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Welcome to drzed’s page.
Contributor score: 206


Comments ...

 +0  (nbme23#9)

My silly mnemonic...

Schizotypal: are your archeTYPAL weirdos (no offense to anyone, just a mnemonic!)

Schizoid: like to avOID people/attention

AvoidANT: generally wANT to like people/attention


 +3  (nbme23#17)

"During strength testing the patient has pain and weakness with abduction, particularly with simultaneous shoulder internal rotation"

This is a descriptive way of describing Neer's impingement sign, which is a (fairly) specific indicator of shoulder cuff tendon impingement; the most commonly impinged tendon of the rotator cuff being supraspinatus of course.


 +3  (nbme23#46)

Lol I was stupid and put increased serum cholesterol concentration because I thought that the fluid loss would lead to a concentration of substances in the ECF (e.g. like how dehydration can trigger gout). RIP.

focus  "The post-burn hypermetabolic response increases the metabolic rate to compensate for the profound water and heat loss severe burn patients suffer. Water loss approaches 4000 milliliters per meter squared burn area per day [38-41]. The body’s natural response to this insult, partially mediated by increased ATP consumption and substrate oxidation, is to raise core and skin temperatures 2°C above normal compared to unburned patients [42]. This response is similar to the response seen during cold acclimatization. In fact, patients that do not mount this response are likely septic and or have exhausted physiologic capabilities to maintain needed body temperature [43]." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3776603/ +2

 +0  (nbme23#6)

Of all these viruses, Hep B is the only one that a child, if infected, would be a chronic carrier. Thus we should screen to make sure that we can prevent future risk of cirrhosis, etc.


 +2  (nbme22#41)

You do not need to memorize a formula to know this, as long as you know the units (which are SO much easier to remember as they are intuitive). The answers are mostly clearance and steady state, which means you can cancel units to see if the answer choice makes sense.

For example, since CL has units of L/min and Css has units of mg/L, then (A) works out because L/min x mg/L = mg/min which is the correct units for infusion rate.

Whereas (B) CL/Css would not work because those units would be L/min / mg/L = L^2/min*mg, which does not make sense.

So if you just cancel some units, you can answer many of the questions.

Huge disclaimer: this won't work with things like half-life, because there is a factor of Ln(2) that has no units, so you have to memorize formulas that have factors before them.


 +11  (nbme22#30)

I tried to use logic to answer this question (I did not know about the hexosamine pathway). Here is my attempt--this is probably wrong somewhere.

I figured that if you want to make glucosamine, you need to combine glucose + an amine group

(A) Arginine I knew was involved in donating nitrogen, but it is in the urea cycle, so I figured this was probably not the answer but it had potential. I figured that the major way this compound removes its nitrogen is through urea, though.

(B) ATP. Since F6P already has the phosphate group, I figured ATP is probably not necessary as the compound in question already has a PO4 group.

(C) Carbamoyl phosphate. I knew this was involved in both the urea cycle and nucleoside synthesis, so this was less likely. It also is the product of a NH3 and CO2 so that means that I wouldn't expect it to donate an amine group

(D) Glutamine I figured has an amine group attached to it ready for donation. I also know that transamination reactions are common with amino acids and alpha-ketoacids (e.g. alpha ketoglutarate with alanine can get you glutamate and a pyruvate via ALT) thus it made sense that an amino acid could donate an amine group.

(E) The only thing I knew about NAG was that it was used in the urea cycle as an allosteric activator of CPS, so I didn't think that it was useful as a donator of nitrogen since its function is to help aid nitrogen excretion.

So then I was stuck between A and D, but based on transamination reactions, I picked D.


 +0  (nbme22#18)

Unfortunately, I chose (C) thinking that the down-regulation of receptors would lead to needing higher doses for efficacy (patient is using a patient controlled pump), however tolerance to miosis does not develop, and thus eventually this side effect would occur.

Could anyone point out where my train of thought is incorrect? I suspect that my assumption of the patient increasing their dose is not warranted?

aag  I also chose this, @drzed but looking back, if there was down-regulation of the receptors then she wouldnt have enough receptors to cause altered mental status and respiratory depression, side effects that you do develop tolerance to. How I would have remembered that morphine is metabolized to other active metabolites is beyond me. Happy studying hope this helps. +1
waterloo  He's also on a controlled analgesic pump. I've been on one before, and basically you can't keep pumping yourself constantly with it. You can hit the button, get a small dose, and then have to wait a bit of time to hit it again. The next time you hit the effect (at least for me) was always the same meaning I wasn't becoming tolerant to it (I was on one for a week). This controlled pump phrase has come up in another exam, which makes me think when they say that they want you to think this isn't someone who's taking alot of meds all the time. I also like aag thought process. +

 +13  (nbme22#50)

I'm a simple man, I see encephalitis and temporal lobe involvment, I click herpes.

asharm10  hahaha true that, overthinking is the reason for getting so many questions wrong +

 +12  (nbme22#45)

(A) aggregates of large atypical lymphocytes = infectious mononucleosis (CD8+ T cells responding to EBV infection in CD21+ B cells)

(B) Granulation tissue containing pseudohyphae and budding yeasts = candidiasis

(C) Intracellular yeasts in macrophages = histoplasmosis

(D) Macrophages containing acid-fast bacilli = mycobacterium

(E) Multinuclear cells containing intranuclear inclusions = cytomegalovirus (or most members of the herpesvirus family)


 +1  (nbme21#44)

If more people have the disease in your population, then the chance of a positive test result actually being positive will increase -- more people have the disease, so you're more likely to be "right"


 +2  (nbme21#17)

Let's say you didn't know methionine was essential.

(A) Alanine -- you can create alanine from the enzyme ALT (alanine aminotransferase), thus this enzyme cannot be essential

(B) Aspartate -- you can create aspartate from the enzyme AST (aspartate aminotransferase), thus this enzyme cannot be essential

(C) Glycine -- this one is low yield, but it is made from serine (serine + THF -> CO2 + Me-THF + glycine). If you didn't know about this, you had a 50/50 shot

(E) Tyrosine -- you can create tyrosine from phenylalanine (unless of course you have phenylketonuria), and thus this cannot be essential.


 +0  (nbme21#14)

Perhaps this is an incorrect way of thinking about this, but I always associate the virulence of Strep pneumo to its capsule, but I only associate the K capsular antigen of E. coli to meningitis (recall that E. coli has other specific virulence factors like fimbriae for UTI).

So basically, I figured that the capsule of Strep pneumo is involved in more disease processes (MOPS) than the capsule of E. coli (mostly meningitis), and thus I chose Strep.

b1ackcoffee  You are right, this is INCORRECT way. Capsule helps in hematogenous spread by protecting from phagocytosis causing sepsis, meningitis, pneumonia, i.e. more systemic infections. +

 +11  (nbme21#1)

mnemonic: schizOID (avOID companionship) vs avoidANT (wANT companionship)


 +1  (nbme21#35)

Perhaps I under-thought this questions, but it is highly unlikely to have HYPER- of anything when consuming large amounts of water, because whatever ion is present is going to get diluted. So in the case of normal gap acidosis from diarrhea, yes there may be an initial hyperchloremia, but the water is going to dilute it out.

Between hypoglycemia and hyponatremia, it is more likely to be hyponatremia because the child had seizures


 +1  (nbme21#18)

SIGECAPS criteria: (1) feeling weepy/overwhelmed, (2) fatigue/irritability, (3) anhedonia, (4) difficulty sleeping, (5) "I feel guilty...", for a period of 6 weeks = meets the criteria for a depressive episode, and since this was in the post partum period, may be post partum depression.

Next best step is to screen for suicidal ideation/thoughts of harming the child.


 +7  (nbme20#48)

First sentence of the stem: he has a 6-week history (e.g. >2 weeks) of depression (1), difficulty sleeping (2), fatigue (3), decreased appetite (4), and poor memory/concentration (5)

For a diagnosis of MDD, you need a 2 week history of 5 of the SIGECAPS symptoms which he meets (he is only missing suicidal ideation and interest in activities). Thus he meets the diagnostic criteria for a major depressive episode, which means that treatment is indicated with an SSRI.

For the other cardiovascular factors, the only ones proven to improve mortality are statins, ACEi, BB (esp. carvedilol in heart failure), and spironolactone. None of those were answer choices, so MDD treatment was the best choice.


 +12  (nbme20#38)

Patient has low serum sodium = hyponatremia.Given that the patient has a LOW URINE OSMOLARITY, it suggests that ADH is NOT active. The only way for someone to have hyponatremia AND a low ADH (in this case) is through psychogenic polydipsia (e.g. if it was SIADH, the urine would be MAXIMALLY concentrated and it is NOT in this case)

(A) would cause central DI -- no ADH means one develops hypernatremia as free water is lost in the urine, thus concentrating the serum.

(B) osmotic diuresis could cause hypernatremia due to loss of free water in the urine

(C) degradation of ADH leads to DI which means one develops hypernatremia

(E) resistance to ADH (nephrogenic DI), again, hypernatremia.

lovebug  thanks for kindful labeling! :) +1




Subcomments ...

submitted by keycompany(296),
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w/cm/i0mltnw.ph9Pbv/w/ip8Csi0.t5.:elocs./nah/2ctr6ngM

rlesO gSin si a sltyoiveitisw,n- cywic-piftoles nifgnid fo Mbenkcroge lotesoserisrlAorci (A)M cciazhtrerdea yb "a llpaepba agtohluh s,sluleesp rdalia arrety liweh hte BP ffuc si fidtalen aovbe lsiotcys pr.useesr"

tI si isslbope ttah r ea)ei:ht heT ei-clcyipftoisw of stih tset seamn it si sloa ebppiaalcl to reriecossasohtl ton( jtus M)Ab) Teh EMNB ctiyceonrrl piislem taht MA is netigbacnelhra iwht oecslrhast.ersoi

bubbles  This was my reasoning, too. I thought this was Mockenberg for sure +  
hello  I don't think think it's a type. According to 2 other comments: "It's atherosclerosis because it said “radial artery is NON-pulsatile BUT REMAINS PALPABLE even as the cuff is inflated”--> normally, you can’t feel the artery when the cuff is overinflated b/c overindlation occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!): "If if something were to not be palpable then it would have to collapse -- atheroclerosis prevents this vessel collapse." +17  
arcanumm  I agree, I just reasoned that atherosclerosis would not be thicker when the lumen is blocked. I don't think they were going for Mockenberg at all. +  
arcanumm  would be thicker +  
drzed  Atherosclerosis isn't common in the radial artery though... it's common in the abdominal aorta + coronary, popliteal, and carotid arteries. I am not going to assume a guy has radial artery atherosclerosis when he is in his 80s without a dyslipidemia syndrome over monckeberg calcification! +  
mdmikek89  This explanation is completely incorrect. Whoever upvoted this is dumb. Pseudohypertension. Pseudohypertension, also known as pseudohypertension in the elderly, noncompressibility artery syndrome, and Osler's sign of pseudohypertension is a falsely elevated blood pressure reading obtained through sphygmomanometry due to calcification of blood vessels which cannot be compressed. +1  
mdmikek89  This is a diffuse calcification. Monckenberg is like PAD with Calcium. Some places have it some places dont. The chance that there is a plaque at the same point as the doctor is feeling for palpation is...well low. Also Monckenberg is a complication of DM Type II. Not in this stem... +  
haydenelise  Would've thanked you for your explanation @mdmike if it hadn't included the "whoever upvoted this is dumb" comment. What a turd lol +4  


submitted by mcl(579),
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oT axpden no tis,h awht we inkht aenshpp iwht 'Porsannisk asedsie (dna ipasikano)rninms si na bmlceinaa wetbene nmpoiaed adn yehleictocaln. tI mkaes orme essen if you kloo at ihst r,aagdim inaygp praitracul ontiettna ot eth tndcirei yaptha.w sLso of aiormidnpecg ()DA rousnne rofm eht ttsainbaus agrni (SNc) suretsl ni tnatocsn iivcoatnta of setoh CAh iertegsnc nsuo,ren hwich eulmttaiyl ulersts in niitnboihi fo aautmlsh rofm ttiinniiga eomt.snevm hfrroeeTe, sguin giraohclcisetnin pleh wtih orpiimsnnisknaa enyroscda to dalo.lh

mcl  Also, you don't wanna use sinemet since that would be counterproductive +2  
drzed  Whaaat? How could increasing levels of dopamine in a psychotic patient possibly be a bad thing? +  


Stellate Ganglion is not involved in the regulation of heart rate: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872892/ Gotta love those shit NBME questions.

drzed  Lol did you read the article: "the right stellate ganglion block (RSGB) decreased heart rate" +2  


submitted by seagull(1404),
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,oS 1/T5-6T2/ era hte ecamytshpit eevll rof eht hrtea. Teh allsetet gglainno are rcciveal siymhtcpate igonnlg.a isTh itnqseou emses mero occrtiern o(r a eghu a)pel ot me. But yhe, I nwko pepole iwll sr.geeiad

dentist  you're right! heart rate is the only option under sympathetic control. +  
drzed  The cervical ganglion is a fusion of the last few cervical levels and the first thoracic level, so it is plausible. +  


submitted by kentuckyfan(43),
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Nieotc atht )A ioBcnhs,ocnrrooitcnt B) nuGlaadrl ectne,oris D) tea,isPsrsli E) atioolnsVaid of knis aer all deurn ipmtacyaapestrh rol.tonc

eTh lyon ihmcayetstp olctron si arhte rt,ea ichhw doulw csairne.e

drzed  Vasodilation of the skin is under sympathetic control as well -- beta-2 receptors when stimulated cause vasodilation (via increase of cAMP in vascular smooth muscle). The key is recognizing that stimulation of a GANGLION of the pns will lead to release of NOREPINEPHRINE, which preferentially stimulates alpha-1 receptors. Those receptors will cause vasoconstriction. If the question asked what happens when you stimulate the adrenal medulla, the answer would be (potentially) vasodilation. This is because the adrenal medulla releases EPINEPHRINE which preferentially stimulates beta-1/2 receptors. +6  
jesusisking  @drzed Awesome explanation except I think sympathetic response induces vasoconstriction in the skin though vasodilation in the muscles! +1  
usmile1  @jesusisking yes you are correct! α1: vasoconstriction in skin and intestine ; β2: vasodilation in skeletal muscle (transmitter: only epinephrine!) +  


submitted by mousie(210),
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yhW no inw?agest I naem I etg tsyEcsa is lypobbar het rudg of hicoec befero na lal thign anced rtayp ol()l btu nodt' nuteasrdnd ywh terhe luowd eb olcd teiixteserm nad no tsnaweig when si FA it syas pyimtearrehh dan bhro???a?d

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. +11  
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. +9  
yotsubato  Because the NBME is full of fuckers. The guy is probably dehydrated so he cant sweat anymore? +18  
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 +8  
monkd  Ketamine acts as a sympathomimetic but oh well. NBME hasn't caught on to ketamine as a drug of recreation :) +4  
usmleuser007  Why not LSD? +  
d_holles  @usmleuser007 LSD doesn't cause HTN and ↑ HR. +1  
sbryant6  @fulminant_life FALSE. KETAMINE CAUSES CARDIOVASCULAR STIMULATION. +9  
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/ +3  
drzed  @sbryant6 you're both saying the same thing. Ketamine has a direct negative inotropic effect on the heart, but it is also a sympathomimetic. You are both correct. +  
paperbackwriter  @drzed Can you please site that? As far as I understand ketamine has a sympathomimetic effect on the CV system --> increased chronotropy and BP. I also don't see how they're saying the same thing. One person said "stimulation" and the other said "depression" +  
nutmeg_liver  People tend to drink a lot of water on MDMA. I just guessed the confusion was a result of hyponatremia (too much free water) but no idea if there's any data saying that people tend to become hyponatremic due to water over-consumption on MDMA lol. +1  
cassdawg  "Despite possessing a direct negative cardiac inotropic effect, ketamine causes dose dependent direct stimulation of the CNS that leads to increased sympathetic nervous system outflow. Consequently, ketamine produces cardiovascular effects that resemble sympathetic nervous system stimulation. Ketamine is associated with increases in systemic and pulmonary blood pressures, heart rate, cardiac output, cardiac work, and myocardial oxygen requirements."(https://www.openanesthesia.org/systemic_effects_of_ketamine/) +  
brise  LSD does cause HTN and tachycardia according to uworld! @d_holles +  


submitted by sajaqua1(519),
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ehT eaptitn hsa a orpri sroyith fo mscheertoyyt hwit lleiaabrt oaholop,posmicy-gerton dan vdecieer tnleexra eabm danitraio ot the pel.vsi heT eitnpat wno siypadsl isnhpoeshrdoyr nda ,rorturyheed hiwt ltdasi elaurtre nonirrwga lr.latieybla The stlkielie oontpi is htat we era nesgei siensoahd ofmr iupeosvr gresyru stccroint the srtr,eeu aicgnsu ish.t

)E arlilehoUt ccamanroi a(sol delcal otsniilnarat lecl mn)icoarac is olsa a iip.slbisyot htaW skeam ihts lneikyul is het nico:oatl bllrate.ai Teh opirr tytycorhesme nda lelbriaat p-oooienchpogtrslmaoy wduol eleva csra eituss on both sdise fo eht bdyo, utb teh dods of lloruhaite oaianrccm rsnaigi aylbitrllae are evry l.mis

)A heT tnaipte adh a rth,mysceteoy os teh sodd of reecurnrt vlcrecia iromaancc are sloa nybecldrii wlo. C) and D) etlhrUar yoolmndac nad truhlrae tlstnniiaaor cell lmapaploi rae in teh rwong lntcoiao ot utancoc rof bralatlie tarhuler irrnognaw iwht euyhdeto.rrr

stinkysulfaeggs  Great explanation - just one addition. The retroperitoneal fibrosis could also be a direct consequence of the external beam radiation. It's linked to both causes. Either way, it's a better fit than urothelial carcinoma (in retrospect). +13  
spow  Why would the onset be 15 years later though? +3  
drzed  I was thinking the same thing @spow. I had put urothelial carcinoma, thinking that a field defect would result in bilateral tumor. +3  


submitted by temmy(126),
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rnAcgdoci to rD ..Sratta comaAricndeona is eth sotm ocmnmo eausc fo ugnl neccra ni laeefm non kessrm.o

drzed  Correction: he says it is the most common in NONSMOKERS and FEMALE SMOKERS. +7  


submitted by krewfoo99(88),
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Wyh wuldo nerpsirfo be the owgnr es?rnaw dlotunW aliauucnmcto fo oxitc ritnsepo useca teh lcel to ounregd ippaotsso ?

ergogenic22  Bortezomib does not directly activate perforin. It directly inhibits the proteasome which → enables CD8+ T cells to initiate apoptosis → via perforin release (in essence a downstream effect). +4  
drzed  Exactly, it triggers the cells to undergo apoptosis which means that it can either be cell mediated (perforin and granzyme via FAS/FASL) OR it could also be through the intrinsic pathway (e.g. mitochondrial; cytochrome c) +  
powerhouseofthecell  Question: But how do CD8 cells have a role in this process exactly in the vignette? Is it saying that when the proteins build up, only then do CD8 cells come and instead of MHC I presenting to proteasomes, they present it to CD8 to initiate apoptosis? +  


submitted by cbrodo(58),
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hTe oriotprse cusmoln uFcl(iscsau Facnusuui/cletusacs isiragcl) ycrra aootmiinfnr ot het nrabi aedrrgign otipr,coponpire b,torvanii vtadseiiniimrc chuto adn .srseurpe ilscyPah axme idnngsfi gsguste a ieolns heer h(et hsoclpanmitai cttar cseriar ciir/nnppaikp nad etremtep,rua and steeh eewr rno.)lma cienS the ntpeita sah anlbrmoa sngniifd ni the rwelo isteemreti,x and romaln nsnfigdi ni the reppu meietixre,st eth wsnrae si sasuFulcci .agislirc sThi is beeusca oiaftnominr fmor dboy eaasr blowe eht eelvl fo 6T si riecdra yb rilgicas dna ornmfioatin morf boyd raeas boaev eth lvele fo T6 is rrdcaie by eaunucst.

kai  kick Goals (gracilis) with your feet Cook and eat (cuneatus) with your hands +3  
temmy  i remember gracilis is for legs by saying i have graciously long legs and they are inside while arms can spread out to remember their orientation on the spinal cord +3  
jess123  I remember it as gracilis = grass so feet haha +4  
link981  Just to add found on page 492 on FA 2018. +  
charcot_bouchard  Hey Temmy, I can spread my legs too :) +  
maxillarythirdmolar  I can't feel GRACIE's ~fine touch~ as she ~vibrates~ my balls. +3  
cat5280  Could someone please explain why you were able to eliminate the spinocerebellar tracts? +1  
drzed  Lmao I remember gracilis because of the gracilis muscle in the legs! +3  
alexxxx30  cat5280...so spinocerebellar tract does 4 things to know 1. proprioception in the Romberg test 2. intention tremor if damaged 3. shin to knee test 4. dysdiadochokinesia (being able to rapidly pronate/supinate the upper extremity) yes the patient has proprioception issues, but the other symptom of vibration loss points us more to a fasciculus gracilis issue. If the patient had presented with proprioception and and intention tremor then we would think spinocerebellar +2  
alexxxx30  adding to my comment^ I would commit these 4 things to memory as I have gotten several questions concerning this topic (there were 2 questions on this exam where spinocerebellar tracts are involved). Memorize them and it might get you 1-2 extra points! +  
solidshake  Just to clarify a point, Spinocerebellar tracts are not tested by the Romberg Test. Romberg tests conscious proprioception that is done by the dorsal columns. Spinocerebellar tracts are used for Unconscious proprioception. Look up tabes dorsalis in First Aid. One of the positive indicators is a positive romberg test, which shows that the dorsal columns have been damaged thus affecting conscious proprioception and thus impaired balanced on standing with the eyes closed +  


submitted by seagull(1404),
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f:.na/kpplyhbisro/i.rg(eiooot/oidgiwPganid/)rtkew_ei

ereH si a lietlt itb on r.egaroefniooHpdp it sphel

jcmed  I'm dropping out +1  
drzed  This question doesn't have to do with proof reading, even though it is mentioned. It is just saying this: you can make all the misfolded proteins you want (e.g. proofreading can be messed up), but it has no relevance to the PROGENY. Why? The progeny of a cell is dependent on DNA replication only--so long as your DNA is perfectly replicated, the progeny will come out perfect. You don't need to worry about RNA to make DNA (unless you're HIV, of course!) +5  


submitted by step420(33),
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naRoviirt bhnisiit 5CY!40P So uyo acn eus it to oobts the tocrnonctiane fo teh eroht storPeea biirtsnioh by gvntenpire rthie mtoimlasbe by 0!YCP54

mousie  who knew +4  
sympathetikey  Right on (thanks sketchy) +6  
mguan1993  MAGIC RACKS is a good mnemonic ive heard for 450 inhibitors (macrolides, amiodarone, grapefruit, cimetidine, RITONAVIR, alcohol (chronic), cipro, ketoconazole, sulfa +3  
criovoly  "CRACK AMIGOS" Cimetidine Ritonavir Amiodarone Ciprofloxacion Ketoconazole Acute alcoholism Macrolides Isoniasid Grapefruit juice Omeprazole Sulfonamides +6  
drzed  Macrolides EXCEPT azithromycin -- they like to trick you with that one. +2  
steatorrhea  chronic alcohol induces 450, acute alcohol inhibits 450 +2  


submitted by sajaqua1(519),
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heT eslnig mtos nipmtrato tginh uobta isth srgos lptayogho si ttha het iesdeas is unulldiort.ma iThs iandciets ssattesema frmo tstdina tsse.i

ievrL cssbsaese era usayul i,unalsgr leldfi with emaryc lyeolw ps,u nad aym shwo a sorfbui asuplce. rrshisiCo otfne shsow a lwleyo lcroo ued ot ytatf engcha sa lewl as aeterrgeinev l,dseoun hcwhi aer ont rsnptee ee.rh A lafoc olndaur alsirpapyeh si a nsgilura omtru fo the i,erlv nad htsi si lalmtonrd.uiu eistHaipt B si a ltetli ehdarr to idsstnuihig aeescbu orfm waht I acn lelt it acn be oamltdliurnu ni soem eacs,s ubt tihs eilvr alos sshow enon of hte rosliessc morf concrih niniamamflto htta woudl ellkyi aancymcpo Hep B. lla,iyFn ew ees no krad tnooodliscair ot idcienat tiianncfro.

monkd  It doesn't explain the sudden death, but I suppose they aren't asking for that! +4  
charcot_bouchard  I hate this type of ques. Here it is. Tell me what it is? +2  
divya  also, a liver infarct is unlikely due to rich dual blood supply. +1  
drzed  @divya Rather, if there was an infarct, it will be hemorrhagic, not pale. +1  
llamastep1  Multiple solid lesions on a healthy liver = meta. I assumed breast wouldn't meta to liver (it's usually GI cancers) but it makes sense since all the blood gets filtered by the liver at some point. TIL! +  


submitted by sugaplum(323),
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asywla bemremer ehtm in reord twih olr,faum I=ESESAIT
adn eht owt on het DEN rae UAODNDI-CT

makinallkindzofgainz  The supraspinatus AB-ducts. The Subscapularis ADDucts +  
makinallkindzofgainz  disregard my comment, I misread what you meant +  
drzed  How are you supposed to remember which S is which? +2  
drschmoctor  @drzed "Supra" = on top, so the 1st S is for supraspinatus. +1  
usmleaspirant2020  according to Physeo : INFraspinatus--EXternal rotaTION------INF-ECTION +  
destinyschild  wow, sugapulm, that mnemonic is gold. you are gold. +1  


submitted by sympathetikey(1252),
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reP AF (.gp )6:63 rinoneCcng resbat .ar..cnce

"cfpAmioaitlinnes/oseovrxprie fo rs/norgegonese ttpreoe rsetrcope ro Beb2r-c H(,2ER naGFE etrep)rco is cmn;oom ER ,⊝ RP ⊝, /aERd2Hnnue ⊝ omrf rome rgie."esgvas

sympathetikey  FA 2019 +4  
meningitis  Why others not it: Anticipation: Trinucleotide repeats; CAG (Huntington), CTG (Myotonic dyst), GAA (ataxia telangiectasia), CGG(Fragile X) Chromosomal rearrangement: Many but can think of Trisomy 21, BCR-Abl, etc Imprinting: Prader willi, angelman Loss of heterozygosity: loss of a single parent's contribution to part of its genome. A common occurrence in cancer, it often indicates the presence of tumor suppressor gene in the lost region. +1  
kai  trinucleotide repeats are not associated with breast cancer Neither are chromosomal rearrangements BRCA1,2 tumor supressor genes are associated with breast cancer, which is why I chose E, but I guess I should have bought the new First Aid.......... +  
charcot_bouchard  GAA is Freidrich Ataxia +4  
tulsigabbard  So is the amplification of the receptors unrelated to BRCA 1, 2? I'm still stuck on this as Sketchy states that breast cancer falls under the "two-hit" model. +  
tallerthanmymom  @tulsigabbard I think one of the keys here is the question stem; " what is the most likely cause of the OVERexpression in this pts tumor cells?" --> I think that the "2-Hit" model would lead to UNDERexpression of a tumor suppression gene rather than overexpression. Whereas amplification would cause OVERexpression of the HER2/estrogen and progesterone receptors. But, I don't think that amplification would be the answer if they were asking about a triple negative cancer. +1  
tallerthanmymom  Also this is on page 632 of FA 2018 for those using that version +  
tulsigabbard  @tallerthanmymom - thank you! +  
drzed  I can understand why @tulsigabbard dropped out of the race--she's taking step 1 soon LOL +1  


submitted by mousie(210),
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ywh osde rameetttn of htyirpdooyh hw(it yvoxreeitlnho mI' mssi)unga enrecsai irks for ?ptmoayyh I coehs it ilsmpy bc ist a oomnmc asevedr cfefte of nasttis btu I on'dt yrlale durdntsaen hwo tntegair orhimhypoitsdy at the saem temi lwoud ahev aitnyhgn to do thiw ti ??? hlpe !lseape

yb_26  They are just asking about side effect of statins, not about treatment of hypothyroidism +5  
mjmejora  Hypothyroidism is just a red herring. +  
ususmle  statins cause both hepatotoxic and mypopathy so I want for hepatotoxic:( I thought usmle expects different stuff +1  
drzed  Statins don't cause 'toxic hepatitis' they just cause a mild asymptomatic rise in LFTs that is reversible with discontinuation of the drug. The more worrisome side effect is of course, myopathy +2  
tyrionwill  statins cause both liver injury and myopathy in a dose related, so kidney failure increases their dose, which leads both liver and muscle risk elevated; Pravastatin is said less liver concerns but the myopathy, so choose myopathy when renal failure. +1  


submitted by thotcandy(74),

i figured it was cocaine or amphetamines so I picked plasma free metanephrines. Why is this not correct?

According to this:

Sympathomimetics: Ephedrine, Pseudoephedrine (Sudafed), Amphetamines, Albuterol (Proventil) can cause positive results in serum metanephrines.

https://www.ncbi.nlm.nih.gov/books/NBK278970/table/pheochromocytoma.table4drug/

drzed  Because a toxicology screen would both answer your question (e.g. that it could be amphetamine abuse) and would also pick up any other drugs that the patient might have been using. So even though the pre-test probability is high for amphetamine use, lets say it was something else, well then the tox screen would pick that up as well. Or lets say that it was simultaneous use of two drugs, same scenario. +2  


submitted by sajaqua1(519),
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In an eyrlled tteaipn hwti istlaedo lvedeaet alklenai seaothshpap ran(lom rsmue ccamiul nad s)otpehahp tsePa'g eeasisd of enbo lshdou eb ta eht otp fo hte firt.eilfedan Tihs ieassed si eud ot lsroyteidguna of latcoeticsso nad ltcasobsitoe avit;icyt fstri na atniiil tsoscoelta ytycthraeipiv s,aehp tenh eisrndeac tobesstalo yitatvic rof a mitrx,eu hnte tacselotsso ur""buont naldeig to eeinolt-ziivnoramra nda itcoesrlc oneb .equpals In tn,aoidid hits can ertcae vieusarertoon unssht in teh esonb hhwci seecesrad aece,nirtss enalgdi to hhig ttupou adaccir frileau a( marilis bmperol can aresi in avoesreotnrui tsfailus rofm dbolo .iiydslas) On sooiytlgh ti lwil ehva a "moi"sca tnear.pt

-)A nrAuasmley enbo ys-ct lelygar a orptdcu of cypirvthyetia fo aos,ttsslceo htis oscruc orem tnofe in het bslm,i adn sohws a syitcc ascep twih okbln-illaoe intoila.d B) nisca-gorAoma ancirmaoosag of the enob si n otsmla uplrey lycit le.isno Tyeh ruocc moer lfnreeyqtu in neuyogr ploe.pe )C Niainc ce-nedfyici I cna nifd ntognih baout tinivamb 3B ceefiincyd givionlnv ben.os B3 cietnecdfi etulsrs in ra,lgplae hiwt hte asilccs hreTe 'sD- tatesrdimi sh(ra caneclke on /C4C3 te)m,dmeaor ,eiaedmnt adn eiarad.hr )E toesmOr-coaas nouFd smotal vicselueyxl ni norueyg eloppe, ihts nobe ortghw rcsuoc at teh htrowg ,etlap alatylircrup ta het xliaorpm edn fo hte bai,it atilsd end of eht eur,fm ro rmoxipla dne fo eht uusehrm ni( the onlg nsebo oaurdn rouy sekne ro at uyro o.h)rsluesd It woshs a rl,aeg dosil gwgoinr smas htat aym sraei the meuortepsi in a rsstnuub ptata/'snmedoCrn g.lneitra )F aiotscPtr a-coinrcma erra fro igneb oen of, fi tno eht nloy eamctaitts bnoe naccer taht is pueryl sa.teolstboci

alexb  Great explanation, except that there was a question in NBME 22 in which the prostatic carcinoma was osteolytic. One of the commenters here looked it up and apparently it's like that 30% of the time or something. So I guess you would have to use the high output HF, normal Ca, high ALP, and mosaic pattern to "play odds" as Goljan would say. +1  
qball  At least they were nice enough to put Paget disease because I had no idea what osteitis deformans is. +1  
drzed  USMLE seems to be moving away from using eponymous names... so it's a good idea to see if there is a descriptive name for diseases. For example, they don't use the word "Wegener" anymore if you have noticed, since it turns out that guy was a nazi. So now they call it by what it is -- granulomatosis with polyangitis. +3  


submitted by momof21234(6),
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het tinetpa hsa assteosb hwchi si resrietvcti lcue( saw uallper qDue)slOL aCp si aerdsceed in crtaiiotcah-rn onitodinsc tsn(triliteai nugl zd e)ct nda omrlna on txrher-iocatac nsidioonct lu(rmsuac ss)suie

usmlecharserssss  how FEV1/FVC is normal i cannot get that +2  
sammyj98  I think this is standard for restrictive lung diseases. In obstructive the airways collapse during expiration so it's hard to expire, but there's a long drawn out end to epiration as little by little it escapes, leading to a decreased FEV1/FVC. In restrictive pt's just aren't able to move and expand their lungs enough, so when they expire it's of a small volume, but there isn't any collapse involved. It's like a normal expiration just with a restricted volume, making the FEV1/FVC normal. +  
spow  @usmlecharserssss In restrictive lung diseases, the ratio is either normal or increased. +  
drzed  And the reason why FEV1/FVC is either normal or increased in restrictive lung disease is very simple: the FEV1 and FVC both decrease because you are restricting airflow, but the FVC will decrease MORE than the FEV1, and thus because the denominator is larger, the fraction either stays normal, or increases slightly Contrast this to obstructive lung disease where you have an obstruction to air FLOW, e.g. the FEV1 will decrease more than the FVC, leading to a low ratio by defition +2  
llamastep1  To add to what @drzed said, fibrosis causes radial traction on the airways therefore increasing FEV1/FVC. Theres a Uworld q on it +  


submitted by sugaplum(323),
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rpiopnamnepenaolylh is na phala atnsoig atth tuielsmast rheltaru ohtoms lsuecm nioconcttr.a - rofm tuo,pdtea veho,ewr ti salo ysas it is otn memcdeoednr tntamtree eynoarm

ugalaxy  α1 stimulation (via α1 agonist) constricts the bladder sphincter thereby, preventing sudden bouts of micturition during coughing/sneezing (abdominal stress). +6  
sammyj98  I thought that B3 stimulation stopped urination +5  
adong  @sammyj98 B3 would facilitate bladder relaxation +  
hvancampen  @sammyj98- were you thinking of oxybutynin? (thats what I thought of!) According to FA, its used for urge incontinence not stress. +1  
drzed  Nah he/she's talking about Beta-3 receptors which are Gs coupled. Gs increases cAMP thus it would cause smooth muscle relaxation -> bladder relaxation! +1  
donttrustmyanswers  From Mayo: "There are no approved medications to specifically treat stress incontinence in the United States. The antidepressant duloxetine (Cymbalta) is used for the treatment of stress incontinence in Europe, however." +1  
nreid4  @hvancampen oxybutynin is an M3 muscarinic antagonist, not B3. +  
alienfever  I thought about B3 agonist as well and got this wrong. I think maybe B3 agonist can be used for bladder (URGENCY incontinence) where the main issue is detrusor over reactivity. In STRESS incontinence however the problem has nothing to do with detrusor, so we use α1 agonist to constrict the sphincter. +1  


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oenArdnsg suace ea.nc nteeotosersT is a etrtbe aswnre tahn eisAantrlndood /cb eth tseentosoeTr si asitodaces whit rupybte, naodseAtrlodni is meor seadtiocas thwi the aenradl agn.dsl

meningitis  I chose Testosterone but I almost chose GnRH because it is surged when starting puberty and therefore increases everything downstream. +10  
temmy  When answering the question, i thought to myself that if GnRH is correct, LH will be too cos GnRH stimulates the Leydig cells via LH to release testosterone. That left testosterone as the best answer because it had the most direct effect. +10  
goaiable  GnRH and LH are increased in a pulsatile fashion at the onset of puberty, so idk if that constitutes as the "rapid increase" that this question is asking for. Tripped me up also. +  
tallerthanmymom  I originally eliminated testosterone and chose androstanediol because women can have Acne Vulgaris too, and Testosterone should not be rising to the same degree. Do I not understand how puberty works? +1  
drzed  Women can still make testosterone though; and androstAnediOL is not the same as androstEnediONE +3  


submitted by lfsuarez(141),
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rtFsi rhaet udons S)(1 is trdegenea yb two etahr avlv:es teh malitr veavl nda rctdisupi avl.ve reylNa lemstuusoani igcsnol of these vlvase amlnylro etgrnsaee a leisgn S1 nuo.sd lnStigtip of eht 1S unsdo si edahr wenh mlarit nad iipuctsrd vealsv elsco at ylsgtlhi ferndteif i,tesm ihtw ulsaluy het lmtiar iocsgln rebofe rpctiduis

yotsubato  Then why the fuck is it describing a mitral valve sound in the tricuspid area +22  
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. +30  
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +4  
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +1  
drzed  It shouldn't matter where you hear a split sound. For example, no matter where you auscultate on the heart, the second heart sound in a healthy individual will always be A2 then P2 (whether you are at the mitral listening post or the aortic listening post) The key is recognizing that the right sided valves in healthy individuals will always close later (e.g. the heart sounds are S1 S2, but more specifically M1 T1 A2 P2). The reason for this is simple: if you take a breath in, you will increase preload on the right side of the heart, and thus the greater volume will cause a delayed closure of the valve. This is physiologic splitting, and is better appreciated in the pulmonary and aortic valves because they are under greater pressure, and thus louder, but it can also be heard in the first heart sound. +9  
alexxxx30  yes agreed!! This question is mostly asking if you understand a few basic things regarding cardio physio. The left side of the heart is the higher pressure side so left sided valves will close first. The right side of the heart is the lower pressure side, which means right sided valves will open first. [Left closes first, Right opens first]...Secondly, it requires you to know what S1 and S2 sounds come from. S1 is the mitral/tricuspid valve closing and S2 is the Aortic/pulmonary valves closing. So really the question asks what is the first component of S1 (mitral or tricuspid closes first). And since we know that the left side will always close first, it must be mitral valve closure. Sorry if that was a long explanation. +10  
jesusisking  Thanks @alexxxx30, you the man! RIP Kobe +  


submitted by lfsuarez(141),
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eH ptsesnre thwi an nmrbalao sinntaeso of hsi fetl andh ahtt sprdase ot tobh ish ftle mar dan cfea. A einlos of hte aolepstcrnt sgyur dluow csaeu tshi as ti it epsoslbenri rfo .nnatsseio

drzed  "you can tell because of the way it is" :) +7  


drzed  That made me want to vomit tbh; I forgot about NMRs until just now. I hated those things. +  


submitted by divya(58),
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i d'ont knthi you need ot ihtkn lla tath cm.hu kool at all het pnooist and hntik of wtah enpapsh hewn heyt sAa ni.,ceer ,B C, D dan F lla nca usaec stirlietntia B edtue.ma sinngecira pleaariylpcr naresistec lieitfedyn e'tdsno.

drzed  Increased lymphatic flow would not cause interstitial edema. +1  
123ojm  but it doesn't say "increase in," it just says "regulatory adjustments in." +1  


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tnaetPi ash tayyiphmocle arve, as cneieddev by ,oryesictytrosh t,yuansrlioscgo dna ahdesheac pam&; einiss.zd EPO is aeedsrcde deu to soryosrtihtyce. sceeeadrD ALP ouldw tncieida LM,C tno .VP

btl_nyc  I thought this was CML. What am I missing that would say CML over PV? +4  
btl_nyc  Nvm, RBCs go down in CML, but everything goes up in PV. +9  
arcanumm  Tricked me. I knew right away that it was PV, but I thought PV would crowd out normal cell creation (e.g. decrease platelets). So apparently crowding out normal cells is just a quality of AML/CML? +1  
drzed  More AML. Remember Sattar always stresses that all the myeloproliferative disorders are expansions of ALL lineages, ESPECIALLY "xx" (depends on which one, for CML it'll be granulocytes, for PV it'll be RBCs etc). They're called MYELOproliferative because all the myeloid linages go up, but one will be increased more than the rest. In this case, it is the RBCs. +3  


submitted by smc213(124),
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oT be pelcotemyl raecl!

shTi aeitptn ash yosnCtiiss a earr aoomautls risseeevc aylmolsos gsaeort redriods dna tmos ocnmmo cesau of niaFocn osrenymd in dcnirhle. yCsonsisti is yietmscs nad lsaed ot ienctys cytlras siepsdot ni eclls dan tisuess otorghuhtu the dby.o

lhAohgut snWislo daeiess can dlae to F,S eth lsatcyrs in the anesocr oeds not leratreco twih loinsWs ieesd.as
reMo if:no /m/c1t//.0rnM6it44cwwnchw.Ps8/osh:1pabt.lgCiv.lpmie/n

highyieldboardswards  Thank you! You are a legend for figuring this out! +  
paulkarr  Appreciate you. +  
drzed  And even if it was Wilson disease, it would have the exact same consequence leading to Fanconi syndrome. +2  
abhishek021196  Fanconi syndrome Generalized reabsorption defect in PCT = Increased excretion of amino acids, glucose, HCO 3 – , and PO 4 3– , and all substances reabsorbed by the PCT May lead to metabolic acidosis (proximal RTA), hypophosphatemia, osteopenia Hereditary defects (eg, Wilson disease, tyrosinemia, glycogen storage disease), ischemia, multiple myeloma, nephrotoxins/drugs (eg, ifosfamide, cisplatin), lead poisoning. Polyuria, renal tubular acidosis type II, growth failure, electrolyte imbalances, hypophosphatemic rickets = Fanconi syndrome (multiple combined dysfunction of the proximal convoluted tubule). +1  


submitted by armymed88(47),
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fO etshe siopotn ,lilbvaeaa Snhcwan slcel lwoud be eth nylo eclsl rtseepn ni hte .SNP eocAsst r,ty ialmgoicr dan lisgoo rae lal CNS lecls aetelSlit llsec are ni eht lemcus dan vsree to adi in ulmsec repria nda oeragitnreen

yb_26  Thats myosatellite cells. Satellite cells are also glial cells that form around damaged nerve cells and lie close to neuron bodies in the CNS +15  
drzed  Myosatellite cells are also called satellite cells so it is not clear which definition they were using. +1  


submitted by iviax94(7),
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rheTe hvea bene a oupelc fo eqnustios oubat iths cotpi no teh wnree esx.ma evI’ nebe nasgrnewi yb uaitqegn dbiiol ot noetersttsoe elevsl nad culrtnano eeicsront to ahhlte of ucavureltas sohseoct(reairsl or )tno. Is ihts ?tcrcero

liverdietrying  When you’re thinking of libido, don’t just equate it to testosterone -- make sure you’re always considering depression! Depression following stroke is common, especially with residual physical disability, so this would decrease his libido. Nocturnal erections equate to “does it actually work?” not just the vasculature but the neural input as well. For example, during prostatectomy damage to the pelvic plexus (nerves) can lead to impotence. There’s nothing to suggest that he has vascular or neurologic erectile dysfunction here, which is why his nocturnal erections are intact. +26  
_pusheen_  @liverdietrying Was it premature to assume he has trouble with erections because of neural damage from the stroke? I put low libido, low nocturnal erections. Is it because the stroke resulted in hemiparesis and not autonomic dysfunction or something like that? +5  
liverdietrying  @pusheen Correct, you won’t classically get impotence after a hemiplegic stroke. His inability to achieve an erection is much more likely to be 2/2 psychosocial effects than organic disease. If this vignette instead said that this had gotten a prostatectomy with resulting damage to the pelvic nerves that allow for erection, then it’d be a more safe choice to put no nocturnal erections. +4  
fast44  Is there a video or somewhere that explains these sexual dysfunctions? This seems to be a topic that keeps repeating on the new exams. +2  
forerofore  well, i though that because he had a stroke he would be likely to have atherosclerosis, which would keep libido high and reduce nocturnal erections, i kinda ignored the whole "he´s depressed" part of the vignette despite understanding the mechanism well. but from a clinical depression point of view, if his arteries are intact, and he is depressed, then libido would be low, and erections present at night. +4  
pg32  I can't remember exactly but I swear the question on NBME 21 the guy's wife had died as well...? Or they had gotten divorced? Either way, he had some psychological baggage as well, but his libido was still normal, and the explanation was that his testosterone would be fine regardless of his depressed mood. So I went with that logic here and missed this question. I don't understand how I am supposed to gauge someone's libido based on vague hints at their mood, especially when in one exam mood does not decrease libido and in the other it does. +  
drzed  @pg32 bro spoilers +2  


submitted by mguan1993(8),
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can oonsmee aepnixl ywh teh nraesw is ont dnraael dng?la I leef kie fi ladearn dlgan swa hte siues etrhe wolud losa eb adcerdsee rticonestcnaon of FSH, L,H dan geostenr r?ghti

mguan1993  ^nvm had a brain fart and go adrenal gland mixed up with anterior pituitary lmao +4  
nor16  ovaries are #1 estrogen producer no estrogen no lubricant = dyspareunia no estrogen and no fsh/lh --> there must be a "higher" problem, up there in the brain +3  
pg32  I agree that hypothalamus is the most logical answer, but if she had overactivation of the adrenal gland (cortisol secreting tumor), that could also inhibit GnRH and cause these same symptoms. +  
drzed  @pg32 the physical examination would not be normal with either a ACTH or cortisol secreting tumor. +  


submitted by armymed88(47),
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wDno ydrenoms 2dn ererimtst eercsn ululyas( nouard 8-1kw16)s sohsw eaedcdres APF, losirte nad scnidaree hGC dna bihiinn .A

fO irsyomt 3//,18211 ownD emSrnydo si the only ot avhe an lvdteeee GCh

makinallkindzofgainz  "Down Syndrome has high HI (hCg and inhibin)" the relationship between the words down/high really stuck for me +1  
drzed  An easy way to remember the other aneuploides is that the "lower" ones (e.g. lower than 21 = 13,18) have "lower" values (e.g. LOW hCg and LOW inhibin) +2  


submitted by pppro(23),
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teaPnti ash .PHB iGve lahpa eon gsntaotina to recude sthomo ecumls tnnocioctar dna eeirlev iiydtflfuc inr.gatnui

d_holles  lol i thought it was some kind of urinary retention problem and put H. +15  
sbryant6  How is H wrong? Oxybutinin or tolterodine treat urinary incontinence by blocking M3 muscarinic acetylcholine receptors --> urinary retention. We're just supposed to assume they are talking about BPH here because he is old? +  
jaxx  I agree. I picked "H" for that same logic. Does anyone know where we should have come to the conclusion that this was BPH? +  
forerofore  they are telling you he's having "difficulty urinating", one of the clinical criteria for BPH is reduced urinary flow rate. this is not incontinence because they are not telling you he leaks at all, just that he pees "a lot" +12  
drzed  Even if he was urinating too much, anticholinergics are contraindicated in the elderly (Beers criteria) +3  
pathogen7  @drzed tI mean techinically alpha-1 blockers are on the Criteria too ... +1  


submitted by pparalpha(83),
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nCa neeoosm eaelsp naiexlp why ti ldwuo not be gylceong oend?petli I uthhtgo the stenoqui saw ltgiank utabo eht rgWuarb mpnhn.ne.ooe. os ywh otn wrdnaeokb fo glcgeyno ot ?esuoclg

I usges it ldwuo nto pielaxn eth m?eead

hello  Glygocen stores are depleted within 24h. This person has signs and symptoms of longterm nutritional deficiences. +2  
raffff  it would not explain the edema, yes +  
drzed  Also the warburg phenomenon has to do with cancers preferentially taking up glucose; there is no indication that he has cancer. +  
haydenelise  The first sentence says that he has lung cancer. +2  


submitted by nwinkelmann(284),
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hsTi leicatr inxalpse teh oyiplhoostgypah e:lwl Ngiv4sowo/s1hhw..3/K/8ikol0tt/bbn.:w4cn/pm.Bn.

Teh ihrtg rneteicvl si iaryrmpil lppuides by the ACR hiwch sola sipluesp hte SA deon dan AV oned %09( of esraht ascebue ythe rea right aidnmto)n, eainlgd ot slos of trlociinctyat of teh hrtig ,dsie dna hstu lduif iulbupd gcnsuai ldeaevet tlnecra svunoe essp.erur Eedeatlv rersspseu in eth lirev nda lratpo ssmety lodwu ldea ot eaaytmgeoplh and efer fuild clmucnauitao in eht meitopuen.r

henoch280  Hellppp. pls why is it not decreased capillary oncotic pressure? +  
whoissaad  @ henoch280 Because there is no change in the levels of protein in the blood. +8  
drzed  theoretically you could develop liver failure from the increase in central venous pressure (e.g. cardiac cirrhosis) and THEN you would develop a decrease in oncotic pressure. +1  


submitted by tissue creep(104),
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niLfgti edah ilewh :orpne 1 hn mSlocaito e:lism 2 h motgnino:oCs 2 nhmsot

pg32  Where do you guys learn that cooing starts at 2 months? It isn't in first aid or boards and beyond so this was an annoying question for me +1  
drschmoctor  @pg32 From being a parent! Otherwise little chance I'd remember all these milestones. +4  
drzed  I'll get right on that @drshmoctor :). If only I could have a kid to memorize all these damn developmental milestones. That would make life easier haha. +6  
snripper  Yeah, I don't see cooing anywhere. +  
teepot123  thankfully a lot of my friends on insta keep posting pics/vids of their babies reaching milestones so im well updated lol +1  
pjpeleven  Mnemonic: "Coo at Two" +1  


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hyw nto d1o?artaim iseoshdo.rsiuc aihritsrt keli .stsosiielityu.yo.ms.3.ennmkdpy2 v estoriiss is a tib vaeriostlrcon

drzed  Need some pulmonary symptoms to make sarcoid convincing. I know in real life people can present with primary neurosarcoid or something crazy but on exams, it'll be classic presentation. No granulomas, hilar lympadenopathy, or interstitial lung disease = probably not sarcoid +1  
peridot  Just curious but if it had been sarcoidosis, would "systemic release of IL-1 and TNF" be an accurate description for the pathogenesis? +  


submitted by welpdedelp(216),
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oS I inkth hatt isues fo istrw oisetexnn /rdona iefnrg dpor udwol be emor idaalr eern.v we,eovrH hetre aws oerm riaxplom nkeasswe, os ti owdul eb .C7

"78- yal htme t"t,rahigs eth tp ndltco'u yal" hemt trag"htsi so it oduwl eb 7C otor

welpdedelp  *As an addition, median nerve involvement would have leaned more toward C8 than C7. +3  
meningitis  Do you have anymore useful mnemonics for brachial plexus? +  
henoch280  FA pg 494 for mnemonics +  
winelover777  Doesn't look like there are many in FA 2019. S1/S2 - Buckle my shoe. L3/L4 - Shut the door. C5/C6 - Pick up sticks. +  
drzed  S2-S4 keeps the penis off the floor :) (cremaster reflex) +  
peridot  What's crazy @drzed is that in FA 2019 it says L1-L2 ("testicles move") on p.498 so I wonder if that changed +  


submitted by rainlad(21),

How do you rule out Protein C deficiency in this case? doesn't that also increase risk of thrombosis and miscarriage?

suckitnbme  @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. +4  
drzed  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. +3  


submitted by seagull(1404),
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iHTs oqutnsie is jsut icariclt k.nhinitg heT lrdeaans are yelaratblil nad ylsemiyarcmlt sl.mla All toher eanrws ihsccoe era otn ylikle to be nvee laytb.llarei rnCace nwo't qayulel apdres in prtecfe meyystrm onr nitefoucsi seacsu lehwi tgiannanimi eth larndae churirette.ac

slim23shady  Will TB be the answer if they'd mentioned the patient from developing world? +  
step1soon  Autoimmune adrenalitis aka addisons disease → adrenals atrophy common cause: 1. developing world: TB 2. Western world:autoimmunne FA 2019 page 334 +14  
drschmoctor  FA 2020 p 349. +  
drzed  I think the cancer reference (C) was with respect to an ACTH secreting tumor, which would symmetrically and bilaterally HYPERTROPHY the adrenals +2  
drzed  ^Just kidding, it says metastatic. My bad! +1  


submitted by seagull(1404),
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iTHs qeutonsi is jsut crilaitc hkngi.nti hTe derlnsaa aer lbailtreyal dan emiamrsylyltc a.lmsl llA hetor rnswae escohic rea nto lileky ot be veen t.ryillbeala arecnC wtn'o euqlayl dprsea ni prectfe memsytry nro oitfisneuc eussca lwihe ntgiamiinna teh daenlar t.aectciruher

slim23shady  Will TB be the answer if they'd mentioned the patient from developing world? +  
step1soon  Autoimmune adrenalitis aka addisons disease → adrenals atrophy common cause: 1. developing world: TB 2. Western world:autoimmunne FA 2019 page 334 +14  
drschmoctor  FA 2020 p 349. +  
drzed  I think the cancer reference (C) was with respect to an ACTH secreting tumor, which would symmetrically and bilaterally HYPERTROPHY the adrenals +2  
drzed  ^Just kidding, it says metastatic. My bad! +1  


submitted by taediggity(30),

So this patient is essentially in hypovolemic shock because he's hemorrhaging blood from the aorta.

A) You'd have increased ADH to conserve volume B) You'd have increased BUN:Cr ratio b/c due to a decrease in blood flow C) Increased TPR naturally due to less pressure on barorecptors D) Decreased Capillary hydrostatic pressure b/c they have decreased volume E) Decreased Carotid sinus firing rate b/c less pressure F) The Answer: RAAS is activated -

drzed  (B) You get an increased BUN:Cr ratio because increased urea absorption at the proximal tubule (conservation of water), but you lose the same amount of Cr since none of it is reabsorbed; thus the ratio increases. +5  
kevin  I may be wrong but I think more of the urea (BUN) would be absorbed in medullary collecting duct in this situation due to ADH; think I saw a question on this in uworld, could pop up +  


submitted by yotsubato(968),
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aWht do uoy eus ot raett Hcepita elaEcppyhn?atoh tsLo.ceula aWth esod tath od, ti csiaeifid NH3 ni the GI tcatr tino N+4H nda opreotsm slso of eht sugnetoiorn rusctodp atht eusca otneehhlapcpya. hsiT is how uyo reeerbmm ihts srpe.sco

carmustine  FA 2019 pg 385 "Triggers --> increased NH3 production & absorption (due to GI bleed, constipation, infection)." +4  
drzed  To add, you can also use rifaximin which will act as a antibiotic decreasing the production of NH3 from gut flora. Same concept. +3  
nevergoingtopost  Lactulose is the correct treatment for hepatic encephalopathy, but it actually acidifies the GI tract (colonic metabolism of lactose → lactate). This favors the NH3 form and decreases NH4+. NH3 is then additionally pulled from the blood into the gut. +  


Orlistat works by inhibiting gastric and pancreatic lipases, the enzymes that break down triglycerides in the intestine.

Don't break things down in the intestines----> osmotic diarrhea

Apparently people use it to lose weight. Who knew. Not me

drzed  I believe it is the only FDA approved weight loss drug and has actually shown efficacy in diabetic patients. +  


Wouldn't telling the patient about the referral do more harm than good?

  1. Pt considers it a bribe and leaves
  2. Ruins study due to placbo effects
  3. Puts doc/hospital at risk for potential legal hassle.

I guess maybe I read it as a study when it really is just a referral but its not that much of a leap to think that this "experimental"" treatment is part of a study

drzed  I think this more of an ethical question (not a legal, or study design problem). Ethically, between the choices of being transparent with your patient, or not, the choice would be to disclose. Disclosing and offering to share would come across as a bribe, so that is less favorable than simply being transparent and putting the patient in charge of their decision. +  


I had no clue where the damage was either, but with that said:

You feel the grass with your feet ––> gracilus

And the arrangement along the spinal cord is similar to the sensory/motor homunculus of the brain where the feet are on the inside/medial and the arms are on the outside/lateral.

drzed  Only in the dorsal columns; this is reversed if the decussation happens within the spinal cord (e.g. the spinothalamic tract has a somatotropic distribution where the proximal extremities are medial) +  


submitted by hyperfukus(75),
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oals ni caes yeht sak reeemmrb hatt eseth rea (PFva'UeAhs dloube nob)sd nda etyh aer bterte tahn tSaadteur atf(osn lbedou sca+dro)bnbs

drzed  PUFA = poly-unsaturated fatty acids in case anyone didn't know the acronym. +4  


submitted by suckitnbme(164),

I was stuck between mitral and aortic and went with aortic because the L ventricle looks enlarged, possibly hinting that the patient had aortic stenosis.

drzed  I went with aortic because it looks like the valve has three cusps, while the mitral valve should only have two. Incorrect logic? +2  


submitted by fatboyslim(38),

(From UW 11852) Some medications including opioids, radiocontrast dyes, and some antibiotics (e.g. vancomycin) can induce and IgE-INDEPENDENT mast cell degranulation by activation of protein kinase A and PI3 kinase, which results in release of histamine, bradykinin, and other chemotactic factors -> diffuse itching, pain, bronchospasm, and localized swee=lling (urticaria).

almondbreeze  just to add : more agents causing such reaction - beta-lactams, sulfonamide, aminoglycoside +  
drzed  Are those IgE dependent, or just allergic reactions (asking because the sketchy for beta-lactam penicillins mention acute interstitial nephritis as an allergic reaction)? +  


submitted by soph(54),
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lal hte treoh spontoi pt lwduo vaeh ue,urts sr.aieov nutresr ehty nwdolut oolk omlrna dan yhte dlouw ehva ioprctah sir.eaov

turtlepenlight  This makes sense, but I was thrown off by the "normal-appearing" b/c wouldn't AIS pts not have pubic hair? +  
drzed  They just say it's a normal appearing 17 year old girl; not that the external genitalia are normal appearing. +1  
teepot123  fa 19 pg 625 +  


submitted by chandlerbas(95),
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uchsobrn rntuotscobi rt spa yxgoen in oleavil n o onitrneg bale ot eretn iotscmah(epr ria rginntee oybd %7(8 ietrognn dan 2%1 ,xegnoy oetnnrgi is so attinormp ionnrgte cb ti si a ryoplo odasebrb ags dan hstu is in rgeahdc of gieknep livloae eengoyx i)ladtnf ni hte eiaovll si erbdsoba tnio eth rooudbgein ldc teh vlemou fo eth la alvevrlioealo loselpac sitp nobaor aestitcslea

bethune  Why is pulmonary hypertension incorrect? +  
samsam3711  PEEP allows the alveoli to remain slightly open with exhalation to prevent atelectasis. Pulmonary Hypertension is going to be related to vascular changes (instead you might see shunting of blood in areas of poor ventilation) +1  
drzed  Pulmonary HTN occurs because of pulmonary vessel vasoconstriction. This can occur d/t multiple factors, but one of the most important ones is hypoxic vasoconstriction that the lungs will undergo (for example, at altitude). In the setting of PEEP, you are ventilating the lungs perfectly; this allows for the pulmonary vessels to open up and not undergo vasoconstriction. Thus, you prevent pulmonary hypertension via hypoxia. +  
peridot  @drzed by your logic, you're arguing for D to be the answer but the correct answer was about preventing atelectasis +  
medstudent  The question is what’s key. The purpose of PEEP is to keep the airway open. The purpose of ventilation with supplemental oxygen can help with preventing pulm HTN. Could be wrong, but that’s what makes sense to me. +  


submitted by uslme123(57),
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rvye stupid ti.usoenq ehT iruvs aws eldainh -- stab hagn edipus wneh yhte slepe dan dl.oro So it rpssdae ot the rnbai cildtyer rmfo het yctoforla yesstm via rargoreted srorntpta uohrhgt evre.sn

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! +  


submitted by sympathetikey(1252),
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ehT leowh ip"kcs ta eth eenlso.ic..ussa eosm elibneg",d edma em hnitk ioP.asissr Sodulh ehva ogen iwth ticciAn tasiroesK aesbd on teh iapntet yrthsio (lost fo sun eoesrux.)p

intcciA srsaKtoei

ianPgrnmlaet lsesion uadecs by nus prxseeuo. lam,Sl ugrho, hoeymteasrut ro rnoiwhsb usleppa qup.slo rea iskR fo moqsusua ellc acirnamco is prinplooarot ot dereeg fo eeltliiaph dyls.saiap

thisisfine   Same - the bleeding thing pushed me over to psoriasis as well. Oops. +5  
temmy  the distribution of the other lesions, forearm, face, ear, scalp..is not characteristic for psoriasis. +6  
hyperfukus  the scalp and ear are actually very common for psoriasis IRL the key is more of the fact that its in areas with UV exposure...actually UV Therapy is found to be helpful in treating some pts w/Psoriasis. Lastly the appearance and lots of things bleed if they were trying to go for auspitz sign it would have tiny dots of bright red blood with slightly touching it +4  
hyperfukus  oh last thing psoriasis itches! they said no itching +4  
drzed  Those locations may be common IRL, but on step 1, if they want you to think psoriasis, the illness script is going to be someone in their 30s (autoimmune age) with symmetric cutaneous plaques that have a silvery scale on the extensor surfaces. In this case, the age and non-classic description (location, type of lesion) made me steer away from psoriasis. +1  


submitted by readit(14),

Why is is not pseudo aneurysm?

"Aortic pseudoaneurysms typically occur as a result of trauma +/- intervention, a considered subset of traumatic aortic injury in the majority of cases. They can be acute or chronic."

https://radiopaedia.org/articles/aortic-pseudoaneurysm?lang=us

readit  *same goes for saccular aneurysm, which also is usually 2/2 trauma +  
samsam3711  In the question stem there is no indication of trauma so it would be hard to just assume that +  
almondbreeze  see my comment above for marfan syndrome. might help +  
drzed  This is because a pseudoaneurysm is between the media and adventitia, and is incited by trauma; a dissection is between the intima and the media and is a result of hypertension causing an intimal tear. The history points toward cocaine -> hypertension rather than penetrating trauma. +  


submitted by h0odtime(46),
  • R Lower quadrantanopia = C/L Parietal Lesion/MCA via Dorsal optic radiation.

  • If top quarter was gone, then it would be C/L temporal lesion via meyer loop.

drzed  the dorsal optic radiation is also known as "baum's loop" +  
icedcoffeeislyfe  FA2020 pg 542 +  


submitted by hayayah(1056),
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erdonycSa iarshytpmpoairdyehr lyus(ula /dt cnhroci nealr r.lfeuai)

Lba ndiingsf ienlcdu ↑ HTP es(onpser ot olw m)lc,cuai ↓ smreu ilacmuc lane(r ali,)uerf ↑ usmer ppsotehah rale(n ,uaelr)fi adn ↑ enilaakl hpeshatopsa PTH( gntaaviitc o.)oealstBsts

haliburton  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. +2  
cr  why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain +  
nala_ula  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. +1  
privatejoker  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. +1  
fatboyslim  @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 +1  
suckitnbme  @privatejoker ALP is included in the standard lab values +  
makinallkindzofgainz  @privatejoker ALP is listed under "Phosphatase (alkaline), serum" in the lab values +1  
pg32  Why does AlkPhos increase in renal osteodystrophy? The PTH would be trying to stimulate bone resorption (increase osteoCLAST activity), not bone formation (osteoBLAST activity). +  
drzed  @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. +1  


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rhrieaaD scsuae sosl of erw,at Na nad cib.aBr rmeRbeem tath daaerrih si a csaeu fo non onian agp btimloeca iadiossc uaecebs eth olss of etrbaiobanc si doemcnpseta by gnracienis elodihrC rsatonoiebrp. So she acn evah apercryhloeihm ro noypmhaertai ued to nkatie fo noyl efre wetra rfo 24 uh.osr uBt hse ahs RUIESSEZ os payinaermhto si tsmo ielykl

drzed  I think the initial hyperchloremia would be quickly diluted out by the large consumption of water, so those two competing processes would likely neutralize the chlorine level, or even make the child hypochloremic. +  


submitted by hayayah(1056),
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Shetctr ro adtiinol fo eht rxvcei dna avigan rae nsgtor liisutm rfo nciyoxto ncsteoeri, meeadtid by lneaur athasywp lcaedl hte ugsnorFe fe.xrel

iAt:elrc cregniupooee:rl.t./inifw/cssnrfns-dtsewtprx/swo/mceeoecciuhecet/c

readit  This is also why ob-gyn's will massage the uterus (which is part of the birth canal) after delivery. It's to get the body to release oxytocin and cause the uterus to contract (to prevent postpartum hemorrhage) +5  
jennybones  Please why is estrogen not the answer, I thought estrogen would upregulate oxytocin receptors and increase oxytocin secretion? +1  
drzed  During pregnancy, oxytocin RECEPTORS are upregulated (by estrogen) as parturition approaches, but the ferugson reflex creates a positive feedback loop where the dilation of the cervix further releases more oxytocin. The inciting event that starts this feedback loop is the dilation of the cervix leading to a direct release of oxytocin, not the presence of more oxytocin receptors. +3  
bbr  To add, the positive feedback loop here is pretty elegant. Basically, it seems like the cervix doesnt want anything in it. When its stretched --> oxytocin --> contract uterus --> push baby --> more stretch at cervix---> more oxytocin (and forward). The positive feedback loop aspect is that oxytocin-based contractions cause more dilation of the cervix (as the baby moves into it!). +  


submitted by hayayah(1056),
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Nti,eco eth semt syas po"resorrcs in hte knis"

3D chloclr(i)ceoaelf rmfo reeosxup of knis t(artusm ebl)saa ot nsu, gneonstii fo ,ihsf ,ilkm t.plnas

2D eaorecocl(f)rgli ofmr ionienstg of a,tnlsp fnig,u asty.es

Bhto etonvcedr ot 5-2HO D3 r(setgoa ro)mf ni lrevi and ot the itveac fmor -1O)52(2H, 3D ac)oll(rtici ni ny.edki

sympathetikey  C is the 3rd letter in the alphabet. Hence, D3 = Cholecalciferol +4  
karljeon  Thanks for the explanation. The question stem made it sound like "what future step will be decreased?" Actual question: "Decreased production of which... is most LIKELY TO OCCUR in this patient?" Maybe NBME needs a grammar Nazi working for them. +8  
bharatpillai  question says "decreased production of which of the following precursors in skin is most likely to occur in this patient? the answer has to be 7-dehydrocholecalciferol! +4  
bharatpillai  7 dehydrocholesterol +2  
brbwhat  Yeah i did the same, but then realised acc to uw flowchart 7dehydrochole.. is converted to cholecalciferol in presence of uv rays. So the decreased precursor would be cholecalciferol since we already have 7 dehydrocholecalciferol not being converted by uvrays Tho the uw chart sites both ergo and chole as dietary sources. +2  
drzed  Wouldn't 7-dehydrocholesterol build up in the skin? Since UV rays convert 7-dehydrocholesterol into cholecalciferol, if you are lacking the conversion, the reactant (7-dehydrocholesterol) should accumulate. +  
brbwhat  They’re asking decreased production of which of the following precursor would occur? 7 dehydrocholestrol builds up, but decreased production of cholecalciferol takes place, which is a precursor in the pathway for vitamin d formation +1  


submitted by mbourne(76),

I think that if they had something like "statin therapy" as an answer choice, we would have an argument for that as it would decrease mortality by helping prevent ANOTHER heart attack. However, I think that anti-depressant therapy will do a LOT to prevent suicide, while omega-3 fatty acids (healthy as they are) wouldn't do AS MUCH to prevent a heart attack.

The question is basically asking, "You can only prescribe one of these to keep this dude alive as long as possible. Which one will have the best chance at accomplishing that?"

Therefore, the answer should be anti-depressant therapy.

bharatpillai  why antidepressant therapy though? there are not enough features given to suggest MDD. He's 56 years old, not an elderly single male so not at the highest "classical" population at risk of suicide? the question is so ambiguous... Given MI, wouldn't chronic alcoholic intake predispose him to dilated cardiomyopathy? +  
neovanilla  I don't believe it's that he has MDD by the clinical definition. It's more that his QoL has probably changed drastically since the MI and MIs are strongly associated with decreased outlook on life, especially considering how common it is to get a second MI soon after the first. I don't know the stats on suicide post-MI, but helping the patient's depression to make him more pro-active to help himself prevent another MI would be better than "a diet high in omega 3 FAs" (at least, this was my justification, as mbourne was saying) +  
drzed  First sentence of the stem: he has a 6-week history (e.g. >2 weeks) of depression (1), difficulty sleeping (2), fatigue (3), decreased appetite (4), and poor memory/concentration (5) For a diagnosis of MDD, you need a 2 week history of 5 of the SIGECAPS symptoms which he meets (he is only missing suicidal ideation and interest in activities). Thus he meets the diagnostic criteria for a major depressive episode, which means that treatment is indicated with an SSRI. +1  


submitted by strugglebus(163),
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sMto of eht tps alsuve were .oralmn Dnnrigki s'atnw gtuooura,es LDL swa ml,di IMB sah inef. He ddi ahve HTN tughho. The isbgegt sikr sorctfa aer eht caft atth he had eeufdsfr na IM nda ttasedr ffrneugsi revsee rispeesdon tgwei(h txnl.ess/oai)y ,uTsh eh si emro ta iksr orf eisc.udi

sohaib111  Won't having an MI be a very big risk factor for another one ? And also if they wanted this answer (the anti-depressant), why would they just add that his LDL is inreasing in the last sentence... +14  
dbg  bc they're SOBs and DOBs +15  
doodimoodi  Yeah, recommended LDL in people with previous heart problem is < 100 jeez +  
asingh  It is because of the timeframe of mortality is 2 yrs, everything else will affect later +5  
benny  mdd increase MI +  
benny  Type 2 diabetes and major depressive disorder (MDD) are independent contributors to cardiovascular disease and to an increased risk of myocardial infarction (MI). +  
drzed  None of the cardiovascular options would improve mortality (statins, ACEi, BB, spironolactone are the ones that have proven mortality benefit). So if they had put one of those, I think I would have chosen that, but given that the rest don't change mortality at all, I went with the antidepressants. +2  
ihatetesting  My thinking was that since he had an MI, a beta blocker would improve mortality, and propranolol is also used as an anxiolytic. +2  


submitted by monoloco(132),
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dcaaEsntpleu nsgsoimra nru ramntap in tnaiepst how hvea on ee,psnl hwhteer cypayihlsl or nnul.ocitlyfa eRlcla( hte aydwrie-ra of easelaqu iskelc llec tisptean pxirenecee askthn to hriet nfctlnouia te.euc)ntsomopyla

sympathetikey  Agreed -- went with E. Coli like a dingus, just because I didn't associate DIC with S. Pneumo. Thought it was too easy. +  
chillqd  Isn't E. Coli also an encapsulated organism? What makes Strep pneumo more likely in this question just because its the more common cause? +23  
studentdo  Pseudomonas aeruginosa is encapsulated as well. I think the right answer has to do with DIC but why? +1  
mgoyo89  The only reason i found was S. pneumo is more common, I went with Pseudomonas because of the "overwhelming sepsis" :( +1  
kard  Everyone is correct about the Encapsulated microbes, but this is one of those of "MOST LIKELY", and by far the most likely is S.Pneumo>>H.infl>N.Mening. (omitting that patients with history of splenectomy must be vaccinated. +1  
djinn  Gram negative are more common in DIC my friends +2  
drzed  Correct me if I am wrong, but I am pretty sure that E. coli is NOT a common cause of pneumonia because it must be aspirated to enter the lung. Thus, only patients with aspiration risk (e.g. stroke, neurogenic conditions) would be at a chance of getting E. coli pneumonia. +1  


submitted by yotsubato(968),
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Thsi etusqoin si hbltuls.i The nwaom oludw omts eyklil be dctacaeinv ot tSerp ne,mpou eyalsiclpe if she adh a eelmytcspo.n

E coil si osla an nldsuapectea ucimebtra ahtt asesuc m,uinoaepn os ahtt is moer elliyk .IOM

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 +1  
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. +  
merpaperple  I thought this too but it seems like Strep pneumo is just more specifically associated with infection in asplenic/sickle cell patients than E. Coli is. Just one of those classic associations. There's a sickle in the Sketchy Strep pneumo sketch, vs. no sickle in the E.Coli sketch. +  
drzed  E. coli causes pneumonia by aspiration, for which this patient had no risk factors. For USMLE, if they don't say the patient is vaccinated, you can assume they are NOT. Just because she has a history of splenectomy following trauma does NOT mean she had to been vaccinated--don't fill in the history for the patient, only use the information they give you. +  
vivijujubebe  also DIC more often seen with G- bacteria right???? That's why I chose E.coli instead of S.pneumonia +1  


submitted by sugaplum(323),
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These awlyas ptdeipr me pu:
+ dPpsyai=loi dnrsepso to ertaw anirpteio,vd wlo mesru Na
+ etnCr=al srdnpeso ot sossvepra,in hgih suemr aN
Neohcgein+ pr = rdsnpeos to hnintg,o omnlar mersu aN

lynn  I think serum Na+ only depends on the patient's access to water. FA19 pg 344 says serum osm is high in both and doesn't mention Na specifically. Spent a while double checking for DI, but low serum Na for polydipsia is definitely correct. +  
drzed  In general, SIADH or polydipsia will cause HYPOnatremia, and DI (central or nephrogenic) will cause HYPERnatremia, but in the latter--as you stated--water access change the serum Na. +  


submitted by monoloco(132),
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hTis is a poahlypsai fo het leeprrueanitlpoo reemnab.m hTe tugs aiterenh into hte oraxht, slualyu no the eflt e,sdi adn lrtseu in aaoppsyihl of teh slgnu b(csaeeu re'they obrhliyr s)rdmpoee.sc

johnthurtjr  Usually on the left because the liver prevents herniation through the right hemidiaphragm +7  
asdfghjkl  aka congenital diaphragmatic hernia +2  
pg32  What's weird to me is that if you usually see air in the intestines on x-ray when they are in the abdomen, why is there no air in the thorax in CDH? The intestines should still have air in them, right? Also, what is filling the abdomen that causes it to appear grayed-out in CDH? +  
drzed  @pg32 You can actually see a gastric bubble if you squint hard enough. Look at where the NG tube is placed; there is a radiolucency to the patient's right of the NG tube which is most likely the stomach. It probably then is radioopaque distally due to the pyloric sphincter, and air having a tendency to rise. +2  
bbr  Any idea what "absence of bowel gas in the abdomen" is referring to? +  
rkdang  my interpretation was absence of bowel gas in abdomen --> the bowel is not in the abdomen --> incomplete formation of pleuroperitoneal membrane bowel gas is a normal finding that you often see on x rays of the abdomen in a normal patient +1  
seba0039  @rkdang is it also abnormal that you cannot see any air in the lungs? This threw me off when I was trying to read the radiograph. +