +1  
pg32  FA says that narcolepsy has nocturnal AND NARCOLEPTIC sleep episodes that start with REM sleep... So is @drdoom correct? FA seems to disagree regarding the daytime sleep pattern. +  


submitted by hayayah(620),

Earliest detectable secondary sexual characteristic is breast bud development in girls, testicular enlargement in boys.

pg32  How did you know this? The Tanner stages in FA simply list pubarche and breast buds developing in the same stage without stating which comes first. Thanks! +  
lynn  @pg32 look at the paragraph above the diagram, it says that exactly. Took me a minute too lol +1  


I do understand that the principal nucleus of the trigeminal nerve is located at the pons. But since this patient is having trigeminal neuralgia wouldn't you be disrupting the pathway involved in pain and temperature, which in this case would be the spinal nucleus (located in the medulla)?

Besides, I found this at an article

A recent hypothesis attributes the pain of trigeminal neuralgia to a central mechanism involving the pars oralis of the spinal trigeminal nucleus.[5]

https://www.ncbi.nlm.nih.gov/books/NBK539729/

pg32  I literally had medulla selected the whole time and then changed it to pons simply because i felt the test writers were just seeing if we knew where the trigeminal nerve was located. bummer because I think your logic is way better. it's what i first thought when i read the case. +