welcome redditors!to snoo-finity ... and beyond!
Welcome to drdoom's page.
Contributor score: 74
School: None
don't just do something, stand there!

Comments ...

 +0  (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.


 +0  (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!

 +1  (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.


 +1  (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."
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].)

 +6  (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"

 +0  (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


 +0  (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


 +2  (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


 +15  (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!
seagull  very well put, thank you

 +3  (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.

 +3  (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


 +2  (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.


 +0  (nbme20#29)

[deleted]


 +0  (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.

 +1  (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.

 +4  (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

 +10  (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.


 -1  (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.
drachenx  hungrybox is a freaking hater
drdoom  @drachenx haha, nah, coming back to this i realize i was probably over-geeking lol

 +1  (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
sympathetikey  He's showing how A & B are incorrect @hungrybox

 +2  (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.”


 +2  (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.


 +0  (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.
drdoom  decreasing respiratory rate = retention of CO2 = vasodilation of brain arteries = more filling of tubes = greater intra-cranial pressure
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!"

 +0  (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.


 +13  (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





Subcomments ...

A medical student shouldn't be the one giving someone a cancer diagnosis. This is a really sensitive issue and the results should be given by someone with higher authority like a resident or attending. At the same time, you shouldn't lie to the patient and say that the results aren't back yet if they are. Best thing to do is deflect the conversation and follow up with the resident..

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! +  


submitted by sattanki(20),

Apparently there is a completely separate spinal cord reflex where direct penile stimulation leads to an erection. This reflex only needs an intact arc in S2-S4, so as long as this region is not injured, an erection can still occur. However, with transection at C8, then the psychogenic erection reflex cannot occur, as this requires descending fibers from the cortex.

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." +2  
seagull  S2-3-4 keeps the penis off the floor +6  
drdoom  Modifying @seagull into iambic pentameter: “S2, S3, and Number 4 / keeps the big ole penis / off the floor” +  


Can anybody explain this one? I put repeated tests because I assumed an 83-year-old woman is an unusual demographic for syphilis.

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. +2  
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 ...? +2  
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. +  
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. +1  
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. +3  
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. +1  
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 +1  
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 +  


my list of spindle type cells and conditions:

  • a. NF-1
  • b. NF-2 ~ Schwannoma (Antoni A) = Cutaneous neurofibroma ~ high cellularity (w/ palisading patterns with interspersing nuclear-free zones called Verocay bodies
  • c. Leiomyoma (uterus & esophagus)
  • d. Mesothelioma (cytokeratin positive)
  • e. Anaplastic Thyroid cancer (biphasic & along with giant cells)
  • f. Medullary Thyroid cancer (can also have polygonal cells)
  • g. Primary cardiac angiosarcoma (malignant vascular spindle cells)
  • h. Osteosarcoma (bone cancer) (pleomorphic cells)
  • i. Meningioma
  • j. Kaposi's Sarcoma (HHV-8) = Slit-like vascular spaces with plump spindle-shaped stromal cells
drdoom  @usmleuser007 to make lists display correctly, try using the plus sign (+) for each "bullet point"; that should work +  
mcl  I love this and I love you +  
usmleuser007  LOL thanks, had to ddo a lot of digging since "spindle cells" are commonly tested +  


1) Analysis of variance is a procedure used for comparing sample means to see if there is sufficient evidence to infer that the means of the corresponding population distributions also differ.

2) Where t-test compare only two distributions, analysis of variance is able to compare many. • What does the one-way part mean? It is one dependent variable (always continuous) and exactly one independent variable (always categorical). A single independent variable can have many levels.

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


submitted by yotsubato(85),

Arent we NOT supposed to use ipratropium in old people?

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. +  
drdoom  discussion of anticholinergics & elderly also discussed at some length (but different context) here: https://www.nbmeanswers.com/exam/nbme22/1288 +  


submitted by drdoom(74),

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. +1  
drachenx  hungrybox is a freaking hater +  
drdoom  @drachenx haha, nah, coming back to this i realize i was probably over-geeking lol +  


submitted by seagull(205),

maybe someone can explain why this is avascular necrosis and not sepsis. It doesn't mention fever or absence of fever. The MRI has a small amount of hypodensity but to get avascular necrosis seems odd/

someduck3  Pg 455 of F.A. mentions that alcoholism can be a cause of avascular necrosis. +1  
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 +1  
yotsubato  He wouldnt be playing golf if he had septic arthritis. Avascular necrosis is a more chronic condition that has a slow onset. +  


submitted by nosancuck(20),

Dam son this lil b got some UMBILICATED Molluscum all up in her bizness

drdoom  tru. +  
meningitis  Pg 164 FA 2019 +  
dr.xx  likely not "lil b" as 2-4 times as many cases are found in whites than in persons of other races +  
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(16),

I feel dumb for asking but can someone explain this? If his parents are of close to normal BMI and are concerned about his weight why would they be allowing his calorie consumption to exceed his energy expenditure? ( AKA letting the kid eat too much and not exercise enough)

meningitis  That's a modern day mystery. +  
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. +  


submitted by mcl(79),

Bonus cadaver diagram, idk why this was on pinterest...........?

drdoom  bonus cadaver diagram via @mcl +  
yotsubato  nurses +  


submitted by beeip(38),

Inability to elevate the palate suggests damage of the vagus nerve.

F. (CN X)

atstillisafraud  I guess F is the vagus nerve. Thanks to NBME I am also training to become a mind reader. +2  
seagull  Thanks to the NBME I have crippling depression +4  
drdoom  bonus cadaver diagram via @mcl +  


submitted by dr.xx(11),

Structures within the outer (lateral) wall of the compartment from superior to inferior: Oculomotor nerve Trochlear nerve Ophthalmic and maxillary branches of the trigeminal nerve Structures passing through the midline (medial) wall: Abducens nerve Internal carotid artery accompanied by the Internal carotid plexus

https://en.wikipedia.org/wiki/Cavernous_sinus



submitted by meningitis(54),

Although it’s about PPV, this researching helped me understand basic phys, I hope this helps everyone in some way.

Takeaway: During PPV, venous return decreases, cardiac output decreases, and heart pressures decrease in the right side of the heart.

Why does PPV decrease venous return?

  • intrathoracic pressure compresses heart, causing blood not to return

Causes for decreased left ventricular output during ventilation:

  • Shifting of intraventricular septum to Left due to increased RV volume
  • Decreased venous return
  • Changes in hearts ability to contract due to positive pressure
  • lack of O2 to heart

Normal compensatory mechanisms for maintaining CO and BP during PPV?

  • increased HR to compensate for decreased SV
  • increased SVR to maintain BP

Other Physiologic responses:

  • Decreased cerebral perfusion pressure (body’s response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels)
  • Decreased renal perfusion (Increased ADH, RAAS, and Patient has renal problems so increased creatinine and uric acid)
  • Possible malnutrition (increased glucose via gluconeogenesis etc.)
meningitis  sorry about the formatting, they were supposed to be bullets not italic. +1  
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(54),

Tanner stages start at TEN years old

Stage I:

  • I is flat, as in flat chest;
  • I is alone, as in no sexual hairs.

Stage II (2): stage II starts at 11 y/o (II look like 11)

  • 2 balls (testicular enlargement)
  • 2 hairs (pubic hairs now appearing)
  • 2 breast buds form

Stage III (3): starts at 13 y/o

  • If you rotate 3, it looks like small breasts (Breast mounds form);
  • If you squiggle the III they look like curly+coarse pubic hair
  • Increased penis length and size can be represented by: II --> III
    (your penis was thin II but now its thicker III)

Stage IV (4): starts at 14 y/o

  • First imagine: The I in IV represents the thigh, and the V in IV looks like the mons pubis between your legs:
    MEANING: you have hair in mons pubis (V) but you have a border detaining the hair from growing into thighs.
  • The V is pointy, as in now the breasts are pointy (raised areola or mound on mound)

Stage V (5): 15 y/o

  • V has no borders detaining hair from growing into thighs (pubic hair + thigh hair)
  • 5 fingers(as in hands) flattening the areolas when grabbing them (areola flatten at this stage and no more "mound on mound")

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +1  
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. +  


submitted by sajaqua1(82),

Male pattern baldness./androgenic alopecia is caused by the effects of dihydrotestosterone (DHT) on the skin of the scalp. Testosterone is converted by the enzyme 5-alpha-reductase into DHT. Finasterideis a 5-a-reductase inhibitor, and so blocks the production of DHT and can halt or even cause some reversal of make pattern baldness. However this same activity may also result in signficant sexual side effects including gynecomastia, erectile dysfunction, ejaculatory dysfunction, and decreased libido.

A) Danazol- a weak androgen with antiestrogenic effects, used in the treatment of endometriosis and fibrocystic breast disease. C) Methyltestosterone- synthetic T, it is used to supplement in testosterone deficiency, or in the treatment of some breast cancers. D) Oxandrolone- an anabolic steroid used to regain weight. E) Stanozolol- another anabolic steroid, with potential used for hereditary angioedema.

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


submitted by bubbles(11),

Wouldn't constriction of peripheral vessels also trigger sphlancnic vasoconstriction, which simulates renal ischemia and causes increased RAAS activity?

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! +2  
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(11),

Wouldn't constriction of peripheral vessels also trigger sphlancnic vasoconstriction, which simulates renal ischemia and causes increased RAAS activity?

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! +2  
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(74),

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! +  


submitted by shaydawn88(2),

I would think resolution involves the stem cells (type II pneumocytes). Is the intact basement membrane the answer because it limits spread?

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 :) +2  
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.) +3  


submitted by drdoom(74),

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. +1  
drdoom  decreasing respiratory rate = retention of CO2 = vasodilation of brain arteries = more filling of tubes = greater intra-cranial pressure +  
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!" +  


submitted by drdoom(74),

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. +1  
drdoom  decreasing respiratory rate = retention of CO2 = vasodilation of brain arteries = more filling of tubes = greater intra-cranial pressure +  
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!" +  


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. +1  
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 +  
meningitis  I guess that's another reason for steroids and doping up. +2  


submitted by drdoom(74),

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  


submitted by drdoom(74),

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." +  
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].) +  


submitted by drdoom(74),

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." +  
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].) +  


submitted by drdoom(74),

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. +1  


Why would it not be anemia of chronic disease with decreased serum transferrin concentration?

lispectedwumbologist  Nevermind I'm stupid as fuck I see my mistake +  
drdoom  be kind to yourself, doc! (it's a long road we're on!) +5  
step1forthewin  Hi, can someone explain the blood smear? isn't it supposed to show hypersegmented neutrophils if it was B12 deficiency? +  
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 +5  
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... +  
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. +  
yotsubato  Thanks NBME, that really helped me.... +  


submitted by keycompany(56),

Nitrogen balance is a measurement of protein metabolism in the body. A negative nitrogen balance indicates muscle loss, as increased amounts of amino acids are being metabolized to produce energy. This increases the amount of nitrogen secreted from the body. Because the amount of nitrogen you are taking in is less than the amount of nitrogen you are secreting, you have a negative nitrogen balance.

This man is malnourished, edematous, cachetic, and has hypoalbuminemia. These clinical findings point to protein malnutrition (Kawashkior Disease), which causes edema due to decreased serum oncotic pressure. Low oncotic pressure in this case is due to protein loss, and hence a negative nitrogen balance.

drdoom  Nice! +  


Everywhere I found (UpToDate and several papers) said the smoking is the biggest risk factor for spontaneous pneumothorax, with body habitus and gender being a lesser risk. Am I just completely misunderstanding the question?

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. +  


Our little friend has a Parvovirus infection, which infects erythroid precursors, causing interruption of erythrocyte production. This is the same way it causes hydrops fetalis in unborn babies and aplastic anemia in sickle cell, etc.

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. +1  
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 +1  


The question stem is describing a mitochondrial disease, which commonly present with lactic acidosis. There is an increase in anaerobic forms of energy production (glycolysis). The mitochondria are faulty, so they can’t use the end product of glycolysis (pyruvate) in TCA. Instead pyruvate is shunted over and is used by LDH (lactate dehydrogenase) to generate pyruvate.

Aside: Recall that LDH uses NADH and generates NAD+. Deficiency of LDH can lead to loss of regeneration of NAD+ and inhibits glycolysis.

drdoom  ... pyruvate is shunted over and is used by LDH (lactate dehydrogenase) to generate lactate*. +  
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. +3  
masonkingcobra  Mitochondria are the powerhouse of the cell +4  
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 +  


Why is duodenal lumen incorrect? I thought pancreatic enzymes (chymotrypsin, carboxypeptidase) would be located here.

colonelred_  Enterokinase actives trypsinogen and is located closer to the intestinal mucosal (“brush border”). +  
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. +  
welpdedelp  http://1.bp.blogspot.com/-UDdBiBiEgec/UzM61mV4pTI/AAAAAAAABRA/_qCG05fliGk/s1600/VBN.PNG +2  
drdoom  Nice schematic, @welpdedelp +  


Hi- I don't have an explanation for this but I am also curious as to why this was the answer.

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. +1  


submitted by nosancuck(20),

Dam son this lil b got some UMBILICATED Molluscum all up in her bizness

drdoom  tru. +  
meningitis  Pg 164 FA 2019 +  
dr.xx  likely not "lil b" as 2-4 times as many cases are found in whites than in persons of other races +  
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(9),

The important thing for most of the ethics questions are to look for the answer where you are being the nicest/most professional while respecting the patient’s autonomy, beneficence, non-maleficence, etc. Most of the choices here were either accusatory or basically being mean to the patient. The correct choice is to help the patient but also motivate them to continue physical therapy and to only use the permit as little as necessary. A similar question (which I think was on NBME 23 -- they are kind of blending together) was the one where the patient had test results that indicated he had cancer but the resident said not to (voluntarily) tell him until the oncologist came in later that day, and the patient asked you about the results. You don’t want to the lie to the patient and say you don’t know or that he doesn’t have cancer, but you also don’t want to be insubordinate to the resident’s (reasonable) request.

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]). +  
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. +  


submitted by aladar50(9),

The important thing for most of the ethics questions are to look for the answer where you are being the nicest/most professional while respecting the patient’s autonomy, beneficence, non-maleficence, etc. Most of the choices here were either accusatory or basically being mean to the patient. The correct choice is to help the patient but also motivate them to continue physical therapy and to only use the permit as little as necessary. A similar question (which I think was on NBME 23 -- they are kind of blending together) was the one where the patient had test results that indicated he had cancer but the resident said not to (voluntarily) tell him until the oncologist came in later that day, and the patient asked you about the results. You don’t want to the lie to the patient and say you don’t know or that he doesn’t have cancer, but you also don’t want to be insubordinate to the resident’s (reasonable) request.

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]). +  
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. +  


submitted by pmnbp(1),

could someone please explain why adenosine is correct?

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. +  


Why is duodenal lumen incorrect? I thought pancreatic enzymes (chymotrypsin, carboxypeptidase) would be located here.

colonelred_  Enterokinase actives trypsinogen and is located closer to the intestinal mucosal (“brush border”). +  
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. +  
welpdedelp  http://1.bp.blogspot.com/-UDdBiBiEgec/UzM61mV4pTI/AAAAAAAABRA/_qCG05fliGk/s1600/VBN.PNG +2  
drdoom  Nice schematic, @welpdedelp +  


You know it’s an enveloped virus since it doesn’t hold up to acid or being dried. You know it causes a fever and a cough, while affecting the larynx. Only virus category that fits all that info is the coronavirus (causes SARS) from that list.

zelderonmorningstar  EBV doesn’t cause fever and cough? +  
zelderonmorningstar  Wow, just checked First Aid and it doesn’t list “cough” as a symptom of EBV. +  
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. +1  
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. +  


I obviously thought that the main thing for capacity is to understand the severity and prognosis of her medical condition BUT I thought this was a trick question because they asked "if the mental examination finding showed..." and the stem failed to mention anything about her orientation to place or time. 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. +