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free120  nbme24  nbme23  nbme22  nbme21  nbme20  nbme19  nbme18  nbme17  nbme16  nbme15  nbme13 
Welcome to notyasupreme’s page.
Contributor score: 3


Comments ...

 +0  (nbme16#21)

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

 +1  (nbme16#48)

I was thinking it could be 22q11 microdeletion because that also would have abnormal organs (heart, thymus, parathyroids) and abnormal face. So, I'm just wondering how you're supposed to definitely know it was Trisomy 21. I had the original answer too, damnit!

nbmeanswersownersucks  I think it's more because a spontaneous microdeletion would not really explain the previous lost pregnancies whereas an unbalanced translocation in the mom could. And I think it could be any of the big trisomies (13, 18, 21) but 21 is most common. +




Subcomments ...

submitted by sahusema(124),
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hatW a GEBGARA .ionsuetq eH was giatne etsafakrb 2 hrsuo gao usjt fein nad now ew rae dssueppo ot aveh teh afylmi ecom ot a sncsesoun obuta a gdenfei etub keil he's on shi tehad dbe? TLLBIUHS

daddyusmle  Did you get the question wrong? +  
notyasupreme  ^ ummm.. chile anyways.. +  


submitted by benzjonez(36),
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olwrUd Qdi 5341 ahs a good ontaxeaipln sa to ohw pauylmnro fosisrbi saneiersc hte aidalr trcoaitn on eht riaway slaw.l

cienfuegos  I think this is it -pulmonary fibrosis increases elastic recoiland widens airway 2/2 increased outward force (radial traction) by fibrotic tissue thus decreasing airflow resistance thus supernormal expiratory flow rates (higher than nl following correction for lung volume) +2  
notyasupreme  ^ Why do I feel like this is literally not english, I have no clue what's being said here. Can someone else explain it? +  


submitted by taway(26),
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hisT qtunsieo si raphdse sy,gnalret tub s'ti nslsetelaiy knsiga thaw" duolw hpnpae fi this mswon'a tiodhhsmyroipy cembea tlcruolonnde oevr eht uecsor fo her ape"ynngc?r

rntuycrel hre TSH is ogdo &-tg;- l-lwcnodeertoll CmTPyHtyLYdsHipIoETAioOhhr ghih STH gt-&;- hre sophriiyoydmth ustm TON be coe-lwontelrlld ed(u ot poduritnis of hte TH/THRT/TS4/3 eioncerdn )isxa

oS, won htta we sadduetrnn that het tioqnuse is saking wta"h ulodw ahpnpe fi hre soyhidiomrhpty aws "od?ltnorlucne

snAew:r csntermii

I ikthn thta this stqounie is sheprad uoat,syrilco utb raf eb it from em to cctiieizr hte ELUMS sgilecinn db..a.ro

yotsubato  I think that this question is phrased atrociously, Just like the rest of the NBME +10  
b1ackcoffee  exactly how does maternal hashimoto can cause cretinism? +  
notyasupreme  @b1ackcoffee, it's not maternal hashimoto, basically you just have to disregard the ENTIRE question stem and the last part of the sentence (if the mom's TSH goes up) means that there's hypothyroidism going on, which causes cretinism. +  


submitted by meningitis(424),
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eWnh ingdsnat ,pu eht doby allromyn vtcaeiats yapihtmctse tsymse ot aovid oittrchotas tnhinpooe.ys

Btu nsice htere si onw na iatdveid tfefce of eth occaerhhoompotmy eresnda,ricg it llwi laed ot a shneonytepri

e:.i( blueDo ionciossrtcvaotn = Pheo genaicsrred + aecpShmtyit my)stes

sympathetikey  Brilliant. +4  
medschul  Would pheo have a normal resting BP though? +4  
meningitis  I was trying to justify these tricky questions but very true medschul.. It shouldn't have normal resting BP. Sometimes it seems these NBME always have a trick up their sleeve. Im getting paranoid lol +  
nala_ula  The reason why the patient probably has normal HTN is because Pheochromocytoma has symptoms that occurs in "spells" - they come and go. Apparently in that moment, when the physician is examining her, she doesn't have the HTN, but like @meningitis explained, so many adrenergic hormones around leads to double the vasoconstriction when the patient stands up. +7  
meningitis  Thank you @nala_ula for your contribution! Really filled in the gap Iwas missing. +1  
nala_ula  No problem! Thank you for all your contributions throughout this page! +1  
mjmejora  I thought the pheochromocytoma was getting squeezed during sitting and releasing the epinephrine then. kinda like how it can happen during manipulation during surgery. Got it right for sorta wrong reasons then oh well. +  
llamastep1  When she sits in the examination table there would be a normal activation of the sympathetic system from the stress of getting examined which is amplified by the pheo. Cheers. +  
sammyj98  UpToDate: Approximately one-half have paroxysmal hypertension; most of the rest have either primary hypertension (formerly called "essential" hypertension) or normal blood pressure. +  
hello_planet  FA 2019 pg. 336 +  
notyasupreme  Damn llama, that is WAYYY too much of an inference. Maybe if they said she was nervous in general or something, but not everyone gets stressed out by a doctor hahaha +  


submitted by saqeer(2),

Remember pheocrhomocytoma leads to high EPO, which leads to polycythemia and flushing seen in this patient

notyasupreme  I thought from the 5 Ps of pheochromocytoma, Pallor was one of them? That's what threw me off from keeping it the same.. Or atleast the anking deck says pallor. +  
saqeer  the way i understand it the pallor is because of the sever vasoconstriction during an episode of catcholamine release but in general anything leading to polycythemia can lead to flushing +  


submitted by cassdawg(610),

Sildenafil is a PDE5 inhibitor that runs the risk of causing hypotension in patients on nitrates due to the synergy of the mechanisms of action. [FA2020 p246]

Nitrates, like nitroglycerin, work by increasing NO production which in turn acts to increase cGMP in smooth muscle causing vasodilation. PDE5 inhibitors act by decreasing the breakdown of cGMP in smooth muscle, enhancing the action of NO to cause vasodilation. Thus, when combined there can be systemic vasodilation that leads to dangerous hypotension.

lee280  For some reason, I had two answers that I felt like both made absolute sense to me. As explained above, that totally came to my mind and I knew this was the case. When I thought about Metoprolol blocking B1 receptors in a patient with an ejection fraction of only 30%, I was thinking this could as well be a contraindication, not sure if it's an absolute one or relative. Now, am I right if I said that Beta-blockers are only contraindicated in acute decompensated HF? and can be used unless otherwise? Someone, please help me clarify this, so then this distinction can come clean in my thoughts. Thanks +2  
notyasupreme  I thought the same thing as you, I think we're just overthinking the most important thing - never give antihypertensive with Viagra lmfao. I totally thought too deep into it. +  


submitted by bingcentipede(129),

Clomiphene is a SERM that antagonizes estrogen receptors in the hypothalamus.

If estrogen is antagonized there, there is decreased negative feedback to improve FSH and LH release to stimulate ovulation. This is very important in PCOS and other disorders with decreased fertility.

notyasupreme  I guess I wasn't sure because it said FSH and LH levels were normal, so I assumed the problem was with progesterone. But I thought too deep into it and should've just went with my gut. +  
feochromocytoma  Clopmiphene is usually the answer for infertility with NORMAL anatomy and NORMAL appearing labs +  
drdoom  very nice +  


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  


submitted by barbados(2),

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. +5  
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... +  


submitted by bingcentipede(129),

IV normal saline will increase hydrostatic pressure in the vasculature. This isotonic solution is freely filtered across the capillaries, which is collected by lymphatics and can be picked up in this experiment.

motherhen  Why does albumin solution not have this effect? +2  
notyasupreme  I think it's because albumin in saline is hypertonic, which would cause the opposite effect of what the experiment was going for. Fluid would go across the capillaries into the vasculature, rather than vice versa. +1  


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 +  


submitted by andro(126),

Fatty Acid degradation
-Occurs in mitochondria or peroxisomes

First step - uptake of the fatty acids by the cell and addition of CoA to them

Second step - Uptake of the Fatty Acyl CoA molecule into the mitochondria by the Carnitine Shuttle *( which involves removal and then addition of the CoA molecule again to the fatty acid once inside the mitochondria)

Once in the mitochondria the fatty acid may undergo , Beta-oxidation ( a process in which a fatty acid is oxidized/cleaved at the Beta carbon to generate Acetyl CoA in several cycles )

An Acyl CoA dehydrogenase catalyzes the initial step .
Look out for Hypoketotic Hypoglycemia in defects of fatty acid degradation

The 2 main subtypes to be aware of are -a problem with the carnitine shuttle ( systemic carnitine deficiency) - or with an Acyl CoA dehydrogenase ( eg MCAD deficiency )

notyasupreme  It's actually funny because the question stem makes it seem like it's an MCAD deficiency (presence of dicarboxylic acid) and all the symptoms, but then treat it with MCAD. Whatever, I got it right but it just felt like a weird question to me. +  
nbmeanswersownersucks  yeah I was confused too but I also think the negative serum carnitine is supposed to help r/o MCAD deficiency since that usually has elevated serum carnitine. +  
baja_blast  If Carnitine was an option here, how could we differentiate this from primary carnitine deficiency? Would it have been possible? +2