welcome redditors!to snoo-finity ... and beyond!
Welcome to nala_ula's page.
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Comments ...

 +1  (nbme21#46)

Toll like receptors are pattern recognition receptors (on innate immunity cells like macrophages) that recognize pathogen associated molecular patterns (PAMPs) and lead to activation of NF-kB. One example of a PAMP is LPS (gram negative bacteria). This leads to secretion of IL-1, IL-6 (cause fever), TNF-a (causes fever and hypotension), Nitric Oxide (causes hypotension).

Complement activation itself leads to hypotension via C3a, as well.

All this can be found on page 133 on FA, as @meningitis pointed out, and page 99 of FA 2019.


 +2  (nbme21#37)

In diabetic ketoacidosis, there is increased acid in the extracellular space. According to FA there is a transcellular shift due to decreased insulin that leads to more H+ entering the cell in exchange for K+. This leads to hyperkalemia with depleted intracellular stores of K+. There is also osmotic diuresis that leads to increased K+ loss in the urine and total body K+ depletion. The question asks that is most likely to decrease with insulin therapy: serum potassium concentration will decrease as K+ is now exchanged for H+ inside the cell.

cienfuegos  Additional UW fun facts regarding Potassium and DKA: use caution giving insulin and IV fluids to dehydrated hyperglycemic because i forces K in cells causing fast decrease of extracellular Potassium, thus give K supplementation even when serum K elevated
linwanrun1357  Why urine K+ does not decrease?

 +4  (nbme21#43)

M. tuberculosis replicates in an unchecked fashion within the alveoli and alveolar macrophages due to virulence factors (cord factor) that prevent macrophage-mediated phagolysosome destruction. After a few weeks, macrophages infected display antigen on MHC II to stimulate T CD4+ cells which leads to an increase in interferon-y (Th1 cytokine) that active macrophages. Activated macrophages can also differentiate into epithelioid histiocytes and coalesce into multinucleated Langhans giant cells that wall off extracellular mycobacteria within granulomas.


 +1  (nbme20#11)

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).





Subcomments ...

submitted by colonelred_(45),

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

shaeking  A strawberry hemangioma is normally pink or red (which is why it is named strawberry). The description has a flat purplish lesion which makes me think of a port wine stain on the face. How do you know to think of strawberry hemangioma over port wine based on this question stem? +1  
sheesher  This sounds more like a nevus simplex, which is very similar to a port wine stain, though it regresses over time. +2  
seagull  the age is key here. Newborns have strawberry hemangiomas typically on their face. Sturge-Weber could also be the case but none of the answer choices matched to that description. +1  
vshummy  I would agree with Sturg Webber nevus flammeus but I also noticed First Aid says it's a non-neoplastic birth mark so I should have known not to pick malignant degeneration or local invasion. Also because capillary hemangiomas don't have to be flat but the nevus flammeus is consistently flat. But I'm also reading on Wiki that the nevus flammeus doesn't regress so they must be trying to describe strawberry hemangioma even though I don't agree with their color choice... +  
nala_ula  Maybe (and I can only hope I'm right and the test makers are not -that much of- sadists) they would have made sure to write "in a cranial nerve 5 (either ophthalmic or maxillary) distribution" if it were Sturge-Weber. +1  


submitted by haliburton(82),

EF2 is translational elogation factor 2, which is necessary for protein synthesis.

sympathetikey  I. Am. So. DUMB. +8  
nala_ula  same :( +1  


submitted by nosancuck(34),

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. +1  
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 +1  
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. +6  
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 +  


submitted by nosancuck(34),

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. +1  
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 +1  
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. +6  
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 +  


submitted by halux(2),

can some one please explain why is the hyperplasia?

beeip  Loss of negative feedback from resected ovaries leads to gonadotroph hyperplasia. +1  
halux  so, the explanation is that in the absence of Estrogen negative feedback inhibition to LH and FSH, this leads to Gonadotrophs Hyperplasia at the Pituitary resulting in elevated LH and FSH secretion levels? I get busted by this one :/ Thanks in advance! +1  
nala_ula  @halux exactly, there's no negative feedback telling them there is an increase in the hormones (since there are no ovaries) so gonadotrophs work in overdrive to keep stimulating the gonads via FSH and LH. +  


submitted by asdfghjkl(1),

Anyone know why IGF-1 wouldn't be increased as well? GHRH is stimulated in hypoglycemic states.

nala_ula  Honestly, it's something that has confused me for a while. Why is it that GH secretion is stimulated by hypoglycemia? I mean, it's literally called growth hormone (for growth!), and hypoglycemia, which is basically a "starvation" state, will stimulate this hormone? +  
shaeking  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3529368/ This might help answer your question. I basically didn't pick IGF-1 because it would increase the uptake of glucose leading to a worsen hypoglycemic state. Didn't have a true reason otherwise. +  
temmy  IGF-1 is regulated by insulin. so it will be decreased because insulin levels are also low. +  
nala_ula  thank you @shaeking! +  
nwinkelmann  I found this and it also explains to a more genetic/cellular level. Essentially, it says that starvation induces some factors that cause GH resistance and IGF1 suppression. +1  
nwinkelmann  Sorry forgot the link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2575072/ +  


Arthropod for sure, but for the record I'm pretty sure this was Chikungunya Virus. Only got this from a UWorld question as I hadn't seen it until then, but apparently the arthralgia is really bad, which is what drew me to the answer.

https://www.cdc.gov/chikungunya/index.html

meningitis  More like Zika Virus (Same a. aegypti vector) since it says she has rash associated to her bone and muscle pain. I had Zika one time (i live in Puerto Rico). Remember also dengue and Zika are Flavivirus. Dengue can cause hemolysis (hemorrhagic), and Zika is associated with Guillen Barre and fetal abnormalities. +6  
nala_ula  I'm shocked that I found a fellow puerto rican on this site! Good luck on your test! +  
namira  dont be shocked! me too! exito! +1  
niboonsh  Dengue is also known as "bone break fever" which makes me think its more likely to be dengue due to the "excruciating pains in joints and muscles". https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4242787/ +2  
dr_jan_itor  I was thinking that its Murine typhus transmitted by fleas +  


submitted by hajj(0),

can anyone explain this? i know median for y is higher by calculation but x has two modes so how come y has higher mode?

lispectedwumbologist  The mode in X is 32 and the mode in Y is 80 +  
lispectedwumbologist  The mode in X is 70 and the mode in Y is 80* +1  
hajj  Thank you! +  
hungrybox  Just checking in so I could feel smart about getting this right despite bombing the rest of the test lmao +2  
usmleuser007  can someone please explain the median in this +  
nala_ula  The median can be known by first assembling the numbers in order from least to greater. If it's an uneven number set, the number in the middle is the median (for example: 4, 10, 12, 20, 27 = median is 12 since this is the number in the middle); if the numbers are even then you have to take the two values in the middle, add them up and divide them by 2 [for example: 4, 10, 12, 12, 20, 27 = (12+12)/2 = 12]. Page 261 on FA 2019 explains it as well. Not sure if I explained it well... good luck on the test, people! +  
dubin johnson  Can someone please explain how the mode for Y than X. Not sure how we got the values above. Thanks! +  
dubin johnson  I mean how is the mode for Y greater than mode for x? +1  
sgarzon15  Mode is the one that repeats the most once you list them in order +  
usmile1  Median would be the BP value that the person in the 50th percentile of each group would have. So for group X, to find the 50th percent value, I added 8 + 12 + 32 = 52, which is right above 50, so the median would be 70 mmHg for group X. Doing the same thing for group Y, 2+8+10+20+ 18 = 58; the 50th percentile would fall in group that had a BP of 90 mmHg. which makes the median higher for group Y. hope that isn't wrong, and helps someone! +4  


submitted by aishu007(1),

can anyone explain why enterococcusfaecalis is the answer here?

priapism  Best I can guess is that both S. aureus and E. faecalis can cause UTI, but S. aureus is described as having clusters where as the other Gm+ cocci are in chains +3  
nala_ula  My doubt here in this question is the fact that Enterococcus faecalis is a normal gut microorganism that causes these different symptoms of sickness after genitoruinary or gastrointestinal procedures... but in this question there is no mention of any procedures. +  
fez_karim  its says chains, so not staph. only other is entero +  
temmy  according to first aid, staph aureus is not one of the high yield bugs for UTIs +  
temmy  uti bugs are E.Coli Staph saprophyticus Klebsiella pneumonia Serratia Marcescens Enterococcus Proteus mirabilis Pseudomonad aeruginosa +  
privatejoker  Where in FA 2019 does it list that C.coccus is specifically in chains? +  
privatejoker  E.Coccus* i mean +  


submitted by hyoscyamine(21),

This is lateral medullary/PICA/Wallenberg syndrome. The woman has damage in the sympathetic chain (sensory syndromes are lateral according to the rule of 4s) resulting in Horner syndrome, spinothalamic tract (pain/temp which are also sensory), and CN IX and CN X dysfunction resulting in the dysphagia/dysarthria (helps us localize to the medulla).

nala_ula  Also, just to add, FA specifies that Nucleus ambiguus effects (dysphagia, hoarseness, decreased gag reflex) are specific to PICA lesions. +1  
cienfuegos  Thanks for the input. I have always found this topic to be tricky and just came across this article that helped me out a ton regarding the rule of 4's hoscyamine mentions above. https://rdcu.be/bLjOB +1  


submitted by hayayah(394),

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. +  


submitted by yotsubato(255),

Why is his Libido normal? It's totally expected that he may have reduced libido after his wife died 2 years ago from some horrible prolonged illness.

nala_ula  perhaps it's more to do with the fact that he can get erections when masturbating, outside of nocturnal erections which are not mediated by sexual desire. So his libido must be intact since he has sexual desire evident in being able to masturbate. +  
nala_ula  At least, that's the way I saw it. +  
home_run_ball  "Testosterone concentration is within the reference range" and the fact that he has no difficulty masturbating = normal libido. Low testosterone would contribute to low libido And if he had low libido he would have difficulty masturbating +  
thisisfine   The way I made the decision about normal vs. decreased libido is also that he presented to his doctor due to difficulty maintaining an erection while trying to have sex - meaning he has the libido to try to have sex. Does that make sense? +1  
btl_nyc  It also says there are no signs of depression, which would cause the low libido after his wife died. +  
temmy  two years is a enough time to mourn...just saying +  
temmy  thisisfine, it makes absolute sense. That is the same way i saw it +  
dr_jan_itor  He misses his wife man, isn't ready for other women. Psychogenic ED. physically hes fine (can crank his meat) +  


submitted by yotsubato(255),

Why is his Libido normal? It's totally expected that he may have reduced libido after his wife died 2 years ago from some horrible prolonged illness.

nala_ula  perhaps it's more to do with the fact that he can get erections when masturbating, outside of nocturnal erections which are not mediated by sexual desire. So his libido must be intact since he has sexual desire evident in being able to masturbate. +  
nala_ula  At least, that's the way I saw it. +  
home_run_ball  "Testosterone concentration is within the reference range" and the fact that he has no difficulty masturbating = normal libido. Low testosterone would contribute to low libido And if he had low libido he would have difficulty masturbating +  
thisisfine   The way I made the decision about normal vs. decreased libido is also that he presented to his doctor due to difficulty maintaining an erection while trying to have sex - meaning he has the libido to try to have sex. Does that make sense? +1  
btl_nyc  It also says there are no signs of depression, which would cause the low libido after his wife died. +  
temmy  two years is a enough time to mourn...just saying +  
temmy  thisisfine, it makes absolute sense. That is the same way i saw it +  
dr_jan_itor  He misses his wife man, isn't ready for other women. Psychogenic ED. physically hes fine (can crank his meat) +  


submitted by yo(24),

This occurred within 6 hours and caused some pulmonary edema and respiratory distress after a transfusion caused by the donor's anti-leukocyte antibodies just destroying the recipients neutrophils and respiratory endothelial cells.

while allergic/anaphylaxis can cause respiratory arrest and shock it has a somewhat different picture, no wheezing, itchiness or whatever and according to first Aid it happens within minutes to 2-3 hours which is at least double what we're seeing here. also beware of IgA deficient people in this choice.

PE, eh I don't think it affects Pao2 that often much according to this super duper high yield resource. but uhh yeah doesn't feel PE kinda question https://emedicine.medscape.com/article/300901-workup#c12

pneomina, right after all the infusion business and no mention of fever or anything? Nah.

go to page 114 of first aid. I'm pretty sure we need to know our infusion/transplant crap because it just keeps coming up in uworld but this whole exam is a crapshoot.

Forgive me if I made a mistake/wrong about anything, I mostly got info from first aid. plz correct if there is a mistake, good luck.

hungrybox  we gonna make it bro +1  
hungrybox  or sis +2  
nala_ula  I did the same, basically went through each one and the time of onset between each. Good luck on your tests!! +  
temmy  i don't think pulmonary embolism will cause bilateral lung infiltrate +1  


submitted by meningitis(150),

When standing up, the body normally activates sympathetic system to avoid orthostatic hypotension.

But since there is now an additive effect of the pheochromocytoma adrenergics, it will lead to a hypertension

(i.e: Double vasoconstriction = Pheo adrenergics + Sympathetic system)

sympathetikey  Brilliant. +1  
medschul  Would pheo have a normal resting BP though? +  
meningitis  I was trying to justify these tricky questions but very true medschul.. It shouldn't have normal resting BP. Sometimes it seems these NBME always have a trick up their sleeve. Im getting paranoid lol +  
nala_ula  The reason why the patient probably has normal HTN is because Pheochromocytoma has symptoms that occurs in "spells" - they come and go. Apparently in that moment, when the physician is examining her, she doesn't have the HTN, but like @meningitis explained, so many adrenergic hormones around leads to double the vasoconstriction when the patient stands up. +5  
meningitis  Thank you @nala_ula for your contribution! Really filled in the gap Iwas missing. +1  
nala_ula  No problem! Thank you for all your contributions throughout this page! +  
mjmejora  I thought the pheochromocytoma was getting squeezed during sitting and releasing the epinephrine then. kinda like how it can happen during manipulation during surgery. Got it right for sorta wrong reasons then oh well. +  


submitted by usmleuser007(110),

just a hunch.... Omeprazole is always the right answer

nala_ula  Famotidine is an H2 blocker which really only stops acid secretion via the stimulation of H+/K+ ATPase by histamine, but it still has vagus and gastrin stimulation. If you use Omeprazole, you get irreversible inhibition of the pump itself which stops the secretion of acid even if there is histamine, gastrin, vagus stimulation. +3  
temmy  what about the healing of her mucosa. Is that not the action of prostaglandin?. That threw me off cos according to FA, misoprostol increases secretion of the gastric mucosa +4  
cry2mucheveryday  same doubt..marked miso +  
sahusema  I guess because misoprostol is more associated with treatment of NSAID related ulcers and PPIs are 1st line DOC for GERD? +1  


submitted by hungrybox(216),

Following a stroke, this patient had weakness of her left face and body, so the stroke must have affected the right side of her brain. B was the only choice on the right side of her brain.

Still confused? Read on...

The voluntary motor fibers (corticospinal tract) descend from the primary motor cortex, cross (decussate) at the medullary pyramids, and then synapse at the anterior motor horn of the spinal level.

Because of decussation at the medullary pyramids, you should make a note of where any stroke occurs. Is it above the medullary pyramids? Then it will affect the side opposite the stroke (contralateral). Is it below the medullary pyramids? Then it will affect the same side as the stroke (ipsilateral).

hungrybox  Woops, E is also on the right side (also remember that imaging is looking up at someone, feet first). But a cerebellar stroke would have caused ataxia. +  
mnemonia  Very nice!! +  
usmleuser007  What gets me is that they mention that Left 2/3 of face is affected. This should indicate a non cortical innervation as most of the cranial nuclei are bilaterally innervated from the left and right hemisphere. If left 2/3 of the face is affected then it should also mean that the lesion is after CN5 nuclei. +1  
yotsubato  @hungrybox Thats not the cerebellum thats the occipital lobe. You would see leftsided homonymous hemianopsia in that lesion +  
mrsmac  To my mind, it is simpler to consider the question first in terms of blood supply distribution. Left sided hemiparesis and weakness of lower 2/3 of face are both indicative of a MCA rupture/stroke (First Aid 2018 pg. 498). Furthermore, since the injury has affected motor function we would be considering the descending tract i.e. lateral corticospinal which courses through the ipsilateral posterior limb of the internal capsule then decussates in the caudal medulla. +1  
mrsmac  You're considering the wrong CN here. CN5 motor function involves muscles of mastication and lower 2/3 of tongue. The nerve in question in this case is CN7/VII Facial n. CNVII UMN injury affects the contralateral side, whereas LMN injury affects ipsilateral (First Aid 2018 pg. 516). i.e. before and after the nucleus in pons respectively. I hope this helps. +1  
nala_ula  Spastic means UMN lesion, since they also don't specify if there is arm or leg weakness, I didn't assume it was MCA stroke. I went with the reasoning that for there to be spastic hemiparesis, there must be damaged to the UMNs and therefore the internal capsule is where these tracts are. +  
champagnesupernova3  Omg this whole discussion is confusing. Internal capsule contains ALL corticospinal and corticobulbar fibers = contralateral hemiparesis and UMN facial lesion +  


I get that this answer choice is the most amicable answer.

But honestly the way they asked the question "it is most appropriate for the physician to address the issue of a feeding tube in which of the following manners"

My reasoning was: well...before the family can even begin to argue what do do don't you have to propose a medical treatment/management strategy? which is why I went with "recommend a tube..."

home_run_ball  Like what is the learning objective of this question? On first aid if you go by the Surrogate decision maker priority: you do spouse first...so like wtf nbme? +5  
uslme123  I think it's because there isn't a legally appointed health care surrogate in this case. The family hierarchy is only an "ethical suggestion." +  
nala_ula  According to first aid, there is an order to who makes decisions when the patient is not able to and hasn't left any directives. My issue was the same as home_run_ball, since they specifically asked about the feeding tube and not "who is supposed to make decisions now" even though that is also warped since the spouse has precedence. +1  


submitted by kchakhabar(17),

What threw me off in this question is the phrase "cells with little cytoplasm that are twice the size of lymphocytes." I though "small cell carcinoma" cannot be that big.

nala_ula  Omg literally the same thought process I had, that phrase through me off! +  
nala_ula  threw* +  


submitted by kchakhabar(17),

What threw me off in this question is the phrase "cells with little cytoplasm that are twice the size of lymphocytes." I though "small cell carcinoma" cannot be that big.

nala_ula  Omg literally the same thought process I had, that phrase through me off! +  
nala_ula  threw* +  


Legionella is common causes of pneumonia superimposed on chronic obstructive pulmonary disease.

asapdoc  Im pretty sure so is strept pneumoniae +2  
usmleuser007  COPD is also exacerbated by Viral infection: Rhinovirus, influenza, parainfluenza; and Bacterial infection: Haemophilus influenzae, Moraxella catarrhalis, Streptococcus. however, the questions gives a hint that it may be legionella = "weekend retreat" which may be associated with this infection +  
loopers  From FA 2017 pg 139: Legionnaires’ disease—severe pneumonia (often unilateral and lobar A ), fever, GI and CNS symptoms. Common in smokers and in **chronic lung disease.** +1  
kentuckyfan  I also believe that the other attendees showed signs of pontiac fever, which is another hint they tried to get at. +1  
luke.10  i did it wrong and chose influenza virus since it is most common infection in COPD but the clue in the Question is that the other attendee didnt get sick since in legionella there is no person to person transmission +  
endochondral   but in Uworld s. pneumo is one of the most common bacterial exacerbation of COPD legionella wasn't even mentioned. How do we rule out s. pneumo ? +1  
nala_ula  maybe because in children s.pneumo causes otitis media? +  
smc213  Another hint made in the Q stem is the location being rural Pennsylvania.... Legionnaires disease was first discovered by the outbreak in 1976 at a convention held in Philadelphia, Pennsylvania. Not sure why I know this fact... +  
hpsbwz  Biggest hint towards legionella to me was that they all were at a residence hall... i.e. where there'd be air conditioners and such. +1  


submitted by meningitis(150),

When standing up, the body normally activates sympathetic system to avoid orthostatic hypotension.

But since there is now an additive effect of the pheochromocytoma adrenergics, it will lead to a hypertension

(i.e: Double vasoconstriction = Pheo adrenergics + Sympathetic system)

sympathetikey  Brilliant. +1  
medschul  Would pheo have a normal resting BP though? +  
meningitis  I was trying to justify these tricky questions but very true medschul.. It shouldn't have normal resting BP. Sometimes it seems these NBME always have a trick up their sleeve. Im getting paranoid lol +  
nala_ula  The reason why the patient probably has normal HTN is because Pheochromocytoma has symptoms that occurs in "spells" - they come and go. Apparently in that moment, when the physician is examining her, she doesn't have the HTN, but like @meningitis explained, so many adrenergic hormones around leads to double the vasoconstriction when the patient stands up. +5  
meningitis  Thank you @nala_ula for your contribution! Really filled in the gap Iwas missing. +1  
nala_ula  No problem! Thank you for all your contributions throughout this page! +  
mjmejora  I thought the pheochromocytoma was getting squeezed during sitting and releasing the epinephrine then. kinda like how it can happen during manipulation during surgery. Got it right for sorta wrong reasons then oh well. +  


submitted by breis(11),

your guess is as good as mine.....................................................................

nala_ula  I spent so long on this question and same... hahaha +  


submitted by asdfghjkl(1),

Anyone know why IGF-1 wouldn't be increased as well? GHRH is stimulated in hypoglycemic states.

nala_ula  Honestly, it's something that has confused me for a while. Why is it that GH secretion is stimulated by hypoglycemia? I mean, it's literally called growth hormone (for growth!), and hypoglycemia, which is basically a "starvation" state, will stimulate this hormone? +  
shaeking  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3529368/ This might help answer your question. I basically didn't pick IGF-1 because it would increase the uptake of glucose leading to a worsen hypoglycemic state. Didn't have a true reason otherwise. +  
temmy  IGF-1 is regulated by insulin. so it will be decreased because insulin levels are also low. +  
nala_ula  thank you @shaeking! +  
nwinkelmann  I found this and it also explains to a more genetic/cellular level. Essentially, it says that starvation induces some factors that cause GH resistance and IGF1 suppression. +1  
nwinkelmann  Sorry forgot the link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2575072/ +  


submitted by thomas(3),

Answer is Astrocyte. Patient has glioblastoma multiforme. Although meningiomas may occur at convexities, meningiomas are benign and often asymptomatic. They may cause h/a seizures, but would be unlikely to cause death w/in 6m of onset of h/a. The size of tumor and course of illness is consistent with the course of GBM

masonkingcobra  Above is obviously incorrect because the answer is Meningeal lol. Here is a link to a good picture: http://neuropathology-web.org/chapter7/chapter7fMiscellaneous.html +1  
kernicterusthefrog  Obviously thomas is disagreeing with the presentation of the question, and I agreed with him! This absolutely sounds like GBM, with rapid onset leading to death, and the symptoms. The question stem leads you to GBM, and the gross image to meningioma (I guess). +1  
kernicterusthefrog  Furthermore, where are the meninges on the gross image form which this (meningioma) grew?! It should at least show the tissue from whence it came! +1  
nala_ula  Had the same problem, got confused since it appeared that the growth was malignant :( +  
sugaplum  FA 2019 pg 514, also agree with everyone. weird presentation. Glios are malignant death within 1 year, meningioma are often asymptomatic or have focal signs. just a gross pathology question at this point +  


submitted by johnthurtjr(48),

I'm not a fan of gross path images and questions that say "look, what is this thing?" - that said meningiomas are the most common brain tumor and this picture is is a good example of one. I had no idea what these things looked like and got it wrong, too. Take a look at this one

johnthurtjr  [Here's more info](http://www.pathologyoutlines.com/topic/cnstumormeningiomageneral.html) +  
meningitis  I got it wrong because I didn't see any apparent Dura mater nor other meninges (The veins aren't being covered by any "shiny layer"), so I thought the tumor was coming from inside the brain and not compressing it like meningiomas usually do. +  
meningitis  But it did follow the common aspect where they are found in between divisions of brain and are circular growths like a ball. +2  
nala_ula  Since it was basically implied that the patient died and "here look at what this is" I thought it was a malignant tumor (glioblastoma)... but I guess it's all about placement. +4  


submitted by celeste(32),

This sounds like Fanconi syndrome. The proximal tubular epithelial cells have a hard time reabsorbing filtrate, so you'll see a loss of phosphate, amino acids, bicarbonate, and glucose.

medschul  Wouldn't Fanconi syndrome also cause hypokalemia though? +2  
yotsubato  Especially considering the fact that the DCT will be working in overdrive to compensate for lost solutes??? +  
nala_ula  This question did not make sense to me at all. I knew it was Fanconi syndrome yet didn't select the obvious answer because it said "follow up examination 1 week after diagnosis". I thought it would already be in treatment... I searched (now) and it says that treatment is basically replenishing was is lost in the urine. So definitely the wording is like wtf to me +  
sugaplum  I was thinking since it affected the PCT that Na resorption would be affected as well? But I guess the other segments will pick up the slack? +  


submitted by haliburton(82),

FA 2017: Infects B cells through CD21. Atypical lymphocytes on peripheral blood smear G —not infected B cells but reactive cytotoxic T cells. ⊕ Monospot test—heterophile antibodies detected by agglutination of sheep or horse RBCs. Use of amoxicillin in mononucleosis can cause characteristic maculopapular rash.

zup  misread the "accounts for" question as what's the reason for the atypical lymphocytes. So I answered "virus infected B lymphocytes." Anyone else misread it like that? +3  
nala_ula  Shit, I misread that too and I noticed it now. Nerves get the best of us! +  


submitted by hayayah(394),

This patient has small cell carcinoma. This type of cancer is associated with paraneoplastic syndromes such as: Cushing Syndrome, SIADH, or antibodies against Ca2+ channels (Lambert-Eaton) or neurons. Amplification of myc oncogenes is also common.

SIADH (Syndrome of inappropriate antidiuretic hormone secretion) is characterized by:

  • Excessive free water retention
  • Euvolemic hyponatremia with continued urinary Na+ excretion
  • Urine osmolality > serum osmolality

Body responds to water retention with aldosterone and ANP and BNP. That is what causes the increased urinary Na+ secretion Žwhich leads to normalization of extracellular fluid volume Žand the euvolemic hyponatremia.

hello  Why would body respond to water retention with ALDO? ALDO would increase water retention... +2  
nala_ula  @hello, the body's response is to decrease Aldosterone since there is increased volume retention and subsequently increased blood pressure. This concept confused me a lot, but I ended up just viewing it as separate responses. First, the increased volume retention leads to increase ANP and BNP secretion that lead to decreased Na+ reabsorption in the tubules (page 294 in FA 2019) and second, this increased volume basically leads to increased pressure so lets also decrease aldosterone so there is no Na+ retention (since water comes with it)... I thought it was counterintuitive to secrete so much Na+ since you're already having decreased serum osmolality (decreased Na+ concentration) because of the water retention, but I'm guessing that this is just another way our body's well intentions end up making us worse XD +5  
compasses  see page 344 FA2019 for SIADH. +  
dickass  author pasted text straight from FA but the arrows didn't copy over, inverting the original meaning +