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Additionally, axillary nerve supplies sensory innervation for lateral aspect of shoulder.
Radial does lateral elbow and musculocutaneous does lateral forearm.
The NBME is full of shit... they also say there's "no trick questions"
I went with aortic because it looks like the valve has three cusps, while the mitral valve should only have two. Incorrect logic?
Yes the superior part supplied by superior thyroid gland which is a branch of external carotid branch.
Superior thyroid artery does supply some blood to the parathyroids through anastomoses but the main vascular supply is from the inferior thyroid artery.
Vibrio species are mostly non-lactose fermenters except Vibrio vulnificus
I thought V.vulnificus could only cause food poisoning from eating shellfish; turns out contact with wound infections causes it too (hence why walking barefoot on the beach is a risk factor)
I think they threw this one in here for all the Sketchy loyalists. Gotta keep us on our feet.
Question stem also implies that the patient has been driving already. "has not had any collisions while driving his personal motor vehicle".
Also 10 years is a really long time. Just didn't seem like a good answer
Went with hepatitis because of his recent surgery. Seen problems like this before where recent surgery means they were given inhaled anesthetic that can cause hepatotoxicity/hepatitis. That, along with the elevated AST/ALT and unconjugated bilirubinemia (signifying liver losing its ability to conjugate bilirubin due to inflammation) made me pick hepatitis. Why is that wrong?
@pg32 AST/ALT are only slightly elevated. The patient also is not particularly symptomatic. He's really not that sick. Hepatoxicity is also most associated with halothane which is no longer used in the US. It would be a different story if the patient had surgery done in a different country (as is common in Uworld questions on this)
I don't know why NBME uses ALT/AST reference ranges from 8-20 u/L when the reference ranges for uworld are 8-40 u/L. So maybe his liver enzymes aren't really elevated since they're below 40
Can someone refute 'surgical trauma'?
Appendix is pretty far anatomically from the bile ducts. Also damage to bile ducts should cause direct hyperbilirubinemia since there's no problem with conjugation versus Gilbert syndrome which causes impairment of UGT
due to pancreatitis
@neovanilla Type 1-hyperchylomicronemia has increased risk of pancreatitis
I don't understand why this isn't hypertriglyceridemia because this also causes acute pancreatitis. Maybe because overproduction of VLDL isn't an answer?
@rainlad Protein C deficiency doesn't cause elevated PT and aPTT. I believe they're both normal and assays for the disease measure protein C activity.
Protein C is an anti-coagulant, so if you lack factor C, then you have MORE clotting factors. This means that the PT and PTT would not be prolonged.
Also another fun fact. Most people in France are infected by Toxo (like 80%) because of how they eat meat. (Very rare)
To add on might be TMI but most people have Toxo but are asymptomatic because its in its latent form as a pseudocyst and its not untill you are immunocompromised that it strikes
This patient also probably got toxo in Brazil
JFYI people in Brazil love to eat rare meat at barbecues
so just to clarify - it's the "symptom-free for 3 months" that rules out thrombosis?
It's moreso that at rest there's no changes, but during exercise there is. Like the pathophys of stable angina.
I think it's more because of the 2-month history of PROGRESSIVE angina sx with exertion. This points to a chronic process rather than an acute event.
Drug-eluting stents prevent re-stenosis (rather than thrombosis) by releasing sirolimus which by blocking cell proliferation.
Why would the second part of that be correct when there is not mention of a DNR?
DNI and DNR are different right? This patient had a DNI. Why would we assume it to be DNR too?
DNI and DNR are indeed different. But it is not the case here. The patient needs to be extubated means she did not sign a DNI or DNR in the first place. I assume her living will is more like terminate supporting treatment in a vegetative state. So there is no need to do resuscitation anyways. But I agree this is not a good question.
"The patient has signed the living will and is consistent with her directives" but the stem doesnt tell has what is in her living will about the extubation? we are extubating on the request of her husband? this is confusing !
I believe this question was not well constructed... it's one of those!
@shayan extubating at request of the husband because he's following what's in her living will. Following that line of thought, the patient probably wanted withdrawal of care if in a vegetative state.
I understood same as @shayan that she wanted to keep intubated... now reading it again I feel extra dumb with my poor reading interpretation skills
@lfsuarez CPR(if the need arises) , for this patient (barb overdose and hospital setting), she will be intubated to get and maintain airway access. However ,she is against any mechanical ventilation as per her living will. Hence, we cannot perform CPR on her.
I too believe DNR and DNI are distinct but UW 1124 says - A DNR order indicates that a patient should not undergo CPR. this includes bls (mouth to mouth breathing, chest compression) as well as advanced cardiac life support (intubation, mechanical ventilation, defibrillation, and administering medications such as vasopressor or epinephrine). Additional wishes such as the desire to not be fed artificially or any other limitation of care can be specified.
Yeah I think it should be MSH
Good to know I wasn't tripping out when I did this question
Not sure why NBME felt like they needed two questions on statin MOA on this form.
because they didn't even realize it because they make insanely low effort practice exams with awful formatting and vague vignettes, yet here we are paying 60 bucks a pop for "high quality" exams, gimme a break. ok i'm done venting
stop whining. no one asked you to buy the exam^
Why does anyone scramble this site? ><
and how about lipoprotein lipase?
and there's no mass in the scrotum, whereas testicular torsion will have that "bag of worms" feel (along with a lack of cremaster reflex)
testicular torsion usually happens in a younger age group
@neels11 I would like to clarify a piece of information. I believe you are confusing Varicocele with Testicular Torsion. Varicocele will present with "bag of worms" feeling. While the absence of cremasteric reflex is a sign of testicular torsion.
This is the classic "loin to groin pain" of nephrolithiasis.
Testicular torsion would also tend to have a unilateral high-riding testicle.
I agree that this nevus simplex and not a strawberry hemeangioma.
Of note, nevus simplex lesions are flat lesions formed from dilated capillaries. Lesions on the face tend to regress while lesions on the back of the neck typically do not.
The main thing that bothers me about this question is that if it is indeed nevus simplex, it's definitely a very non-typical presentation. Nevus simplex most commonly occurs on he back of the neck/midline locations plus they are pink in color.
The lesion described in this question is purplish (not pink) and it appears on the right side of the face (ie. neither back of neck nor midline). We can definitely rule out nevus flammeus because that is only seen in the setting of Sturge-Weber syndrome, which this patient has no signs of. We can also rule out strawberry hemangioma because such a lesion would be raised, not flat.
To add to that, I guess in the NBME world you can not have a nevus flammeus if there is no Sturge-Weber syndrome, in the real world most nevus flammeus are not associated with Sturge-Weber syndrome, but if a patient has Sturge-Weber syndrome then he is very likely to have a nevus flammeus
The funny thing is that the image seems to show that the spindle did in fact form.
They showed the mitotic spindle is formed, so paclitaxel would be ok, but for vincristine, the damn thing would not even form
Yep. They tried to throw you off with the picture, but the wording in the stem says its a "photomicrograph" -- not exposed to plane polarized light, where you would see the negative birefringence.
Why is NBME so mean to us. Do those mean a lot in clinic？
@linwanrun1357 I highly doubt you would be looking at your own joint fluid aspirates instead of sending it to the lab.
what those yellow white nodules signify?
In clinic gout is typically a clinical diagnosis. If you can treat w/ NSAIDs instead of aspirate you would do that. You would aspirate if you are considering septic arthritis so you can get culture. I don't think anyone aspirate for heck of it.
@nnp, the yellow white nodules are tophus which is a sign of chronic gout, characterized histologically by aggregates of uric acid crystals, can show up as skin nodules most commonly on external ear, olecranon bursa or achilles tendon (pg 467 FA 2020)
Also wouldn't mammography be secondary prevention since you'd look for asymptomatic disease already present?
USPSTF recommends starting screening at age 50. 40 by patient choice if there's risk factors.
@_yeetmasterflex thats a good point i didnt think about that
Is there a situation where you would pick fibromuscular dysplasia over atherosclerosis if given both options? Thanks for your help!
Atherosclerosis affects PROXIMAL 1/3 of renal artery
Fibromuscular dysplasia affects DISTAL 2/3 of renal artery
Why is there ↓ size in both kidneys? This threw me off
@gonyyong : Maybe because narrowed renal a. d/t atherosclerosis led to renal hypoperfusion and decrease in size?
Fibromuscular dysplasia occurs in young females according to Sattar Pg 67, 2018.
Normally you will see Fibromuscular dysplasia in a young female 18-35 with high or resistant hypertension. She is older has a history type II DM predispose you to vascular disease and normal to moderate elevation in BP
@gonyyong there's bilateral renal artery stenosis. The decrease in size of both kidneys should be from atrophy due to lack of renal blood flow.
1 year ago, she did not present any physical or Lab abnormalities. This means she must not suffer fibromuscular dysplasia, otherwise she must have presented renal abnormalities for a long long time, or even before DM-2.
a little surprised that atherosclerosis leading to bilateral renal artery stenosis and shrunken kidneys could happen that quickly after everything was A okay the year prior
How does telling an "embarrassed kid" that he will have big tits for 12-18 months help?!
my exact thought, telling him that it will last for somewhere around a year and a half doesnt seem so reassuring
I thought it was reassuring in that the kid is being told this isn't permanent as well as that this isn't something serious. It's important to inform him about the prognosis.
"don't worry your gynecomastia isn't permanent, but the mental scars from the bullying you will receive in HS definitely will be :) good luck!"
What is the gynecomastia is from a prolactinoma?
@therealslimshady the gynecomastia is from the sudden surge of testosterone during puberty being converted into estrogen => more breast tissue.
My breasts are not rubbery nodules, thank you very much!
if its a metaplasia, then how it be normal ? I mean Metaplasia is not normal?
i got it confused bc the question stated that there was a mass in one lobe of lung and i didn't knew that squamous metaplasia also presents as a mass in lung. i missed that on biopsy they were clearly stating squamous metaplasia.
@shayan The term "normal" in the answer is used to indicate that the cells appear normal (meaning appropriate size/architecture/appearance). Remember that metaplasia is a normal response to stress.
Metaplasia is not normal (in the sense that you only have metaplasia as a reaction to stress, but under not under normal circumstances), but the cells in metaplasia are normal. When they become abnormal, you get dysplasia.
metaplasia also can lead to cancer FA p206 2019
Dysplasia is not cancer since it is, in theory, still reversible. Only when it becomes irreversible is it a carcinoma.
because they mention scattered fragments of foreign material (pt presents 2 months after c-section, sutures are either removed in 1 week or dissolve in few weeks (depends on type of suture material)
I think it IS a foreign body granuloma. The sutures are supposed to be removed or dissolve but sometimes one gets left in. The question says foreign material and sutures are often polarizable.
I think it's because Bethanechol acts on M3 receptors which can treat her urinary problems but it might exacerbate her asthma symptoms since there are M3 receptors on the lungs.
I definitely had to read this question multiple times to understand it.
I read it like 6 times and gave up
I definitely had to read this question multiple times to still not understand it
It's so obscure of a test that wikipedia only has 4 sentences on it.
FA2020 added the Ham test to PNH I believe!
Whoops no sorry I am wrong. They did add something called the EMA test to spherocytosis though.
Ham test has been replaced by flow cytometry now. So fck off, NBME.
I remember it like this: PNH occurs at night due to mild respiratory acidosis (slower respiratory rate), which activates complement which destroys RBCs. The test is essentially doing the same thing, putting cells into an acidic environment -> dead RBCs.
Ugh. Of course they dont put schwann cells as a choice. So I pick oligodendrocytes like a dumbass
Schwann cells = PNS
Oligodendrocytes = CNS
NBME loves their neural crest cells
How much do they pay these testwriters anyway? I can use a thesaurus too
@suckitnbme they do love their neural crest cells, I have chosen neural crest cells for every single answer choice I see it in and I believe I gotten 90% of them correct, if something doesn't click or you don't know, I would keep neural crest cells as a very possible answer lol
Thanks, I was wondering why EPO was not correct. So EPO synthesis would be stimulated in case of blood loss? its just wrong becase they ask specifically what is going to be produced in the bone marrow?
@lilyo yes because it's specifically asking what the bone marrow is synthesizing. EPO would also be upregulated but this happens in the kidneys.
Great video! Very, very solid review of brainstem anatomy.
This image was surprisingly interpretable for NBME standards
and the fact that all you needed to know was the side of the lesion to answer tbh lmao, but other than that localizing to medulla wasn't hard.
Actually, they were quite nice. You didn't even have to know what side. There was no option for left medulla.
If they were measuring risk shouldn't it be a cohort study though? By looking at first aid..
They both can determine risk. Key here is the time efficiency of case-control studies when compared to cohort.
Case-control only determines odds ratio which is not calculating risk. In rare diseases the odds ratio can be used as an estimate of the risk ratio however.
crescent sign is a finding on radiographs that is associated with avascular necrosis, NOT aneurysms !!!
what you're seeing is Calcification of wall of the aortic aneurysm
@happysingh - Thank you. You are correct indeed.
Adding on, this patient is a >65 yo Male with a 120 pack year smoking history. Both are significant risk factors for AAA.
Specifically stratified squamous epithelium I believe.
All the other answer choices make you come across as an asshole. Easy way to ace ethics questions is to just not be an asshole
I would be a bigger asshole when the family came I'n after I pulled the plug...opps...but the friend said
The patient has no wife, children, or close relatives...
@lispectedwumbologist this is going to be my technique, because I've gotten a couple of these wrong, but I completely agree with everyone else's sentiments of suspicion of going off what a friend said without any confirmation about state of advance directives, etc. It's really dumb.
With these questions; you have to take what NBME says at face value. If it says no family, he really does have no family. This friend is also claiming that the 78 y/o said this about himself, so we know it's the patients wishes rather than someone else's wishes for him. (A son saying he can't let go of his father yet despite the patient's DNR type of situation).
I think the point here isn't that we would take the patient off the ventilator because the friend said so. The answer is saying "Thank you for your input, we will take that into consideration." It's completely non-committal.
they say no close relatives, which means he could have remote relatives, relatives must be asked before listening to a stranger/friend's words.....
Yeah the negative EtOH screen threw me off
Why cant it be early alzheimers and hippocampus? She could easily have been a former prominent physician and member of city council. Am i supposed to assume that simply because shes disheveled and poor hygeine that she must be an alcoholic homeless person? It also mentions no symptoms of nystagmus, ataxia, etc.
it said broad based gait and nystagmus
She is/was an alcoholic and appears pretty much homeless, just not drunk at this moment.
@ dr janitor. The question says "physical exam shows a broad-based gait and nystagmus."
NBME questions also stereotype the shit out of their patients
I think we're assuming that we eradicated the leukemia with the chemo. However at the same time a lot of normal stem cells were also killed off so we give GCSF to help recovery especially since they have an infection.
Also agree the narrowing of the lumen plus the pic is pointing towards Crohn's. The acute systemic sx of fever and chills is what made me go with diverticulitis (along with the hx of increasing constipation).
Why does the question say there is NARROWING OF THE LUMEN? Does that happen in diverticulitis? I went with Chron's at the last second against my better judgment because Chron's can cause strictures/narrowing of the lumen.
FA 2020 pg.383
Most common area for Diverticulosis to take place is the sigmoid colon and diverticulitis can cause obstruction (inflammatory stenosis). The key here is recognizing the risk factors (>60, chronic constipation) and signs of acute inflammation (fever, chills and LLQ pain).
also remember that in renal failure, 1-alpha-hydroxylase activity is down, so there will be less activation of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is a key mechanism causing hypocalcemia.
why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain
Increased phosphate, since the kidneys aren't working well, leads to the release of fibroblast growth factor 23 from bone, which decreases calcitriol production and decreased calcium absorption. The increase in phosphate and the decrease in calcium lead to secondary hyperparathyroidism.
Probably a dumb question but how do we definitively know that the ALP is elevated if they give us no reference range in the lab values or Q stem? Everything stated above definitely makes sense from a physiological standpoint, I was just curious.
@cr the question asked "the patient's BONE PAIN is most likely caused by which of the following?" Increased levels of 25-hydroxycholecalciferol might exist in that patient, but it wouldn't cause bone pain. PTH causes bone pain because of bone resorption
@privatejoker ALP is included in the standard lab values
@privatejoker ALP is listed under "Phosphatase (alkaline), serum" in the lab values
Why does AlkPhos increase in renal osteodystrophy? The PTH would be trying to stimulate bone resorption (increase osteoCLAST activity), not bone formation (osteoBLAST activity).
@pg32 the only way to stimulate an osteoclast in this case (e.g. via PTH) is by stimulating osteoblasts first (thru RANKL/RANK interaction), thus ALP increases.
"live-born offspring" ← baited
why is it 50% females tho?
felt like an idiot after i figured out why i got this wrong.
This isn't exactly right as males can still be born as evidenced by individuals III 6,9,11. This basically an x-linked recessive disease. A carrier mother can still pass her normal X chromosome to a son (50% chance). It's just that the other 50% chance of passing an affected X chromosome results in death of the fetus in utero. Thus all males actually born will not be affected.
@suckitnbme, Correct, but if you're a live-born male, you 100% for sure do NOT have the disease, so the chance of a live-born male "being affected" is 0.
@suckitnbme it's not X-linked recessive, otherwise every single son would be affected and therefore have died in utero. It's X-linked dominant
correct @spow affected females= X linked Dominant
Chancroid is described as an ulcer.. whilst in this question they mentioned "vesicles". Pretty much only herpes is vesicular
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 :)
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.
for chancroid, there may be a mention of inguinal lymphadenopathy
Also with chancroid questions they want you to differentiate it between chancroid and syphilis, (eg. Painful vs. painless) and is usually described as a much larger ulcer that is painful (not vesicular as in this question)
Also believe that chancroid does not presents with systemic symptoms like in this vignette.
did you get scabies from "burrows" and "night itching"
My question is where do you get scabies originally? I knew it was transmitted person-to-person, but thought it has to originate somewhere (a pet possibly?) so I went with pets. The internet only seems to say that you get scabies from another person with scabies, so the question remains: where do people contract scabies from?
@pg32 , long quote:
+ "Sarcoptes scabiei mites seek the source of stimuli originating from the host when they are off the host but in close proximity to it. This behavior may facilitate their finding a host if they are dislodged from it and contaminate the host environment. Thus, direct contact with an infested host may not be required for humans and other mammals to become infected with S. scabiei. In the case of human scabies, live mites in bedding, furniture, toys, and clothing can be a source of infection. Sarcoptes scabiei var. hominis have been recovered from laundry bins in a nursing home." + from here: https://parasitesandvectors.biomedcentral.com/articles/10.1186/s13071-017-2234-1
to summarize leafhouse: Fomites
FA 2020 p.161
"transmission through skin-to-skin contact (most common) or via
So, this says sympathetic also spared and hypothalamus also spared. Then what was wrong with this clinical case??
i think the sympathetic system is actually impaired b/c it's cut before it can "outflow"...at least it's the only way this makes sense
I agree. I think the question stem is saying the sympathetics were lesioned. Not that they were spared.
I think it’s because meningiomas are able to calcify (aka sometimes they have psamomma bodies). I got this question wrong too but I totally did not completely register that the tumor was in the dura (interhemispheric fissure + central sulcus). Hope that helps!
the only reason I got this right was because they described the tumour as being near the falx cerebri.
Other hints include being described as round and seen in a female. Both indicative of Meningioma
also meningiomas typically present with seizures or focal neurological signs
I thought enhancing meant it uptakes contrast. Meningiomas are commonly enhancing lesions per Radiopaedia.
I get Parvo has tropism for RBC precursors, but wouldn’t it take 120 days to manifest?
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.
@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.
He can drop from 11 to 10 hgb easily
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??
@is2076 check my comment to @hello I thought the same thing for a sec too :)
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
@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.
@Is3076 another point is that malar rash refers to the butterfly rash on the cheeks that is commonly seen in lupus, so the face is NOT spared.
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.
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...
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.
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.
why not detail the long-therm health effects of smoking?
@ 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.
Also because the patient states he already knows smoking hurts him in the long run so it may come off as lecturing on something he already knows. I view this as what is the least-judgmental way to facilitate the patient moving on to the next step of the stages of change model largely of their own volition.
i choose the option c which is initiate a pulmunary function test. why is that a wrong choice?
@usmlehulk - he's asymptomatic, knows it is not good for him in the long run, but is not quite ready to make a change. It is best to talk with him about the pros/cons of cessation so that maybe he will make the decision to quit smoking soon.
Ordering a pulmonary function test is not going to be useful. Let's say it's decreased. Ok, so what? It doesn't change management in this patient right now.
Think of it as motivational interviewing
Still don't like the answer given that the patient already stated that he knows that it can do him harm in the long run. It seems like overkill.
Wouldn't nitrates be a faster acting drug here? That was my take-away anyway. One is more acute, the other for long term maintenance.
I also believe it's because CCBs have minimal effect on venous beds and would not cause a significant decrease on preload.
decrease of cardiac preload is another word of Venodilation, so Nitrates primarly venodilators. CCB dilate arteria more than veins
also, verapamil is the one that causes constipation. But Verampamil is non-dyhydropiridine, so it works more on the heart than the vessels
You should be able to rule it out by the normal Thrombin time. Abnormal fibrinogen would have increased PT/PTT but also increased Thrombin time because the entire pathway is compromised by the inability of fibrinogen to be cleaved to functioning fibrin.