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Welcome to drdoom’s page.
Contributor score: 819
don't just do something, stand there!

Comments ...

 +2  (nbme18#6)

Responding to @azibird’s comment:

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.


 +1  (nbme19#40)
  • A: Broca’s
  • B: Premotor
  • C: Motor
  • D: Somatosensory

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!

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.


 +4  (nbme18#28)

Responding to @azibird’s comment:

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

The tricuspid murmur gets worse with inspiration because when you ask someone to take a good, deep breath, the diaphraghm (a very strong muscle, indeed) pulls the entire thoracic cage down and outward (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.

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 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”).

heart sound areas => https://images.app.goo.gl/2F1wUeppSd9vL2os9


 +0  (step2ck_form7#3)

“It’s awfully quiet in these here pages ...” 🌵🤠

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 -3  (step2ck_form6#3)

“It’s awfully quiet in these here pages ...” 🌵🤠

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 +4  (nbme24#46)

The CFTR protein is a transmembrane protein. Like all proteins, its translation begins in the cytosol; that said, CFTR contains an N-terminus “signal sequence”, which means as it is being translated, it (and the ribosome making it!) will be transported to the Endoplasmic Reticulum.^footnote!

As it gets translated, its hydrophobic motifs will emerge, which embeds the CFTR protein within the phospholipid bilayer of the ER itself! That means the protein will never again be found “in the cytosol” because it gets threaded through the bilayer (which is, in fact, how all transmembrane proteins become transmembrane proteins at the cell surface -- they have to be made into transmembrane proteins in the ER first!).

So, yes, ultimately, these misfolded proteins will be directed toward a proteasome for degradation/recycling, but that will happen as a little vesicle (or “liposome”); the misfolded protein, in this case, is not water-soluble (since, by definition, it has hydrophobic motifs which get “threaded through” a bilayer to create the transmembrane pattern), which means you won’t find it in the cytosol.


\ footnote! \ The hitching of active* ribosomes to the Endoplasmic Reticulum is why we call that area of ER “rough Endoplasmic Reticulum (rER)”; on electron microscopy, that section was bespeckled with little dots; later, we (humans) discovered that these dots were ribosomes!

\ * \ By “active ribosomes”, I just mean ribosomes in the process of converting mRNA to protein! (What we call “translation” ;)

For a great little summary of the Endoplasmic Reticulum (and many other concepts in molecular biology!), see this from Alberts’ Molecular Biology of the Cell:
https://www.ncbi.nlm.nih.gov/books/NBK26841/#A2204

drdoom  ^ I'm just re-stating in one comment what I wrote in multiple subcomments above: https://nbmeanswers.com/exam/nbme24/939#1379 +

 +1  (nbme23#35)

The prevailing rule of American medicine (and law) is individual autonomy, otherwise known as liberty. In American law, no other person, professional or otherwise, is granted “default access” or privilege to another person’s body—that includes the physician! (It even includes spouses! That’s why, in American law, you can be married to someone and still be charged with sexual assault/rape; marriage ≠ your spouse surrendering “bodily rights”.) The physician must receive consent from “a (conscious) person” before they become “a (conscious) patient”. In the same way, the person (now, patient) must give consent before anyone else is permitted to be involved in his or her care—spouses included!


 +1  (nbme21#40)

Accuracy means the data points are dispersed, but when you take the mean of those points, that mean (“sample mean”) is nearby the population mean (“true mean”). Data points are “more precise” if the dispersion across data points is smaller than some other set of data points (notice how this is a comparison and not an “absolute” statement); precision says nothing about how close the average of the data points are to the “true mean.”

Keep in mind that accuracy and precision are relative descriptors; you can’t say “so-and-so is precise”; no, you can only say “such-and-such is more precise than so-and-so” or “so-and-so is more accurate than such-and-such.” So, in this case, we can infer that NBME considers “men at the urologist” to have BUNs that are closer to each other (more clustered; more precise; less dispersed) than the BUNs of “men at mall.”

Here’s a nice image:
https://medbullets.com/images/precision-vs-accuracy.jpg


 +3  (free120#27)

The reason something is an “autosomal recessive” disease is because the protein encoded by the gene (of which you have two alleles, of course) does something where as long as you make SOME protein, your body should be okay.

That’s kind of vague, so take the case of Cystic Fibrosis: you don’t present with Cystic Fibrosis if you have at least one functional allele -- that’s because CFTR protein is a protein that (in the case of bronchiole tissue) moves Cl- from inside cells to the outside lumen, which brings with it H2O and keeps the bronchiole lumen nice and watery, and fluid and non-viscous and non-pluggy.

So long as you make enough of this protein, you don’t “need” both alleles to be good; the good allele can “make up for” (make enough of the protein product to compensate for) the “broken allele.” So, once again, understanding the pathophys of a disease allows you to reason through and predict things like disease penetrance and expressivity.


 +8  (nbme21#40)

This might be a more intuitive framework for drug trial phases.

Phase 1 / First you give only to healthy people. You cannot test a new therapy on individuals who are already “sick.” How would you distinguish adverse drug effect from complication of the disease? In the beginning you simply have to prove that the drug doesn’t cause problems in normal individuals. You can’t prove that if your initial study includes “non-normal” humans.

Phase 2 / Second, you give only to the sick. This lets you to determine if the drug has any benefit whatsoever in the intended audience. If it does not provide benefit, there is “no reason” to advance to the next stage.

Phase 3 / Third, you must prove that the drug not only provides a benefit but is actually better than the current standard. (“Head-to-head” trial; random controlled trial.)

Phase 4 / If you pass the third stage, you can release your product to market but must surveil for longterm effects which could not be captured by the earlier, shorter-stage phases.

spaceboy98  This is the kinda shit we need more of. Awesome explanation man, I wish they wrote FA like this +2

 +10  (nbme22#47)

You have to think about it this way: the basement membrane is the “scaffolding” on which [restorative] healing occurs. So, yes, stem cells (type II pneumocytes) would be involved in that healing process but they couldn’t restore the normal architecture (“no abnormalities”) without the ‘skeleton’ of the basement membrane telling them where to go, in what direction to grow, which way is “up”, etc. If the basement membrane is destroyed, you can still get healing, but it won’t be organized healing -- it’ll be disorganized healing, which does not appear as normal tissue. (Disorganized healing is better than no healing, but without a BM, the regenerating cells don’t have any “direction” and therefore can’t restore the normal architecture.)

drdoom  by "restorative" i mean healing which restores the previous (and normal) tissue architecture. for that to happen, you need an intact basement membrane! +2
nwinkelmann  Yes, this a great summary to the post by @bubbles and the article he posted! Another way to think of the question is not, what causes repair, but what causes irreversible injury/fibrosis. That article explained an experiment that showed TGF-beta was necessary to initiate fibrosis, but if BM was intact and TGF-beta was removed, the fibrosis didn't persist, i.e. intact BM is protective against TGF-beta. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/ +

 +2  (nbme22#41)

If I gave you a bucket of spontaneous pneumo patients -- and you reached your hand in there and pulled one out -- what scenario would be more common: In your hand you have a smoker or in your hand you have a thin male? It’s the latter.


 +5  (nbme22#41)

You have to think about this using the concept of CONDITIONAL PROBABILITY. Another way to ask this type of question is like this: “I show you a patient with spontaneous pneumothorax. Which other thing is most likely to be true about that person?” Or you can phrase it these ways:

  • Given a CONDITION (spontaneous pneumo), what other finding is most likely to be the case?
  • Given a pool of people with spontaneous pneumothorax, what other thing is most likely to be true about them?

In other words, of all people who end up with spontaneous pneumo, the most common other thing about them is that they are MALE & THIN.

If I gave you a bucket of spontaneous pneumo patients -- and you reached your hand in there and pulled one out -- what scenario would be more common: In your hand you have a smoker or in your hand you have a thin male? It’s the latter.

someduck3  Is this the best approach to all of the "strongest predisposing risk factor" type questions? +
drdoom  There is a town of 1,000 men. Nine hundred of them work as lawyers. The other 100 are engineers. Tom is from this town. He rides his bike to work. In his free time, he likes solving math puzzles. He built his own computer. What is Tom's occupation most likely to be? Answer: Tom is most likely to be a lawyer! Don't let assumptions distract you from the overwhelming force of sheer probability! "Given that Tom is from this town, his most likely occupation (from the available data) = lawyer." +4
drdoom  There is a town of 1,000 spontaneous pneumo patients. Six hundred are tall, thin and male. The other 400 are something else. Two hundred of the 1,000 smoke cigarettes. The other 800 do not. What risk factor is most strongly associated with spontaneous pneumo? (Answer: Not being a smoker! ... because out of 1,000 people, the most common trait is NOT smoking [800 members].) +4
impostersyndromel1000  this is WILD! thanks guy +3
belleng  beautiful! also, i think about odds ratio vs. relative risk...odds ratio is retrospective of case-control studies to find risk factor or exposure that correlates with grater ratio of disease. relative risk is an estimation of incidence in the future when looking at different cohort studies. +
drdoom  @impostersyndrome I love me some probability and statistics. Glad my rant was useful :P +
hyperfukus  @drdoom i hate it which is why your rant was extremely useful lol i learned a ton thanks dr.doom! +1
dubywow  I caught he was thin. The only reason I didn't pick Gender and body habitus is because he was not overly tall (5'10"). I talked myself out of it because I thought the body habitus was too "normal" because he was not both thin AND tall. Got to keep telling myself to not think too hard on these. Thanks for the explanation. +1
taediggity  It isn't just that this person has Ehlers Danlos and they're more prone to spontaneous pneumo??? +1

 +24  (nbme22#34)

Calculations for dad. The probability of the father being a carrier is 2/3 since it is known that he doesn’t have the disease. Then the probability of him passing it on to his kid is 1/2, thus:

  • Probability of dad being carrier = 2/3
  • Probability of dad passing on disease allele = 1/2

Calculations for mom. With the Hardy-Weinberg Principle, you can figure out the probability of the mother being a carrier:

q = sqrt(1/40,000) = 1/200

So, 2pq = 2 * 1/200 * 199/200, which is approx 1/100.

For the child to get the allele from mom, two things need to happen: (1) mom must be a carrier [“heterozygote”] and (2) mom must pass the allele to child:

  • Probability of mom being carrier = 1/100
  • Probability of mom passing on disease allele = 1/2

Puting it all together. Now, combine all together:

= (probability of dad being carrier) * (probability of dad passing on disease allele) * (probability of mom being carrier) * (probability of mom passing on disease allele)

= 2/3 * 1/2 * 1/100 * 1/2
= 1 in 600

kernicterusthefrog  To quote Thorgy Thor, drag queen: "ew, Jesus, gross" +37
niboonsh  This question makes me want to vomit +11
drdoom  lol +
5thgencephalosporin  okay wow +

 +3  (nbme22#37)

Here’s another very nice one that superimposes the pathway onto a simplified brainstem drawing (nice for the anatomical relations):

https://webeye.ophth.uiowa.edu/eyeforum/cases-i/case252/Fig2-INO-LRG.png

Source article:

https://webeye.ophth.uiowa.edu/eyeforum/cases/252-internuclear-ophthalmoplegia.htm

To see even more, try google image search on “medial longitudinal fasciculus”:

https://www.google.com/search?q=medial+longitudinal+fasciculus&tbm=isch

endochondral1  what is A and B in this pic? i knew it was dorsal pons ipsilateral but i just didn't know what part that was on the pic? +
nwinkelmann  A and B are the superior cerebellar peduncles.http://what-when-how.com/wp-content/uploads/2012/04/tmp15F2.jpg +

 +1  (nbme22#37)

Nice schematic of how horizontal gaze is coordinated through the abducens/MLF/oculomotor pathway:

https://n.neurology.org/content/neurology/70/17/e57/F1.large.jpg

In the diagram, the system is coordinating gaze toward pt’s left, which (conveniently) is the same as in the stem.

Source article: https://n.neurology.org/content/70/17/e57


 +13  (nbme24#45)

The stem is describing sequelae of posterior inferior cerebellar artery occlusion, resulting in Wallenberg syndrome. Here’s a nice schematic of the affected nuclei and brain stem regions:

https://i.ytimg.com/vi/A8S3B9p1t_g/maxresdefault.jpg

... and a 6-minute YouTube video that walks you through it:

https://www.youtube.com/watch?v=A8S3B9p1t_g

nbme4unme  Great video! Very, very solid review of brainstem anatomy. +
suckitnbme  This image was surprisingly interpretable for NBME standards +12
aneurysmclip  and the fact that all you needed to know was the side of the lesion to answer tbh lmao, but other than that localizing to medulla wasn't hard. +4
medguru2295  Actually, they were quite nice. You didn't even have to know what side. There was no option for left medulla. +3

 +82  (nbme24#2)

After the cuff is tied, the cells and tissue distal to the cuff will continue consuming ATP (ATP->ADP), but no fresh blood will be delivered to “clear” what will be an accumulating amount of ADP and other metabolites. ADP (=Adenosine) is itself a proxy of consumption and drives vasodilation of arteries! (Evolution is smart!) Increasing ADP/Adenosine in a “local environment” is a signal to the body that a lot of consumption is occurring there; thus, arteries and arterioles naturally dilate to increase blood flow rates and “sweep away” metabolic byproducts.

lispectedwumbologist  You're a good man. Thank you. +
drdoom  So glad it helped! +1
seagull  very well put, thank you +1
aisel1787  gold. thank you! +
pediculushumanus  beautiful explanation! +2
rockodude  this explanation was on par with Dr. Sattar IMO +1

 +49  (nbme24#48)

The duodenal lumen (and pancreatic proteases like CHYMOTRYPSIN) is the site where pancreatic enzymes (“endopeptidases”) cleave large polypeptides into smaller bits (=dipeptides,tripeptides). It is at the BRUSH BORDER where the smallest kinds of peptides (dipeptides,tripeptides) are broken down into their amino acids, which finally can be co-transported with Na+ into the intestinal cell.

I think about it this way:

  • stomach acid denatures and “opens up” proteins (without specific cleavage);
  • pancreatic enzymes then cleave denatured polypeptides into smaller bits;
  • brush border enzymes finally break down tiniest peptides into absorbable amino acids.
regularstudent  Isn't the brush border still part of the intestinal lumen? Don't the amino acids enter into the intestinal cell (the "intestinal mucosa")? +
drdoom  @regularstudent No, the lumen is literally the cavity—the empty space. +

 +7  (nbme24#25)

EBV is not a “respiratory virus” -- it’s a B cell virus. It infects B cells; not laryngeal cells.

Even though you might associate it with the “upper respiratory tract” (=kissing disease), it doesn’t cause respiratory inflammation since that’s not its trope. B cells are its trope! That’s why EBV is implicated in Burkitt Lymphoma, hairy leukoplakia and other blood cancers. (EBV is also known as “lymphocryptovirus” -- it was originally discovered “hiding” in lymphocytes of monkeys.) So, EBV = think B cells. From the MeSH library:

The type species of LYMPHOCRYPTOVIRUS, subfamily GAMMAHERPESVIRINAE, infecting B-cells in humans. It is thought to be the causative agent of INFECTIOUS MONONUCLEOSIS and is strongly associated with oral hairy leukoplakia (LEUKOPLAKIA, HAIRY;), BURKITT LYMPHOMA; and other malignancies.

https://meshb-prev.nlm.nih.gov/record/ui?name=HERPESVIRUS%204,%20HUMAN


 +9  (nbme21#39)

Stem actually states, “On questioning, the patient does not know the date [time], the name of the hospital [place], or the name of her nurse who had just introduced himself [person].” So, pt is disoriented to time and place (Choice A); that is definitely concerning -- as would be depressed mood (Choice E) and the other choices -- but “inability to understand severity and prognosis” is the most concerning since that is the very definition of capacity. Inability to understand = lack of capacity.

lovebug  you explain very clearly. THX!!! +
drdoom  thanks lovebug! +

 -2  (nbme20#29)

[deleted]


 +2  (nbme21#21)

Also consider this great description from the NIH’s MeSH database:

INCIDENCE: The number of new cases of a given disease during a given period in a specified population. It also is used for the rate at which new events occur in a defined population. It is differentiated from PREVALENCE, which refers to all cases, new or old, in the population at a given time.

https://meshb.nlm.nih.gov/record/ui?ui=D015994

questioneverything  The prevalence of chlamydia in this group would be 0. It is not a chronic disease. +

 +10  (nbme21#21)

Don’t forget that incidence is the number of new cases which emerge in an unaffected population. Incidence is trying to get at the question -> “In a given year, how many new people develop this disease?”

In other words, you cannot count people who already have the disease. You have to exclude those people from your calculation. You want to know, among all the people out there who DO NOT have the disease, how many times this year was someone (newly) diagnosed?

Said differently still, you don’t want to “double-count” people who developed the disease before your study. As an epidemiologist, that would screw up your sense of how infective or transmissible a disease is. You want to know, “from time1 to time2 how many new cases emerged?”

questioneverything  You would count the total risk pool. Chlamydia is not a chronic disease so you would treat those 500 people and they would return to the risk pool. +1
drdoom  But you would first have to determine that they CLEARED the infection. What if you gave them tx and then they come back and say, "doc i got the chlamydia" -- is this a new case or did the tx fail? You're assuming it cleared but maybe it didn't. That's why you want to EXCLUDE from the start anyone who might already have disease of interest. +7

 +20  (nbme21#21)

2,500 students ... but you find out during your initial screen that 500 already have the disease. So, strikeout those people. That leaves 2,000 students who don’t have the disease.

Over the course of 1 year, you discover 200 students developed the infection. Thus:

200 new cases / 2,000 people who didn’t have the disease when you started your study = 10 percent

Tricky, tricky NBME ...

sympathetikey  Ah, I see. Thank you! +
niboonsh  Im mad at how simple this question actually is +7
sahusema  Incidence is measured from those AT RISK. People with the disease are not considered to be at risk. So 2500 - 500 = 2000 people at-risk. Of those 2000, within one year 200 develop the disease. So 200/2000 of the at-risk population develop the disease. 20/2000 = 10% = incidence +3
daddyusmle  fuck im retarded +2

 +46  (nbme21#49)

The synthesis of virtually all proteins (mRNA->peptide) occurs in the cytoplasm.[1] That’s where all ribosomes reside, after all. Ribosomes, which are mostly just rRNA (~2/3 rRNA + 1/3 protein*, by weight), are assembled in the nucleus but only do their stuff once they get to the cytoplasm.

For a protein to leave its original hometown of the cytosol and become a resident of the nucleus or, sayyyyyy, the endoplasmic reticulum, it needs to have a little string of amino acids which shout “I belong in the nucleus!” or “I belong in the endoplasmic reticulum!”

Proteins ultimately destined for the ER contain an unimaginatively named string of amino acids known as “signal sequence,” which, for the purposes of the Step 1, is always at the N-terminus. The signal sequence tells other cytosolic proteins, “Hey! Take me (and the rest of the peptide of which I am part) to the ER!”

In the absence of this signal, a protein will remain in its “default” home of the cytosol.

Here’s a nice schematic showing the flow of proteins from initial synthesis to final destinations:


Endnotes

  1. “The synthesis of virtually all proteins in the cell begins on ribosomes in the cytosol.” (Essential Cell Biology, Alberts et al., 2014, p. 492)

*If you really want your mind blown, consider that even the protein subunits that make up that 1/3 of a ribosome are themselves initially synthesized in the cytosol; later, they are transported back into the nucleus via the nuclear pore.

qball  Awesome explanation. Now explain it to me like I'm 5. +8
drdoom  All baby peptides are born in the cytosol. But some baby peptides have a birthmark at their N-terminus. The birthmark tells a special mailman that this baby needs to be delivered somewhere else. If you chop off the birthmark — or erase it somehow — the mailman never knows to take baby to its true home. The end. Now go to sleep or Santa won’t bring your presents. +36

 +0  (nbme21#28)

Here’s one way to process-of-eliminate “decreased hydrogen-bond formation”: I’m not a big fan of this line of reasoning, but technically alanine as a side group has more hydrogens* for potential hydrogen bonding than glycine:

alanine: —CH3
glycine: —H

So, “technically,” alanine would permit more hydrogen-bond formation, which might allow you to eliminate that choice.

That said, it seems almost impossible to rule out (without very technical knowledge or some provided experimental data) that the slightly larger alanine does not impair hydrogen bonding between collagen molecules via steric (spatial) interference. In simpler terms, since alanine is larger, you would think that it must somehow interfere with the hydrogen-bonding that occurs with the wild-type glycine.

---
*Strictly speaking, it’s not the number of hydrogens but also the strength of the dipole that facilitates hydrogen bonding: a hydrogen bound to a strongly electronegative molecule like fluorine will “appear” more positive and, thus, hydrogen-bond more strongly with a nearby oxygen (compared with a hydrogen connected to carbon, for example).

Further reading:

  1. https://www.chem.purdue.edu/gchelp/liquids/hbond.html
hungrybox  Appreciate the effort but this is far too long to be useful. +21
drachenx  hungrybox is a freaking hater +
drdoom  @drachenx haha, nah, coming back to this i realize i was probably over-geeking lol +
blueberrymuffinbabey  isn't the hydrogen bonding dependent on the hydroxylated proline and lysine? so that wouldn't really be the issue here since those aren't the aas being altered? +
drdoom  @blueberry According to Alberts’ MBoC (see Tangents at right), hydroxylysine and hydroxyproline contribute hydrogen bonds that form between the chains (“interchain”, as opposed to intra-chain; the chains, of course, are separate polypeptides; that is, separate collagen proteins; and interactions between separate chains [separate polypeptides] is what we call “quaternary structure”; see Tangent above). And in this case, as you point out, the stem describes a Gly->Ala substitution. That seems to mean two things: (1) the three separate collagen polypeptides will not “pack [as] tightly” to form the triple helix (=quaternary structure) we all know and love and (2) proline rings will fail to layer quite as snugly, compromising the helical conformation that defines an alpha chain (=secondary structure; the shapes that form within a single polypeptide). +
tadki38097  also you can't H bond with carbon, it's not polar enough +

 +8  (nbme21#23)

Vasoconstriction (narrowing of a tube) will cause the flow rate to increase through that tube, which decreases radial/outward pressure. The faster a fluid moves through a tube, the less “outward” force it exerts. (This is known as the Venturi effect.)

hungrybox  not seeing how this is relevant +8
sympathetikey  He's showing how A & B are incorrect @hungrybox +7
nerdstewiegriffin  what a moron @hungrybox is !! +2
leaf_house  MCAT flashbacks on this image +1

 +11  (nbme20#6)

This is an interesting one. I like to remember it this way: in people with narcolepsy, all the “right kinds” of sleep are happening at all the “wrong times” of day. During the day, when a power nap would typically throw you immediately into REM, this kid is only entering Stage 1 or 2 (lightest sleep = slightest noises jar him back to reality). At night, when he should peacefully drift into Stage 1, 2, and so on, he instead completely zonks out. Classic narcolepsy.

From UpToDate: “Narcolepsy can be conceptualized as a disorder of sleep-wake control in which elements of sleep intrude into wakefulness and elements of wakefulness intrude into sleep.”

chextra  Isn't REM a rather light sleep stage? Brain waves during REM are very similar to awake states. I think you even wake up briefly in the middle of REM sleep. I don't think FA gave me a great understanding of narcolepsy, but I see it as going from awake to REM (light) for any kind of sleep, daytime or night time. +
sammyj98  I'm definitely not ace on this subject, but I think the brain waves present in REM are similar to wakefulness because of the dreaming component. I think of it as though the brain has to go through a process of hypnotizing the body into a state of relaxation, and then properly paralyzing it, and then it can simulate wakefulness (dreaming) to go through with it's defragging of the hard drive. So REM is actually the deepest sleep because the body is fully paralyzed. Please someone correct me, this is probably an inacurrate perspective. +3
pg32  FA says that narcolepsy has nocturnal AND NARCOLEPTIC sleep episodes that start with REM sleep... So is @drdoom correct? FA seems to disagree regarding the daytime sleep pattern. +3

 +16  (nbme20#11)

As described in the question stem, this mutation occurs within an intron (a gene segment which is transcribed [DNA->RNA] but not translated). RNA splicing enzyme(s) grab RNA and “loop it”; an intron is cut out and the exons on either side of the intron are adjoined, like this:

exon1—intron—exon2 => exon1—exon2

Typically, this splicing occurs at the very edges of the intron (what I denoted with the “—” character). But in our case, a mutation within the intron is causing RNA splicing enzyme to recognize a new site: the splicer cuts within the intron (instead of at the very edge, as it should). So, we get something that looks like this:

exon1—intr—exon2

That’s a totally different mRNA molecule, and it's going to make our β-globin protein look (and behave) awfully strange.

drdanielr  I remember that in the pre-mRNA, the splicing sites of the intron where the spliceosome attaches are surrounded by "GU---AG" like "guac", so here the homologous DNA to this strand would be transcribed into "gu............ag......" and this would create a 3' slice site too soon +4
vivarin  if this is supposed to be pre-mRNA, why are there T's in the sequence? I'm so confused by this for some reason +8
sars  This is the gene (DNA), not heterogenous mRNA. +

 +1  (nbme20#15)

The more general principle: endothelia vasodilate in the presence of high CO2; you gotta get rid of that acid somehow! Can’t let it accumulate, as lower pH within a “micro-environment” affects structure/efficiency of enzymes, proteins, etc. The more acidic a local environment, the more you expect nearby vasculature to dilate (as a means of increasing flow rate, thereby ferrying off accumulate acid).

The anesthesiologist can exploit this mechanism. By hyperventilating (blowing off CO2), the brain vasculature senses a low CO2 / “hunky-dory state,” which requires no vasodilation. In other words, the vasculature does not need to continue the ATP-consuming practice of synthesizing Nitric Oxide (NO).

hello  But, the Q-stem states the anesthesiologist is HYPOventilating the patient. +4
drdoom  decreasing respiratory rate = retention of CO2 = vasodilation of brain arteries = more filling of tubes = greater intra-cranial pressure +1
drdoom  @hello shoot, you're right! i ended my explanation with the example of HYPERventilation when i should have done the opposite! (sorry!) ... edit: "By HYPOventilating (retaining CO2), the brain vasculature senses a high CO2 environment and vasodilates = increases intra-cranial filling and pressure!" +3
dulxy071  @drdoom could you please elaborate on your point. +

 +2  (nbme19#13)

This is essentially a formal logic question. Logically speaking, the question asks us to identify a mechanism that tumor suppressors have which proto-oncogenes do not. In other words, what is a mechanism shared by all known tumor suppressors but not shared by any known proto-oncogenes? For that reason, it can’t be phosphorylation; sure, phosphorylation is a mechanism of tumor suppressors but it’s also a mechanism of many known proto-oncogenes.


 +9  (nbme19#4)

Inability to maintain an erection = erectile dysfunction. So now the question is "Why?"

Fatigue, difficulty sleeping, difficulty concentrating is starting to sound like depression. "Difficulty concentrating" might be interpreted as impaired executive function or the beginnings of vascular-related dementia (dementia related to small but numerous cerebral infarcts), but on Step 1 dementia will be blatant (i.e., "lost his way home," "wandering," etc.).

Depression is actually common after a debilitating event like stroke, as you might expect. With depression comes a loss of sexual interest and desire—that is decreased libido.

One can make the argument that a "vascular patient" might have some issues with his "pipes" (arteriosclerosis, parasympathetic/sympathetic dysfunction) and, for this reason, nocturnal erection should be decreased; but note that nothing is mentioned about long-standing vascular disease (no hx of hypertension).

As a result, the best answer choice here is C. (Libido decreased but nocturnal erections normal.) The big question I have is, how the heck does this guy know he's hard when he's asleep!!? :p

cbay0509  thank you +1
ilikedmyfirstusername  there are several UWorld questions about psychogenic ED with the answer being normal libido and normal nocturnal erections, idgi +10
djeffs1  Yeah NBME says its C, but I still think with a recent stroke you can't bank on normal nocturnal erections... +
drdoom  @djeffs nocturnal erections happen at the level of the spinal cord (S2–S4)! a “brain stroke” (UMN damage or “cortical damage”) would not kill your ability to have nocturnal erections! https://en.wikipedia.org/wiki/Nocturnal_penile_tumescence#Mechanism +
drjo  fatigue, difficulty sleeping and concentrating could be depression or hypothyroidism both of which can cause decreased libido +
jurrutia  @djeffs1 when you say NBME say's it's C, how do you know that's the official answer? Did NBME post the answers somewhere? +
djeffs1  in the versions I purchased from them they highlight the correct answer in the test review +




Subcomments ...

submitted by szsnikaa(6),

This question is a rather interesting one. While pharyngitis with viral or bacterial etiologies have very similar clinical presentations, there are a few subtle hints that make Throat Culture the more likely answer regardless of the CENTOR score in this Vignette.

September. The seasonality of Group A Strep (GAS) pharyngitis is usually between winter & early spring. Viral pharyngitis, although all year round, is more common in the colder months.

The main objective of a primary care physician is distinguishing which patients have a higher likelihood of GAS infection vs. viral and because there is a significant overlap between the 2 etiologies, clinical judgment alone is not accurate in diagnosing GAS infections often leading to overtreatment with antimicrobial therapy.

Throat culture is the gold standard in diagnosing GAS. This is done in this scenario, despite the negative rapid test (Sensitivity 70% - 90%), because of the suspicion of viral etiology as well as the avoidance of overtreatment. Throat culture is the most appropriate next step in this case.

drdoom  😍😍😍 +  


submitted by welpdedelp(219),

She met the Centor criteria for empiric antibiotics, why was is culture?



submitted by szsnikaa(6),

This patient has a testicular mass. Let's examine a few differentials as we go through the answer choices.

Germinal Cell Tumor (Testicular Tumor) + Usually painless but dull/achy/heavy sensation; palpation of SOLID mass + No change in size when supine + No transillumination

Dilated pampiniform venous plexus (Varicocele) + Usually painless; "Bag of worms" + Reduced swelling when supine + No transillumination

Cystic Dilation of the effect ductules (Spermatocele) + Typically painless; fluctuant swelling of upper testicular pole + No change in size when supine + Does transilluminate

Fluid accumulation within the tunica vaginalis testis (Hydrocele) + Often painless; fluctuant swelling of scrotum + May/May not change in size wrt position + Does transilluminate

Vascular Trauma (Hematocele/Ruptured Testis) + Extremely painful & tender; visible hematoma + May/May not change in size wrt position + No transillumination

drdoom  your account has been upgraded to: ATTENDING +  


submitted by cassdawg(959),

First order elimination: a constant FRACTION of drug is metabolized per unit time (i.e. elimination rate is proportional to the drug concentration)

This differs from zero order elimination where a constant amount of drug is metabolized per unit time (i.e. rate stays constant)

In this question:

  • In two hours, 2.5 mg of 12.5 mg is metabolized, which is a fraction of 2.5/12.5 = 0.2 or 20%
  • Thus, in another two hours, another 20% will be metabolized since this is first-order elimination
  • 20% of 10 is 2 and 10-2 = 8

FA2020 p232

m0niagui  how will it work if this followed a zero order elimination? +  
drdoom  @m0niagui Zero-order would like like this: 12.5mg—10mg—7.5mg—5mg—2.5mg—0mg (this assumes 2.5mg is eliminated per unit time) +2  


submitted by step7777(0),

Of note, osteosarcoma also is the only bone tumor with a biphasic epidemiological distribution. More common in adolescents, but can also occur in elderly.

drdoom  also known as “bimodal” (since distribution shows two modes: in the second decade of life and the eighth) +  


submitted by brise(45),

Can anyone explain why complement C5-9 is listed?

drdoom  don't have the stem in front of me but the Fc “handle” of antibody allows for opsonization (by macrophages and other APCs) but more immediately it activates circulating complement -> terminating in the formation of the Membrane Attack Complex. MAC is great way to kill nonself intruders without having to wait for macrophages to mature or neutrophils to arrive. FAST ACTIN’ TANACTIN! +1  
brise  Thank you so much! +1  


Elimination

(a) ARDS is bilateral

(b) aspiration PNA is too quick (4 hours!) and is usually consolidated

(c) fat embolism is more common with long bone fractures (e.g., femur) -- if you hear chest is bruised, think chest first

(d) hemothorax is usually more acute, but I suppose possible especially if you're thinking flail chest with sharp ribs causing puncture. But, x-ray would be more consolidated

(e) pulmonary contusion fits. You have trauma, initially normal ABG, chest bruising, and unilateral diffuse consolidation a few hours later

drdoom  very neat. very structured. to-the-point, practical breakdowns. but also great use of typographical elements ... 🤔 too neat for emergency medicine. maybe gen surg? too good natured for ob/gyn .. hmmm, maybe future peds surg? okay, that's my final answer: peds surg. +1  
drdoom  no, wait .. i’m revising to peds specialty. probably peds nephro. final answer. +1  


Elimination

(a) ARDS is bilateral

(b) aspiration PNA is too quick (4 hours!) and is usually consolidated

(c) fat embolism is more common with long bone fractures (e.g., femur) -- if you hear chest is bruised, think chest first

(d) hemothorax is usually more acute, but I suppose possible especially if you're thinking flail chest with sharp ribs causing puncture. But, x-ray would be more consolidated

(e) pulmonary contusion fits. You have trauma, initially normal ABG, chest bruising, and unilateral diffuse consolidation a few hours later

drdoom  very neat. very structured. to-the-point, practical breakdowns. but also great use of typographical elements ... 🤔 too neat for emergency medicine. maybe gen surg? too good natured for ob/gyn .. hmmm, maybe future peds surg? okay, that's my final answer: peds surg. +1  
drdoom  no, wait .. i’m revising to peds specialty. probably peds nephro. final answer. +1  


I took the approach of 10 year history DM --> Chronic DM complications = 1. Nonenzymatic Glycosylation (NEG) 2. Osmotic Damage.

Osmotic Damage can lead to neuropathy and autonomic degeneration. Fecal incontinence can be indicative of autonomic damage (parasympathetics = rest + digest = poop; There was a UWorld Q about constipation + parasympathetics - can't remember ID Sorry).

A. Dysuria --> Not related to NEG or osmotic damage

C. Inability to climb stairs --> Motor > sensory, so unlikely NEG or osmotic

D. Night-time leg cramps --> Claudication/PAD can present with symptoms that are worse at night when legs are horizontal with height, however this isn't cramping pain, which hints to an MSK problem or RLS.

E - Sciatica --> Not related to NEG or Osmotic Damage.

That leaves us with B --> Erections are obtained by pointing, shooting, and squeezing (parasympathetics, sympathetics, somatic). Impotence specifically is failure to obtain erection = failure to point = failure of parasympathetics = autonomic instability secondary to osmotic damage

Reference = FA2018 - page 344

drdoom  damn this write-up beautiful +  


submitted by xxabi(252),
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I aws nduer het snemrpoisi hatt tihs was na aicotr istisdco,ne ude to "eersev shect p"ian as lwle sa eht esfal nemlu ni hte aort.a dAn HTN is the #1 kirs crofta orf ocitar dcnoiet.sis eoSeomn crretoc me if m'i ognw,r but I hitnk siht is tcaoir deitsscoin rteahr nhta raciot muysanre.

chefcurry  I believe so, FA 2018 pg 299 +3  
ergogenic22  It is dissection "extra lumen in the media of the proximal aorta" = "a longitudinal intimal (tunica intima) tear with dissection of blood through the media of the aortic wall" ... answer is still hypertension +2  
breis  FA 2019: 301 +  
pg32  First Aid says that aortic dissection causes widening of the mediastinum and is due to an intimal tear, so I thought it wasn't an aortic dissection. Can anyone help me understand why First Aid was wrong in this case? Thanks! +3  
nephroguy  @pg32 The question stems states that there is no widening of the Aorta, not the mediastinum. Widening of the mediastinum is seen in dissection while widening of the aorta is seen in aneurysm. Also the intimal tear creates a false lumen between the intima and media. Hope that helps! +9  
j44n  https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.118.312436 pictures worth a 1,000 character limit +  


The other comment is partially incorrect. If the drug molecules dissolve in blood, they do not have an anesthetic effect. If they have a low blood solubility, they do NOT dissolve in blood well which leads to a faster anesthetic effect.

The potency is related to the lipid solubility because the drug has to be lipid soluble to cross the blood-brain barrier. A drug with a higher lipid solubility will be able to reach a therapeutic dose in the brain at a lower administered dose, so lower lipid solubility = more potent.

This question asked about a quick induction time, so we want a drug with a low blood solubility so the drug will not dissolve in the blood and will more quickly cross into the brain.

In other terms, a low blood:gas partition coefficient = low blood solubility = short induction time.

As an aside, I strongly disagree with putting this site behind a large paywall given that all of the content on this site is user-generated. The site owner is profiting entirely off of the work of others, and I refuse to support him. I was able to comment without paying for a subscription, otherwise I would have left entirely at this point.

hello_planet  Ugh, it appears you can't edit comments. I meant that a higher lipid solubility = more potent. +1  
drdoom  nice explanation! +1  


Patient is suffering from Schizophrenia (1 year of symptoms). Treatment is with anti-psychotics (Risperidone: Atypical antipsychtic)

nbmeanswersownersucks  In case anyone considered Lithium because you thought she had Bipolar with psychotic features, her depressed and sad mood is more likely explained by the negative symptoms of schizophrenia and she would also need current symptoms of/a past history of mania for a diagnosis of Bipolar. +  
drdoom  ah, interesting: so you cannot diagnose bipolar without an episode of mania (either at presentation or some point in the past). nice. +  


submitted by seagull(1443),

WTF is this x-ray. I would be better off pepper-spraying myself in the eyes and looking at a good x-ray than this shit.

I do not even begin to see spondlolololisthesis here.

drdoom  will you be my attending? +2  


submitted by drdoom(819),
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tyIiablni to iimannat an icotneer = ecilteer ysfodnuitcn. oS now eth ntqouies si h"y"?W

,eaigFut fylfuctidi egspe,nli fiyfdtiluc ngccattnoeirn si srgnaitt to sudno eikl sroinedpse. "yclitfuDif gncieaontrc"tn hmigt eb rtenipdteer as dmaeirip veceixetu niftuonc ro het nbsngeingi of aetscu-lareldvra tenimead nmdtaeei( earldte to laslm tbu oumesunr cebalrre ,nic)afsrt tbu no pteS 1 anemedit lliw be antlabt .i.,(e tol"s sih yaw mho",e ""iennra,wgd ..ec)t

epeornsisD si acllatuy ncoomm retfa a ebidnigtaitl nteve iekl s,okrte as uyo ghmit xpcte.e itWh enrposseid mseoc a loss of aeusxl ntrsetei and —ieehsdtrta si edcsdreea biolid.

One anc emka eht utaenmrg atth a lsuc"arav ptn"taie hgmti evha osme ussise htwi ihs spei""p eeiaiosrrscolr,t(s pphetyh/scsataiptcrymatemai inoynfudct)s n,ad orf shit n,sorae taurlcnno neoitrce husdol eb eeddsacre; tbu noet htat notghni si ioedmnetn abotu nggiao-tnslnd aslcurav dseiaes n(o xh fo etrenyio)psnh.

sA a u,tesrl the etsb ewarsn ehccio rehe is C. (idoiLb eadsdcere utb unlncrtao ctrsnoiee lrmno).a The ibg eotsuiqn I avhe ,si owh hte ckeh sdeo tshi ygu onwk she' rdah ehwn se'h es?!!aepl :p

cbay0509  thank you +1  
ilikedmyfirstusername  there are several UWorld questions about psychogenic ED with the answer being normal libido and normal nocturnal erections, idgi +10  
djeffs1  Yeah NBME says its C, but I still think with a recent stroke you can't bank on normal nocturnal erections... +  
drdoom  @djeffs nocturnal erections happen at the level of the spinal cord (S2–S4)! a “brain stroke” (UMN damage or “cortical damage”) would not kill your ability to have nocturnal erections! https://en.wikipedia.org/wiki/Nocturnal_penile_tumescence#Mechanism +  
drjo  fatigue, difficulty sleeping and concentrating could be depression or hypothyroidism both of which can cause decreased libido +  
jurrutia  @djeffs1 when you say NBME say's it's C, how do you know that's the official answer? Did NBME post the answers somewhere? +  
djeffs1  in the versions I purchased from them they highlight the correct answer in the test review +  


submitted by sphazhang(0),

does anyone understand why the parathyroid hormone concentration is so high when this is supposed to be an iatrogenic hypoparathyroidism question? this really threw me off

drdoom  Inadvertent and abrupt ligation of an artery kills the blood supply to tissue (ISCHEMIA). The tissue (parathyroid gland) will begin to undergo necrosis, releasing its contents, which, in this case, includes a boatload of PTH. +1  


This question is actually a lot deeper than it looks. It is not about "when do you treat thrombocytopenia", which you DO treat when they have bleeding like in the question. This question is about management of ALL which has specific guidelines. According to uptodate, as long as platelet levels are about 20,000 in ALL, you are good to go for a bone biopsy.

drdoom  very nice +  


submitted by mcl(586),
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hsiT giame si .lseuuf tNoe htta teh isnat sdue askme lenymi erpapa a.rkd

ettVnieg si capytil ofr sirska'Pnon essdiea. rAea D si eth tstbasanui .iarng

oznefu  Oh nice! Thanks! +  
bend_nbme_over  Great image thanks! Even though it was an MSU link :P Go Blue! +  
apurva  Saved My life +1  
john198  is this link only for MSU students??? , I can't access it . +  


submitted by pingra(2),

I thought of this as a giant physiologic shunt (ie, due to the pneumothorax there is no ventilation to an entire lung, as a consequence you retain CO2) - not sure if this is the actual mechanism but it helped me get this question right

hopefully this helps!

drdoom  this definitely makes sense to me, especially if it happens “acutely”/suddenly. if someone gets a lung or lobe removed, e.g., cancer, my guess is that the reminaing lung would “remodel” over time and recoup at least some of that lost surface area — in the same way new anastomoses form in the weeks or months after near-complete artery blockage (as guided by VEGF elaboration) +  
drdoom  but in the case where it happens “all of sudden”, i totally agree you’re going to get CO2 retention +  


submitted by pingra(2),

I thought of this as a giant physiologic shunt (ie, due to the pneumothorax there is no ventilation to an entire lung, as a consequence you retain CO2) - not sure if this is the actual mechanism but it helped me get this question right

hopefully this helps!

drdoom  this definitely makes sense to me, especially if it happens “acutely”/suddenly. if someone gets a lung or lobe removed, e.g., cancer, my guess is that the reminaing lung would “remodel” over time and recoup at least some of that lost surface area — in the same way new anastomoses form in the weeks or months after near-complete artery blockage (as guided by VEGF elaboration) +  
drdoom  but in the case where it happens “all of sudden”, i totally agree you’re going to get CO2 retention +  


submitted by sugaplum(326),

These are symptoms of acute benzo withdrawl

drdoom  holy cow you are crushing it right now. frickin POWER SESSION +1  


submitted by sugaplum(326),

sclera injection and munchies

In the words of afroman. I was gonnna go to work....but then I got high...

drdoom  I was gonna get up and find the broom but then I got high .. +1  


submitted by madojo(163),
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I o'tnd okwn fi tish aws the irhgt wya i tutoghh botau it tub i beemreermd Ath.K.HL.eC . gistnh taht aecus tsnaavlodioi ni eaktlels sumlce

C - ,oC2 H - +,H -A seeadnoni, L - ectaatl K- +K

drdoom  This is great; these are all proxies of catabolism, i.e., "net" ATP consumption! (ATP->ADP) +1  
drdoom  Potassium might be the one that doesn't seem to fit but recall that cells have an H+/K+ antiporter: cells can act as a "sink" for high blood H+; they "take up" H+ (from blood, into cell) but "in exchange" they have to put out a K+ (to maintain a normal electro-gradient). So, as blood acid starts to creep up, cells actually "attempt" to bring it back to equilibrium by sucking up H+ (and putting out K+, which, as you surely recall ;), is the predominant cation within cells). +3  
misterdoctor69  @drdoom, would you also venture to say that there is increased Na+/K+ ATPase activity in an increased metabolic state which might also contribute to greater K+ efflux into the blood? +  
drdoom  @misterdoctor69, no. Potassium flow is driven by its chemical gradient (from inside cell, where its concentration is high, to outside). If K+ efflux is increased, the best culprit would be the H+/K+ antiporter (which “takes up” a proton, but has to “surrender” a potassium, in an attempt to remove acid from the blood — acidic blood, of course, being an inevitable outcome of revved metabolic state: net ATP consumption & high CO2 production). +  


submitted by beetbox(1),

Can someone explain more on how to tackle these types of questions? I suck at these questions for real... To me, he sounded pretty sane and reasonable (does not wish to waste other people's money). Sure he might be under slight depression judging how he has a terminal illness and his statement on how nobody cares for him. But unless he is incoherent or displaying magical thinking, signs of loss of memory etc., why should he be evaluated on decision-making capacity?

drdoom  in medical parlance, you can be so depressed that you're actually cognitively impaired. this is known as pseudodementia. thus, you need to figure out: “is this guy so depressed we can deem him incompetent to make decisions?” +  
rockodude  he says he has an invention to cure arthritis in 6 months he'll be back.. not normal imo. at least for this question thats the line that made me think does this person have capacity +  


submitted by keycompany(301),
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olFw atRe = iecyltoV x S-nCirsstcoloae reaA

2 cm^2 x 02 cem/cs x 60 cnsi/em x 1 ,/L0100 ^3cm = 42. mniL/

0,010 ^cm3 = 1 L

seagull  Well, I missed this one. I don't even feel bad. +58  
link981  @keycompany a small typo, 100 cm^3 = 1 L not 1000cm^3. 1000 mL^3= 1 L +  
hello  @keycompany how did you edit your original comment to fix your typo? +  
winelover777  Pretty sure @keycompany was correct. 1 L = 1000 cm^3. Otherwise the answer would be 24. +3  
drdoom  1 centimeter is a distance. (A line.) +  
drdoom  If we multiply a line by another line, we get a surface area. (A piece of paper.) +  
drdoom  If we multiply the piece of paper by another line, we get volume. (A cube. A box.) +  
drdoom  If we fill the box with a fluid, we will have 1 mL of this fluid. +  
drdoom  If we have a thousand of these boxes, we have 1 L of fluid. +  
drdoom  1,ooo mL = 1 Liter = 1,ooo centimeter³ +  


submitted by keycompany(301),
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olFw eRta = ltVioyce x oersol-SsictanC aerA

2 ^cm2 x 20 mc/ces x 60 mn/scei x 1 0,/00L1 ^m3c = .24 iLm/n

0,001 3^cm = 1 L

seagull  Well, I missed this one. I don't even feel bad. +58  
link981  @keycompany a small typo, 100 cm^3 = 1 L not 1000cm^3. 1000 mL^3= 1 L +  
hello  @keycompany how did you edit your original comment to fix your typo? +  
winelover777  Pretty sure @keycompany was correct. 1 L = 1000 cm^3. Otherwise the answer would be 24. +3  
drdoom  1 centimeter is a distance. (A line.) +  
drdoom  If we multiply a line by another line, we get a surface area. (A piece of paper.) +  
drdoom  If we multiply the piece of paper by another line, we get volume. (A cube. A box.) +  
drdoom  If we fill the box with a fluid, we will have 1 mL of this fluid. +  
drdoom  If we have a thousand of these boxes, we have 1 L of fluid. +  
drdoom  1,ooo mL = 1 Liter = 1,ooo centimeter³ +  


submitted by keycompany(301),
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owFl Reta = ecoyVlit x CissSo-anrocelt arAe

2 ^2cm x 02 esc/cm x 60 icns/me x 1 L00/10, m3^c = 2.4 /mniL

00,10 3cm^ = 1 L

seagull  Well, I missed this one. I don't even feel bad. +58  
link981  @keycompany a small typo, 100 cm^3 = 1 L not 1000cm^3. 1000 mL^3= 1 L +  
hello  @keycompany how did you edit your original comment to fix your typo? +  
winelover777  Pretty sure @keycompany was correct. 1 L = 1000 cm^3. Otherwise the answer would be 24. +3  
drdoom  1 centimeter is a distance. (A line.) +  
drdoom  If we multiply a line by another line, we get a surface area. (A piece of paper.) +  
drdoom  If we multiply the piece of paper by another line, we get volume. (A cube. A box.) +  
drdoom  If we fill the box with a fluid, we will have 1 mL of this fluid. +  
drdoom  If we have a thousand of these boxes, we have 1 L of fluid. +  
drdoom  1,ooo mL = 1 Liter = 1,ooo centimeter³ +  


submitted by keycompany(301),
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olFw taRe = leoctyiV x -cteiCsnoalSsro Area

2 c^m2 x 20 scme/c x 06 nmc/ies x 1 0L01/,0 mc3^ = 42. imn/L

0010, c^m3 = 1 L

seagull  Well, I missed this one. I don't even feel bad. +58  
link981  @keycompany a small typo, 100 cm^3 = 1 L not 1000cm^3. 1000 mL^3= 1 L +  
hello  @keycompany how did you edit your original comment to fix your typo? +  
winelover777  Pretty sure @keycompany was correct. 1 L = 1000 cm^3. Otherwise the answer would be 24. +3  
drdoom  1 centimeter is a distance. (A line.) +  
drdoom  If we multiply a line by another line, we get a surface area. (A piece of paper.) +  
drdoom  If we multiply the piece of paper by another line, we get volume. (A cube. A box.) +  
drdoom  If we fill the box with a fluid, we will have 1 mL of this fluid. +  
drdoom  If we have a thousand of these boxes, we have 1 L of fluid. +  
drdoom  1,ooo mL = 1 Liter = 1,ooo centimeter³ +  


submitted by keycompany(301),
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Fowl eRta = itecoylV x aisCoSrsectoln- Area

2 ^2cm x 02 escm/c x 60 cneis/m x 1 /L,0100 mc^3 = 4.2 iL/nm

00,10 m^c3 = 1 L

seagull  Well, I missed this one. I don't even feel bad. +58  
link981  @keycompany a small typo, 100 cm^3 = 1 L not 1000cm^3. 1000 mL^3= 1 L +  
hello  @keycompany how did you edit your original comment to fix your typo? +  
winelover777  Pretty sure @keycompany was correct. 1 L = 1000 cm^3. Otherwise the answer would be 24. +3  
drdoom  1 centimeter is a distance. (A line.) +  
drdoom  If we multiply a line by another line, we get a surface area. (A piece of paper.) +  
drdoom  If we multiply the piece of paper by another line, we get volume. (A cube. A box.) +  
drdoom  If we fill the box with a fluid, we will have 1 mL of this fluid. +  
drdoom  If we have a thousand of these boxes, we have 1 L of fluid. +  
drdoom  1,ooo mL = 1 Liter = 1,ooo centimeter³ +  


submitted by keycompany(301),
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olwF tRea = Vetloyic x ientsCsar-oSlco aAer

2 m^c2 x 20 csc/me x 60 mencis/ x 1 ,/1L000 ^3cm = .24 /mLin

0,100 m^c3 = 1 L

seagull  Well, I missed this one. I don't even feel bad. +58  
link981  @keycompany a small typo, 100 cm^3 = 1 L not 1000cm^3. 1000 mL^3= 1 L +  
hello  @keycompany how did you edit your original comment to fix your typo? +  
winelover777  Pretty sure @keycompany was correct. 1 L = 1000 cm^3. Otherwise the answer would be 24. +3  
drdoom  1 centimeter is a distance. (A line.) +  
drdoom  If we multiply a line by another line, we get a surface area. (A piece of paper.) +  
drdoom  If we multiply the piece of paper by another line, we get volume. (A cube. A box.) +  
drdoom  If we fill the box with a fluid, we will have 1 mL of this fluid. +  
drdoom  If we have a thousand of these boxes, we have 1 L of fluid. +  
drdoom  1,ooo mL = 1 Liter = 1,ooo centimeter³ +  


submitted by tinydoc(223),

https://www.mayoclinic.org/tests-procedures/pap-smear/expert-answers/pap-smear/faq-20057782#:~:text=If%20you're%20a%20virgin,lower%20end%20of%20your%20uterus.

Patients often think that not sexually active is only for vaginal intercourse and might not think that it counts. Also HPV isn't the only risk factor for HPV (smoking, fam hx etc.). Obviously the risk is a lot lower but they should still consider getting tested.

drdoom  I’ll take “More unpleasant things about being a virgin” for 200, Alex. +1  


submitted by johnthurtjr(139),
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rs'eeh a olgoge

johnthurtjr  FTR I had no idea this was a thing, and was pretty disappointed in myself when the google search had it in big bold letters right in my face. +3  
drdoom  via @johnthurtjr link: "Testosterone and other androgens have an erythropoietic stimulating effect that can cause polycythemia, which manifests as an increase in hemoglobin, hematocrit, or red blood cell count." https://www.medscape.com/viewarticle/773465 +3  
meningitis  I guess that's another reason for steroids and doping up. +7  
drschmoctor  For once I feel like I've been led astray by Pathoma. My instinct was to go with hemoglobin, but I talked myself out of it after remembering Dr. Sattar saying that the reason why women have lower hemoglobin is due to menstruation. +2  
fexx  F U testosterone! and F U NBME 22 question +1  
schep  I only knew this because there are three (at least three, maybe more that I don't know) contraindications to giving testosterone replacement therapy: +OSA +prostate cancer +hematocrit >50% +2  
drdoom  ^ linkify @drdoom https://www.medscape.com/viewarticle/773465 +  


submitted by syoung07(21),

if you are 68 and still dating Palmala Handerson, your libido isnt low my friends.

drdoom  amen +  


submitted by cbreland(62),

If you knew that basement membrane disruption prevents restoration of normal tissue (repeat from another NBME), then you missed this because you didn't know what "preclude" means.

Missing questions I miss due to lack of vocab and grammar, you love to see it

cbreland  Say a prayer for me +  
drdoom  you can include. you can exclude. or you can altogether preclude. +1  
drdoom  all these words, along with “claudication”, share the same Latin root: clud = claud (to shut) +  
dhpainte22  Missed it for the same reason :( +1  


submitted by cbreland(62),

If you knew that basement membrane disruption prevents restoration of normal tissue (repeat from another NBME), then you missed this because you didn't know what "preclude" means.

Missing questions I miss due to lack of vocab and grammar, you love to see it

cbreland  Say a prayer for me +  
drdoom  you can include. you can exclude. or you can altogether preclude. +1  
drdoom  all these words, along with “claudication”, share the same Latin root: clud = claud (to shut) +  
dhpainte22  Missed it for the same reason :( +1  


submitted by haozhier(16),

Can someone please explain to me: If the posterior 1/3 of the tongue is developed from 3rd and 4th pharyngeal arches, why is it wrong to choose pharyngeal arch?

therealslimshady  Welcome to NBME +2  
mutteringly  First time? (meme) +1  
drdoom  That would be like choosing “blastula” if it were an option: it's not wrong but there's a more precise answer. +  
pontiacfever  That is wrong. They're indicating towards thyroglossal duct/thyroid which originates from Pharyngeal pouch not arch. secondly, they're asking that the mass originated from which structure. So, as we know it is associated to foramen cecum which is related to tongue. +  
drdoom  @pontiacfever, i believe you’re responding to @haozhier’s original comment, yes? +  
pontiacfever  @drdoom, yes the original comment by @haozhier +1  


submitted by j44n(42),

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

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. +  


submitted by haozhier(16),

Can someone please explain to me: If the posterior 1/3 of the tongue is developed from 3rd and 4th pharyngeal arches, why is it wrong to choose pharyngeal arch?

therealslimshady  Welcome to NBME +2  
mutteringly  First time? (meme) +1  
drdoom  That would be like choosing “blastula” if it were an option: it's not wrong but there's a more precise answer. +  
pontiacfever  That is wrong. They're indicating towards thyroglossal duct/thyroid which originates from Pharyngeal pouch not arch. secondly, they're asking that the mass originated from which structure. So, as we know it is associated to foramen cecum which is related to tongue. +  
drdoom  @pontiacfever, i believe you’re responding to @haozhier’s original comment, yes? +  
pontiacfever  @drdoom, yes the original comment by @haozhier +1  


submitted by azibird(162),

This is the most poorly drawn cell diagram. I see zero ribosomes, so I figured F was the smooth endoplasmic reticulum. However, now I can see that the curved organelle is the golgi apparatus and F must represent the whole endoplasmic reticulum.

I believe plasma membrane proteins are synthesized in the rough endoplasmic reticulum.

FA2020 p46 Rough endoplasmic reticulum Site of synthesis of secretory (exported) proteins and of N-linked oligosaccharide addition to lysosomal and other proteins.

Free ribosomes—unattached to any membrane; site of synthesis of cytosolic, peroxisomal, and mitochondrial proteins.

Smooth endoplasmic reticulum Site of steroid synthesis and detoxification of drugs and poisons. Lacks surface ribosomes. Location of glucose-6-phosphatase (last step of glycogenolysis).

nbmeanswersownersucks  I was under the impression that translation of transmembrane proteins begins with ribosomes in the cytoplasm that then translocate to the rough ER once the signal sequence is reached by the ribosome? i.e. technically translation begins in the cytoplasm but finishes in the rough ER. Am I wrong about that? +4  
nbmeanswersownersucks  It was UWORLD 6544 about insulin translation. They state that the translation is initiated in the cytoplasm then relocates to the RER (d/t the signal sequence) and is finished there. So is there a difference in translation steps for proteins that are excreted like insulin and transmembrane proteins? +2  
nsinghey  Same, I am not sure about this. My best guess is that since insulin is not a functional protein, it is not synthesized in the RER (even though it it excreted from the cell). Actual proteins are made in the RER +2  
kevster123  I just put F cause it said transmembrane domains and I know the rough ER got a lot of balls on it that translate it through and to translate through the balls you're passing through membranes. +  
drdoom  @nbmeanswersownersucks @nsinghey et al. There is extensive discussion of this on an NBME 24 thread. This link will take you to the comments (just don't scroll up to spoil the answer for yourself!): https://nbmeanswers.com/exam/nbme24/939#1379 +  
drdoom  also, this thread from NBME 21 discusses cell transport more generally (same warnings apply! don't scroll up!): https://nbmeanswers.com/exam/nbme21/742#257 +  
brise  The question is saying where is it initially produced? It is produced in the RER, therefore F. Not asking where it's production starts- asking where is it produced etc. +1  


submitted by azibird(162),

This is the most poorly drawn cell diagram. I see zero ribosomes, so I figured F was the smooth endoplasmic reticulum. However, now I can see that the curved organelle is the golgi apparatus and F must represent the whole endoplasmic reticulum.

I believe plasma membrane proteins are synthesized in the rough endoplasmic reticulum.

FA2020 p46 Rough endoplasmic reticulum Site of synthesis of secretory (exported) proteins and of N-linked oligosaccharide addition to lysosomal and other proteins.

Free ribosomes—unattached to any membrane; site of synthesis of cytosolic, peroxisomal, and mitochondrial proteins.

Smooth endoplasmic reticulum Site of steroid synthesis and detoxification of drugs and poisons. Lacks surface ribosomes. Location of glucose-6-phosphatase (last step of glycogenolysis).

nbmeanswersownersucks  I was under the impression that translation of transmembrane proteins begins with ribosomes in the cytoplasm that then translocate to the rough ER once the signal sequence is reached by the ribosome? i.e. technically translation begins in the cytoplasm but finishes in the rough ER. Am I wrong about that? +4  
nbmeanswersownersucks  It was UWORLD 6544 about insulin translation. They state that the translation is initiated in the cytoplasm then relocates to the RER (d/t the signal sequence) and is finished there. So is there a difference in translation steps for proteins that are excreted like insulin and transmembrane proteins? +2  
nsinghey  Same, I am not sure about this. My best guess is that since insulin is not a functional protein, it is not synthesized in the RER (even though it it excreted from the cell). Actual proteins are made in the RER +2  
kevster123  I just put F cause it said transmembrane domains and I know the rough ER got a lot of balls on it that translate it through and to translate through the balls you're passing through membranes. +  
drdoom  @nbmeanswersownersucks @nsinghey et al. There is extensive discussion of this on an NBME 24 thread. This link will take you to the comments (just don't scroll up to spoil the answer for yourself!): https://nbmeanswers.com/exam/nbme24/939#1379 +  
drdoom  also, this thread from NBME 21 discusses cell transport more generally (same warnings apply! don't scroll up!): https://nbmeanswers.com/exam/nbme21/742#257 +  
brise  The question is saying where is it initially produced? It is produced in the RER, therefore F. Not asking where it's production starts- asking where is it produced etc. +1  


submitted by vshummy(156),
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I nhikt mreo gnl,elraey ioeptnr ndligfo hneaspp ta hte RER dna the mtes syas eht pneirto esdtno’ ldof lerppr.yo ciclla,eSpyfi eht tsom mcomon FC tmnatiou si a olfdmedis oeptnir dna the teonrip is eirandte in eht ERR adn tno anstrtroped to the elcl barnemme - AF 0912 pg 6.0

uroosisyed5  Which makes sense if we think about the pathophys of elevated Cl- and Na intracellularly. Both of these ions go up inside the cells due to the retention of the misfolded proteins in the RER. +  
lilyo  I actually disagree with this reasoning. The pathophysiology in CFTR is not due to accumulation of misfolded proteins. It is due to decreased/absent ATP gated transmembrane Chloride channel. According to Uworld, the miscoded protein is detected by the Endoplasmic Reticulum. The abnormal protein is targeted for destruction by the proteasome and never reaches the cell surface. There is NO retention of misfolded protein, there is degradation of misfolded protein and therefore absence of chloride channels on the membrane. This is what leads to impaired removal of salt from the sweat as well as decreased NaCl in mucus. I dont think the answer should be ER. Can anyone tell me if I am missing something here that makes the answer ER as opposed to cytoplasm? Because the way I see if is misfolded proteins go form the ER into the cytoplasm to reach the proteasome and then be destructed. Uworld questions ID are 805, 802, 1514, and 1939. +15  
drdoom  @lilyo The CFTR is a transmembrane protein. Like all proteins, its translation begins in the cytosol; that said, CFTR contains an N-terminus “signal sequence”, which means as it is being translated, it (and the ribosome making it!) will be transported to the Endoplasmic Reticulum.^footnote! As it gets translated, its hydrophobic motifs will emerge, which embeds the CFTR protein within the phospholipid bilayer of the ER itself! That means the protein will never again be found “in the cytosol” because it gets threaded through the bilayer (which is, in fact, how all transmembrane proteins become transmembrane proteins at the cell surface -- they have to be made into transmembrane proteins in the ER first!). +8  
drdoom  @lilyo (continued) So, yes, ultimately, these misfolded proteins will be directed toward a proteasome for degradation/recycling, but that will happen as a little vesicle (or “liposome”); the misfolded protein, in this case, is not water-soluble (since, by definition, it has hydrophobic motifs which get “threaded through” a bilayer to create the transmembrane pattern), which means you won’t find it in the cytosol. +5  
drdoom  ^footnote! : The movement of active* ribosomes from the cytosol to the Endoplasmic Reticulum is why we call that area of ER “rough Endoplasmic Reticulum (rER)”; on electron microscopy, that section was bespeckled with little dots; later, we (humans) discovered that these dots were ribosomes! +1  
drdoom  * By “active ribosomes”, I just mean ribosomes in the process of converting mRNA to protein! (What we call “translation” ;) +1  
wrongcareer69  How many goddamn ways are they going to test us on CF. I'm so over this! +2  
furqanka  also in FA, under alpha 1 antitrypsin, its says 'Misfolded gene product protein aggregates in hepatocellular ER". might be the same concept. +3  
joanmanuel26  According to Kaplan; All proteins that are synthesized in the ER must fold correctly in order to be transported to the golgi aparatus and then to their final destinations. If the mutation cause a misfolded protein, the result will be the loss of the protein function and, in some cases, accumulation of the protein in the ER. +  
drdoom  @lilyo Thinking about this more. You will not find the (misfolded) protein in the cytosol. The misfolded protein may be inside a proteasome—and a proteasome may live in the cytosol—but the misfolded protein itself will never appear in the cytosol. The products of its degradation might (constituent amino acids or small peptides) but if you had an antibody for the misfolded protein and asked it “Where is the misfolded protein?”, the antibody would answer: “Most of what I could find appears to be in the rER.” +  


submitted by drdoom(819),
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eTh CFRT epinrot is a srnamremnbaet pnio.ret eikL lal rtpeison, tsi laisarottnn gebnsi in eth st;coyol taht ai,sd RCFT antsconi na neur-Nsimt sgn“ial unecqsee,” hchwi sanme sa ti is igebn tatlrsaned, ti ad(n the moorsibe manigk !)ti ilwl be taorpdnters ot teh ocnElimapds m^.tecuulRi!otfeonot

sA it segt ,tlaastdren sti ihboorhpycd imtsof llwi eerm,eg iwchh ebdmse het RCFT npoerti thiwin the dphiopiholps bryaiel of the ER stefli! ahtT senam eht ropenit wlli neerv aiagn be udfno “in eth tclo”soy saeuceb ti gste eedrhtad uhohtgr het iyrblea ci(hhw ,si ni atfc, hwo all enrnsrmaabtem stpenroi eoembc rmternbaenmsa eotprisn ta eht elcl ceurfsa -- they heav to eb amed toin beemnrmrstana onepsrti in eht ER st!.ifr)

oS, yes, lm,atuytiel seteh mdlsodfie rnsoeipt lwil be eriectdd rwdoat a eaometrsop for glade,onirendiargcct/y tub atth liwl ppahen sa a tillet seevlci (or ”lomip“o)s;e teh selfdodim ,nrtoepi ni htsi scea, is otn tsowl-eeuarbl csn,i(e yb idioinen,tf ti ahs opohchrydbi fistmo chwhi get hedr“daet ”hgrthuo a briylea ot aeterc the anrmntremsbea tpnt)a,er ichwh mesna yuo o’wtn ifnd it in eht tos.yloc


\ otfooen!t \ heT inihthcg of *vtceia emrbsoosi to the apnEidomlsc ilRtumcue si yhw we clal ttah aaer of RE ohr“ug Epicnomdsal ectilRuum ;”)R(Er no olneertc c,icsoormpy ttha cnsoeit aws plekecbeds twhi illett tos;d rel,at we um)anhs( isdrdeceov ttah ethse dtos eewr mb!esiosor

\ * \ yB ca“veti ”oseb,sromi I stuj eamn mesosbiro ni eth sosperc fo ctennovgri NAmR to neoi!rpt tahW( we lcal nar”tnast“lio ;)

For a eragt letilt uyrmsam fo eth mcEpnidoasl ilmceuutR na(d namy rohet cnptecso ni ermulcola o,ygoil!)b ese tsih rfmo ’lbtAers elulaMroc oBoygil fo the Clel:
wmwoBkw/.AiiohKn4lNs..0#bp.1/no//2t2:/86bhngs2ct4v

drdoom  ^ I'm just re-stating in one comment what I wrote in multiple subcomments above: https://nbmeanswers.com/exam/nbme24/939#1379 +  


submitted by lfcdave182(31),

Cold temperature: Causes peripheral vasoconstriction and central vasodilation

  • Increased central blood volume --> Lower ADH due to increased blood volume through kidneys
  • Increased central blood volme --> leads to atrial stretching, increased preload --> Increased ANP release
passplease  what organs are considered "central"? I initially thought that the kidneys would not be getting more blood with most of the blood flow going to the lungs and heart +1  
brise  Same :( +  
drdoom  the kidneys are the lungs for waste products that can't be expelled via your breathe. (another way of saying this is: the lungs are like the kidneys of your mouth: instead of urinating out of your mouth, you "pee out" CO2 in the form of expired air.) tl;dr the kidneys are very vital organs!! +1  


submitted by apurva(68),

THIS IS KAPOSI's SARCOMA ==> give antineoplastic

"THIS IS JUST TO LENGTHEN THIS ANSWER, NEVER EVER PAY THIS SITE, EDUCATION SHOULD BE FREE FOR ALL!"

michaelshain2  It's unfortunate that I had to pay in order to get these answer explanations. They aren't as informative/thorough on freenbme :/ +3  
jamaicabliz  So annoyed, I thought it was asking us to recognize that it could also be Bacillary Angiomatosis from Bartonella, which also presents in the immunocompromised... So any different study materials stress the importance of differentiating them, given they look very similar. +2  
drdoom  @apurva tell that to my loan officer!😝😂😂 +  
cbreland  Between this and bacillary angiomatosis, I think it came down to Kaposi being more likely with a HIV patient and also the lesions being purple +  
jsanmiguel415  It says that "in addition to treatment with highly active antiretroviral therapy" which makes me think this is HHV-8 -> Kaposi sarcoma. Bartonella is bacterial and would be treated with azithro + doxy +  


submitted by ergogenic22(303),
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looC dan ealp etteirxseim rluse tou tivrieisbtud uesasc oe(ngrc,ueni hi,xpsaanaly set.p)ci

loHyomivcep uldwo bseecdir a rceopss of meovul sols bed(ngeil or oer)dhtiydan nda lwuod ton nlapiex hte arecsckl ro uaulrgj eivn oteisinnds.

o'ntd be trhnwo off by hte romlna ahetr n.dssou

baja_blast  Raise your hand if you were also thrown off by the normal heart sounds. +6  
jmd2020  I think this question is poorly constructed. Cardiogenic shock would result in an INCREASE in SVR - this woman's BP is 70/40... +1  
drdoom  @jmd2020 low BP does not mean the SVR isn't increased — it /is/ increased! it's just that the heart is so effed up that even massively increased SVR is not enough to maintain good pressure +2  
drdoom  another way to explain: imagine you are losing blood volume at a constant rate (someone punched a tube into your aorta and draining you like a pig); at first, your heart would beat stronger (ionotropy) and faster (chronotropy) to maintain BP; at the same time, all your arterioles would constrict to maintain blood flow rates (and perfusion) to vital tissues ... but at some point you will have lost so much blood that all the ionotropy, chronotropy & SVR in the world could not save you or your BP .. your BP will plummet no matter what compensatory mechanisms your body has up its sleeve. +3  
drjo  Jugular venous distension clued me into cardiogenic shock (heart isn't pumping well resulting in back up) vs the others listed, esp since obstructive shock isn't an answer choice +  


submitted by ergogenic22(303),
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ooCl dna leap metxieeitsr rleus tou iiuridebsttv ssueac ic(orgeenu,n aanxy,ialhsp si.pcet)

polmoyeciHv ludwo dscieerb a peoscsr of lovemu olss be(dglnie or yrndeotdhia) nda wdluo ont piaxenl teh lescrcak or gulaurj inve ssiteno.nid

dt'no eb rnhwto fof by het oranlm ertha s.nsudo

baja_blast  Raise your hand if you were also thrown off by the normal heart sounds. +6  
jmd2020  I think this question is poorly constructed. Cardiogenic shock would result in an INCREASE in SVR - this woman's BP is 70/40... +1  
drdoom  @jmd2020 low BP does not mean the SVR isn't increased — it /is/ increased! it's just that the heart is so effed up that even massively increased SVR is not enough to maintain good pressure +2  
drdoom  another way to explain: imagine you are losing blood volume at a constant rate (someone punched a tube into your aorta and draining you like a pig); at first, your heart would beat stronger (ionotropy) and faster (chronotropy) to maintain BP; at the same time, all your arterioles would constrict to maintain blood flow rates (and perfusion) to vital tissues ... but at some point you will have lost so much blood that all the ionotropy, chronotropy & SVR in the world could not save you or your BP .. your BP will plummet no matter what compensatory mechanisms your body has up its sleeve. +3  
drjo  Jugular venous distension clued me into cardiogenic shock (heart isn't pumping well resulting in back up) vs the others listed, esp since obstructive shock isn't an answer choice +  


submitted by step_prep(48),
  • Tricky, nuanced question because contraindication to patient receiving a lung resection is if their residual FEV1 will be less than 800 mL following the surgery

  • Normal FEV1 in a healthy woman is typically around 3 L, so in this patient is likely close to 750 mL since she has an FEV1 that is 25% of predicted; therefore, this patient would likely not be able to tolerate any sort of lung resection because she is already barely hanging on in terms of her ventilatory capabilities

  • Could also approach this question through process of elimination because ABG shows mild CO2 retention (seen in many COPD patients), ejection fraction cut-off for surgery often <35%, cardiac stress test was normal and patient has had DVTs for a long time

https://step-prep.org/

drdoom  very nice +  


submitted by googaga(1),

Testing testing 123. This is a test post to see if things un scram ble by typing a comment. Thanks.

drdoom  i respect this attempt but i don't think it works that way +  


submitted by hello(302),
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yWh 'snti thsi a hoortc y?stud

drdoom  This is a cohort study! (Since it involves splitting people into "groups"; group = cohort.) But the stem asks what "best describes" the design. So, yes, it's a cohort study but a more precise ("more specific") description is Open-label. In other words, "Open-label clinical trial" is a type of cohort study, and, in this case, "Open-label" is a more precise description of what is described in the stem. +7  
drdoom  For a more technical explanation of "Cohort studies", see the definition from the National Library of Medicine: https://meshb.nlm.nih.gov/record/ui?ui=D015331 +1  
angelaq11  It is a cohort, just as @drdoom said, but it isn't an "Observational" one. +2  
pg32  It's actually not a cohort study, imo. In a cohort you find people with an exposure and see if they develop some outcome. In this experiment, people were RANDOMLY ASSIGNED to the different exposures. That doesn't happen in cohorts. +7  
pg32  It may be a cohort in that these people are in groups, but for the purposes of Step 1, I don't think we will deal with typical "Cohort" studies in which participants are randomly assigned. +2  
ashli777  you don't administer an intervention in a cohort study, you just observe what happens. it is an observational study. +  
drdoom  ^ i retract my earlier subcomment! thanks @ashli777 and @pg32 — you guys are right that cohorts do not intervene! in two senses: (1) there is no treatment intervention and (2) there is no “assignment” intervention (either randomly or by selection; that is, investigators do not DESIGN or DETERMINE how groups are formed, even if that means random determination by computer). +1  


submitted by drdoom(819),
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Smte caytlaul ,attess “nO ,intsunegioq the atnipet does not wkon het aedt [m]iet, eht amen of eth soiptlah cl]ap[e, ro teh amen fo rhe usnre who dha sjut cuirenodtd lmifseh snoepr][”. oS, pt is dteieinrdos to ietm nad eclpa h(Cieoc A;) htta si fnietleiyd nnrccionge -- as uodlw eb edspderes oodm (oCchie )E and eth eroht ocsheic -- utb ya“ibitlni to ndrtenadus syveirte dan sgnosip”ro si eht tsmo gcrionnecn iensc thta is the yver inetdfoini of t.ciyaacp ntIbiiayl to enadsdtrun = lcka fo ypati.cac

lovebug  you explain very clearly. THX!!! +  
drdoom  thanks lovebug! +  


submitted by lovebug(13),

really curious about why not (C) Suggest that the couple to a therapist together.? T.T

drdoom  thou shall not punt nor refer thy patient to another +4  
lovebug  Oh, thank you! +  
drdoom  yeah, think about it this way: the Step exams are here to certify “this person can practice medicine in your state without supervision.” even the most worshipped and glorified neurosurgeons have to pass the Steps. that’s because, at the end of the day, all responsibility (and liability) falls on the physician of record. “the buck stops here,” as they say. so, the Step needs to assess that you can make a decision when no one else is around. it couldn’t do that if it allowed you to choose “refer this problem to someone else.” +2  
csalib2  @drdoom fantastic point. never thought of it that way. +  
lovebug  @drdoom THX! very sweet explanation! +  


submitted by bingcentipede(219),

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. +1  
feochromocytoma  Clopmiphene is usually the answer for infertility with NORMAL anatomy and NORMAL appearing labs +  
drdoom  very nice +  
cheesetouch  FA18 p 637 +  


submitted by lovebug(13),

really curious about why not (C) Suggest that the couple to a therapist together.? T.T

drdoom  thou shall not punt nor refer thy patient to another +4  
lovebug  Oh, thank you! +  
drdoom  yeah, think about it this way: the Step exams are here to certify “this person can practice medicine in your state without supervision.” even the most worshipped and glorified neurosurgeons have to pass the Steps. that’s because, at the end of the day, all responsibility (and liability) falls on the physician of record. “the buck stops here,” as they say. so, the Step needs to assess that you can make a decision when no one else is around. it couldn’t do that if it allowed you to choose “refer this problem to someone else.” +2  
csalib2  @drdoom fantastic point. never thought of it that way. +  
lovebug  @drdoom THX! very sweet explanation! +  


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. +  


submitted by deberawr(4),

i got this question right only because when i worked as a med assistant in a derm office before med school, the dermatologist looked at my skin and asked me if i was eating a lot of carrots because my skin looked more orange than usual

drdoom  and precisely how many pounds of carrots were you eating? +  


submitted by cassdawg(959),

"Simple rules of the brainstem" (credit to our anatomy gods at UofL for organizing, also this image is fucking great for visual learners):

  1. There are 4 structures always in the ‘midline‘ beginning with M
    • Motor pathway (or corticospinal tract): damage results in contralateral weakness of the arm and leg
    • Medial Lemniscus: damage results in contralateral loss of vibration and proprioception in the arm and leg
    • Medial longitudinal fasciculus: damage results in ipsilateral inter-nuclear ophthalmoplegia (failure of adduction of the ipsilateral eye towards the nose and nystagmus in the opposite eye as it looks laterally)
    • Motor nucleus and nerve: damage results in ipsilateral loss of the cranial nerve that is affected (III, IV, VI or XII)

  2. There are 4 structures to the ‘side‘ (lateral) beginning with S
    • Spinocerebellar pathway: damage results in ipsilateral ataxia of the arm and leg
    • Spinothalamic pathway: damage results in contralateral alteration of pain and temperature affecting the arm, leg and rarely the trunk
    • Sensory nucleus of CN V: damage results in ipsilateral alteration of pain and temperature on the face in the distribution of CN V (this nucleus is a long vertical structure that extends in the lateral aspect of the pons down into the medulla)
    • Sympathetic pathway: damage results in ipsilateral Horner’s syndrome, that is partial ptosis and a small pupil (miosis)

  3. The rule of CN 4’s (also found in FA2020 p504)
    • 4 cranial nerves in the medulla (IX-XII)
    • 4 in the pons (V-VIII)
    • 4 above the pons (2 in the midbrain= III, IV, 2 in the cortex= I, II)
    • The 4 motor nuclei that are in the midline are those that divide equally into 12 (except I and II), including III, IV, VI and XII (V, VII, IX and XII are in the lateral brainstem)
cassdawg  Sorry for the formatting fuck up +  
drdoom  @cassdawg best to avoid doing nested lists. website doesn't seem to like that :P better to start a “brand new” list for each little subsection kinda thing :) p.s. congrats on your MVP of the Year Award! +1  


submitted by medstruggle(12),
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Wyh is ti not irovnaa focelill sel?cl I ghtutho the eamlfe gnloaa of ltireoS dan deLyig si oae/agnrltaushc lcse.l

colonelred_  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +7  
brethren_md  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +4  
sympathetikey  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +5  
s1q3t3  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +11  
masonkingcobra  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +3  
mcl  Wait, but did anyone mention that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen??? +37  
mcl  But seriously though, pathology outlines says sertoli-leydig tumor "may be suspected clinically in a young patient presenting with a combination of virilization, elevated testosterone levels and ovarian / pelvic mass on imaging studies." As for follicle cell tumors, granulosa cell tumors usually occur in adults and would cause elevated levels of estrogens. Theca cell tumor would also primarily produce estrogens. Putting the links at the end since idk if they're gonna turn out right lol Link pathology outlines for sertoli leydig granulosa cell tumor theca cell tumor +12  
bigjimbo  LOL +  
fallenistand  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +5  
medpsychosis  So after doing some intense research, UPtoDate, PubMed, an intense literature review on the topic I have come to the final conclusion that...... ...... ...... ...... Wait for it.... ..... ..... Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +9  
charcot_bouchard  Hello, i just want to add that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
giggidy  Hold up, so I'm confused - I read all the posts above but I still am unsure - are sertoli-leydig cells notorious for producing androgen? +4  
subclaviansteele  Hold the phone.....Females can get sertoli leydig cell tumors which are notorious for producing androgen? TIL TL;DR - Females can get sertoli leydig cell tumors = high androgens +  
cinnapie  I just found a recent study on PubMed saying "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" +2  
youssefa  Hahahahaha ya'll just bored +9  
water  Bored? you wouldn't think so if you knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +5  
nbmehelp  I dont get it +  
redvelvet  how don't you get it that females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen? +1  
drmomo  what if this means..... females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen +  
sunshinesweetheart  hahahaha this made my day #futurephysicians #lowkeyidiots +  
sunshinesweetheart  @medstruggle look up placental aromatase deficiency (p. 625 FA 2019), it would have a different presentation +  
deathbystep1  i am sure i would ace STEP 1 if i only knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +2  
noplanb  Wait... I might actually never forget this now lol +3  
drmohandes  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +1  
lilmonkey  Don't forget that females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens! You're welcome! +  
drpatinoire  Now I get it that females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens. Thank you very much.. So why choose Sertoli-Leydig cell tumor again? +  
dr_ligma  The reason is because females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens! This is easy to remember, as you can remember it through the simple mnemonic "FCGSLCTWANFPLOA" which stands for "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen!" +17  
minion7  after receiving a f*king score..... this post made me smile and thanks to the statement-- females can get sertoli-leydig cell tumours, which are notorious for producing lots of androgen! +1  
djtallahassee  My worthless self put adrenal zona fasciculate but now I will never forget that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
medguru2295  Wait..... so can females get Sertoli Leydig cells that produce androgens then?????? +  
peqmd  Going to snapshot this to my anki deck card: "females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of {{c1::androgens}}" +1  
paperbackwriter  Watch me f*ck up the fact that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgens on the real deal. +2  
alexxxx30  just made sure to add to my notes "Females can get sertoli leydig cell tumors, which are notorious for producing lots of androgens" +2  
peridot  I also just wanna add that if you look on in FA on p.696969, you'll see that they'll mention "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" +  
mbate4  According to the literature [lol] females can get sertoli-leydig cell tumors, which are notorious for producing lots of antigens +  
drdoom  the tradition lives on +1  
jamaicabliz  Wait... so for clarification, is it that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen? Or that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen?? HELP +  
abkapoor  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen sorry for bad Englesh +  
faus305  Sertoli-leydig cells are notorious for producing lots of androgens, females can get these. +  
djeffs1  the fact that a bunch of medstudents can get so weird about how females can get sertoli-leydig cell tumors: notorious for producing lots of androgens- just made my week!! I love you guys +  


submitted by m-ice(326),
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shTi amn has spsulu ,udsopxaar a gisn in ihwch ooldb eusrserp eecssdear ialadltcyrs uinrdg rinonpsaii.t sPluus aurpsodxa si a iacslcs ings fo elrdaipicar ea.dmtopna

enWh fludi fnot(e )loodb ash doleop rdnuao eth erta,h hte trahe lssegrgtu to dxapen and fill with lood.b ishT eebocsm a gegibr pomelrb rfo the ithgr niecevrtl urgdin tnrn,soiaipi eacsebu het rthgi deis of eht rhate esierevc dreacnsei seonuv rrnute ngirud triiipo.snna Bauecse heert si fdilu ptenivegnr het girht velrtecin mofr xpingndae r,wauotd teh ylon eohrt elpac it anc npxaed to democtmcoaa si by uihgspn on the etm,ups isnirgnhk eth zies fo eht flet v.tierlnce hsiT sucsea edcaesrde PB ewhn hte flet nvrlectie ncrcsotta nriugd ttah riacdca cy.elc

sajaqua1  In addition to causing pulsus paradoxus, we see jugular venous distension, and muffled/distant heart sounds (hard to hear through the cardiac tamponade). https://radiopaedia.org/articles/beck-triad?lang=us +3  
drdoom  ^ linkify https://radiopaedia.org/articles/beck-triad?lang=us +  


submitted by cheesetouch(95),

Pheochromocytomas are tumors of the adrenal medulla, derived from chromaffin cells of the neural crest. In regards to the image, A is possibly the capsule allowing E to be the adrenal medulla? Here are some web images, sorry I can't solve this mystery, zoinks. https://lh3.googleusercontent.com/proxy/TtqGfP9U5W_

drdoom  ^ broken links +  
cheesetouch  Sorry! I wasn't able to find a replacement. +  


submitted by drdoom(819),
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heT uelanodd unelm da(n enraatpcci tseospera ikle RYOCYSN)PHMIT si teh seit wrhee tpneacraic zsymene s(”epdeta“sod)nipe aecelv large ppieesdployt into searllm tbsi (i,ipdptitpestde.=pesrei)d tI si at eth HRBSU ODRRBE ewher eth etslamls kndis fo pitsdepe )ttp(reeddiei,epdipptssi rae kbeorn dwno tion heirt monia is,cad iwchh fanllyi nca be arepdt-torcnos htwi Na+ noit hte tisaliennt lc.le

I hnkit uoatb ti stih a:yw

  • stocamh iacd taduneers nad sn“poe pu” reptonis uthtw(oi piecsicf )vlg;eceaa
  • intccaerpa mzeyens ehtn vacele eetudndra tipdyleosppe tnoi erllsam ;sitb
  • ursbh rdbero zesymen faniyll bkaer ndow tnietis depetips inot alrbbobsea omina d.asci
regularstudent  Isn't the brush border still part of the intestinal lumen? Don't the amino acids enter into the intestinal cell (the "intestinal mucosa")? +  
drdoom  @regularstudent No, the lumen is literally the cavity—the empty space. +  


submitted by azibird(162),

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. +3  
cbreland  I had it down between the correct answer and "your son is average". Picked the wrong one. As stated by @drdoom, the stem says you have already reassured that everything is fine. It would be a good time to get extra info from mom instead of say the same thing over again. Really the question gave us the answer (I still picked wrong, but we'll do better on test day!) +1  


submitted by hungrybox(977),

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. +  


submitted by hungrybox(977),

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. +  


submitted by hungrybox(977),

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. +  


submitted by hungrybox(977),

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. +  


submitted by hungrybox(977),

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. +  


submitted by hungrybox(977),

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. +  


submitted by azibird(162),

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. +3  
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”). +  
cancelstep  Similar to what's been said, but here's how I answered: Agree that a pancystolic murmur at LL Sternal Border is tricuspid regurgitation, increases with inspiration because increased right ventricle preload would increase amount of regurgitation. PMI in sub-xiphoid area means that the strongest contraction is happening sub-xiphoid which has to be due to right ventricular hypertrophy (left ventricular hypertrophy would push PMI towards axilla). Diffuse, scattered wheezes bilaterally are probably indicative of COPD from history of smoking which would cause a secondary pulmonary hypertension due to hypoxemia and vasoconstriction in the lungs (primary is idiopathic, most commonly occurs in younger/middle-aged females). So this explains why you have RVH. Pulmonary edema would be crackles on lung auscultation and would point to Left HF, but not the case here. Also, BP 150/80 in a 68-year old without any medication is definitely high, but not causing AS. Peripheral/liver edema = RHF +2  


submitted by azibird(162),

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. +3  
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”). +  
cancelstep  Similar to what's been said, but here's how I answered: Agree that a pancystolic murmur at LL Sternal Border is tricuspid regurgitation, increases with inspiration because increased right ventricle preload would increase amount of regurgitation. PMI in sub-xiphoid area means that the strongest contraction is happening sub-xiphoid which has to be due to right ventricular hypertrophy (left ventricular hypertrophy would push PMI towards axilla). Diffuse, scattered wheezes bilaterally are probably indicative of COPD from history of smoking which would cause a secondary pulmonary hypertension due to hypoxemia and vasoconstriction in the lungs (primary is idiopathic, most commonly occurs in younger/middle-aged females). So this explains why you have RVH. Pulmonary edema would be crackles on lung auscultation and would point to Left HF, but not the case here. Also, BP 150/80 in a 68-year old without any medication is definitely high, but not causing AS. Peripheral/liver edema = RHF +2  


submitted by azibird(162),

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. +3  
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”). +  
cancelstep  Similar to what's been said, but here's how I answered: Agree that a pancystolic murmur at LL Sternal Border is tricuspid regurgitation, increases with inspiration because increased right ventricle preload would increase amount of regurgitation. PMI in sub-xiphoid area means that the strongest contraction is happening sub-xiphoid which has to be due to right ventricular hypertrophy (left ventricular hypertrophy would push PMI towards axilla). Diffuse, scattered wheezes bilaterally are probably indicative of COPD from history of smoking which would cause a secondary pulmonary hypertension due to hypoxemia and vasoconstriction in the lungs (primary is idiopathic, most commonly occurs in younger/middle-aged females). So this explains why you have RVH. Pulmonary edema would be crackles on lung auscultation and would point to Left HF, but not the case here. Also, BP 150/80 in a 68-year old without any medication is definitely high, but not causing AS. Peripheral/liver edema = RHF +2  


Where do you get off selling peoples comments I understand you built the platform but charging $5 a month for something that was built by users that thought it was free for everyone. You should be ashamed of yourself.

blueberriesyum  People are going to move to a different platform now that this isn't free anymore. +1  
azibird  Oh shit, is that what's happening? Someone explain. I was wondering why there are so many questions missing, is that related? +  
thisshouldbefree  @azibird i dont think the missing questions is related to that as i dont think ppl would delete them +1  
drdoom  @thisshouldbefree after you pass a certain score threshold, you can add missing questions via a form on the main exam pages +  
pelparente  Yah it sucks that they are charging now, but I'm assuming they have to pay hosting fees for the website. It is basically going to cost you at most 10 bucks for your dedicated period, which isn't terrible, and good on them if they make a bit of money for having this idea. That's capitalism. I would love for it to be free, but please don't delete your comments if you posted something... I still need to study and these answers don't seem to be aggregated anywhere else. @not_greedy_like_you make another website that is free then get this content on there and create competition so they have to go back to free in order to have anyone on here if you feel so strongly. +  


submitted by mousie(211),
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lphe hwti this eno ..peasle.. si itsh esbueac eh has TpGhrye DAN ltrehsColeo ADN nyios.corhcml. nyol LL cydfciieen idax neplwoul lla of eseth idg?fnins I escoh DLL R cdiieycnef eacusbe I eugss I ghouht ti dlwuo uecas lla fo ehmt to esnraiec tbu is hits ypte of nicdeyfeci lnyo aoasitcsde with ihhg DLL?

sympathetikey  First off, do yourself a favor and check this out - https://www.youtube.com/watch?v=NJYNf-Jcclo The LDL receptor is found on peripheral tissues. It recognizes B100 on LDL, IDL, and VLDL (secreted from the liver). Therefore, an issue with that would cause an increase in those, but mainly LDL. Since in this question we see that Triglycerides and Chylomicrons are elevated, that points towards a different problem. That problem is in the Lipoprotein Lipase receptor. This is the receptor that allows tissues to degrade TGs in Chylomicrons. So, if it's not working, you get increased TGs and Chylomicrons. Additionally, you get eruptive xanthomas, which are the yellow white papules the question refers to. +8  
davidw  There is much easier way go to page 94 in first aid. This kid has Type 1 Hyper-Chylomicronemia which is I) Increased Chylomicrons, Increase TG and Increased Cholesterol. It can be either Lipoprotein Lipase or Apolipoprotein CII Deficiency +12  
bulgaine  The video sympathetikey referred to only mentions pancreatitis in type IV but according to page 94 of FA 2019 it is also present in type I Hyper-chylomicronemia which is what the question stem is referring to with the abdominal pain, vomiting and increased amylase activity +  
dentist  thats not the only difference in that video.... +  
paulkarr  Pixorize has a set of videos on all the lipid disorders that made it a breeze to answer. Pixorize is basically sketchy but for biochem and other basic science subjects. +2  
futurelatinadr  Pancreatitis was a huge clue for me to think of hyperchylomicronemia +  


submitted by yotsubato(979),
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lWel taths a rellay deucr yaw to eerncs ofr ..snpsidoree.

champagnesupernova3  There's really no other way to say it without using euphemisms +2  
drdoom  You can’t rule out suicidal thoughts via inference. +  
drdoom  LAWYER: Did you ask the patient if she was suicidal? DOCTOR: Well, um, no, not exactly — but, I mean, she seemed okay .. +  
drdoom  LAWYER: So, a patient walks into your office, you suspect post partum depression — a diagnosis with known suicide risk — and you didn't ask if she was suicidal? +  
drdoom  DOCTOR: gulp +  
beetbox  @drdoom wow ok now this will stick to me forever. Always ask your patient so I can avoid lawsuits! +1  


submitted by yotsubato(979),
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eWll tatsh a lleayr educr way to scneer rof .sr.donpe.sei

champagnesupernova3  There's really no other way to say it without using euphemisms +2  
drdoom  You can’t rule out suicidal thoughts via inference. +  
drdoom  LAWYER: Did you ask the patient if she was suicidal? DOCTOR: Well, um, no, not exactly — but, I mean, she seemed okay .. +  
drdoom  LAWYER: So, a patient walks into your office, you suspect post partum depression — a diagnosis with known suicide risk — and you didn't ask if she was suicidal? +  
drdoom  DOCTOR: gulp +  
beetbox  @drdoom wow ok now this will stick to me forever. Always ask your patient so I can avoid lawsuits! +1  


submitted by yotsubato(979),
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ellW sttha a lalery ecdru awy ot nceers orf ..snedsr.poei

champagnesupernova3  There's really no other way to say it without using euphemisms +2  
drdoom  You can’t rule out suicidal thoughts via inference. +  
drdoom  LAWYER: Did you ask the patient if she was suicidal? DOCTOR: Well, um, no, not exactly — but, I mean, she seemed okay .. +  
drdoom  LAWYER: So, a patient walks into your office, you suspect post partum depression — a diagnosis with known suicide risk — and you didn't ask if she was suicidal? +  
drdoom  DOCTOR: gulp +  
beetbox  @drdoom wow ok now this will stick to me forever. Always ask your patient so I can avoid lawsuits! +1  


submitted by bbr(23),

"Has it come as a surprise to you how hard parenting is? Many people feel that way." I don't think this validates their feelings, and it would make someone feel badly if you said "hey everyone deals with this shit". Also this answer focused on parenting, rather than the psychiatric concern (postpartum depression).

"im concerned about how bad you've been feeling lately". I think this does acknowledge their feelings, and does show that the physician is engaged. Yes, its blunt. But at its worst, its still more complete than the other ones.

Tough question based on you're reading style.

drdoom  if a disease or syndrome has known risk of suicide, and you fail to assess for it, that's negligence brotha (“if you suspect, you must protect!”) +  


submitted by yotsubato(979),
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leWl thats a elalyr cerud ayw to nrecse rof .e.ssirdone.p

champagnesupernova3  There's really no other way to say it without using euphemisms +2  
drdoom  You can’t rule out suicidal thoughts via inference. +  
drdoom  LAWYER: Did you ask the patient if she was suicidal? DOCTOR: Well, um, no, not exactly — but, I mean, she seemed okay .. +  
drdoom  LAWYER: So, a patient walks into your office, you suspect post partum depression — a diagnosis with known suicide risk — and you didn't ask if she was suicidal? +  
drdoom  DOCTOR: gulp +  
beetbox  @drdoom wow ok now this will stick to me forever. Always ask your patient so I can avoid lawsuits! +1  


submitted by cassdawg(959),

Cimetidine is one of the cytochrome p450 inhibitors which would allow increase of the concentration of diazepam to toxic levels by inhibiting its elimination. (https://en.wikipedia.org/wiki/Diazepam)

SICKFACES.COM when I Am Really drinking Grapefruit Juice (FA2020 p252)

drdoom  sickfaces.com is down again .. +4  
zalzale96  I low key expected a porn site to open when I click that link :p +6  
feochromocytoma  Also a reminder that alcohol can be both an inducer AND inhibitor of the P450 - - - Chronic alcohol is an inducer of P450 Acute alcohol is an inhibitor of P450 +1  


submitted by mattnatomy(41),
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I viebeel hits si rnrfergie to dgitum noaoritlmta. Due to eppiorrm gonpiiiostn of olewb (no teh htgir s.)ide ddsLa sabdn cncnoet eht aglre sintentei ot the il.rev

anC aled :to

  1. luluvosV

  2. eudlDano osbittuocnr

3. SAM oucnclOsi -- 'Im ggeusisn dsabe no eth nersaw to hte iesonqut

meningitis  Yes, the question clicked for me when I realized the ligament was on the RT side instead of LT so I thought of Volvulus. Image of ligament of treitz: https://media.springernature.com/original/springer-static/image/chp:10.1007/978-3-642-13327-5_17/MediaObjects/978-3-642-13327-5_17_Fig3_HTML.gif +3  
hyperfukus  So Volvulus regardless in baby or adult is gonna cause SMA prob + Duodenal Obstruction: d/t Ladd bands im gonna go back and remember those associations :) +1  
pg32  Yeah, recall that the midgut rotates AROUND THE SMA in development. If you can recognize that the ligament of Treitz is on the wrong side (right) then you know you have a malrotation issue. Then you recall the midgut rotates around the SMA and you pick that answer out of pure association recall and get it right. Nice. +1  


submitted by yo(79),
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nsipsyiglrur godo ntleanoaixp nda cptirue nudof on htis ti.se geotmisnh angol het lesni fo itucnmnratiio exefrl aa(k lbdreda si lufl nda uyo pssi elxre)f si geon so the teenafrf risfeb ynarcgir eht nigsla ahtt het lderadb is ulfl ntea'r r.onwkgi toshe sebfri rea rdireac ni het ilvcep servne

:/s/pttc//ueogpytocst.uptewpcdoirol.notw/rgodiyirto-mmixwis/rur/cbe

yo  if still confused, a better explanation can be found here https://courses.washington.edu/conj/bess/urination/urination.html +19  
hyoscyamine  i found this image to be helpful in remembering which nerves do what on which receptor. https://i.ytimg.com/vi/JwaeWXhklio/maxresdefault.jpg +7  
drdoom  ^ linkify hyoscyamine https://i.ytimg.com/vi/JwaeWXhklio/maxresdefault.jpg +  


submitted by yo(79),
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srsgruilypin doog eaonalxtpin adn upeitrc udnfo on hsti eist. tghsemino noalg eth esnli of cotumnirtniai efrlxe kaa( ldadrbe si ulfl dan uyo issp elxer)f si noge so eht eeffatnr fbisre grcaryin het alsign thta teh adberdl si full aent'r .girnkwo tsoeh feisrb are cdrraie in teh pvlice snevre

/tp/ts:emoooesuiuwryo/yitt-sbop/mtto.//citrwrepwi/crg.roxidpgldnucc

yo  if still confused, a better explanation can be found here https://courses.washington.edu/conj/bess/urination/urination.html +19  
hyoscyamine  i found this image to be helpful in remembering which nerves do what on which receptor. https://i.ytimg.com/vi/JwaeWXhklio/maxresdefault.jpg +7  
drdoom  ^ linkify hyoscyamine https://i.ytimg.com/vi/JwaeWXhklio/maxresdefault.jpg +  


submitted by nwinkelmann(285),
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I dnuof a iteucrp sgwionh het sriimsotnnsa by wto tzrsgueooyhe ahalp aeiasltsamh ttiar inaas eid)ec-oilnst( etpra,ns nad foiddeim it to salo oshw eht nriiheantce by tow zosegyretuoh ahlap eslstmiaaah rinaafc eonlrsed-i)an(tt nat.pers Here uyo g:o /wO8i1m/=oJtqhsv7eoW.Iwu9dptv9JlTPUonEige12gcdhoHrpd4e.R:cTnQ?dV/w

makinallkindzofgainz  broken link +1  
drdoom  broken link +  


submitted by andro(173),

Graft Vs Host disease

Look out for Skin involvement - maculopapular rash
Enteric involvement - diarrhea and or cramping , abdominal pain .. nausea/vomiting
Hepatic dysfunction - jaundice

*** The skin , liver and intestines are the most involved affected organs

drdoom  basic science of GVHD https://youtu.be/he2vfNZDfbY?t=522 +3  
bingcentipede  Graft vs. Host disease - type IV hypersensitivity response, but this is the only one where the graft (T cells) are attacking the recipient (cells). Additionally, GvH dz is very common (at least in questions) in BONE MARROW TRANSPLANTS (also liver, but BMTs seems to pop up a lot) +  


submitted by jesusisking(16),

Tumbleweed

drdoom  need more cowboys in these here parts .. +2  


submitted by hungrybox(977),

A: Anal carcinoma | Would not be so acute

B: Anal fissure

C: External hemorrhoid | Correct!

D: Human papillomavirus infection

E: Skin tag


picture from the problem

picture showing most answers

*couldn't find a good image for anal carcinoma, if someone wants to share one that would be great

drdoom  wowee that’s a lot of butthole .. +7  
hungrybox  hawt +1  
underd0g  Why isn't this HPV given the sexual history? +1  
prosopagnosia  Anal fissure and Anal carcinoma - would present with rectal bleeding which our patient denies. HPV could lead to anal carcinoma and the image isn't similar to the morphology of condylomata acuminata. External hemorrhoid is the only one that presents with rectal pain (due to somatic innervation from the pudendal nerve) and no bleeding. +1  


Amniotic fluid phospholipid analysis is used for testing fetal lung maturity via measuring surfactant production.

Fetal echocardiography would reveal any congenital heart defects if present, but would not be diagnostic of Downs syndrome

Fetal ultrasound First-trimester ultrasound commonly shows increased nuchal translucency and hypoplastic nasal bone. But I feel this is used more commonly in older women who might have chromosomal dysgenesis as the cause of downs syndrome

Fetal biopsy Pretty invasive technique, when we have a lesser invasive and more specific test available.

drdoom  [system mailer] your account has been upgraded: FORMAT NINJA +  


submitted by thomas(1),
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wrAsen is tsye.ctAro ntPtiea has malsiolobatg .lmfmteoiur tAulhhgo sgonainmmei yam cuocr ta sntcexvei,io mgsmninaeio aer bgenin and etfon sacymoamittp. Tyeh mya eacus a/h zserse,ui ubt lowud be nlukieyl ot csaeu edath wn/i 6m of nseto fo ha/. Teh eszi fo mtruo and suorec of lessnil is stonisctne htwi het eroucs of MGB

masonkingcobra  Above is obviously incorrect because the answer is Meningeal lol. Here is a link to a good picture: http://neuropathology-web.org/chapter7/chapter7fMiscellaneous.html +24  
kernicterusthefrog  Obviously thomas is disagreeing with the presentation of the question, and I agreed with him! This absolutely sounds like GBM, with rapid onset leading to death, and the symptoms. The question stem leads you to GBM, and the gross image to meningioma (I guess). +2  
kernicterusthefrog  Furthermore, where are the meninges on the gross image form which this (meningioma) grew?! It should at least show the tissue from whence it came! +1  
nala_ula  Had the same problem, got confused since it appeared that the growth was malignant :( +  
sugaplum  FA 2019 pg 514, also agree with everyone. weird presentation. Glios are malignant death within 1 year, meningioma are often asymptomatic or have focal signs. just a gross pathology question at this point +  
garima  ı think she died bc of pressure or something guys, its obviously round shaped benign lesion, its also extra axial not like GBM. she had this maybe years before death +2  


submitted by johnthurtjr(139),
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I'm not a naf fo sorgs atph maigse and sseoitunq that sya l",koo htaw is thsi tgn?ih" - atth aids nmsaeimingo aer teh osmt omcmno rabni urmot nad stih cutrpie si si a ogod leamxep of o.en I dha on diae waht etehs sngith ookeld eilk adn otg it nwrgo, o.to akTe a ookl at this one

johnthurtjr  [Here's more info](http://www.pathologyoutlines.com/topic/cnstumormeningiomageneral.html) +1  
meningitis  I got it wrong because I didn't see any apparent Dura mater nor other meninges (The veins aren't being covered by any "shiny layer"), so I thought the tumor was coming from inside the brain and not compressing it like meningiomas usually do. +3  
meningitis  But it did follow the common aspect where they are found in between divisions of brain and are circular growths like a ball. +7  
nala_ula  Since it was basically implied that the patient died and "here look at what this is" I thought it was a malignant tumor (glioblastoma)... but I guess it's all about placement. +11  
thelupuswolf  GBM would be in the perenchyma. Devine podcast said if they show you a gross picture of the bottom of the brain then it's a hemangioblastoma bc it's most often cerebellar. But this one wasn't cerebellar so I went ahead with meningioma (FA says external to brain parenchyma as well) +2  
vivijujubebe  GBM would have necrosis and bleeding whereas the ball-shaped tumor in the picture looks smooth and very benign...even tho I have no idea how someone can die so suddenly from meningioma +  
seba0039  Minor correction, but I do not think that Meningiomas are the most common brain tumor; they are the most common benign brain tumor of adults (Pathoma), but I'm not sure if they're the most common overall. +  


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arOl eceilvs h(tin )htin. ntrlsiiBge ilrsuacve onlise no teh dhan. oN e,fevr otn garei.t-pciopxna Tish is sHrpee (oyu yam ebmremre tndtssie ngettgi tchpriee wiltwho in uroy ,edstusi which si wtah this .i)s otMs lfsko tge H1VS sa ciherlnd, huhtgo ybilousvo ton lal aer impmyota.cst VSH is a lraeg -auoen,dedltsrbd renail DAN .usvri

jiya   why cant this be hand foot and mouth disease cause of coxsache +7  
drachenx  Also thought it was Hand-foot-mouth an RNA virus but I did consider Herpes. Changed because I thought Hand foot and mouth would be more common. +  
llamastep1  Hand foot mouth usualy involves all 3 places (hands, feet and mouth/perioral area) and the lesions on the hand arent localized to just one finger. +2  
aneurysmclip  Hand foot mouth disease affects palms and soles. ref: FA 2019 - 150 +3  
raffff  wouldnt the history also be different for coxsakie +  
focus  I think this image is trying to show the "dew drops on a rose petal" sign on Hermes, the god of Herpes on Sketchy Micro +1  
drpee  Google some images of HF&M disease. The small blisters look very different from herpetic whitlow. +  
drdoom  ^ ... some images of HF&M disease ... +  


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arOl sveclei (tnhi )h.int rnltegBsii rlsiueacv enoils no hte dhna. oN freve, nto .nxpi-gerpiotaca hisT is esrpeH y(uo may emeembrr sensittd tteggni herpcite whwlito ni yrou ess,tuid ichwh is what htsi ).is tosM oksfl etg VH1S as nihdlcr,e hughot byosloiuv tno all rea mcyimot.tpsa HSV si a eagrl ld-snaro,ubedtde arilne NDA v.uisr

jiya   why cant this be hand foot and mouth disease cause of coxsache +7  
drachenx  Also thought it was Hand-foot-mouth an RNA virus but I did consider Herpes. Changed because I thought Hand foot and mouth would be more common. +  
llamastep1  Hand foot mouth usualy involves all 3 places (hands, feet and mouth/perioral area) and the lesions on the hand arent localized to just one finger. +2  
aneurysmclip  Hand foot mouth disease affects palms and soles. ref: FA 2019 - 150 +3  
raffff  wouldnt the history also be different for coxsakie +  
focus  I think this image is trying to show the "dew drops on a rose petal" sign on Hermes, the god of Herpes on Sketchy Micro +1  
drpee  Google some images of HF&M disease. The small blisters look very different from herpetic whitlow. +  
drdoom  ^ ... some images of HF&M disease ... +  


submitted by mcl(586),
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Sicen 'reoyu oingsl lal uyor cbarbi tnoi uryo ,pee oyu owlud xepetc het pH to eb roem anek.illa sAol, siecn trhee si edsrdaeec H+a/+N tao,tnpir hrete si esls dmuiso erdabrosbe and ereerohtf rnciadees slso fo rfee diflu to the r.enui

joker4eva76  Why wouldn't this be similar to a Type 2 RTA where urinary pH <5.5? +1  
mcl  I can't remember exactly what the question was asking off the top of my head, I think it was asking about relative to normal? But I think you're right in that the alpha intercalated cells (AIC) can still dump H+ into the urine and acidify it to an extent. And, like in RTA2, I don't know that the action of the AIC would be able to overcome the bicarb and acidify the urine enough for it to be the usual pH, so the urine should still be more alkaline compared to baseline. Kinda sucks, pH less than 5.5 should technically be acidic but it's alkaline for pee. +  
mcl  JK, normal urine pH is around 4-8, but I guess they consider closer to 5.5 on the more alkaline side...? I guess I would go more off that the alpha intercalated cells can't completely compensate for the amount of bicarb in the pee due to the CA inhibitor, not so much the actual pH. +  
meningitis  Anhydrase inhibitors also affect the anhydrase inhibitors that are used in the AIC in order to excrete the H+. Here is a link: http://pedclerk.bsd.uchicago.edu/sites/pedclerk.uchicago.edu/files/uploads/distal_0.png +4  
mcl  ohhhhhhhhhhhhhhhhhhhhhhh my god duh yes thank you <3 +1  
meningitis  Lol yw!! +  


submitted by hello(302),
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alnGoj adh a rluecet hatt denonmeti tath "If a taipnte has teg,raoclahra verwei evrey rgud rhee'ty ktngia cseni naym gudrs eucas rreoaha".cgatl

heT lony gitnh fo oepsbisl lnvraceee in ihst sQtem- si htat ehs eksta a i,toeicndam efrteheor eht naswer of gr"du fft"cee is het ostm eilykl sraeno rof reh lehgatocra.ar

hungrybox  I still think this question is pretty BS. But having studied some more, I think it's less BS than I originally thought. Pathoma gives the three major causes of galactorrhea as nipple stimulation, prolactinoma of anterior pituitary, and drugs (see 16.1 - Breast Pathology). Only drug effect is an answer choice for this question. +5  
hungrybox  To put another way - before you try to go through every answer choice, asking yourself "would this cause galactorrhea?" Instead, ask yourself, "What are the causes of galactorrhea?" According to Dr. Sattar, they are "nipple stimulation, prolactinoma of anterior pituitary, and drugs." +2  
hungrybox  The question doesn't say anything that would point you toward nipple stimulation, like "it only seems to appear when she puts on a shirt/plays sports/runs/etc." It also makes no mention of bitemporal blindness (which would point you to an anterior pituitary tumor), so you can rule out prolactinoma. The only option left is drug effect. +2  
drdoom  hungrybox’s full comment (below) here: https://nbmeanswers.com/exam/nbme20/410#3907 +1  


submitted by hungrybox(977),

Pathoma gives the three major causes of galactorrhea as nipple stimulation, prolactinoma of anterior pituitary, and drugs (see 16.1 - Breast Pathology). Only drug effect is an answer choice for this question.

To put another way - before you try to go through every answer choice, asking yourself "would this cause galactorrhea?" Instead, ask yourself, "What are the causes of galactorrhea?" According to Dr. Sattar, they are "nipple stimulation, prolactinoma of anterior pituitary, and drugs."

The question doesn't say anything that would point you toward nipple stimulation, like "it only seems to appear when she puts on a shirt/plays sports/runs/etc."† So you can rule out nipple stimulation.

It also makes no mention of bitemporal blindness (which would point you to an anterior pituitary tumor), so you can rule out prolactinoma. The only option left is drug effect.


I've never seen anything like this on a question but I assume the NBME would word it in some convoluted way like that.


I initially wrote this as a subcomment, but I feel like it deserves its own comment. I was never really satisfied with any of the explanations for this problem, and I finally arrived at one that makes the most sense to me.

hungrybox  Oh, and besides, nipple stimulation and prolactinoma aren't even answers lol +  
drdoom  [system mailer] your account has been upgraded: FORMAT NINJA +1  


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 +  


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 +  


submitted by arkanaftus(12),

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. +8  


submitted by irgunner(13),

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. +1  


submitted by sahusema(138),
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.Reasoac An aimlntramyfo aalcif skin orrdidse ctarzcaeirhde by eaymturhetos espapul and suulept utb on ooncme.sde aMy eb aicoaedsts htwi acafil gslhuinf in enesrsop ot tlanxeer smiutil ge(, ,hloclao ahet).

qball  https://en.wikipedia.org/wiki/Rosacea#/media/File:Rosacea.jpg for that quick picture. +3  
drdoom  and many, many more: https://www.google.com/search?q=rosacea&tbm=isch :) +  
icedcoffeeislyfe  FA2020 pg 477 +  


submitted by drdoom(819),
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Teh isnssyeth fo lvurltyia lal psntroie teip)pe-NdmRAg(&;t crsouc ni eth otacmypls.[]1 s’Ttah erwhe lla erbmsoois ,reised earft lal. seoi,sbmoR iwchh aer stmyol jstu NArR (3/2~ rRAN + 13/ e*pnrtoi, by eit),ghw ear easdebslm in het uculsen btu lony do thier tsuff cnoe heyt teg ot het csyo.ltpam

For a orenitp to aeevl sti orgainil ohmeotnw fo hte otosylc and oemceb a dresenti of the enclsuu ,or ayyysy,yy the damieclnpso uc,umrilet ti sneed ot ahev a lteitl tgnisr fo mnioa dicas hicwh uohst “I gnloeb in eht !c”sluneu ro I“ nlegob in the eimcladsopn leuiumcr”!t

toPesrni eluatmlyit netiesdd rfo the RE ncioatn na agiimuvatnlynei amden rgstin fo iaonm csdia knonw as gan“ils e”euqce,sn ihhcw, rof the sseprpuo fo hte petS ,1 si slwyaa at the enNrts.u-im eTh ingasl esqcneeu stlle etrho slociotcy nies,rpto y“He! eakT em da(n teh rtse fo eht etipedp of hcihw I am r)tpa to the E”!R

In hte bnascee of hsti aigsn,l a itenorp lwli mirnae ni its tfluae“”d home of eth t.olsocy

r&eessuoqr;H a ienc icescmath inhsgwo eht wofl fo trnespoi ofrm iinlita syshsteni ot lfnai dttsnis:oiean


enodsntE

  1. “eTh sieysnhts fo lrayvtuli lal siptroen in hte cell bgiens no rbsiomose in hte l”ooysct. (anistseEl eCll loBiogy, stebAlr te a,.l ,4201 .p )924

fI* you lyelra nwta ruoy idmn bo,nlw rcosenid hatt veen the opteinr btnisuus atht mkae pu htat 1/3 of a meobosir aer hstemleves itlanilyi yhdssnzetie in het ;oocylts l,ater tehy rea ernpotsdrta akcb toni eht ulcesnu via the arelunc o.rpe

qball  Awesome explanation. Now explain it to me like I'm 5. +8  
drdoom  All baby peptides are born in the cytosol. But some baby peptides have a birthmark at their N-terminus. The birthmark tells a special mailman that this baby needs to be delivered somewhere else. If you chop off the birthmark — or erase it somehow — the mailman never knows to take baby to its true home. The end. Now go to sleep or Santa won’t bring your presents. +36  


C and D are never really the right answers on ethics questions. B is out because nurses are not specifically trained to do this), you're left with A and E. Because her blood pressure is 90/60, pulse is 120, she's bleeding out and this is an emergency. The other facility is 2 hours away. Asking the patient if she'd allow the exam wouldn't hurt, wouldn't it? It doesn't say "forcefully examine her", it says ask. If she says no, then you'd have no other choice but to let her bleed out on the 2 hour drive to her family obstetrician.

drdoom  dude you’re on point with these close readings of the stems! Lit(erature) major? +  


When proteins being made in the ER misfold, they accumulate in the ER, which then triggers them to be spit out into the cytosol and become degraded by proteasomes. Thus, the accumulation of the misfolded protein in the ER is required for them to ultimately be tagged by ubiquitin and be degraded in proteasomes.

Even if you argue that they will be accumulating in the cytosol because proteasomes are in the cytosol, the question is asking where are the proteins accumulating, not being degraded. So they can't accumulate in proteasomes, because they are destroyed in them.

drdoom  nice catch with the “accumulating” remark! qq, when you say “triggers them to be spit out into the cytosol”, do you have a source for that? don't recall learning that anywhere myself. thx! +1  
therealslimshady  I can't remember where I read this but it stuck with me, I think it was a cell bio book +  


submitted by mdmikek89(1),

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  


submitted by castlblack(50),

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?

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). +  
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. +  
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´´. +  
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. +  
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. +  
drdoom  no worries! +  
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. +  
amy  what about the long steamy bath? He also sweat a lot, and profuse sweating is going to cause hyponatremia? +  


submitted by castlblack(50),

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?

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). +  
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. +  
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´´. +  
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. +  
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. +  
drdoom  no worries! +  
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. +  
amy  what about the long steamy bath? He also sweat a lot, and profuse sweating is going to cause hyponatremia? +  


drdoom  ^ link broken +  


submitted by rainlad(22),

my approach to this question was to eliminate all the answer choices that mentioned specificity or sensitivity, since the data here did not provide information about any sort of screening test.

that left me with two possible answer choices: I eliminated the one about consistency of other studies, since no other studies were mentioned in the question stem.

not sure if I oversimplified things, but it led me to the right answer!

makinallkindzofgainz  this is exactly how I reasoned through it. Were we correct in our line of thinking? We'll never knooooow +  
qball  But will you ever know on the real thing? +1  
drdoom  but will you ever know in real life? you may do the right thing (given time constraints, & information available), but outcome is bad; maybe you do the wrong thing, but the outcome is good (despite your decision). how to know the difference? +3  


submitted by hayayah(1057),
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LV tdpepos ,rowignk uperesrs kbdcae pu itno umpl cutrii.c mlPu rtcucii rhgoyul is adem fo 3 spar""t - eth pacalsre,ili reitntltiisa ec,sap dna the loaeilv.

In cirdgianoce soc,hk eht txear bolod eisenrcas rayclapli atyhsiordct resupers, ivgrndi dulif ntio eth rtaiitnilste cps.ea omCeaprd ot teh ao,eillv eth ttiinlistaer aecsp now sah eorm lduif th(su omre rtiinateilts itsoydhcrta rrpesuse and sels toccoin pseuesrr due to roiat fo ilduf to enro,i)tp dan sa a eusltr of hist gaanlninbuc fo oc,resf ilfdu vsemo nito the loaeliv g-&t-; norpmalyu me.ead



submitted by snoochi95(1),

How come you couldnt say "I dont know, but the oncologist will be seeing you later today"? Is it because technically you are ~lying~ to the patient?

drdoom  Not “technically” but actually! To say “I don’t know” when you *do* know is as lyin’ as it gets! Just remember, before a state issues you a license to practice medicine in their backyard, they look to the National Board of Medical Examiners and ask, “Should we trust this person to practice medicine here?” The NBME is in the business of telling states, “Yes, we believe this person knows enough to practice morally and competently.” Answer ethics questions with this in mind. +4  
pseudo_mona  Besides technically lying, it also probably isn't a good idea to drop the word "oncologist" to a patient before they hear they have cancer, especially as a student who can't answer any further questions about the biopsy results. +10  
usmile1  @pseudo_ shit I just realized that telling them that the oncologist will be seeing them, is essentially telling them they have cancer. Additionally, you can't lie and say you don't know. no Idea what I was thinking when I took this. +9  


submitted by medstruggle(12),
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yhW si uadndole numle ro?tcrcine I tghouht ncitpaarec ymeesnz yip,(ynocstmrh rposipxacdebetya) lwduo eb lcoated ere.h

colonelred_  Enterokinase actives trypsinogen and is located closer to the intestinal mucosal (“brush border”). +1  
drdoom  Yeah, @colonelred is right. @medstruggle: the duodenal lumen (and the pancreatic /proteases/ you mention) is the site where pancreatic enzymes (“endopeptidases”) cleave large polypeptides into smaller bits. It is at the BRUSH BORDER where the smallest kinds of peptides (dipeptides, tripeptides) are broken down into their amino acids, which finally can be co-transported with Na+ into the intestinal cell. I think about it this way: stomach acid denatures and “opens up” proteins (without any specific cleavage); pancreatic enzymes then cleave denatured polypeptides into smaller bits; brush border enzymes finally break down tiny peptides into absorbable amino acids. +3  
drdoom  Nice schematic, @welpdedelp +  


Can anyone explain what does "lost her pep" means?

drdoom  `pep` actually comes from `pepper`; to `pepper` something (including a food dish!) is to make it more vigorous, to give it more kick, to vitalize it. so, to “lose one’s pep” is to lose one’s vitality, feel fatigued, feel lackluster, etc. https://www.etymonline.com/word/pep +1  


FA 2020: 463

Causes of avascular necrosis: CASTS Bend LEGS. +Corticosteroids +Alcoholism +Sickle cell disease +Trauma +SLE

+“the Bends” (caisson/decompression disease) +LEgg-Calvé- Perthes disease (idiopathic) +Gaucher disease +Slipped capital femoral epiphysis

drdoom  for bulleted lists, be sure to follow the plus sign with a space! :) +2  


submitted by madojo(163),

Know your STD's baby ;-) (going through every other choice on this question):

  • Bacterial vaginosis caused by gardnerella vaginallis. Se a thin, off white discharge and fishy smell (fish in the garden). There's no inflammation Lab findings: pH greater than 4.5 (just like trichomoniasis), and a positive whiff test with KOH. Stem will say something about malodorous discharge and show the infamous CLUE CELLS if we are lucky. Not the answer for this question obviously because we would not expect vesicles with this bacterial disease.

  • Candidiasis is going to be your thick cottage cheese discharge, with inflammation. normal pH see pseudohyphae. Treat with topical nystatin, or oral fluconazole unless you're pregnant than use Clotrimazole. Again not going to see any vesicles.

  • Chancroid per uworld is associated with Haemophilus ducreyi you will have a Deep purulent painful ulcer with suppurative lymphadenitis. Will be told that patient has painful inguinal nodes, there may be multiple deep ulcers with gray-yellow exudate. You do cry with H. duCRYi This wouldn't be true for what our patient has in this question because we aren't told of any inguinal adenopathy. a link to a chancroid VDA

  • Chlamydia trachomatis causes lymphogranuloma venereum which is small shallow ulcers, painless, but then the large painful coalesced inguinal lymph nodes aka BUBOES. Compared with gonnorhea the discharge is more thinner and watery. Again not the case here as its painful and no mention of any BUBOOESS. The discharge in gonorrhea is more thicker. Both lead to PID, treat for both because confection is common. With both patient may have some sort of pain or burning sensation upon urination. Sterile pyuria though for both.

  • Condyloma accuminatum is a manifestation of HPV 6 + 11 (genital warts). They look like big cauliflowers. This is in contrast to Condyloma lata that you see in syphillis which is just a flatter latte brown looking macule.

  • Genital Herpes (the answer to the question) will present with multiple painful superficial vesicles or ulcerations with constitutional symptoms (fever, malaise) Just fits better than all the other choices I ran through.

  • Syphillis is the painless chancre. UW describes it as a single, indurated well circumscribed ulcer, with a clean base. See corkscrew organisms on DF microscopy. Keep in mind other painless ulcers are lymphogranuloma venereum of clamydia (but the buboes are whats painful not the ulcer), and granuloma inguinale (donovanosis - klebsiella granulomatis) but whats hallmark about this one is that its painless without lymphadenopathy

In short, be safe.

drdoom  this write-up is AWESOME ... but it also made me vomit. +  
b1ackcoffee  This is awesome, writeup, not the stds. +  
lovebug  FA 2019 pg 184. I summed up @madojo's comment! this patient have "multiple, tender vesicles and ulcer". and scant vaginal discharge. A) Bacterial vaginosis -> NO vesicle -> r/o B) Candidiasis -> NO vesicle -> r/o C) Chancroid -> should have Inguinal Adenopathy -> r/o D) C. trachomatis -> have Large painful inguinal LN -> r/o E) Condyloma acuminata -> Big Cauliflower -> r/o F) Gental herpes -> YES!!! G) Gonorrhea -> NO Vesicle, creamy prulent discharge -> r/o H) C. trachomatis again (same as D) -> r/o I) Syphilis -> painless chancre -> r/o J) Trichomoniasis -> strawberry cervix, motile in wet prep -> r/o thanks @madojo! +  


FA 2020, page 127:

Encapsulated bacteria are opsonized and then cleared by spleen. Asplenic patients have decreased opsonizing ability and an increased risk for severe infections.

They need vaccines to protect against Neisseria meningitidis, Streptococcus Pneumoniae, Haemophilus influenza

mnemonic: "No Spleen Here"

regardless I got this one wrong because of a 50/50 guess between strep and e. coli. I guess they wanted you to recognize that he was at risk for S. pneumonia sepsis and therefore needed to be vaccinated, whereas there's not much you can do to protect him from E. coli other than wash your hands lol

drdoom  ^ voted best username +  
mambaforstep  ^^what he/she said. FA 2019 pg 127 +  
meryen13  its not e coli not because you couldn't vaccinate the pt but because he was in an accident and the chances of infection with s. pneumo is higher. page 186 FA 2020: splenic pt: s.pneumo >> H. influenza b> N meningitidis +  


submitted by hayayah(1057),
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uepyrHteca apnatlnrts eecrnojti rsoucc hiwnit ismtneu d/t netesixpigr- piirenetc boisedtani taht rceat to drono tainegn pe(ty II iieyrtysvhteinps ac,netri)o attciaev tcopeenl.mm

mcl  [Useful figures illustrating transplant rejection](https://www.stomponstep1.com/transplant-rejection-hyperacute-acute-chronic-graft-versus-host/) +  
drdoom  ^ via @mcl [Useful figures illustrating transplant rejection](https://www.stomponstep1.com/transplant-rejection-hyperacute-acute-chronic-graft-versus-host/ +1  


Why would you give GMCSF to someone with AML?? Isn't the whole goal of treatment to knock out the granulocytes? I feel like giving someone GMCSF after they were JUST treated for AML is asking for a relapse but what the hell do I know.

drdoom  The problem in AML (acute myeloid leukemia) is that precursor cells “get stuck” on their way to becoming (mature) granulocytes. Giving GM–CSF “pushes” them toward a more differentiated state and, because they divide as they mature, the cells become vulnerable to drugs that disrupt cell division (replication): “Granulocyte–macrophage colony-stimulating factor (GM–CSF) can stimulate proliferation of leukemic blasts and sensitize these cells to the cytotoxic effects of S-phase–specific drugs.” https://www.nature.com/articles/2402368 +3  


submitted by qfever(43),

Does anyone know what are A, C, D? For C not sure if it's pointing to the ribosomes on RER.

(I'm assuming E is glycogen granules based on a comment below!)

drdoom  see @jinzo’s comment above +  


submitted by brookly_(0),
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I htotugh ilaumbi igev ersi ot bliecaomt kalsasilo can... onesome raeeaobtl ?

drdoom  Remember, bulimia itself does not mean “purging”; it means “ox-hunger”. It is purging (e.g., intentional vomiting, laxative abuse, diuretic abuse, excessive exercise, or extreme fasting) which creates metabolic disturbance. The type of disturbance depends on your preferred route of “exit”. +1  


submitted by lilyo(69),
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I had het mesa eoqnsuit gredgianr is.th I nwok ttah ntaerelx oidoerrsmhh arlery lebed dna intlraen dmshireroho ptreens as iasnepls egbldein so in ym dnmi I ewkn I was genib ksead aubto nnrtlaie oorhm.sdihre Hrve,ewo uesporri -cage-l;&ttr frinreio ectersmein it;-vn-&ge tpoarl en,vi cna aoenyn ltel me why the wsearn saw oserupir eraltc nad not nfrierio eecsnr?eitm

dubywow  Because the wording sucks. It's a confusing way to word the question. I too was confused what direct tributaries was referring to and chose Inferior mesenteric because I suck and also because this question sucks. Really its asking where are the hemorrhoids? They are on/from the superior rectals even though those veins feed to Inferior mesenteric. +3  
drdoom  Defining tributary: https://i.imgur.com/2zDxPbW.png Nice images make the term easier to recall. Smaller streams "pay tribute" to larger rivers (by flowing into them). +5  


submitted by sympathetikey(1265),
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r:uceoS egse.wtMtiiihelnki:./ipodiay//krnwp/

nimyel" spesde eht niioarnsmsts of lercitlaec selsuimp dlealc cnitoa tosateplni loang aietmyelnd sxoan yb nisualnigt eth xoan dan ginerdcu aonxla enrbmmae caiaeatnpcc"

littletreetrunk  I think this makes total sense, but how does it not ALSO stop fast axonal transport? +3  
laminin  axonal transport is transport of organelles bidirectionally along the axon in the cytoplasm since myelin is on the outside of the axon demyelination doesn't affect this process. source: https://en.wikipedia.org/wiki/Axonal_transport "Axonal transport, also called axoplasmic transport or axoplasmic flow, is a cellular process responsible for movement of mitochondria, lipids, synaptic vesicles, proteins, and other cell parts to and from a neuron's cell body, through the cytoplasm of its axon." +3  
yotsubato  axonal transport is mediated by kinesin and dynein. Microtubule toxins like vincristine block these +3  
drdoom  @littletreetrunk "axonal transport" is movement of bulk goods via microtubules (which run from soma to terminus); ions, on the other hand, move in an "electrical wave" that we call an action potential! no axonal (microtubular) transport required! in other words, de-myelination will have no effect on the transport of bulk goods; but it will really mess up how fast "electrical waves" traverse the neuron! +  


submitted by beeip(123),
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I hmgit eb hte only prosen on tehar woh gto isth eon gnrw,o ubt relrassged:

T"TI iyassanl sdienluc verey jtecsbu woh si ndmiazedor ocncidagr to edzdmranio attetenrm stinag.ensm It nerosig neacnomcipol,n otplorco s,tadiiveno wihdtwa,arl adn ihyngnat taht phpneas reaft ozoa"mrdantiin.[]1

yo  You're not. I also goofed. +19  
seagull  https://www.youtube.com/watch?v=Kps3VzbykFQ This video is a pretty decent explination worth your time on the subject. +2  
hungrybox  I got it right but I was only like 50% sure. So I appreciate it. +  
drdoom  ^ linkifying @seagull: https://www.youtube.com/watch?v=Kps3VzbykFQ +2  
teepot123  ^ same video above used when I analysed my form 20 q which I got incorrect at time, its very clear at explaining this, helping me get it correct on this form +  


submitted by tinydoc(223),
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fsritanc odwul eb a emor ihperlerap gdwee saphe

secbsa tndulwo eb niiseavv to eht snuoirrgnud raae i thkin.

uqmsuosa lecl is ermo aclrynlte laeocdt

na'swt 1%00 reus ubt taths het sbte nsearw tosulghh stuidp to evgi 0 stpyomms and ustj a eciur,pt tonginh ekli an auclat llicniac soearnci

tsl19  Squamous cell is centrally located and has cavitation, which you can see in the pic. Similar to this one: https://webpath.med.utah.edu/LUNGHTML/LUNG068.html +5  
drdoom  ^ linkifying: https://webpath.med.utah.edu/LUNGHTML/LUNG068.html +4  
zevvyt  I also didn't choose infarct cuz i think the lung would have a red infarct. +  


submitted by madojo(163),
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I do'tn kwon fi stih aws hte igthr awy i thouthg utaob ti tub i mrdemreeeb L..eKhH A.t.C ginsht atth acseu lsnitaodaovi ni lleasetk emucls

C - 2,Co H - ,+H -A ense,dioan L - taalect K- +K

drdoom  This is great; these are all proxies of catabolism, i.e., "net" ATP consumption! (ATP->ADP) +1  
drdoom  Potassium might be the one that doesn't seem to fit but recall that cells have an H+/K+ antiporter: cells can act as a "sink" for high blood H+; they "take up" H+ (from blood, into cell) but "in exchange" they have to put out a K+ (to maintain a normal electro-gradient). So, as blood acid starts to creep up, cells actually "attempt" to bring it back to equilibrium by sucking up H+ (and putting out K+, which, as you surely recall ;), is the predominant cation within cells). +3  
misterdoctor69  @drdoom, would you also venture to say that there is increased Na+/K+ ATPase activity in an increased metabolic state which might also contribute to greater K+ efflux into the blood? +  
drdoom  @misterdoctor69, no. Potassium flow is driven by its chemical gradient (from inside cell, where its concentration is high, to outside). If K+ efflux is increased, the best culprit would be the H+/K+ antiporter (which “takes up” a proton, but has to “surrender” a potassium, in an attempt to remove acid from the blood — acidic blood, of course, being an inevitable outcome of revved metabolic state: net ATP consumption & high CO2 production). +  


submitted by madojo(163),
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I ntod' kwon fi hits was het htgri way i oughtht tuoab it tbu i eeeerrbdmm e.K.HL.C htA. ighnst atth cusea odaanvistlio in laekltse scluem

C - Co2, H - +,H -A nnoee,aids L - ctletaa K- +K

drdoom  This is great; these are all proxies of catabolism, i.e., "net" ATP consumption! (ATP->ADP) +1  
drdoom  Potassium might be the one that doesn't seem to fit but recall that cells have an H+/K+ antiporter: cells can act as a "sink" for high blood H+; they "take up" H+ (from blood, into cell) but "in exchange" they have to put out a K+ (to maintain a normal electro-gradient). So, as blood acid starts to creep up, cells actually "attempt" to bring it back to equilibrium by sucking up H+ (and putting out K+, which, as you surely recall ;), is the predominant cation within cells). +3  
misterdoctor69  @drdoom, would you also venture to say that there is increased Na+/K+ ATPase activity in an increased metabolic state which might also contribute to greater K+ efflux into the blood? +  
drdoom  @misterdoctor69, no. Potassium flow is driven by its chemical gradient (from inside cell, where its concentration is high, to outside). If K+ efflux is increased, the best culprit would be the H+/K+ antiporter (which “takes up” a proton, but has to “surrender” a potassium, in an attempt to remove acid from the blood — acidic blood, of course, being an inevitable outcome of revved metabolic state: net ATP consumption & high CO2 production). +  


What makes this coxsackie virus over Adenovirus? Both cause myocarditis which would be seen on autopsy? Is it just more common to get coxsackie?

drdoom  the general consensus appears to be that Coxsackie is more common than Adenovirus, but i haven’t come across any papers or textbooks that would agree (they only mention “Coxsackie” and “Adenovirus” as associations with myocarditis) +1  
bharatpillai  there specifically is a question on uworld in which a young woman gets viral myocarditis with sore throat and the answer to that is adenovirus. i think thats why many people (including me) got it wrong :( +  


submitted by brolycow(27),
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He has htera fieurla which adels to a dreseeca ni ralen loobd lofw adn pelrrean aeoa.iztm nI rlpaneer ,ietaozma U:CrNB raito si t=g&; ;02 inivcoAtat of eht ARSA sstyem eud ot het lrpaeenr mzoiaate masne ahtt the ecps vgar is ghih ta 510.2 nda eh si nliodgh noot oudsmi os yriuarn miuosd lliw be wol t,l2(;&0 aFEN %.;&t1l)

figprincess  did you figure out the the ratio by actually divding out the numbers since the q didn't give it as a ratio? also what resource tells us what prerenal spec gravity should be? +  
brolycow  I just usually remember from class that spec grav 1.001-1.010 is considered dilute urine, and anything 1.025 and above is concentrated. For this question specifically, I think I remember there only being one option that even had the ratio >=20, all of the others were like 15 or less, so just have to rule them out. +7  
benzjonez  Very helpful video for acute kidney injury: https://www.youtube.com/watch?v=bMp6IxDKK2Q +8  
notadoctor  Another explanation that helped me is that inability to concentrate the urine means something is wrong with the kidneys. If you have dilute urine, or the spec gravity is between 1.001-1.010 in someone with low urine output it suggests something is wrong with the concentration mechanisms of the kidney. Because this person had congestive heart failure we were already looking for something that matched up with prerenal azotemia so we can pretty much get rid of all the answer choices that suggest other azotemias. Then finally to get the precise answer I looked at the BUN/Cr ratio which you would expect to be high(>= 20). +  
mikay92  Would fully recommend the OnlineMedEd video on AKI. Goes through the differential, lab results, treatment, etc in a very clear and concise manner. +  
drdoom  repost via @benzjonez -> https://www.youtube.com/watch?v=bMp6IxDKK2Q +  
drdoom  @mikay92 is this the OnlineMedEd video you're referring to? -> https://youtu.be/EWFgzVtMN50 +1  
drdoom  aha! there is an updated AKI video but you need an OnlineMedEd (free) account to view it: https://onlinemeded.org/spa/nephrology/acute-kidney-injury/acquire +  
popofo  I understand that BUN:Cr > 20 if renal perfusion is repaired, but in heart failure wouldn't there be increased secretion of ANP/BNP from the atria that pushes up the sodium excretion? +  


submitted by brolycow(27),
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eH ahs aetrh aurlife hhiwc elasd ot a srdeceea ni arnel ldobo flow dna elarrpne ao.timaez In prenlera ezaai,otm :BUCNr riaot is &=;tg 20; oiinavtctA fo het RSAA esmtys deu to hte replrnae iaetmzoa enmsa ahtt het spec rgva is hhig at .5012 nad he is lgdionh ootn disomu os ruaryin midsuo ilwl be olw ;0&(tl2, NFEa .)1tl%&;

figprincess  did you figure out the the ratio by actually divding out the numbers since the q didn't give it as a ratio? also what resource tells us what prerenal spec gravity should be? +  
brolycow  I just usually remember from class that spec grav 1.001-1.010 is considered dilute urine, and anything 1.025 and above is concentrated. For this question specifically, I think I remember there only being one option that even had the ratio >=20, all of the others were like 15 or less, so just have to rule them out. +7  
benzjonez  Very helpful video for acute kidney injury: https://www.youtube.com/watch?v=bMp6IxDKK2Q +8  
notadoctor  Another explanation that helped me is that inability to concentrate the urine means something is wrong with the kidneys. If you have dilute urine, or the spec gravity is between 1.001-1.010 in someone with low urine output it suggests something is wrong with the concentration mechanisms of the kidney. Because this person had congestive heart failure we were already looking for something that matched up with prerenal azotemia so we can pretty much get rid of all the answer choices that suggest other azotemias. Then finally to get the precise answer I looked at the BUN/Cr ratio which you would expect to be high(>= 20). +  
mikay92  Would fully recommend the OnlineMedEd video on AKI. Goes through the differential, lab results, treatment, etc in a very clear and concise manner. +  
drdoom  repost via @benzjonez -> https://www.youtube.com/watch?v=bMp6IxDKK2Q +  
drdoom  @mikay92 is this the OnlineMedEd video you're referring to? -> https://youtu.be/EWFgzVtMN50 +1  
drdoom  aha! there is an updated AKI video but you need an OnlineMedEd (free) account to view it: https://onlinemeded.org/spa/nephrology/acute-kidney-injury/acquire +  
popofo  I understand that BUN:Cr > 20 if renal perfusion is repaired, but in heart failure wouldn't there be increased secretion of ANP/BNP from the atria that pushes up the sodium excretion? +  


submitted by brolycow(27),
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He ahs rhaet ueirfal ichhw eldas to a edasecer in rlane boold ofwl adn elraprne za.etaiom In lenerpar itoe,azam :rCBNU iaort si ;t=&g 0;2 iAavttconi fo teh ARAS ymesst edu ot teh pnrlreea eaiomzat manes that eht ecsp agvr si ghhi at .5201 adn eh si iolghdn oont udomis so rynaiur sudoim iwll eb low ;l,(2t0& FEaN &1lt);.%

figprincess  did you figure out the the ratio by actually divding out the numbers since the q didn't give it as a ratio? also what resource tells us what prerenal spec gravity should be? +  
brolycow  I just usually remember from class that spec grav 1.001-1.010 is considered dilute urine, and anything 1.025 and above is concentrated. For this question specifically, I think I remember there only being one option that even had the ratio >=20, all of the others were like 15 or less, so just have to rule them out. +7  
benzjonez  Very helpful video for acute kidney injury: https://www.youtube.com/watch?v=bMp6IxDKK2Q +8  
notadoctor  Another explanation that helped me is that inability to concentrate the urine means something is wrong with the kidneys. If you have dilute urine, or the spec gravity is between 1.001-1.010 in someone with low urine output it suggests something is wrong with the concentration mechanisms of the kidney. Because this person had congestive heart failure we were already looking for something that matched up with prerenal azotemia so we can pretty much get rid of all the answer choices that suggest other azotemias. Then finally to get the precise answer I looked at the BUN/Cr ratio which you would expect to be high(>= 20). +  
mikay92  Would fully recommend the OnlineMedEd video on AKI. Goes through the differential, lab results, treatment, etc in a very clear and concise manner. +  
drdoom  repost via @benzjonez -> https://www.youtube.com/watch?v=bMp6IxDKK2Q +  
drdoom  @mikay92 is this the OnlineMedEd video you're referring to? -> https://youtu.be/EWFgzVtMN50 +1  
drdoom  aha! there is an updated AKI video but you need an OnlineMedEd (free) account to view it: https://onlinemeded.org/spa/nephrology/acute-kidney-injury/acquire +  
popofo  I understand that BUN:Cr > 20 if renal perfusion is repaired, but in heart failure wouldn't there be increased secretion of ANP/BNP from the atria that pushes up the sodium excretion? +  


submitted by mahitha(0),

Can anyone PLZZ explain how lymes disesa has memory problems and depressed mood?

drdoom  Chronic inflammation, and the persistent elaboration of cytokines that go along with it, can cause all sorts of unusual and nonspecific problems, including cognitive compromise. (Just imagine how you might feel if you had low-grade fever for, say, a decade.) Patients who have suffered significant cardio- or cerebrovascular “events” report depressed mood following the event. My guess is that the memory problems can be from chronic inflammation or as a result of spirochete vasculitis which, over time, results in a kind of vascular dementia (“multi-infarct”). You see spirochete vasculitis (of the thoracic aorta), as well as vascular dementia, in another famous spirochete, Treponema pallidum, the culprit behind Syphilis. +3  


submitted by drdoom(819),
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re’seH neo way to -omrtps-eniiecfoales daed“srcee deodnbr-gyonh tn:omaofi”r ’mI tno a igb anf fo sith neil of eair,nsong ubt lclainhytce lnanaei as a idse ropug ash eomr dnshgr*yoe rof oetnpilta groenhyd gbiondn nath nielygc:

inaln:ea 3CH—
:ylgenic H—

S,o thliyec“a”c,nl nailaen lduow rpietm emor ne-grodhyodnb ir,foaotnm hcwhi hgtim llaow uyo ot leeimniat htat ecco.ih

ahTt a,isd ti essem molsta eiismoblps ot rlue otu uhtow(ti ryve acnliethc gondleekw ro esmo ordiepvd xenplamtreei adta) ahtt eth yghlstil relrga eanailn sedo otn iaiprm engohrdy dogninb ebwetne alclogen leouseclm avi ectisr ptsi)aa(l frneretnce.ie In sirmepl et,mrs csien anniale si e,ragrl you lwduo hiknt ttha ti umst whoesom teerifnre hwti het doyrnionegb-gdhn taht csucro with eth lye-tpwid igeycnl.

---
*lrytSict ksne,pagi s’it tno eht rmnbeu of dnorgsyeh tbu soal eht rntthgse fo hte ldpeoi atht taitcielasf gdoeyrhn dnnbo:ig a roedgnyh oubnd ot a tnglsory ctvaongeetreeil ecuellmo klei onfulire wlli ar“”epap reom optveiis adn, shut, rnn-gdobhoyde ermo ostlnryg hitw a neybra yoxeng orca(pdme hwit a hryendgo encecotnd ot rbnac,o for eae.l)mpx

hFreurt genidar:

  1. mcuodbs:l/dtu/u//hneiqw.wdiu.erlcmwhp.hdpe.s/httghlpe
hungrybox  Appreciate the effort but this is far too long to be useful. +21  
drachenx  hungrybox is a freaking hater +  
drdoom  @drachenx haha, nah, coming back to this i realize i was probably over-geeking lol +  
blueberrymuffinbabey  isn't the hydrogen bonding dependent on the hydroxylated proline and lysine? so that wouldn't really be the issue here since those aren't the aas being altered? +  
drdoom  @blueberry According to Alberts’ MBoC (see Tangents at right), hydroxylysine and hydroxyproline contribute hydrogen bonds that form between the chains (“interchain”, as opposed to intra-chain; the chains, of course, are separate polypeptides; that is, separate collagen proteins; and interactions between separate chains [separate polypeptides] is what we call “quaternary structure”; see Tangent above). And in this case, as you point out, the stem describes a Gly->Ala substitution. That seems to mean two things: (1) the three separate collagen polypeptides will not “pack [as] tightly” to form the triple helix (=quaternary structure) we all know and love and (2) proline rings will fail to layer quite as snugly, compromising the helical conformation that defines an alpha chain (=secondary structure; the shapes that form within a single polypeptide). +  
tadki38097  also you can't H bond with carbon, it's not polar enough +  


submitted by gabstep(14),
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nufdo isth in sor:bbni the cilgoioard dan lghtocsoii panrtte fo sfbiirso si dreefrre ot as uasul slinattiitre naenmupio, hwchi is rruqeied ofr teh donssaigi fo I.PF

drdoom  pneumonitis* +  
drdoom  ^nevermind! +  


submitted by gabstep(14),
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fondu isht ni in:srbob eth igaolrcido nad gloiiotshc etrantp fo oisbifrs is erdrreef to as usalu istlnrteatii moinuapen, iwhhc is ueeidrrq rfo eht aisndoigs fo F.PI

drdoom  pneumonitis* +  
drdoom  ^nevermind! +  


submitted by mikay92(0),
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idD eynano esle fdni sith ensqouti llfunaipy loopyr tewirn?t I ptesn os logn sujt ityngr to rfueig uot ahwt eth hcek tyhe eerw k.sniag

I'ts sa if thye 'odnt ntwa us ot od w.lle..

drdoom  I don’t think the NBME ever “intends” to write an ambiguous or poorly worded stem. What they want to do is write questions whose response choices are not “blatantly obvious” but which do have a single, “most correct” choice. That’s actually surprisingly difficult! If the correct choice were “obvious”, the test would not be doing a good job assessing anyone’s ability to make subtle judgment calls (an important skill, one might argue, in the morass that is the real world); this is also the reason they eschew “buzzwords”, generally. If a stem has two or more choices that are “equally correct”, the same lapse has occurred: they would be failing to assess the capacity to make subtle judgment calls. +  
drdoom  All that said, please see this perfect metaphorical description of all Step 1 questions: reddit.com/r/step1/comments/4jegfu/took_step_1_wanted_to_share +1  


submitted by mikay92(0),
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Ddi yenoan esle dnif htsi oeqntius fnyuapill rpoylo tinr?wte I setpn os nlgo utsj tnrigy ot igfreu out awht eht cehk ehty ewer gkn.ais

'tIs as if tyhe to'dn nwat su ot od .w.e.ll

drdoom  I don’t think the NBME ever “intends” to write an ambiguous or poorly worded stem. What they want to do is write questions whose response choices are not “blatantly obvious” but which do have a single, “most correct” choice. That’s actually surprisingly difficult! If the correct choice were “obvious”, the test would not be doing a good job assessing anyone’s ability to make subtle judgment calls (an important skill, one might argue, in the morass that is the real world); this is also the reason they eschew “buzzwords”, generally. If a stem has two or more choices that are “equally correct”, the same lapse has occurred: they would be failing to assess the capacity to make subtle judgment calls. +  
drdoom  All that said, please see this perfect metaphorical description of all Step 1 questions: reddit.com/r/step1/comments/4jegfu/took_step_1_wanted_to_share +1  


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yM otugthh psoescr wsa that mpsurta-pot beigednl si yuslual ltdaree ot the ueu,trs dna ucmh of het pvclei iarecvs is sdpupeil by nsehbrac fo hte nitlrean licia ta.ryre

neonem  This sounds like a case of acute endometritis. In any case, uterus is supplied by uterine artery (branch of internal iliac artery) with collateral flow from ovarian artery (comes right off aorta). I don't think there are any branches of external iliac artery into the pelvis; it becomes femoral artery once it passes under inguinal ligament. +4  
tsl19  Here's a picture that I found helpful [Female Reproductive Tract arterial supply] (https://teachmeanatomy.info/wp-content/uploads/Blood-Supply-to-Female-Reproductive-Tract.jpg) +14  
sympathetikey  @tsl - Thank you! +  
step1soon  uworld Qid:11908 +  


drdoom  great schematic. +  
qball  Just to add, the ovarian artery branches from the aorta as well. +1  


submitted by vshummy(156),
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I hnitk rmoe egrnyle,al etpnior ogfnldi hppsnea ta teh ERR adn eht mest ysas the noetrpi ’ndoest ldfo pyrrolep. cSaelflyii,pc the tsom nmcoom FC uittmaon si a oledsmdfi intrpeo adn eth rtepino is inteeard ni teh RER nda tno rdretpatosn ot the ellc nmmeaerb - AF 0291 pg 6.0

uroosisyed5  Which makes sense if we think about the pathophys of elevated Cl- and Na intracellularly. Both of these ions go up inside the cells due to the retention of the misfolded proteins in the RER. +  
lilyo  I actually disagree with this reasoning. The pathophysiology in CFTR is not due to accumulation of misfolded proteins. It is due to decreased/absent ATP gated transmembrane Chloride channel. According to Uworld, the miscoded protein is detected by the Endoplasmic Reticulum. The abnormal protein is targeted for destruction by the proteasome and never reaches the cell surface. There is NO retention of misfolded protein, there is degradation of misfolded protein and therefore absence of chloride channels on the membrane. This is what leads to impaired removal of salt from the sweat as well as decreased NaCl in mucus. I dont think the answer should be ER. Can anyone tell me if I am missing something here that makes the answer ER as opposed to cytoplasm? Because the way I see if is misfolded proteins go form the ER into the cytoplasm to reach the proteasome and then be destructed. Uworld questions ID are 805, 802, 1514, and 1939. +15  
drdoom  @lilyo The CFTR is a transmembrane protein. Like all proteins, its translation begins in the cytosol; that said, CFTR contains an N-terminus “signal sequence”, which means as it is being translated, it (and the ribosome making it!) will be transported to the Endoplasmic Reticulum.^footnote! As it gets translated, its hydrophobic motifs will emerge, which embeds the CFTR protein within the phospholipid bilayer of the ER itself! That means the protein will never again be found “in the cytosol” because it gets threaded through the bilayer (which is, in fact, how all transmembrane proteins become transmembrane proteins at the cell surface -- they have to be made into transmembrane proteins in the ER first!). +8  
drdoom  @lilyo (continued) So, yes, ultimately, these misfolded proteins will be directed toward a proteasome for degradation/recycling, but that will happen as a little vesicle (or “liposome”); the misfolded protein, in this case, is not water-soluble (since, by definition, it has hydrophobic motifs which get “threaded through” a bilayer to create the transmembrane pattern), which means you won’t find it in the cytosol. +5  
drdoom  ^footnote! : The movement of active* ribosomes from the cytosol to the Endoplasmic Reticulum is why we call that area of ER “rough Endoplasmic Reticulum (rER)”; on electron microscopy, that section was bespeckled with little dots; later, we (humans) discovered that these dots were ribosomes! +1  
drdoom  * By “active ribosomes”, I just mean ribosomes in the process of converting mRNA to protein! (What we call “translation” ;) +1  
wrongcareer69  How many goddamn ways are they going to test us on CF. I'm so over this! +2  
furqanka  also in FA, under alpha 1 antitrypsin, its says 'Misfolded gene product protein aggregates in hepatocellular ER". might be the same concept. +3  
joanmanuel26  According to Kaplan; All proteins that are synthesized in the ER must fold correctly in order to be transported to the golgi aparatus and then to their final destinations. If the mutation cause a misfolded protein, the result will be the loss of the protein function and, in some cases, accumulation of the protein in the ER. +  
drdoom  @lilyo Thinking about this more. You will not find the (misfolded) protein in the cytosol. The misfolded protein may be inside a proteasome—and a proteasome may live in the cytosol—but the misfolded protein itself will never appear in the cytosol. The products of its degradation might (constituent amino acids or small peptides) but if you had an antibody for the misfolded protein and asked it “Where is the misfolded protein?”, the antibody would answer: “Most of what I could find appears to be in the rER.” +  


submitted by vshummy(156),
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I kthni emor nell,ageyr eonprti gfnldio phepasn ta eth RRE dna the emst says the teporni ’etsdon dlof yprerl.op ccyelfpliSa,i hte sotm oncomm FC mtnotiau si a dfsomledi oprietn nad teh noreipt si eeinratd in eth ERR and tno ntorpadsert to teh cell mnbrmaee - AF 1920 gp .60

uroosisyed5  Which makes sense if we think about the pathophys of elevated Cl- and Na intracellularly. Both of these ions go up inside the cells due to the retention of the misfolded proteins in the RER. +  
lilyo  I actually disagree with this reasoning. The pathophysiology in CFTR is not due to accumulation of misfolded proteins. It is due to decreased/absent ATP gated transmembrane Chloride channel. According to Uworld, the miscoded protein is detected by the Endoplasmic Reticulum. The abnormal protein is targeted for destruction by the proteasome and never reaches the cell surface. There is NO retention of misfolded protein, there is degradation of misfolded protein and therefore absence of chloride channels on the membrane. This is what leads to impaired removal of salt from the sweat as well as decreased NaCl in mucus. I dont think the answer should be ER. Can anyone tell me if I am missing something here that makes the answer ER as opposed to cytoplasm? Because the way I see if is misfolded proteins go form the ER into the cytoplasm to reach the proteasome and then be destructed. Uworld questions ID are 805, 802, 1514, and 1939. +15  
drdoom  @lilyo The CFTR is a transmembrane protein. Like all proteins, its translation begins in the cytosol; that said, CFTR contains an N-terminus “signal sequence”, which means as it is being translated, it (and the ribosome making it!) will be transported to the Endoplasmic Reticulum.^footnote! As it gets translated, its hydrophobic motifs will emerge, which embeds the CFTR protein within the phospholipid bilayer of the ER itself! That means the protein will never again be found “in the cytosol” because it gets threaded through the bilayer (which is, in fact, how all transmembrane proteins become transmembrane proteins at the cell surface -- they have to be made into transmembrane proteins in the ER first!). +8  
drdoom  @lilyo (continued) So, yes, ultimately, these misfolded proteins will be directed toward a proteasome for degradation/recycling, but that will happen as a little vesicle (or “liposome”); the misfolded protein, in this case, is not water-soluble (since, by definition, it has hydrophobic motifs which get “threaded through” a bilayer to create the transmembrane pattern), which means you won’t find it in the cytosol. +5  
drdoom  ^footnote! : The movement of active* ribosomes from the cytosol to the Endoplasmic Reticulum is why we call that area of ER “rough Endoplasmic Reticulum (rER)”; on electron microscopy, that section was bespeckled with little dots; later, we (humans) discovered that these dots were ribosomes! +1  
drdoom  * By “active ribosomes”, I just mean ribosomes in the process of converting mRNA to protein! (What we call “translation” ;) +1  
wrongcareer69  How many goddamn ways are they going to test us on CF. I'm so over this! +2  
furqanka  also in FA, under alpha 1 antitrypsin, its says 'Misfolded gene product protein aggregates in hepatocellular ER". might be the same concept. +3  
joanmanuel26  According to Kaplan; All proteins that are synthesized in the ER must fold correctly in order to be transported to the golgi aparatus and then to their final destinations. If the mutation cause a misfolded protein, the result will be the loss of the protein function and, in some cases, accumulation of the protein in the ER. +  
drdoom  @lilyo Thinking about this more. You will not find the (misfolded) protein in the cytosol. The misfolded protein may be inside a proteasome—and a proteasome may live in the cytosol—but the misfolded protein itself will never appear in the cytosol. The products of its degradation might (constituent amino acids or small peptides) but if you had an antibody for the misfolded protein and asked it “Where is the misfolded protein?”, the antibody would answer: “Most of what I could find appears to be in the rER.” +  


submitted by vshummy(156),
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I nihtk mreo ale,gneylr teoprin gfilnod aphpsen at teh RER and eht tsem syas hte eptonir nosted’ fldo oyp.elrpr Salecfcypiil, het ostm omnocm FC nttmiaou is a idesldomf ptoiner dna hte oertnpi is trneeaid ni the ERR nda ont dtnrtasoerp ot eht ecll meamnrbe - AF 1920 gp 60.

uroosisyed5  Which makes sense if we think about the pathophys of elevated Cl- and Na intracellularly. Both of these ions go up inside the cells due to the retention of the misfolded proteins in the RER. +  
lilyo  I actually disagree with this reasoning. The pathophysiology in CFTR is not due to accumulation of misfolded proteins. It is due to decreased/absent ATP gated transmembrane Chloride channel. According to Uworld, the miscoded protein is detected by the Endoplasmic Reticulum. The abnormal protein is targeted for destruction by the proteasome and never reaches the cell surface. There is NO retention of misfolded protein, there is degradation of misfolded protein and therefore absence of chloride channels on the membrane. This is what leads to impaired removal of salt from the sweat as well as decreased NaCl in mucus. I dont think the answer should be ER. Can anyone tell me if I am missing something here that makes the answer ER as opposed to cytoplasm? Because the way I see if is misfolded proteins go form the ER into the cytoplasm to reach the proteasome and then be destructed. Uworld questions ID are 805, 802, 1514, and 1939. +15  
drdoom  @lilyo The CFTR is a transmembrane protein. Like all proteins, its translation begins in the cytosol; that said, CFTR contains an N-terminus “signal sequence”, which means as it is being translated, it (and the ribosome making it!) will be transported to the Endoplasmic Reticulum.^footnote! As it gets translated, its hydrophobic motifs will emerge, which embeds the CFTR protein within the phospholipid bilayer of the ER itself! That means the protein will never again be found “in the cytosol” because it gets threaded through the bilayer (which is, in fact, how all transmembrane proteins become transmembrane proteins at the cell surface -- they have to be made into transmembrane proteins in the ER first!). +8  
drdoom  @lilyo (continued) So, yes, ultimately, these misfolded proteins will be directed toward a proteasome for degradation/recycling, but that will happen as a little vesicle (or “liposome”); the misfolded protein, in this case, is not water-soluble (since, by definition, it has hydrophobic motifs which get “threaded through” a bilayer to create the transmembrane pattern), which means you won’t find it in the cytosol. +5  
drdoom  ^footnote! : The movement of active* ribosomes from the cytosol to the Endoplasmic Reticulum is why we call that area of ER “rough Endoplasmic Reticulum (rER)”; on electron microscopy, that section was bespeckled with little dots; later, we (humans) discovered that these dots were ribosomes! +1  
drdoom  * By “active ribosomes”, I just mean ribosomes in the process of converting mRNA to protein! (What we call “translation” ;) +1  
wrongcareer69  How many goddamn ways are they going to test us on CF. I'm so over this! +2  
furqanka  also in FA, under alpha 1 antitrypsin, its says 'Misfolded gene product protein aggregates in hepatocellular ER". might be the same concept. +3  
joanmanuel26  According to Kaplan; All proteins that are synthesized in the ER must fold correctly in order to be transported to the golgi aparatus and then to their final destinations. If the mutation cause a misfolded protein, the result will be the loss of the protein function and, in some cases, accumulation of the protein in the ER. +  
drdoom  @lilyo Thinking about this more. You will not find the (misfolded) protein in the cytosol. The misfolded protein may be inside a proteasome—and a proteasome may live in the cytosol—but the misfolded protein itself will never appear in the cytosol. The products of its degradation might (constituent amino acids or small peptides) but if you had an antibody for the misfolded protein and asked it “Where is the misfolded protein?”, the antibody would answer: “Most of what I could find appears to be in the rER.” +  


submitted by vshummy(156),
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I thnki emor alre,enylg rnpieot ndligof spphnae ta het ERR dan eht smte sysa hte nptoeri dtoe’ns ldfo pyre.olpr ycie,clSlfpai eth tosm mnocom CF ntmauoti is a dlsemiodf iotrpen adn teh eoriptn is iedertan ni hte RRE adn nto resnarpotdt ot the lcel banemmre - FA 0219 pg 60.

uroosisyed5  Which makes sense if we think about the pathophys of elevated Cl- and Na intracellularly. Both of these ions go up inside the cells due to the retention of the misfolded proteins in the RER. +  
lilyo  I actually disagree with this reasoning. The pathophysiology in CFTR is not due to accumulation of misfolded proteins. It is due to decreased/absent ATP gated transmembrane Chloride channel. According to Uworld, the miscoded protein is detected by the Endoplasmic Reticulum. The abnormal protein is targeted for destruction by the proteasome and never reaches the cell surface. There is NO retention of misfolded protein, there is degradation of misfolded protein and therefore absence of chloride channels on the membrane. This is what leads to impaired removal of salt from the sweat as well as decreased NaCl in mucus. I dont think the answer should be ER. Can anyone tell me if I am missing something here that makes the answer ER as opposed to cytoplasm? Because the way I see if is misfolded proteins go form the ER into the cytoplasm to reach the proteasome and then be destructed. Uworld questions ID are 805, 802, 1514, and 1939. +15  
drdoom  @lilyo The CFTR is a transmembrane protein. Like all proteins, its translation begins in the cytosol; that said, CFTR contains an N-terminus “signal sequence”, which means as it is being translated, it (and the ribosome making it!) will be transported to the Endoplasmic Reticulum.^footnote! As it gets translated, its hydrophobic motifs will emerge, which embeds the CFTR protein within the phospholipid bilayer of the ER itself! That means the protein will never again be found “in the cytosol” because it gets threaded through the bilayer (which is, in fact, how all transmembrane proteins become transmembrane proteins at the cell surface -- they have to be made into transmembrane proteins in the ER first!). +8  
drdoom  @lilyo (continued) So, yes, ultimately, these misfolded proteins will be directed toward a proteasome for degradation/recycling, but that will happen as a little vesicle (or “liposome”); the misfolded protein, in this case, is not water-soluble (since, by definition, it has hydrophobic motifs which get “threaded through” a bilayer to create the transmembrane pattern), which means you won’t find it in the cytosol. +5  
drdoom  ^footnote! : The movement of active* ribosomes from the cytosol to the Endoplasmic Reticulum is why we call that area of ER “rough Endoplasmic Reticulum (rER)”; on electron microscopy, that section was bespeckled with little dots; later, we (humans) discovered that these dots were ribosomes! +1  
drdoom  * By “active ribosomes”, I just mean ribosomes in the process of converting mRNA to protein! (What we call “translation” ;) +1  
wrongcareer69  How many goddamn ways are they going to test us on CF. I'm so over this! +2  
furqanka  also in FA, under alpha 1 antitrypsin, its says 'Misfolded gene product protein aggregates in hepatocellular ER". might be the same concept. +3  
joanmanuel26  According to Kaplan; All proteins that are synthesized in the ER must fold correctly in order to be transported to the golgi aparatus and then to their final destinations. If the mutation cause a misfolded protein, the result will be the loss of the protein function and, in some cases, accumulation of the protein in the ER. +  
drdoom  @lilyo Thinking about this more. You will not find the (misfolded) protein in the cytosol. The misfolded protein may be inside a proteasome—and a proteasome may live in the cytosol—but the misfolded protein itself will never appear in the cytosol. The products of its degradation might (constituent amino acids or small peptides) but if you had an antibody for the misfolded protein and asked it “Where is the misfolded protein?”, the antibody would answer: “Most of what I could find appears to be in the rER.” +  


submitted by kdckjn(0),
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hwy erthe si byoalptiirb fo hartfe igben a rrearci is 23/

drdoom  We assume this is a recessive disease. In other words, you manifest the disease if you inherit a disease allele, d, from your mother and a disease allele, d, from your father, giving you an allele pairing denoted by dd. dd = you have the disease. The father does not have the disease; this means his genotype can only be 1 of three things: DD, Dd, or dD. That is, DD = D from his dad, D from his mom; Dd = D from his dad, d from his mom; or dD = d from his dad, D from his mom. Notice that in only two of these 3 possibilities does the father (potentially) have a disease allele (d) that he might pass on to his progeny. +  


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wmha0atl3/f.p1twpp5ot//0:a/3f0.r/0w1psg4h./52

^^^a uefulbait eatlb taht owshs sffecta no eoecleylttr vselle in vatelaisx vs drctesiui vs igtnvo.im

idcrcgonA ot the betal, sit dhra to eltl ceiritud sv vtilaxae buase by sremu tscreetlleoy noa.el ehT eruni tlesycotlere lwdou eldkamry rffdei in thta diceirut iwll veha icderenas CKN/a/l dna tavisxlae dwuol olwlof teh ospptioe dtern cerdeasd.)e( vHeerwo, twih eth tfac ahtt UBN si senigianrc and atth ew can tlle ht'rese a octlamebi aslaoslik htwi ysreoatrrip sciadsio iamosepc,otnn ew acn bte on tdusrciie over iaxvlst.ea

EARXT NFOI rofm the laebt ni teh knli oe:vab

inmgo:tVi K[ c]ed C[l e]dc 3[HCO i]nc Hp[ ]nci
iv:aasetLx [K ecd] C[l nic or dce] 3CH[O cde or nic] pH[ dec or cn]i
Drui esi:ct K[ ce]d lC[ ]edc O3H[C in]c [pH ]cni

nI ienur fro t,nimgiov lCK/aN/ will lla be Ieeacendd sr renui rof ieaxatvl as,bue NK/a lliw eb dr.asceeed lC is ormlna or Idseeedca.n r einur rof erctduii suaeb: laCK//N will lla be enrdiseac

end(wAr aYng ofr s)rtnPiede

drdoom  table -> https://imgur.com/vyJZV55 +2  
nootnootpenguinn  The last sentence is nice touch!!! +2  


submitted by hello(302),
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at'hWs teh sehymscoe dpspsoeu to eb a eulc a?otbu Deso hits epittan vhea ?CID oDse CID aaslwy auces pvoeyhomcil hk?soc

drdoom  Disseminated intravascular coagulation (DIC) is a syndromic definition. (See tangent.) It does not “always” lead to shock but shock is definitely a possible sequela (since, by definition, DIC = “systemic thrombotic process”; anything systemic should get you a little worried), and so a patient with DIC should be monitored closely! +  


submitted by usmle11a(73),
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ok eth ywa i kldooe ta sthi :swa

eyour ont 01%0 eusr hes wsa kcdtaate ron do yuo awtn to be the neospr engitll eth nhsadub seh na rkctatae os uyo re:eomv B C

golianwl mhi in ithw hte ntetp,ia ogd knwso waht tath ygu ahs iddenh hwti mih osal oyu ilwl ekma a eghu sence : A

eht nylo thgin ot do is be icmtipalod sa lopepe nokw yteh rneta laewldo ni eht tmnaetrte arae nda by thta uoy rusaes reh stf.aye

drdoom  The prevailing rule of American medicine (and law) is individual autonomy. No other person, professional or otherwise, is granted “default access” or privilege to another person’s body—that includes the physician! The physician must receive consent from a (conscious) “person” before they become “a patient”. In the same way, the person (now, the patient) must give consent before anyone else is permitted to be involved in her care—spouses included! +1  
llamastep1  Alright we got it! lol +1  
123ojm  B and C are actually wrong because they put the patient in danger for when she is discharged and has to return home. she probably has things she needs in their home (eg passport, money, etc) and if the husband knows she has told you about the abuse she is at risk of being killed. +  


submitted by dr.xx(144),
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igrh.t eh tobeaylusl tusm mnaeri in hte gwnatii aear so ttah eh si at danh ot tatkca his wfei rnheewev hre axem d.sen go !MENB

meningitis  I guess it was all about not offering battering information in order to not make matters worse since he will figure out that the wife told on him.. Also, its a HUGE STRETCH but the only reason I thought he should stay in the waiting room was just in case the wife died they could detain him and call the police for questioning. +10  
temmy  Also, he should stay there because his wife did not grant him the permission to see him. Patients requests trumps. +  
nephcard  Doctor should not believe what wife told her. There may be some other reason for injury so batttering information should not be provided. But her wish of not letting her husband in should be fulfilled +2  
charcot_bouchard  No. In real life patient lies. In Board ques they always tell the truth. Unless they make it very obvious. in fact its a board ques rule. So u believe her untill proven otherwise. +3  
drdoom  The prevailing rule of American medicine and law is individual autonomy. No other person is granted “default access” or privilege to another person’s body—that includes the physician! The physician must receive consent from a (conscious) “person” before they become “a patient”. In the same way, the person (the patient) must give consent before anyone else is permitted to be involved in her care, spouses included! +  


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Teh etsinoqu ysas yeht tnd'o epsnsrod to casdtani ETHN skas hicwh you to iiedtynf cihwh rudg is the smot tveeffeic at srpnpsuegsi adci cdtuipo,nro TON hatw het tsom efcieetvf iadtnac is. ehT nwaers si PP.sI'

I llwi ys,a ehrveow, I aws oolinkg rof osiegthnm leik eictootder.

drdoom  lucid. nice catch. +1  
maddy1994  WHY not blockage of h2 receptors +3  
krewfoo99  @maddy1994. PPI are more effective than H2 blockers in suppression of gastric acid +1  


submitted by hello(302),
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yWh tnsi' sith a ohtcro sy?dtu

drdoom  This is a cohort study! (Since it involves splitting people into "groups"; group = cohort.) But the stem asks what "best describes" the design. So, yes, it's a cohort study but a more precise ("more specific") description is Open-label. In other words, "Open-label clinical trial" is a type of cohort study, and, in this case, "Open-label" is a more precise description of what is described in the stem. +7  
drdoom  For a more technical explanation of "Cohort studies", see the definition from the National Library of Medicine: https://meshb.nlm.nih.gov/record/ui?ui=D015331 +1  
angelaq11  It is a cohort, just as @drdoom said, but it isn't an "Observational" one. +2  
pg32  It's actually not a cohort study, imo. In a cohort you find people with an exposure and see if they develop some outcome. In this experiment, people were RANDOMLY ASSIGNED to the different exposures. That doesn't happen in cohorts. +7  
pg32  It may be a cohort in that these people are in groups, but for the purposes of Step 1, I don't think we will deal with typical "Cohort" studies in which participants are randomly assigned. +2  
ashli777  you don't administer an intervention in a cohort study, you just observe what happens. it is an observational study. +  
drdoom  ^ i retract my earlier subcomment! thanks @ashli777 and @pg32 — you guys are right that cohorts do not intervene! in two senses: (1) there is no treatment intervention and (2) there is no “assignment” intervention (either randomly or by selection; that is, investigators do not DESIGN or DETERMINE how groups are formed, even if that means random determination by computer). +1  


submitted by hello(302),
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Wyh s'nit shti a otorhc tudys?

drdoom  This is a cohort study! (Since it involves splitting people into "groups"; group = cohort.) But the stem asks what "best describes" the design. So, yes, it's a cohort study but a more precise ("more specific") description is Open-label. In other words, "Open-label clinical trial" is a type of cohort study, and, in this case, "Open-label" is a more precise description of what is described in the stem. +7  
drdoom  For a more technical explanation of "Cohort studies", see the definition from the National Library of Medicine: https://meshb.nlm.nih.gov/record/ui?ui=D015331 +1  
angelaq11  It is a cohort, just as @drdoom said, but it isn't an "Observational" one. +2  
pg32  It's actually not a cohort study, imo. In a cohort you find people with an exposure and see if they develop some outcome. In this experiment, people were RANDOMLY ASSIGNED to the different exposures. That doesn't happen in cohorts. +7  
pg32  It may be a cohort in that these people are in groups, but for the purposes of Step 1, I don't think we will deal with typical "Cohort" studies in which participants are randomly assigned. +2  
ashli777  you don't administer an intervention in a cohort study, you just observe what happens. it is an observational study. +  
drdoom  ^ i retract my earlier subcomment! thanks @ashli777 and @pg32 — you guys are right that cohorts do not intervene! in two senses: (1) there is no treatment intervention and (2) there is no “assignment” intervention (either randomly or by selection; that is, investigators do not DESIGN or DETERMINE how groups are formed, even if that means random determination by computer). +1  


submitted by lauri(-2),
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I CTONAN EWIV ETH TEENIR UQ.IOTNES SI ITHS ARL?NMO

trichotillomaniac  Hi Lauri, this is normal. We can't post the whole question due to copy right laws but you can almost always find the question you are looking for and the answer to by going to the form and then Ctrl + find -ing the age of the patient and other key words or the answer! +6  
drdoom  HI LAURI. THANK YOU FOR DEMONSTRATING YOUR PROFICIENCY WITH ALL-CAP COMPOSITION! +4  


submitted by drdoom(819),
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Coclnlsauait fro add. The byoliribpat of teh ahretf bigen a ircerar si 23/ scnei ti is wnokn atht eh ’eodsnt veha het esiaed.s ehnT eth ribptyoailb fo mhi sasngip it no to ihs ikd is 21,/ tuh:s

  • biibtPoraly of dda igbne arercri = /32
  • otyiilbrabP of add nsiagsp on iseeasd aeelll = 21/

lcisnoaualCt fro omm. thWi the yiebWgrnHrdea- lcipPe,rni uyo nca ieufrg tou het tpilriyboba fo hte emhrto giben a i:rerrac

q = 100r,(/)0tq04s = 00/12

So, 2qp = 2 * /2010 * 20/1990, hihwc si xpapro 01/.01

oFr the ihcld to egt eht elleal mrfo o,mm wto shtnig ende to hppa:ne ()1 mmo tsmu be a eacrirr h“yo[tzeoe”e]grt dna (2) mom mtus spsa the aleell ot c:hlid

  • ibPbolratyi fo mom ingbe rciarre = 1/100
  • bbilaytroPi of mom gsaspni on aseseid llleea = /12

Pguitn ti lla otterghe. ,Nwo ebinomc lal ehegor:tt

= (yibpabriolt of dda ebign cr)rreai * brbpiltayo(i of dad sgnaspi no sedseia )lleale * by(patiliorb of omm niegb eci)arrr * priatlb(ioby fo mom apnigss on iessdea l)ellae

= /32 * /12 * 1/010 * 12/
= 1 ni 060

kernicterusthefrog  To quote Thorgy Thor, drag queen: "ew, Jesus, gross" +37  
niboonsh  This question makes me want to vomit +11  
drdoom  lol +  
5thgencephalosporin  okay wow +  


submitted by dr.xx(144),
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In oasiidso,scr lerycaehmaipc nlayorlm pespesssru het seeelra fo THP dna foeehrret het nprocdutoi fo oaicrcitll h1y,recd5i)yifod,a-collx(2hlcroe utb in odiassosrci nad ehrot traousagulonm as,seesdi etdcaativ nouenaormcl sllce lricar(puytla aocp)haresmg in het lung dna lpmyh esdon durcepo lticlaoicr a-oe(xl5hei2oirocl,dccyh)1ydrlf fomr olaiiclcd eaoxyrh)frhcdl5c2(ll-ocieoy npddeintnee of T.PH

e-r.iaolttnchrecntahsocaiadywswpsen/-oste/ptdnmt:toaw/eluoasim.upsguec/m-

dr.xx  ~~In sarcoidosis,~~ +  
hello  Probably a typo in the first 2 words of the explanation -- not sure what they meant to say instead +  
drdoom  I believe @dr.xx meant to strikeout "In sarcoidosis" from his comment; double-tilde is the markdown plaintext that usually accomplishes that. +  


submitted by dentist(50),
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reytpt godo uamsrmy

drdoom  welcome, O great physician of the skull and oral cavity. we revere your intricate understandings of the face, jaw, maxilla and all their tiny and hidden foramina. teach us your ways. +6  


submitted by sunny(4),
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why si siht tno a rscos canisetlo v?yresu ... escin ew aer iganks at a ulacrrtiap teim

drdoom  As Aristotle once quipped, “A ‘single-point in time’ doth not a cross-sectional study make.” The design of a cross-sectional study would not define “ahead of time” two cohorts (two groups); said another way, a cross-sectional design would not “split people into two groups.” In the design of a cross-sectional study there is only “one group”, and then you ask all members of that group some question (“Do you have asthma?”). At the end of a cross-sectional study, the authors will be able to make a statement like this: “We called 10,000 phone numbers with area code 415 at random and asked ‘Do you take Drug X?’ 500 responded ‘I don’t know’, 633 responded ‘Yes’, and 8,867 responded ’No’.” +16  
castlblack  That is interesting. I think the question is phrased ambiguously. I interpreted the question stem to say that they called random people and sorted them into hemorrhagic stroke pts vs controls after the fact using an ORAL questionnaire. Therefore the question would be " Did you have a stroke?" Yes = 702 or no = 1376. And thus would be a cross-sectional study. I see now that the questionnaire must be paper and contacted from some unstated list of drug X recipients. +  


submitted by nwinkelmann(285),
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I ilrtllaye ujst azrdeile ywh shit uqetonis ouncdfes me os cuhm (nad Iv'e ertdi to eurgif it otu a oelcup fo eit,ms )o.ll I elt het iloclquloa iednionitf of uibmali .i(e. gnmvtiio) istck in my dnim, htta I gfotor het tlcaua ideaclm iefnoiidtn = manorl IBM 1(g8t);& + iegbn igntae dna ignprug whee(r pirungg ludco eb nddcuei mingitov or iituerdc sue or alevaxit eus n/drao eisevxces )xre.eesic oS aly,rle hwat stih tesqiuon aws gasnik is implys awth si eht otetclryeel elaacbn of sxeicevse ?aedirahr EGE!Z I dmae it os mchu erardh in my adhe wnhe trigny to asewrn ti yligaoil.nr

rarDaeih sscaue nonioan-n apg i(..e cproeleyhimh)cr bcoitmlae sdi.oisac oolSt tynlrmeiopdna osntacni C-OH3 dna +,K so vxecsiese reaadhri = exsisceev ssol fo O3CH- dna K+. hlieodrC slleev in hte eurms wlil be eiearcdsn due ot eth anmlor -3/CClH-O lieibiuumr,q os sa eenvagti ehargc tsdpiesisa ude to sols fo OHC3,- -lC llwi ecesnira crtginorce teh agonip-.na

drdoom  Bulimia comes from Greek "ravenous hunger"; the term is a literal concatenation of the words for ox (bous) + hunger (limos). So, in Greek, bou-limia is literally "ox hunger", which is a nod to how the word is used in medicine = perpetual and insatiable appetite for food (the very "opposite" of vomiting). +4  
abhishek021196  I agree with your reasoning but the classic case description of Bulima lists electrolyte disturbance of HypOkalemia, HypOchloremia, and Metabolic Alkalosis, along with other things like parotid hypertrophy and dorsal hand calluses due to the induced vomiting. I tripped up there. :/ FA 20 Pg 567 +  
llamastep1  Take home lesson: reasoning > memorizing +2  


submitted by ellomon(-2),
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tnosQeui ,assy htta a duyts is onde ot amueers reau iornegnt ni nme dega 5.6 htaW fo hte logfwionl wssenar ridedovp ash ANCTIUCERA and ECREPSI emuasers

I od arege hatt fro a gilhyh ecepisr taneememsru uyo ende a bgi urgop so yruo dtanrsad rorre fo teh mane is lwroe .ie( eniiasnrcg the dtyus o).pewr

TUB

Age is eylalr mttpoiarn eerh, incse eoeplp dgae 65 REA UUAYLSL ELDHEDUSC ot the origotlus , nehec a TCIAANNREU sarmuee dowul be epoelp not from arevage aeg 56 t-&;g men gigno to a alcol ihpgpnos etcne.r hTsi rpuog oesd otn cfltere eth ergvaea NBU htat uoy dwulo ndfi ni a 65 eary ldo aeml go,urp so eht

NERWAS I:S 500 MEN MROF A TILS FO NSTATIPE GIOENUNDGR A IREOTNU TAHEHL ENISNCGER AT A ACOLL NGIOHSPP TRNEEC t;&g- EIRUNAANCT DNA CSEEIPR g-&;t soeD not etferlc ltuyr teh NBU name of 65 yaer ldo smael tub it seod it islryepce whit( wol dasartdn rreor of eanm, essl vnitdoiea of tlru)sse

I hpoe im h,tirg if im ont eplsea nplxeai em .wyh :( !!

drdoom  Accuracy means the data points are dispersed, but when you take the mean of those points, that mean (“sample mean”) is nearby the population mean (“true mean”). Data points are “more precise” if the dispersion across data points is smaller than some other set of data points (notice how this is a comparison and not an “absolute” statement); precision says nothing about how close the average of the data points are to the “true mean.” +  
drdoom  Keep in mind that “accuracy” and “precision” are relative descriptors; you can’t say “so-and-so is precise”; no, you can only say “such-and-such is more precise than so-and-so” or “so-and-so is more accurate than such-and-such.” So, in this case, we can infer that NBME considers “men at the urologist” to have BUNs that are closer to each other (more clustered; more precise; less dispersed) than the BUNs of “men at mall.” Here’s a nice image: https://medbullets.com/images/precision-vs-accuracy.jpg +  


submitted by ellomon(-2),
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Qnieutos ay,ss thta a tyuds si eond ot ereasum areu enortngi in men aedg 5.6 thaW fo teh ngfllooiw rsswnae oidpdver sha AIAEUCNCRT dan RSECPEI eaumssre

I od aeegr atth for a higylh iceespr numeetmsera oyu eden a gbi ogrup so ruoy tdnsdaar orerr of eht aenm is lwoer i(e. nsgiiecrna eth uydst rpw.)eo

UBT

eAg is aeyllr oattmripn e,reh cesin eoelpp gaed 56 AER ULAYLSU CHDEDELSU to teh lsiugotro , enech a NAAINTRCEU eremasu olduw eb epelop otn frmo veearag gea 65 -t;&g nme igogn to a colla pohnspgi ren.tce This ogurp deso not ftelcer hte agveare NUB ttah uoy olduw nifd in a 65 yare lod mela u,pgor os the

SRNEWA :SI 005 MNE FOMR A SITL FO INTSTPAE RNGIODNEUG A ITNEORU HAETLH RSEENCNGI TA A LACLO NPHIOPGS NCETER g&t;- AENUTANRCI DNA RCIESPE -g&;t oeDs ont eecftrl tlryu eht NUB nmea of 56 eyar ldo mlaes but ti esdo ti relpeyisc ti(wh lwo rddstaan orerr fo n,ema lses edativino of ler)usts

I ehop mi rihgt, fi im tno speale pnialxe me hwy. :( !!

drdoom  Accuracy means the data points are dispersed, but when you take the mean of those points, that mean (“sample mean”) is nearby the population mean (“true mean”). Data points are “more precise” if the dispersion across data points is smaller than some other set of data points (notice how this is a comparison and not an “absolute” statement); precision says nothing about how close the average of the data points are to the “true mean.” +  
drdoom  Keep in mind that “accuracy” and “precision” are relative descriptors; you can’t say “so-and-so is precise”; no, you can only say “such-and-such is more precise than so-and-so” or “so-and-so is more accurate than such-and-such.” So, in this case, we can infer that NBME considers “men at the urologist” to have BUNs that are closer to each other (more clustered; more precise; less dispersed) than the BUNs of “men at mall.” Here’s a nice image: https://medbullets.com/images/precision-vs-accuracy.jpg +  


submitted by seagull(1443),
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yhW u?esnsapnoto 'eHs gnnggeia ni na teviac tospr itwh na sedicnear sikr of uatTrmiac .yrjuni oS ew laeylr ujst seumas seh nto jduerni cuebeas eth emst osdent cyedltri asy 'esh nijru?ed Tehse tnsseqiuo eald ot oto yamn aispnmsu.ots (ni ym oipnn)oi

nc1992  Spontaneous pneumothorax, as a condition, is significantly more likely than a traumatic pneumothorax from just about anything but a car crash (ok maybe if he was in a fight). The car crash or a stabbing is also more probable overall but there's no point in inferring something that isn't provided +1  
nwinkelmann  I picked the traumatic injury also. After reading these comments I looked into it further. Traumatic pneumos occur because of blunt or penetrating chest trauma, and I found that the MCC form of blunt trauma (>70%) is motor vehicle acidents that cause significant trauma (i.e. rib fractures) or even blast trauma. Although it didn't say there were no chest wall fractures, at the same time it didn't indicate any rib fractures, which would be most like to cause the traumatic injury pneumo in the patient's case. +1  
drdoom  The stem makes no mention of trauma. +  
hyperfukus  i guess the issue is that you have to assume what they mean by "strongest predisposing risk factor for this patient's condition" I think this is dumb bc the answer is completely different based on what you consider this patient's "CONDITION" to be? either way he has a pneumothorax so if you wan to know what caused that its prob him being active or bumping into someone but if you consider the etiology of the pneumothorax then its the bleb and that is from him being a skinny dude/smoker i went to this b/c he's also only 5/10 that's not tall in my head they could have been nicer and made him 6'1 at least...also i feel like i saw a lot of q's back in the day when i first learned this with a presentation of the person like tripping or something dumb but they already had the bleb and then got the pneumothorax +  


submitted by drdoom(819),
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ouY aveh ot khnit bauot tshi usngi teh cptnoce fo OANNIICODLT LABTI.OPBIRY renoAth way ot aks thsi ptey of nuitqeso is ilek :iths “I swoh you a aetpint iwth nsastouonpe uopx.aetmnhor hihWc eroth nhgti si stmo keylil to be ertu about ttah neor?p”s rO uoy nac sharpe ti eseht :aysw

  • ieGvn a DCOIINNTO (ponotnsesua uenmpo,) wtha toehr nngidfi si ostm liykle to be het c?eas
  • Gvnie a oopl of eelopp whit nsotasenopu uoeoam,htpnxr hawt toerh tingh is otms iyklel ot be uetr obtua thm?e

nI rohte wdsor, fo lla olpeep owh nde pu twih ostueopsann pne,oum eth msot monocm rtheo inhgt atoub etmh is atht etyh aer AMLE pa;m& HTI.N

fI I gave uyo a ukectb fo eoanpstuosn oupenm ietsapnt -- dna yuo eraecdh ruoy dhan ni rthee nad dllpeu one otu -- waht orseanic duowl be moer omcnm:o nI yuro ahnd uyo aveh a esrmok or ni yuro ahdn uyo evah a hitn am?le t’Is hte rtael.t

someduck3  Is this the best approach to all of the "strongest predisposing risk factor" type questions? +  
drdoom  There is a town of 1,000 men. Nine hundred of them work as lawyers. The other 100 are engineers. Tom is from this town. He rides his bike to work. In his free time, he likes solving math puzzles. He built his own computer. What is Tom's occupation most likely to be? Answer: Tom is most likely to be a lawyer! Don't let assumptions distract you from the overwhelming force of sheer probability! "Given that Tom is from this town, his most likely occupation (from the available data) = lawyer." +4  
drdoom  There is a town of 1,000 spontaneous pneumo patients. Six hundred are tall, thin and male. The other 400 are something else. Two hundred of the 1,000 smoke cigarettes. The other 800 do not. What risk factor is most strongly associated with spontaneous pneumo? (Answer: Not being a smoker! ... because out of 1,000 people, the most common trait is NOT smoking [800 members].) +4  
impostersyndromel1000  this is WILD! thanks guy +3  
belleng  beautiful! also, i think about odds ratio vs. relative risk...odds ratio is retrospective of case-control studies to find risk factor or exposure that correlates with grater ratio of disease. relative risk is an estimation of incidence in the future when looking at different cohort studies. +  
drdoom  @impostersyndrome I love me some probability and statistics. Glad my rant was useful :P +  
hyperfukus  @drdoom i hate it which is why your rant was extremely useful lol i learned a ton thanks dr.doom! +1  
dubywow  I caught he was thin. The only reason I didn't pick Gender and body habitus is because he was not overly tall (5'10"). I talked myself out of it because I thought the body habitus was too "normal" because he was not both thin AND tall. Got to keep telling myself to not think too hard on these. Thanks for the explanation. +1  
taediggity  It isn't just that this person has Ehlers Danlos and they're more prone to spontaneous pneumo??? +1  


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aiNccrot use rfo tcuaely lpiuafn oisndoinct si btho srbanoelae dna atiot.nprm reS-trhmot esu yaitmmidle(e isrscluop)ga-t sdoe ont eald to enmgortl- edepcnndee (or os loepep avhe tguhoh.t…) nAd ,yse gudrs sdtcaid ohldus aslo evceeir nitsarocc to olctrno pn.ia

drdoom  prefer “patients with hx of substance abuse” over more conveniently typed but less redemptive “drug addict” +11  
sugaplum  I don't see why switching her to oral pain meds when she is ready would be incorrect. Clearly she is worried about being on the pain meds, I feel making a proclamation that she has a low risk of addiction would be profiling just because she doesn't have a history. The opioid epidemic also affects people who didn't have a previous history of drug abuse. Just a thought, not trying to push any buttons. Maybe I am thinking to hard about this, but I don't see the clear A vs B line for this question. +44  
nbme4unme  @sugaplum I thought the exact same thing as you and chose the acetaminophen answer accordingly. I maintain that I am correct, my score be damned! +6  
sushizuka  I had a similar question on UW and the explanation stated that the correct answer choice was the only one that addressed the patient's concern and answered her question. The rest were just alternative treatments, so they were incorrect. But I too answered with oral pain meds. +5  
angelaq11  couldn't agree more with you all. I chose acetaminophen because opioid abuse is NO joke. The crisis is still going strong because of answers like this... +1  
houseppary  I ruled out oral acetaminophen because they described in great detail the severity of her injuries, and indicated that she wasn't even fully conscious/aware when she asked this question about opioids. Rather than expose her to more pain, and possibly worsen her long-term pain prognosis, by switching to acetaminophen too early, in this case it makes sense to keep her comfortable because she's very seriously injured and not even fully lucid. It's kind to reassure her in this case. +2  
anastomoses  I appreciate all of the passion for the opioid crisis, and the wording of the answer is definitely not ideal. However, PAIN is also very real, and there is no way acetaminophen alone would cut it in a case like this, not "as soon as she can take medications orally." Maybe I'm lucky to have 6 months in clinicals before STEP or had a mom who just went through urgent spine surgery for breast cancer mets, but there is a time and place for opioids and this is clearly one of them. Thank you for coming to my ted talk. +3  
llamastep1  I agree with anastomoses, cmon guys have you ever had serious pain? oral acetaminophen is NOT enough for that type of pain. +2  
sora  I r/o oral acetaminophen b/c she's post-op for major GI surgeries so you might want to avoid PO meds for a while +  
melchior  As argument against the oral acetaminophen answer choice, it says "switch the patient to oral acetaminophen boldas soon as she can take the medication orallybold" This means you're just waiting for her swallowing inability from the facial fracture surgery to come back, which might not have much to do with her pain, and so it seems somewhat arbitrary. +  
drpee  Maybe logically/clinically A is true, but this seems like a "patient communication" question to me and I could NEVER imagine A being a good way to phrase this point IRL. +2  


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tiyCcs sirofbsi si an umaaoolst ecevrsise sdieeas iivvgolnn CFTR (chwhi encdoes eth CFTR p,oeirn)t hwihc eamsn oyu eend a bduloe tih to rsxsepe eth is.dseea fI eth ntigeec stte nloy kcpeid up o,en hnte it mtus eavh desims hte reoht.

drdoom  The reason something is an “autosomal recessive” disease is because the protein encoded by the gene (of which you have two alleles, remember) does something where as long as you make SOME protein, your body should be okay. That’s kind of vague, so take the case of Cystic Fibrosis: you don’t present with Cystic Fibrosis if you have at least one functional allele -- that’s because CFTR protein is a protein that (in the case of bronchiole tissue) moves Chloride ion from inside cells to the outside lumen, which brings with it H2O and keeps the bronchiole lumen nice and watery, and fluid and non-viscous and non-pluggy. So long as you make enough of this protein, you don’t “need” both alleles to be good; the good allele can “make up for” (make enough of the protein product) to compensate for the “broken allele.” So, once again, understanding the pathophys of a disease allows you to reason through and predict things like disease penetrance and expressivity. +3  


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fctiiycpeiS is who fetno oruy sett si tgihr abuot ppoeel wtutohi het sesdia:e

= TN / N(T + F)P
= 59 / 5+5(9)
= 5%9

drdoom  Put another way: Of all the people who are disease-free, how many (of those people) did you catch? In this case, there are 100 people who are disease-free; our test labeled 95 of those people as “disease-free”, but our test also called 5 of those people “positive”; so our test is good (sort of) but not that good. +1  
drdoom  Also note how specificity only answers questions about people WITHOUT THE DISEASE; it only “deals with” people who are disease-free. (Sensitivity is the opposite: it is a formula which only deals with people WITH THE DISEASE. I think understanding that is better than coming up with some crazy Snout-Spout-Spin mnemonic, which I never remember anyway.) +  


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eiitpycicSf is ohw eoftn yrou ttse is rgiht tuboa opepel uthitow hte s:ieadse

= TN / (NT + F)P
= 59 / 595+()
= 95%

drdoom  Put another way: Of all the people who are disease-free, how many (of those people) did you catch? In this case, there are 100 people who are disease-free; our test labeled 95 of those people as “disease-free”, but our test also called 5 of those people “positive”; so our test is good (sort of) but not that good. +1  
drdoom  Also note how specificity only answers questions about people WITHOUT THE DISEASE; it only “deals with” people who are disease-free. (Sensitivity is the opposite: it is a formula which only deals with people WITH THE DISEASE. I think understanding that is better than coming up with some crazy Snout-Spout-Spin mnemonic, which I never remember anyway.) +  


submitted by niboonsh(338),
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aCn nsomoee epxinal eth fneeedrcfi etwnebe .C (eeralse fo rdotse dyrihot mohnero mrfo a diyrtoh nagdl rndailfitte yb s)ylpcoyethm dna .D eaeRs(el fo tyrihdo meoronh mrof a oamtsympohlu tdriyoh .dalgn

drdoom  @niboonsh, ending a comment with a question mark will make it appear on the "comments seeking answers" lists +4  
nwinkelmann  A lymphomatous thyroid gland can either be due to primary thyroid lymphoma (which is almost always NHL, but is very rare) or due to Hashimoto's thyroid progression. Hashimoto's thyroiditis = lymphocytic infiltrate with germinal B cells and Hurthle cells, which upon continued stimulation, can lead to mutation/malignant transformation to B cell lymphoma. These, I believe, would still present with hypothyroidism, and thus would have low T4 and high TSH (opposite of this patient). +1  


submitted by drdre(21),
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ePga 506 AF 9201 ssidcbree shee.chaad

rlCuest

  • aUealinrlt
  • 15 mnsi ot 3 hurso
  • atiPbelrori aipn whit mnriailatoc and ehnarrorih
  • Tx: tarmatpuSni

Mi naegri

  • iaaUrllnte
  • 4 to 72 suorh
  • ualgsitnP ianp tihw ,naesau phia,ohotpbo boaphpn,iooh may heav aru"a"
  • NC ,V inemnseg or dlboo eesslv tarnioirti
  • x:T DAISS,N tnptiras, eornrymeiiadothdg

inTones

  • rilaeltBa
  • 4 ot 6 uhsor
  • klBdi-nae apin
  • x:T ,ssalaigenc ,ASSIDN nncheaiemaotp

drdre  yay formatting fail +  
drdoom  @drdre, next time try hitting enter twice ("start a new paragraph") before beginning a list. +  
temmy  cluster mostly seen in men +1  


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A cmealid nttused 'tusnlohd eb hte neo ignigv eonmeso a cnrace nagsiisdo. Tsih si a rlylae ivtnieess seisu and the tuslers sudlho be eingv yb eneomos with heirhg huytairot kiel a tsrindee ro gtneidnt.a tA eht asme te,mi you ntho'dlus ile to eth enitpat dna sya taht eth etlrsus ate'rn akbc ety fi yeht ra.e tBes tinhg ot od is dtceelf teh scontinoearv adn lofowl pu twih eht e.etris.nd

drdoom  It isn’t so much “someone with higher authority” as it is someone with a license! Without a license, an individual is not permitted legally to provide clinical interpretations, as that would constitute the (unlawful) practice of medicine! +20  


submitted by sattanki(69),
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neApltpary hreet si a ycelmtpoel reapates ispnal ocrd flerex rehew retdci ielnep lsaimitnuto asdel ot an en.ocitre shiT eflrex ynol dnese an aticnt rca in 2,-SS4 os sa glno as isth ieongr si tno jr,niedu na reeitnoc can lislt co.ucr reHovew, thiw teanrosintc at C8, ethn hte oechypgisnc etnoceir erlefx ocnnta cuc,or sa shti qsriuree dnecingesd irebfs from het ecxtro.

lsmarshall  Just saw a good summary of nerves/vessels involved saying, "pelvic parasympathetic fibers from S2-S4 can cause cavernous arteriole vasodilation via the cavernous nerve without of central stimulation." +7  
seagull  S2-3-4 keeps the penis off the floor +36  
drdoom  Modifying @seagull into iambic pentameter: “S2, S3, and Number 4 / keeps the big ole penis / off the floor” +1  
myoclonictonicbionic  I can assure you the validity of answer (speaking from experience) +2  
raddad  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4896089/ Under the "autonomic control" header +1  
llamastep1  I've always wondered how quadraplegics got it up. I guess their girls help em lol +  


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Cna bnadyyo nalxeip htis o?en I tup dpeeetra stest seueabc I amdssue na lye8r-3a-od nwaom is na nluausu hgcadorpemi rfo .ilypsish

m-ice  83 might seem an uncommon age, but we don't know for sure her sexual history. She only recently (8 months ago) started showing some signs of mild cognitive impairment. She has all these results implying that she has syphilis, so the most likely answer is that she has syphilis, so we should speak to her privately about her sexual history. The tests don't necessarily means she got syphilis very recently, it's possible she's had syphilis for a while and never got treated. +5  
mousie  I understand that she could possibly have syphilis but I also put repeat tests because I know there are a few things that can cause false positive VRDLs but if she also has a + RPR does this make a FP less likely? And also if she has mild cognitive impairment you still discuss with her not her daughter correct ...? +4  
m-ice  This definitely could be a false positive, but before we want to consider it to be a false positive, we should talk to the patient about it privately. Assuming that it's a false positive before asking the patient about it could delay treatment of her syphilis. There's a chance she didn't want to disclose her sexual history in front of her daughter or maybe she was embarrassed or didn't think it was important to mention. And you're absolutely right, she only has mild cognitive impairment, so we most definitely should talk to the patient alone without her daughter first. +4  
seagull  She has dementia. She doesn't have the capacity to determine her own care (23/20 MME). I feel the daughter should have the word on the care since Grandma likely doesn't have the capacity to understand her actions. +5  
sajaqua1  From what I remember, dementia is typically a combination of impaired memory *and* impaired thought processes. There is nothing to indicate that the patient has impaired thought processes, and the memory impairment is only mild. The patient can still reasonably said to be competent, and so her private information should be discussed with her alone. +12  
yotsubato  Elder care homes or elderly communities actually have a high rate of STDs. Turns out, when you put a bunch of divorced/widowed adults together in a community they have sex. +10  
yotsubato  Additionally, you should respect the privacy of a competent adult with "Mild memory" impairment. I know I could have mild memory impairment considering the crap I forget studying for step 1 +13  
drdoom  @seagull dementia ≠ absence of competence -- the two are separate concepts and have to be evaluated independently. see https://meshb.nlm.nih.gov/record/ui?ui=D003704 and https://meshb.nlm.nih.gov/record/ui?ui=D016743 +3  
wowo  also important to note, d) repeated tests is also incorrect as the microhemagglutination assay is a confirmatory treponemal test (along the same lines as FTA-ABS) https://www.uofmhealth.org/health-library/hw5839 +5  
sunshinesweetheart  also.... I think we can assume that "repeated tests" means repeat VRDL, not "additional tests to rule out false positives" +2  
imtiredofstudying  the entire point of this question is that when you see an STD in an unexpected demographic (children, elderly), THINK SEXUAL ABUSE +  


submitted by usmleuser007(377),
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ym silt of nlsidpe ytpe cslle nda ctoiidsonn:

  • .a -NF1
  • b. -2NF ~ aShnnamwoc nn(Aiot )A = eutCunsoa bmauiorfeonr ~ ghih yalrceltiul w(/ idnsiagapl ratnpets wthi pisengtnriers -nafrrlceeue sozne blon&;aselcapyVercd bsdoie
  • .c Liamyooem (suutre a&;pm ouagh)sspe
  • d. Mhsetiolomae ca(noyeirttk s)vtieipo
  • e. caaAlspitn hrdoiTy cnaecr aiischpb( pa&m; ngola ithw ngtia )lcsel
  • .f dalyMuelr Toihrdy cnerca n(ac saol hvea pnoyglloa ec)lls
  • g. rraPiym rdaciac grcaianmosoa tanmng(ali rlvusaac nsidepl leslc)
  • h. csetrmoOsoaa (enbo a)erncc eihpmop(rlco e)scll
  • .i ineMiaognm
  • .j ss'pKoai oSarcam 8VH()-H = iktl-Siel acauvslr specas whit umplp -enahddpisslep ratslmo clles
drdoom  @usmleuser007 to make lists display correctly, try using the plus sign (+) for each "bullet point"; that should work +1  
mcl  I love this and I love you +7  
usmleuser007  LOL thanks, had to ddo a lot of digging since "spindle cells" are commonly tested +3  
leaf_house  @uslmeuser007 "MAMML PONNK" is the best I can do with that +  


submitted by usmleuser007(377),
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1) syilAnas fo rviancae is a orduecpre seud ofr iomrgcanp amespl ensam to ees if rteeh is siufcenfit ceednvei to rnife tath het smnea of eth nncorpdsoirge patlunpooi itsuirbsotidn lsoa edi.frf

2) ehWre ttest- repacom lony wto bnroitduisi,ts ysnialas of ecairvan si albe to premoac my.na • thWa seod eth e-wnoya ptar n?ame tI is eon denenetpd rbvilaae slaa(yw iscuuoo)tnn adn eclytax eon ptdidneenen ivbleraa l(aasyw ae)catog.cril A lisegn edpeednnnit rielaabv acn heav mnay l.veles

drdoom  via @usmleuser007 https://www.slideshare.net/adsarwar/anova-and-ttest +  


submitted by yotsubato(979),
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rAent we TNO uedpsops to esu itarimuoprp in odl ?pepleo

amirmullick3  Who said not to use it in old people? Remember "I pray that tio can breathe soon" and tio is an old uncle in spanish but its also the other drug, tiotrropium. +2  
drdoom  discussion of anticholinergics & elderly also discussed at some length (but different context) here: https://www.nbmeanswers.com/exam/nbme22/1288 +  
guillo12  Ipratropium does not penetrate the blood-brain barrier, so I think this is why it can be given to old people. https://www.rxlist.com/duoneb-drug.htm#clinpharm +4  


submitted by drdoom(819),
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’ersHe eon ywa ot -aieoetrsfimns-eploc eerac“dsed ed-nhdoyobrng ”fmoiora:nt ’Im tno a ibg nfa fo shti neli fo rnaiegon,s btu ltniachlecy naliean sa a iesd pgour hsa meor dnh*serogy rfo ettaolipn goerndhy dgionnb htan glcieny:

:einlnaa CH—3
ely:ncgi H—

o,S h”“yailltnec,c iaennla wdulo emrtip rmoe bno-ddgyheonr ,onafirmot cihwh mtghi lwloa ouy to aeimtieln atth i.eccoh

athT ,adis it eemss tsoalm imbslspoie ot uerl uot titu(hwo yerv eachnlcit kdoweenlg or emos drdveiop epexnraeimtl t)ada ahtt the igthllys ralrge ilneana sedo tno iarmpi drngehyo odbignn teewneb ogcanlel lcuelseom avi esritc i)pastl(a .nicnfrereete In smriepl ,msetr csnie lnainea si lraegr, yuo odwlu thnki htta it tums moosweh ernietefr itwh hte dinn-godbgnorhye ahtt ouccrs twhi eth wtpeyil-d cglieyn.

---
ritS*yclt aipsgn,ke s’it ton the rnbume of gndsrohye but osla eht tnrhtesg fo eht dieolp htat isaaicttefl ygdnhore oinnb:dg a nhrgdoey bundo to a lystngor oeratigcevenlet celeluom eikl forlnieu ilwl ap”par“e eomr tipoesvi d,an ,uhts -ydoeodbhnrgn oemr losrtgny htiw a byrnea xnogey rmaocdep( ihwt a ydghroen ceodcnnte ot cnra,ob rof pea)xlem.

uFtehrr radegni:

  1. ilh/eountmldcuq//:hedgwp.uhhrilcb.ep.wstd//u.whmeptds
hungrybox  Appreciate the effort but this is far too long to be useful. +21  
drachenx  hungrybox is a freaking hater +  
drdoom  @drachenx haha, nah, coming back to this i realize i was probably over-geeking lol +  
blueberrymuffinbabey  isn't the hydrogen bonding dependent on the hydroxylated proline and lysine? so that wouldn't really be the issue here since those aren't the aas being altered? +  
drdoom  @blueberry According to Alberts’ MBoC (see Tangents at right), hydroxylysine and hydroxyproline contribute hydrogen bonds that form between the chains (“interchain”, as opposed to intra-chain; the chains, of course, are separate polypeptides; that is, separate collagen proteins; and interactions between separate chains [separate polypeptides] is what we call “quaternary structure”; see Tangent above). And in this case, as you point out, the stem describes a Gly->Ala substitution. That seems to mean two things: (1) the three separate collagen polypeptides will not “pack [as] tightly” to form the triple helix (=quaternary structure) we all know and love and (2) proline rings will fail to layer quite as snugly, compromising the helical conformation that defines an alpha chain (=secondary structure; the shapes that form within a single polypeptide). +  
tadki38097  also you can't H bond with carbon, it's not polar enough +  


submitted by seagull(1443),
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baeym eomoens can iaxenlp why sthi si acrlvuaas srsoenic and ont sisesp. tI etosn'd ntimeno ferev or enesacb fo .verfe Teh IMR sha a malls monuta of eidypysthon btu ot gte raauaclvs nocesisr emses do/d

someduck3  Pg 455 of F.A. mentions that alcoholism can be a cause of avascular necrosis. +5  
meningitis  I think the small dark area on the left head of femur and the darkened neck are the avascular sites. Neck: http://img.medscapestatic.com/pi/meds/ckb/15/19515tn.jpg Head: (obvious lesion on the RT femur, but similar discrete lesion on the left as seen on the practice NBME) http://radsource.us/wp-content/uploads/2005/11/1a.jpg +3  
yotsubato  He wouldnt be playing golf if he had septic arthritis. Avascular necrosis is a more chronic condition that has a slow onset. +3  


submitted by nosancuck(85),
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Dam nso itsh ill b gto oems IMEIDBCLATU Mmlusuloc all pu ni hre ezsbnis

drdoom  tru. +  
meningitis  Pg 164 FA 2019 +1  
dr.xx  likely not "lil b" as 2-4 times as many cases are found in whites than in persons of other races +7  
drdoom  lil b not a referent of race; cf. lil boo, lil baybay, lil bowow, &c. +  
dr.xx  I disagree. Google "lil b" for images. See what you may discover. +  


submitted by aesalmon(81),
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I fele mbdu orf ksnaig ubt nca eoesnmo naxipel sih?t fI sih rnspeat are of seclo ot alonmr IMB dan rae eccnnoder utoab sih ihetgw hwy dwuol they be lginwola ihs oiecarl oitpncsounm to ecexde sih ryeneg pertxuede?in ( AKA eitgntl hte kdi ate too mcuh dna nto xecsreie )ohugen

meningitis  That's a modern day mystery. +16  
drdoom  The prompt is only asking "what's the likely cause of obesity?" It's not that they're "allowing" him to eat more than exercise. (Few parents can monitor their kids that closely!) The prompt is only asking what's the most likely explanation for his 95th percentile weight and BMI (given that he otherwise appears normal); in the United States, the most likely explanation is eating way more than you expend. +1  
niboonsh  aka 'merica #firstworldproblems +4  
makinallkindzofgainz  If you are obese, it's because you have consumed calories in excess of your energy expenditure, end of story. (there are factors that affect your energy expenditure, but the simple statement is 100% true, unless you want to argue against the laws of thermodynamics). A is the only correct answer. +1  
tulsigabbard  This answer hit too close to home. +4  
castlblack  I think the reason they point out the average weight of the parents is because leptin disorders are inherited. It helps you eliminate that answer choice. +1  


submitted by mcl(586),
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sBuno dcvreaa armagid, kid ywh this wsa no .stt..irn.?...ep.e...

drdoom  bonus cadaver diagram via @mcl +  
yotsubato  nurses +4  
faus305  Cause it's cute unlike the monstrosities they always put on the NBMEs +  


submitted by beeip(123),
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niytiaIbl ot letvaee the ltaape setssggu dgmeaa fo eth svuag r.evne

.F NC( X)

atstillisafraud  I guess F is the vagus nerve. Thanks to NBME I am also training to become a mind reader. +31  
seagull  Thanks to the NBME I have crippling depression +38  
drdoom  bonus cadaver diagram via @mcl +2  


submitted by dr.xx(144),
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tsrctureuS iithwn hte otrue )aea(rltl awll fo eht tmermantocp rfmo spouerir to looOreotruo mii:crnf heeTcraoerv lnr ehtvepOirnmahcl nda rxllymiaa sahbnerc fo eth trmliigane ucurt retnvreesS gspanis guorhht the mndliie )almde(i asbul:wcd nleA arl rInneenevt atcodri yrreta encpdcmoaia by het nleatnrI crtdiao peuslx

niaiwehe.//wsi.idoe/oariu:tvpnnsiCps/t_krsukg



submitted by meningitis(512),
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lghohtAu is’t about VPP, sith ergeirchsna lhpeed me ndnersuadt bicsa hy,sp I eohp tish selph eenorvye ni oesm yaw.

:ywaakeaT guriDn VP,P uevnos nterru ,eeedrssca iacrdca outtup raece,edss dan reath rperesssu eseraced ni het rhgti dies fo the ahrte.

hyW soed PVP aedecser sunove erur?tn

  • crtocaihrtina rerusesp srcemssoep e,thar gnuscai olobd not to rutren

Csaues orf seedcaedr telf nlruaiverct tuputo uinrdg ita:oltiennv

  • fngSthii of cnirviaaenrltutr setpum to tfLe eud to ceidresna RV vlmoeu
  • caseredDe nuevos utrrne
  • nahsegC ni shreat ibytial to tctcorna due to sipeivto seurespr
  • klac of O2 to ehatr

Nlmrao meytoascronp amsemncihs rfo mginaininta CO dna BP nuidrg VP?P

  • crensdiea HR to metepaocsn orf redceedsa SV
  • deareincs RSV to iiatnnma BP

hOret cyloioPhisg ns:eeossrp

  • seardeecD errcebal sfnuipore sueepsrr ’(bosdy spensroe ot a alfl ni CPP is ot eairs essyctmi odblo userspre adn dliaet abreclre odbol ee)vsssl
  • eresceadD leran pisefourn ecn(sedrIa H,AD ,RAAS adn etaPint has eraln pseorlmb os ersdeinac eniitenrac and icru c)dia
  • ePlbssio uiairmlontnt sdrac(iene scleuog aiv nlsionugegecoes tce).
meningitis  sorry about the formatting, they were supposed to be bullets not italic. +26  
drdoom  looks good to me! ;) instead of asterisks try using the plus sign for unordered lists; the system gets confused sometimes because the asterisk is also for italics 😊 +1  
meningitis  Yeah, I noticed :s Oh, I didnt know the + sign did that! Very much appreciated, I will try that next time. +1  


submitted by meningitis(512),
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Tennra atsges srtta at TEN sraey dol

gaSte : I

  • I is atfl, sa in laft scteh;
  • I is aloe,n as ni no elausx ahris.

tegaS II :2)( agste II statrs ta 11 /yo I(I okol leik 1 )1

  • 2 slabl sue(clattir )nretnlmegea
  • 2 shira (ibcup srhai onw agp)nreiap
  • 2 etbasr sudb fomr

Sgeta III :()3 astrts ta 13 yo/

  • If uyo etatro ,3 it oskol klie llsma stesabr setrBa( sodmnu fmo)r;
  • fI uoy ggsqileu hte III ethy olko kiel cruoyeas+lcr picub rhai
  • seracneId eipns enlhtg nad izse anc be eeesndrrpet yb: II --g&t; III
    yo(ur iespn swa hnti II ubt nwo sti hcierkt )III

agtSe VI ():4 rsttas ta 14 y/o

  • tFirs nage:iim eTh I ni IV eeesnrsrtp the h,htgi nad hte V ni IV olosk eikl eth mson psubi bteenew ruoy g:sel
    ME: ANGNI oyu evah iarh ni snom spiub ()V utb ouy eahv a rdober dgineatni eth hria mrof roingwg iont s.gthhi
  • The V is itpon,y sa in onw the astbsre rea iypotn (ersdai oeaalr or oudnm no ondmu)

Sgeta V (:)5 15 o/y

  • V ash on rsredbo eintganid iarh mfro gniwogr niot hsigth ubcp(i airh + thigh )ahri
  • 5 saegfirn(s in dnhsa) taentglfin het saoarle ewhn bigargnb meth r(eaoal nttefla ta hsit gteas nda on remo nou"md no )u"mnod

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +17  
gh889  According to FA2019, stage 2 ends at 11, stage 3 starts 11.5-13, and stage 4 starts at 13-15, where did you get your info from? +  
meningitis  You can change it to ENDS at 11, ENDS at 13, ENDS at 14... I simply have it as a range just like you stated in a couple of them. The importance is in how the kid presents because he/she will have some things mature but others not, the age will vary in questions. +  
endochondral1  stage 3 breast mound is for females not males btw +2  
endochondral1  see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females +  
angelaq11  this is just too funny, I LOVE it! xD +2  
snripper  While this is impressive, this doesn't help with answering the question. +1  
yng  Pseudogynecomastia (False gynecomastia): this has nothing to do with puberty or hormones. Simple d/t the fast some guys have extra fat in chest area, making it look like they have breasts. The boy weight at 60 percentile while height at 50 percentile. +  


submitted by sajaqua1(524),
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leMa tpnaert osleenrngbd/.iadnsca oapciale si dsuace yb het fesftce of etrnesdeohdisorttoy H)DT( on het kins fo het s.capl Teortsesetno si tencoevrd yb eht zmyeen ahalsrdeap-cet-u5 toni .HDT iFiedtrnsiase a e-dartec-s5au tbrihn,oii dna so bsckol hte rdiuntoopc of THD adn acn halt or vene usace esom rseearvl fo emak paerntt dssna.leb eeowvrH ihst maes vtiaitcy yam lsao urtesl in gtnfnciias aseulx eisd etscfef cniingudl ctyeao,gnasim rceeilet ud,nfitonsyc aatylrujcoe fs,inutdncoy nda cddseeear oi.bldi

)A zloDa-na a akew ndegnaro hwti ricgotaneentsi efftce,s esud in teh ttanermet of mroietsoisden dan csrbioityfc ebtras ai.eesds C) t-ylesteehrtoMnetso nhettysci ,T it is dseu to ppelunmste in eeetostnsort i,edcieycfn or in het tnearmtte of eoms rbaset acsern.c )D raOoeo-xldnn na aaiobcln tidrose sued to aigern tiwehg. E) oao-olnzSlt noetrha obinalac toe,rdsi twih itnolatep udse rof adeiyrhret omn.aieeadg

sajaqua1  I am embarrassed by these typos. +1  
drdoom  lol +  


submitted by bubbles(67),
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'nutldWo rnonsicttcio fo arplhpriee lvssees oals irregtg lcihnspnca oirsoctvnco,saint wichh sutmleasi nelar aheisicm and sacesu ainsedcer SAAR it?acvtiy

drdoom  Constriction of peripheral (cutaneous) arterioles/capillaries in response to cold surroundings is an attempt to reduce heat loss & maintain internal body temp; it is not at all coupled with splanchnic vasoconstriction. In fact, the peripheral vasoconstriction is trying to “re-route” blood to more internal/visceral compartments; simultaneous splanchnic vasoconstriction would impede that very process! +49  
bubbles  Ah, okay! I got led off track because I had a bunch of super hard practice questions asking about hepatorenal syndrome and how the constriction of sphlancnic vessels might trigger renal ischemia. Do you know if there would ever be a time when sphlancnic vasoconstriction occur outside of hepatorenal syndrome? +  
drdoom  @bubbles i would think only in cases of catastrophic shock (when the body is doing everything it can to maintain central tension; pressure to vital organs like heart,kidneys); in those cases, i could see the body sacrificing visceral flow as an "option of last resort" +  


submitted by bubbles(67),
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Wntulo'd nioctorisnct fo rraelpipeh esselvs olas grgetri napcsnclih isr,nsvaicooctnto hihwc ltsusmiae erlan haiescim dna sceusa diernaesc ARSA iy?vticta

drdoom  Constriction of peripheral (cutaneous) arterioles/capillaries in response to cold surroundings is an attempt to reduce heat loss & maintain internal body temp; it is not at all coupled with splanchnic vasoconstriction. In fact, the peripheral vasoconstriction is trying to “re-route” blood to more internal/visceral compartments; simultaneous splanchnic vasoconstriction would impede that very process! +49  
bubbles  Ah, okay! I got led off track because I had a bunch of super hard practice questions asking about hepatorenal syndrome and how the constriction of sphlancnic vessels might trigger renal ischemia. Do you know if there would ever be a time when sphlancnic vasoconstriction occur outside of hepatorenal syndrome? +  
drdoom  @bubbles i would think only in cases of catastrophic shock (when the body is doing everything it can to maintain central tension; pressure to vital organs like heart,kidneys); in those cases, i could see the body sacrificing visceral flow as an "option of last resort" +  


submitted by drdoom(819),
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uoY aevh ot tinkh uoatb it htsi wya: teh nebastme rnebamme si eht ga”ociln“dfsf on hhwci ]totasvrree[i ihganel o.rccus oS, e,ys emst lelcs e(ytp II peunetocmsy) oluwd eb vnvldieo in ttha ghlanie psocers but ethy tlocn’du streoer teh oralnm chcereutirta o(n“ erao”atsi)blmni uwttiho the okees’tn‘l fo hte besetmna ebemmnar llintge thme eehrw to ,og in htwa coiednirt ot rowg, hicwh ywa si pu,“” et.c If eth mebtenas beemnrma is ,eysdoertd yuo nca iltsl etg aengil,h utb it to’wn be dnezogria naghlei -- till’ eb ozedigndarsi liea,nhg hihcw soed not paarep as mrlnao eustsi. ae(sgDrizinod hilngea is trtebe atnh no eniahl,g btu owttiuh a BM, hte rnrngieeaget llecs ’otdn evah any ie“noict”dr dna rtfroheee antc’ reroste hte onrlam e.trtruca)cieh

drdoom  by "restorative" i mean healing which restores the previous (and normal) tissue architecture. for that to happen, you need an intact basement membrane! +2  
nwinkelmann  Yes, this a great summary to the post by @bubbles and the article he posted! Another way to think of the question is not, what causes repair, but what causes irreversible injury/fibrosis. That article explained an experiment that showed TGF-beta was necessary to initiate fibrosis, but if BM was intact and TGF-beta was removed, the fibrosis didn't persist, i.e. intact BM is protective against TGF-beta. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/ +  


submitted by shaydawn88(8),
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I oulwd itkhn leuortison ilesvovn the tsme elcls pty(e II nseto)uepmyc. sI eht tnicat bmtasene neeabmrm the wasner cebueas it iitmls edasp?r

aesalmon  I would also like to know if anyone can answer this question - I saw it as a Sattar "one day, one week, one month" kind of question. Its probably very simple but I still don't get it +  
bubbles  I posted a new comment explaining: basement membrane integrity is the strongest determinant of full fx recovery following pulmonary insult :) +5  
drdoom  You have to think about it this way: the basement membrane is the “scaffolding” on which [restorative] healing occurs. So, yes, stem cells (type II pneumocytes) would be involved in that healing process but they couldn’t restore the *normal* architecture (“no abnormalities”) without the ‘skeleton’ of the basement membrane telling them where to go, in what direction to grow, which way is “up”, etc. If the basement membrane is destroyed, you can still get healing, but it won’t be organized healing -- it’ll be *disorganized* healing, which does not appear as normal tissue. (Disorganized healing is better than no healing, but without a BM, the regenerating cells don’t have any “direction” and therefore can’t restore the normal architecture.) +8  
nwinkelmann  Yes, this a great summary to the post by @bubbles and the article he posted! Another way to think of the question is not, what causes repair, but what causes irreversible injury/fibrosis. That article explained an experiment that showed TGF-beta was necessary to initiate fibrosis, but if BM was intact and TGF-beta was removed, the fibrosis didn't persist, i.e. intact BM is protective against TGF-beta. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/ +  


submitted by drdoom(819),
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Teh omer eganler :lrcippeni oeeltidhan tesdalaiov ni eth ersnecpe of gihh O;C2 uyo ttago teg rdi of ttah caid wsoe!hmo taCn’ tel it tcu,calmaeu sa oewlr pH htniiw a “”metrnncn-irimoeov setffca ccteeryi/cfeurntsiuf of eensymz, sntripo,e cet. hTe emro icaicd a acllo o,vmirnenetn hte eomr uyo texcep ybnrea tuucsrlveaa ot iateld a(s a esmna fo sngeacinri fwlo ,atre breheyt nergrfiy ffo cctuelmaau dic.a)

heT tsatloiheinoegss anc oxlpite htsi shaeicnm.m yB tayngpithrvleeni gl(oibnw fof ,)O2C eht nbria ucsalrvaeut sensse a low CO2 / dhr-kuo“nyy es,ta”t ihchw eurrqesi on saloin.davtoi In toreh sro,dw the elcuaruvtas sdeo ton ende to tuonneic teh PTnc-nmuogsiA tciacerp of syegznitnish triNci dOexi (ON.)

hello  But, the Q-stem states the anesthesiologist is HYPOventilating the patient. +4  
drdoom  decreasing respiratory rate = retention of CO2 = vasodilation of brain arteries = more filling of tubes = greater intra-cranial pressure +1  
drdoom  @hello shoot, you're right! i ended my explanation with the example of HYPERventilation when i should have done the opposite! (sorry!) ... edit: "By HYPOventilating (retaining CO2), the brain vasculature senses a high CO2 environment and vasodilates = increases intra-cranial filling and pressure!" +3  
dulxy071  @drdoom could you please elaborate on your point. +  


submitted by drdoom(819),
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hTe more garnlee plpnier:ic eonaehlidt aavtoelsid in the rnceepes of ghih ;OC2 ouy agott etg dir of taht dica wsho!ome ’Cnat tle it eclamc,auut sa lerwo Hp iitnwh a rmo”n“m-onitceenrvi fefacst utirct/eueficeyfcsnr fo eznmye,s e,prsotin t.ce hTe rmoe iaccid a calol e,mveotnrinn het reom uoy epxect nebrya svelacuatru ot telaid as( a nsame of rgceaninsi oflw raet, yrebteh geyfrirn off aucealcutm ai.)cd

The ogeiilsostsnaeht cna txpielo sith .meashcnmi By avripetynignethl (golniwb off )OC,2 teh aibrn clvataeuurs nsesse a owl CO2 / ryo“ky-duhn ”a,ttes hhicw reiuqers on nsdooaiailvt. In trheo r,swod eth uretcsualav deso nto eend ot innutoec eth TumPncsiogA-n cripacet of iygsshtnznei iritcN dxeiO (NO.)

hello  But, the Q-stem states the anesthesiologist is HYPOventilating the patient. +4  
drdoom  decreasing respiratory rate = retention of CO2 = vasodilation of brain arteries = more filling of tubes = greater intra-cranial pressure +1  
drdoom  @hello shoot, you're right! i ended my explanation with the example of HYPERventilation when i should have done the opposite! (sorry!) ... edit: "By HYPOventilating (retaining CO2), the brain vasculature senses a high CO2 environment and vasodilates = increases intra-cranial filling and pressure!" +3  
dulxy071  @drdoom could you please elaborate on your point. +  


submitted by johnthurtjr(139),
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eh'esr a oleogg

johnthurtjr  FTR I had no idea this was a thing, and was pretty disappointed in myself when the google search had it in big bold letters right in my face. +3  
drdoom  via @johnthurtjr link: "Testosterone and other androgens have an erythropoietic stimulating effect that can cause polycythemia, which manifests as an increase in hemoglobin, hematocrit, or red blood cell count." https://www.medscape.com/viewarticle/773465 +3  
meningitis  I guess that's another reason for steroids and doping up. +7  
drschmoctor  For once I feel like I've been led astray by Pathoma. My instinct was to go with hemoglobin, but I talked myself out of it after remembering Dr. Sattar saying that the reason why women have lower hemoglobin is due to menstruation. +2  
fexx  F U testosterone! and F U NBME 22 question +1  
schep  I only knew this because there are three (at least three, maybe more that I don't know) contraindications to giving testosterone replacement therapy: +OSA +prostate cancer +hematocrit >50% +2  
drdoom  ^ linkify @drdoom https://www.medscape.com/viewarticle/773465 +  


submitted by drdoom(819),
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rfAte teh fucf is e,dit teh ellsc dan sisute atsidl to het cffu lilw nioutcne ucnsgnoim APT (-Pg&A;TPtAD), ubt no sferh boldo iwll eb eveireddl to “lca”re hatw lliw eb an acacngltuimu uoanmt of APD nad horet tebo.alimste ADP (A)ionee=dsn is letifs a xrypo fo tniosmpuocn and deirsv iosldinoaatv fo iet!rrase univotolE( si t)mr!as Igscnranie /edoeAAiDnPns ni a l“clao nrnemto”evni si a lisang ot teh odyb htta a lto of pisnonumtco si riorucncg reeth; thsu, esierart and ritsloeaer latrluayn iadetl to sinceare dloob folw atesr and pw“see ”wyaa lmtoacbei py.ctdbruso

lispectedwumbologist  You're a good man. Thank you. +  
drdoom  So glad it helped! +1  
seagull  very well put, thank you +1  
eosinophil_council  Great! +  
aisel1787  gold. thank you! +  
pediculushumanus  beautiful explanation! +2  
rockodude  this explanation was on par with Dr. Sattar IMO +1  


submitted by drdoom(819),
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uYo ehav to nithk otuba shti usgin the noectcp of LOADNCIITNO AOYLTPIIBBR. ehortAn awy to aks hsti teyp fo qitnoeus si ilke s:hit I“ ohws uoy a teinpat htiw sseanptouno ptmohaexruno. ichhW orthe intgh is omts ekilly to eb rtue ouabt ttha ?psno”er rO uyo anc rhpesa ti htees s:way

  • evniG a DOTCIONNI (ntonsueaosp muopne,) wtha horte nfnigid is mots elylki ot be hte a?ces
  • ineGv a olpo fo eopple with uoepnnasost thonpmxur,aeo ahwt hrote thgni is tsmo ilylek to eb ruet uaobt th?me

In threo dsrow, fo lal ppeeol woh edn pu twhi uopenssotan pomeun, hte smot nmmcoo tohre itnhg ouabt thme si that yhte rea AELM p;a&m HI.TN

fI I aegv ouy a ckubet fo sspenutnooa nepomu ttinesap -- dna uyo eacdreh oyur dnha ni ehetr and leuldp eno uto -- wtah oaeirncs duwlo eb rmoe ommnoc: In uyro adnh yuo hvae a rmokes ro in uroy andh yuo aveh a tinh e?mla tIs’ the .eltrta

someduck3  Is this the best approach to all of the "strongest predisposing risk factor" type questions? +  
drdoom  There is a town of 1,000 men. Nine hundred of them work as lawyers. The other 100 are engineers. Tom is from this town. He rides his bike to work. In his free time, he likes solving math puzzles. He built his own computer. What is Tom's occupation most likely to be? Answer: Tom is most likely to be a lawyer! Don't let assumptions distract you from the overwhelming force of sheer probability! "Given that Tom is from this town, his most likely occupation (from the available data) = lawyer." +4  
drdoom  There is a town of 1,000 spontaneous pneumo patients. Six hundred are tall, thin and male. The other 400 are something else. Two hundred of the 1,000 smoke cigarettes. The other 800 do not. What risk factor is most strongly associated with spontaneous pneumo? (Answer: Not being a smoker! ... because out of 1,000 people, the most common trait is NOT smoking [800 members].) +4  
impostersyndromel1000  this is WILD! thanks guy +3  
belleng  beautiful! also, i think about odds ratio vs. relative risk...odds ratio is retrospective of case-control studies to find risk factor or exposure that correlates with grater ratio of disease. relative risk is an estimation of incidence in the future when looking at different cohort studies. +  
drdoom  @impostersyndrome I love me some probability and statistics. Glad my rant was useful :P +  
hyperfukus  @drdoom i hate it which is why your rant was extremely useful lol i learned a ton thanks dr.doom! +1  
dubywow  I caught he was thin. The only reason I didn't pick Gender and body habitus is because he was not overly tall (5'10"). I talked myself out of it because I thought the body habitus was too "normal" because he was not both thin AND tall. Got to keep telling myself to not think too hard on these. Thanks for the explanation. +1  
taediggity  It isn't just that this person has Ehlers Danlos and they're more prone to spontaneous pneumo??? +1  


submitted by drdoom(819),
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uoY heav ot ihtnk uobat siht gsnui teh tpeoncc of TNOLNDCAOII ROBAILYIT.BP eAontrh awy to sak iths yept fo qitoesnu is ekli st:ih I“ ohws ouy a pttniea ihwt oanptsuneos m.auperxontho cWihh eotrh ihtng is tmso ilylek to eb tuer obtua ttha o?”psren Or you acn phrsae it ethes y:was

  • enGvi a CTININODO (peonusasotn eumpon), athw treoh nginfid si mtso ilkely to be hte ?asec
  • veinG a olpo fo leoppe htiw naeospunsot thomonx,pruae twah oehrt tinhg is omst iklely ot eb urte outab h?tem

In otrhe wrosd, of lla olpeep woh den pu wthi notnsepuaso puoe,mn het mtos mmoonc hreot hignt butao htem si atht yteh rea MLAE &;pam HNT.I

If I eagv oyu a butkec of tspsnoenauo eopumn aeitptsn -- dna ouy chareed uyro dnah ni etrhe dna pulled noe tou -- whta eaosnicr uwlod eb orem oo:nmmc In oruy hdan ouy eahv a ksmeor ro in yoru danh you aevh a htni ?lema ’Its the etlrat.

someduck3  Is this the best approach to all of the "strongest predisposing risk factor" type questions? +  
drdoom  There is a town of 1,000 men. Nine hundred of them work as lawyers. The other 100 are engineers. Tom is from this town. He rides his bike to work. In his free time, he likes solving math puzzles. He built his own computer. What is Tom's occupation most likely to be? Answer: Tom is most likely to be a lawyer! Don't let assumptions distract you from the overwhelming force of sheer probability! "Given that Tom is from this town, his most likely occupation (from the available data) = lawyer." +4  
drdoom  There is a town of 1,000 spontaneous pneumo patients. Six hundred are tall, thin and male. The other 400 are something else. Two hundred of the 1,000 smoke cigarettes. The other 800 do not. What risk factor is most strongly associated with spontaneous pneumo? (Answer: Not being a smoker! ... because out of 1,000 people, the most common trait is NOT smoking [800 members].) +4  
impostersyndromel1000  this is WILD! thanks guy +3  
belleng  beautiful! also, i think about odds ratio vs. relative risk...odds ratio is retrospective of case-control studies to find risk factor or exposure that correlates with grater ratio of disease. relative risk is an estimation of incidence in the future when looking at different cohort studies. +  
drdoom  @impostersyndrome I love me some probability and statistics. Glad my rant was useful :P +  
hyperfukus  @drdoom i hate it which is why your rant was extremely useful lol i learned a ton thanks dr.doom! +1  
dubywow  I caught he was thin. The only reason I didn't pick Gender and body habitus is because he was not overly tall (5'10"). I talked myself out of it because I thought the body habitus was too "normal" because he was not both thin AND tall. Got to keep telling myself to not think too hard on these. Thanks for the explanation. +1  
taediggity  It isn't just that this person has Ehlers Danlos and they're more prone to spontaneous pneumo??? +1  


submitted by drdoom(819),
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Dt’on gefrot taht icenecidn is teh rumben fo wne aessc hichw gmreee ni an eacuffdent aontpupiol. Iiecndenc si nryitg ot teg ta hte teoinuqs g&;t- In“ a veing ,erya ohw namy ewn poeepl epvedlo ihts di”es?esa

nI trhoe rdow,s uyo ntncao cnotu olepep how dreaaly heva hte eaidses. Yuo aveh to deluecx oseht eplpeo mrof oruy cunaalotc.li Yuo atnw to wnk,o agmon lla the eoeppl otu reeht ohw OD ONT heva teh adssiee, ohw aymn iemst tsih ryae swa oeseonm elwny() nidoad?ges

Sadi lyrentfdefi lsl,it you dtno’ ntwa to et”olcu“nudb-o eloppe owh pedolveed eht saidsee erfobe ryou y.ustd sA na imes,iptodegoil htat wloud wsecr up oyru ssnee fo who nvitieecf ro riitambesslns a seaeids s.i uoY atwn ot nokw, f“rom mtei1 to emit2 owh ymna ewn esasc eerdm”g?e

questioneverything  You would count the total risk pool. Chlamydia is not a chronic disease so you would treat those 500 people and they would return to the risk pool. +1  
drdoom  But you would first have to determine that they CLEARED the infection. What if you gave them tx and then they come back and say, "doc i got the chlamydia" -- is this a new case or did the tx fail? You're assuming it cleared but maybe it didn't. That's why you want to EXCLUDE from the start anyone who might already have disease of interest. +7  


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Wyh wolud ti tno be eamani fo icrhnoc eiassde hiwt derescead semru ennrriafstr oncaor?eintcnt

lispectedwumbologist  Nevermind I'm stupid as fuck I see my mistake +1  
drdoom  be kind to yourself, doc! (it's a long road we're on!) +20  
step1forthewin  Hi, can someone explain the blood smear? isn't it supposed to show hypersegmented neutrophils if it was B12 deficiency? +1  
loftybirdman  I think the blood smear is showing a lone lymphocyte, which should be the same size as a normal RBC. You can see the RBCs in this smear are bigger than that ->macrocytic ->B12 deficiency +22  
seagull  maybe i'm new to the game. but isn't the answer folate deficiency and not B12? Also, i though it was anemia of chronic disease as well. +  
vshummy  Lispectedwumbologist, please explain your mistake? Lol because that seems like a respectible answer to me... +9  
gonyyong  It's a B12 deficiency Ileum is where B12 is reabsorbed, folate is jejunum The blood smear is showing enlarged RBCs Methionine synthase does this conversion, using cofactor B12 +  
uslme123  Anemia of chronic disease is a microcytic anemia -- I believe this is why they put a lymphocyte on the side -- so we could see that it was a macrocytic anemia. +2  
yotsubato  Thanks NBME, that really helped me.... +1  
keshvi  the question was relatively easy, but the picture was so misguiding i felt! i thought it looked like microcytic RBCs. I guess the key is, that they clearly mentioned distal ileum. and that is THE site for B12 absorption. +6  
sahusema  I didn't even register that was a lymphocyte. I thought I was seeing target cells so I was confused AF +  
drschmoctor  Leave it to NBME to find the palest macrocytes on the planet. +4  
zevvyt  so i guess size is more important than color cause those are hypochromatic as fuck +  


submitted by keycompany(301),
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intreogN aclbnea is a ramenmsuete of erptnoi btelaimoms in het .bydo A aetgeivn ogientnr abalenc seainicdt mecusl loss, sa nrsdeicae aunomst fo onami dcsia ear negib etimebloazd to depcuor erne.gy Tihs criesasen teh tuanmo fo gonertin ecsretde form teh yob.d eusaecB het unmtao fo netongir uyo rea tgiakn in si sles tnah eth muonta fo ngortine uyo are ecirgntes, ouy eahv a etvnagie otignner abeancl.

hiTs nam is eushod,irnaml mdsueate,o ci,chtcea and ash iboy.mnaiaepulmh Tehes liniaccl nisifndg oipnt to tinproe oniunttmairl k(aKworahsi a)issDee, whhci sacesu mdaee eud to dsraeedec sremu ooctcin esu.rreps owL incooct spresrue in sthi case is edu ot entpoir os,sl and eechn a atienvge tnionegr cnebal.a

drdoom  Nice! +18  
dubywow  I knew your last sentence and suspected Kwashiorkor. It's just everything else I did not know. I have not heard or thought of muscle/protein changes in terms of "nitrogen balance" before... and that's why I got this wrong. Nice explanation! +3  
macrohphage95  I agree with you in first part but i dont think it has any relation to kwashirkor. It is simply due to cachexia which causes muscle destruction through the proteasome pathway .. +3  
zevvyt  also, it says that his albumin is low. +  


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vhyewrEere I unfod epU(ToDat and rlevsae reasp)p dsia eht ignomks si eth bgteisg iksr rcoaft rof anoptessuno reotouamn,pxh ithw boyd subthai and gedner nbgei a elsres sik.r mA I jsut emoplcyetl namdtgnsudsreini het esoqi?ntu

imresident2020  Yes smoking is a risk factor but not the best option among the choices given. Check FA, it says that it occurs more in tall thin young males. Smoking isn’t even mentioned. Tall & thin males are more at risk because they have more negative intrapleural pressure. Check Uworld for this. +  
drdoom  You have to think about this using the concept of CONDITIONAL PROBABILITY. Another way to ask this type of question is like this: “I show you a patient with spontaneous pneumothorax. Which other thing is most likely to be true about this patient?” Said a different way: Given a CONDITION [spontaneous pneumo], what other finding is most likely to be the case? Still other words: Given a pool of people with spontaneous pneumothorax, what other thing is most likely to be true about them? In other words, of all people who end up with spontaneous pneumo, the most common other thing about them is that they are MALE & THIN. If I gave you a bucket of spontaneous pneumo patients -- and you reached your hand in there and pulled one out -- what scenario would be more common: In your hand you have a smoker or in your hand you have a thin male? The latter. +  
cocoxaurus  Rupture of pulmonary blebs are a common cause of spontaneous pneumothorax in young adult males that are tall and thin. I know it's also associated with smoking, but gender and body habitus seemed like the more likely answer here since the patient is a young male. +1  


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urO litlte ifrned has a viarPvrsuo fioi,ecntn whhci icfnset roihrdtey ,cspusorrre asngciu epriiotutnrn fo otyehtceryr opcuitno.rd iTsh is the msea ayw it csaeus rsphdoy saetlfi ni unbnor eiasbb adn ipataslc anmaei ni liscek l,cel .cet

gainsgutsglory  I get Parvo has tropism for RBC precursors, but wouldn’t it take 120 days to manifest? +  
keycompany  RBCs don’t just spill out of the bone marrow every 4 months on the dot. Erythropoesis is a constant process. If you get a parvo virus on “Day 1” then the RBCs that were synthesized 120 days before “Day 1” will need to be replaced. They can’t be because of parvovirus. This leads to symptomatic anemia within 5 days because the RBCs that were synthesized 125-120 days before the infection are not being replaced. +23  
drdoom  @gainsgutsglory @keycompany It seems unlikely that “1 week” of illness can explain such a large drop in Hb. It seems more likely that parvo begins to destroy erythroid precursors LONG BEFORE it manifests clinically as “red cheeks, rash, fever,” etc. Might be overkill to do the math, but back-of-the-envelope: 7 days of 120 day lifespan -> represents ~6 percent of RBC mass. Seems unlikely that failure to replenish 6 percent of total RBC mass would result in the Hb drop observed. +  
yotsubato  He can drop from 11 to 10 hgb easily +3  
ls3076  Apologies if this is completely left-field, but I didn't think this was Parvovirus. Parvo would affect face. Notably, patient has fever and THEN rash, which is more indicative of Roseola. Thoughts?? +4  
hyperfukus  @is2076 check my comment to @hello I thought the same thing for a sec too :) +  
hyperfukus  also i think you guys are thinking of hb in adults in this q it says hb is 10g/dL(N=11-15) so it's not relatively insanely low +  
angelaq11  @Is3076 I completely agree with @hyperfukus and I think that thinking of Roseola isn't crazy, but remember that usually with Roseola you get from 3-5 days of high fever, THEN fever is completely gone accompanied by a rash. This question says that the patient has a history of 4 days of rash and 7 days of fever, but never mentioned that the fever subsided before the appearance of the rash. And Roseola is not supposed to present with anemia. +3  
suckitnbme  @Is3076 another point is that malar rash refers to the butterfly rash on the cheeks that is commonly seen in lupus, so the face is NOT spared. +  
mdmikek89  Honestly y'all lmao First line...RED CHEEKS AND RASH Malar Erythema --- Hello? Rash - Eventually it may extend to the arms, trunk, thighs and buttocks, where the rash has a pink, lacy, slightly raised appearance Hemoglobin is 1 g/dL below normal. This is Parvo B19 -- SLAPPED CHEEK. I swear man, y'all make this easy nonsence. WAY to hard. +1  


submitted by joker4eva76(25),
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hTe ntoqseui etsm si dengbirsci a iohinoltmacrd es,iadse cwhhi ocommlny psetren thiw altcci aico.isds herTe si na ecnreais ni oreiabanc sofmr of genrey dipotocurn siylgol(ys).c hTe aoitcirdohmn are uatlf,y os thye t’can sue teh nde pocurtd fo lcygsoliys trpv(yuae) ni .TAC dstnIea yuatrvpe is ushtend eorv and is dsue by DLH (atlcaet oshner)dgedeay ot erngetea pu.yravte

sA:die ceRlla taht HDL ssue NAHD and gnteeasre DA.+N cfyneicDei of LHD cna aled ot osls of ateegeionrnr of D+NA nad tihbisni sl.lyicgyso

drdoom  ... pyruvate is shunted over and is used by LDH (lactate dehydrogenase) to generate lactate*. +3  
chris07  It's hinted in the answer, but I would like to clarify: max O2 consumption is decreased because O2 is consumed in the Electron Transport Chain, which occurs in the mitochondria. With the mitochondria not working, the ETC cannot work, and thus there is less demand for Oxygen. +17  
masonkingcobra  Mitochondria are the powerhouse of the cell +51  
uslme123  Apparently ragged red fibers are the result of coarse subsarcolemmal or intermyofibrillar mitochondrial accumulations.. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/mitochondrial-myopathy +2  
mnemonicsfordayz  As @chris07 said, less O2 is being consumed in the ETC... but I also was thinking that the diaphragm is a muscle and if the mitochondria in her diaphragm are also not functioning, then she's not breathing properly and less O2 is being inhaled and therefore decreasing her oxygen consumption. Is that totally off base or am I just grasping at straws here? +  


submitted by medstruggle(12),
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Why si oeandlud uemnl ocre?nitrc I gthouht rcpceiaatn emeyzsn htnyys(roic,pm poyraiba)secxtped ulodw eb taodlec .eerh

colonelred_  Enterokinase actives trypsinogen and is located closer to the intestinal mucosal (“brush border”). +1  
drdoom  Yeah, @colonelred is right. @medstruggle: the duodenal lumen (and the pancreatic /proteases/ you mention) is the site where pancreatic enzymes (“endopeptidases”) cleave large polypeptides into smaller bits. It is at the BRUSH BORDER where the smallest kinds of peptides (dipeptides, tripeptides) are broken down into their amino acids, which finally can be co-transported with Na+ into the intestinal cell. I think about it this way: stomach acid denatures and “opens up” proteins (without any specific cleavage); pancreatic enzymes then cleave denatured polypeptides into smaller bits; brush border enzymes finally break down tiny peptides into absorbable amino acids. +3  
drdoom  Nice schematic, @welpdedelp +  


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-iH I 'tdon ehav na lnnipotaexa rof htis ubt I am lsoa ruuosci as ot hyw hist swa hte enasw.r

drdoom  via @hyoscyamine: FA pg.372. Squamous cell carcinoma occurs in the upper 2/3 of esophagus whereas adenocarcinoma occurs in the distal 1/3. Since this was in the mid esophagus, its squamous cell carcinoma. Key feature of squamous cell carcinoma is keratin pearls. +17  
hyperfukus  idk why my dumbass didn't put foci of keratinization and pearls together lmao +1  


submitted by nosancuck(85),
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Dma ons ihts lil b tgo eosm UDCLEBTAIMI oclsmuuMl lla pu in ehr szsbien

drdoom  tru. +  
meningitis  Pg 164 FA 2019 +1  
dr.xx  likely not "lil b" as 2-4 times as many cases are found in whites than in persons of other races +7  
drdoom  lil b not a referent of race; cf. lil boo, lil baybay, lil bowow, &c. +  
dr.xx  I disagree. Google "lil b" for images. See what you may discover. +  


submitted by aladar50(40),
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heT otitrmnap nitgh orf smto fo eth etschi oeqntssiu rae to look rof eth srnwae where uoy era bengi het sti/nocsetm sioelnfropas ihlew trpiescneg hte nis’petat tuo,aonym ,fnceiebecen nnlemeacen,ofic- t.ce toMs of hte oihcesc ehre were eeihrt artysoccua ro cbsiallya nbieg mnea ot teh .tnepiat hTe crrotce hiceco si to hple het ttpaine but slao emoaivtt etmh to iuncneto lchpsyia yeparht dan to lyon use eth pmreit as ilttel sa serya.snce A siialmr oqtesuin (cihwh I hknit wsa no MNEB 32 -- yeth era indk of igednbnl th)oetreg aws eth neo ehwer hte anetitp adh ttse sstrlue tath tidaicdne eh hda necarc tbu eth sneertid asid not to rlylt)nau(voi tell mhi tunil the oosnoticlg mcea in tarel ahtt y,ad adn eht pnettai ekdsa uoy aoubt eth lresstu. uoY ont’d watn ot eht ile ot eht paitnet dna sya uyo otdn’ knwo or atth eh eonsdt’ ehav rane,cc ubt uyo sola o’tdn antw ot be nbistnaorueid ot eth rn’dsteise aelb)onr(sae rq.eeuts

drdoom  @aladar Your response is good but it’s actually mistaken: You *never* lie to patients. Period. In medicine, it’s our inclination not to be insubordinate to a “superior” (even if the request sounds reasonable -- “let’s not inform the patient until the oncologist comes”) but *your* relationship with *your* patient takes precedence over your relationship with a colleague or a supervisor. So, when a patient asks you a question directly, (1) you must not lie and (2) for the purposes of Step 1, you mustn’t avoid providing an answer to the question (either by deferring to someone else or by “pulling a politician” [providing a response which does not address the original question]). +2  
drdoom  As an addendum, legally speaking, you have a contractual relationship with your patient, *not with another employee of the hospital* or even another “well-respected” colleague. This is why, from a legal as well as moral standpoint, your relationship with someone for whom you provide medical care takes precedence over “collegial relationships” (i.e., relationships with colleagues, other providers, or employers). +  
imnotarobotbut  @drdoom, it's not about lying to the patient but it would be wrong for an inexperienced medical student to give the patient their cancer diagnosis, or for a doctor to give a cancer diagnosis if they feel that the patient should be seen by oncology. In fact, the correct answer that the question that was referred to by aladar50 says that you do NOT give the patient their cancer diagnosis even if they asked you directly about it. +1  
charcot_bouchard  Dont give it to him. DOnt lie to him that yyou dont know. Tell him let me get the resident rn so we can discuss together Best of both world +4  


submitted by aladar50(40),
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heT mnpitorta hgnti orf stom fo the etihsc untosesiq aer ot okol rof het nrswea eerhw uoy ear gibne het cnsettoim/s erplasoisfon ehwil egenscrtpi teh it’psnaet omy,uatno eeeecf,cibnn onelenaecfn-ic,m etc. Msot fo eth soccehi hree rewe iehrte aocucsyrat or bllaacysi negbi enma to het teni.pat hTe ectocrr ichoec is ot pleh hte intpaet utb sola etmatovi htem ot noectnui slphyaci thyapre nad to lyno sue teh trpiem sa elittl as nyce.srsea A simlari qeusnoti cwi(hh I inthk wsa no NEMB 32 -- htey rea dikn fo nnbeldgi hot)erget swa hte eon wreeh eth etpitna dha ttse ltreuss ttah diciedtan eh had caencr btu hte erntsdei isad otn to ayur)lvlot(ni tlel imh itlnu eht consotolgi emca in teral atth da,y dna het teianpt dseka ouy obtau the rsl.esut You o’tnd ntaw ot hte lie ot eht eptiant nda yas ouy tdo’n nwko ro atth he tdo’esn vhea narec,c ubt yuo osal t’nod twna to eb rtsainiuenbdo to teh ntseerdsi’ abran)seel(o tsq.reue

drdoom  @aladar Your response is good but it’s actually mistaken: You *never* lie to patients. Period. In medicine, it’s our inclination not to be insubordinate to a “superior” (even if the request sounds reasonable -- “let’s not inform the patient until the oncologist comes”) but *your* relationship with *your* patient takes precedence over your relationship with a colleague or a supervisor. So, when a patient asks you a question directly, (1) you must not lie and (2) for the purposes of Step 1, you mustn’t avoid providing an answer to the question (either by deferring to someone else or by “pulling a politician” [providing a response which does not address the original question]). +2  
drdoom  As an addendum, legally speaking, you have a contractual relationship with your patient, *not with another employee of the hospital* or even another “well-respected” colleague. This is why, from a legal as well as moral standpoint, your relationship with someone for whom you provide medical care takes precedence over “collegial relationships” (i.e., relationships with colleagues, other providers, or employers). +  
imnotarobotbut  @drdoom, it's not about lying to the patient but it would be wrong for an inexperienced medical student to give the patient their cancer diagnosis, or for a doctor to give a cancer diagnosis if they feel that the patient should be seen by oncology. In fact, the correct answer that the question that was referred to by aladar50 says that you do NOT give the patient their cancer diagnosis even if they asked you directly about it. +1  
charcot_bouchard  Dont give it to him. DOnt lie to him that yyou dont know. Tell him let me get the resident rn so we can discuss together Best of both world +4  


submitted by pmnbp(2),
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uldco nomoese alspee anilpex hwy eieosnand is rerto?cc

drdoom  After the cuff is tied, the cells and tissue distal to the cuff will continue consuming ATP (ATP->ADP), but no fresh blood will be delivered to “clear” what will be an accumulating amount of ADP and other metabolites. ADP (=Adenosine) is itself a proxy of consumption and drives vasodilation of arteries! (Evolution is smart!) Increasing ADP/Adenosine in a “local environment” is a signal to the body that a lot of consumption is occurring there; thus, arteries and arterioles naturally dilate to increase blood flow rates and “sweep away” metabolic byproducts. +1  


submitted by medstruggle(12),
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Wyh is oaelndud lemun rnroc?icet I htohtug eaatircpnc eeyzmsn (omycpshntr,iy aiy)arxoptcsedebp odwul be odcalte .eher

colonelred_  Enterokinase actives trypsinogen and is located closer to the intestinal mucosal (“brush border”). +1  
drdoom  Yeah, @colonelred is right. @medstruggle: the duodenal lumen (and the pancreatic /proteases/ you mention) is the site where pancreatic enzymes (“endopeptidases”) cleave large polypeptides into smaller bits. It is at the BRUSH BORDER where the smallest kinds of peptides (dipeptides, tripeptides) are broken down into their amino acids, which finally can be co-transported with Na+ into the intestinal cell. I think about it this way: stomach acid denatures and “opens up” proteins (without any specific cleavage); pancreatic enzymes then cleave denatured polypeptides into smaller bits; brush border enzymes finally break down tiny peptides into absorbable amino acids. +3  
drdoom  Nice schematic, @welpdedelp +  


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uoY know ist’ na neodvpeel uvirs neics ti tsdoe’n olhd pu to icad or bigne ri.ded Yuo knwo it csaues a vrfee dan a hgouc, hielw gfecanfti eht any.rlx ylnO isvur atrcgoey hatt fits lal thta ifno si eth ncroivrsuao aesu(sc RSS)A fomr ttha i.stl

zelderonmorningstar  EBV doesn’t cause fever and cough? +1  
zelderonmorningstar  Wow, just checked First Aid and it doesn’t list “cough” as a symptom of EBV. +4  
drdoom  EBV is not a “respiratory virus”; it’s a *B cell virus*. Even though you might associate it with the “upper respiratory tract” (=kissing disease), it doesn’t cause respiratory inflammation since that’s not its trope. B cells are its trope! That’s why EBV is implicated in Burkitt Lymphoma, hairy leukoplakia and other blood cancers. (EBV is also known as “lymphocryptovirus” -- it was originally discovered “hiding” in *lymphocytes* of monkeys.) So, EBV = think B cells. +27  
fulminant_life  EBV does cause pharyngeal and laryngeal inflammation along with fever, malaise, and cough and LAD. The only thing that pointed me away from mono and towards coronavirus was the patients age. +7  
nbmehelp  Can someone explain what not holding up to acid or being dried has to do with being enveloped? +  
yb_26  @nbmehelp, the envelope consists of phospholipids and glycoproteins => heat, acid, detergents, drying - all of that can dissolve the lipid bilayer membranes => viruses will loss their infectivity (because they need an envelope for two reasons - to protect them against host immune system, and to attach to host cells surface in order to infect them) +9  
lowyield  @yb_26 does that mean that non-enveloped viruses hold up better to acid/dryness? +2  
rina  yes enveloped viruses are easier to kill (see post from drsquarepants: https://www.nbmeanswers.com/exam/nbme23/1161). also i think the "when dried" might refer to the fact that coronavirus is spread by respiratory droplets (don't even need to read first aid can just read the news at this point!) +3  


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I bsyilvuoo ththguo ahtt the iamn ihtng orf yticacap si ot ntdursdean the yvtersie and insgopors fo rhe dlmciea incooindt UTB I gtthuoh itsh aws a itrck uqoesnit uasbeec htey sdaek i"f eth tlnmae iaoimxnanet nfignid woeds.h".. adn the esmt fdilae to tenonim yhitnang tuoba ehr nritotaeoni to elpca ro iet.m dmbu

drdoom  Stem actually states, “On questioning, the patient does not know the date [time], the name of the hospital [place], or the name of her nurse who had just introduced himself [person].” So, pt *is* actually disoriented to time and place (Choice A). That is definitely concerning -- as would be depressed mood (Choice E) and the other choices -- but “inability to understand severity and prognosis” is **the most concerning** since that is the very definition of capacity. Inability to understand = lack of capacity. +  
sahusema  So by the logic of the question, if someone understands the severity of their medical condition AND happens to also be disorientated to place and time. Go ahead and do sx on them, it's fine. +2