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Welcome to j44nโ€™s page.
Contributor score: 141


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 +0  visit this page (nbme20#49)
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I hated everything about these answer choices

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 +4  visit this page (nbme17#0)
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Dr. Sattar for the win, this is a reperfusion injury. The cells dont have ATP so they cant run reduction reactions when they get 02 again. Its like being bankrupt they cant "pay" for thing like glutathione system etc so they get a build up of free radicals and free radicals cause lipid peroxidation

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 +0  visit this page (nbme17#49)
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this was kind of a garbage question because she's still having normal periods, she hasnt hit menopause yet but shes close. What sells it it the BMI of 27 which is techncially overweight (normal BMI ends at 25) so the elevated fat is causing her to have hyperplasia from all the estrone coming from her fat. So during her proliferative phase the added estrogen from her fat is causing it to be overdone

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 +1  visit this page (nbme17#50)
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you cant blame anyone for your being late. You have to deflect and stay broad because it creates a distrust in the medical system all the other ones place blame else where or make you look like the encounter isnt a priority

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thegout  idk why this wasnt as obvious to me, i picked the apology followed by this wont be long. I thought if i apologise and bring up her being late, it might just trigger her further if she really is late. +2
whoopthereitis  I put that answer too, I think that by saying "but this won't take long" can be considered as you promising the patient something that you can't guarantee. And also like you are going to rush the experience afterward because of your mistake or tardiness whatever. +1

 +1  visit this page (nbme17#29)
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the semantics of this question made me want to put my fist through my laptop screen

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 +0  visit this page (nbme17#40)
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this lady has eithe OCD or an anxiety disorder both first line for tx is an SSRI-> she washes her hands 30x a day and wakes the poor baby up 14 times a night. She's got multiple repetitive behaviors that aren't productive to solving the perceived problem

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 +0  visit this page (nbme20#17)
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Possible causes of galactorrhea include: Medications, such as certain sedatives, antidepressants, antipsychotics and high blood pressure drugs. Opioid use. Herbal supplements, such as fennel, anise or fenugreek seed

^ from the mayo clinic.... emphasis on the HTN drugs

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 +2  visit this page (nbme19#0)
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the way I approached this was that it didnt increase the amount of substrate to reach vmax so it couldnt have been any kind of comp inhib, also the efficacy is the same so it couldnt be an allosteric inhib

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 +0  visit this page (nbme19#39)
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I picked the adrenal glands because cortisol has a permissive effect on blood pressure and gluconeo

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 +1  visit this page (nbme24#18)
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I hate these so much these questions give me MCAT PTSD

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 -1  visit this page (nbme24#35)
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Just another piss poor government institution cutting corners. If you've done NBME 18 and seen the cell diagram figure it is the literal pinnacle

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drdoom  the NBME is a private, for-profit corporation. individual U.S. states use its products (i.e., the certification it gives you when you pass their exams) to determine your eligibility to practice in their state. but they are not a government entity. +1

 +0  visit this page (nbme24#4)
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For as much money as the NBME scams off of us they really do give you the most HEINOUS figures... if you've done NBME 18 there's a cell diagram that looks like the test writers toddler drew.

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 +0  visit this page (nbme24#30)
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AT-II is the main stimulator of aldosterone release. This is kind of bull shit because that was the answer to one of the other NBME questions in ACTH cushing's disease "wHaT pArT oF tHe GlAnD iSn'T eNlArGed?"

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 +0  visit this page (nbme24#50)
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this is how I looked at it extra cellular osmoles> intracellular so it will pull the h20 out.... then the high osmotic pull of the sugar overwhelming the SGL2 transporter in the kidney will pull the h20 out of the body dehydrating the extracellular compartment

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j44n  also the brain/CNS/neurons have the highest affinity GLUT transporters.... thats why giving glucagon brings someone out of hypoglycemia when theyre passed out. The glucagon increases the blood sugar and it goes straight to the brain restoring concious +

 +0  visit this page (nbme24#19)
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The only reason I got this right is because I did a study for a practice on surgery cancelation rates and when we did lit review I read a paper that in middle eastern countries in areas where they are very very conservative muslim a lot of surgeries get canceled because their husbands dictate all of their care or can't be there to see their wives during the surgery. I think they're just wanting you to see the cultural difference and be aware of it. Which unless you haven read that one specific paper is like trying to see something with the sun in your eyes. Not defending the NBME but this question was garbage and almost as much bull shit as the platelet question

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 +0  visit this page (nbme24#5)
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I got thrown off because there's an arrow point to the three unaffected daughters (with an affected father) so I thought XLR because they'd be carriers. And there was no generation skipping so that made me think AR

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Subcomments ...

submitted by flapjacks(110), visit this page
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My reasoning for this question:

  • In both situations, you see a cyclical increase in pain before receiving the injection. This could be seen if the effect was wearing off; however, if you notice, there is a decrease in pain before the injection is even given. I believe this implies that something inherent about the injection is providing pain relief.
  • Furthermore, both curves follow the same path with an eventual decrease in pain, regardless of intervention.
  • Maybe an additional point - I am not questioning their pain, but fibromyalgia typically shows no abnormal lab results in addition to typically coexisting with some form of mental pathology. I don't think placebo being demonstrated is far off.
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j44n  I agree that was my though process, except i didnt notice the decrease before the injection, good eye! also the other answers didnt really apply regression toward the mean is the phenomenon that arises if a random variable is extreme on its first or first few measurements but closer to the mean or average on further measurements and there was no way for us to know about confounding or their selection procedures so from that we couldn't really know about the types of errors they made +3


submitted by beastaran1(2), visit this page
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Believe this one is tubulointerstitial fibrosis of the kidney:

medullary cystic disease is characterized by autosomal dominant inheritance pattern progressive and slow impairment in renal function that ultimately results in end-stage renal disease no or minimal proteinuria with a bland urine sediment medullary cysts on renal ultrasound in most cases medullary cysts are not present can see shrunken kidneys on ultrasound

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makepoopinggreatagain  Tubular atrophy (hint: dilated ureter/calyx in image) โ†“ Posterior urethral valves is the 1 cause of bladder obstruction in males ...Diagnosed by hydronephrosis and thick walled bladder +
nbmeanswersownersucks  this can't be posterior urethral valve because then both kidneys would be effected. +9
j44n  I agree its the medullary cystic kindey disease-> FA19-592 talks about it +


submitted by motherhen(69), visit this page
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Are these gottron's papules from dermatomyositis? Pareaneoplastic syndrome from adenocarcinoma, esp ovarian?

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j44n  it is not. The pt has a history of being immunocompromised. Also, gottron's are over the hands and dermatomysitis can present with a rash over the eyelid as well! There is also no history muscle weakness at the proximal muscles (shoudler/ hip area) and no mention of an elevated creatine kinase! - hope this helps :) +2


submitted by nwinkelmann(366), visit this page
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Does anyone have a good explanation for why decreased levels of inhibin is wrong? From my understanding, inhibin and activin work together, in that inhibin binds and blocks activin leading to decreased feedback on hypothalamus and activin increases FSH and GnRH production.. thus, if you decrease inhibin then you would have increased activin which would lead to increased GnRH and FSH, right? I found one article talking about it in regards to puberty, but it seems to be a hypothesis/not confirmed at this point... is that why? But still... how do I rule it out on a test?

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yb_26  I also picked decreased inhibin. may be it was one of the "experimental questions", which are not even counted on the real exam +2
artist90  Inceased FSH will lead to spermatogenesis and spermiogenesis NOT Increase in Testosterone which is causing increased Height of this pt +7
artist90  Inhibin B only has negative feeback on FSH not GnRH. see the diagram on the topic of semineferous tubules in FA. Testosterone has a negative feedback on BOTH LH and GnRH +3
usmile1  Kind of like how nocturnal pulsatile GNRH release occurs during sleep to stimulate growth (FA page327), the same thing happens for puberty. Pg 325 in FA, "pulsatile GnRH leads to puberty and fertility." It doesn't explicitly state during sleep, but pulsatile release of GnRH leading to pulsatile release of LH and FSH will lead to puberty. Puberty starts in the brain, its onset really has nothing to do with decreased inhibin levels which happens in the testes. hope that makes sense! +4
sars  From what I understand, inhibin is only released by granulosa cells when FSH levels are high. This is a boy. Next off, this question is about puberty, which is due to pulsatile GnRH leading to large amounts of LH and FSH, leading to large amounts of dihydrotestosterone (males) and estradiol (females), and eventually secondary characteristics of puberty. The increased pulse of estrogen and testosterone leads to GH release, which is metabolized into IGF-1 in the liver. This leads to long bone growth from what I understand, which is not much. +1
cassdawg  @sars inhibin B is also released by sertoli cells in males and will feedback to inhibit FSH release, its not just a female thing. Also, there is actually an inhibin B pubertal surge in both females and males that corresponds to maturation of the granulosa and sertoli cells, respectively. Hormones are wack. https://pubmed.ncbi.nlm.nih.gov/15319819/ +1
j44n  I think youre just supposed to see that he's starting puberty and know that the nocturnal pulses are involved +1


submitted by madojo(212), visit this page
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https://www.sketchymedical.com/products/catalog

CORONAVIRUS SKETCHY

positive sense RNA virus, sun crown corona king wearing robe - encapsulated helical virus - spiraling road, helical trees sneezing and blowing king - common cold with bronchiol tree on king pointing to SARS and middle east respiratory syndrome (acute bronchitis)

This virus replicates in the cytoplasm thats why King is outside his castle (nucleus)

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j44n  I'm so glad i dont have to take step one once they discover all this shit about the new corona strain. +


submitted by cassdawg(1781), visit this page
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My dumb ass thought ketonemia was like anemia of ketones or something and thus meant low ketones so I almost put fatty acid oxidation (hypoketotic hypoglycemia). FYI ketonemia is high ketones.

Defects in fatty acid oxidation would also be corrected with the sugar additions so even if you suck at medical vocab you could rule it out.

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j44n  if it was glycolysis they wouldnt be able to metabolize the galactose either, a defect in glycogen breakdown/glycogenolysis would't effect the immediate metabolism of a monosacharide it would effect the long term storage of it. I don't think we were supposed to know what disease this is I think we were just supposed to think about the metabolism of the three sugars in question. Hexokinase only converts fructose when it is extremely overloaded with fructose(it has a low affinity for it... they'll never say that so lets say "high Km"). Glycogen synthesis happens over time and he had poor feeding for 3 days so his glycogen would already be gone and he would be immediately symptomatic the second his blood glucose dropped +


submitted by lsmarshall(465), visit this page
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Synaptobrevin is the target of tetanospasmin (tetanus toxin); muscle spasms are characteristic. Only other answer you might consider is Acetylcholinesterase since he is a farmer and buzzwords often carry us to the promised land... but symptoms of a cholinergic storm are absent.

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vshummy  Synaptobrevin is a SNARE protein. Why they couldnโ€™t just give us SNARE Iโ€™ll never know. +52
yotsubato  Cause they're dicks, and they watched sketchy to make sure our buzzwords were removed from the exam +53
yotsubato  Oh and they read FA and did UW to make sure its not in there either +42
soph  This toxin binds to the presynaptic membrane of the neuromuscular junction and is internalized and transported retroaxonally to the spinal cord. Enzymatically, tetanus toxin is a zinc metalloprotease that cleaves the protein synaptobrevin, an integral neurovesicle protein involved in membrane fusion. Without membrane fusion, the release of inhibitory neurotransmitters glycine and GABA is blocked. -rx questions! +6
qfever  So out of curiosity I checked out B) N-Acetylneuraminic acid It's sialic acid typical NBME +2
alexxxx30  shocked they haven't started calling a "farmworker" a "drudge" <-- word I pulled from thesaurus. +3
snripper  "You shouldn't memorize buzzwords. You gotta learn how to think." Lemme pick another random ass word that doesn't have anything to do with critical thinking skills and use it instead. +10
mw126  Just as an FYI, there are multiple "SNARE" Proteins. Syntaxin, SNAP 25, Synaptobrevin (VAMP). From google it looks like Tetanospasmin cleaves Synaptobrevin (VAMP). Botulism toxin has multiple serotypes that target any of the SNARE proteins. +2
wrongcareer69  Here's one fact I won't forget: Step 1 testwriters are incels +4
baja_blast  FML +
j44n  its not an ACH-E inhib because he doesnt have dumbell signs +
flvent2120  I'm not even mad I got this wrong +
ooooopss  Buzzwords often carry us to the promised land im dyingggg. It's 9pm and I'm cracking up LOL +


submitted by sympathetikey(1600), visit this page
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As per Pathoma,

"Vascular permeability occurs at the post-capillary venule"

This is why, when you have edema, you would have gaps in the venules.

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j44n  that was my exact reasoning +3


submitted by lsmarshall(465), visit this page
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MHC class 1 peptide antigen processing > "Antigen peptides loaded onto MHC I in RER after delivery via TAP (transporter associated with antigen processing)" - First Aid 2019.

Bare lymphocyte syndrome type 2 (BLS II; affecting MHC II) is due to mutations in genes that code for transcription factors that normally regulate the expression (gene transcription) of the MHC II genes. Bare lymphocyte syndrome type 1 (BLS I; affecting MHC I), is much more rare, and is associated with TAP deficiencies.

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tyrionwill  in the question, it says absence of MHC-I presenting cells. I guess the meaning is lack of MHC-I. IF TAP is missing or dysfunction (bare lym syn type-1), MHC-I should be there, however Ag cannot be loaded to the MHC-I. Can anyone help me to understand more. +1
peridot  @tyrionwill From wiki: "The TAP proteins are involved in pumping degraded cytosolic peptides across the endoplasmic reticulum membrane so they can bind HLA class I. Once the peptide:HLA class I complex forms, it is transported to the membrane of the cell. However, a defect in the TAP proteins prevents pumping of peptides into the endoplasmic reticulum so no peptide:HLA class I complexes form, and therefore, no HLA class I is expressed on the membrane. Just like BLS II, the defect isn't in the MHC protein, but rather another accessory protein." +1
j44n  i hate this question because MHCI is on all nucleated cells. So this person is literally a bag of RBC's +1
soccerfan23  @j44n Not quite. It's true that MHC I is on all nucleated cells. Because of the TAP mutation, these cells don't express MHC I on their membranes. But these cells still exist. That is what is meant when the vignette says "flow cytometry shows absence of class I MHC-expressing cells. +1


submitted by seagull(1933), visit this page
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at BMI 15 not only has she never had a period but she never had a meal.

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sympathetikey  You're on fire man lol +2
monkey  How the fuck is it not related to anorexia nervosa is beyond me. +4
avarkey  the blind vaginal pouch points away from it being anorexia related +5
j44n  Its actually a man, there's no DHT to to dev the external genitals. +1
am4140  @monkey - with real anorexia, she wouldnโ€™t necessarily have boobs either. If sheโ€™s got boobs she has the nutrition to develop boobs. That was my thought. +
freckles  the patient is actually what ever gender they want to identify as. If this was a 5 alpha reductase deficiency the patient would have experienced masculinization of external genitalia during puberty when testosterone levels increase significantly. The pt most likely has Androgen Insensitivity Syndrome. +7
weirdmed51  BLIND VAGINAL POUCH = never ever ever in anorexia nervosa! It is an anatomical defect, hence not psych prob. +


submitted by suckitnbme(239), visit this page
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Tfw NBME said there's no repeats on 23 and 24 and then you get a repeat.

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j44n  The NBME is full of shit... they also say there's "no trick questions" +3


submitted by j44n(141), visit this page
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this is how I looked at it extra cellular osmoles> intracellular so it will pull the h20 out.... then the high osmotic pull of the sugar overwhelming the SGL2 transporter in the kidney will pull the h20 out of the body dehydrating the extracellular compartment

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j44n  also the brain/CNS/neurons have the highest affinity GLUT transporters.... thats why giving glucagon brings someone out of hypoglycemia when theyre passed out. The glucagon increases the blood sugar and it goes straight to the brain restoring concious +


submitted by misterdoctor69(70), visit this page
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Mixed up cytoscopy with culposcopy so I put HPV. Insert upsidedownsmileyface.jpg

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j44n  if it makes you feel better I miss ID'd the PCT not once but twice on this exam +3
tobias  Same!I was so confused by why I got the answers wrong. +2


submitted by enbeemee(12), visit this page
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i get why it's hyporeflexia, but why not fibrillations? it's also an LMN sign

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et-tu-bromocriptine  Imagine a simple reflex arc: you have an afferent neuron, some interneuron shenanigans, and an efferent neuron (aka LMN neuron). If you damage the LMN, you will get hyporeflexia (due to damaged reflex arc) and fibrillations (because your LMN won't be able to effectively contract muscle on command). However, if you damage the afferent part of the arc, you will still get a damaged reflex arc (hyporeflexia), but your motor neuron will still be able to do its stimulating effectively, so your muscles won't show weak contractions when stimulated by a higher pathway. Kinda confusing but I hope I made it a tad simpler! +18
eli_medina9  https://imgur.com/1z4OF4l Gonna piggy back off your comment and just post this kaplan image +12
hungrybox  Very helpful image, thanks bro +
j44n  its not a efferent motor neuron its the sensory/afferent branch +


submitted by sympathetikey(1600), visit this page
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Everyone who got this question right is a cop. เผผโŒโ– ู„อŸโ– เผฝ

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dr_ligma  Fkn narcs +2
j44n  whippet_gang +


submitted by sweetmed(157), visit this page
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Testicular torsion mostly happens in young boys, rarely in adults. Also the pain started at the flanks, which is not how torsion pain starts.

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j44n  I actually had testicular torsion and my pain started in my appendix area and by the time I got to the hospital it localized to my testicle +3


submitted by colonelred_(124), visit this page
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The diagnosis is strawberry hemangioma, commonly happens in kids, often resolves on its own as they get older.

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shaeking  A strawberry hemangioma is normally pink or red (which is why it is named strawberry). The description has a flat purplish lesion which makes me think of a port wine stain on the face. How do you know to think of strawberry hemangioma over port wine based on this question stem? +4
seagull  the age is key here. Newborns have strawberry hemangiomas typically on their face. Sturge-Weber could also be the case but none of the answer choices matched to that description. +1
vshummy  I would agree with Sturg Webber nevus flammeus but I also noticed First Aid says it's a non-neoplastic birth mark so I should have known not to pick malignant degeneration or local invasion. Also because capillary hemangiomas don't have to be flat but the nevus flammeus is consistently flat. But I'm also reading on Wiki that the nevus flammeus doesn't regress so they must be trying to describe strawberry hemangioma even though I don't agree with their color choice... +
nala_ula  Maybe (and I can only hope I'm right and the test makers are not -that much of- sadists) they would have made sure to write "in a cranial nerve 5 (either ophthalmic or maxillary) distribution" if it were Sturge-Weber. +1
j44n  this is literally on every NBME along with the 10,000 ways to not get a boner +1


submitted by thisshouldbefree(51), visit this page
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I get these VERY often. I seem to get them only after eating something that can damage the mucosa in my mouth such as hard chips (Tostitos, very jagged very pain). These are NOT cold sores (HSV). This is simply a aphthous ulcer; they can be stress induced (studying for hard test). they are very painful and do reoccur. there are no associated sx with them.

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j44n  they're also caused by stress. I got 3 in my mouth the day after Prometric canceled my test for the 3rd time! +15
ih8payingfordis  In layman terms, these things are called canker sores. I also get them on my tongue sometimes - super painful especially when it makes contact with anything salty. Just like @thisshouldbefree, it's usually preceded by mucosa damage (ie biting my tongue accidentally while eating) +2
xmen  test in 2 weeks. i have them now +1
drdoom  The physiological corollary of psychological โ€œstressโ€ is cortisol and its many cousins (corticosteroids, et cetera). Cortisol suppresses the โ€œnormalโ€ but energetically costly process of dermal maintenance and growth (basal stem cell division, skin + epidermal turnover, including in the mucosa). So, in the presence of high โ€œstressโ€, normal mucosal maintenance is sacrificed. This is because some other, more important existential threat is happening in the body. The result is stuff like aphthous ulcers, since your body is literally neglecting your mucosa, allowing it to โ€œthin outโ€ to preserve energy to address some other major systemic issue. +1
drdoom  From https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5181654/?report=classic: The glucocorticoid receptor (GR) is highly expressed in the basal cells but it is barely detectable in the other layers of the epidermis (22). The localization of the GR in basal corneocytes, as well as the negative effects of glucocorticoids on keratinocyte growth factor and type-I and-III collagen gene expression (23โ€“26) suggest that endogenous cortisol in CS suppresses not only wound healing but also normal skin growth and turnover. +
drdoom  ^ btw, CS = Cushing Syndrome (hypercortisolism) +
jbrito718  Herpangia would occur in the posterior oropharynx--> caused by Coxsakie A NOT HSV +
meryen13  I have some in my mouth rn... 2 weeks to my step... they can be food or stress induced and its more common in some regions more than others. in Middle East and Asia it seems to be common. +


submitted by jucapami(14), visit this page
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x-ray corresponds to a tension pneumothorax = imminent respiratory failure if untreated. Right lung is fully collapsed, increasing intra-thoracic pressure, imparing O2 exchange (due to mass effect toward left lung, and collapsed right one), hence accumulating CO2 (in blood), inducing respiratory acidosis.

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j44n  how is it a tension if there is not tracheal deviation? +2
djeffs1  I can see that its resp. Acidosis, but wouldn't the most risky potential complication be diffuse alveolar damage (If you arent able to reinflate sometime? +
sexymexican888  @j44n honestly you cant even see the damn trachea on this! lol +


submitted by centeno(3), visit this page
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I thought that the cognitive impairment could be the manifestation of neurosyphilis. In addition, the doctor should talk directly to the patient to check for sexual abuse.

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j44n  The maximum MMSE score is 30 points. A score of 20 to 24 suggests mild dementia, 13 to 20 suggests moderate dementia, and less than 12 indicates severe dementia. On average, the MMSE score of a person with Alzheimer's declines about two to four points each year. she only has mild dementia. I had to look this up she could still retain her capacity +1


submitted by lamhtu(139), visit this page
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Platelet adherence and platelet aggregation are different things and this diferrence MATTERS A LOT. Fuck you, NBME. These differences supposedly matter on some questions and not on others. Where is the consistency? Hello?

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hungrybox  Agreed. This is so fucking stupid. +
hungrybox  "Aspirin inhibits platelet aggregation and produces a mild bleeding defect by inhibiting cyclooxygenase, a platelet enzyme that is required for TXA2 synthesis." literally straight from Big Robbins +1
susyars  Im gonna upvote this bc i love to be right +7
regularstudent  It's always a horrible, horrible feeling to pick the wrong answer that you know they think is right. Amazing job NBME... +5
j44n  yeah i thought adherence was the GP1B receptor that's already on the platelet +1
j44n  im also glad we're getting exposed to this horse shit now and now when I'm in a testing center about to put my fist through a screen. +2
jurrutia  GPiib/iiia receptor is not inhibited by aspirin. Aspirin prevents the upregulation of GPiib/iiia which is not the same as inhibiting the receptor itself. +2
jj375  @jurrutia I think you are thinking of Clopidogrel, prasugrel, and ticlopidine which downregulate GP2b3a expression. Aspirin inhibits COX therefore inhibiting TXA2 and platelet aggregation. +
jbrito718  This is whaat I call a FUCKBOY question +


submitted by susyars(41), visit this page
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Im gonna fight this one because AGGREGATION is mediated by expression of Gp IIb/IIIa.

If your platelet increases TXA2 that means is gonna upregulate AGGREGATION by which receptor? ... Duh

Once Im done with this test and become a Pathologist Im gonna send you a copy of my journal and research on platelet aggregation mediated by TXA2 and Gp IIb/IIIa and also im gonna go over every single WTF NBME question and prove them so wrong

Maybe i should change my username before submitting this

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corgilobacter  Dr. Tio Goljan Jr. In the house everyone. CLAPS +
susyars  Tio Goljan would be so proud of me +
j44n  I agree TXA2 up-regulates the GP2b3A receptor that mediates aggregation. +


submitted by lamhtu(139), visit this page
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Platelet adherence and platelet aggregation are different things and this diferrence MATTERS A LOT. Fuck you, NBME. These differences supposedly matter on some questions and not on others. Where is the consistency? Hello?

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hungrybox  Agreed. This is so fucking stupid. +
hungrybox  "Aspirin inhibits platelet aggregation and produces a mild bleeding defect by inhibiting cyclooxygenase, a platelet enzyme that is required for TXA2 synthesis." literally straight from Big Robbins +1
susyars  Im gonna upvote this bc i love to be right +7
regularstudent  It's always a horrible, horrible feeling to pick the wrong answer that you know they think is right. Amazing job NBME... +5
j44n  yeah i thought adherence was the GP1B receptor that's already on the platelet +1
j44n  im also glad we're getting exposed to this horse shit now and now when I'm in a testing center about to put my fist through a screen. +2
jurrutia  GPiib/iiia receptor is not inhibited by aspirin. Aspirin prevents the upregulation of GPiib/iiia which is not the same as inhibiting the receptor itself. +2
jj375  @jurrutia I think you are thinking of Clopidogrel, prasugrel, and ticlopidine which downregulate GP2b3a expression. Aspirin inhibits COX therefore inhibiting TXA2 and platelet aggregation. +
jbrito718  This is whaat I call a FUCKBOY question +


submitted by gonyyong(131), visit this page
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Wasn't sure about others, but mammography for general population isn't recommended until 40

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_yeetmasterflex  Also wouldn't mammography be secondary prevention since you'd look for asymptomatic disease already present? +24
suckitnbme  USPSTF recommends starting screening at age 50. 40 by patient choice if there's risk factors. +2
j44n  @_yeetmasterflex thats a good point i didnt think about that +


submitted by snoodle(36), visit this page
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just wanted to add that questions that ask small details like this make me want to carve my eyeballs out

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j44n  This is the shit that keeps me up at night +6
jbrito718  I just realized its asking about MITOTIC cyclins +


submitted by krewfoo99(115), visit this page
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Lung volume will decrease in obesity hypoventilation syndrome. Even though this patient is obese, he has all the clinical features of sleep apnea

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j44n  also the lung volume would't have an "episodic" decrease. It would be constant due to the weight on their chest. +


submitted by medstruggle(21), visit this page
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Whats the difference between โ€œheterozygous null mutation in B globin geneโ€ and โ€œheterozygous mutation known to cause 50% decrease in B globin gene function of one alleleโ€?

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welpdedelp  I interpreted "null" as meaning full deletion while the other heterozygous mutations was only a 50% decrease in the function. One child would inherit 1 null mutation and 1 50% mutation, which would leave them with a 25% functional gene. +18
j44n  A thal is the deletion, B thal is mutations on promoters or splice sites. +


submitted by medstruggle(21), visit this page
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Can someone please explain this? What is the diagnosis here?

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welpdedelp  I thought it just as it was, polyneuropathy is supposed to be a burning pain affecting the extremities, he might have acute intermittent porphyria. He was too young and didn't fit ALS due to the rapid onset. No loss of pain in the arms so it couldn't be syringomelia. Wasn't asymmetric so couldn't be polio. Didn't have anything resembling Parkinson. +5
j44n  I got tripped up on this too. I think what youre supposed to see is multiple areas of nerve damage on the motor tracts and proprioception is a senory component, so instead of saying they feel burning, they cant tell where their limbs are in 3D space. If they said burning you wouldn't have to know all the other 4 possible answer choices to get to this one. +


submitted by susyars(41), visit this page
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From a girls perspective, is really hard to understand this penis/erection physiology questions

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john055  hahaha. thats hilarious lol +
thisshouldbefree  from a males perspective it is really hard to understand the mensural cycle +10
j44n  I'm a man.... and i still miss every boner question +1


submitted by sattanki(82), visit this page
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There are two mechanisms of regulating renal blood flow, the myogenic mechanism and tubulo-glomerular feedback. This question asks purely about the myogenic mechanism, which is where the afferent arteriole controls blood flow based purely off blood pressure entering the kidney, which is why decreased afferent arteriolar resistance is the best answer (the arteriole is dilating in response to the decreased blood flow in attempt to maintain normal blood flow to the kidney).

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nwinkelmann  Man... I took this WAY TOO FAR, lol. I totally didn't recognize the clue of GFR and RPF as staying the same to tell me it was talking about normal, physiologic autoregulation. Silly mistake! +7
j44n  I agree. All I saw was a stenosed artery and ATII constriction +


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