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Welcome to drdoom’s page.
Contributor score: 804
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" +35
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

 +81  (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

 +48  (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. +
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 +7
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. +

 +3  (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.


 +8  (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 cassdawg(930),

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) +1  


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(44),

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(248),
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I swa nerdu hte iprmsonise tath isht wsa an coirta s,soncitdie eud ot "reevse tcseh pi"an as lewl sa het aesfl nlume ni teh ot.ara nAd THN is het #1 kris atcrfo rfo iratco toediis.ncs omeoeSn errocct me if im' orn,gw but I nihkt hsti is rtioac snetcsodii tahrer thna riocat rymsneau.

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(1391),

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? +  


submitted by drdoom(804),
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tiyInibal ot naiaitmn an coiretne = recietel uyofiscnntd. So onw eth nqtoiesu si h?Wy""

Fu,aegti dicftiflyu sleipne,g fdyuitilcf rtncacogneint si tinrtasg to dnsou klei orseiendps. lucffiy"iDt ecgrti"nconatn mtgih eb ndeerrpttei as diemiarp xuiveecet ucontinf or eht ebggnsinni of edlavrtusalcae-r eandmeit mtdneie(a daretel ot llmas tub sreunumo errlaebc sincta),fr btu on Setp 1 eintdaem wlli eb atlbnat e(i.., o"stl his wya "oemh, n,wgin"rdea" e)t..c

ineDprseso si aulylcta mmocno etarf a ldetibiiagtn veent ikel reks,ot sa ouy thgim xp.ceet tiWh nessoredpi cmsoe a lsos fo uelsax isetenrt and ieadtteh—rs is eeedarcsd obdiil.

nOe nac eamk hte mrtenuag thta a ulavc"asr p"iatnet htgmi vhea omes eussis with hsi pes"p"i slr(eirreiosct,osa sipaimctpehatamrthyetayc/sp oytdfcin)uns n,da for hsit ,soerna orctnulan cntieroe suodhl be saeeecdrd; utb etno thta nhongit si ndeemonti tabuo oinsntln-gagd scvalrua ssieead o(n hx fo rnhpoeesy)tin.

As a l,urtes the sbet awrsen ecchoi ereh is C. (Lobiid esrdceeda utb otcaurnln toseenirc aomn)r.l The big teosuinq I eahv ,si owh the cehk esod stih gyu nkow 'hes hrad hewn hs'e !a!?epesl 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(578),
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sThi emaig is lues.uf oNte htat eth snita ueds kmsae mieyln eppaar akr.d

engtiVte is aipcylt rof arkPn'snios edsi.sae Area D is eth bittanuass a.ingr

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(323),

These are symptoms of acute benzo withdrawl

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


submitted by sugaplum(323),

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(157),
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I dnt'o onkw if iths wsa eht rihgt awy i tuhogth abuot ti tub i mereeebdmr etL..H. AhK.C gntish ahtt eacus ilatdovsonia in telealsk uslcme

C - ,2oC H - +,H -A ,odsienena L - catltea -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(0),

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(294),
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lwoF tRae = telyocVi x -ltcrnSaessCooi reAa

2 ^cm2 x 02 msc/ec x 06 se/inmc x 1 ,1/L000 m^c3 = 24. Lmin/

1000, 3m^c = 1 L

seagull  Well, I missed this one. I don't even feel bad. +53  
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(294),
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wloF eRta = ytcloeVi x otsasCecrSino-l Arae

2 2m^c x 02 /eccsm x 06 smni/ce x 1 000,L1/ mc3^ = 42. mn/Li

,1000 cm^3 = 1 L

seagull  Well, I missed this one. I don't even feel bad. +53  
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(294),
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owFl Raet = tcVlyoie x nstSicsr-aCleoo aAer

2 ^2cm x 02 m/cecs x 06 im/scne x 1 /0001L, ^mc3 = .42 L/inm

,0010 ^3mc = 1 L

seagull  Well, I missed this one. I don't even feel bad. +53  
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(294),
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wlFo tRea = leyVctio x ssaoSCrel-cniot Aear

2 2c^m x 02 ccmse/ x 60 msnice/ x 1 001,/L0 mc^3 = .42 imL/n

100,0 3^mc = 1 L

seagull  Well, I missed this one. I don't even feel bad. +53  
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(294),
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wlFo Reta = eoytilcV x aicestoS-Csrlno eraA

2 m^2c x 02 ec/smc x 60 nic/ems x 1 1,00L0/ ^mc3 = 24. nLim/

,0001 ^3cm = 1 L

seagull  Well, I missed this one. I don't even feel bad. +53  
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(294),
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Flwo teRa = lcyiteoV x oo-lsenicstrSCa areA

2 m2c^ x 02 ce/cms x 60 c/msine x 1 0/00,L1 ^m3c = .42 nmLi/

0001, ^3cm = 1 L

seagull  Well, I missed this one. I don't even feel bad. +53  
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(138),
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e'sehr a goloeg

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(20),

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

drdoom  amen +  


submitted by cbreland(59),

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(59),

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(15),

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(38),

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(15),

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(158),

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. +  


submitted by azibird(158),

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. +  


submitted by vshummy(152),
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I itnhk emro le,rlegyna rointep onglfid phnpesa at eth ERR dna het emts asys eht etronip ontsed’ dfol .prerlpoy l,cfliySeacip eht msto mconmo FC umoantti si a lmsieoddf eiportn dna the nteorip is einedrta ni het RRE and ton tetrodnpras ot teh llec nerambem - AF 9012 gp 0.6

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. +2  
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(804),
unscramble the site ⋅ remove ads ⋅ become a member ($39/month)

The CRTF rniepto si a smraematrbnne iptr.eon Leki all ,rnpseiot ist tasnolnrita bensig ni het yooclst; htat ,isad RCFT asiotcnn na umtNries-n ngalis“ ,cn”eueseq ihhcw eanms as ti si bigne dtntaasl,re it n(da eht rbiesmoo mginak i)t! will be pnedarrsott ot eht dcEaplsonmi l^.tRicmeuu!tnooeoft

As it setg ltntedaa,rs sit odhcoprybhi ofmits wlli m,eeerg hihcw bsemed het TCFR prtoien nwihit the dshpoihpoilp yliabre fo het ER esflt!i tahT saemn het irepnto lwil enrev aniga be foudn ni“ the lytsoo”c eaubesc ti stge erdhtade rouhthg het ielbray cihw(h i,s in cfa,t woh lal raaeemrmbnsnt ontsirpe eemocb raemembnstnra tioersnp ta hte elcl sfcuare -- thye hvae to be meda tion emeanrmtnasbr sptoerni ni eht RE .)ts!rfi

So, s,ey melil,taytu shtee iesdlfomd esrtionp illw eb ecrddeti odwtra a ootaeprmes ofr dgn/drocai,ereiaygctln btu hatt liwl hppaen sa a elitlt scievel ro( ls“pmoi”eo); hte eldsofdmi ,pentiro in tish ca,se si nto etsalure-lbwo ec,nsi( by niefditni,o ti sah dyborhiohpc fimtos wchih etg dheart“de tughr”oh a yraibel ot ecreta eht mnseamatnebrr )ae,rtnpt whihc maesn yuo ow’tn nfdi ti ni het ts.lcoyo


\ f!toenoot \ The inhthgci of iv*eact rmbssoioe to teh apdicsmoEln tlRiuucme si hyw we lcla atth aear of RE ru“hgo dEcinmoaspl Rcteumuil RE;(r”) no onectlre ymprscoc,io htat tsnoeci was cskbdeleep with etiltl o;sdt rla,et ew hsn(ma)u oideverscd atth ethes dsot rwee moirbsos!e

\ * \ yB vti“cae o”siosebr,m I stuj eamn obermisos in eth sosecpr of nnivocetgr NRAm to pinte!or (tWah we lcal tasnori”t“lan ;)

orF a rgtea teltil rmasmyu of eth Epmodcaslni umRuetilc (dan mayn rteoh topccens in eloarumcl !),obiyogl ees shti rfmo lrbtsAe’ luleoarcM oBliyog fo eth eCll:
B/hilcwnw20v#sn26m:o1.tbh4.8A2/.npNtK/sbow/gk/i.4o

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(30),

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(300),
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oloC and epla eeetsirtixm lrues tuo isdtiuivrteb scusae eei(ognnru,c nyxihpaasal, s)ptci.e

lHyicmoeopv wlodu beredcsi a psecors of vumeol loss dln(iebge or ardnihdt)eoy and ldouw nto epanlxi the ccrlskae ro jluaurg vine ds.toeinnsi

dt'no be otwrhn off yb the lamorn htear su.nsod

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. +2  
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(300),
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oCol nda leap xeeiritmets uerls tou idtvreubtiis seacsu oc,uen(rneig spyixan,hlaa )ie.tspc

pcvoioeyHlm wodlu eciredsb a rssceop of umeovl olss ibelgn(de or ddnyo)aietrh and ulowd nto nxpleia eht klccears or ualurjg nvie .inosistdne

dtno' be trowhn fof yb teh nlraom treha usosnd.

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. +2  
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(47),
  • 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(300),
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hWy nt'is ihst a oorcth y?tdsu

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(804),
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eSmt aatlulcy ,tesats n“O nt,egqiusnio eth atteipn edso tno wkno the tdea []emti, hte aenm of teh hlotpisa ][elcpa, ro hte maen fo hre enrus woh adh tusj otndrdceui hfseilm pes[onr]”. ,So pt is ddiiotnrese to ietm and pecla eCiho(c ;)A htat si tielfienyd cirngnenoc -- sa udlow be eedsrpsed odmo Ccoe(ih E) nda eht horte oicechs -- tbu “iitibyaln to srundenatd yieverts nda gsorsin”op si eht mots neingoncrc ceins tath is the evyr etniinfiod of taccay.pi tylnbiiIa ot unretdsdan = ackl of itapcc.ay

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(209),

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 +  


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(930),

"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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Why is it otn aravnio ofeclill cllse? I thghout het eefaml noalag of Setilro nad geiydL si gl/tehsaaranocu sc.ell

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(317),
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Tshi nma hsa puussl osardpxu,a a igns in wihch oblod sruesrep ecdsseaer alcirylsdta urnidg sp.itirionna Pususl daruxsapo is a saclcsi ngis fo cdreiairlpa atopm.neda

Wenh fuldi tnoe(f olobd) has oploed rdnuoa eht herat, eth rehta sergsgutl ot eapdxn nad lilf htiw blodo. iThs cobsmee a grgeib relmbpo ofr het tghir rieevtnlc igrndu onriisitap,n seaecbu hte hitgr sdie fo hte earht eevceirs eensrciad unsveo rrnteu ndrugi p.irionainst Bsuceae heter is lifdu gepnvietrn eht higtr vnceetirl fomr panxeingd tard,uow eth ynlo terho plcae ti can pexadn to odmctmeaaoc is yb pnsghui on eht mup,set nshgikrin het esiz fo teh eftl .rniletevc shiT saesuc aededesrc BP wehn het flte cvtnlreie atrotccsn ugnrid that crciaad .eylcc

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(87),

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(804),
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Teh luodndae leunm dn(a ranccpatie sstaperoe ikle RYINTYSMCHO)P si hte ites ehwre naicatcerp yenmsez (ta“”de)iesdppnseo leaevc learg poptsdeeplyi noti rlalmse tbis ie,s)rpepp=dsitdteiiedp(.t tI si ta teh URBSH DRBOER reehw teh semalstl knsdi of spetdipe tpid)sptped,rspeiite(edi rea nebork dwon tion ihtre oimna ,siacd ichhw yfllnai can be orednracotsp-t twhi +aN tion eht ntintealsi el.lc

I kthin utabo ti shti :ayw

  • stcmaho diac sudnraete adn psen“o ”up rpseotni iwtt(uoh spcifcie l);eceavga
  • nticreacap ysenezm then elacev neutrdeda ylteepopsdip toni aersmll bt;si
  • rbuhs odrber smeeynz iflanly bkrae wdno ntities ptsdeepi toni eoblarbasb aiomn sda.ci
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(158),

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(963),

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(963),

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(963),

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(963),

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(963),

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(963),

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(158),

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(158),

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(158),

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(209),
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ephl whit isth one e....pasel is shti esebacu eh sah TrpGyhe DAN toeeollCshr DAN niomlc.h.corsy lony LL fcnidiycee lulaxdwpnioe lal of thsee sfdi?inng I eochs LLD R neiefcidyc cbsauee I ugess I hhuotg ti oldwu esuca lla fo hmte to resnacie utb si hsit eypt fo iyeicedcnf lyon isdtsoaeac iwth gihh LLD?

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(963),
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lWle htats a aylerl rudce way ot nescer rof ep.is.ders.on

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 +  


submitted by yotsubato(963),
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lWel sthat a aelrly rduec way to ceersn rfo .oesprn.si.de

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 +  


submitted by yotsubato(963),
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lleW ttahs a allrye druec yaw to ersnce orf i.pe..dnesors

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 +  


submitted by bbr(22),

"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(963),
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ellW httsa a eyllar ecurd ywa to ecrnse rof .r..ienospdse

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 +  


submitted by cassdawg(930),

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 +5  
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 eivebel iths is rfineerrg to gtdumi toraitmnaol. Deu ot mrpropei tniiigpsoon of bwleo no( eht hitgr )de.is sdadL asnbd nntccoe eht lrgea eneittsin to eth .ervil

aCn ldae :to

  1. sovVlulu

  2. ueoDndla subottocnri

3. ASM nclsOciuo -- 'Im sueignsg bdsae no eth wraesn ot hte niqsteou

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(77),
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nisruiglryps odog xelptaannio dan cuipret nudof on tsih .iest ehgmnsoit noalg hte ilsne fo tricionianmut flxree (kaa derblda is ulfl nda yuo spsi fr)exle si ogne os eth efnatref fserbi yncrigra het galsni ahtt the lbdeard is full rt'ane wionkgr. estho erifbs aer iecrard in eth ilvecp nverse

tsp:t//doiuwrmcerspdoocwpttibuiuooi/mxgilcc/nrw-ttr.r/t/yeops/ygo.e

yo  if still confused, a better explanation can be found here https://courses.washington.edu/conj/bess/urination/urination.html +17  
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(77),
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usiyirlpgnrs odgo pelnanoaitx dan icptrue doufn no sith sti.e minhoetsg lgano het lenis fo iiartcimnnotu eflrex ak(a bdraled is llfu nda uyo spsi refxe)l is ngoe so teh tffnerae sribfe gircynar eht lgnias ttah teh dalebrd is lflu e'nart rw.oigkn sohet rbesif aer riecard ni eth pvlcei reevns

/t:tsp/otbiwnde/i/ugimr/wtor/cwpttouroi/ei-.ccglcepmysptxysdour.oor

yo  if still confused, a better explanation can be found here https://courses.washington.edu/conj/bess/urination/urination.html +17  
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(282),
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I fdnuo a upicrte nogwhsi hte nisrnimsasot by owt eghyrouzesto lhpaa slmiaheaast rtati ansia eli)iesd(t-con tnarpe,s and dmiefdio it to laos ohws eth niitacehenr yb tow hgzsoetureoy aplah msletashaia icafarn aote(t-n)lidrsne pat.esnr ereH yuo go: 7odPIeed./Woo/uowwcggnh9:1/d2=venm1sO9tii?4rHvlhRtqQpE.TJJUVdpw8Tc

makinallkindzofgainz  broken link +1  
drdoom  broken link +  


submitted by andro(169),

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(15),

Tumbleweed

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


submitted by hungrybox(963),

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(0),
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rAnswe is cyestAtro. nittPae sha boiloalamtsg mor.iuftlme hgluothA iongnsmimae mya ccuor at vsionec,ietx mensnaogiim rae eingbn dan eftno acyts.mapmito hTye aym aceus ah/ es,zusrei utb wodlu eb uieyllkn to ecaus edhat w/in m6 fo esnot of a/.h The eizs of omrut nad ocruse fo nelslis si nistsetnoc tiwh het rcesou of BGM

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(138),
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I'm not a anf fo gssro hpta asmige adn seqsonuti ahtt ysa ,o"kol what si tish nth?ig" - taht asdi nmsgaonimie rea teh msot cmnoom rainb rtoum dan tish eritpuc si is a dogo mpeelxa fo e.on I hda no adie ahwt heset nshgit eklood ikel adn tog ti wn,rog too. aeTk a oklo ta iths oen

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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laOr esvliec ti(hn i.n)th iegsriltBn elsrivauc nsleoi no het nh.da oN erv,fe ton egnp-potxiariac. hsTi si seeprH uyo( yam ermembre iesttnsd tngtieg preiceht owhwlit ni uory de,sitsu hwcih is twha thsi )s.i osMt loksf etg 1VSH as hldinc,er hgtuoh vosolybiu nto lal aer tmoyatmisp.c VSH is a rlgae dtser-nboe,uldda anierl DAN vr.uis

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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rlOa elscvie nhit( .ntih) igBnitslre ersiluvac linoes on hte nh.da No rf,eev not paitnpecox.gai-r sihT si spreeH uyo( yam rreeembm nesdsitt iegtntg retipehc ohiwwtl ni your s,teuisd hchwi si htaw itsh is). tsoM flkso tge HVS1 as ,nelrchdi ohught bvsoyoliu not lal are att.micpmyso SHV is a alrge -o,tednualdbsder lneiar ADN .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 ... +  


submitted by mcl(578),
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cSien eruy'o lsoing lla uryo bcriba iton oury pee, uoy luowd tcexep teh Hp ot eb more iaal.nkle l,soA nesic htree is rsedadece +H+/aN tiptran,o eerth si lsse misduo deaebrrosb adn eetrofhre discearne slso fo eerf lifdu ot eht unrie.

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(300),
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aojGln ahd a cutreel htat nditmenoe htat I"f a tanitpe has ,hatlcerraoag eweriv yerve gudr t'yehre gaintk escni naym gsrud scaeu rghe"aar.tclao

hTe lyon nhtig fo lsiseopb lenceeavr ni shit -tQems is taht seh tksea a atmocidein, eferetrho het snrwae fo g"dru e"efcft si the most elyikl sonear orf ehr clhrreaaogt.a

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(963),

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(137),
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co.easRa An mrltiamoyfan ailacf insk eirdosrd errzehadcicat by ethoymtrasue apuelps nda etuuspl but no .eomdoecns ayM be odsaestcai htwi iaalcf gnsuhfil in psnreose ot ltxernea imusitl (,eg holoa,lc t.a)eh

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(804),
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hTe syseshnti fo ilyuartvl lla ospritne pdtNgtmAee)R&-;(ip rsccou in het tam.pcsoly1][ ’shTta weehr lla ssmoirbeo edsir,e freat lal. msosbiRo,e whcih era lmtsyo just rRAN /(32~ rANR + 13/ ,*enoptri yb ,ehgti)w rae adsbmlese ni teh slceunu tbu ynol od hrtie futsf neoc teyh tge to eht opsmlac.yt

Fro a potenri to veeal tsi onilriga ewmoohtn fo hte sytoclo adn bemoec a neetsrdi of the enusucl or, ,sayyyyyy the ilpamcnesod uimerltuc, it seden to ehva a ltteli itrgns of miaon cdsia cwihh htsou I“ eonlgb in the !sueulcn” ro I“ bolgen in het dncieapslmo elr”!ciuutm

tsiroenP itmyleluat ieesddtn rfo eth ER nnacoit an imtuannelyiaivg mnead gtrins fo oanmi isacd onnwk as sl“inga ceseu”n,qe h,hiwc rfo het esruospp of hte tSpe ,1 si ayalws ta eht sn-.Nretuim eTh snilga sequence lselt throe coolscity osrtpi,ne e!“yH Teak em dna( eht etrs fo teh tdpeiep of ichhw I am rt)pa to hte !E”R

In het aeesncb of isht l,ngasi a tnreipo lwil aenmri in its fat”ueld“ hmeo fo teh ooylc.st

qor&ssru;eeH a cnie cmahcseti sgohwni het owfl fo epsitron mfor inailit hstniysse to lfina :stitanidneos


Etsedonn

  1. eT“h sitsenysh fo trilvyalu all esrontpi in eth clel segnib on rsbmsooie ni the locos.t”y (Essaitlen Clle giBloyo, slAretb te al., 4012, p. )942

*If uoy yelarl wnat uory imdn wl,bno desricno ahtt neve the ptioern tbniuuss ttah amke up htta 1/3 of a rbmeoiso rea selestemhv yiilnatil eehdiyztsns in eht toco;yls terla, yhet aer sanopdterrt cabk iont teh cnuuels avi het clurnea pr.oe

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(0),

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(21),

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(1056),
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LV ppodste wokngi,r perruses dbckae up toni mulp c.ciutir lmPu ctiiucr uhrgoyl is meda fo 3 s""tapr - the aiapeicrls,l tsttairielin easc,p nda eht ovilale.

In dnieciocgar ,hkosc teh xater dloob ircsneesa alylacrpi dsotytachir preuessr, nvdirgi lufid into eth ttieisnriatl acpes. mCoredap ot teh aeivol,l het titlnrseaiit cpaes own sah mroe ldifu htu(s ermo rliiatisntet rottiychads eurrseps nad slse otncoic psusrere deu ot troia fo filud to ipn)otr,e adn as a strelu fo ihst ablnnugianc fo escorf, diufl eovms tnoi eth lavoeil g&-;-t aroyunpml ee.adm



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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hWy si ddalnuoe unelm ?orrncceit I hoghutt anirectapc eesmyzn pomth(iycs,nyr iyd)srpaoeabcetxp oduwl eb odlceta .hree

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(157),

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(1056),
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uHcrpyteea lnprasattn jcnotreie cosucr hinitw mtinseu dt/ xsrie-getnip niritcepe taidoesinb thta eactr to odonr itnange epyt( II isyehtnyristpiev e,catirno) ctatieav pnecelm.mot

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(42),

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),

I thought bulimia give rise to metabolic alkalosis ...can someone elaborate ?

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 dha teh asem uisnqoet igagnerdr st.hi I kown that elrtaxen mrodhehoisr arrley dbele dan intalern dmorirhsohe nrpsete as neapsils ideelbgn os in ym mndi I knew I aws ibeng deska obuta inalenrt .hrosmhediro Hrwevoe, ueripors ca-gre-;l&tt eoirifnr erstnemcei t;-vegin&- oaprlt nive, cna yoanen ltle me hwy eht nsrewa asw sirerpuo lectra nda tno iorenfri ertscmeei?n

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(1248),
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ueS:cro iktyhdnsiiar/pge/M:ewkelopni/..iw/it

n"yimle sesped the oaimnsitssrn of leaerctlci siepumls laledc cnoita entoasltip loang lmiaeydten nsaxo yb igntainuls eth xoan and ienrucdg olnaax nrbemema tneicacpcaa"

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 ghitm be het onyl enosrp on rheta woh got iths eon ,wrgno ubt rrsegsl:aed

T"TI ilsysnaa delinscu verye bejutsc owh si dmineoarzd oncicdrga to diamrzdone nattteerm mts.aegnsni It srieong ,nnpomcnloaeci oclporto etsvai,oind haalwtwrd,i and hygtanin ttah pehpasn ferta dmoion"znir.ata1][

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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rtncfsai dowlu eb a erom iherpleapr degew hpaes

basesc luodwtn eb invisvea ot the nuurdnigsro eraa i .nhkit

umssqoua clle si omre lctnarley eodtcal

a'wtsn 10%0 urse tub ttash eth steb arswen htulhosg tuidps to giev 0 sostympm adn ujst a c,tepuir hotnnig elki an aatluc aillicnc rnaieocs

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(157),
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I n'odt wonk if shit swa teh rhtig ayw i gthouth ubota it but i eederemmrb ..LAhH..e KCt ntshgi atht esauc nodliiaasotv in keelstal luesmc

C - o2C, H - ,+H -A anseonedi, L - ttecaal 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(157),
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I o'dnt nwko if sthi swa eht rthgi yaw i ohgutht btoau it ubt i mrmbeerdee ..Hht.ACL.eK gthisn hatt asuec navoodtalsii ni llteeska umcesl

C - ,oC2 H - +H, -A sdaoniee,n L - aatlcet -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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eH ash rehta auelifr hhciw eldas to a seredeca in narel odobl owlf dna perelnra atmaozei. In palenrre eat,aomzi rNBUC: irtoa is &;g=t 20; itovtacAni fo teh ASAR sysemt deu ot hte plraeenr zaeoitam mnsea thta teh spec avrg is hgih at 02.51 and he si lgodnhi noto musido os arniyur omiusd liwl be lwo 0(tl&;,2 ENFa .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 +7  
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 sha treha friulae wihhc daesl ot a edereasc ni anrle boldo wlof nda earrnple aeaizo.mt In plrearne em,aiotaz UBNC:r otari is gt&=; 20; tAoinictav of hte SAAR sysmte due to eth lreaenpr itzomaae sname hatt eth scep vgar si hghi at 0215. and he si nlgdohi ntoo umsdoi os rinyrua musdoi liwl eb wlo (0t2l&,; NEaF )t1;l%&.

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 +7  
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 atreh ruielaf hhiwc ledsa ot a sacdreee in arlne olodb lfow adn lepnerar .omeitzaa nI lrraepen aoi,mteaz rUBC:N atroi si t;g&= ;02 tiotcivAna of eth ASAR mtyses eud to hte pelarren ioaaezmt nemsa htta hte sepc rvga is high ta 102.5 dan he si igonlhd oton idumos so iynrrua omdsui iwll be olw 0lt;2,(& EaNF tl)&.1%;

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 +7  
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. +2  


submitted by drdoom(804),
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s’Here noe ayw ot cis-tfno-epsleariome drds“eacee ehyrbd-ongond inarmot”:fo mI’ otn a ibg nfa fo shti ieln fo gnasrnioe, tbu llantyhicec elanina sa a edis orugp ahs orem oeryg*shdn for otiptalen gyrdoehn dbignon ahtn ncgeliy:

aa:nelni —3CH
y:egincl H—

So, i”le“tcalhn,cy enialna uoldw miretp oemr nnebg-hdoodry rfoaim,not hihwc gtimh awlol you ot imealntie taht o.hiecc

tTha a,isd it smese lmatso ipomelsisb ot eulr uot thwotu(i eryv icechtlan wgoenkeld or semo dpvirdeo extrneimapel tada) hatt hte yslilgth gerral eilnaan sdoe otn aripim yodhrgen ndbiong etweenb alnocelg cuesemoll avi ritecs t(ialap)s ir.necenerfte In islrmep ,stmer sniec ilanane si e,ragrl uyo wdolu tkhni taht ti utms woemosh erfnteeri hwti het gogr-noeniydbdnh atht uscorc twih the pwle-idyt gycelin.

---
Sty*cirtl gans,peki ’tis not hte umbnre of odgyhrens but laos eht hetrngts fo eth dlpioe ttah iftslctaiae hedgynor odg:ibnn a gynhedor bonud to a stgryoln eolcetrngaeeitv oucleeml klie neirfolu liwl “aarep”p moer opetsvii adn, tu,sh hgrbonn-dyedo rome ylntsrog iwht a rbneya gexyno dmprec(ao htiw a dgehrnoy notccened ot ora,bcn rfo ma)p.elxe

hFurret enig:dar

  1. u.suuehwbimdlrcl/:hmheptlhqi/thutewoppdsd.gn/./dce.w/
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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odfun htsi in sin:orbb eht idralgcoio and soglhioict pntaert of rbfssiio si rerreedf ot as luuas naiistilertt opmaniuen, hichw is ierdqure rof eht adogsiisn fo .PFI

drdoom  pneumonitis* +  
drdoom  ^nevermind! +  


submitted by gabstep(14),
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dnouf ihst ni bs:irnob het ioirclgoad dan othcgsoiil tapnter fo rbiofiss is erredref ot sa ulasu tltiisrntaie omnneaipu, which si redqeiur fro teh gisnaiosd fo IFP.

drdoom  pneumonitis* +  
drdoom  ^nevermind! +  


submitted by mikay92(0),

Did anyone else find this question painfully poorly written? I spent so long just trying to figure out what the heck they were asking.

It's as if they don't want us to do well...

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),

Did anyone else find this question painfully poorly written? I spent so long just trying to figure out what the heck they were asking.

It's as if they don't want us to do well...

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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My uothgth ercsspo saw atth oumrt-taspp liendbge si ulsualy adelret ot eth ,utesru nad muhc of hte cpeilv ivsecar si ippeldsu by anhrbecs of eht irtalenn ciali re.ryta

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(152),
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I ihnkt more ,lyeeagnlr tinpeor loidgfn hpsnaep at hte ERR nad hte stem asys het iotrnep teno’sd dolf ro.leppyr fycaielcSlpi, hte sotm nmcoom FC antmiuto is a sedidmlof preoint dan eth nerotip is itdnaree ni the RRE adn tno partndsrote to hte clle bearmemn - AF 9210 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. +2  
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(152),
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I itnkh mreo lnlyga,eer oiptenr gfniold psaepnh at eth RER dna teh mest says eth etnroip endos’t lodf oy.rprelp Scyfll,iiaecp het sotm ocmnmo FC imtnuoat is a odsefmild neirpto nad hte roipten is trneidae ni hte RER adn ont odtasneprrt to eth elcl banmreem - FA 0129 pg 06.

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. +2  
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(152),
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I inthk reom la,neregyl reoptin ilgdnof seppahn at hte RRE and hte etms says hte reotnip edosn’t lfdo yelp.rpro Sfaic,icyellp hte mtso mconom FC autnimto is a mdsideolf ertoinp dna the ionpter si irandtee in eth RER dan otn ndsptroaret ot eht lcel mneamebr - AF 9021 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. +2  
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(152),
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I hktni remo le,rnlegay inetrpo oildfgn neasphp ta eth RRE dan eht mtse sysa het proenti s’tndeo fold rrpoylep. al,flcScpeiyi teh otms oncomm CF otmntaui is a dlmoseidf npoetri dna hte onrepit is ietdearn ni eht ERR nda otn rnsdrtotepa ot eht llce embrenam - AF 2109 gp 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. +2  
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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wyh tehre is tbiiboyrpla of afhtre eignb a arrcrei is 32/

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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413m1hrt0/p/fp.5p5/2lo//00wa:3sg0pfwt./.hataw

^a^^ laibefuut etbal thta wohss efcatfs no lltyeeertoc elesvl in itlaavxse sv cisretidu vs nm.vitigo

dicocgnAr ot the ebtl,a sit hard ot ellt deuitric sv xlevitaa abues yb usemr tyecslerlote le.ona ehT urein otetscllreey wdoul mykedrla eidffr ni htat rdueciti lilw eahv easridecn a//KClN nda axsvaielt udolw wollfo eth otpeipos dnetr (dereae)c.sd Hrw,eove wthi het aftc atth UBN si icegirsnna and ttha we anc lelt ethrs'e a mtoeliacb klssilaoa with eaproiyrsrt cidasois ptoioec,smann we can tbe on deiuctirs orev lvisxeaat.

TRXEA IFON rmfo het albet in teh ilkn aeb:ov

i:mgoiVnt [K ced] l[C dec] C3H[O ]inc p[H ]cni
a vaxtLi:se K[ c]de Cl[ nic ro d]ce HOC[3 cde ro i]cn pH[ ced or ni]c
ri Dcitsue: K[ edc] [Cl ecd] [3HCO ]nic [pH inc]

nI eiunr fro vini,mgot NaKC/l/ illw lla eb d ecdIensrea nirue ofr valateix ba,eus NKa/ wlil eb dcesedear. Cl is onamlr or Isracdne.e de rneui rfo duteiric :esuba a/NCl/K illw all eb aredicnse

w(erAnd agYn ofr rie)esPdnt

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


submitted by hello(300),
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h'asWt teh syhoeescm esupposd to eb a cleu u?obat eDos shit paeitnt evah I?DC Dose CID waylas euasc lcvheoyoipm c?kosh

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 the yaw i eoolkd at stih saw:

eoruy nto %001 srue hes aws eataktcd onr do uoy ntwa to eb hte nrosep nglltei eth nushabd ehs an caatktre os uoy :reeovm B C

ollnwagi imh in whit het aip,entt odg onwks twah ttha ugy ahs nddehi whti mih aslo uoy will amek a uhge eesnc : A

the ynlo tnhig ot do si eb pacimdilto as eoelpp onwk ythe ernat doellwa in eth eremnttat eraa dna yb atth uyo aesurs rhe ayefst.

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(142),
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hgt.ir he eltyaoulbs ustm ainrem in eth aginwti eaar so atth he is ta hdan ot ackatt ish fwie hneveewr hre exma .dsen og MNE!B

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 +1  
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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heT eqotisnu says tyeh dto'n npdsroes to acitsadn HNET sksa hchwi ouy to nfyieitd hcwih gdur is het tsom icfeevetf at ruespssgnip cida pit,onurdoc OTN ahwt eht omst ceifetefv aatcind i.s The aswner si .I'PsP

I lilw ysa, hrewv,eo I wsa nokloig orf tienghsmo keil ocetrde.toi

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(300),
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Wyh n'sit hsti a tohrco yudst?

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(300),
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yhW 'stni isth a ctoroh sd?tyu

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 ANNTOC WVIE HET REETNI TQNIUSO.E IS SHIT ORMNLA?

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(804),
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liautosnlCca for add. Teh tbyioabplir of het eahrtf geibn a ercirar si 2/3 isecn ti si nnokw atth eh te’dosn vhea het seaesi.d Thne hte btriapbioly fo ihm spnsiga ti no to ihs idk si /2,1 s:thu

  • lbtaobriiPy fo dda igenb icrarer = 23/
  • iolyrbabiPt of dad gsinsap on sdaeies eellal = 21/

Ctlcuiaolsan rfo mmo. tihW the eegrHWnb-ayird i,Pinpcrel ouy can ufiger tuo het tbbyoiairlp of eth oerhmt gienb a aic:rrer

q = 0/t(0sr040)1q, = 1/200

o,S pq2 = 2 * 0012/ * 990/102, wchhi is aoprxp 1100./

roF the hlicd to etg het llleea orfm om,m otw sgniht ened to :pepnha (1) mmo tums eb a erirarc ehrzoytt[]oee“”g and 2)( omm mstu pass the lleeal to :lhdic

  • iPoabyrblit of mmo bigen rriecra = 0011/
  • ioiybbrtalP fo omm napgiss on sesaide eealll = 12/

ngiPtu ti lla tgerhtoe. ,woN omceibn lal rh:tegeto

= otlbyira(pbi fo add nbige )rcreari * bpaiyibrl(to of add ssngapi on esesadi leeall) * y(boribpilta of omm gebin rcrarei) * tbilbyri(poa of mom aspgsin no eaiessd lllaee)

= /32 * 21/ * 011/0 * 1/2
= 1 ni 600

kernicterusthefrog  To quote Thorgy Thor, drag queen: "ew, Jesus, gross" +35  
niboonsh  This question makes me want to vomit +11  
drdoom  lol +  
5thgencephalosporin  okay wow +  


submitted by dr.xx(142),
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nI iiossdar,sco eamcacyhpleri olramlyn espsspurse teh rseeale fo PTH and eroerheft teh cnotroidup of lcolatirci ,(yiceocei5hhloloxc),y1dl-r2rdaf btu in ssrciosaodi dan oterh olugtsaoruamn idaee,sss cttaeaivd nrcoamnlueo sllce (aylpalctruir )mhapcergsao in eht lgun nad mhlyp soend crpoude atcriollci d(oaflyehcc2y15rl,delc)ii-xoorh mrfo allciidco -cc)ryel5chfyrxilaloe2(odho deneetpidnn of .THP

twpccuhmsraiyapto-cweed.mh/:nanesgesos-eoanmulotitwusair.ttecnapt/ld/s/-o

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(49),
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rtyetp ogod yrsmmua

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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yhw is hist ont a ocssr oeanstlic uysver? ... csnie ew rae iasgnk ta a pirulacrta temi

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(282),
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I tyallrlei sutj lzeeadir wyh shti unesotqi nsefcoud em so mhcu a(nd e'vI drtie to greuif it tuo a upolce fo ,iesmt ol).l I let eht loquoclali noifnieidt of liubima .ie(. ovm)ginti ikcst ni my n,mdi htat I oorftg teh tclaau daiclme ifnotnidie = nmaolr MIB )g&1t(8; + engib etgina nad ignugpr re(hwe grpguin loduc eb dcnieud imivontg or tideucri ues or lxaetvia use arndo/ xeciesves .iexsr)cee So rl,laye waht tish isutnoqe aws aginsk si slmiyp ahwt si eht elceottryel enblaac fo xesviseec ai?rerdha GZEE! I deam ti os cumh ardehr ni my eadh hewn grytin ot raewns ti .yoiinrlgal

raehriaD scasue onoinnn-a gap .ie(. yr)cecohilhpmer cobetmlai os.acdiis olotS tailonyemnprd ioantcsn CO3H- and +K, so xvsceseei dhrareia = eveescxsi osls of C-3OH adn K.+ lCoehidr elvles in hte esmru lilw eb searnceid ude to het lnmroa C3CO-l/H- ii,buimurlqe os sa gnavteei hrgace teipssadsi eud to loss fo C3-,HO lC- iwll cnreaeis ocerctgrni het i.p-naoagn

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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onusietQ ,sasy thta a utysd is deno ot asemreu uear ogenitnr ni emn aegd 5.6 taWh of teh iolnlfgow nswsare irpedvdo ash ARCUEAINTC nda PCEIERS ssmeurea

I od ereag tath rfo a hyghli percies utmsrnaeeme you deen a gbi orgup os yrou ntdrasad rrreo fo teh eamn si lwore i.(e gnsinrceia teh ytuds pwro).e

UTB

geA is aelylr iranopmtt eeh,r since lppeeo gdea 56 EAR SLYULUA EDUDCSELH ot eht srgtlooiu , eechn a CTRAANUNIE eemsaru udlwo be lpepeo otn ormf ergaaev gae 65 t-&;g nem ggnio ot a llcoa gpohpisn eenrtc. Tsih grpou sedo otn rlfceet eht rgveaae NUB tath uoy uwold nfid ni a 56 eyar lod alme pgor,u os het

NASWER IS: 500 MEN MORF A ISTL OF TSNPAIET GUNINGDORE A TEUORNI HELTAH IREEGNSNC AT A LOCAL SINPPHOG NCTEER -g;t& UITEANCNRA AND SPIECRE ;t&-g eosD otn tclrfee ltryu het UBN mena fo 65 arye ldo emsal tbu ti odes it rlsyipcee i(thw owl ntdraasd orrer fo a,nme slse tviendoia fo relss)ut

I pheo im thgri, if im otn peaels penalix me 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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soQenitu ,sysa taht a tuysd is eodn to esemrau uear etrnoign in emn aedg 65. hWta fo the wlifonlgo nswrase drvidpeo has CIAEANCRTU nad IECREPS rsauesem

I do rgeea htta rfo a hyhlig eecsrip auemeesnmtr oyu ndee a gib ruopg os royu dtsanadr rrroe fo eht enma si lorwe e(i. gancnrisie hte dytsu roewp).

UBT

eAg si yelrla taotmnpri ,reeh censi opplee deag 65 ERA LUYUALS DEECDULSH to eth outgslroi , neech a IAEUTRNANC aseemur loduw eb polepe ton mfor rgaveea age 56 &;t-g men gigon ot a aolcl phpnsoig cernte. hsTi porgu oesd ont eeltfcr eht eraaegv NUB ttah you wuodl fdin in a 65 raye dlo alem ugorp, os het

WNSERA :SI 500 ENM OFRM A TLSI FO INETSAPT GNEORNDIUG A IUROTNE TEHAHL SRNNCIEEG AT A ALOCL POGSHIPN ENTCER ;g&-t NANEUCTAIR ADN EPIESCR g-t;& Dsoe otn eceltrf lytur het UBN anem of 65 year dlo eslam btu it edso ti eyiscpelr iwh(t lwo rnddasta rorre of nma,e sesl ivitondea of ts)ulres

I hpoe im rht,gi fi im ont laseep nxeplai em .yhw (: !!

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(1391),
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Why unoso?sptaen sHe' neggangi in na icatve tposr wthi an cidneeras isrk of iTctrauam u.irnyj So we earlly jsut sseuam hes otn ijdrenu euseabc hte setm endots tieycdlr yas she' ndrue?ji sheeT essitoqun aled to too mnya u.sposanismt n(i my oipnin)o

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(804),
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You heva ot ithkn atuob this uigns het oectpnc of ODICONINATL .IYIBPORATLB Atnehor ayw ot ksa thsi etyp fo tiuosneq si leik :hist I“ wsho ouy a pteinat htwi enspntuosoa nrmpoax.houte ihWhc herot htgin is toms lkiley to eb tuer oatub ahtt ”spr?neo rO uoy nca ehspar it sthee :yaws

  • einGv a CNIOTONID (npusatonoes opneum), twah htroe inngdif is smot lkelyi to eb eth ?caes
  • enivG a olpo of oleppe iwht topossaenun ueono,mrpaxht htaw htore ihtng is tmos ilekly to be urte botau ?tehm

nI hrtoe rwdso, fo lla leepop woh dne pu ithw oaesutsnpno eunpmo, the osmt mmocon herot tnghi oautb etmh si taht ythe aer LAME a;p&m NTI.H

fI I gvea yuo a ukcteb fo sosneunpota monupe pniatste -- dna ouy acheerd oury hnad in etehr nda llpdeu noe otu -- thaw saiorecn lwdou eb emor o:ocmnm In oyur hdna uoy haev a rmkeso ro in royu hnad oyu vhea a thni ae?lm s’tI het ettrl.a

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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Ncacitro eus rfo aletyuc unaflip nosidticon si tohb noelasareb dna trpoai.tnm m-rtreoSth seu eiaemdmly(ti gs-t)ucipslaor odes otn elda to glmoe-nrt eddneepecn (ro so peleop vhae thtog.u)…h nAd s,ye rgdus tsddcia dhlosu soal ciereev rontacsci to otnlcro ipa.n

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. +43  
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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tsyicC sbfosrii is an slotmuoaa icsrevese esdseai vinigolvn FTRC wihhc( needsoc teh FRTC tnieo,rp) hwihc nesma oyu ende a oldbeu tih ot exrpses hte edssiae. fI hte eicegtn etts lyon dicpek pu eno, hten it umts evah imesds het te.ohr

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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fySictpiice si who otefn ruyo tets is ihgrt utoba opplee iowtuth teh easdies:

= NT / N(T + FP)
= 59 / )59(5+
= 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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fSceiipciyt is hwo fnote uryo sett si ghitr oautb eppole twuhoti the asiede:s

= NT / N(T + P)F
= 59 / 9(5)5+
= 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.) +  


submitted by niboonsh(336),
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anC esnoeom xainelp het ecfnrdfiee nbeweet C. laseree( fo rstdeo yohrdit enhoorm rofm a yhordit ldgan infeltirtda yb yemtoy)chlsp dan .D elseRea( fo tdyoirh hrmnooe fomr a uosplyahommt hrdiyto 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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eaPg 560 AF 9120 ecrsbdsie hedac.esha

truCels

  • rllaaitenU
  • 15 nmsi ot 3 sourh
  • troilPebira pnia ihtw ltiroiancma adn raohrenhri
  • Tx: aSrtpnimtau

eMngri ia

  • nlUiralate
  • 4 ot 27 ourhs
  • lPaintgus pani twhi naua,es hp,aohtiopbo iaooohhppbn, aym heva aar"u"
  • NC V, nnegemis or boodl sveles itinarrito
  • :xT ANS,SDI tn,parits oehrgdiietarnyodm

onseTni

  • eaiaBtllr
  • 4 to 6 hours
  • laeiknBd- ipan
  • :xT aiesnlc,ags SN,ISDA noptmnahiacee

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 deiamcl unesttd tu'nlshdo eb eth noe invigg nmeseoo a ncacer igia.sosdn Tsih si a ealryl vitsiseen ssuei dan eth selurst hdslou eb engvi by soeeomn tihw heghir utrhaiyot lkie a teendirs ro d.tanientg tA het maes i,met ouy snhodlu't lei to eht taientp nad ays taht teh surtels arnte' kcba tey if they .rea tesB tghin to od si cdteelf het rvncoenaoits nad ofwoll pu tiwh teh rin.tes.ed

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(68),
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prepnyAalt etreh is a leletcyopm asarpeet plansi orcd felrxe eewhr ierdct pinlee tuanitlmsoi sdeal ot an rneiocet. hsiT relexf lyon ndsee na tantci rac ni S2-S,4 so as goln sa isth oenrig is not dujneri, na nitrcoee anc tlsli rcuo.c v,eeHowr itwh oacrnettisn at ,C8 nthe teh geohycnspci ereincot eexflr nnocat cuoc,r as isth reeriusq ednnegdsci ifsrbe mrof eth .xrtoce

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 +35  
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 +  
llamastep1  I've always wondered how quadraplegics got it up. I guess their girls help em lol +  


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naC aybonyd pleniax shti n?eo I upt erdteepa setst eeaubsc I esduams an -yeo8adl-r3 mnawo is an uauunsl decmprgihoa for s.lpiihsy

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(370),
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ym ltsi of sdlpein pyet lcsle nda ic:soiondnt

  • .a -N1F
  • b. NF2- ~ nacShnwmao itnno(A A) = snuteuaoC aormrinfbeuo ~ gihh elyarclluti /w( niapsdlagi epsntrat iwht ispegtnnsrire arluef-enrce oznse cydepllsVnab;rcoae& disobe
  • c. oymoiLmae es(truu & sphg)eousa
  • d. maithoeolseM (ytircotneak vt)eoiips
  • e. sctipnalaA Tiydhor arnecc aiibhsp(c ;&pma agonl htwi ngtia lcels)
  • .f lMeluydra riyoThd eracnc (nac salo eahv llgpoyona )elscl
  • g. rPmyari daarcci ncaaoosgamir aamgnn(tli rcuavsal ndlpsei clels)
  • h. seorsatacOom ebn(o )crncea lom(perhpico )llecs
  • .i iMemnoiagn
  • j. Koiss'ap mSracao HH()8V- = ii-eSlklt arsauvlc cspsae itwh lpupm hiadlpepn-dses tsmolar sllce
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 +4  
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(370),
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)1 inaAysls fo ianrveca is a uedpreorc dsue orf rgpcnoami amleps mnesa ot ees fi eerht si fuisciftne cvedeein to rneif htta eht manse fo eht ecsodrgrpnnoi tnluappooi tdiursitoisbn asol .fdeifr

2) eherW tt-set pecmaro nylo wot rit,bonsiituds nisaylas fo cnraviea is ealb ot aoecrpm yn.ma • athW deso teh -ywenoa tpra ne?ma tI is noe eependdtn eblivaar sawyl(a cnutnosuoi) and xcyalte eno detpninnede eaabvrli sw(ylaa cialc)aoge.rt A slgine tnedpedeinn aberlavi nac ahve naym l.leesv

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


submitted by yotsubato(963),
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Arten ew TNO updespos to use mioaitrprpu ni odl lepep?o

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(804),
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rseH’e neo yaw ot plreostmafoienec-i-s e“asreddec oo-rbdngheynd roiamnt:o”f ’Im ont a gbi anf fo hsti lnie fo gnsnr,aoei but iycnacthell eananil as a dise gpuro sha omre rdy*egnohs rfo tptianleo orheygdn ndigbon tnha nlcyeig:

laina:en 3HC—
lye:nicg —H

,oS y“h,ntcl”eilca aanleni odulw rietpm mroe oergndhdboy-n ,oaironmft whihc hitmg olalw yuo ot iateleinm hatt c.oehci

athT ,siad it smees amolts piolssbmei ot uler tou ttow(iuh vyre ceitlhcna oklneedwg ro mose pdvdiroe rimapnleetex )data ahtt eth htyllisg ergrla liannae osde ton raimip dhonrgey ogbnind neetebw glonecla elucolsem aiv etcrsi ast(p)ail teefrri.enecn In eismrpl ,strem cnise aaelnni is rare,lg yuo uldow ikhtn ttah ti stum shoowme eetfirner ihwt the ynbegdhrn-nigood atth corsuc hwit eth e-dpliytw cniegyl.

---
ittSrlc*y ikg,spena sti’ ton eht mnubre of ngehoydsr btu losa eht getrhsnt of eht dolepi ahtt ieaitlasftc godhreny bnndg:oi a erygodnh udbno to a tnslrygo cetlerngoetaeiv lleeoumc ekli ouirnelf lwli ”pap“era mero voiiespt na,d tsh,u nynbrdeh-doog ermo ogtlrsny iwht a naebry nygxeo copaed(mr twih a ghdeyorn edneccont to ra,nobc orf emaex)p.l

Freuhrt :erngiad

  1. /mswdcpdhwew//l.utneqhrg.dlt.pidlbeuipoh:c.mutehh/u/s
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(1391),
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aebym ooesnme nac eialxnp yhw tsih si arasvualc rosseinc nda otn sses.pi tI 'enosdt etonimn eefrv or nbesaec of f.erev eTh RIM ahs a laslm ontaum fo deypisoyhnt btu ot egt lcavuraas scnesior esmse /dod

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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amD sno shit lli b got emos ABICLEMTIUD olmMulcus lla up ni rhe ebsnzsi

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 +6  
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 lfee bmud orf ngskai but nac seoonem pxlaein it?sh fI sih taenrsp rae fo esloc ot lonmar MBI and are roecnecdn autbo ihs wigeth wyh uolwd tyhe eb ngwoiall ihs eoliarc oiosptcnmnu to xdeece hsi neyreg dureenextip? ( AAK intglte teh ikd ate oto hucm nad not rceeesxi gne)hou

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(578),
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nBsuo ecvaard darmgia, idk why hist asw on ..e...tns...pr?i.t..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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Ityniilba to tveeela the paelta tuseggss agedam of eth uvasg nr.eev

F. CN( 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 +37  
drdoom  bonus cadaver diagram via @mcl +2  


submitted by dr.xx(142),
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retuucrsSt tiiwnh eth teruo el)(lraat alwl of hte nmtorptcema from ourisper to milrOi rcooe:onrtfou rareolerThce nv nvcelhmtprai Oeh nad almraiylx abehcrns fo the lnriitagem tvru tSrsreceeun spnagis trohuhg teh lnimied lm)id(ea bc wdAua:nllse ennlvIe trerna tcdrioa traeyr pdcmoaeanci by teh alnIetrn ctriado ulpxes

w/oteiurviiCnti.nunhka.asswsr/kpgeeop/dsi_/i:



submitted by meningitis(500),
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lgohhtAu ’sit utboa VP,P htsi egnsecrairh edhepl em nedsnadurt abcsi yphs, I ehop this hslep eeyrnvoe ni osem .ayw

wT:ekayaa uDnrig ,PVP vosune rnrtue sasercdee, rcaacid totuup ecd,erseas and trhae pusresrse sraedcee ni eht rtigh edsi of teh arhet.

yhW dose VPP eesardce eovnus etrr?nu

  • haatiotncircr esprseur essmoepsrc r,taeh iausncg loodb not ot rrutne

usCeas fro esarddeec eftl vlcniterrua upttou urgind anvni:etolti

  • tSighfni fo tnntrvelcrraiuia psetum to fetL eud ot dnaercsie RV oevuml
  • seeedcDar usvnoe tenurr
  • gasChen in arehts yblitia to onactcrt eud ot tsviipeo eprusres
  • kacl fo O2 ot etarh

olrmNa eoconmyrptsa hnscamiesm rfo agtianmnini CO nad BP ruidgn ?PVP

  • ncadsieer HR to senamptcoe orf ercadesed VS
  • srindceea SRV ot niiantam BP

hertO yooighPcsil :seresnops

  • Decasrdee ercrblae rfinpsoue rerspeus ’oy(bds posneesr ot a afll in PPC si to sarei stmeicsy dbloo espusrre dan datlei lbercrae ldobo )esvsles
  • arcsDeede aenrl orsfpniue ceIsa(redn HD,A R,SAA dna ntteaPi hsa arnel esborpml os nacdeeisr inecnairet nda criu adic)
  • osbsliPe nralotitmiun edcsnia(re leocsug via nioselsgeceugno t)c.e
meningitis  sorry about the formatting, they were supposed to be bullets not italic. +23  
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(500),
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Taenrn aetsgs rstat at TEN yrase ldo

tgSae I:

  • I is ftla, as in laft th;esc
  • I is ,aenol as in on alxuse aish.r

tSgea II ():2 eatgs II sattrs ta 11 /yo II( look klie )11

  • 2 lblas lttui(erasc rntene)emgal
  • 2 haris pb(iuc ashir onw eanig)rpap
  • 2 batser bdus omrf

agteS III 3:() tsstra at 13 /o y

  • If yuo traeot ,3 ti kloos ilek lsmla bstraes s(eaBtr domnus r)f;om
  • fI ouy iqegsglu eht III eyht loko kiel orc+aeulrcys cuibp hira
  • edInsecra npsei hltnge dan iezs can be peteseenrrd by: II &-g;t- III
    ru(oy isepn saw ihnt II btu own sti tkehirc II)I

teSga IV )(:4 atrsts ta 14 oy/

  • itFsr ianegmi: hTe I ni VI eepssnrtre eth hti,hg dan the V ni IV ooskl keli eth mson pisub eewetbn uyro ls:eg
    I MANEG:N you heav riah ni nmos bupis V() tbu oyu avhe a rbrode teaigndni het rahi mrfo owrngig iotn t.hihsg
  • Teh V is piyn,to as in own eth easbstr rae pniyto isde(ra elroaa ro mnuod no m)onud

teSag V (:)5 15 oy/

  • V ash no besdrro itnengida iahr mrfo nggrwoi into stighh (pbuic airh + ihthg )irah
  • 5 re(snaifgs ni ah)sdn ltninftage teh slaaoer wehn aigbrngb ehtm e(orlaa aenltft at siht gaest dan on rmoe dnuo"m no do")mnu

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +15  
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(518),
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aMle rnpatet dgisneosban/.nlcerda elioaacp si esdcau yb het ffesetc of shsneoyetdioeottrrd D)H(T on hte sikn of eth salpc. Tsteseotnreo is dntocreev yb teh eyzemn acrtle--ae5udpash tino .HDT iieritasdsFen a st5u-ec-eaard tioibnhi,r nda os ckobls hte ooicuptnrd fo THD nad anc talh ro vene scaeu meos reevlsar fo amke ntpetra ensadbs.l reowevH hsti msea tviiyact yma olas treslu in fcintnagsi sualex esdi eesftcf lnciiugnd tyagimnc,saoe cireltee dfintnuc,soy raajyutlcoe ncio,snydtfu nda aesdrdece dbi.ilo

)A noa-Dzal a wkae dngoeanr htwi ainntortecegsi efec,tsf eusd in het artnemtte fo enoiesmotirds nda ftricioycbs atsbre ia.deses C) otnMyse-etertethsol cinsteyht ,T it is sdeu to mseplueptn in ostreeetnost icenc,edify ro ni hte nttaermet of seom beastr rnccesa. )D o-lOenoraxnd an abioalcn eotisrd edsu to inaegr gwiteh. )E tnoSazlool- aohntre iolbanac dtirseo, twih aeilttnpo usde orf aetreydhir edaigm.naeo

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


submitted by bubbles(66),
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lont'Wdu ostrnoniccit of eeparprihl eesslsv olsa regirtg snnlcaphic aoinntic,oscsovtr hcwhi tliseuams nlrea haiecmsi and acessu rcensdeia ARAS i?ytitcav

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! +46  
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(66),
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'Wodtnlu nocctroitsni fo eihprlprae elsvses sloa trggrie nihlnsaccp itcsntc,sovinroao ihchw sisaumelt renla hiaseicm dna sscuea eerdinasc RASA citi?vtya

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! +46  
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(804),
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Yuo vhea to khtni batuo it tihs wya: hte enaembts bnermame is teh lda“cignfofs” on cwhih esi]ravt[erto gaenhil c.urcso ,oS esy, etms lcels tepy( II uncptyesom)e owlud be oenidvlv ni atth nagielh scoersp btu eyht d’noltcu teesorr the lonarm tcrcireaethu “no( l)airamibnot”se iuwthto eth t‘son’kele of eth etbmnsea anemrbme letlgin temh ehrew ot ,og in htwa nteidiorc to g,owr iwchh ayw is up,”“ te.c If hte nbtesaem enrmebma si eset,roydd yuo nca tlisl gte hngli,ae but it nwo’t eb neogazrid hngilae -- tll’i be iizgordenasd ngihe,la wcihh oeds ont prpeaa sa ormnla eusi.st roiizns(egadD egniahl si rbttee tnah on aienl,hg ubt ihtwuto a M,B teh reiegtnngear ecsll n’otd eahv nya ”ciodirten“ nad htefrreeo tc’an eeosrtr het lornma .rcettuhrcae)i

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 dowlu khtin snoirleotu vvielson hte tems slcle y(etp II tsmun.yo)pece Is teh ntatci teaenmbs narmeemb eht sawnre ebaescu it iltsmi ?adesrp

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(804),
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heT omer aerleng lpi:rpecni lodtneheai oataivseld in the seeenrpc of hgih 2;CO uoy totag etg idr fo ahtt diac !woehosm Cta’n tle it luamu,tceca sa lwroe Hp witnih a mrc”em“i-oenirntvon afsceft cciffsu/iectryntueer fo sm,eyezn tpinrsoe, e.ct Teh mroe icicda a llaoc mei,vtrennno eht oerm oyu xcepet byrnea vasrlteacuu to ildtea s(a a ansme of scnngraeii fwol ,eart brtehey eifrrnyg off lacmuuaetc )id.ca

Teh onsistgeiltoaseh can etxilop sthi c.hnmmaies By lnhtrpyigteavine og(ibnwl ffo )2CO, hte brian ulcesaavrut nssese a wol 2CO / yodr“-nkhyu te,s”at hwhic seueirqr no tsnolovia.adi In orhet ows,rd het csaeuultrva oeds otn need ot ncounite the AicmusoTP-ngn ctpecrai fo ignitzssyenh Nirtci dOexi N(O.)

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(804),
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Teh orem naeeglr lpriicpne: denhalotie odesatlvai ni hte sreepecn fo gihh ;C2O ouy togta tge idr fo that caid oeshmow! a’tCn tle it cueuaam,clt as oelwr pH hniwti a mvn-”“croieonirtenm tffesac cyneeericutrfiuf/cst of neyzsm,e onptesri, tec. Teh omer iicdca a llcoa ov,mnietenrn teh eomr you exeptc eayrnb clurtsaaveu ot aitlde sa( a aenms of cnsreniiga lfow ea,rt erbhety ifergyrn off ecacautmlu )c.iad

hTe ieetssonoaitshgl anc eilpoxt thsi mcnem.asih yB ilhirnpegettynav nwoblg(i off ,)CO2 het ibnra uauavsctrel ssseen a wol OC2 / uod-yrkyh“n a”tets, hchiw esrrquei no vidinatool.sa nI eroht drow,s het vtaselruuac dsoe tno nede to oucentni hte mgAPTnsc-unio crapitec fo tzsnhiseying criiNt xdeiO (N).O

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(138),
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h'eers a gleoog

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(804),
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retAf eht fcuf si ,eidt hte sllce adn tsusie lidtsa ot eht uffc iwll noeuintc uigmnnosc APT (&tDTAP-P;Ag), tbu no eshfr olobd lwil be eilrdveed to “”ecrla thwa wlli eb na acluuciamgnt tnoamu of PDA dna eroth isloeetatmb. PAD =os)edAnni(e is etfsil a pxroy fo tocmsuoinpn nda iedrvs ooinadasivtl of reit!ares ltovEon(ui si )strma! aeIsninrgc AsinoD/AdneeP in a “oclla tmneeov”irnn si a anigls ot eht yodb hatt a lto of umcnopnosti si ucrcorign hee;tr u,hts reitresa dan esrtiorale llturnaya deatil to rceenias oolbd flow rtaes nad pee“sw awya” aeoiclbmt o.dcbsutryp

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(804),
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You haev to ithkn boatu hits ugnsi eht cctoenp of NCDOOTLAINI RLIBIAYBOTP. hrneotA ywa ot ask htis ptey fo suontieq si iekl h:tsi “I hwso uoy a ettpani ithw potneossanu uhmtrooaexnp. hichW eorht hitng is mtos iklely to eb etur uboat hatt prn”oes? Or oyu nca phsrae ti eehst as:yw

  • inGev a TONNCIIOD (nnsaoteupos mepnou), hawt other ingidnf si smto lilkye ot be eht sa?ec
  • invGe a oopl of lppeoe ithw putosnnaoes orx,tunepaomh ahwt retho tihng is somt ylekil to be erut aubot mh?et

nI ohrte rwosd, of all oelepp ohw ned up hwit tpsuasoneno uopm,ne eth tmos monomc horte tngih uboat ethm is htta tyeh ear MALE ;a&pm ITH.N

If I eagv ouy a ectkbu fo poeusaostnn oeupmn itpseant -- adn ouy daecher royu adhn ni heert and lduepl one otu -- wtha cirnsaeo dluow be omer om:omnc In your hnda uoy vahe a kemors ro ni oury hadn you vhea a ntih e?lma ’stI the t.tlare

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(804),
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uoY vahe ot knith bauot ihts sginu hte etccnop of NLDOIOTCNIA BYTRI.AOBLIP erAonht ayw ot aks sthi tyep of suenoitq is leik t:his I“ owsh uyo a atnetip htwi enoopnsusat meatrpxnh.oou ihcWh hetor itgnh is msto ilelky ot eb tuer batou that pe?sn”ro rO oyu cna spehra it tshee wsya:

  • neiGv a NTDICONOI (onasupesotn mponeu,) hwta hteor gidfinn si toms eilkly to eb hte sa?ec
  • vGeni a oolp fo ploeep thwi unteopsonas ,nmohrueaotxp thaw thore hgtni si otsm lkilye to be uret oatub ?temh

nI herto rsdwo, of lla pepoel how edn up hiwt onsuaonepts ,eumnpo the most monmco toehr nigth uotab tehm si atht ethy rae LEMA pa;m& TINH.

fI I veag uoy a tbucek of atsnpouosen eunomp snteaipt -- dna yuo eecrhda ouyr andh ni treeh adn upledl eon otu -- thwa rinscaeo uwold be oerm moocn:m In your hand uyo avhe a emrkso or ni oury dnah uoy ahve a ihtn aml?e t’Is eth tr.ltea

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(804),
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ontD’ trefog taht idnnecice is hte ebnmru fo enw asces chihw eregme ni na afteeunfcd lntopiaupo. cceIndnei is ingryt ot tge ta eth suoetqin &t;-g “In a nveig ,yrea who amny wen eolppe poeedvl hits ee?ss”ida

nI toher ordsw, you ocnant octnu peoepl who ladraey avhe the aisedes. ouY eavh to luxeedc eosht oepelp rfmo rouy ocnlu.aitcal Yuo tawn ot k,won omnga all teh epeopl uot erteh woh OD NOT hvea teh sesidae, ohw mnay mseti ihts reya wsa oosenem lneyw() ?anidoesdg

aSdi edrtnfyielf s,litl uoy tdn’o natw ot ou-nlce“dob”tu lepoep ohw dpeelovde eht adesesi ebroef uryo su.dyt As na ooiteli,igmpdse htat lduwo rcsew up yuor sseen of hwo ficvetein or rbastmlisinse a seeidas .is You want to ,nkow “morf iemt1 ot miet2 who ynma enw sasce rge?dmee”

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. +  
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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hyW ulwdo ti not be aaniem fo ochinrc ieaedss tihw reseadced umesr rsnnrafrtie noctnocrnit?ea

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  


submitted by keycompany(294),
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nitgreNo lanbeca si a esnmuteearm fo irpnote oblitasmem in eht d.ybo A teigvean griennto lcabean adincesti emuscl ,sosl sa aenrsiced otmusan of oiman sdaci aer gbine oalebzmdeti ot reucpod eryge.n ihsT isncreaes hte oamutn fo etorginn tecdrese mrof het b.yod eauBecs het mtnauo of eirnnotg uoy are nkitag ni is essl hnta teh otmuan fo oignenrt uoy ear tcsrneige, uyo aveh a nietavge nritoneg aclbnea.

hsiT amn si udnasimhelor, mtdeoasu,e t,ichaecc adn hsa mlmhauei.apoiynb Tehes ialcnlci gfnnsiid pinto to npteiro uloaiirmtnnt (koswrhaiKa eDias)se, whihc sscaue eedam deu to aereddecs usmre oncctio psreru.es wLo ccnoiot reespusr in siht saec is eud ot ieonptr ,slso and neche a vgnieate otngeirn cnla.bea

drdoom  Nice! +15  
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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whrveyeerE I dnfou UDt(Tpaoe nad saeevrl papse)r asid eth gsmokni is teh itegsgb riks afotcr ofr upnsoenosat maeuhootrn,px tiwh ydbo bhtaisu nad rednge ienbg a rleses ik.rs mA I tsju lolptcymee adnrndiunsstgiem the nueqtso?i

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 ttleil edirfn sah a arPvsviuor f,nconeiti hwchi eticsnf iorrtyedh rupcsresr,o ugnacis etnnriutrpio fo teeyhrocryt rpnucioot.d ihTs is teh esma ayw it easucs hyrdpso ialtefs ni brnuon ebabis dna ltiaacsp eiaanm ni sciekl e,llc ce.t

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. +20  
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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The qtsnouei mset si bcsiegirnd a ahidtomirocln saesi,ed iwchh mylomonc sprteen ihwt calcti casoisd.i hreTe is na arneecis ni ibrcnoaea mrofs of erengy dopnoircut yyislsg.lco() hTe dtniiomohcar are utayl,f so ethy catn’ seu the ned odtcpur of sycgyisoll aetvr)pu(y in TC.A ndsIaet rtvaypeu si dtnuhes orev dan is sude yb LDH ta(atecl yohdre)aeedgns ot eeeartng teavyr.pu

Ai:eds claleR atht DHL uess HNAD dna ngeeetasr DA.+N yeiiecfDcn fo HLD nca dael ot ossl fo ierotnaenerg fo DA+N nad bsihtini solygcls.yi

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 +50  
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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Wyh is odluaden mlnue tccnirer?o I huhgtot acrpaeictn yeemzns ym,irscoynph(t daiptxposbearyce) lduwo be ltocdae eh.er

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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-Hi I ont'd veah na etinlanaopx fro isth ubt I ma osla iruusoc as ot why hist was the e.wnrsa

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 nos isht lli b tgo msoe MICDEUBTILA clluMuosm all up in reh esisnbz

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 +6  
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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The anitotrpm ihtgn rfo smto of het estcih sensuqoti aer ot loko for eth easrnw hreew uyo ear gbien the tscenmsto/i easfooprslin hilwe ecpsrtgein the et’tnaisp muoyo,nat cbee,fnnciee ncemecnlaoef-,in cte. sotM fo teh chcsoie ehre rwee eitehr ocrctyasua or bslaaycil ebnig maen to het ta.ietpn Teh ctecorr cheoic si ot hlpe teh atientp but loas tevoatmi meht to euincnot ciplhsya aerhpyt nda ot nlyo use the itperm as leltit as ecenasrs.y A aimislr instueqo hi(cwh I nikht was on BMNE 32 -- ethy rae nkdi fo gdebinln ohgtrte)e swa teh one hreew het itptean ahd etts sltsuer atht dtnaiecid he dha cencar tbu teh dteesnir sdia ont to tonayvll(r)iu ellt imh itlun eth sctooiglon mace ni rleta atth ,ady adn hte ntpieat kdeas you atobu het .uslrtse Yuo dt’no tawn to the lei to teh tnaetip adn yas you ’tdon wnko or ahtt eh tsne’od heva ac,ercn ubt yuo lsao dt’on twna ot be tibneiadnusor to teh neiesstr’d esblano()are equ.ters

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 atromntpi ihtng rfo otsm fo eht schtie noustesiq era ot look rfo the rsenwa wehre uoy ear ibegn eht tmoeistcns/ irefasospnlo lehiw etgecsnirp het ’etaitsnp moa,ntyuo eefnnebcec,i eenfei,cnnm-calo tc.e toMs of hte soehcic ereh ewre eirhet atyrscacou or islcalbay geibn naem ot eth t.itenpa eTh orectrc hiccoe si ot phle eth pentati utb lsoa oemttiva ehtm to oneintuc lcsayphi rphyaet dan to loyn use hte rmteip sa elittl as ensyr.csea A misliar sqnteiuo hiwh(c I tkhin asw on MBNE 23 -- eyth ear knid fo lenibdng teohetg)r asw teh noe hreew hte attpien ahd etst rtelsus htta dacnitdei he dha ecancr but hte reeisntd isad ton ot lvtalonru)(yi llet hmi unitl het ooitolsngc mcea ni lerat tath d,ya and eth etaintp aesdk yuo utbao hte sus.rlte Yuo ’tond want ot the eli ot teh ntpiaet dan ays uyo otnd’ kwno or ttha eh oedtsn’ vhea c,cnaer tub yuo aslo ’dotn antw ot eb stnbroadinuie to eth sdeisne’tr o)ealasrne(b etuqsr.e

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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cudlo enmeoos alepes nlxiaep yhw eeisanndo si ccroer?t

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 ddalneou elnmu trrncceoi? I huhottg ncairteapc ynmseez cmpsi(yhorn,yt eotybcdsirappea)x dlwou be tdlecoa 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 +  


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uoY wnko t’is na poedveeln survi nicse it dotsn’e dlho pu ot idac ro bengi ire.dd oYu wnko it csusea a ervef and a hgou,c wheli naitecfgf eth yalx.nr Oyln irsvu ceatroyg tath sift lal taht fnoi is hte rosanviruoc cse(aus RSSA) romf htta sl.ti

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 lbvoyiosu ogthhut tath the naim gntih for aytcapic is ot eartdnunsd eth ervyiest nad rsinopogs fo ehr aimdcel onioicndt TUB I tuoghht tsih asw a crkit uteisqno esueabc yeth adske i"f the atlemn xnaatieonmi giindfn .hdo.e"ws. nad the tesm daifel to ntemoni athiyngn utbao ehr iertaoinotn ot cplae ro .iemt dumb

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