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Welcome to uslme123’s page.
Contributor score: 66


Comments ...

 +4  (nbme23#39)
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Tshi iteoqsun mkeas no eness to em. eSh sha an eeyrletxm olw ingpone upesrser ety ash ssngi of aencredis nriaclaairtn ssrre.peu diD htey enma ot ptu 23 cm ?2?H???????0

uslme123  Standard lab values are incorrect, way to go NBME. +3
wutuwantbruv  I think they mean to put mm Hg. Normal CSF pressure is about 100-180 mm H20 which equates to about 8-15 mm Hg. +3
alexb  I lost a bit of time wondering about that ugh lol +1
mjmejora  I thought there must be an obstruction in the ventricles somewhere preventing csf from getting to the spine. so pressure is low in spinal tap but in the head it must be really high. +2
donttrustmyanswers  Does anyone have clarification on this question? +
llamastep1  Pseudo tumor cerebri can have normal ICP. Who knew +
tyrionwill  Hi, mjmejora, MRI did not see anything abnormality, couldn't this mean that there was no obstruction in the ventricles? +1

 -14  (nbme21#20)
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evyr stuipd e.otsquin The rvuis saw hendail -- atbs nhag iedspu nhwe tyeh lepes adn lrdo.o So it praedss to het anbir idcrtlye mofr hte raoloctyf mesyst aiv aeetdgrror taotsprrn grhuoth .reenvs

niboonsh  yea, aeresol transmission via bat poop in caves +
len49  How do you know the virus was inhaled? Doesn't mention it. Moreover, non-bite/scratch transmission is extremely rare. +
makinallkindzofgainz  You get rabies by being bitten, not by inhaling it +
drzed  She was probably bitten by a bat; many times the bite is not recognized ('unapparent bites'), and thus the CDC recommends that even if you think you have been bitten by a bat (or that you COULD have been bitten), you should go and get active/passive immunization immediately. +
mangotango  Sketchy (and Zanki) says you can get rabies via animal bites OR aerosol transmission. In the U.S. it's most commonly through bats. It could also be through skunks (Western U.S.) or foxes/raccoons (Eastern U.S.). I remember this by thinking about how skunks smell so bad! +
shieldmaiden  But the question is "how it got to the brain" not how she got it, so the best answer is through the nerves +

 +1  (nbme21#35)
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VAFs' = narcedies icdarac B T.utotpuU htis 'ntsi enw for htsi r?esnop I wive tihs as a rteah atht sha iylflan eubng to lfia -- dreseaecd vceietfef yraocrlicut evmluo --;tg& eendrisca R.VS

tBu i eguss oyu na'tc have B oefreb A -- vwethear --\

happyhib_  his bp was something like 130/50; with diastolic around 50 I figured he couldnt have increased SVR because his diastolic would be higher? +1
trazobone  I had this same reasoning I completely glossed over the BP 🤦🏻‍♀️ +




Subcomments ...

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yWh odwul ti tno be imaane fo hrnocic seaides hwit adercedse usemr nfranetrirs n?coientanocrt

lispectedwumbologist  Nevermind I'm stupid as fuck I see my mistake +2  
drdoom  be kind to yourself, doc! (it's a long road we're on!) +21  
step1forthewin  Hi, can someone explain the blood smear? isn't it supposed to show hypersegmented neutrophils if it was B12 deficiency? +1  
loftybirdman  I think the blood smear is showing a lone lymphocyte, which should be the same size as a normal RBC. You can see the RBCs in this smear are bigger than that ->macrocytic ->B12 deficiency +23  
seagull  maybe i'm new to the game. but isn't the answer folate deficiency and not B12? Also, i though it was anemia of chronic disease as well. +  
vshummy  Lispectedwumbologist, please explain your mistake? Lol because that seems like a respectible answer to me... +9  
gonyyong  It's a B12 deficiency Ileum is where B12 is reabsorbed, folate is jejunum The blood smear is showing enlarged RBCs Methionine synthase does this conversion, using cofactor B12 +1  
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. +3  
yotsubato  Thanks NBME, that really helped me.... +1  
keshvi  the question was relatively easy, but the picture was so misguiding i felt! i thought it looked like microcytic RBCs. I guess the key is, that they clearly mentioned distal ileum. and that is THE site for B12 absorption. +6  
sahusema  I didn't even register that was a lymphocyte. I thought I was seeing target cells so I was confused AF +  
drschmoctor  Leave it to NBME to find the palest macrocytes on the planet. +5  
zevvyt  so i guess size is more important than color cause those are hypochromatic as fuck +  
yesa  The NUCLEUS of a lymphocyte should be the same size as a normal RBC, which is not the case here. Under normal circumstances RBCs are not as big as lymphocytes, so this is truly extraordinary = megaloblastic anemia. +  


submitted by lsmarshall(417),
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ebePciro"dn dan dgiseohh- aysslelctai ibitnih eairbsptorno of uric cadi in amilpxor clotuvndoe tlbueu ls(oa tshinibi ctinseore fo .ieii)lnlpcn" - trsFi idA 2901

uslme123  so ............... +10  
adisdiadochokinetic  So probenecid is the best answer here because they only specified acetylsalicylic acid, not the dosage, and low-dose acetylsalicylic acid has the opposite effect. +8  


submitted by welpdedelp(227),
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hwen a olfcilel edtns'o rupuetr (aka tauovlian)no nhet it iwll form a tyc.s

uslme123  n premenopausal women, simple adnexal cysts (image 1) that are <3 cm in diameter typically represent normal follicles or may be a corpus luteal cyst (these may appear simple or complex) and may be considered a normal finding. Even when up to 5 cm in diameter, these simple cysts are so commonly due to normal menstrual physiology that the Society of Radiologists in Ultrasound (SRU) does not recommend follow-up when asymptomatic +8  


submitted by keycompany(310),
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nCa osbmyeod seelpa xaielnp who ninniongzio aanodiirt sha na innoziig e.cfeft

uslme123  "technically non-ionizing, can produce photochemical reactions that are damaging to molecules by means other than simple heat. Since these reactions are often very similar to those caused by ionizing radiation, often the entire UV spectrum is considered to be equivalent to ionization radiation in its interaction with many systems (including biological systems)." -- https://en.wikipedia.org/wiki/Non-ionizing_radiation#Near_ultraviolet_radiation I'm guessing NBME reads wiki lmao? +3  


submitted by sympathetikey(1368),
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dMa ta eflmys orf gnagchni my naewsr.

utlyaF glcio aedm em erwdno if tgntiih rouy eahd ludow csdaue dnaecreis ICP os, kile a shcuing lu,rce you uwodl egt rasndeeci aguVs eervn cititavy dna bmeya cdyaabarrdi + tpoho.nnsyei tuB I esugs the AASR ystesm lwduo hvea todcraceeunt ttah dan aedcus itrcoscsniatoovn eorv 42 hu,osr so peHiovlmcoy okshc si ilynifeetd het estb cieoc.h

alsAyw uhsldo og itwh eth svuooib reansw ):

seagull  I had the idea that this was a neurogenic shock and increasing intracranial pressure could affect the vagus too. I think the question really wants us to go that direction. +13  
uslme123  The Cushing reflex leads to bradycardia! +4  
purdude  Wait I'm confused. I thought hypovolemic shock leads to an increased SVR? +2  
littletreetrunk  apparently, there's a thing called sympathetic escape that can happen after a while (i.e. he's been out for 24 hours): Accumulation of tissue metabolic vasodilator substances impairs sympathetic-mediated vasoconstriction, which leads to loss of vascular tone, progressive hypotension and organ hypoperfusion. +  
littletreetrunk  also also if he hit his head he could have loss of sympathetic outflow from a hypoxic medulla which could lead to vasodilation, which further reduces arterial pressure, but this was a hard one for me lol. I also put increased ICP wah. +  
catch-22  Any lack of sympathetic outflow/increased vagal outflow should reduce HR, not increase it. Further, you would expect brainstem signs if there was hypoxia to the brainstem. For example, if you had damage to the solitary nucleus, you wouldn't be able to regulate your HR in response to reduced BP. Since this patient has reduced BP and increased HR, this indicates that the primary disturbance is likely the reduced BP. He's also been in a desert for 24+ hours so. +3  
charcot_bouchard  In a patient who develops hypotension following high-energy trauma, neurogenic shock is a diagnosis of exclusion that is made after hypovolemic and obstructive cardiogenic shock have been ruled out! Plus Absent Bradycardia rules it out +2  


submitted by hayayah(1079),
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Ffimelrzobi is a bt,afeir edsu for inlwoerg GT s.lvele

mousie  I also chose Gemfibrozil too because its the best TG lowering drug listed but I can see where there might be some red flags for this drug in the way they asked the question... 40 year old obese woman with some upper abdominal pain ..... HELLO GALL STONES which is a common adverse outcome of Fibrates. +10  
uslme123  Well I didn't wanna give a fat, forty, female, that smokes a fibrate. So a statin, for me, was the best next option. +9  
whoissaad  Used same reasoning to choose statins. Fibrates are the main drug of choice for hypertriglyceridemia but given her symptoms, statins made more sense. Why do they do this to us... +  
roaaaj  what a tricky question! there are multiple factors should be taken in consideration.. she has triglyceridemia which put her in risk of pancreatitis, and most importantly atherosclerotic disease, and all of that would outweigh the risk of giving her gallstone. +  
paulkarr  Yeah I had statins selected initially because "statins are always the answer" but when I saw them stating first line "recently diagnosed with hyper TG" I figured this follow-up was purely to address that. So Fibrate is the best move. +2  


submitted by joker4eva76(26),
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heT seoutnqi mtse si gbdrieicsn a aoliointrmdhc ,sedieas hhiwc olmnmyoc snetrep ithw ciatcl doaic.sis hreTe si an rsniecae ni aieborcna rmofs of eygner codruntipo s)yg(lsolci.y heT nrcamdiooith rea ,fluayt os thye atn’c ues teh den tcodpru of sogsllyicy tp()vaueyr in TCA. Idsenat utyervpa si hsetund oerv dna is uesd yb HLD (ltataec ysreeoengda)dh ot eenaegtr aryt.eupv

dAies: laRcel taht DLH ssue NHAD and tnesagere AN+.D cfnDicyeie of LDH acn lade ot lsso of annegireotre fo +AND nda isnthiib coly.sigysl

drdoom  ... pyruvate is shunted over and is used by LDH (lactate dehydrogenase) to generate lactate*. +3  
chris07  It's hinted in the answer, but I would like to clarify: max O2 consumption is decreased because O2 is consumed in the Electron Transport Chain, which occurs in the mitochondria. With the mitochondria not working, the ETC cannot work, and thus there is less demand for Oxygen. +18  
masonkingcobra  Mitochondria are the powerhouse of the cell +54  
uslme123  Apparently ragged red fibers are the result of coarse subsarcolemmal or intermyofibrillar mitochondrial accumulations.. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/mitochondrial-myopathy +3  
mnemonicsfordayz  As @chris07 said, less O2 is being consumed in the ETC... but I also was thinking that the diaphragm is a muscle and if the mitochondria in her diaphragm are also not functioning, then she's not breathing properly and less O2 is being inhaled and therefore decreasing her oxygen consumption. Is that totally off base or am I just grasping at straws here? +  


submitted by uslme123(66),
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Tish etnsuioq kames on nssee ot m.e She sah na reteylmex low openngi rrepessu tey ahs gsnis of arcsiedne irncniaaalrt psresreu. diD tehy maen ot tpu 32 cm ?0????2????H

uslme123  Standard lab values are incorrect, way to go NBME. +3  
wutuwantbruv  I think they mean to put mm Hg. Normal CSF pressure is about 100-180 mm H20 which equates to about 8-15 mm Hg. +3  
alexb  I lost a bit of time wondering about that ugh lol +1  
mjmejora  I thought there must be an obstruction in the ventricles somewhere preventing csf from getting to the spine. so pressure is low in spinal tap but in the head it must be really high. +2  
donttrustmyanswers  Does anyone have clarification on this question? +  
llamastep1  Pseudo tumor cerebri can have normal ICP. Who knew +  
tyrionwill  Hi, mjmejora, MRI did not see anything abnormality, couldn't this mean that there was no obstruction in the ventricles? +1  


submitted by sajaqua1(535),
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a,noGaiscmtey erdisp itmngoaaa, nad asdyhipgonom sa( ewll as armalp he)tmeary rea lal gissn fo sexces rengt.soe ehT evrli ni pnastite tihw ipeatch iedases is impaider dan os nactno elcra ntseegro cl.yusfineitf xSi 12 zo esber ayild 2(7 oz, or hlfa a o)aglln is oto muh,c adn is dyreosigtn his lvri.e

uslme123  No hepatosplenomegaly, ascites, or edema through me off. We that being said, I shied away from cirrhosis. I thought that he showed signed of depression, so I went with the thyroid. But who's to say he isn't injection anabolic steroids?! +6  
catch-22  The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum. +12  
notadoctor  He likely has hepatitis B/C given his history of intravenous drug use. I believe both can have liver dysfunction but may or may not have ascites, whereas the type of damage we would expect from alcohol that would match this presentation would also show ascites. +  
charcot_bouchard  For Ascities u need to have portal HTN. Thats a must. (unless exudative cause like Malignancy) +2  
paulkarr  For anyone who needs it; the FA photo is kinda burned into my mind for these questions. NBME has some weird infatuation with this clinical presentation.. FA (2019) Pg: 383 "Cirrhosis and Portal HTN". +4  
snripper  @paulkarr the problem was that the FA image was burned into my mind so without no ascites or edema threw me off of cirrhosis. +  
tyrionwill  cirrhosis doesn't present hepatomegaly, instead, the liver could be shrunken. +1  
avocadotoast  Cirrhosis (most likely due to alcoholism in this patient) leads to an increase in sex hormone binding globulin, causing a relative increase in estrogen compared to androgens. Cirrhosis doesn't always have to present with ascites and adema. I agree with @catch-22 that liver disease is a spectrum. This patient does not have ascites because his liver is still able to produce enough albumin to maintain oncotic pressure in the blood. +1  


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ts’I ceuta llhoaco icsotompunn os attyf cgneha omre .elliky laerllCu leglnwis nstcdeiia aooichllc htesatipi wchih riuqeesr nrcicho hlcoola upitoncosnm See( AF 1209 gp 53)8. tA tslea ath’st hte lcigo I sedu to pkic ftayt c.gneha

seagull  Seems like fatty change would require more than 1 weekend. I choose swelling since it's reversible and seems like something with a quick onset. +42  
nc1992  I think it's just a bad question. It should be "on weekends" +16  
uslme123  https://webpath.med.utah.edu/LIVEHTML/LIVER145.html +21  
uslme123  So his hepatocytes aren't dying ( ballon degeneration ) vs just damaged/increased FA synthesis due to increased NADH/citrate +1  
sympathetikey  @seagull I agree! +  
et-tu-bromocriptine  It's not in pathoma, but I have it written in (so he or Dr. Ryan may have mentioned it) - Alcoholic hepatitis is generally seen in binge drinkers WITH A LONG HISTORY OF CONSUMPTION. +  
linwanrun1357  Do NOT think the answer of this question is right. Cell swelling make more sense! +1  
fkstpashls  some asshole in suspenders and a bowtie definitely wrote this q, as I've seen both acute swelling and fatty change be used to describe one episode of drinking. +14  
msw  short term ingestion of as much as 80gm of alcohol (six beers) over one to several days generally produces mild , reversible hepatic steatosis . from big robin 8th edition page 858. Basically to develop alcoholic hepatitis with cellular swelling etc you have to have sustained long term ingestion of alcohol while steatosis can develop with a single six cap . hope that helps . ps i got it wrong too . +1  
msw  six pack8 +  
mariame  After even moderate intake of alcohol, lipid droplets accumulate in hepatocytes increasing with amount and chronicity of alcohol intake. (...) Fatty change is completely reversible if there is abstention from further intake of alcohol. The swelling is caused by accumulation of fat, water and proteins. Therefore this will occur later. From big Robins 9th pg842. +  


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Its’ tecua hlooacl noponticsum so fatyt egchan mreo klleyi. elaClrlu lewnlgis nsietadci lialccooh aphtiesti chiwh reuireqs rcochin loalhco tnpumnoisco (eSe AF 0219 gp 5.3)8 tA lesta atht’s teh ioglc I duse ot pkci tyaft ecngha.

seagull  Seems like fatty change would require more than 1 weekend. I choose swelling since it's reversible and seems like something with a quick onset. +42  
nc1992  I think it's just a bad question. It should be "on weekends" +16  
uslme123  https://webpath.med.utah.edu/LIVEHTML/LIVER145.html +21  
uslme123  So his hepatocytes aren't dying ( ballon degeneration ) vs just damaged/increased FA synthesis due to increased NADH/citrate +1  
sympathetikey  @seagull I agree! +  
et-tu-bromocriptine  It's not in pathoma, but I have it written in (so he or Dr. Ryan may have mentioned it) - Alcoholic hepatitis is generally seen in binge drinkers WITH A LONG HISTORY OF CONSUMPTION. +  
linwanrun1357  Do NOT think the answer of this question is right. Cell swelling make more sense! +1  
fkstpashls  some asshole in suspenders and a bowtie definitely wrote this q, as I've seen both acute swelling and fatty change be used to describe one episode of drinking. +14  
msw  short term ingestion of as much as 80gm of alcohol (six beers) over one to several days generally produces mild , reversible hepatic steatosis . from big robin 8th edition page 858. Basically to develop alcoholic hepatitis with cellular swelling etc you have to have sustained long term ingestion of alcohol while steatosis can develop with a single six cap . hope that helps . ps i got it wrong too . +1  
msw  six pack8 +  
mariame  After even moderate intake of alcohol, lipid droplets accumulate in hepatocytes increasing with amount and chronicity of alcohol intake. (...) Fatty change is completely reversible if there is abstention from further intake of alcohol. The swelling is caused by accumulation of fat, water and proteins. Therefore this will occur later. From big Robins 9th pg842. +  


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My tgohuth aws ttha isht si mcednie sputhy rfom oleus on[ a sieu,rc rash yoln on het krtn,u rgia]taalhr

tshgTuoh?

s,noytlHe enev fi it is udeeng was eth eams sanwre rhgus ejoim

uslme123  I did too ... but It looks like the timing fits better for denge. +  


submitted by liltr(23),
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I ecohso VPM ,oot btu hist s’titeanp imna smypotm is coghu lony uigrnd isxcree.e hiTs si remo cnvetiaiid of deexrcise deaiatscso .masath Yuo coudl see rohentsss of etharb ni MVP unirgd x,iceeser but onicogsh MPV aeslve teh hcuog anucectoudn fo.r

.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. +15  
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" +6  
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? +2  
cienfuegos  Just noticed that he has FHx, game changer. +1  
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) +1  
pg32  Isn't exercise induced asthma usually found in people running outside, especially in cold weather? I feel like that is how it is always presented in NBME questions, so this threw me off. Not to mention the MVP. +  
happyhib_  it took me a little; the FHx really pushed me to exercise induced. I was also looking at malingering but there wasnt a real reason to push me to this (as a doctor it would be sad to be like hes faking it becasue he doesnt want to play sports with out being sure first; led me away because there wasnt enough pointing there). Also MVP could be slightly benign and is very common and usually no Sx and his lungs were clear as was rest of exam. All pushed to Asthma +  
mittelschmerz  I think MVP on its own shouldnt cause SoB with cough (in a question, I'm sure it could in the real world). In the world of NBME questions where you need to follow the physiology perfectly, you would need some degree of MR that lead to LV dysfunction/vol overload, and theres no pulmonary edema nor an S3 that point us towards that. Malingering would have to be faked for gain, and theres no external gain here or evidence that he's faking symptoms. You would also need to r/o physical illness before diagnosing malingering, which hasnt been done. Cold weather is certainly known for exacerbating EIA and are the exam buzzwords, but any exercise can absolutely be a trigger +2  


submitted by liltr(23),
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I oohsec MPV to,o but shti eps’tntai mina yopmtsm is cohug oynl guindr ieecerx.s shTi si orme avicniited of xesercdei dtcaaiesos hmsata. uoY coldu ese thsesosnr of bearht ni MVP nrgdui er,eesxci tbu scoginoh VMP asvele eth uhogc uecatocundn .rof

.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. +15  
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" +6  
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? +2  
cienfuegos  Just noticed that he has FHx, game changer. +1  
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) +1  
pg32  Isn't exercise induced asthma usually found in people running outside, especially in cold weather? I feel like that is how it is always presented in NBME questions, so this threw me off. Not to mention the MVP. +  
happyhib_  it took me a little; the FHx really pushed me to exercise induced. I was also looking at malingering but there wasnt a real reason to push me to this (as a doctor it would be sad to be like hes faking it becasue he doesnt want to play sports with out being sure first; led me away because there wasnt enough pointing there). Also MVP could be slightly benign and is very common and usually no Sx and his lungs were clear as was rest of exam. All pushed to Asthma +  
mittelschmerz  I think MVP on its own shouldnt cause SoB with cough (in a question, I'm sure it could in the real world). In the world of NBME questions where you need to follow the physiology perfectly, you would need some degree of MR that lead to LV dysfunction/vol overload, and theres no pulmonary edema nor an S3 that point us towards that. Malingering would have to be faked for gain, and theres no external gain here or evidence that he's faking symptoms. You would also need to r/o physical illness before diagnosing malingering, which hasnt been done. Cold weather is certainly known for exacerbating EIA and are the exam buzzwords, but any exercise can absolutely be a trigger +2  


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I egt tath shit seanwr ccehio is het tsom amcleaib rw.nesa

Btu oyhsentl eht ayw hyte dsaek eht eoitnqus ti" is stom epratoparip rof teh ipsnyhcai to srddaes the ssuei fo a eifengd bute ni chhiw of teh goilwlfon mennrs"a

yM eigorsann a:sw ellbow..erf.e teh ylaimf can enev ibegn ot reaug hawt od do ndo't uoy heva to soropep a lieacdm gmtatrtaenetn/amenme tasyrg?et wihch is hwy I wtne whit me"mecnord a bt"..u.e

home_run_ball  Like what is the learning objective of this question? On first aid if you go by the Surrogate decision maker priority: you do spouse first...so like wtf nbme? +13  
uslme123  I think it's because there isn't a legally appointed health care surrogate in this case. The family hierarchy is only an "ethical suggestion." +1  
nala_ula  According to first aid, there is an order to who makes decisions when the patient is not able to and hasn't left any directives. My issue was the same as home_run_ball, since they specifically asked about the feeding tube and not "who is supposed to make decisions now" even though that is also warped since the spouse has precedence. +2  
badstudent  If you look at the wording for the rest of the recommend a tube option ("because feeding will be more efficient and prevent starvation") it seems like you would be persuading the family to move forward with a feeding tube for their ease and convenience rather than proceeding with a feeding tube to avoid the possible dangers of an aspiration pneumonia. A family that is visiting daily likely doesn't mind any challenges associated with feeding. Instead it would be more important to recommend a feeding tube to avoid risk. Dumb questions for sure, just wanted to explain why i ruled that answer out. +  


submitted by hayayah(1079),
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saCe fo soosarer.otrciellsi

pysHacpertli issoletilrorarcoes leiovvns nhkiectgni of essevl lwla by ilaasehpypr of sothmo sculem s(ni-iok'onn ae)pc'ranape

  • eensocnueCq of gmnntiala rinosnepethy &;1g1/028t0( /w uaect neogd-anr daaeg)m
  • tuRslse ni eerudcd lsesve crlbiae with n-anedorg iihcmeas
  • ayM dale to irboifdni isscenor fo eht vlssee lawl htiw eahrh;ormge lasaisyccll ceuass uetca aelrn laiefur ()FAR htiw a cathrstcacriie ttl'fbe-ien'a cnearpeapa
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 =/ +16  
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); +23  
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) +7  
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 +  


submitted by hayayah(1079),
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aMni usscae of rnael ytaerr nisotses:

  • oiotAechrrsltec i—raesqllxmuaopp 1/dr3 ln fraoe rer,tya usyuall in ldero ms,lea .merksos

  • sFcrurmlbiauo staalyiasdpdl—is /dr23 laoen fr trarye or tmeglsaen arb,chnse uals uyluongy ro elemidagd-d emasfle.

Lab veuasl sadbe ff:o

  1. tSeoinss essardcee dbloo wfol to mslguel.rou
  2. toJaeuglralxmur asaatppur G()AJ rnospesd yb rgcteenis eni,nr hihwc tcsneorv etoinneagsgnino ot negnsaitino .I
  3. toginiAnsne I si nctrveeod to toainesingn II T(AII) yb otasnnignie gnocnvtrie ynezme AC(E i-n- nu)gls
  4. AIIT ieasrs odolb rssurpee by )1( ngctinrocta iartareolr hosomt ls,muce sinercaign tatol raperehlpi sacseniert adn ()2 rtgmoonip lanrdae lersaee fo oeled,naotsr hcwhi serascien orapiesrobnt fo iodusm he(wre N+a egso H2O ilwl llfo)wo in het atldis ceoovlutnd tlbeuu n(ipngaedx plamsa ue.lovm) naC eadl to eapamhkoily (enes ni het blas orf htsi to)iequns
  5. dsLae to NHT iwht ansereidc asaplm nenri nad trlauailen rhytaop e(du ot lwo ldboo )wlfo of eth fdaceetf knedyi; intrhee tareefu is eesn in rpmiayr nentohseipry
uslme123  So both causes would result in increased aldo and MR is the only way to differentiate the two? +2  
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. +8  
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. +4