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submitted by scoresloth(3), visit this page
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FA 202 page 441 Vincristine, areflexia, peripheral neuritis, constipation,

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helppls  would inhibition of synaptic vesicle endocytosis have to do with SNARE proteins? (botulism?) +
scoresloth  Snare proteins are for fusion of vesicles. Microtubule depolymerization stops movement required for endocytosis I think. +


submitted by brise(86), visit this page
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Does anyone know why decreased left ventricular stroke volume work is wrong? Would'n stroke volume decrease with increased afterload?

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brise  WOW, OMG IT SAYS STROKE WORK -_- NEVERMIND UGH +3
helppls  I put down stroke work because I was thinking about decompensated heart failure, could this not be a potential answer? +
madamestep  @helppls that was my thought too. But maybe the baroreceptor adaptation comes first... +


submitted by topgunber(68), visit this page
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Hep C - RNA virus (not enveloped) (picorna family + ssRNA).

Viruses are intracellular- so their products are displayed on MHCI molecules (using tap1/tap2 to shuttle the viral proteins broken down by proteosome) and are shipped to the cell surface of infected cells. Since this is MHC I we know CD8+ t cells (cytotoxic T lymphocytes) are responsible for attacking the infected cells.

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helppls  Would the self peptides be an auto-immune response? (autoimmune can be cause by either CD8 or CD4 correct?) +


submitted by azibird(279), visit this page
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Who else came here after getting triggered by this answer?

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yousif11  This question did not age well +23
helppls  I'm going to be taking Step with this song stuck in my head lol +


submitted by proteinbound123(3), visit this page
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Beneficence: health care providers have a duty to be of a benefit to the patient and should take positive steps to prevent and to remove harm from the patient.

Consent for minors (FA2020 pg 265): Consent should be obtained from parents, except for Emergency Medicine.

This is a case where the Principle of Beneficence is given priority over the principle of respect for the patient's autonomy. In Emergency Medicine, the patient is incapacitated by the grave nature of accident or illness, we presume that the reasonable person (in this case, the patient's parents) would want to be treated aggressively, and we rush to provide beneficent intervention by stemming the bleeding, mending the broken or suturing the wounded.

So by the Principle of Beneficence, the surgery was indicated and by the same principle, the doctor proceeded without permission because it was a case of Emergency Medicine.

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misterdoctor69  What I found strange about the question was that the parents were even contacted for consent to begin with..when, as you clearly stated, consent isn't needed for emergency medicine. In the hypothetical scenario where the parents were able to be reached and they said, "No, don't do the procedure," what would happen next? +2
yousif7000  I think you'll proceed anyway since the parents refusal is kinda considered as child abuse at this point +
helppls  I was a little confused, I assumed that proceeding with the surgery would prevent further complications (herniation). Thus preventing harm = nonmaleficence? +2


submitted by castlblack(78), visit this page
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I have read all the comments, but none explain why hyponatremia is wrong. There is definitely Na+ in stool....thats why sugar+salt is rehydration for peds diarrheal sickness. Low Na+ causes low EVV explaining the low BP, high HR, pallor, and dehydration. Is it correct but just not as correct as C?

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waterloo  I Dont know what you mean by low EVV. But here's my thought process. This pt lost lots of water, and when someone takes a laxative causing them to have diarrhea that will lead to metabolic acidosis. A buffering mechanism for the decreased bicarb in the blood is for H+ to leave cells and K+ to go into the cells. So he has to have hypokalemia (low K+ in serum). They gave him IV fluids, so his BP should be headed back to normal. I would think his RAAS will chill out. But it takes time to correct the acidosis, you're kidney won't just immediately stop reabs bicarb so you're body will still be buffering against the acidosis (H+ out of cell, K+ in). +2
waterloo  sorry, I wrote increased bicarb, I meant DECREASED bicarb in the blood. And also should have written "you're kidney won't just immediately START reabs new bicarb" My Bad, wasn't trying to add to confusion. +1
drdoom  i think by `EVV` author meant `ECV` (extracellular volume). @waterloo, appreciate the explanation but think something is off: loss of HCO3- via diarrhea should result in acidemia, which would oppose the presumption of ‌``H+ leaving cell, K+ going in´´. +2
waterloo  hey so sorry, I must have been super tired posting this. Can't believe I made so many mistakes. Read over it again, and it sounds like gibberish. Wish there was a way to delete. My bad. +1
waterloo  I think I tried to explain too hard. Looking at this question again, I think really the only this is when you lose that much volume, you lose bicarb and K+. Nothing really to do with acid-base. My b. +1
drdoom  no worries! +1
castlblack  EVV = effective vascular volume. Thank you for trying to help but I still don't understand. I still agree with my above mechanism as correct. Whether or not it's most correct idk. +1
amy  what about the long steamy bath? He also sweat a lot, and profuse sweating is going to cause hyponatremia? +1
helppls  thats what I was thinking as well^^^ I figured he was sweating out a lot of NaCl +1
icrieeverytiem  The Q mentions that he feels better after an infusion of fluids so I assumed any hyponatremia that he had must've been resolved. +1


submitted by sacredazn(101), visit this page
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The concept is a convoluted way of asking if you knew how VDJ recombination works, which is that it is actually an example of altering the DNA of the B/T lymphocyte.

Southern blot technique: So when they use a probe against some region, and outputting a size of 1.5 kb or 6 kb, this is telling you the size of the DNA fragment in each cell (doesn’t matter if they say J probe or constant region probe, they’re just saying they’re targeting some nucleotide sequence found in the Ig locus/TCR beta chain locus respectively for B/T cells).

I think the confusing part could be wondering how you know whether you’re partly through rearrangement (answer choices B thru D) or if it hasn’t occurred at all yet (correct answer). Here, the concept is that B cells undergo V(D)J rearrangement in the bone marrow, while T cells do it in the thymus, and it all happens at once. So a plasma cell in the blood like in Multiple Myeloma would have fully undergone recombination, while a T cell in the blood could either be fully educated (and have finished VDJ recombination) or immature (hasn’t started VDJ).

Since the T cell gene was 6 kb and definitely bigger than the 1.5 kb gene, the T cell hasn’t undergone recombination yet.

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trichotillomaniac  very nice explanation! +29
nwinkelmann  This was awesome! Made so much sense and hopefully I will be able to think that critically about questions in the future (because I NEVER would have come up with this on my own, hah). +5
eacv  OMG! THANK YOU. I DIDNT KNOW ANYTHING about this!! Hope this is not testesd on real examen :p +5
ajss  wow! this explanation was awesome! thanks! +
mrglass  Also the T-cell V-D-J segments are not the same as the B-cell V-D-J segments. Therefore a B-cell J segment southern blot would look for whether the B-cell site VDJ segment in a T-cell, which would always non-rearranged. +6
mynamejeff  Thank you! So is this because multiple myeloma produces excessive monoclonal light chain Ig? Is this the 1.5 kb gene? Whereas, T-cells that have not gone through differentiation yet and their J region includes everything (VDJ) vs. just VJ in the light chain? (FA 2020 pg 104) +
peridot  This explanation is amazing! However, to fully understand another step of what the question is getting at, please take a look at @highyieldboardswards's and/or @mrglass' explanation as well - a very important addition!! +1
skonys  My logic was wrong but my answer correct. I am suffering from success. +
fhegedus  wow! this is amazing! thank you! +


submitted by scrambledeggs(17), visit this page
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This lady had preterm premature rupture of membranes. She had a genital tract infection, which is a risk factor for PPROM.

From Uptodate: Many of the microorganisms that colonize the lower genital tract have the capacity to produce phospholipases, which can stimulate the production of prostaglandins and thereby lead to the onset of uterine contractions. In addition, the host's immune response to bacterial invasion of the endocervix and/or fetal membranes leads to the production of multiple inflammatory mediators that can cause localized weakening of the fetal membranes and result in PPROM.

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alimd  did you pay fucking $30? +2
cheesetouch  some institutions give students UpToDate access +6
cbreland  I knew that misoprostol (PGE1) can be used for abortions by forcing uterine contractions, so I figured the answer had something to do with prostaglandins +11
rthavranek  I knew prostaglandins increased uterine contraction, but I also thought PGE2 caused cervical ripening and since there was a closed cervix, I eliminated that choice. I had no idea what was going on so I just picked oxytocin since that would increase uterine tone without dilation, though my reasoning seems to be incorrect +2
utap2001  Great, the above message deserve $30. +
notyasupreme  I think also it said that the fetus releases oxytocin and steroids, which I guess is stupid wording that makes it not right. Anyways, fuck the curve on NBME 18 :) +4
okokok1  if anyone didn't know what "PPROM" stood for it is: Preterm Premature Rupture Of Membranes" +4
aakb  I was between the prostaglandin answer and stressed fetal production and release of oxytocin and the reason I didn't pick oxytocin was if the cervical os is closed (membranes ruptured 32 hrs ago and contractions been going on for 12) and there's no effacement, it didn't seem like that baby actually wanted to come out so I thought that's not what's happening here. Plus mom has a fever so inflamed maternal decidua seemed to fit. +2
helppls  If there was an increase in Pgs why did she not have a ripened cervix? +
leemax  read it again guys-option E-stressed fetal production and release of OXYTOCIN. good nbme,got me there! +1
gabriellerenai  I think a key thing is that oxytocin is never the primary initiator of labor even in full term labor (it mainly controls Phase 3 and 4): via up to date - "It is unlikely that oxytocin provides the trigger for the initiation of labor, but the release of oxytocin during labor results in more forceful uterine contractions and undoubtedly facilitates delivery of the fetus and placenta." +3
gabriellerenai  and their question was what is the primary stimulus +
epiglotitties  @leemax doesn't the fetus produce oxytocin? and its clearly stressed, a fetal heart rate of 210 is high isnt it? Still don't get why that couldnt be the answer.. +
fatboyslim  I got this wrong and chose oxytocin. But now I recall a UW question saying oxytocin receptors on the uterus don't play much of a role in uterine contractions until about the late 3rd trimester. This fetus is 27 weeks gestation. +


submitted by blueberriesyum(28), visit this page
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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.

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flapjacks  If you know the story of Phineas Gage, it can help +6
helppls  How do you tell the difference from a frontal lobe issue and Kluver Bucy Syndrome? +1
nikitasr27  I would say the emotional and language part. The frontal lobe is very involved in emotions and the limbic system as well as in complex language concepts. Kluver Bucy would lack these aspects as the individual is “indifferent” to everything (no fear, no emotions) just like my ex +3
randi  Kluver-bucy is also marked by specific behaviors like hyperphagia, hyperorality, hypersexuality. Apparently can also be associated with HSV-1 encephalitis FA2019 p499. +1
chaosawaits  What am I looking at? From what viewpoint am I looking? Can anyone identify the labels? I have A is olfactory tract, C/D are optic nerves, E/F are optic tracts, G/H are substantia nigra of midbrain & still I am totally lost. +1
chaosawaits  I imagine that we are viewing the front of the brain from underneath and slightly angled to expose the midbrain more easily. Obviously B is the frontal lobe. But what are I and J? +
an1  @chaosawaits I think J might be the partial lobe. the only thing confusing me is that B is the frontal lobe with the amygdala is actually in the temporal lobe... +
an1  I take that back, I thought it was Kluver body for a second but its just frontal lobe stuff lol +
pakimd  can anyone explain why this is kluver bucy and not frontotemporal dementia? +
doida  it is not kluver, it is frontal lobe dementia +
thatmd  I and J are the temporal lobes +


submitted by hungrybox(1277), visit this page
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Morphine stimulates mu opioid receptors to provide the desired effect of analgesia, but in doing so can also precipitate many undesired effects.  This patient has multiple signs of opioid toxicity, including miosis (ie, pinpoint pupils), respiratory depression (evidenced by slow respiratory rate and respiratory acidosis), and CNS depression (eg, somnolence, coma).  Morphine is primarily metabolized by the liver via glucuronidation to form 2 major metabolites.  These metabolites, morphine-3-glucoronide and morphine-6-glucoronide, then undergo renal elimination via excretion in the urine.  Because the metabolites are metabolically active, renal dysfunction can lead to metabolite accumulation and opioid toxicity.  Morphine-6-glucoronide is particularly responsible for toxicity, acting as a more potent mu opioid receptor agonist than morphine itself.

Due to its metabolically active and renally cleared metabolites, morphine requires careful monitoring when used in patients with renal dysfunction.  When opioid pain control is needed in such patients, fentanyl or hydromorphone is often preferred as these drugs are predominantly hepatically cleared.

Source: UW18563

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caramel  I got this answer through the process of elimination. I figured that A/C/D would NOT cause the pt to have an overdose. And with B, she wasn't using it chronically (3 days..) +
helppls  What drugs inhibit their own metabolism? +
letitb  Carbamazepine i think ^ +1


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