welcome redditors!to snoo-finity ... and beyond!
Welcome to yotsubato's page.
Contributor score: 255
School:


Comments ...

 -1  (nbme24#45)

Cool another question taken from the list of things not in FA

charcot_bouchard  Actually it is in FA. FA 19 Page 100 - Antigen loaded onto MHC1 in RER after delivery via TAP transporter.... Remember FA is that friend who always say I told you so.
yotsubato  But not in this context

 +1  (nbme24#6)

ALT and AST are enzymes within hepatocytes. Without hepatocyte damage, you wont have elevations.

Alkaline phosphatase is present in all tissues throughout the entire body, but is particularly concentrated in the liver, bile duct, kidney, bone, intestinal mucosa and placenta.


 +2  (nbme24#49)

Cold air induces asthma attacks.

Decreasing course load wont help

Taking steroids is too much for now

Moving back to the dorms is not viable

Air cleaners dont work enough

Dont get rid of the Good Boye

Smoking indoors is disgusting

sherry  Stress can actually be a trigger for asthma. I think the problem here is that she has alwasys carried a heavy course, while the disease just started recently.

 +0  (nbme24#13)

Why is the patient not in pain. I wouldnt expect Incarcerated hernia to present with zero pain, but 1 week of constipation and swelling.

yotsubato  Incarcerated hernia. If the contents of the hernia become trapped in the weak point in the abdominal wall, it can obstruct the bowel, leading to severe pain, nausea, vomiting, and the inability to have a bowel movement or pass gas. Like really? Why is he not in pain?
medschul  I thought that inguinal hernias were reducible?
fahmed14  could be a femoral hernia as they are more likely to cause incarceration. They do, however, present more often in females. (FA 2019- 364)
wowo  incarcerated, not strangulated, thus no pain as there's no serious tissue damage/ischemia. Incarcerated hernias may progress to strangulated in which case he would have pain Under section, "complications" https://www.amboss.com/us/knowledge/Inguinal_hernia

 +1  (nbme24#41)

Kind of tricky question. The hypnozoites are chloroquine resistant. But the species may not be.

P. Falciparum is resistant and looks like a banana, but you dont know if the malaria in the RBC is falciparum or not.


 +3  (nbme24#29)

Amyloid A : seen in chronic inflammatory conditions, deposition of amyloid in tissues

B2 microglobulin: associated with ESRD and long term dialysis

Neurofilament protein: Form the cytoskeleton of neurons (in healthy individuals)

Presenilin: associated with familial alzheimers disease


 +1  (nbme23#49)

Although acetaminophen (Tylenol) is not considered an NSAID, it too may provoke an aspirin-like sensitivity.

meningitis  For that same reason (not an NSAID) it doesn't reduce inflammation so it cant be used for Gout.
meningitis  And I think Indomethacin is associated with anaphylactic reactions in patients with aspirin-sensitive asthma and aspirin allergies. Can anyone confirm?
link981  How many other's like me didn't see "allergic to aspirin"? FML
hyperfukus  OMFG me too i just got so mad and questioned my whole life at least its cuz i can't read not bc i don't understand :(((((

 +0  (nbme23#27)

"Children exhibit behavior incongruent with their age and development" in sexual abuse.


 +11  (nbme23#10)

Was it just me, or did "age at onset in years" appear RIGHT above the number of patients, rather than the mean. Which confused me for a good 3 minutes.

fulminant_life  Definitely was the same for me. I was so confused for like 5 mins
d_holles  dude i almost didn't get the question bc of this ... i thought the age of onset was the actual age of onset (36)
mellowpenguins  Are you serious. NBME strikes again with shitty formatting.
yex  OMG!! Now I just realized that. Super confused and also thought onset of age was 36. :-/
monkey  what is 36 supposed to be?
thomasburton  Think the number of people in that group

 +6  (nbme23#11)

Yeah sure, lets give the guy who wants to keep his dick working and be attractive towards women Finasteride and completely ruin his testosterone levels and give him a limp dick, man boobs, and decreased performance in sports.

Sometimes the NBME really just makes me ask Why?

Topical minoxidil would be way better but no they wont put that as a choice


 +0  (nbme23#23)

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
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

 +5  (nbme23#9)

This is a question about patient privacy. The patient here is the child. The proxy for the patient is the mother and father. They must know whats wrong. Sister and mother are just lookyloos, and parents may not want to tell them (stupid I know, but whatever) so you send them out and then tell the parents the situation.

dr.xx  agreed
thepromise  so you're not gonna conceal the abnormality and act like its their fault? since they touched it last
tinydoc  How on earth would they expect the parents to conceal a malformed upper extremity from the grandmother and the aunt of the child in a family that is close enough to allow these people to be in the room during the delivery. As always the ethics questions seem to make sense in retrospect, but always seem to have a ludicrous action on your part that you wouldnt do in practice.

 +1  (nbme23#12)

Murmur that is louder with reduced venous return => Hypertrophic cardiomyopathy

HOCM is due to mutations encoding sarcomeres such as myosin binding protein C and beta myosin heavy chain.

btl_nyc  So I thought this was Marfan's because the murmur from HOCM is at the left sternal border, but Marfan's is a defect in fibrillin, not in collagen.

 +14  (nbme23#48)

So for Candida we can use

Azoles (fluconazole) (inhibit CYP450 demethylation)

Amphotercin B (pore formation in fungal cell membrane)

Caspofungin (prevent crosslinking of beta glucans in cell wall)

or Nysatin for oral or esophageal cases (pore formation)

This question is saying that she is taking an ORAL drug to treat candida vaginitis.

Amphotercin is IV

Caspofungin is also IV

so we're left with azoles

Azoles inhibit synthesis of ergosterol by inhibiting CYP 450 that converts lanosterol to ergosterol.


 +0  (nbme23#42)

This patient is unresponsive to many antiacids. They dont specify which ones, but the question is basically asking which antiacid is the strongest. That would be PPIs, which inhibit gastric H K ATPase

yb_26  PPIs are not antacids!

 +2  (nbme23#25)

Transfusion reactions are mediated by Type II hypersensitivity reactions. These occur due to preformed antibodies that bind to the foreign antigen (AB group on RBC) and lead to hemolysis by NK cells. This is a form of Antibody dependent cellular cytotoxicity.


 +3  (nbme23#41)

So this question is describing a guy having difficulty externally rotating his arm while the forearm is flexed. He is able to supinate while his arm is extended (because of the supinator muscle and biceps). In the rotator cuff, only the infraspinatus performs external rotation, so that is the best choice.

Biceps works fine here

Subscapularis performs internal rotation.

Supraspinatus performs abduction

Triceps provides extension of forearm.

bigjimbo  technically rotator cuff infraspinatous and teres minor do ER (but teres minor is not a answer choice0

 +1  (nbme22#45)

Why cant this be laxatives? Both would cause metabolic alkalosis with hypokalemia... ?

sup  Laxatives would cause an anion gap metabolic acidosis due to loss of bicarbonate in the stool. You would see hypokalemia though as seen in this question.

 +1  (nbme22#40)

Pancrealipase is basically "Pancreatic Enzymes" in fancy pants NBME world


 +5  (nbme22#31)

In biology, phase variation is a method for dealing with rapidly varying environments without requiring random mutation. It involves the variation of protein expression, frequently in an on-off fashion, within different parts of a bacterial population. As such the phenotype can switch at frequencies that are much higher (sometimes >1%) than classical mutation rates. Phase variation contributes to virulence by generating heterogeneity. Although it has been most commonly studied in the context of immune evasion, it is observed in many other areas as well and is employed by various types of bacteria, including Salmonella species.

https://www.wikiwand.com/en/Phase_variation

whoissaad  is it the same thing as antigenic variation?
dorsomedial_nucleus  No, antigenic variation involves genomic rearrangement Phase variation can be thought of as MORE or LESS of something. An on/off switch. No DNA is being rearranged, just under or overexpressed in response to the environment.

 +2  (nbme22#35)

p53 is mutated and cant bind the TATA box, so what happens to transcription of inhibitory proteins?

Is basically what this question is trying to ask...

So no TATA box promoter => Decreased binding of RNA polymerase

link981  You said it, they are "trying" to ask. Should use better grammar.
titanesxvi  This is on first aid, and says that the promoter region is where RNApolymerase binds

 +1  (nbme22#28)

Interosseous muscles are innervated by the ulnar nerve.

Flexion of the foot is innervated by tibial nerve


 +1  (nbme22#41)

What happens when you go into cold water? You pee.

How does this happen.

Vasoconstriction of vessels to preserve heat, pulls water into vasculature due to decreased hydrostatic pressure in vessels. Volume goes up, ADH goes down, ANP goes up due to increased volume.


 +1  (nbme22#1)

Celiac: doesnt make sense, it comes out of the root of the aorta and ends instantly. Thats not getting caught up in the volvulus alone.

Left/right colic: thats all IMA branches, thats uninvolved in the situation.

Umbilical: that getting occluded is physiologic after birth.

Whats left is SMA: which goes right above the duodenum, so i would imagine a duodenal volvulus would involve the SMA easily.


 +1  (nbme22#8)

Its a diuretic, so volume is increased.

HCO3 is increased because acetazolamide reduces reabsorption of HCO3.

pH is increased, because HCO3- is a weak base, so it sucks up stray hydrogen ions in the urine.


 +0  (nbme22#49)

"MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is a prodrug to the neurotoxin MPP+, which causes permanent symptoms of Parkinson's disease by destroying dopaminergic neurons in the substantia nigra of the brain. It has been used to study disease models in various animal studies." Wiki

ilikecheese  pg 508 FA 2019
sbryant6  I thought this was testing "lead pipe rigidity" aka Neuroleptic Malignant Syndrome and its connection to dopamine. Had no clue what MPTP was and got it right still. Probably wrong train of thought though.

 +3  (nbme22#31)

What do you use to treat Hepatic Encephalopathy? Lactulose. What does that do, it acidifies NH3 in the GI tract into NH4+ and promotes loss of the nitrogenous products that cause encephalopathy. This is how you remember this process.


 +2  (nbme22#9)

Area C is where the gap junctions between cardiac myocytes are. Gap Junctions are found on the plasma membrane of the cardiac myocyte.

The question is basically asking where the plasma membrane is with a bunch of biochem mumbojumbo you dont have to understand.


 +3  (nbme21#38)

The patient has Neutropenic fever. GSCF will restore his neutrophils.

yotsubato  His RBC and platelets are low, but at acceptable levels for someone undergoing chemotherapy.

 +3  (nbme21#18)

Well thats a really crude way to screen for depression...

champagnesupernova3  There's really no other way to say it without using euphemisms

 +0  (nbme21#33)

Why is his Libido normal? It's totally expected that he may have reduced libido after his wife died 2 years ago from some horrible prolonged illness.

nala_ula  perhaps it's more to do with the fact that he can get erections when masturbating, outside of nocturnal erections which are not mediated by sexual desire. So his libido must be intact since he has sexual desire evident in being able to masturbate.
nala_ula  At least, that's the way I saw it.
home_run_ball  "Testosterone concentration is within the reference range" and the fact that he has no difficulty masturbating = normal libido. Low testosterone would contribute to low libido And if he had low libido he would have difficulty masturbating
thisisfine   The way I made the decision about normal vs. decreased libido is also that he presented to his doctor due to difficulty maintaining an erection while trying to have sex - meaning he has the libido to try to have sex. Does that make sense?
btl_nyc  It also says there are no signs of depression, which would cause the low libido after his wife died.
temmy  two years is a enough time to mourn...just saying
temmy  thisisfine, it makes absolute sense. That is the same way i saw it
dr_jan_itor  He misses his wife man, isn't ready for other women. Psychogenic ED. physically hes fine (can crank his meat)

 +0  (nbme21#39)

Why is this NOT chancroid? Theres nothing here that rules it out.

drachenx  Chancroid is described as an ulcer.. whilst in this question they mentioned "vesicles". Pretty much only herpes is vesicular
whoissaad  They mentioned ulcers too. I chose chancroid as well, couldn't find a clue to rule it out. Also thought "discharge" was pointing you towards a bacterial infection. But guess I'm wrong :)
emmy2k21  I think NBME/USMLE writers make the assumption the patient is in America unless specified otherwise. Chancroid is not common in the US. If the question stem mentions a developing country, then chancroid can make your differential list.

 +1  (nbme21#35)

Bullshit memorization question. You have to know that the single NRTI that causes pancreatitis is didanosine.

Page 203 FA2019


 -4  (nbme21#14)

She has Bernard Soulier Disease page 419 of first aid 2019

sympathetikey  That's a genetic deficiency of GP1b -- not antibody related
alexandramda  In Berard Soulierd you have a Defect in adhesion. decreases GpIb and decreased platelet-to-vWF adhesion. Labs: abnormal ristocetin test, large platelets.

 +7  (nbme21#25)

This question is stupid. Water intake for a healthy individual is 2.0 L a day.


 +0  (nbme20#14)

This question is bullshit. The woman would most likely be vaccinated to Strep pneumo, especially if she had a splenectomy.

E coli is also an encapsulated bacterium that causes pneumonia, so that is more likely IMO.

sugaplum  I agree with you, only possible logic for their answer: the qualifier asplenic makes the "ShIN" pathogens more likely, even though Ecoli can cause gram negative sepsis and DIC. FA 2019 pg 127 Also it says s pneumo causes sepsis specifically in asplenic patients Pg 136
lmfaoayeitslit  To be honest, the only reason I got this right (because I really was thinking E.Coli as well), is that I ended up remembering the MOPS part of the Sketchy, and I couldn't remember if he said that it was the number 1 cause of all of them or not, and ended up clicking it. It's pretty shitty they don't offer explanations for these.

 +1  (nbme20#1)

"physicians should always encourage healthy minor-guardian communication."

Also you're going to do some serious things to cure this girl's disease, leading up to amputation. You cant hide that from her.

djjix  Non sense ... you can hide the amputation from her
charcot_bouchard  Just show her one leg twice.

 +1  (nbme20#7)

It cant be Bacterial abscess (Nocardia) because shes taking TMP SMX.

It cant be toxo, because she has one lesion and is also taking TMP SMX which should improve her symptoms.

Glioblastoma is a disease of older individuals

Metastatic disease that mets to the brain is unlikely at this age.

CNS lymphoma is common in HIV AIDS patients, so that is the most likely choice.


 +1  (nbme20#21)

"Do no harm"

Starving the baby or withholding food is doing harm. At this point you provide palliative care until the death of the baby. If the parents decide to "pull the plug" then they can do it, but as the doctor thats not your choice.

cry2mucheveryday  Why not 'give foods according to normal caloric requirement'?
hpsbwz  @cry2mucheveryday because feeding to the caloric may be too much or too little for this baby. considering the baby's crying only resolves with food, if you've already reached the limit, are you just not going to feed the baby? that's how i thought of it. "maintain comfort" is the key phrase.

 +6  (nbme20#42)

Bifid carotid pulses are seen in Aortic stenosis or regurgitation

Carotid Bruit is heard with atherosclerosis of common carotid artery

Slow rising decreased volume carotid pulse is characteristic of aortic stenosis.

Cannon waves are seen in complete AV block, as right ventricle and atria contract independently.


 +2  (nbme19#27)

What was confusing for me in this question was that he has an acute presentation. That didnt make sense to me... He lived 74 years with renal artery stenosis and now has hypertension because of it!?





Subcomments ...

submitted by yotsubato(255),

Cool another question taken from the list of things not in FA

charcot_bouchard  Actually it is in FA. FA 19 Page 100 - Antigen loaded onto MHC1 in RER after delivery via TAP transporter.... Remember FA is that friend who always say I told you so. +2  
yotsubato  But not in this context +1  


submitted by mousie(82),

is this subacute endocarditis associated Membrano-proliferative GN?

jus2234  The question describes how he had a strep infection 15 days ago, and now this is poststreptococcal glomeruloneprhitis, which can also be described as proliferative glomerulonephritis +7  
seagull  The question would be too fair if it just said PSGN. Instead we need to smell our own farts first. +26  
yotsubato  And they used terminology NOT found in FA +5  
water  who said they were limited to FA? +1  
nbmehelp  FA uses the common nomenclature and the fact most of our other resources use the same nomenclature for this, I think we can agree that is is the accepted terms. If they're gonna decide not to use the nomenclature that most medical students are taught then they should provide their own study materials at that point for us to use. The test shouldn't be this convoluted for no reason. +1  


submitted by mcl(202),

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

drdoom  bonus cadaver diagram via @mcl +  
yotsubato  nurses +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!) +7  
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 +8  
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.... +  
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. +2  
sahusema  I didn't even register that was a lymphocyte. I thought I was seeing target cells so I was confused AF +  


Why is the answer “granulation tissue”? I thought after 14 days you have a fully formed scar.

colonelred_  If you go back and look at the image you can see that it was highly vascular which is characteristic of granulation tissue. Scar tissue formation will be closer to 1 month, plus you will see lots of fibrosis on histology. +3  
sympathetikey  It's a bit misleading, for me, since you do see fibrosis intermixed with the granulation tissue, but granulation tissue was a better answer. +  
haliburton  According to FA 2017: 3-14d: Macrophages, then granulation tissue at margins. 2wk to several months: Contracted scar complete. Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus). i'm getting pretty frustrated with NBME contradictions to FA, and FA omissions of content. this stuff is hard enough to get straight as it is. +  
yotsubato  Thats cause the NBME exam writers read FA, then make questions not fit in with FA +1  
trichotillomaniac  This fits the timeline laid out in Pathoma! 1-3 wks = granulation tissue with plump fibroblasts, collagen, and blood vessels +1  


submitted by neonem(251),

Cerebellopontine angle mass = Vestibular schwannoma (AKA acoustic neuroma). Derived from Schwann cells, which are of neural crest origin.

yotsubato  Ugh. Of course they dont put schwann cells as a choice. So I pick oligodendrocytes like a dumbass +9  
subclaviansteele  Same^ +  


submitted by lsmarshall(191),

I thought this was a trick question since skin cancers are the most common type of cancers overall. But actually among HIV patients, HIV-related cancers are much more common than non-HIV-related cancers (even skin cancers). EBV-induced primary CNS lymphoma is the only option that is AIDs-defining illness/cancer.

medskool123  why not hep B? i guess another whats the better answer ones... Just rem reading that it was more common with aids pts.. anyone have an idea about this? +1  
haliburton  Yes, I think CNS lymphoma as an AIDS defining illness wins the day. My thought was since SHE has AIDS it is most likely from IVDA, which has a high risk of HBV that could go undiagnosed for a long time. at 32, that might not be long enough to have HBV and get HCC (but with no immune system...?) +1  
yotsubato  God damn this is such BULLSHIT... +6  
trichotillomaniac  Why you gotta do me dirty like this NBME +  


submitted by seagull(413),

A- primary motor cortex = wrong side of body (deficit of UMN on left side body)

B - Thalamus = sensory information conduit - motor deficits unlikely to originate from here

C - Pons - CNs 8,7,6,5, likely result in "locked in syndrome" or complete loss of motor function on right side + facial features.

D. Vermis - central body coordination. Damage results in ataxia

Not complete but maybe helpful..

yotsubato  C - Pons - CNs 8,7,6,5, likely result in "locked in syndrome" or complete loss of motor function on LEFT side + RIGHT sided facial features. Decussation occurs in medulla +1  


submitted by lsmarshall(191),

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

vshummy  Synaptobrevin is a SNARE protein. Why they couldn’t just give us SNARE I’ll never know. +13  
yotsubato  Cause they're dicks, and they watched sketchy to make sure our buzzwords were removed from the exam +9  
yotsubato  Oh and they read FA and did UW to make sure its not in there either +7  
soph  This toxin binds to the presynaptic membrane of the neuromuscular junction and is internalized and transported retroaxonally to the spinal cord. Enzymatically, tetanus toxin is a zinc metalloprotease that cleaves the protein synaptobrevin, an integral neurovesicle protein involved in membrane fusion. Without membrane fusion, the release of inhibitory neurotransmitters glycine and GABA is blocked. -rx questions! +1  


submitted by lsmarshall(191),

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

vshummy  Synaptobrevin is a SNARE protein. Why they couldn’t just give us SNARE I’ll never know. +13  
yotsubato  Cause they're dicks, and they watched sketchy to make sure our buzzwords were removed from the exam +9  
yotsubato  Oh and they read FA and did UW to make sure its not in there either +7  
soph  This toxin binds to the presynaptic membrane of the neuromuscular junction and is internalized and transported retroaxonally to the spinal cord. Enzymatically, tetanus toxin is a zinc metalloprotease that cleaves the protein synaptobrevin, an integral neurovesicle protein involved in membrane fusion. Without membrane fusion, the release of inhibitory neurotransmitters glycine and GABA is blocked. -rx questions! +1  


Thank you NBME for the high quality pictures. It makes these exams stress free and enjoyable.

sympathetikey  Feels bad man. +2  
zoggybiscuits  Those Sclera sure look blue. wow. +  
yotsubato  the same girl shows up on so many NBME exams its not even funny. Its just like that poor kidney that's cut in half that shows up in all kidney questions. +2  


submitted by colonelred_(45),

Looked it up and found that because you’re in a supine position for a long time you’re going to have increased venous return which leads to increased CO. This negatively feedsback on RAAS, leading to decreased aldosterone. As a result, you’re going to have increased diuresis which leads to decreased blood and plasma volume.

medstruggle  Doesn’t supine position compress IVC leading to decreased venous return? (This is the pathophys of supine hypotension syndrome.) There was a UWorld questions about this ... +2  
tea-cats-biscuits  @medstruggle *Supine position* decreases blood pooling in the legs and decreases the effect of gravity. *Supine hypotension syndrome*, on the other hand, seems specific to a pregnant female, since the gravid uterus will compress the IVC; in an average pt, there wouldn’t be the same postural compression. +1  
welpdedelp  this was the exact same reasoning I used, but I thought the RAAS would inactivate which would lead to less aldosterone and less sodium retention +1  
yotsubato  You gotta be preggers to compress your IVC +  
nwinkelmann  Could you also think of it in a purely "rest/digest" vs "fight/fright/flight" response, i.e. you're PNS is active, so your HR and subsequently your CO is less? But the explanation given above does make sense. Also because I think just saying someone is one bed rest leaves a lot up for interpretation, maybe not with this patient because his pelvis is broken, but lots of people on bed rest aren't lying flat.... ? +1  
urachus  wouldnt low aldosterone cause low plasma sodium? choice B +  


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. +5  
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. +2  
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 +4  
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 +1  
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 +1  
sunshinesweetheart  also.... I think we can assume that "repeated tests" means repeat VRDL, not "additional tests to rule out false positives" +  


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. +5  
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. +2  
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 +4  
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 +1  
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 +1  
sunshinesweetheart  also.... I think we can assume that "repeated tests" means repeat VRDL, not "additional tests to rule out false positives" +  


submitted by mousie(82),

A Teen with injection of both conjunctiva = weed could also be abusing other drugs Is 12 years old and four months just too old and too long of a time for it to be impetigo? I narrowed it down to these two and guessed but... I wasn't sure I could eliminate it.

medskool123  I picked impetigo because of the gold stippling... I guess I took that as honey crusted lesions. F*ck NBME. +1  
yotsubato  Huffing gold spray paint. A la the chrome huffers in Mad Max +3  
subclaviansteele  LOL I think that might be what they were going for here. Gold spray paint. +1  
et-tu-bromocriptine  Anyone know what may be causing his weight loss and unwillingness to eat? I thought too much into it and put "mercury poisoning", since I thought the heavy metal's abdominal symptoms may have caused him to not want to eat. ¯_(ツ)_/¯ +  


submitted by yotsubato(255),

Why is the patient not in pain. I wouldnt expect Incarcerated hernia to present with zero pain, but 1 week of constipation and swelling.

yotsubato  Incarcerated hernia. If the contents of the hernia become trapped in the weak point in the abdominal wall, it can obstruct the bowel, leading to severe pain, nausea, vomiting, and the inability to have a bowel movement or pass gas. Like really? Why is he not in pain? +1  
medschul  I thought that inguinal hernias were reducible? +  
fahmed14  could be a femoral hernia as they are more likely to cause incarceration. They do, however, present more often in females. (FA 2019- 364) +  
wowo  incarcerated, not strangulated, thus no pain as there's no serious tissue damage/ischemia. Incarcerated hernias may progress to strangulated in which case he would have pain Under section, "complications" https://www.amboss.com/us/knowledge/Inguinal_hernia +  


submitted by majic(0),

THE MOST COMMON route of Toxo transmission in adults in the USA is ingestion of undercooked pork. Even if cat litter is an option, undercooked pork is still more common.

yotsubato  Also another fun fact. Most people in France are infected by Toxo (like 80%) because of how they eat meat. (Very rare) +1  


submitted by wired-in(25),

Maintenance dose formula is (CssCltau)/F where Css is steady-state target plasma conc. of drug, Cl is clearance, tau is dosage interval & F is bioavailability.

Neither dosage interval nor bioavailability is given, so ignoring those & plugging in the numbers (careful to convert units to mg/kg/day): (12 ug/mL * 1 mg/1000 ug) * (0.09 L/hr/kg * 1000 mL/1 L * 24 hr/1 day) = 25.92 mg/kg/day

...which isn't any of the answer choices listed. They must have rounded 0.09 L/hr/kg to 0.1 L/hr/kg, and doing so gives exactly 28.8 mg/kg/day (choice C)

lispectedwumbologist  That's so infuriating I stared at this question for 20 minutes thinking I did something wrong +17  
hyoid  ^^^^^ +2  
seagull  lol..my math never worked either. I also just chose the closest number. also, screw this question author for doing that. +2  
praderwilli  Big mad +3  
ht3  this is why you never waste 7 minutes on a question.... because of shit like this +4  
yotsubato  Why the FUCK did they not just give us a clearance of 0.1 if they're going to fuckin round it anyways... +5  
bigjimbo  JOKES +  
cr  in ur maths, why did u put 24h/1day and not 1day/24h? if the given Cl was 0.09L/hr/kg. I know it just is a math question, but i´d appreciate if someone could explain it. +  
d_holles  LMAO games NBME plays +  
hyperfukus  magic math!!!!! how TF r we supposed to know when they round and when they don't like wtf im so pissed someone please tell me step isn't like this...with such precise decimal answers and a calculator fxn you would assume they wanted an actual answer! +  
jean_young2019  OMG, I've got the 25.92 mg/kg/day, which isn't any of the answer choices listed. So I chose the D 51.8, because 51.8 is double of 25.9......I thought I must have make a mistake during the calculation ...... +  


submitted by sympathetikey(301),

Source: https://en.wikipedia.org/wiki/Myelin

"myelin speeds the transmission of electrical impulses called action potentials along myelinated axons by insulating the axon and reducing axonal membrane capacitance"

littletreetrunk  I think this makes total sense, but how does it not ALSO stop fast axonal transport? +2  
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." +1  
yotsubato  axonal transport is mediated by kinesin and dynein. Microtubule toxins like vincristine block these +2  


Can anyone explain how 10cm H20 positive PEEP leads to Peak Inspiratory PA, End Tidal PA, Peak Inspiratory Pip and End Tidal Pip all being positive?

tea-cats-biscuits  In PEEP, bc of how mechanical ventilation works, all the inspiration part of breathing is done by the machine actively pushing air into the lungs. As a result, there is no negative pressures in the system compared to the normal lung which needs the negative inter-pleural pressure to draw air in. +9  
yotsubato  " As a result, there is no negative pressures in the system compared to the normal lung which needs the negative inter-pleural pressure to draw air in. " Thats totally what threw me off. TIL +  


submitted by welpdedelp(74),

30* 0.15. Think about it, there is x flow with an oxygen concentration of y--so to find out the delivery you just multiply them together.

yotsubato  One of those questions too simple to believe its actually the right answer +7  
mimi21  Right, I was like this is too simple lol ! im not sure if this is also a good tip but I tend to look at the units they are asking for and double check my math to make sure I end up with them. +2  
osgood-schlatter  what equation is it exactly? +  


submitted by sakbarh(4),

She has many cardiovascular risk factors and likely suffered a stroke of the basilar artery causing locked in syndrome. According to FA this can cause a lesion at the pons, medullar, or lower midbrain -- however anatomically the basilar artery runs right on top of the pons so proximity most likely makes it the right answer.

mousie  The Boards and Beyond video of SC strokes was really helpful at explaining this if you are a video kind of person! +  
yotsubato  What pushed me away from pons was "dysarthric speech" which implied she still could speak to some degree.... which made me pick medulla. +1  
mimi21  I think FA may be misleading. Primarily it will effect the Pons because that is where the majority of the Basilar Artery is located. and I guess it could effect the other locations? but everywhere I have looked Locked-in syndrome is an issue with the Pons. But someone please continue to clarify, cause I was a bit tripped up at first with this question +  
cbrodo  Although FA says it can be pons, medulla, or lower midbrain, "locked-in" syndrome generally arises from BL pons lesions. Another way you can rule out medulla and midbrain in this question is the ocular movement findings. Since the patient has impaired horizontal gaze BL, you can conclude that the Abducens nuclei are involved on both sides. The abducens nuclei are located in the pons. +7  
gh889  USMLE secrets also states that it is most commonly in the pons Bates states that locked-in syndrome preserves consciousness but these patients have limited speaking ability +  


submitted by mousie(82),

Why no sweating? I mean I get Ecstasy is probably the drug of choice before an all night dance party (lol) but don't understand why there would be cold extremities and no sweating when is FA it says hyperthermia and rhabdo????

sympathetikey  FA says, "euphoria, disinhibition, hyperactivity, distorted sensory and time perception, bruxism. Lifethreatening effects include hypertension, tachycardia, hyperthermia, hyponatremia, serotonin syndrome." So I think they wanted you to see Sinus Tachy and jump for MDMA. Idk why Ketamine couldn't also potentially be correct though. +1  
amorah  I picked ketamine because it said no diaphoresis. But if you need to find a reason, I guess the half life of ketamine might rule it out. Remember from sketchy, ketamine is used for anaesthesia induction, so probably won't keep the HR and BP high for 8 hrs. In fact, its action is ~10-15 mins-ish iv. +2  
yotsubato  Because the NBME is full of fuckers. The guy is probably dehydrated so he cant sweat anymore? +1  
fulminant_life  you wouldnt see tachycardia with ketamine. It causes cardiovascular depression but honestly i saw " all-night dance party" picked the mdma answer and moved on lol +3  
monkd  Ketamine acts as a sympathomimetic but oh well. NBME hasn't caught on to ketamine as a drug of recreation :) +  
usmleuser007  Why not LSD? +  
d_holles  @usmleuser007 LSD doesn't cause HTN and ↑ HR. +  
sbryant6  @fulminant_life FALSE. KETAMINE CAUSES CARDIOVASCULAR STIMULATION. +1  
dashou19  Take a look at why the patient has pale and cold extremities. "Mechanistic clinical studies indicate that the MDMA-induced elevations in body temperature in humans partially depend on the MDMA-induced release of norepinephrine and involve enhanced metabolic heat generation and cutaneous vasoconstriction, resulting in impaired heat dissipation." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5008716/ +  


submitted by lfsuarez(65),

First heart sound (S1) is generated by two heart valves: the mitral valve and tricuspid valve. Nearly simultaneous closing of these valves normally generates a single S1 sound. Splitting of the S1 sound is heard when mitral and tricuspid valves close at slightly different times, with usually the mitral closing before tricuspid

yotsubato  Then why the fuck is it describing a mitral valve sound in the tricuspid area +4  
dr.xx  it's describing a splitting S1 — consisting of mitral and tricuspid valve closure — that is best heard at the tricuspid (left lower sternal border) and mitral (cardiac apex) listening posts. +2  


submitted by sajaqua1(198),

Wouldn't total AV nodal ablation destroy to autorhythmicity of the pacemaker? That would mean that below the AV node the rhythm would be provided by a ventricular foci, and those usually create wide QRS complexes.

haliburton  that was my reasoning as well. guess not. +  
yotsubato  Shitty NBME grammar strikes again. +  
charcot_bouchard  No. No guys. Bundle of his located below AV node and it can generate impulse. it calls junction escape rhythm and narrow complex. Below this is purkinje, bundle branch & ventricular muscle. those are wide complex +  


submitted by aladar50(17),

For the ECG, I initially thought it was 2nd degree Type 1 because it seemed that the PR intervals were increasing until a beat was dropped, but if you look at it closely, some of the P waves were hidden in the QRS complexes. If you notice that, then you can see that there were regular P waves and regular QRS complexes, but there was a complete dissociation between them which means it was 3rd degree heart block, so the answer was ablation near the AV node.

yotsubato  answer was ablation near the AV node. No it wasnt. It was ablation OF THE AV node itself. Which faked me out. +1  


submitted by seagull(413),

This is a type II Renal Tubular Acidosis. My Medical School Never taught this to me. Did you also go to poverty med school? I'm surprised they even gave us toilet paper.

mousie  haha mine didn't either. But they usually leave out most high yield info so, to be expected I guess. +1  
yotsubato  I didnt have physiology in my medical school. None, zip, zero, none. Nor did I have biochem. They said "you learned all this shit in undergrad, youll memorize it again for step 1 and forget it promptly" and then just moved on. +1  


submitted by seagull(413),

What a terrible picture. They they covered up part of it with lines. WTF

sympathetikey  Agreed. +  
catch-22  Start at the pontomedullary junction and count from superior to inferiorly (or medially to laterally): VI, VII, VIII, IX. +  
yotsubato  I looked at the left side (cause the nerves arent frazzled up). Saw 7 and 8 come out together nicely. Then picked the right sided version of 8 +  
lolmedlol  why is it not H or I on the right side; the stem says he has hearing loss on the right side, so the lesion should be ipsilateral no? +1  
catch-22  You're looking at the ventral aspect of the brainstem. +2  
catch-22  ^Also, you know it's the ventral aspect because you can see the medullary pyramids. +  
amarousis  think of the belly of the pons as a pregnant lady. so you're looking at the front of her +1  
hello  which letter is CN IX in this diagram? +  


submitted by seagull(413),

This patient is tripping balls. Better do a drug screen which seems obvious.

sympathetikey  When the answer is so obvious that you pick a stupid answer instead of it. DOH +4  
jooceman739  Funny thing I noticed is "he is alert and cooperative. He appears to be in pain" So he was so high that he was alert and cooperative during the basal ganglia hemorrhage +2  
yotsubato  @sympathetikey That fucking guy who drinks 2 six packs a day with liver failure got me like that. +  
yogi  probably the "drug" have to be a stimulant or a hallucinogen which causes HTN & Tachycardia. +2  
charcot_bouchard  Lol. I got the right answer but took long time +  
goodkarmaonly  The patient's B.P. and pulse are raised + Bilateral dilated pupils = Most likely use of a stimulant Thats how I reasoned it anyways +  


submitted by sajaqua1(198),

Because the baby's mother has Type 1 Diabetes mellitus, it is plausible that they had elevated blood glucose levels during or shortly before birth. Insulin does not cross the placenta, but glucose does, so during birth the neonate would have been hyperglycemic. This would lead to the neonatal pancreas releasing insulin, driving glucose into cells and turning down gluconeogenesis; this is why the baby is hypoglycemic right now.

B) Decreased glycogen concentration- I don't know the glycogen concentration compared to an adult patient, but a decrease in glycogen concentration would indicate glycogen/glucose release, which would not be a hypoglycemic state. C) Decreased glycogen synthase activity- decreased glycogen synthase activity indicates energy catabolism, and would lead to higher serum glucose levels. D) Decreased serum insulin concentration- decreased serum insulin would lead to higher levels of glucose in serum. E) Increased serum insulin-like growth factor- IGF does not bind nearly as well to insulin receptors as insulin does, and so would have to be in extremely high concentrations to have this effect. IGF is associated with somatic growth and muscle development.

yotsubato  His glycogen concentration is high, since he's been hyperglycemic with lots of insulin until birth. +3  
alexb  Also explains why he's 12 pounds. +1  


Malaria can impair hepatic gluconeogenesis and can also consume glucose for its own metabolic demands.

yotsubato  Truly a bull shit question... Its not in FA, Sketchy or Pathoma +14  
meningitis  I will try to remember this by associating it with P. vivax, that stay in the liver (liver=gluconeogenesis). Thank you @thomasalterman. +2  


submitted by seagull(413),

Why is this not HUS? How did you guys approach the question?

joonam  I think if this was HUS (d/t a bacterial infection) the leukocyte count would be abnormal (11k<) +  
yotsubato  normochromic normocytic RBC thats why. You would see schistocytes +1  


submitted by medstudied(2),

Why is it azithromycin not doxycycline? According to sketchy, you treat chlamydia with macrolides/doxy +ceftriaxone. You treat neisseria gonorrhea with ceftriaxone+azithromycin+doxycycline.

​Not sure what this question is testing -- is it wanting us to know that gonorrhea has to be treated as well? In that case, doxy would work for both according to sketchy ... Any other reasonings appreciated!

dr_salface  The patient in the stem is pregnant! The question wants to see if you know that doxy is a teratogen. Tetracyclines in general like to bind to fetal bone/teeth which can impair development. +5  
dr_salface  As a side note, treating chlamydia alone only requires macrolides or doxy. Treating gonorrhea alone only requires ceftriaxone or macrolides. The reason sketchy includes all three is because you usually treat one infection and co-treat the other. +  
yotsubato  Theres a crow in the chlamydia sketchy. You can use Macrolides, OR Ceftriaxone, OR Doxycycline. Most doctors in real life just give the azithromycin z pack (which kicks ass cause its one drug 5 doses thats it) +1  


submitted by dr.xx(39),

The most common and severe form of autosomal dominant polycystic kidney disease (ADPKD) results from mutations in PKD1, encoding polycystin-1 (PC1)..

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4348948/

yotsubato  Here we thank FA for failing us yet again. Giving us PKD1, but not polycystin. I got the question right but I just guessed it because nothing else made sense. +3  
usmleuser007  Autosomal dominant polycystic kidney disease 1) occurs in patients with mutations in the gene (PKD1) encoding polycystin-1 (PC1). 2) PC1 is a complex polytopic membrane protein expressed in cilia that undergoes autoproteolytic cleavage at a G protein–coupled receptor proteolytic site (GPS). 3) A quarter of PKD1 mutations are missense variants, though it is not clear how these mutations promote disease. 4) GPS cleavage is required for PC1 trafficking to cilia. 5) A common feature among a subset of pathogenic missense mutations is a resulting failure of PC1 to traffic to cilia regardless of GPS cleavage. 6) Missense mutation in the gene encoding polycystin-2 (PC2) that prevented this protein from properly trafficking to cilia.  +1  


submitted by lnsetick(33),

How are you able to tell that the CT slice is not at the level of duodenum?

zelderonmorningstar  I think the small intestine narrows as you go along, so jejunum would most likely intuss into the duodenum. +  
yotsubato  Duodenum is fixed to the retroperitoneal wall, and also has lots of named vessels attached to it, along with the pancreaticobiliary duct and ampulla. It cant really intussuscept. +  
gh889  You should also know that the duodenum is almost purely on the right side of the body +4  


submitted by seagull(413),

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. +4  
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. +2  


submitted by just_1more(1),

I got that it needed to be a potassium sparing diuretic. Is there a reason it cannot be an aldosterone antagonist? I chose blocks basolateral K+ channels as these decrease the basolateral K+/Na+/ATPase because the wording of the correct answer did not make sense to me -- assuming they were going for an ENaC blocker (and that decreased luminal permeability indicates that Na+ would be remaining in the lumen, not remaining in the principal cell as I originally thought).

luckeroo  I think the reason it’s a potassium-sparing diuretic rather than an aldosterone antagonist has less to do with why the aldosterone antagonist cannot be used and more to do with the fact that a potassium-sparing diuretic would be more of a “first-line” adjunctive diuretic treatment. +1  
luckeroo  As for the answer choice, potassium sparing diuretics achieve their overall anti-aldosterone effect by competitively inhibiting aldosterone receptors on the interstitial side (decreasing the Na/K-ATPase effect of shunting Na into the blood), thereby decreasing the gradient for sodium to enter the cell from the luminal aspect, blocking ENaC. +1  
yotsubato  There is no such thing as "Basolateral K Channel" there is only basolateral Sodium Potassium Pumps which are controlled by aldosterone. FA pg 573 +5  
nwinkelmann  @yotsubato LOL.... why didn't I think of it that what?! (by the way, that LOL is for me). The only basolateral K channel is the nephron (based on the first aid picture) is in the thick ascending limb of the loop of henle. +  
hello  Spironolactone and eplerenone are potassium-sparing diurectics that inhibit the Na/K ATPase, so I'm not sure what @luckeroo is referring to. Spironolactone and aplerenone are both ALDO antagonists. Na/K ATPase is found on the basolateral membrane. None of the answer choices fit with this. Amiloride and triamterene are also potassium-sparing diuretics; their mechanism is to block ENaC channels on the luminal membrane, this is choice "B." +1  


submitted by joker4eva76(10),

Could also use the patient's age to make the differential. Age is a risk factor related to breast cancer (common in post-menopausal women, unless there's a history of breast cancer in the family).

Fibrocystic changes and fibroadenomas are usually common in premenopausal women.

No discharge noted, so it's not an intraductal papilloma.

yotsubato  Intraductal papillomas are also under the areola +1  


submitted by iviax94(5),

I figured they were trying to get at the life expectancy of an RBC, but wouldn’t supplemental O2 technically replace the CO bound to RBCs? FA even mentions that CO binds competitively to RBCs, and isn’t that the whole point of giving hyperbaric/100% O2?

nc1992  First aid has a lot of errors +  
yotsubato  Thats not an error though. Thats the actual reason behind giving hyperbartic O2 for CO poisoning... +  


submitted by hipster_do(2),

I think this was referring to reverse transcriptase, and the only two viruses I knew that used them were HepB and HIV/retroviruses. Given the context I picked HIV/retroviruses which are SS + sense. This was kind of weird though since the virus was “new” ... but I’ve learned that “new” usually means very little on these tests.

yotsubato  "New" means made up fantasyland virus +1  
yotsubato  Also Hep B is a ssDNA virus that goes to RNA, then is reverse transcribed to dsDNA +  


submitted by hipster_do(2),

I think this was referring to reverse transcriptase, and the only two viruses I knew that used them were HepB and HIV/retroviruses. Given the context I picked HIV/retroviruses which are SS + sense. This was kind of weird though since the virus was “new” ... but I’ve learned that “new” usually means very little on these tests.

yotsubato  "New" means made up fantasyland virus +1  
yotsubato  Also Hep B is a ssDNA virus that goes to RNA, then is reverse transcribed to dsDNA +  


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. +2  
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  
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?? +2  
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. +  


submitted by marbledoc(0),

Why would you ask the patient to identify the pros and cons? I don’t get the approach here!

someduck3  There was a question about this in Uworld. for *stubborn* patients who are "not ready to quit" just yet you use the motivational approach. The technique acronym is OARS: Open ended questions, Affirmation, Reflect, Summarize. +2  
yotsubato  Additionally the guy himself says "I know smoking is bad for me" Like he knows its bad, he doesnt care, but give him nicotine replacement and maybe he'll quit... +1  
usmleuser007  I didn't think nicotine replacement was a good answer choice b/c if he isn't ready to quit then why would he agree to use alternatives. +  
usmleuser007  People who smoke and are addicted like the feel of the cigs and environmental ques. Using replacements would be more challenging. The second best answer choice would have been Rx. +  
titanesxvi  why not detail the long-therm health effects of smoking? +  
seracen  @ titanesxvi: I assume because they always like the most "open ended" response. If you start detailing the long term effects, the patient might interpret that as attempting to convince, and might resist or feel pressured. By having the patient elucidate what they consider pros and cons, you allow it to be an open discussion. +  


submitted by seagull(413),

out of curiosity, how may people knew this? (dont be shy to say you did or didnt?)

My poverty education didn't ingrain this in me.

johnthurtjr  I did not +  
nlkrueger  i did not lol +  
ht3  you're definitely not alone lol +  
yotsubato  no idea +  
yotsubato  And its not in FA, so fuck it IMO +  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +4  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +2  
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +  
jaxx  Not a clue. This was so random. +  
wolvarien  I did not +  
ls3076  no way +  
hyperfukus  no clue +  
mkreamy  this made me feel a lot better. also, no fucking clue +  


submitted by seagull(413),

out of curiosity, how may people knew this? (dont be shy to say you did or didnt?)

My poverty education didn't ingrain this in me.

johnthurtjr  I did not +  
nlkrueger  i did not lol +  
ht3  you're definitely not alone lol +  
yotsubato  no idea +  
yotsubato  And its not in FA, so fuck it IMO +  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +4  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +2  
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +  
jaxx  Not a clue. This was so random. +  
wolvarien  I did not +  
ls3076  no way +  
hyperfukus  no clue +  
mkreamy  this made me feel a lot better. also, no fucking clue +  


Tamoxifen has to be metabolized via first pass metabolism to an active metabolite (endoxifen). The patient has decreased concentrations of the metabolized product indicating that the patient’s pair of cytochrome P450 alleles aren’t metabolizing tamoxifen correctly. The question is asking what the chances are the sister has the same genotype, which would be 25% --> 1/2 * 1/2 = 1/4

medschul  How do we know the parents are not homozygous +1  
yotsubato  Chances are they are not unless they had or are incestuous +  


submitted by joha961(13),

Maintenance dose = (Css * CL * t) / F

... where t is elapsed time between doses (not relevant here since it’s continuous infusion) and F is bioavailability (which is 100% or 1.0 here because it’s given IV).

​Contrast with loading dose:

(Css * Vd) / F

... where Vd is volume of distribution.

yotsubato  So do we just have to memorize this... +1  
gh889  yep +1  


submitted by haliburton(82),

kaposi sarcoma. HHV8. violaceous (purple) lesions. advanced HIV CD4 < 200 (WHO).

yotsubato  Yeah thats the easy part. But the histology is whats hard +  


I got it down to bleomycin & chlorambucil and went with chlorambucil (sounded like “bu”sulfan ... lol) because I thought bleomycin was for testicular cancer/Hodgkins lymphoma. I later found out that chlorambucil is actually a preferred treatment for CLL! Is it because chlorambucil causes severe immunosuppression? So you wouldn’t be giving it to a 72 yo man in the first place?

yotsubato  Bleomycin is the big boy of cancer treatment. I've never heard of chlorambucil and its not in FA. +  


submitted by yotsubato(255),

The patient has Neutropenic fever. GSCF will restore his neutrophils.

yotsubato  His RBC and platelets are low, but at acceptable levels for someone undergoing chemotherapy. +1  


submitted by liltr(11),

I choose MVP too, but this patient’s main symptom is cough only during exercise. This is more indicative of exercised associated asthma. You could see shortness of breath in MVP during exercise, but choosing MVP leaves the cough unaccounted for.

.ooo.   I agree! Also, At the end of the stem, the question is which of the following best explain the patients symptoms? Not physical exam findings. Since this patient is coming in with a chief complaint of SOB while playing sports exercise induced asthma is the best choice. Hopefully that helps. +6  
uslme123  I mean... couldn't increased BP during exercise worsen his MVP and give him SOB? +  
uslme123  (by causing slight regurg) +1  
yotsubato  "Lungs are clear to auscultation" +3  
sahusema  But wouldn't choosing exercise-induced asthma leave the murmur unaccounted for? +  
cienfuegos  I incorrectly chose malingering and am wondering if the fact that he presented (although it doesn't state who brought him in/confirmed his symptoms while exercising) makes this less likely despite the fact that he clearly states "I don't want to play anymore" which could be interpreted as a secondary gain? Also, regarding the MVP, I'm wondering if the fact that these are usually benign should have factored into our decision to rule it out? Thoughts? +1  
cienfuegos  Just noticed that he has FHx, game changer. +  
kimcharito  clear lungs, they try to say no cardiogenic Pulm. edema, means is not due to MVP shortness of breath while doing sports and no shortness at rest makes me to think more asthma induced by exercise) +  


submitted by lnsetick(33),

I just remember Sattar saying MVP tends to be asymptomatic. Also, I think the kid complained specifically of coughing, and that made me really lean away from MVP.

yo  he also has a family history of asthma. that's shit is genetic. +1 for asthma. +1  
yotsubato  Cheif complaint is SOB during exercise with coughing. Mitral valve prolapse is not going to do that so I picked asthma as well. +1  


submitted by hungrybox(216),

other answers:

inhibition of H2 receptors: (for GERD) prevent gastric acid secretion (cimetidine,

inhibition of phosphodiesterases (PDE):

  • theophylline (asthma) inhibits cAMP PDE
  • -nafils (dick pills) for ED inhibit cGMP PDE

β2 agonists: (for asthma) cause bronchodilation

  • albuterol (short acting - A for Acute)
  • salmeterol, formoterol (long acting - prophylaxis)

(idk lymphocyte membrane stabilization)

hungrybox  H2 blockers are the -tidines +1  
yotsubato  > dickpills lol +6  
temmy  hungrybox, you are a life saver +1  
cienfuegos  Via FA: take H2 before you dine, think "table for 2" to remember H2 +  


submitted by haliburton(82),

from AAFP ED of mixed organic and psychogenic origin is common. Psychogenic causes are more likely when the patient has normal erections with masturbation or when nocturnal penile tumescence is normal.

yotsubato  Couldnt a psychogenic cause reduce libido? +  
home_run_ball  "Testosterone concentration is within the reference range" and the fact that he has no difficulty masturbating = normal libido. Low testosterone would contribute to low libido And if he had low libido he would have difficulty masturbating +5  
home_run_ball  whoops meant to comment on the other comment +  


submitted by taway(7),

This question is phrased strangely, but it's essentially asking "what would happen if this woman's hypothyroidism became uncontrolled over the course of her pregnancy?"

currently her TSH is good --> well-controlled hypothryoidism HYPOTHETICAL high TSH --> her hypothyroidism must NOT be well-controlled (due to disruption of the T3/T4/TRH/TSH endocrine axis)

So, now that we understand that the question is asking "what would happen if her hypothyroidism was uncontrolled?"

Answer: cretinism

I think that this question is phrased atrociously, but far be it from me to criticize the USMLE licensing board...

yotsubato  I think that this question is phrased atrociously, Just like the rest of the NBME +2  


Autoimmune thyroiditis (aka Hashimoto) + pregnant--> Think about possibility of fetal hypothyroidism due to antibody mediated maternal hypothyroidism. Leads to Cretinism. Findings in infant are the 6'P (Pot belly, Pale, Puffy face, Protruding umbilicus, Protuberant tongue, and Poor Brain development.

neonem  I don't understand the last part of this question stem though... if the mother's TSH *increases* during pregnancy? Wouldn't this further increase her (and/or the fetus's) production of T4 and thus counteract the hypothyroidism? +  
poojaym  @neonem no. Autoimmune hypothyroidism is a destruction of the thyroid gland, and a decrease in production of T3/T4. An increase in TSH means that there is not enough T3/T4 to inhibit TRH, and so TSH is being released to stimulate the thyroid gland. +3  
arezpr  TSH, T3, T4 and thyroglobulin cannot cross the placental barrier. +  
chamaleo  @arezpr although those hormones can't cross, the autoantibodies from Hashimoto's can +  
yotsubato  The baby has its own TSH though +  
sbryant6  TSH comes from the pituitary, and act on the thyroid. Autoantibodies attack the thyroid, so TSH doesn't work. +  
kimcharito  no goiter then? +  


yotsubato  How is that NOT posterior to middle concha? bad question +2  
sympathetikey  @yotsubato - That would have been if it was the spehnoid sinus (I got it wrong too btw) +  
niboonsh  this is a good video if u need a visual https://www.youtube.com/watch?v=mf7rY1VNy70 +1  
sahusema  Sphenoethmoidal RECESS not sphenoethmoidal SINUS +  


submitted by aishu007(1),

Elevations in body temperature occur when concentrations of prostaglandin E(2) (PGE(2)) increase within certain areas of the brain.These elevations alter the firing rate of neurons that control thermoregulation in the hypothalamus.. It is now clear that most antipyretics work by inhibiting the enzyme cyclooxygenase and reducing the levels of PGE(2) within the hypothalamus.

https://www.ncbi.nlm.nih.gov/pubmed/11566461

yotsubato  Ugh, again a concept NOT in UFAP anywhere. Bites me in the ass every time +3  
epr94  pg213 FA2019 +2  


submitted by notadoctor(56),

This question was asking about the adverse effects of proton pump inhibitors especially given previous kidney issues. PPIs decrease serum Mg and serum Ca absorption and can increase the risk of fracture (especially in the elderly).

yotsubato  PPI therapy *begins* the day she presents. She has not taken PPI before +4  
notadoctor  You're right, I missed that! +  
naught  MEN 1 is pituitary (monitor cortisol), pancreas, parathyroid (monitor calcium) but is not the ask of this question. +  


submitted by nosancuck(34),

Yo dis B got NO INTERNAL FEMALE ORGANS

Why dat!???

We be lookin at someone with an SRY from dere Y chromie! Dey be a Y chromie Homie so they be makin some Testis Determinin Factor which I be sure makes some nice lil ANTI MULLERIAN FACTOR so dey aint got that Female Internal Tract u know what i be sayin

And since wimminz is da DEFAULT they stil be gettin dose pussy lips and breastes

meningitis  The above explanation is correct (disregarding the hard to read and unprofessional dialect) but just in case anyone was wondering: chromatin-negative= Just a quick way of knowing it was a boy. The term applies to the nuclei of cells in normal males as well as those in individuals with certain chromosomal abnormalities +11  
yotsubato  Turner syndrome patients are also chromatin negative as well though.... +3  
sympathetikey  I didn't know a complication post-meningitis was lack of humor. +2  
sympathetikey  Ah, didn't read the last line. Yeah, that is taking it a bit far +1  
niboonsh  yall are haters. this is the first explanation that has ever made sense to me +2  
arkmoses  https://www.youtube.com/watch?v=yuXL-3eoB-o&t=77s Interesting syndrome watching this helped me to put it into real life perspective, interesting points they have no pubic hair/body hair, they apparently also dont smell, and breast size is usually increased... +  
whoissaad  How does chormatin-negative indicate a normal cell? Isn't chormatin just condensed DNA? +1  
cienfuegos  According to this paper most individuals with Turner Syndrome are chromatin negative: "One of the initial laboratory procedures used to confirm or rule out this diagnosis involves a sex chromatin determination from a buccal smear. Cells from the lining of the mouth are stained for the presence or absence of X-chromatin or Barr bodies, which represent a portion of an inactivated X chromosome. The typical Turner’s syndrome patient, who has 45 chromosomes and only one sex chromosome (an X), has no Barr bodies and is, therefore, X-chromatin negative. This abnormal X-chromatin negative finding in the majority of Turner’s syndrome females is similar to the result found in a normal male, who also has only one X chromosome, and differs from the X-chromatin positive condition observed in the normal female, who has two X chromosomes. Occasionally, the patient with features of Turner’s syndrome is found to be X-chromatin positive." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6233891/ +  
hyperfukus  i really hate haters this is awesome! +  


submitted by haliburton(82),

FA 2017: Chronic hypoxic pulmonary vasoconstriction results in pulmonary hypertension and RVH.

yotsubato  Yeah but in a chronic case this guy would produce more RBC and not be hypoxic anymore. +1  


submitted by hayayah(394),

Cysteine-cysteine chemokine receptor 5 (CCR5) is a protein found on the surface of CD4 cells.

yotsubato  Note, this is NOT in FA +  
sbryant6  It is in UWorld. +  


submitted by cantaloupe5(35),

This one was tricky but I think you could’ve done this one without knowledge of NMDA receptors. Stem told you that glutamate activates both non-NMDA and NMDA receptors but it activated only non-NMDA receptors in the early phase. That means NMDA receptors activate after non-NMDA receptors. That means something was delaying NMDA receptor activating and the only answer that made sense as the Mg inhibiting NMDA at resting potential. Once the cell is depolarized by non-NMDA receptors, NMDA receptors can be activated.

hungrybox  I forgot/didn't know this factoid and narrowed it to the correct answer and a wrong answer. Guess which one I chose? +4  
yotsubato  >That means something was delaying NMDA receptor activating and the only answer that made sense as the Mg inhibiting NMDA at resting potential. What makes the fasting gating kinetics choice incorrect then? +2  
imgdoc  NMDA receptors are both voltage gated and ligand gated channels. Glutamate and aspartate are endogenous ligands for this receptor. Binding of one of the ligands is required to open the channel thus it exhibits characteristics of a ligand channel. If Em (membrane potential) is more negative than -70 mV, binding of the ligand does NOT open the channel (Mg2+ block on the NMDA receptor). IF Em is less negative than -70 mV binding of the ligand opens the channel (even though no Mg2+ block at this Em, channel will not open without ligand binding. Out of the answer choices only NMDA receptors blocked by Mg2+ makes sense. Hope this helps. +1  
divya  sweet explanation imgdoc +  


submitted by tinydoc(53),

Type 1 Familial Dyslipidemia (pg. 94 FA 19 )

increased TG ---> pancreatitis Eruptice / pruritis Xanthomas and HSM

Can be caused by Lipoprotien lipase or Apoprotien CII deficiency

they said that LPL is fine so its APO CII

Heparin seperates LPL from Herparin Sulfate Moeity on Vasc Endothelium allowing us to test its function in the lab.

I got it wrong too - Stupid Rote memorization recall Question.

masonkingcobra  I think you need to know that ApoCII activates LPL not necessarily know the disease +2  
yotsubato  Knowing the disease makes it easier to remember the details though +  


submitted by priapism(3),

Per First Aid: antibodies against ABO blood types tend to be IgM or IgG, which is why the answer is IgG + complement and not IgA + complement

yotsubato  IgA also has no role in any hypersensitivity reaction +1  
divya  hi. where is this given in first aid? +  


euthyroid sick syndrome is sometimes called "low T3 syndrome." Also you know that the patient is euthyroid because her T4 and TSH are within the reference range. She is sick.

yotsubato  This is not in FA btw. +3  
niboonsh  https://www.ncbi.nlm.nih.gov/books/NBK482219/ probably caused by her recurrent pneumonia +1  
eacv  I though in this one as a sick sinus syndrome hahaha in UW. +  


submitted by aesalmon(35),

I went back and watched this section on pathoma after getting the question wrong - Dr. Sattar says that Chondromas and Chondrosarcomas arise in the MEDULLA, and not the cortex. However the question stem states that there is "thickening of the diaphysis and disruption of the CORTEX with focal area of increased calcification", ???

yotsubato  It arises in the medulla and *passes* through the cortex because its invasive and malignant. +1  


submitted by hungrybox(216),

Following a stroke, this patient had weakness of her left face and body, so the stroke must have affected the right side of her brain. B was the only choice on the right side of her brain.

Still confused? Read on...

The voluntary motor fibers (corticospinal tract) descend from the primary motor cortex, cross (decussate) at the medullary pyramids, and then synapse at the anterior motor horn of the spinal level.

Because of decussation at the medullary pyramids, you should make a note of where any stroke occurs. Is it above the medullary pyramids? Then it will affect the side opposite the stroke (contralateral). Is it below the medullary pyramids? Then it will affect the same side as the stroke (ipsilateral).

hungrybox  Woops, E is also on the right side (also remember that imaging is looking up at someone, feet first). But a cerebellar stroke would have caused ataxia. +  
mnemonia  Very nice!! +  
usmleuser007  What gets me is that they mention that Left 2/3 of face is affected. This should indicate a non cortical innervation as most of the cranial nuclei are bilaterally innervated from the left and right hemisphere. If left 2/3 of the face is affected then it should also mean that the lesion is after CN5 nuclei. +1  
yotsubato  @hungrybox Thats not the cerebellum thats the occipital lobe. You would see leftsided homonymous hemianopsia in that lesion +  
mrsmac  To my mind, it is simpler to consider the question first in terms of blood supply distribution. Left sided hemiparesis and weakness of lower 2/3 of face are both indicative of a MCA rupture/stroke (First Aid 2018 pg. 498). Furthermore, since the injury has affected motor function we would be considering the descending tract i.e. lateral corticospinal which courses through the ipsilateral posterior limb of the internal capsule then decussates in the caudal medulla. +1  
mrsmac  You're considering the wrong CN here. CN5 motor function involves muscles of mastication and lower 2/3 of tongue. The nerve in question in this case is CN7/VII Facial n. CNVII UMN injury affects the contralateral side, whereas LMN injury affects ipsilateral (First Aid 2018 pg. 516). i.e. before and after the nucleus in pons respectively. I hope this helps. +1  
nala_ula  Spastic means UMN lesion, since they also don't specify if there is arm or leg weakness, I didn't assume it was MCA stroke. I went with the reasoning that for there to be spastic hemiparesis, there must be damaged to the UMNs and therefore the internal capsule is where these tracts are. +  
champagnesupernova3  Omg this whole discussion is confusing. Internal capsule contains ALL corticospinal and corticobulbar fibers = contralateral hemiparesis and UMN facial lesion +  


submitted by sympathetikey(301),

Choice A. would have been correct if this patient was immunocompromised. Per First Aid, "If CD4 <100, Bartonella...Findings: Neutrophilic Inflammation.

However, as this patient has a competent immune system, buzz words are stellate necrotizing granulomas.

yotsubato  Everyones choice A is different. +  
sugaplum  they mean- Diffuse neutrophil infiltration +  
macrohphage95  what does stellate necrotizng granuloma means ? +  


submitted by laminin(6),

can someone explain why it says he has an 'intact' PTH concentration...is it to let us know that the PTH concentration is a result of pathology? and what's his dx? thanks!

yotsubato  I swear they make up some of this stuff. Like whats up with the thirst, urination, and peptic ulcer diseases. +2  
redvelvet  hypercalcemia can cause nephrogenic diabetes inspidus; so thirst, urination. hypercalcemia can also cause peptic ulcer disease. His symptoms are all about hypercalcemia due to hyperparathyroidism. +1  
namira  "Hypercalcemia can cause renal dysfunction such as nephrogenic diabetes insipidus (NDI), but the mechanisms underlying hypercalcemia-induced NDI are not well understood." https://www.kidney-international.org/article/S0085-2538(16)30704-9/fulltext +  


submitted by killme(3),

The concept being tested is "what does PTH do that leads to hypercalcemia" https://i.ibb.co/sKPdVj3/image.png

yotsubato  ugh, bullshit. I was trying to figure out an actual disease process here. +1  
rio19111  its primary hyperparathyroidism caused by parathyroid adenoma. addition of the peptic ulcer suggest Zollinger ---> MEN1 but none of that is imp because that's not what they are asking. All they are asking for is the function of PTH. +1  


submitted by xxabi(90),

Bronchogenic carcinoma = lung cancer

That being said, lung adenocarcinoma specifically is associated with hypertrophic osteoarthropathy, which is a paraneoplastic syndrome characterized by digital clubbing, arthralgia, joint effusions, and periostosis of tubular bones

luke.10  why not systemic scleroderma since i did this question wrong and i chose systemic sclerosis scleroderma , can someone explain that ? +1  
kernicterusthefrog  My best guess answer to that @luke.10 is that: a) there's no mention of any skin involvement (which there would be in order to be scleroderma) b) Scleroderma shows pitting in the nails, not clubbing c) There would be collagen deposition with fibrosis, not hypertrophy of the bone at joints Saying that, I also got this wrong! (but put RA...) so I'm not claiming to "get this" Hope my thought process helps, though! +1  
yotsubato  This is in FA 2019 page 229 +2  
larascon  I agree with @kernicterusthefrog on this one, Bronchogenic carcinoma = lung cancer. Squamous cell carcinoma gives you hypercalcemia (new bone formation; maybe?), commonly found in SMOKERS ... +2  


submitted by celeste(32),

This sounds like Fanconi syndrome. The proximal tubular epithelial cells have a hard time reabsorbing filtrate, so you'll see a loss of phosphate, amino acids, bicarbonate, and glucose.

medschul  Wouldn't Fanconi syndrome also cause hypokalemia though? +2  
yotsubato  Especially considering the fact that the DCT will be working in overdrive to compensate for lost solutes??? +  
nala_ula  This question did not make sense to me at all. I knew it was Fanconi syndrome yet didn't select the obvious answer because it said "follow up examination 1 week after diagnosis". I thought it would already be in treatment... I searched (now) and it says that treatment is basically replenishing was is lost in the urine. So definitely the wording is like wtf to me +  
sugaplum  I was thinking since it affected the PCT that Na resorption would be affected as well? But I guess the other segments will pick up the slack? +  


submitted by beeip(62),

Thought this would be something regarding "bariatric surgery," but nope, just "no starchy foods, because you're pre-diabetic."

hello  Yep, seems that because the patient has prediabetes, he should avoid eating excessive starchy foods. +  
yotsubato  such a BS question IMO +3  
yotsubato  such a BS question IMO +  
breis  I put nuts thinking of "fats" and that with a bariatric surgery they may have problems with absorption.. +2  
teetime  This isn't right because the bariatric surgery will cure the prediabetes. It's dumping. +  
dr_jan_itor  Why should he avoid eating excessive starchy foods? To avoid gaining weight? It doesn't matter what macronutrients he eats if they are calorie controlled. +  


submitted by beeip(62),

Thought this would be something regarding "bariatric surgery," but nope, just "no starchy foods, because you're pre-diabetic."

hello  Yep, seems that because the patient has prediabetes, he should avoid eating excessive starchy foods. +  
yotsubato  such a BS question IMO +3  
yotsubato  such a BS question IMO +  
breis  I put nuts thinking of "fats" and that with a bariatric surgery they may have problems with absorption.. +2  
teetime  This isn't right because the bariatric surgery will cure the prediabetes. It's dumping. +  
dr_jan_itor  Why should he avoid eating excessive starchy foods? To avoid gaining weight? It doesn't matter what macronutrients he eats if they are calorie controlled. +  


submitted by neonem(251),

Shigella causes an inflammatory diarrhea; it produces a toxin and can invade tissue directly. In addition, it is resistant to acid, so it has a characteristically low infective dose (~10 organisms), which facilitates its fecal-oral (person-to-person) spread especially in settings where hygiene may be compromised, such as in daycare or institutional housing. It can be differentiated from E. Coli (EHEC) because E Coli doesn't have as much person-to-person spread and only causes GI damage by the shiga-like toxin, not direct invasion. Therefore, EHEC wouldn't facilitate as strong of a neutrophilic response.

yotsubato  I assumed all the kids in the daycare had the same lunch, thus got food poisoning, thus all got EHEC. +  


In psychogenic polydipsia, serum sodium is low, and after water deprivation test, urine osmolality is increased. Urine osmolality does not increase with vasopressin injection

In nephrogenic diabetes insipidus, serum sodium is high and there is no change/mild increase in urine osmolality after water deprivation

yotsubato  This patient does not undergo a water deprivation test +5  
niboonsh  Compulsive water drinking or psychogenic polydipsia is now increasingly seen in psychiatric populations. Effects of increased water intake can lead to hyponatremia causing symptoms of nausea, vomiting, seizures, delirium and can even be life threatening if not recognized and managed early. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5579464/ +2  
missi19998  Just wondering why it in not resistance to ADH action of vasopressin +  
amarousis  because he would be hypernatremic with no ADH. can't resorb any water +1  
minhphuongpnt07  low osm/urine, low os/plasma => psychogenic polydipsia +  


submitted by strugglebus(69),

Nowhere have I been able to find why the hell this is a thing.

yotsubato  Its not in FA, Sketchy, or Pathoma, or U world. I knew it wasnt cancer because its bilateral. And Diabetes made no sense to me. So I just threw down Drug effect and walked away. +1  
breis  same^^^ +  
feliperamirez  The only possible explanation I think is that she was under a K sparing diuretic, such as spironolactone (which would lead to gynecomastia). +  


submitted by hayayah(394),

Renovascular disease is the most common cause of 2° HTN in adults. Can be d/t ischemia from renal stenosis or microvascular disease. Can hear renal bruits lateral to umbilicus.

Main causes of renal artery stenosis:

  • Atherosclerotic plaques—proximal 1/3rd of renal artery, usually in older males, smokers.

  • Fibromuscular dysplasia—distal 2/3rd of renal artery or segmental branches, usually young or middle-aged females.

Lab values based off:

  1. Stenosis decreases blood flow to glomerulus.
  2. Juxtaglomerular apparatus (JGA) responds by secreting renin, which converts angiotensinogen to angiotensin I.
  3. Angiotensin I is converted to angiotensin II (ATII) by angiotensin converting enzyme (ACE --in lungs)
  4. ATII raises blood pressure by (1) contracting arteriolar smooth muscle, increasing total peripheral resistance and (2) promoting adrenal release of aldosterone, which increases reabsorption of sodium (where Na+ goes H2O will follow) in the distal convoluted tubule (expanding plasma volume). Can lead to hypokalemia (seen in the labs for this question)
  5. Leads to HTN with increased plasma renin and unilateral atrophy (due to low blood flow) of the affected kidney; neither feature is seen in primary hypertension
uslme123  So both causes would result in increased aldo and MR is the only way to differentiate the two? +1  
hello  @USMLE123 I think both are causes of renal artery stenosis and that could be seen via MR angiography. It is asking what could help DIAGNOSE this patient -- and her most likely cause of the findings is fibromuscular dysplasia. So, yes, MR angiography would look different for the 2 different etiologies and thus could can be used to differentiate the two from one another. However, epidemiologically, we are looking to diagnose her with the suspected most probable cause. +1  
yotsubato  @USLME123 I think measuring Aldosterone is an incorrect answer because you already know its increased due to low K. Knowing she has high Aldosterone wouldnt provide you evidence for a final diagnosis. +2  


submitted by hayayah(394),

Capitate and lunate are in the center of the palm. Capitate is not an option, so lunate is the answer.

Dislocation of lunate may cause acute carpal tunnel syndrome.

yotsubato  Lunate is the only carpal bone that is frequently dislocated. Scaphoid is frequently fractured. Hook of hamate is also frequently fractured. +1  
redvelvet  and also point tenderness in the anatomical snuffbox may indicate a scaphoid fracture. +1  


submitted by strugglebus(69),

OK, so if I remember correctly this is the one that shows the inheritance pattern. mitochondrial is also passed by the mother; however, it can have variable expressivity and incomplete penetrance, which is why some members were not affected.

hyoscyamine  Also, question said there was a deficiency in NADH dehydrogenase activity which is another fancy way of saying complex I in the mitochondria. +4  
yotsubato  That unaffected male really threw me off... : ( +4  
charcot_bouchard  It was pure MELAS description. the unaffected male threw me off +2  


submitted by hayayah(394),

Inguinal hernias are usually reducible, femoral hernias are not.

This is an indirect inguinal hernia. It enters internal inguinal ring lateral to inferior epigastric vessels and is superior to the inguinal ligament.

Caused by failure of processus vaginalis to close (can form hydrocele). May be noticed in infants or discovered in adulthood. Much more common in males.

yotsubato  Heres a good picture to help with the concept. https://www.google.com/url?sa=i&source=images&cd=&ved=2ahUKEwjVkIi0yN7iAhWLjqQKHbeXCTUQjRx6BAgBEAU&url=https%3A%2F%2Fwww.herniaclinic.co.nz%2Finformation%2Ftypes-of-hernias%2F&psig=AOvVaw2BzGtQLvSmUN8ymhdvETG5&ust=1560244112252834 +2  
sbryant6  Note that direct inguinal hernias typically happen in older adults. This question presents a younger baby, so it is more like to be indirect. +1  


submitted by hayayah(394),

Case of arteriolosclerosis.

Hyperplastic arteriolosclerosis involves thickening of vessel wall by hyperplasia of smooth muscle ('onion-skin appearance')

  • Consequence of malignant hypertension (>180/120 w/ acute end-organ damage)
  • Results in reduced vessel caliber with end-organ ischemia
  • May lead to fibrinoid necrosis of the vessel wall with hemorrhage; classically causes acute renal failure (ARF) with a characteristic 'flea-bitten' appearance
masonkingcobra  From Robbin's: Fibromuscular dysplasia is a focal irregular thickening of the walls of medium-sized and large muscular arteries due to a combination of medial and intimal hyperplasia and fibrosis. It can manifest at any age but occurs most frequently in young women. The focal wall thickening results in luminal stenosis or can be associated with abnormal vessel spasm that reduces vascular flow; in the renal arteries, it can lead to renovascular hypertension. Between the focal segments of thickened wall, the artery often also exhibits medial attenuation; vascular outpouchings can develop in these portions of the vessel and sometimes rupture. +  
asapdoc  I thought this was a weirdly worded answer. I immediately ( stupidly) crossed of fibromuscular dysplasia since it wasnt a younger women =/ +4  
uslme123  I was thinking malignant nephrosclerosis ... but I guess you'd get hyperplastic arteries first -_- +  
hello  The answer choice is fibromuscular HYPERplasia - I think this is different from fibromuscular DYSplasia (seen in young women); +7  
yotsubato  hello is right. Fibromuscular hyperplasia is thickening of the muscular layer of the arteriole in response to chronic hypertension (as the question stem implies) +2  
smc213  Fibromuscular Hyperplasia vs Dysplasia...... are supposedly the SAME thing with multiple names. Fibromuscular dysplasia, also known as fibromuscular hyperplasia, medial hyperplasia, or arterial dysplasia, is a relatively uncommon multifocal arterial disease of unknown cause, characterized by nonatherosclerotic abnormalities involving the smooth muscle, fibrous and elastic tissue, of small- to medium-sized arterial walls. http://www.medlink.com/article/fibromuscular_dysplasia +1  
smc213  *sorry I had to post this because it was confusing!!!*Fibromuscular dysplasia is most common in women between the ages of 40 of and 60, but the condition can also occur in children and the elderly. The majority (more than 90%) of patients with FMD are women. However, men can also have FMD, and those who do have a higher risk of complications such as aneurysms (bulging) or dissections (tears) in the arteries. https://my.clevelandclinic.org/health/diseases/17001-fibromuscular-dysplasia-fmd +1  
momina_amjad  These questions are driving me crazy- fibromuscular dysplasia/hyperplasia is the same thing, and it is NOT this presentation and it doesn't refer to arteriolosclerosis seen in malignant HTN! Is the HTN a cause, or a consequence? I read it as being the cause (uncontrolled HTN for many years) If it was the consequence, the presentation is still not classical! -_- +1  
charcot_bouchard  Poor controlled HTN is the cause here +  
charcot_bouchard  Also guys if u take it as Fibromuscular dysplasia resulting in RAS none of the answer choice matches +