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Comments ...

 +0  (nbme23#3)

By default you should use intention to treat analysis b/c it's the most conservative.

 +0  (nbme23#32)

You can answer by process of elimination. "Competitive interactions" makes you think stimulatory NT. Cross out GABA and glycine. In the cortex so glutamate. Metabotropic would mean there's second messengers involved and the receptor would not transmit calcium. Hence NMDA.

 +0  (nbme23#27)

If you're confused by the systolic murmur look at FA2019 p.288. ASD can cause systolic ejection murmurs in the pulmonic location (can think of it as increase turbulent flow).

Of course the more important thing is fixed splitting so SMASH away.

 +0  (nbme23#45)

In addition to what has already been said I think an important point in the question was regulatory adjustments which points more towards arteriolar regulation.

 +0  (nbme23#44)

tricky image but question is asking more specifically about his visual complaints which is just "double vision" so IR entrapment is the best answer

 +1  (nbme23#10)

I don't think you're supposed to know any complicated niche piece of knowledge. You have to infer that the pt has a skin lesion and is therefore prone to skin infections, most commonly from Staph aureus.

 +2  (nbme22#49)

the patient is pregnant so not doxy. azithro is alternative (see sketchy vid)

 +4  (nbme22#44)

Dicumarol is in the coumarin family which includes warfarin. It helps if you think about warfarin's brand name Coumadin. Coumadin, coumarin, dicumarol...all the other derivatives have COUM it in some fashion

 +2  (nbme22#45)

neuroendocrine cells doesn't always mean neural crest

 +3  (nbme22#38)

literally know every single name they can possibly call this

djtallahassee  literally a new name every nbme

 +0  (nbme22#2)

from uworld: fibrates activate PPAR-alpha to increase LPL and decrease VLDL production

 +1  (nbme22#46)

uworld says somewhere that testosterone increases hematocrit, increases LDL, and decreases HDL

 +1  (nbme22#43)

got confused by the systolic pulsation of the liver but basically regurgitant blood from RV will go into RA > IVC > hepatic veins

 +1  (nbme22#8)

the question can easily be misinterpreted. it's asking for urinary pH, urinary bicarb, and urinary volume

 +0  (nbme22#30)

hit the kidney so retroperitoneal. leaves only the duodenum and splenic flexure. kidneys are more lateral structures so splenic flexure (at turn of descending colon)

 +0  (nbme22#7)

Pretty much if they can masturbate or get it up alone in any way their nocturnal tumescence should be normal meaning that their innervation and reflex pathways are all intact. Libido aka sex drive from what I’ve seen so far is altered by depression. So like in the question on NBME 21 the stem stated that screening for depression was negative which is why libido would also be normal in this case. If there’s ever a Q with a depressed guy and normal lab values and physical exam, most likely gonna be decreased libido with normal night erections - courtesy of /u/diffuseaxonalinjury

 +1  (nbme22#30)

you need to add an amine (nitrogen) and most biochem processes from sugar --> amine requires glutamine

 +0  (nbme22#35)

Super annoying they are using the same picture BUT you can answer with process of elimination. No mass in the picture so not nephroblastomatosis or RCC. 4 year old so not amyloidosis. Stem does not really cue you into membranous GN. Instead it talks about UTIs which would have inflammatory processes --> interstitial inflammation.

 +0  (nbme21#26)

Cecum is intraperitoneal even though it's part of the ascending colon

 +3  (nbme21#8)

Euthyroid sick syndrome = levels of T3 and/or T4 are abnormal, but the thyroid gland does not appear to be dysfunctional. The classical phenotype of this condition is often seen in starvation, critical illness, or patients in the intensive care unit. The most common hormone pattern is low total and free T3, elevated rT3, and normal T4 and TSH levels.

 +0  (nbme21#39)

FA19 p.233 cortisol has a permissive effect on catecholamines

 +0  (nbme21#25)

unequal BP/pulses in the arms is a big key for aortic dissection

 +2  (nbme18#18)

Increased pressure is in the Bowman space (NOT the glomerular capillaries) so the only pathology listed that would cause backward build up of pressure is BPH

Subcomments ...

submitted by sugaplum(122),

phenylpropanolamine is an alpha agonist that stimulates urethral smooth muscle contraction. - from uptodate, however, it also says it is not recommended treatment anymore

ugalaxy  α1 stimulation (via α1 agonist) constricts the bladder sphincter thereby, preventing sudden bouts of micturition during coughing/sneezing (abdominal stress). +5  
sammyj98  I thought that B3 stimulation stopped urination +4  
adong  @sammyj98 B3 would facilitate bladder relaxation +  
hvancampen  @sammyj98- were you thinking of oxybutynin? (thats what I thought of!) According to FA, its used for urge incontinence not stress. +  
drzed  Nah he/she's talking about Beta-3 receptors which are Gs coupled. Gs increases cAMP thus it would cause smooth muscle relaxation -> bladder relaxation! +  
donttrustmyanswers  From Mayo: "There are no approved medications to specifically treat stress incontinence in the United States. The antidepressant duloxetine (Cymbalta) is used for the treatment of stress incontinence in Europe, however." +1  

submitted by hayayah(599),

Coloboma is an eye abnormality that occurs before birth. They're missing pieces of tissue in structures that form the eye.

  • Colobomas affecting the iris, which result in a "keyhole" appearance of the pupil, generally do not lead to vision loss.

  • Colobomas involving the retina result in vision loss in specific parts of the visual field.

  • Large retinal colobomas or those affecting the optic nerve can cause low vision, which means vision loss that cannot be completely corrected with glasses or contact lenses.

mousie  thanks for this explanation! +  
macrohphage95  can any one explain to me why not lens ? +  
krewfoo99  @macrophage95 Lens are an interal part of the refractive power of the eye. Without the lens the image would not be formed on the retina, thus leading to visual loss +2  
qfever  Do anyone know why not choroid? +  
adong  @qfever, no choroid would also be more detrimental to vision since it supplies blood to the retina +2  

submitted by alexb(31),

Since there were "small amounts of meconium" I thought it couldn't be atresia. Turns out atresia isn't always absence of lumen, it can also be abnormal narrowing of lumen, allowing just a small amount to pass through...

adong  I don't think that's true, atresia literally means closure/absence of the lumen. I also got tripped up by the meconium but that could be just GI epithelium that was shed while in utero etc. I wouldn't change your definition of atresia. +1  

submitted by pitaziki(-2),

Why is the answer fibularis brevis and not fibularis tertius? How do you distinguish between the two from this vignette?

gainsgutsglory  tertius is an anterior muscle and overlays the dorsum of foot as it fans out to the toes. Does not relate to the lateral malleolus. +  
adong  wrong question to post on agree with above +  

submitted by gh889(55),

From ShoryukenHadooken on reddit:

What the question is getting at is the sympathetic chain was spared. It was a terrible way of wording it.

Your anterior hypothalamus is responsible for cooling features and is under parasympathetic control. A lesion would cause hyperthermia.

Your posterior hypothalamus is responsible for heating when you're cold and to generate the Fever response and is under sympathetic control. A lesion would cause hypothermia.

In this question it is simply asking a person gets sick, hypothalamus was spared, what happens.

Answer: hypothalamus will still be able to elevate set body temperature to battle infection.

Hint: IF they give a question similar to this but reworded to include a lesion of the sympathetic fibers or of the hypothalamus, you would in turn NOT be able to generate a fever response to infection. The hypothalamus would be entirely under parasympathetic control

This adds more context to the fact the Q states that the sympathetics was spared

oslerweberrendu  So, this says sympathetic also spared and hypothalamus also spared. Then what was wrong with this clinical case?? +  
adong  i think the sympathetic system is actually impaired b/c it's cut before it can "outflow"...at least it's the only way this makes sense +1  
suckitnbme  I agree. I think the question stem is saying the sympathetics were lesioned. Not that they were spared. +2  

submitted by sinforslide(23),

Male internal genitalia -> Intact SRY , testes, and testosterone.

No female internal genitalia -> Presence of MIF (antimullerian hormone) and intact Sertoli cell function.

Female external genitalia -> No androgen present, which is required for male external genitalia formation.

d_holles  Not sure I understand why T is wrong, but DHT is correct. +  
d_holles  I thought about this some more -- DHT forms external genitalia while T forms 'male genital ducts'. That's why the correct answer is DHT, not T, since the PT had +ext genitalia, but -internal genitalia. I was thinking that the PT had CAIS, but that would lead to testes only w/o male genital ducts. See FA2019 p608. +2  
d_holles  *I meant -ext genitalia, +int genitalia +  
adong  T is wrong because you still need T to make the internal male organs which he has based off the MRI +1  

If both HCTZ and loop diuretics were provided as an answer choice, further clue that hctz would be the answer choice is the presentation of the patient "feeling funny". This suggests hypercalcemia (psychiatric overtones) which is a side effect unique to HCTZ.

adong  there wasn't any loop diuretics... +  
the_enigma28  Good explanation!! +  

submitted by hello(145),

The Q stem states FOXO is a transcription factor that responds to insulin signaling by altering the transcription of metabolic genes --> therefore, FOXO is a transcription factor involved in metabolism. This should make sense because insulin-receptor activation has a role in regulating metabolism.

This Q asks about reversible ways that insulin reguates FOXO transcrption factor activity.

Ubiquitin-mediated proteolysis is irreversible. Eliminate all choices except for B, D, and H.

Insulin-receptors function through PI3K signaling. PI3K signaling involves phosphorylation of serine --> serine phosphorylation is a reversible process. Eliminate H. FYI: protein/amino acid phosphorylation is always reversible.

You are left with choices B and D.

FOXO is a transcription factor --> transcription factors mediate gene activity by shuttling between the cytoplasm and nucleus. Regulating the location of FOXO transcription factor (i.e. cytoplasm vs. nucleus) will therefore reversibly modulate FOXO-mediated metabolic gene activity.

This leaves you with the correct answer: Choice B.

adong  A better way to think about it is insulin acts through MAPK which is a serine/threonine kinase +  

submitted by strugglebus(96),

Lysine is used in elastin and collagen cross linking; it is cross linked by lysyl oxidase to make collagen fibers

charcot_bouchard  Thats my brother from UFAP mother +1  
smpate  but glycine and proline are used in elastin too. Seems like you'd have to know about desmosine though that's not in first aid. Or maybe you can infer lysine since it's charged and is probably more important in maintaining stability? +  
adong  the only thing we know about cross-linking is with LYSYL oxidase, hence lysine +1  

submitted by aj32803(1),

Uworld specifically says that Psoas abscess means the patient will prefer flexion to avoid stretching the muscle. That's why Psoas did not make sense to me since the patient preferred extension, which would be stretching out the muscle.

On the other hand it's right on the vertebra and it's associated with TB.

adong  it's confusing but i think b/c psoas acts to flex at the hip, staying completely flat would keep the muscle from being contracted. uworld is talking about the psoas test which would end up hyperextending the psoas muscle which would elicit pain (psoas test can also be done with active flexion against pressure which would explain the not wanting to flex). +  
kamilia20  First ideal to my mind is that:patient is a TB, TB prefer psoas +  

submitted by dr_jan_itor(40),

Can anyone answer why this one can't be F. Beta thalasemia major? I was thinking becaues of his anemia and the "european descent" which includes the mediteranian europeans. Unless NMBE writers think that european only means the ones with extra white people lol

dickass  European implies northern european (they even specified the patient was a person of pallor), mediterranean descent is usually implied by country of origin or by straight-out writing 'mediterranean'. +  
poisonivy  The MCV is normal, thalassemias are microcytic anemias, that hint helps to rule out the thalassemias. However, I got it wrong, not sure why it cannot be a homozygous mutation in the ankyrin gene +1  
adong  @poisonivy, other commenter pointed out it's autosomal dominant so best answer would be heterozygous +  

submitted by ye2019(1),

Physical exams showed tenderness of costophrenic angles, which are the places where the diaphragm (-phrenic) meets the ribs (costo-). Not the Costovertebral angle tenderness that we think to hint renal disease.I got confused with this point.

adong  honestly think this was a typo. hot trash +  
neovanilla  Assuming it was not a typo, how would the costophrenic angles be tender in this condition? ...From crying...? +  

submitted by step1soon(26),

Anything upper lip + above → basal cell carcinoma

Anything lower lip → Squamous cell carcinoma

FA 2019 -pg 473

adong  it's saying upper vs lower lip. this pt has it on the nose +  

This is LITERALLY the same photo they used to describe the 4-year-old boy with diffuse cortical necrosis from NBME 18. Can someone explain what's going on here

lancestephenson  *Tubular atrophy, not cortical necrosis lol +  
charcot_bouchard  Can u fuckers talk about spoilers +1  
adong  same photo because the end gross pathology is the same. whether it's due to cancer or whatever the 4 year old boy had (some sort of obstruction IIRC) it ends with atrophy of the kidneys +  

This is how my brain farted while I was doing this question.... I wanted to choose TBG deficiency, but I kept thinking that if TBG is deficient, that means there are less or no binding proteins in the blood. And how can the free T4 be normal? Shouldn't free T4 increase if there were less T4 binding protein? ...

adong  free T4 wouldn't increase because it would be sensed by the pituitary and TSH would drop until free T4 normalizes +