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Comments ...

 +2  (free120#24)

external carotid branch supplies the superior parathyroid glands as well........?

yng  Yes the superior part supplied by superior thyroid gland which is a branch of external carotid branch.
llamastep1  No they do not, parathyroids are supplied by the inferior thyroid arteries. https://teachmeanatomy.info/neck/viscera/parathyroid-glands/
suckitnbme  Superior thyroid artery does supply some blood to the parathyroids through anastomoses but the main vascular supply is from the inferior thyroid artery.

 +0  (nbme18#23)

CONcentric - CONstricts ventricle

ECCentric - ECCpands ventricle (expands)

jmangels  Also, he's an endurance athlete. It would most likely be a physiological adaptation. "Volume overload-induced cardiac hypertrophy is known as eccentric hypertrophy. In endurance training, the volume load is a predominant factor; therefore, the endurance-trained heart develops eccentric hypertrophy" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2300466/

 +1  (nbme23#35)

One of the questions in the uworld practice test 2 actually touched on this.

motivational interviewing: indication
  • substance use disorders
  • other behaviors in patients who are not ready to change
  • acknowledge resistance to change
  • address discrepancies between behavior and long term goals
  • enhance motivation to change
  • nonjudgmental
Technique (OARS)
  • Ask Open-ended questions (encourage further discussion)
  • Give Affirmations
  • Reflect and Summarize main points

 +2  (nbme20#13)

found this online: https://academic.oup.com/rheumap/article/2/1/rky009/5040548

Hypertrophic pulmonary osteoarthropathy (HPOA) is a syndrome characterized by the triad of periostitis, digital clubbing and painful arthropathy of the large joints, especially involving the lower limbs. Clubbing is characterized by bulbous enlargement of terminal segments of the fingers and toes due to proliferation of subungual connective tissue.

primary... is a rare hereditary condition.

A majority of cases (>90%) of secondary HPOA are associated with pulmonary malignancies [6] or chronic suppurative pulmonary diseases.

Pulmonary malignancies, including primary [7], metastatic lung cancer and intrathoracic lymphoma, account for 80% of cases of secondary HPOA. Adenocarcinoma of the lung is the most frequent and small cell carcinoma is the least frequent histopathologic type of lung cancer associated with HPOA [7].

other associated extrathoracic malignancies include nasopharyngeal carcinoma, renal cell carcinoma, oesophageal cancer, gastric tumour [8], pancreatic cancer, breast phyllodes tumour [9], melanoma, thyroid cancer, osteosarcoma and intestinal lymphoma.

Various rheumatologic conditions, including RA [10], AS [11], polyarteritis nodosa, SLE [12], Takayasu disease [13], sarcoidosis, APS and Mediterranean fever are known to be associated with this condition as well.

Pulmonary conditions such as cystic fibrosis, tuberculosis, idiopathic pulmonary fibrosis [14] and lung transplantation have also been associated with HPOA.

 +0  (nbme24#8)

is no one else concerned about the fact that theyre giving a beta 2 agonist to a woman whos 28 weeks pregnant.......?

yobo13  Beta 2 agonists relax the uterus so this would be okay, right?
med4fun  inhaled drugs do not have as much of systemic affect and B-agonists are used often in pregnancy for asthma control. SABAS are deemed safe but there are increased birth defects with long acting B-agonists.

 +1  (nbme24#24)

Probenecid makes you Pee

Colchicine clenches your microtubules

 +24  (nbme24#30)

this question makes me want to eat an e coli cookie and hope i bleed out

 +4  (nbme22#36)

tri-CyCliC antidepressent - anti C holinergic, C ant stand up (a1 block), C ardiotoxic (prolong qt by messing w na channels)

waterloo  that's cool and all but there are so many side affects when it comes to TCAs. H1 antagonism, reduced libido, convulsions.

 +1  (nbme22#15)

Can someone explain the difference between C. (release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes) and D. (Release of thyroid hormone from a lymphomatous thyroid gland.

drdoom  @niboonsh, ending a comment with a question mark will make it appear on the "comments seeking answers" lists
nwinkelmann  A lymphomatous thyroid gland can either be due to primary thyroid lymphoma (which is almost always NHL, but is very rare) or due to 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. These, I believe, would still present with hypothyroidism, and thus would have low T4 and high TSH (opposite of this patient).

 +0  (nbme22#20)

I am confusion. why wouldnt this be a cross over study?

shokay  there is no washout period and the order of drugs given isn't switched

 +0  (nbme22#5)

My guess is that they are referring to Retrovirus (HIV/HTLV)- a single stranded positive sense linear RNA. Retroviruses are known to carry reverse transcriptase (RNA-dependent DNA-polymerase). The encephalitis is what threw me off cuz I automatically thought of the many negative sense RNA viruses that cause encephalitis (like arenavirus or bunyavirus). Apparently there have been a few causes of HTLV causing encephalitis... maybe this is what they were trying to get at? Idk but i just spent way too much time on this damn question https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5878187/

 +1  (nbme22#19)

https://www.ncbi.nlm.nih.gov/pubmed/15599631 The horseshoe kidney was detected before surgery in 12 patients (80%) by ultrasonography, angiography, computed tomography (CT) or excretory urography. Angiography revealed multiple or anomalous renal arteries in 8 of 12 patients studied preoperatively

 +2  (nbme22#47)

This is a case of acute transplant rejection. weeks to months after the transplant, recipient cd8 and/or cd4 t cells are activated against the donor (a type 4 HSR) and the donor starts making antibodies against the transplant. This presents as a vasculitis with dense interstitial lymphocytic infiltrates. (FA2018 pg 119)

ls3076  Actually was confused about this due to a UW explanation. UW said acute txp rejection has two types - humoral and humoral and cellular. Humoral has Neutrophilic infiltrate + necrotizing vasculitis while cellular has lymphocytosis. Can anyone simplify/explain this please?
apurva  We usually look for c4d complement for humoral response in acute graft rejection. Because c4d makes covalent bond with the endothelium can can be found on staining because it is long lasting.

 -1  (nbme21#34)

The obliques do the opposite action of their name. Inferior oblique moves the eye UP and OUT (extortion, elevation, ABduction). Since the question says that there is a fracture involving the orbital floor, that automatically rules out D (medial rectus and inferior oblique), leaving the only logical answer to be the inferior rectus and inferior oblique. https://www.youtube.com/watch?v=lWKkHWWDIEI

aishu007  hi, but inferior oblique moves up and in and not out

 +4  (nbme21#26)

i think of this as ole farmer joe on his actinic farm picking karats (carrots) (actinic keratosis)

usmlecharserssssss  says everyone after discovering that actually answer is not psoriasis

 +0  (nbme21#32)

my understanding of this is from pathoma - Interstitial (atypical) pneumonia - caused by diffuse interstitial infiltrates. Can be caused by Mycoplasma pneumo, RSV, chlamydia pneumo, influenza, coxiella burentii

athenathefirst  Yeah but how does that help you choose Usual interstital pneumonia?

 +12  (nbme21#40)


phase one - is it Safe?

phase 2 - does it Work?

phase 3 - any Improvements?

phase 4 - stay on the Market?

 +3  (nbme21#38)

i got this question right but why couldnt it be ginko biloba?

nor16  and why no therapy, i.e. cognitive training`
jessica_kaushal  first step is to make the patient's environment accomodating for the patient.
jessica_kaushal  first step is to make the patient's environment accomodating for the patient.
tryntofigritout  Because this is a western medicine test. Even though it has shown great protection against AD and memory protection, this test won't allow that. I initially clicked on ginko but thought to myself... na this test doesn't accept an eastern idea. so clicked on the one I know they wanted me to say, and I got it right. ha

 +9  (nbme21#35)

this was a dumb question. the mneumonic "DIDanosine causes pancreaDIDis" is useful here

 +34  (nbme21#45)

https://www.youtube.com/watch?v=4-DuvwoH2zQ if ur lazy like me, this is a good refresher video

d_holles  Amazing video dude. Somehow never learned this in neuro lol.
aag  Awesome video! Is this why you can give Mg2+ to eclampsia patients, because if so, mind goddamn blown.

 +2  (nbme20#17)

" Other classes of medications that cause hyperprolactinemia include antidepressants, antihypertensive agents, and drugs that increase bowel motility. Hyperprolactinemia caused by medications is commonly symptomatic, causing galactorrhea, menstrual disturbance, and impotence. It is Important to ensure that hyperprolactinemia in an Individual patient is due to medication and not to a structural lesion in the hypothalamic/pituitary area; this can be accomplished by (1) stopping the medication temporarily to determine whether prolactin levels return to normal, (2) switching to a medication that does not cause hyperprolactinemia "


"Non-dose-dependent side effects — Although low-dose therapy seems to minimize the metabolic complications induced by a thiazide or thiazide-like diuretic, it may not necessarily eliminate other side effects. As an example, as many as 25 percent of men treated with 25 mg/day of chlorthalidone develop a decline in sexual function [34]. Sleep disturbances can also occur, particularly if the patient is on a low-sodium diet [34]. How these problems occur is not known."


 +4  (nbme20#47)

https://www.youtube.com/watch?v=WGWFFN01qkA succinylcholine usually has v fast duration of action bcuz metabolized by plasma pseudocholinesterase. With atypical pseudocholinesterase, decreased metabolism of succinylcholine and thus causes a prolonged duration of action of succinylcholine ----> APNEA

chandlerbas  i love that mosquito and then SLAP

Subcomments ...

submitted by lsmarshall(314),

"Parasternal heave (lift) occurs during right ventricular hypertrophy (i.e. enlargement) or very rarely severe left atrial enlargement." RV hypertrophy can be seen so easily because the RV is at the anterior surface of the chest.

In this patient blood from LA to LV decreases in saturation, so it is going somehwere. From the O2 sat. we can deduce there is probably a VSD (increased RV pressure would cause RVH and parasternal heave). Furthermor, the vignette is likely describing tetralogy of fallot (caused by anterosuperior displacement of the infundibular septum). In Tet spells, RV outflow is too obstructed and patient gets cyanosis and R>L shunting Squats increase SVR, decreasing R>L shunting, putting more blood through pulmonary circuit and relieving cyanosis.

seagull  i'm pretty sure your a prof and not a student. +8  
nor16  nevertheless, we are greatful for explanation! +  
niboonsh  I remember seeing a question describe parasternal lift in the context of pulm htn. still got this wrong tho fml +  
anotherstudent  Did my question have a typo? It says O2 saturation in the right ventricle is 70, which is equal to the Right atrium and vena cava. It says the O2 saturation in the left ventricle is 82%, which is a decrease from the LA (95) but not equal to the RV, which is why I thought there wasn't a VSD, I assumed there was a weird shunt from the LV to some other part. Will O2 saturation not always equalize? +  
pseudomonalisa  This is a right to left VSD due to the pulmonic stenosis present in Tetralogy of Fallot. O2 sat will be low (70) in the right ventricle, and from there it'll enter the left ventricle and mix with freshly oxygenated blood coming from the left atrium (95). Because of the mixing, the O2 sat of blood in the left ventricle will be somewhere in the middle of 70 and 95 (82 in this case). You're correct, though, that most other VSDs are left to right and you'd see greater O2 sat in the right ventricle in that case (not sure if it equalizes with the left ventricle though). +  

Can someone please clarify the answer. Is decreased adherence same as decreased aggregation? Wouldn;t inhibition of the IIb/IIIa receptor prevent aggregation?

xxabi  I'm not completely sure...but I think its because its aspirin, and aspirin doesn't work on IIb/IIIa receptors. That's why i picked decreased adherence of platelets, figured that was the closest thing to decreased aggregation that still made sense with aspirin's mechanism of action. Hope that helps! +  
ihavenolife  Aspirin irreversibly inhibits COX which leads to decreased TXA2. TXA2 normally is a vasoconstrictor and induces platelet aggregation, so aspirin inhibits platelet aggregation by downplaying TXA2 not by interacting with IIb/IIIa receptor. (Source FA and UWorld) +12  
fallenistand  In this case, inhibition of COX-1 by aspirin will also reduce the amount of precursors for vascular prostacyclin synthesis, provided, for example, from adhering platelets https://www.ncbi.nlm.nih.gov/pubmed/9263351 +1  
niboonsh  inhibition of IIb/IIIa receptor is the moa of a completely separate class of drugs - Glycoprotein IIb/IIIa (abciximab, eptifabide, tirofiban) +  
t123  Bad question - TXA2 upregulates GpIIb/IIIa on platelets. So aspirin inhibits their expression. +  
mdrahimi7  You know that platelet sticking to collagen or injured endothelial cell is platelet adhesion then platelets when more and more platelet accumulate on that that is primary platelet plaque and when fibrin on that secondary platelet or hemostatic plague formation occurs . Now as aspirin inhibit the formation of prostaglandin like thromboxane a2 this thromboxane a2 is acting as vaso constrictor and attract platelet to come to that area for thrombosis formation right so platelet aggregation doesn't occur it mean their adherence decrease to each other but if we say that glycoprotein inhibition leads to inhibition platelet aggregation it is true but this is not the mechanism of aspirin it is done by drugs like abciximab. +  

submitted by neonem(451),

NRTIs are the main HIV therapy drug that can cause bone marrow suppression (not as common with NNRTIs). This class includes zidovudine, didanosine, emtricitabine, lamivudine, stavudine, abacavir. Zidovudine is most known for this side effect.

Nelfinavir = protease inhibitor azithromycin = aminoglycoside (not really used for HIV) pentamidine = another antimicrobial, mostly used for pneumocystis I think? Lamivudine = another NRTI but less known for bone marrow suppression

adisdiadochokinetic  Azithromycin is a macrolide, not an aminoglycoside FYI, and its use in HIV is primarily as prophylaxis at very low CD4 counts for, among other things, the mycobacterium avium complex. +5  
nbmehelp  How would we have known to choose Zidovudine over Lamivudine tho +5  
mjmejora  @nbmehelp the sketchy with Princess Izolde (Zidovudine) eating bone marrow was my only tip off +6  
niboonsh  you have ero bone marrow if you take idovudine +1  
niboonsh  the z's were supposed to be bold idk what happened. you have Zero bone marrow if you take Zidovudine +4  
t123  Zidovudine is also a very early NRTI developed. As a good rule of thumb, older drugs have worse side effects +2  
therealslimshady  Zidovudine Zaps your bone marrow (sorry) +1  

submitted by neonem(451),

NRTIs are the main HIV therapy drug that can cause bone marrow suppression (not as common with NNRTIs). This class includes zidovudine, didanosine, emtricitabine, lamivudine, stavudine, abacavir. Zidovudine is most known for this side effect.

Nelfinavir = protease inhibitor azithromycin = aminoglycoside (not really used for HIV) pentamidine = another antimicrobial, mostly used for pneumocystis I think? Lamivudine = another NRTI but less known for bone marrow suppression

adisdiadochokinetic  Azithromycin is a macrolide, not an aminoglycoside FYI, and its use in HIV is primarily as prophylaxis at very low CD4 counts for, among other things, the mycobacterium avium complex. +5  
nbmehelp  How would we have known to choose Zidovudine over Lamivudine tho +5  
mjmejora  @nbmehelp the sketchy with Princess Izolde (Zidovudine) eating bone marrow was my only tip off +6  
niboonsh  you have ero bone marrow if you take idovudine +1  
niboonsh  the z's were supposed to be bold idk what happened. you have Zero bone marrow if you take Zidovudine +4  
t123  Zidovudine is also a very early NRTI developed. As a good rule of thumb, older drugs have worse side effects +2  
therealslimshady  Zidovudine Zaps your bone marrow (sorry) +1  

submitted by m-ice(236),

The patient needs medical attention immediately, which eliminates obtaining a court order, or transferring her. A nurse does not have the same training and qualifications as a physician, so it would be inappropriate to ask them to examine the patient. Asking the hospital chaplain again could be inappropriate, and would take more time. Therefore, the best option among those given is to ask the patient if she will allow with her husband present.

sympathetikey  Garbage question. +37  
masonkingcobra  So two men is better than one apparently +19  
zoggybiscuits  GarBAGE! ? +1  
bigjimbo  gĂĄrbĂĄgĂ© +3  
fulminant_life  this question is garbage. She doesnt want to be examined by a male how would the presence of her husband make any difference in that respect? +6  
dr.xx  I guess this is a garbage question because what hospital, even small and rural, does not have a female physician on staff. NBME take notice -- this is the 2010s not 1970s. https://images.app.goo.gl/xBL4cK31ta7nG4L39 +6  
medpsychosis  The question here focuses on a specific issue which is the patient's religious conservative beliefs vs. urgency of the situation. A physician is required to respect the patient's autonomy while also balancing between beneficence and non-maleficence. The answer choice where the physician asks the patient if it would be ok to perform the exam with the husband present is an attempt to respect the conservative religious belief of the patient (not being exposed or alone with another man in the absence of her husband) while also allowing the physician to provide necessary medical treatment that could be life saving for her and or the child. Again, this allows for the patient to practice autonomy as she has the right to say no. +10  
sahusema  I showed this question to my parents and they said "this is the kind of stuff you study all day?" smh +14  
sherry  I totally agree this is a garbage question. I personally think there is more garbage question on new NBME forms than the previous ones...they can argue in any way. I feel like they were just trying to make people struggle on bad options when everybody knows what they were trying to ask. +  
niboonsh  This question is a3othobillah +4  
sunshinesweetheart  this question is really not that garbage....actually easy points I was grateful for... yall are just clearly ignorant about Islam. educate yourselves, brethren, just as this exam is trying to get you to do. but yeah I agree there should be an option for female physician lol +3  
drmohandes  I think this NBME24 is a waste of $60. On one hand we have these types of questions, that have 0 connection to our week-month-year-long studying. On the other hand we have "Synaptobrevin" instead of SNARE, because f*ck coming up with good questions. +8  
myoclonictonicbionic  @sunshinesweetheart I actually have studied the religion tremendously and there a clear consensus among all Muslims that in the case of an emergency, it is completely allowed to have someone from the opposite gender examine you. I think this actually represents how ignorant the exam writers are of Islam. +5  

submitted by neonem(451),

Falling on outstretched hand: scaphoid is most common one to be fractured, lunate is most common to be dislocated. Lunate dislocation can cause acute carpal tunnel syndrome.

Think of the mnemonic "Straight Line To Pinky, Here Comes The Thumb" for the bones of the palm, drawing a football shape starting below the thumb MCP joint adjacent to the radius, then moving to your medial wrist, and then back to the thumb.

Scaphoid, lunate, triquetrum, pisiform, hamate, capitate, trapezoid, trapezium. The lunate looks like it's posteriorly dislocated here.

sympathetikey  Yep. I didn't even look at the X-ray. +4  
dr.xx  loonies love lunate +2  
wes79  she landed on her "right hand", but the X-ray is showing a left hand?? +  
wes79  i legit have no idea whats going on in that xray lol +5  
nbme4unme  X-ray confused the hell out of me, I was going to put lunate based on Q stem but ended up putting Pisiform because it looks like that's what's messed up in the photo? Should have ignored the picture haha. +  
nwinkelmann  for @dr.xx, love your mnemonic. I added to it, or at least found an explanation on why it works. "loonies love lunate" and "loonies" are "dislocated" from reality. +3  
doctorevil  She Looks Too Pretty, Try To Catch Her is a mnemonic that works for me. +  
niboonsh  Some Lovers Try Positions That They Cant Handle +4  

submitted by cinnapie(13),

Why does every NBME have one or two erection related questions??

youssefa  Cause we all know what bout to happen to us in this exam :D +18  
niboonsh  lmfaooooooo +  
corgilobacter  erections are a very hard subject +  

submitted by usmleuser007(279),

Some other endocrine like cells and disorders for reference:

  1. Salt-and-pepper chromatin (fine granular cytoplasm) in Endocrine tumors:

  2. Medullary thyroid carcinoma

  3. neuroendocrine tumors and pheochromocytoma
  4. Carcinoid Tumor (serotonin) --- (also has sheets of uniform cells)
  5. Small Cell Carcinoma of lungs = Small, blue cells with scant cytoplasm and granular chromatin) = flat, oval-shaped cells with scant cytoplasm and hyperchromatic nuclei

  6. Small Blue Cells

  7. Ewing sarcoma (anaplastic malignant tumor)
  8. SCC of lungs
  9. flat, oval-shaped cells with scant cytoplasm and hyperchromatic nuclei
happysingh  i've never heard of " 6. Small Blue Cells" cancer / tumor / carcinoma .... +1  
niboonsh  might want to look at fa pg 665 +  

submitted by roygbiv(17),

Why could this not be extravascular hemolysis? In FA it says acute hemolytic transfusion reaction can be due to ABO incompatibility or extravascular hemolysis.

niboonsh  because extravascular hemolysis is associated w jaundice. Intravascular hemolysis would have hemoglobinuria but that's not an answer +  
niboonsh  i mean that is the answer lol +  
krewfoo99  According to pathoma: Intrvascular haemolysis will lead to haemoglobin binding to haptoglobin. This complex will travel to the kidneys and be excreted. This will lead to red colored urine and haemosiduria (Note: This can also lead to acute tubular necrosis) Extravascular haemolysis is when macrophages break down the RBC. Then the Haeme is converted to biliverdin then bilirubin and conjugated in liver, and then excreted. +3  
paperbackwriter  If you look under the "clinical presentation" column of the blood transfusion reactions chart (pg114), it says that hemoglobinuria is with intravascular hemolysis and jaundice is with extravascular. Makes sense because with extravascular hemolysis your splenic macrophages are are chewing up the RBCs and sequestering it in the spleen so you don't get "spillover" -- i.e. clean urine. +1  

submitted by roygbiv(17),

Why could this not be extravascular hemolysis? In FA it says acute hemolytic transfusion reaction can be due to ABO incompatibility or extravascular hemolysis.

niboonsh  because extravascular hemolysis is associated w jaundice. Intravascular hemolysis would have hemoglobinuria but that's not an answer +  
niboonsh  i mean that is the answer lol +  
krewfoo99  According to pathoma: Intrvascular haemolysis will lead to haemoglobin binding to haptoglobin. This complex will travel to the kidneys and be excreted. This will lead to red colored urine and haemosiduria (Note: This can also lead to acute tubular necrosis) Extravascular haemolysis is when macrophages break down the RBC. Then the Haeme is converted to biliverdin then bilirubin and conjugated in liver, and then excreted. +3  
paperbackwriter  If you look under the "clinical presentation" column of the blood transfusion reactions chart (pg114), it says that hemoglobinuria is with intravascular hemolysis and jaundice is with extravascular. Makes sense because with extravascular hemolysis your splenic macrophages are are chewing up the RBCs and sequestering it in the spleen so you don't get "spillover" -- i.e. clean urine. +1  

It said it was fatal to males in utero, and the question asked about live born offspring. Since the males aren’t being born in the first place, I said 50% females and 0% males.

hungrybox  fuck i got baited +22  
jcrll  "live-born offspring" ← baited +8  
sympathetikey  Same :/ +  
arkmoses  smh +  
niboonsh  why is it 50% females tho? +2  
imgdoc  felt like an idiot after i figured out why i got this wrong. +1  
temmy  oh shit! +  
suckitnbme  This isn't exactly right as males can still be born as evidenced by individuals III 6,9,11. This basically an x-linked recessive disease. A carrier mother can still pass her normal X chromosome to a son (50% chance). It's just that the other 50% chance of passing an affected X chromosome results in death of the fetus in utero. Thus all males actually born will not be affected. +2  
makinallkindzofgainz  @suckitnbme, Correct, but if you're a live-born male, you 100% for sure do NOT have the disease, so the chance of a live-born male "being affected" is 0. +1  
spow  @suckitnbme it's not X-linked recessive, otherwise every single son would be affected and therefore have died in utero. It's X-linked dominant +1  
qball  Jail-baited +  

submitted by drdoom(467),

Calculations for dad. The probability of the father being a carrier is 2/3 since it is known that he doesn’t have the disease. Then the probability of him passing it on to his kid is 1/2, thus:

  • Probability of dad being carrier = 2/3
  • Probability of dad passing on disease allele = 1/2

Calculations for mom. With the Hardy-Weinberg Principle, you can figure out the probability of the mother being a carrier:

q = sqrt(1/40,000) = 1/200

So, 2pq = 2 * 1/200 * 199/200, which is approx 1/100.

For the child to get the allele from mom, two things need to happen: (1) mom must be a carrier [“heterozygote”] and (2) mom must pass the allele to child:

  • Probability of mom being carrier = 1/100
  • Probability of mom passing on disease allele = 1/2

Puting it all together. Now, combine all together:

= (probability of dad being carrier) * (probability of dad passing on disease allele) * (probability of mom being carrier) * (probability of mom passing on disease allele)

= 2/3 * 1/2 * 1/100 * 1/2
= 1 in 600

kernicterusthefrog  To quote Thorgy Thor, drag queen: "ew, Jesus, gross" +5  
niboonsh  This question makes me want to vomit +5  
drdoom  lol +  

submitted by aesalmon(65),

I feel dumb for asking but can someone explain this? If his parents are of close to normal BMI and are concerned about his weight why would they be allowing his calorie consumption to exceed his energy expenditure? ( AKA letting the kid eat too much and not exercise enough)

meningitis  That's a modern day mystery. +9  
drdoom  The prompt is only asking "what's the likely cause of obesity?" It's not that they're "allowing" him to eat more than exercise. (Few parents can monitor their kids that closely!) The prompt is only asking what's the most likely explanation for his 95th percentile weight and BMI (given that he otherwise appears normal); in the United States, the most likely explanation is eating way more than you expend. +  
niboonsh  aka 'merica #firstworldproblems +4  
makinallkindzofgainz  If you are obese, it's because you have consumed calories in excess of your energy expenditure, end of story. (there are factors that affect your energy expenditure, but the simple statement is 100% true, unless you want to argue against the laws of thermodynamics). A is the only correct answer. +1  
tulsigabbard  This answer hit too close to home. +1  
castlblack  I think the reason they point out the average weight of the parents is because leptin disorders are inherited. It helps you eliminate that answer choice. +  

meningiomas count as enhancing lesions? (this comment needs to be more than 50 characters apparently.)

goldenwakosu  I think it’s because meningiomas are able to calcify (aka sometimes they have psamomma bodies). I got this question wrong too but I totally did not completely register that the tumor was in the dura (interhemispheric fissure + central sulcus). Hope that helps! +1  
pipter  the only reason I got this right was because they described the tumour as being near the falx cerebri. +2  
fcambridge  Other hints include being described as round and seen in a female. Both indicative of Meningioma +6  
niboonsh  also meningiomas typically present with seizures or focal neurological signs +  
suckitnbme  I thought enhancing meant it uptakes contrast. Meningiomas are commonly enhancing lesions per Radiopaedia. +  

submitted by seagull(839),

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

My poverty education didn't ingrain this in me.

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

submitted by bubbles(51),

Has anybody found a good explanation for this histology? I genuinely have no idea what I'm looking at.

meningitis  This is common in Klinefelter.. think of the equivalent of Streaked ovaries seen in Turners. White streaks, red/pink material of hyaline, and hyperplasia of Leydig cells. Just remember: It doesn't look like normal structured testicle histology (No organized seminiferous tubules with Sertoli cells around) +9  
niboonsh  https://www.pathologyoutlines.com/topic/testisklinefelter.html these pictures are kinda similar +2  

submitted by bubbles(51),

Sorry if I'm being dense...why does this woman have diarrhea due to statins, diet, and exercise? I didn't really understand what they were asking for here to be honest.

.ooo.   I believe they were asking what the most common effect of statins, which is GI upset (including diarrhea). Rarely you can have hepatotoxicity and myopathy but neither of these are a side effect in the answer choices. Hopefully this helps! +1  
niboonsh  Theyre asking about the most common side effect of Orlistat - which is really fatty diarrhea +1  
asharm10  Orlistat is not a statin drug, it basically inhibits pancreatic lipase so that you absorb less fatm drug is used for weight loss. So when you are not absorbing fat you are inviting diarrhea. +1  

submitted by bubbles(51),

Can someone explain properly how we know that this trait follows Mendelian genetics and is autosomal recessive and furthermore how the parents were heterozygous?

I guessed a lot on this question and got lucky :(

niboonsh  Autosomal Dominant disorders usually present as defects in structural genes, where as Autosomal Recessive disorders usually present as enzyme deficiencies. P450 is an enzyme, so we are probably dealing with an autosomal recessive disorder. furthermore, the question states there was a "homozygous presence of p450.....". In autosomal recessive problemos, parents are usually heterozygous, meaning that 1/4 of their kiddos will be affected (aka homozygous), 1/2 of the kids will be carriers, and 1/4 of their kids will be unaffected. +14  
nwinkelmann  Is this how we should attack this probelm?: First clue stating endoxifen is active metabolite of Tamoxifen should make us recognize this undering first pass hepatic CYP450 metabolism? Once we know that, the fact that the metabolite is decrease suggests an enzyme defect, which is supported by patient's homozygous enzyme alleles. Then use the general rule that enzyme defects are AR whereas structural protein defects are AD inheritance patters. Once we know the pattern, think that most common transmission of AR comes from two carrier parents. So offspring alleles = 25% homozygous normal, 50% heterozygous carrier, and 25% homozygous affected, thus sister has a 25% of having the same alleles as patient (i.e. homozygous CYP450 2D6*4)? +6  
impostersyndromel1000  we had the exact same thought process, so i too am hoping this is the correct way to approach it get reasoning friend +  
ajss  thanks for this explanation, I totally forgot about AR patterns are most likely enzymes deficiencies, this kind of make the question easier if you approach it that way, thanks +  

submitted by meatus(1),

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

niboonsh  the question is asking what would happen to the URINARY ph, bicarb, and volume. dont worry, i misread the question too -_- +8  
link981  Also misread the question, thought about the lab volumes of the BLOOD smh +5  
hyperfukus  yooooo me too!!! this is the second NBME i did this on they purposely don't write urine on the arrow categories to mess u up i swear!!! AHHHHHH +2  
medulla  missed this question for the same reason .. still pissed +2  
osler_weber_rendu  I DID NOT READ "URINARY" OH NOOOOOO. Im so dumb. +2  

submitted by k_tron_3000(24),

The description of bilateral lower limb loss of vibration implies DCML damage, and the absent DTRs + Romberg seem to me to be implying that he possibly has tabes dorsalis from syphilis (or something very similar in presentation).

As for the other answers, A is wrong because his motor function is intact, B is wrong because pain and temperature deficits are not mentioned, C is wrong because it implies a specific nerve is entrapped, but he has lost bilateral sensation in his entire lower extremities

D is the trickiest, and I’m not 100% sure, but I would think radiculopathy of the anterior (ventral) roots would cause motor deficits since they carry motor efferents. You might also expect that motor dysfunction to be unilateral, since it would be unlikely to have a problem with the nerve roots on both sides. also the DCML is not located near the anterior roots of the spinal cord, so if the anterior roots were affected you really wouldn’t expect to see vibratory loss.

So basically process of elimination, I do feel like sensory neuropathy is an extremely vague answer though and I wasn’t a fan of the question.

keycompany  This is a great rationale. I would like to add on that D is wrong because Radicular Neuropathy of the anterior lumbar roots would (1) be painful [radicular neuropathy is characterized by radiating pain (hence the word “Radicular”); this patient has numbness and tingling, not pain] and (2) because the anterior lumbar roots are the motor roots and do not carry sensory innervation. This patient is having a problem with his dorsal spinal cord (not anterior/ventral). +16  
hello  Want to clarify that "radiculopathy" is not synonymous with pain. Radiculopathy can cause pain, weakness, or numbness. I think the only reason Choice D. was incorrect because it discussed the "anterior lumbar roots", which would affect motor function. +10  
niboonsh  Radiculopathy is damage to the actual nerve itself, wouldnt that make it a LMN lesion and babinski would be negative? +1  
link981  Great explanation guys +  
usmel2020  UW QID: 12035 explains what you are testing with Romberg sign +  

submitted by sirminalot(-78),


niboonsh  this is disgusting. +1  

yotsubato  How is that NOT posterior to middle concha? bad question +5  
sympathetikey  @yotsubato - That would have been if it was the spehnoid sinus (I got it wrong too btw) +2  
niboonsh  this is a good video if u need a visual https://www.youtube.com/watch?v=mf7rY1VNy70 +3  
sahusema  Sphenoethmoidal RECESS not sphenoethmoidal SINUS +2  

submitted by whossayin(13),

the question was very poorly worded in my opinion, anybody else agree?

niboonsh  yea it was a dumbass question, whoever is writing these questions is undoubtedly a crazy genius but homeboy (or homegirl...homeperson?) needs a few grammar lessons. +2  
yex  I agree. We know that it is a teratogen, but how does that question directs you to think about teratogenic effects instead of something physiologic? +5  
dr_jan_itor  The questions in the NBMEs by default are reject questions. So highly selective to be awful questsions. I am recieving regular heads up that the stems on the real thing lately are like 10-12 lines long. So these questions are not anywhere near like the test. NBME has f'd us good for this particular round of practice forms. +  

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.


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. +7  
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/ +13  
dr_jan_itor  I was thinking that its Murine typhus transmitted by fleas +  
monique  I would say this is more likely scenario of either Dengue or Chikungunya, not Zika virus. Excruciating pain is common in those, not in Zika. Zika has milder symptoms of those three infection. +1  
jakeperalta  Can confirm that Chikungunya's arthralgia is pretty horrible, from personal experience. +  
almondbreeze  UW: co-infection with chikungunya virus with dengue virus can occure bc Aedes mosquito is a vector of both Chiungunya, dengue, and zika +  

submitted by drdoom(467),

2,500 students ... but you find out during your initial screen that 500 already have the disease. So, strikeout those people. That leaves 2,000 students who don’t have the disease.

Over the course of 1 year, you discover 200 students developed the infection. Thus:

200 new cases / 2,000 people who didn’t have the disease when you started your study = 10 percent

Tricky, tricky NBME ...

sympathetikey  Ah, I see. Thank you! +  
niboonsh  Im mad at how simple this question actually is +2  
sahusema  Incidence is measured from those AT RISK. People with the disease are not considered to be at risk. So 2500 - 500 = 2000 people at-risk. Of those 2000, within one year 200 develop the disease. So 200/2000 of the at-risk population develop the disease. 20/2000 = 10% = incidence +2  
daddyusmle  fuck im retarded +  

submitted by nosancuck(63),


Why dat!???

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

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

meningitis  The above explanation is correct (disregarding the hard to read and unprofessional dialect) but just in case anyone was wondering: chromatin-negative= Just a quick way of knowing it was a boy. The term applies to the nuclei of cells in normal males as well as those in individuals with certain chromosomal abnormalities +13  
yotsubato  Turner syndrome patients are also chromatin negative as well though.... +3  
sympathetikey  I didn't know a complication post-meningitis was lack of humor. +2  
sympathetikey  Ah, didn't read the last line. Yeah, that is taking it a bit far +3  
niboonsh  yall are haters. this is the first explanation that has ever made sense to me +4  
arkmoses  https://www.youtube.com/watch?v=yuXL-3eoB-o&t=77s Interesting syndrome watching this helped me to put it into real life perspective, interesting points they have no pubic hair/body hair, they apparently also dont smell, and breast size is usually increased... +1  
whoissaad  How does chormatin-negative indicate a normal cell? Isn't chormatin just condensed DNA? +1  
cienfuegos  According to this paper most individuals with Turner Syndrome are chromatin negative: "One of the initial laboratory procedures used to confirm or rule out this diagnosis involves a sex chromatin determination from a buccal smear. Cells from the lining of the mouth are stained for the presence or absence of X-chromatin or Barr bodies, which represent a portion of an inactivated X chromosome. The typical Turner’s syndrome patient, who has 45 chromosomes and only one sex chromosome (an X), has no Barr bodies and is, therefore, X-chromatin negative. This abnormal X-chromatin negative finding in the majority of Turner’s syndrome females is similar to the result found in a normal male, who also has only one X chromosome, and differs from the X-chromatin positive condition observed in the normal female, who has two X chromosomes. Occasionally, the patient with features of Turner’s syndrome is found to be X-chromatin positive." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6233891/ +1  
hyperfukus  i really hate haters this is awesome! +1  
selectuw  to add to the above, free testosterone is aromatized to estrogen leading to breast development +  

submitted by mcl(453),

Per p608 in FA 2019, SRY on Y chromosome results in development of testes. DHT results in development of male external genitalia (and the prostate).

mrsmac  No sertoli cells or lack of mullerian inhibitory factor makes more sense. bc there is both male and female internal genitalia but only male external genatalia. and karyotype would show 46XY. First Aid 2018 pg. 604 - the "Sexual Differentiation" charge delineates exactly this. If it were 5areductase deficiency the child would have testicles and scrotum, which in this case is absence. Hope this makes sense. Please let me know if you disagree and why. Thanks. +  
mixmasta  I believe the tricky part is that they don't mention the status of the Male external genitalia. Pg. 605 from FA ( bottom portion) shows the external development of the Male/Female genitalia; you see DHT is need for male. Furthermore, pg. 604 (SEXUAL DIFFERENTIATION) DHT is also needed for Male external development. +  
niboonsh  My understanding of this is that the diagnosis is 5alpha reductase deficiency because the newborn has female external (aka ambiguous) with male internal (aka "male genital ducts"). According to FA, leydig cells produce testosterone, which can either stimulate the mesonephric duct to form the INTERNAL male genitals (as see in the pt). Testosterone can also be acted on by 5alpha reductase to become Dihydrotestosterone, which forms the male EXTERNAL genitalia. Since this kid has "female" genitals, but has male insides and is 46XY, id say this is a simple case of 5alpha reductase deficiency. No sertoli cells or no MIF would present as both female and male internal (because MIF typically inhibits differentiation of female internal) and male external genitalia (bcuz leydig cells are unaffected) +13  

submitted by uslme123(22),

very stupid question. The virus was inhaled -- bats hang upside when they sleep and drool. So it spreads to the brain directly from the olfactory system via retrograde transport through nerves.

niboonsh  yea, aeresol transmission via bat poop in caves +  
len49  How do you know the virus was inhaled? Doesn't mention it. Moreover, non-bite/scratch transmission is extremely rare. +  
makinallkindzofgainz  You get rabies by being bitten, not by inhaling it +  
drzed  She was probably bitten by a bat; many times the bite is not recognized ('unapparent bites'), and thus the CDC recommends that even if you think you have been bitten by a bat (or that you COULD have been bitten), you should go and get active/passive immunization immediately. +  

submitted by mcl(453),

Methionine is an essential amino acid. All others listed are not.

scalpelofthenorth  Pg 81 Tyrosine is listed as an essential AA. Should be tryptophan for those who got this wrong like me. +  
neonem  But tyrosine can come from phenylalanine, so it's not really essential right? +  
gh889  in FA2019, it is listed as Tryptophan, not Tyrosine. That was corrected. +1  
usmleuser007  Note: Tyrosine is ONLY essential with PKU in children +  
niboonsh  bro FA2018 lists tyrosine as an essential AA. They played us. +1  

submitted by calcium196(10),

Ubiquitin-mediated proteolysis is not reversibly affected by insulin. The question asks for reversible ways that insulin affects it, and ubiquitination would lead to degradation via proteases, which is not reversible. Nuclear/cytoplasmic shunting makes sense because FOXO is a transcription factor, so it can’t do its job if it is in the cytoplasm!

meningitis  Thank you for your explanation! One question: How about the serine phosphorylation? Is it answered by pure memorization that the FOXO TF is serine phosphorylated, or is it a general fact that all TF's are serine-threonine phosphorylated? +  
tsl19  I'm not sure, but it may be as simple as this: ubiquitin-mediated proteolysis is irreversible, but both N/C shuttling and phosphorylation are generally reversible processes. +  
didelphus  I also guessed that FOXO must be a part of the PI3K pathway, since insulin regulates metabolism through PI3K and the question stem specifically mentions that. Phosphorylation is a major part of that pathway, so even indirectly phosphorylation would regulate FOXO. Frustrating question. +7  
niboonsh  yes, FOXO is affected downstream of the activation of PI3K. This is a really good video that explains the whole cascade https://www.youtube.com/watch?v=ewgLd9N3s-4 +1  
alexb  According to wikipedia (https://en.wikipedia.org/wiki/FOXO1) phosphorylation of FOXO1 is irreversible. This is referring to phosphorylation of serine residues on FOXO by Akt, which occurs in response to insulin. But the NBME answer suggests it's reversible. What's up? +1  
almondbreeze  could wiki be wrong on phosphorylation being irreversible? according to this article, it is a reversible process: regulation of FoxO transcription factors by reversible phosphorylation and acetylation (https://www.sciencedirect.com/science/article/pii/S0167488911000735#s0010) some wiki info, however, is helpful : In its un-phosphorylated state, FOXO1 is localized to the nucleus, where it binds to the insulin response sequence located in the promoter for glucose 6-phosphatase and increases its rate of transcription. FOXO1, through increasing transcription of glucose-6-phosphatase, indirectly increases the rate of hepatic glucose production.[19] However, when FOXO1 is phosphorylated by Akt on Thr-24, Ser-256, and Ser-319, it is excluded from the nucleus, where it is then ubiquitinated and degraded. The phosphorylation of FOXO1 by Akt subsequently decreases the hepatic glucose production through a decrease in transcription of glucose 6-phosphatase. +  
leaf_house  It seems like the phosphorylation from Akt leads to destruction, but maybe the assumption is that that phosphorylation step (excluding every other step of ubiquitin-proteosome pathway) is reversible, where proteolysis is final. @niboonsh video is good but doesn't split this one. +  

submitted by usmleuser007(279),

Can someone please explain why can't alcohol be correct in this setting?

niboonsh  rhinorrhea is specific to withdrawal from opioids (aka heroin). Look at page 554 in FA2018 +9  
dr_jan_itor  what if the alcoholic just has a concurrent rhinovirus infection ;) +3  

tinidazole preferred due to single dose

sweetmed  or metronidazole +  
niboonsh  what would his diagnosis be tho? +  
lostweightthxnorovirus  @niboonsh Giardia I believe. the trophozoite is pictured in the problem and has a classic "shield-like" appearance. FA 2019 pg. 155 has more information and the sketchy for it was really good! +1  
nwinkelmann  Per FA, DOC for giardia = metronidazole. MOA of metronidazole = formation of toxic free radical metabolites in the bacterial cell wall that damage DNA making it bactericidal and antiprotozoal. Metro treats = GET GAP = giardia, entamoeba, trichomonas, Gardnerella, anaerobes (below diaphragm), and H. pylori (as an alternative to amoxicillin in PCN allergy). Adverse effects = disulfiram-like reaction, HA, and metallic taste. I didn't know what Tinidazole is, and found out it is of the same drug class as Metronidazole, so makes sense why it would also be used for Giardia. For the purpose of the UMSLE 1, though, I think metronidazole would be DOC (especially because tinidazole isn't in FA). +1  
mannywillsee  This little bug has has a face, and now you can't unsee it either! +  

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. +7  
niboonsh  https://www.ncbi.nlm.nih.gov/books/NBK482219/ probably caused by her recurrent pneumonia +3  
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 taway(22),

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! +5  
niboonsh  i am confusion +1  
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. +4  
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  

In psychogenic polydipsia, serum sodium is low, and after water deprivation test, urine osmolality is increased. Urine osmolality does not increase with vasopressin injection

In nephrogenic diabetes insipidus, serum sodium is high and there is no change/mild increase in urine osmolality after water deprivation

yotsubato  This patient does not undergo a water deprivation test +9  
niboonsh  Compulsive water drinking or psychogenic polydipsia is now increasingly seen in psychiatric populations. Effects of increased water intake can lead to hyponatremia causing symptoms of nausea, vomiting, seizures, delirium and can even be life threatening if not recognized and managed early. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5579464/ +7  
missi19998  Just wondering why it in not resistance to ADH action of vasopressin +  
amarousis  because he would be hypernatremic with no ADH. can't resorb any water +1  
minhphuongpnt07  low osm/urine, low os/plasma => psychogenic polydipsia +  
benitezmena  In this question the pt had a normal urine osm (80) a low urine osm would be <50mosmol/kg. +  
euchromatin69  u world 212 +  

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