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“Arrggg, here be fellow mateys seeking an explanation!”




... anechakfspb is asking for clarification on nbme23
 +0  upvote downvote
submitted by anechakfspb(2)

Why couldn't it be inhibition of gastric muscarinic (M1) receptors? Wouldn't that be the most effective overall?

... shutch94 is asking for clarification on nbme22
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submitted by shutch94(0)

I get that bleeding time is a measurement of platelet function. Is clotting time a measurement of the coagulation cascade (PTT/PT)?

drdoom  yes, that's correct. +
... rohan225 is asking for clarification on free120
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submitted by rohan225(0)

Why is the answer carrier status unknown? Why can't the mother be homozygous? Duchennes is X linked recessive.

dkhan123  not sure but here is my logic: -Male sibling of patient has died from Duchenne, confirming mother MUST BE either affected or a carrier. -Mother does NOT have the Duchenne phenotype, but has elevated enzymes, suggesting she is a carrier. The Duchenne average life expectancy is 26. Also the question is written such that it implies the mother does not have the Duchenne phenotype and the elevated enzyme level is due to the carrier status of Duchenne and not an unrelated illness. -Lastly, the daughter has normal enzyme levels. This could be due to two possible scenarios, either she inherited the Duchenne gene and has inactivated it, or she never inherited the gene to begin with. +
... ilikedmyfirstusername is asking for clarification on free120
 +0  upvote downvote
submitted by ilikedmyfirstusername(1)

Why not superoxide dismutase? Its the step right in between NADPH (chronic granulomatous disease) and MPO

ilikedmyfirstusername  I guess that could potentially manifest as an even worse phenotype in SCID? +
... masn8cc is asking for clarification on nbme18
 +1  upvote downvote
submitted by masn8cc(1)

Can someone explain how they r/o aortic stenosis? because that could enlarge the LA and give the same sx of hoarseness etc. And the murmur also fits with AS

... chadgas is asking for clarification on nbme18
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submitted by chadgas(0)

Did anyone have any difficulty deciding between C and E? I knew it was a Vitamin D deficiency, but doesn't calcitriol feedback to decrease PTH production?

... gandon is asking for clarification on nbme23
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submitted by gandon(0)

what drug acts on C?

... boostcap23 is asking for clarification on nbme24
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submitted by boostcap23(23)

This mentioned anywhere in FA or other board prep resources or just supposed to be common knowledge lol?

... md_caffeiner is asking for clarification on nbme18
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submitted by md_caffeiner(35)

yo sketchy veterans.

do you remember that loping back and forth lop eared rabbit that was increasing the phasic segmentation and therefore icreasing stool transit time?

This is it now.

... peteandplop is asking for clarification on nbme20
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submitted by peteandplop(10)

Can anyone explain why it's not anxiolytic? My logic was this dude has a bum ticker from previous MI, and his HR was 104/min--which can't be good for the old heart. I went w/a anxiolytic to bring his HR and anxiety under control.

Would an antidepressant do the same, thus, is it a better answer, or cover a wider range of symptoms?

... jessikasanz is asking for clarification on nbme22
 +0  upvote downvote
submitted by jessikasanz(3)

What does Zidovudine act on? It is a rev transcriptase inhibitor. Resistance often occurs at site of drug activity.

... baja_blast is asking for clarification on nbme15
 +0  upvote downvote
submitted by baja_blast(28)

Anyone know why this was Hydronephrosis and not Staghorn Calculus??

hchairston  There are no calculi in the image. The image shows a dilated ureter, you know it's a ureter because there is an opening into the hilum of the kidney. +
... anechakfspb is asking for clarification on nbme22
 +1  upvote downvote
submitted by anechakfspb(2)

Why couldn't it be retroperitoneal idiopathic fibrosis?

... notyasupreme is asking for clarification on nbme16
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submitted by notyasupreme(2)

Just wondering if someone could explain the difference between collagen and elastin for this one? I thought either or could be used for tensile strength. Anyone have clarification, don't know why collagen is the best answer!

notyasupreme  Lol, never mind I realize, it's a scar and that's type III collagen! +1
... tbarbacc95 is asking for clarification on nbme24
 +0  upvote downvote
submitted by tbarbacc95(0)

Anyone else think that B was on the proximal straight tubule?

boostcap23  Yupp :( +1
... azibird is asking for clarification on free120
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submitted by azibird(63)

How can we differentiate RSV from the common cold? Is it the bilateral, diffuse wheezes and expiratory rhonchi? Along with the intercostal retractions, signifying significant respiratory problems?

nbmeanswersownersucks  I was initially thinking it was rhinovirus too but in retrospect I think the wheezes etc make RSV more likely +
... azibird is asking for clarification on free120
 +1  upvote downvote
submitted by azibird(63)

This patient has a mixed hyperbilirubinemia. How could Gilbert syndrome, cause direct bilirubin to increase? The syndrome is caused by mildly decreased UDP-glucuronosyltransferase conjugation and impaired bilirubin uptake. So there's absolutely no way it could increase direct bilirubin! I thought this must mean that there was an obstruction or extravascular hemolysis.

... icedcoffeeislyfe is asking for clarification on free120
 +0  upvote downvote
submitted by icedcoffeeislyfe(25)

Is the decrease in baroreceptor output due to the body adapting to the hypertension?

azibird  Apparently. "Baroreceptor activity is reset during sustained increases in blood pressure so that in patients with essential hypertension, baroreceptor responsiveness is maintained." "It is a universally accepted phenomenon that vascular baroreceptors reset to operate at higher pressure levels in hypertension." Okay, so they can reset to normal levels, but wouldn't this patient already have undergone their reset? Why would the receptors further decrease? I thought that eventually their LV would hypertrophy and fail, leading to decreased stroke work. https://www.ahajournals.org/doi/full/10.1161/01.HYP.0000160355.93303.72 https://pubmed.ncbi.nlm.nih.gov/3042363/ +1
azibird  From Costanzo Physiology: "The sensitivity of the baroreceptors can be altered by disease. For example, in chronic hypertension (elevated blood pressure), the baroreceptors do not “see” the elevated blood pressure as abnormal. In such cases, the hypertension will be maintained, rather than corrected, by the baroreceptor reflex. The mechanism of this defect is either decreased sensitivity of the baroreceptors to increases in arterial pressure or an increase in the blood pressure set point of the brain stem centers." +4
mangomango  Hypertensive heart disease causes concentric LVH - impaired diastolic function, preserved ejection fraction +
... motherhen is asking for clarification on nbme16
 +1  upvote downvote
submitted by motherhen(4)

In other words, what is the active product of the thyroid gland that is needed for normal development? Only thyroxine, iodine and thyroglobulin are in the thyroid gland. Of these, thyroxine is the active hormone produced that would affect development.

... maria_danieli is asking for clarification on nbme24
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submitted by maria_danieli(0)

So does someone know what is phase 0 for? It was an option... somathing like "let me see if i can study this thing?"

cheesetouch  via google - A Phase 0 study gives no data on safety or efficacy, being by definition a dose too low to cause any therapeutic effect. Drug development companies carry out Phase 0 studies to rank drug candidates in order to decide which has the best pharmacokinetic parameters in humans to take forward into further development. +
boostcap23  Phase 0 is an extremely small dose (1% of normal) given to easily rule out any harmful effects. Basically used as a quick way to eliminate further trails/research on drugs that don't work. +1
... barbados is asking for clarification on nbme16
 +1  upvote downvote
submitted by barbados(1)

Did anyone else feel like the question should have been more specific as in saying "just before the consumption of a meal"? As in saying she has high ghrelin = high hunger just before she eats so point B?

lee280  I agree, at the start, I got a bit confused because I felt like the question was probably less specific than it would have been, but NBME being NBME this is really expected. When you think about it more closely, once you consume the meal then ghrelin will peak and start dropping. +3
notyasupreme  I agree, I had B at first but then thought too deep into it. I thought if she ATE a meal, she'd be full and low ghrelin. Annoying to get a question wrong on something so simple. +
radzio1  Also got this question wrong. A really bad explanation what they want from the curve... +
... diplococci is asking for clarification on nbme24
 +1  upvote downvote
submitted by diplococci(1)

I was confused because UW 19280 says pulmonary artery systolic pressure will be increased to maintain forward movement of blood. How does this not lead to pulmonary vascular resistance being increased?

boostcap23  Pressure doesn't necessarily equal increased vascular resistance. Pulmonary resistance regulation mainly increases in areas of hypoxia, and decreases in well-oxygenated area's to send blood to well ventilated areas, nothing to do with an acute MI. In fact in MI there is vasodilation of apical capillaries and the V/Q ratio will approach 1 to accommodate the extra blood. In this patient, you can see his systemic blood pressure is low yet his systemic vascular resistance is high (due to sympathetic constriction of vessels in response to low CO). I just thought of it like how in normal resting state ventilation is wasted at the apex so in a volume overloaded state that extra blood could go up to the apex. +1
... avocadotoast is asking for clarification on nbme23
 +2  upvote downvote
submitted by avocadotoast(2)

Boards and Beyond has a good flow chart for ambiguous genitalia. If the patient is XX - do they have mullerian structures? If yes, it's CAH (increased androgens). If they patient is XY - do they have mullerian structures? If yes, gonadal dysgenesis (no MIH). If no, then it could be due to abnormal androgen receptors, CAH, or low DHT.

... azibird is asking for clarification on nbme18
 +1  upvote downvote
submitted by azibird(63)

Follow-up vs support group?

The only thing that saved me was the ancient Step 1 adage: "Never refer!"

Especially when the answer to another question in the same exam was "Encourage the patient to participate in a support group for persons with her condition"

I mean REALLY! The only difference is that they used the word "encourage" instead of refer. Exact same answer.

... azibird is asking for clarification on nbme18
 +0  upvote downvote
submitted by azibird(63)

Can someone explain the physical findings?

"Cardiac examination shows a grade 2/6 pansystolic murmur heard best at the lower left sternal border, which increaes on inspiration. The point of maximal impulse is palpated in the sub-xiphoid area S1 and S2 sounds are distant"

I don't understand how any of these would correspond to cor pulmonale.

drdoom  Backfilling of blood from the lungs into the R ventricle is stretching out the R side (dilation) and also remodeling the heart via hypertrophy (the heart has to pack on mass to eject the ever greater amount of blood piling up from lungs). Dilation of the R ventricle “pulls apart” the leaves of the tricuspid valve=``lower left sternal border``; when the heart is in systole, the tricuspid valves don’t make good contact and blood rushes from high pressure compartment (RV) to the low pressure (RA) == ``pansystolic murmur`` +
drdoom  The tricuspid murmur gets worse with inspiration because when you ask someone to take a good, deep breath, the diaphragm (a very strong muscle, indeed) pulls the entire thoracic cage down and out (expansion) — including the heart! Because the heart “gets pulled from all directions”, the tricuspid leaflets make even less contact == bigger hole == more pronounced murmur during systole. +2
drdoom  The point of maximal impulse (the heart apex) is way below the xiphoid because this guy’s heart is so big from the years of dilation and hypertrophy — that’s also why the S2 sounds are distant: the great vessels (and their valves) are buried even deeper than usual, so you can’t hear them snapping shut (aortic & pulmonic valves; S2=“dub”). +
... azibird is asking for clarification on nbme18
 +1  upvote downvote
submitted by azibird(63)

What is going on here? The mother is not the patient, why are we exploring this further when the son is completely normal? I get it that we would say this if the patient were concerned, but he's not and he's normal so why don't we just tell her that everything is normal? Exploring further will probably make the patient feel worse.

drdoom  Another way to read the stem is like this: “Assume you will make a statement that assures mom that boy is fine. What other statement do you want to make?” Since we’re *already* assuring mom, the best next thing is to ask an open-ended question. There’s a reason for this. As a physician, you really don’t want to say more than what you are (1) sure of or (2) obliged to. “Accept him as he is” = judgy. “He’s not going to get any taller” = you don’t know this for sure. +
... hungrybox is asking for clarification on nbme19
 +0  upvote downvote
submitted by hungrybox(770)

I put C because I thought that the weakness of the lower 2/3 face meant there was something more going on than just speech problems from Broca's aphasia.

Can anyone tell me why I'm wrong?

drdoom  A: Broca’s +
drdoom  B: Premotor +
drdoom  C: Motor +
drdoom  D: Somatosensory +
drdoom  Damage to C (motor) wouldn’t explain *fluency* problems. Fluency (=Latin ``flow``; the ease with which the brain formulates words). Slurred speech is your brain knowing and formulating the words easy but your mouth muscles not co-operating! +
drdoom  So, dis-fluency ≠ slurred speech. This gentleman is dis-fluent in the same way you’re dis-fluent when you visit Paris: your brain struggles to formulate French words in the first place! The only lesion that explains that in your native tongue is a lesion to the language synthesis center = Broca’s area. +
... usmleboy is asking for clarification on nbme22
 +1  upvote downvote
submitted by usmleboy(7)

LOL. I thought they were asking for Urinary pH, but blood bicarb and blood volume.

Who in their right mind would ask for urinary pH, urinary bicarb, and urinary blood volume by saying ".... urinary pH, bicarbonate and volume"

Am I crazy?

... passplease is asking for clarification on nbme16
 -1  upvote downvote
submitted by passplease(6)

Why not a tear in the sciatic nerve? especially since it radiates down to the leg

cassdawg  My main thoughts on this is that an actual tear in the sciatic nerve is extremely difficult and further it would present with motor weakness to the muscles innervated by the sciatic nerve as well (the hamsrtings and adductor magnus, FA2020 p452). The sciatica pain that you are referring to is more common with injury to the nerve via herniated disc. +1
... azibird is asking for clarification on nbme24
 +6  upvote downvote
submitted by azibird(63)

Who else came here after getting triggered by this answer?

... wherearetheanswers is asking for clarification on nbme19
 +1  upvote downvote
submitted by wherearetheanswers(9)

The kidneys make glucose too? 6 years of studying science and no one mentions the kidneys.

... euphoria is asking for clarification on nbme21
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submitted by euphoria(1)

i have answered this question right, but why there is mid systolic murmur in the stem?

mittelschmerz  He also has MVP, but asthma is more likely to cause this symptomatology and he has a family hx. +1
euphoria  Thank you very much bro :-) +1
... cuteaf is asking for clarification on nbme23
 +0  upvote downvote
submitted by cuteaf(4)

Why is it not answer " Postatic venous plexus to the the internal iliac veins" I thought the route of metastases to the spine is prostate plexus -> internal iliac veins -> vertebral plexus??

... azibird is asking for clarification on nbme24
 +0  upvote downvote
submitted by azibird(63)

Why are there lots of RBCs but few RBC casts? That made me think about a post tubule process.

boostcap23  Any amount of RBC casts is an abnormality and indicates tubular pathology. Normally should have none. Just like how even a single neutrophil in CSF is abnormal. +1
... russnels is asking for clarification on step2ck_form7
 +0  upvote downvote
submitted by russnels(2)

Why would this not be ABO incompatibility? Is Rh incompatibility just more common?

boostcap23  Yes for newborns specifically Rh incompatibility is more likely and also much more severe (see pg 405 FA 2020). ABO incompatibility would produce only mild jaundice and is actually quite common. +1
... russnels is asking for clarification on step2ck_form7
 +0  upvote downvote
submitted by russnels(2)

Anybody have any good insights as to what is going on here? Does surgery somehow cause hypokalemia? Or does this have to do with digoxin toxicity? I'm not sure how surgery fits in. Thanks in advance!

misscorona  Looking at UpToDate, hypokalemia is listed as one of few postoperative electrolyte abnormalities. Surgical stress releases aldosterone which leads to hypokalemia. Hypokalemia is a known cause of premature ventricular contractions. Digoxin toxicity can cause premature ventricular contractions but it seems like this patient was on these medications prior to surgery and this may be less likely contributor. Side note, digoxin can lead to hyperkalemia. +
... russnels is asking for clarification on step2ck_form7
 +0  upvote downvote
submitted by russnels(2)

My understanding was that both IUDs and OCP can reduce risk of ovarian epithelial cancer. Anybody know why OCPs are better than IUDs?

... russnels is asking for clarification on step2ck_form7
 +1  upvote downvote
submitted by russnels(2)

Would this be x-linked agammaglobulinemia? With a BTK gene mutaiton?

misscorona  I would agree. X-linked agammaglobulinemia is associated with recurrent sinopulmonary infections with encapsulated organisms which are all the organisms mentioned in the question stem. +
... russnels is asking for clarification on step2ck_form7
 +0  upvote downvote
submitted by russnels(2)

I'm not sure what they were going for on this question. Is it that bilateral varicoceles are the only answer correlated with decreased sperm count? Maybe testicular atrophy? Doesn't mention anything about the testes, so not sure what to think.

... russnels is asking for clarification on step2ck_form7
 +0  upvote downvote
submitted by russnels(2)

Anything else here pointing to Fat Embolism Syndrome other than the long bone fracture? Is "fluffy infiltrates" pathognomonic for FES? Why could it not also be ARDS?

... russnels is asking for clarification on step2ck_form7
 +1  upvote downvote
submitted by russnels(2)

Is this sarcoidosis? I think that accounts for the erythema nodosum, hypercalcemia, and hilar findings.

... russnels is asking for clarification on step2ck_form7
 +0  upvote downvote
submitted by russnels(2)

I'm guessing she had a chylothorax seeing that the answer was triglycerides? Anything jumping out at anyone that points to that?

... athenathefirst is asking for clarification on nbme13
 +0  upvote downvote
submitted by athenathefirst(2)

Why is this VSD? Is it just because she is 3 years old? I was stuck between MVP, VSD.

... nootnootpenguinn is asking for clarification on nbme22
 +1  upvote downvote
submitted by nootnootpenguinn(5)

Why are his labs normal?

Protein electrophoresis is to r/o MM. What are the others trying to rule out? Also, if it was prostate adenocarcinoma, wouldn't there be elevated PSA in the urine (which might result abnormal UA)?

lsp1992  Urinalysis provides a microscopic examination of urine, which would tell you about the presence of RBC, WBC, casts, crystals, epithelial cells, and a chemical test for nitrites, bili, urobilinogen, ph, specific gravity, proteins, glucose, blood, and ketones. PSA is a specific protein that would be found in the blood, and a lab test that would have to be ordered specifically. +
... azibird is asking for clarification on nbme23
 +2  upvote downvote
submitted by azibird(63)

What is the educational objective of this question? To see if we know that radiation doesn't stick? Not that cool.

... azibird is asking for clarification on nbme23
 +2  upvote downvote
submitted by azibird(63)

Why is there a decreased FVC? There is a mass pressing on her trachea, how could that possible affect lung volume? If we give her enough time, why couldn't she take in a full breath?

... achrondroplease is asking for clarification on nbme23
 +0  upvote downvote
submitted by achrondroplease(2)

Why can this not be MEN 1? And the increased serum calcium be a result of increased PTH release from parathyroid?

azibird  None of the answers are parathyroid. +
... bbr is asking for clarification on nbme21
 +0  upvote downvote
submitted by bbr(15)

I'm still confused, where is this guys problem occuring? Is that he is unable to urinate, or that he has overflow incontinence? Getting lost in these nerves.

... mynamejeff is asking for clarification on nbme24
 +0  upvote downvote
submitted by mynamejeff(0)

I think E is also viable... 1/4 is B/B and another 1/4 is B/B+ . The B/B+ is B-thalassemia minor where B chain is underproduced (functions normally) and is usually asymptomatic, per FA (2020 pg. 418).

Thoughts?

Also, my understanding on B-thalassemia from Dr. Sattar and first aid is that it's not set in stone that B+ is 50% production. It seems to vary.

syringomyelia1  E says 1/2 not 1/4 +
... bmilt34 is asking for clarification on nbme23
 +0  upvote downvote
submitted by bmilt34(1)

Some things ive noticed for these types of questions? 1) dont be a dick (b, d, e) 2) dont differ to some other person (a)

... mamed is asking for clarification on nbme18
 +1  upvote downvote
submitted by mamed(4)

What is the neoplastic chondrocytes filling lacunes?

mumenrider4ever  I think that's a chondrosarcoma (tumor of malignant chondrocytes, found in the pelvis, proximal femur and humerus, FA 2020 pg. 465) +1
... mamed is asking for clarification on nbme18
 +0  upvote downvote
submitted by mamed(4)

Was anyone thinking about answer choice E- PTH hormone production? I was in between a Vitamin D and Calcium deficiency with the no milk. I ended up going with vitamin D (thank you sketchy) but couldn't rule out a calcium deficiency in my mind.

... stefanmil is asking for clarification on nbme21
 +2  upvote downvote
submitted by stefanmil(2)

Why we have deposits in the glomerular membrane. It supposed to be subepithelial - spike and dome - granulations, right?

lovebug  @stefanmil Yap. you're right. I think "Spike and dome" @ EM. and Diffuse capillary and GBM thickening in @ LM. +
... nafilnaf is asking for clarification on nbme20
 +0  upvote downvote
submitted by nafilnaf(0)

What does she have? My assumption was that she was getting NRTIs for HIV/AIDS which get phosphorylated by HOST thymidine kinases and the mechanism for viral resistance is mutations in reverse transcriptase

azibird  I think she has chickenpox, caused by varicella-zoster virus. From FA 2020 p 183: "Vesicular rash begins on trunk; spreads to face D and extremities with lesions of different stages" +2
... clamshell27 is asking for clarification on nbme23
 +0  upvote downvote
submitted by clamshell27(0)

Can anyone explain why bicipital tendonitis is incorrect?

... xw1984 is asking for clarification on nbme24
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submitted by xw1984(1)

English is not my first language, but would it be possible that adherence is not equivalent to adhesion and somehow interchangeable to aggregation? I feel like doing a reading comprehension test, not USMLE.

... lsp1992 is asking for clarification on nbme16
 +1  upvote downvote
submitted by lsp1992(10)

Can someone please explain what we're seeing on the histo slide? I chose the correct answer because I was thinking fungus because of the immunocompromise and neutropenia (and I thought PAS was used for aspergillus), but I don't see anything fungus-related on that slide.

cassdawg  I think this is Blastomyces (broad based buds) where the darker pink are the blastomyces budding. Here are some similar slides: https://images.slideplayer.com/25/7691707/slides/slide_39.jpg https://www.gettyimages.co.uk/detail/photo/blastomycosis-in-the-brain-caused-by-the-high-res-stock-photography/vis303384 It could also be cryptococcus potentially (https://www.omicsonline.org/publication-images/diagnostic-pathology-budding-cryptococci-3-139-g005.png) but I think the bud bases are too broad and there is no clearing/visible capsule that cryptococcus is notable for. Either way you treat both systemic mycoses with amphotericin. +2
passplease  How did you eliminate CMV? +
cassdawg  For me, CMV would have the characteristic "owl eye intranuclear inclusion" cells on biopsy but would be less likely to show anything in pleural fluid (i.e. thoracocentesis would not be used to diagnose CMV). Further CMV pneumonitis is an atypical/interstitial pneumonitis (diffuse patchy infiltrates on CXR, FA2020 p683) and he has a lower lobe consolidation with pleural effusion (more characteristic of fungal pneumonia). +1
... tinyhorse is asking for clarification on nbme17
 +3  upvote downvote
submitted by tinyhorse(3)

Frankly pretty floored that anybody thought that this question contained enough information for someone to confidently answer it.

The question has you assume that both parents are heterozygotes at the locus. Why? I assume I'm missing some esoteric fact about P450 allele frequencies.

flapjacks  I got lucky guessing the same % chance that siblings share HLA markers +2
baja_blast  I agree with OP seriously no idea how anyone could have gotten this right without totally guessing it. Am I missing something here?? +
... aoa05 is asking for clarification on nbme16
 +0  upvote downvote
submitted by aoa05(11)

A high stepping gate implies distal more than proximal weakness. Hammer toes are a finding in Charcot-Marie-Tooth (hereditary motor and sensory) neuropathies, most of which also feature demyelination of peripheral myelin sheaths. Slowing of nerve conduction velocities could have demonstrated the same thing less invasively.?

notyasupreme  Ask me why I thought this was Friedreich Ataxia and not CMT fml lol +
... cassdawg is asking for clarification on nbme17
 +1  upvote downvote
submitted by cassdawg(548)
  • Clinical trial Phase I - healthy volunteers asking is it safe [FA2020 p256]
  • Phase II is small # people with the disease - does it work, optimal dosing, side effects?
  • Phase III is larger # with disease - is it good or better? (randomized controlled trial phase)
  • Phase IV - postmarketing surveillance
... blueberriesyum is asking for clarification on nbme19
 +4  upvote downvote
submitted by blueberriesyum(6)

A 70 year old develops a progressive disinhibition syndrome with episodes of emotional outbursts, inappropriate use of language, and socially inappropriate behavior. Where is the most likely damage?

Answer: Frontal lobe disinhibition.

Bilateral amygdala (medial temporal lobe) would've been affected if it was Kluver Bucy Syndrome.

flapjacks  If you know the story of Phineas Gage, it can help +4
... icedcoffeeislyfe is asking for clarification on nbme19
 +2  upvote downvote
submitted by icedcoffeeislyfe(25)

FA2020 pg 48

retrograde transport= dynein

anterograde transport= kinesin

REaDY? AttacK!

... usmleboy is asking for clarification on nbme20
 +2  upvote downvote
submitted by usmleboy(7)

I just want to add that I hate this question and I am not sure why the NBME loves to use the worst grammar imaginable.

We all know strawberry hemangiomas spontaneously involute after 5-8 years... why don't they just ask this? Why do they insist on ambiguity of phrases? Why are my board exams trying to trick me with poor english?

Rant over.

... fatboyslim is asking for clarification on nbme20
 +0  upvote downvote
submitted by fatboyslim(25)

I chose Aspirin. So aspirin is a non-reversible inhibitor of COX-1 and 2 which should decrease TXA2 levels, and according to FA 2020 page 485, TXA2 causes platelet aggregation and increases vascular tone...I'm guessing the overall combined effect of COX 1 & 2 inhibition will cause a net effect of either vasoconstriction or no change to vascular tone?

spaceboy98  Me too. i thought aspirin blocking off the TXA2 production would allow for vasodialation. +1
... jesusisking is asking for clarification on step2ck_form7
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submitted by jesusisking(10)

Did anyone else think autonomic insufficiency given the diabetes? I know it was previously well controlled but still a 10 year history

... brise is asking for clarification on nbme15
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submitted by brise(31)

I thought that a child with down syndrome under the age of 5, had a chance of getting acute megakaryoblastic leukemia? and over 5, acute lymphoblastic leukemia?

mittelschmerz  I was stuck between those as well. My thought process was that megakaryocytosis would be mature megakaryocytes though, which would not happen in a megakaryoblastic leukemia since they are stuck in the blast stage. That left only lymphoblasts, and I presume while one may be MORE likely age 5, a patient with Down Syndrome is still at higher risk for both. +1
cassdawg  "Megaloblastosis" as in the answer choices refers to megaloblastic anemia in B12 and folate deficiency, so it is not associated with megakaryocytes or megakaryoblastic anemia! Hope this helps! +3
... greentea733 is asking for clarification on nbme24
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submitted by greentea733(10)

Why wouldn't the body down-regulate the conversion of FT4 into FT3? Is that conversion just constitutively activated? Since FT3 is more potent than T4, it would make sense for the body to turn that conversion down...that was my reasoning...obviously not correct, but idk why that wouldn't be the case. Anyone have insight?

maria_danieli  i thought the same... i remember that T3 conversion is somehow regulated but evidently not in this case +
sars  Peripheral conversion of free T4 to T3 is done by 5-deiodinase. From what I know, only way to decrease this conversion is via b-blockers, glucocorticoids, propylthiouracil, and potassium iodide (lugols). I believe this was mentioned in the sketchy pharm vid as well. +
sars  Peripheral conversion of free T4 to T3 is done by 5-deiodinase. From what I know, only way to decrease this conversion is via b-blockers, glucocorticoids, propylthiouracil, and potassium iodide (lugols). I believe this was mentioned in the sketchy pharm vid as well. +
sars  4th blocking agent isn't lugols, its iodinated radiocontrast dye! Sorry for that mistake. +
cassdawg  "T3 is derived from peripheral conversion of T4... normal plasma T3 levels are obtained in athyreotic patients treated with sufficient T4 to achieve high-normal plasma (F)T4 levels. Administration of T4 to hypothyroid rats to achieve normal plasma T4 levels results in subnormal plasma T3 levels not only because of the lack of T3 secretion but also because of a decreased T3 production by D1 in peripheral tissues, since this enzyme is under positive control of T3 itself". (https://www.ncbi.nlm.nih.gov/books/NBK285545/) i.e. because he is taking SUPRATHERAPEUTIC T4 his T3 is NORMAL. If he was taking NORMAL T4 then he would have DECREASED T3. Pretty sure the normal T4/decreased T3 thing is in another NBME test or UWorld somewhere. +
cassdawg  ^Sorry to add, her is suprasupratherapeutic so his T3 is elevated. Essentially in a normal hypothyroid patient they are given supratherapeutic T4 to get normal T3 since T3 is the hormone with the action. Apologies if anything is confusing. +
... b1ackcoffee is asking for clarification on nbme22
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submitted by b1ackcoffee(24)

my problem with this, why can't it be similar to Hep B (circular DNA)? virus is new or hypothetical.

andro  Hep B - is " partially " Double stranded and not fully double stranded . Double stranded Circular does not necessarily denote Hep B even though the virus has a reverse transcriptase . I think they wanted you to pay attention to this . And besides the obvious fact that Hepatitis viruses cause inflammation of the Hepar ( liver) and not encephalon ( brain) +
... 123ojm is asking for clarification on nbme23
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submitted by 123ojm(7)

Which structure is letter F pointing to in the diagram?

andro  Cerebral Peduncles +1
... zevvyt is asking for clarification on nbme22
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submitted by zevvyt(16)

You dont really need to know the murmur to get the question right, but I'm confused about the murmur. It sounds like Mitral Regurgitation. So why is it in the left sternal border and not the apex?

... geekymle is asking for clarification on nbme16
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submitted by geekymle(7)

i tried but i'm not able to reason this question. can anyone please help me on this?

sunnyd  I found a good explanation in the discussion here: https://forums.studentdoctor.net/threads/nbme-16-help.1059939/page-2 +
geekymle  thank you! it was the wording of the question which got me!! +1
andro  I think there were two possible ways of approaching this. The first was by appreciating that the tumor cells ( which release Growth Hormone ) would express growth hormone releasing hormone receptors GHRH receptors - GHRH uses the Gs signalling pathway ( Net effect an increase in cAMP from the increased activity of adenyl cyclase ) The second and more straight forward approach From the stem of the question already they told us we are dealing with an overactivation of the G alpha stimulatory subunit . If the GTPase aint working ( meaning it cant be inactivated ) , the effect would be an increase in the activity of adenyl cyclase +3
... vivarin is asking for clarification on nbme20
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submitted by vivarin(4)

in hereditary hemorrhagic telangiectasia would you have normal or low platelets?

andro  You would have normal platelets : It is a a problem with the structure of the vessels that leads to the sequela ( vasculopathy) +1
... monique is asking for clarification on nbme22
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submitted by monique(4)

Does anyone know where I can find this information on FIRST Aid 2020? I can not find it . Thanks for posting the answer!

... cassdawg is asking for clarification on nbme19
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submitted by cassdawg(548)

I am assuming this is just something we are expected to know; tubular reabsorption requires the most oxygen because it would consume the most ATP out of the processes in the kidney?

waitingonprometric  I believe this is correct--assuming that active transport of solutes at the thick ascending limb and active transport of solutes (secondary to Na/K pump) at the PCT consumes O2 at highest rate b/c of ATP use. Since tubular reabsorption always happening...very high use of O2 relative to the other answer choices that occur sporadically in response to body homeostatic changes? Note: glomerular filtration is always happening, but that's passive movement through fenestrated capillaries (i.e. no ATP used). +1
... al1234 is asking for clarification on nbme24
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submitted by al1234(1)

If it had stated a 'Rare Cancer' I would have thought case control. But it said common cancer.... Any thoughts on this?

... mittelschmerz is asking for clarification on nbme15
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submitted by mittelschmerz(9)

How do you know for sure that this is incomplete penetrance and not gonadal mosaicism? Dont both allow an AD disease to be transmitted by a phenotypically non-expressing carrier?

nissimhazkour1  my line of thinking is that gonadal mosaicism is much less likely considering there is a family history of the disease. If there was no family history then a gonadal mutation causing mosaicism is possible, but taking into consideration how there is a clear AD inheritance, it must be that the person inherited the disorder but is not expressing the phenotype. hope this helps! +
mittelschmerz  Yes thanks! That feels like it should have been so obvious in retrospect, ugh. +
... zevvyt is asking for clarification on nbme21
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submitted by zevvyt(16)

Of all the things they can test us on, they're testing our fucking Gadar??

peridot  Don't mean to be an eager beaver but I thought it was pretty cool to get tested on our gaydar! I think that's an important thing to pick up on. As for their answer choices, I'm not always the biggest fan of those since I think there's more than one right way to do something... +
... weenathon is asking for clarification on nbme20
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submitted by weenathon(21)

Anybody know why fatty acid degradation doesn't play a role?

andro  The question specifically asks for a process in myocytes Fatty Acids ( Triglycerides ) are primarily stored in adipocytes . It is from adipocytes, that the fat can be mobilized for use by other cells . Loss of adipocytes can decrease the width of the calf , but then again we are talking about mechanisms of muscle atrophy and the most important mechanisms for this is ubiquitination - breakdown of the cytoskeleton proteins +
... newrose is asking for clarification on nbme24
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submitted by newrose(8)

Can someone clarify why Prostacyclin was wrong? I knew the CHALK thing but for some reason had trouble ruling out prostacyclin since it's a vasodilator

cassdawg  My best answer for this is that the best answer is adenosine because it is asking for which is involved in the mechanism of reactive hyperemia (which involves similar mechanisms to autoregulation) of blood flow, which involves CHALK. While vasodilators like PGI2 (protacyclin) are vasodilators it is released at a base level by the lungs and endothelium, and releasedat higher levels in instances such as inflammation. Prostacyclin is not released in reactive hyperemia. If you want a refresher about active v reactive hyperemia: https://slideplayer.com/slide/2541224/9/images/3/Arteriole+Resistance%3A+Control+of+Local+Blood+Flow.jpg. They are both mediated by metabolic intermediates. as mentioned above. +
... stepwarrior is asking for clarification on nbme20
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submitted by stepwarrior(8)

Wouldn't chronic alcoholism also reduce available NAD and thus inhibit pyruvate decarboxylation by PDH?

andro  It may also potentially do that , But that has no connection with our patients current symptoms - perifollicular hyperkeratosis and hemorrhages . Inhbition of PDH would be more relevant if they were talking about Alcoholic Lactic Acidosis or decreased energy in alcoholics +
... stepwarrior is asking for clarification on nbme20
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submitted by stepwarrior(8)

You're just going to diss the son like that right in front of him?

splanchnic  made an account to upvote this +4
snoodle  I agree - I was stuck between this and "Was he under any unusual stress at home/school or did he have any problems with a gf when all of this started?" and I chose the latter. I didn't want to choose this because why would you want to call the son frightening in front of the son?! I didn't want to choose the answer I chose, either, because you aren't supposed to imply he's straight :/ annoying af +
... kllrsouth is asking for clarification on nbme16
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submitted by kllrsouth(0)

Couldn't the answer also be IL-2? Why can't you use cyclosporine in this patient with RA?

andro  First thing to note is that methotrexate has been shown to have the most activity of the non biological DMARDS in reducing erosions in RA . It is typically used in combination with another DMARD . Our Patient is not responding to our best Therapy for erosive RA ---- This is refractory RA . The algorithm generally used in Tx of R.A is that if non biological DMARDS have failed , as in our Pts , Biological therapy is initiated eg - Monoclonal antibodies against TNF alpha ( adalimumab ) or decoy receptors to TNF alpha ( etarnecept ) +2
... misterdoctor69 is asking for clarification on nbme24
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submitted by misterdoctor69(17)

Anyone else got thrown off by their use of HNPCC rather than Lynch syndrome?

... misterdoctor69 is asking for clarification on nbme24
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submitted by misterdoctor69(17)

How come melanocytes:basal keratinocytes don't also have a desmosomal connection (in addition to their E-cadherin link)?

vivijujubebe  melanocyte is not part of the epidermal structure. they're at the epidermal-dermal junction and they produce melanin which is transported to the epidermal +
... skip_lesions is asking for clarification on nbme21
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submitted by skip_lesions(8)

Can't histamine also cause swelling or is it just not involved in the pathology of gout?

zevvyt  yes. Histamine causes vasodilation and increased vessel permeability. But it's not involved in Gout. Gout is more about Neutrophils and Macrophages activating eachother and not really about Mast cells. +2
... b1ackcoffee is asking for clarification on free120
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submitted by b1ackcoffee(24)

Any good material for this and lymph node drainage in general? Is this common knowledge or low yield stuff?

... b1ackcoffee is asking for clarification on free120
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submitted by b1ackcoffee(24)

confused why this is not autonomic dysfunction or hyponatremia due to sweating and why is this orthostatic hypotension?

mamed  Not sure if this is correct thinking but how I got this right was: 1. She is hypovolemic 2. Likely retaining salt so water follows (ADH or just renal dynamics in general). This is how I ruled our hypokalemia and hyponatremia 3. If she is hyponatremic b/c sweating then why wouldn't she also be hypokalemic? so both have to wrong because both can't be right 4. Volume depletion ==> orthostatic hypotension +
blah  I thought that orthostatic hypotension was more of a chronic condition, but I fooled myself into believing that. +
... b1ackcoffee is asking for clarification on free120
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submitted by b1ackcoffee(24)

I am wondering which parasite is this actually? --

b1ackcoffee  @mdmofongo I know this. But which parasite is this? +
drblu92  The parasite is most likely Trichuris trichiura (human whipworm). Trichuriasis is often asymptomatic and adult forms can reach 2 cm in length (visible with naked eye). A lot more common in tropical areas but there have been cases in the southeastern US (ex: Kentucky). All other GI worms would present with either a fever or a cough. Treat with mebendazole or albendazole. +4
... amy is asking for clarification on nbme22
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submitted by amy(0)

HHV8 belongs to Herpesviridae family. Is it true that all members of this family have multinucleate cell with intranuclear inclusion body? HSV and VZV(cowry type A inclusion), EBV and CMV(owl-eye internuclear inclusion) certainly have them. Did anyone pick E for this reason?

... peridot is asking for clarification on nbme22
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submitted by peridot(33)

While I understand why it's hyperplastic arteriosclerosis and how it classically occurs with HTN, I was wondering why it couldn't be berry aneurysm? Is it because the question is asking which is "most likely", making C the better answer? Thank you.

mannan  Berry Aneurysm is not CAUSED by HTN. It's caused by weakening of the arterial wall (at bifurcations). Hypertensive disease exacerbates them and causes the clinical picture of SAH (worst headache of life) when they rupture. Hope that helps -- Reference: FA CNS pathology, aneurysms. +1
usmleboy  Actually according to Goljan this is incorrect. Berry aneurysms are caused by hypertension. The weakening of the wall (no tunica media) at bifurcations is inherent in human anatomy. Basically you have to have elevated BP to cause the dilation, outside of the inherited connective tissue disorders. Hence why PKD has the berry association. However, these aneurysms present with extremely prolonged HTN, whereas our guy in this Q only has a 1 year history. The key to answering this question is recognizing that this is MALIGNANT hypertension that is relatively acute in onset. Malignant HTN = hyperplastic arteriolosclerosis (onion rings). +
... skip_lesions is asking for clarification on nbme22
 +1  upvote downvote
submitted by skip_lesions(8)

Why would there be hyperkalemia if total body potassium is decreased in DKA?

drdoom  super high blood glucose; super high glucose spillage into urine; lots of peeing = volume depleted (“osmotic diuresis”) +
alphatnf  because insulin normally stimulates Na/K ATPase, which sequesters K inside cell. lack of insulin means that there will be more K outside of the cell causing hyperkalemia. however, you are still total body K depleted due to osmotic diuresis. so the hyperkalemia is mainly due to a shift of K from the intracellular (where the vast majority of your K is inside your body is) to the extracellular space. +
alphatnf  *where the vast majority of your K is inside your body +
... pharmtomed is asking for clarification on nbme20
 +1  upvote downvote
submitted by pharmtomed(1)

Could anyone help me on why this couldn't be C (facial portion of the homonculus in the primary motor cortex)? It explicitly mentions motor issues with the face - not just speech. I understand why it would be Broca's - that's what I put originally. But the last sentence mentioning motor disruption caused me to change my answer. Thanks.

jaeyphf  I didn't even think about the motor part during the question, but it might be related to the homonculus (FA 2020 pg 502). Motor and sensory areas of the lower face generally fall towards the lower half of the brain. Answers B/C/D would probably show some hand or arm involvement. +1
bbr  I know this isnt a great answer, but I was assuming that they wanted us to "play the game" and decide broca/wernicke. It seems set up for us answering that type of question. Going off buzzwords like "fluency", "phrase length", "comphrension". +1
... 123ojm is asking for clarification on nbme24
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submitted by 123ojm(7)

Specifically didn't choose coronavirus due to the evidence that COVID-19 is spread fecal-orally. How does it get through the GI tract if it's inactivated by pH < 6? Can someone explain why my thinking is wrong?

hello  ...COVID-19 is transmitted via respiratory droplets. +2
123ojm  Right but some research has come out saying it's also spread fecal-orally. So I'm wondering what I'm missing in this question. +
tyrionwill  Don't trust US CDC in this pandemic. They always downplayed the truth. Cronavirus does spread mainly by droplets, when they drop, they contaminate the surface, then fecal-oral could be a second pathway. Wearing mask, social distancing are both to prevent a droplet. +
boostcap23  I thought covid used to be low yield when this test was made and they didn't mention helical so I didn't pick it smh I'm an idiot. +1
... trump2020 is asking for clarification on free120
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submitted by trump2020(4)

How do we know the inferior aspect of the tube doesnt rupture, releasing fluid down in between the layers of the broad ligament?

melchior  What is special about the Pouch of Douglas is that it is the lowest point of the peritoneal cavity, so even if blood gets in between the layers of the broad ligament (which I agree with you, it looks like it should), I bet it somehow makes its way down to the Pouch of Douglas due to gravity. +2
... joanmadd is asking for clarification on nbme21
 +1  upvote downvote
submitted by joanmadd(4)

I know that small cell carcinoma wasn't an option in this question, but would there be any possible way to distinguish small cell from squamous cell on this specific gross pathology?

... irgunner is asking for clarification on nbme23
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submitted by irgunner(8)

I was thinking signal sequence on the N-terminal end that would direct the protein into the RER to be then implanted into the plasma membrane. I guess transmembrane region is the better more specific answer?

drdoom  A bilayer has hydrophobic tails (polar head + nonpolar tails). If the N-terminus could be embedded in there, it would also have to be hydrophobic; but if an N-terminus were hydrophobic, it wouldn't dissolve well in the cytosol (=mostly water). In fact, an N-terminus probably wouldn't dissolve at all. If it were hydrophobic, it would aggregate with other, nearby N-terminuses (or other hydrophobic motifs). But if that happened, shuttle proteins couldn't recognize N-terminuses in the first place (they wouldn't be sterically accessible), nor deliver them to the rER. +
... arkanaftus is asking for clarification on nbme20
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submitted by arkanaftus(8)

Is it appropriate to ask a question about the structure which is absent on the picture? It was super confusing! How can you say it was not a defect of the tissue cut?

drdoom  why did this get downvoted? +
weenathon  The missing structure is the cerebral peduncle (also called the crus cerebri). You can tell it is a good slice and not a weird cut because of the symmetry of the rest of the midbrain structures. Everything is symmetrical except the cerebral peduncles, with the left one missing. I also think it's a safe bet to say it's not a random piece of tissue missing because tissue artifact is not one of the choices. +5
... therealslimshady is asking for clarification on nbme24
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submitted by therealslimshady(11)

Given the diagnosis of AAA, why did he have syncope? I was first thinking it was from rupture, but his blood pressure is not hypotensive, so how could he get syncope from that.

Or maybe the AAA was compressing the inferior vena cava, causing syncope?

... mdmikek89 is asking for clarification on nbme22
 -3  upvote downvote
submitted by mdmikek89(-4)

Spindle cells....sarcoma or carcinoma

Kaposi *Sarcoma*...

Why y'all make this shit so complicated?

drdoom  This explanation only begs the question. (It's a tautology.) +1
... haozhier is asking for clarification on nbme21
 +3  upvote downvote
submitted by haozhier(8)

Why is it not hypoglycemia?? Hypoglycemia can also lead to seizure

cuthbertallg0od  Same thoughts here, and I think hypoglycemia occurs earlier in kids/infants than in adults (like 8 hours?) -- maybe just more likely to be hyponatremia since Na+ lost in the diarrhea... +1
fbehzadi  I think mostly the fact that 24 is not gonna reduce his glucose to the point of causing a seizure. +
fbehzadi  24 hours* +