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Welcome to drzed’s page.
Contributor score: 220


Comments ...

 +1  (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.


 +3  (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.


 +12  (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"


 +3  (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.


 +9  (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(310),
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.s9hc/ctt/lpw8/6./.5n:p/2tolihmbC0Pwne.rwagiM/cm0nisv

serlO niSg is a ewty,ssi-tiilvon wciefsoyl-ctpi ndfinig fo Mgocbnkere srrseerAosiciololt ()MA hiacdcrteezra by "a aplbplae hgluhato eslselpu,s driala rrtyea lwehi hte PB ucff si tliedfan eovba oslitcsy eerp"rs.su

It si isspbleo htta trh)a i:ee Teh cocip-tiiewslfy fo tsih etst esnma it is loas aclbepliap ot sshteolrcsoaire (ton jstu AbM )) eTh EMBN itcelryrnco imilesp ttha MA is habternaingcle tihw siroetsseoa.lhcr

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! +  
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(599),
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oT epnaxd no is,th tahw we nhikt apshnpe ihtw 'Poinkrsans edeisas a(nd iimnnsipnaak)rso si an lebncaaim eneetbw omdnaeip adn cheonci.aetlyl tI keasm eomr nsese fi ouy olko at shit argimda, pagyin pacratiurl onntttiae to teh dtnriice pah.atwy Lsos of icenrdoiagmp (DA) unsnoer from hte uainasbstt argni N(S)c tsleurs ni antocstn noittavcia fo tseoh ACh egncsiert e,nnuors chhiw eylautlimt surltes in hiitonbnii fo thulmsaa rfmo gntiiantii stenevm.mo fhore,rTee nusig cgoicrsninltaeih pleh whti anpisnarioknmsi yacondrse ot dl.aohl

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(1567),
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,oS T-6//251T rae the hemtcsptiay vleel rfo hte .hrate eTh talsleet iognlgan aer viarccel cyastpemiht alogngi.n ihTs oseiunqt semes mroe cctrenroi (or a uegh p)lae to em. uBt ehy, I nkow ppeole lliw rgsi.adee

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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Nceoti thta A) tro,ocoocBtsinnrhcni )B dulanaGlr nsicreo,te )D ts,rliaPsise E) idsiolnoataV fo nkis rae lal ruden pipaaatrsyectmh lornco.t

heT lyno tsmpeicahty olnrtoc is raeth a,ert whcih duolw ace.ienrs

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. +8  
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(218),
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Why on t?isngeaw I enam I get Ecasyts si bypboarl teh rugd of hoccei efrobe an lal nthgi cneda yrtpa )lo(l utb o'tdn atdnrdeuns hyw ereth oldwu be dcol eietxtismer and on gateiswn hewn is AF ti yass ihatepryrhme adn o???r?dbha

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. +11  
yotsubato  Because the NBME is full of fuckers. The guy is probably dehydrated so he cant sweat anymore? +19  
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(533),
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eTh nitetap hsa a ropir tyiohsr of eycttmsyhore tiwh baerialtl hpgceon,oitpmosayrool- nda evcideer arexntle emba torianida ot hte sivp.el Teh nitteap onw lsdsipay hohoerdryspins dan teoeurr,rdhy whti datsil rteraelu ogawrrnni lllrbyteaai. Teh iskeelilt oopitn is ttha ew ear negesi doihsesan omrf seuripov sryergu troctncis hte ee,srtur icuasng i.hst

E) ltliaoehUr mniacocar sla(o elcdla tntrnaaislio llce nocrmaai)c si asol a oiyislisp.bt Waht skame htis uinekyll si hte :lotaocin eatbliarl. eTh irorp ycsortteyehm nda aarelbilt gppo-tymsoalniorhocoe lwoud aleev asrc etsusi no btoh edsis fo eht oyd,b btu eht sdod fo alieorluht comircaan igrains rblaaltleyi are vyer li.ms

)A hTe itneapt had a hytytrse,mcoe so eth sodd of retuecrrn arlvccei niramccoa aer slao liednycbir olw. )C and D) etrrahUl oncdomlay dan eurlhatr ralsinottain llce pllipmaoa rea in eth wngro otcoilan ot ncoatuc orf tileabral rlhtauer nwroniarg wtih oehutr.errdy

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(130),
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rnccgiAdo to rD ta.at.rS omrecaioacAnnd is teh smto cmonom ecasu of ugln necrac ni efaeml nno osemks.r

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


submitted by krewfoo99(93),
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hyW dwolu rirpnsoef be eht ngwro sae?nrw dWlunot aniuctcauoml fo iotcx rsinptoe suaec eht llec ot ergonud spaotsoip ?

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? +  
flexatronn  @powerhouseofthecell so it all goes back to basic immuno (i got this wrong and put apoptosis as well) but after reviewing relevant anki cards, i now get it. So proteasomes break down tagged proteins within the cell (endogenous). The breakdown products get taken up by transport associated with antigen processing (TAP) and brought to the rough ER. The breakdown products are then loaded onto MHC I molecules and brought to the surface of the cell. When thinking about MHC I, think about CD8+ T cells (FA MHC 1 x 8 = CD8. Now to summarize, when using a proteasome inhibitor, you're blocking that tagging and MHC I loading process. As stated before, CD8 recognizes MHC I (which won't happen when using these drugs) +  


submitted by cbrodo(60),
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hTe sertopori snomulc saicsFulc(u nieaua/lcustucFcuss lgiiracs) racry ifroonminta ot the rnabi agnrdgrie p,ooporireitncp ,binoviart ircavmntdeiisi cuoht nda suserepr. hylciPas xmea idnfnigs gsutgse a lisnoe erhe t(he laasphmtcoini rtatc caiserr niirpcaipnkp/ adn rrtatpum,eee dan heets were lron)am. enSci the attnpei sah laanrobm isfnndgi ni the rwelo reximetesti, dna lrmaon ifisndng in het euppr eiemstrt,iex eht ernwas is ulsucsFcai cir.ilsga ihsT si becuase oamnritfino ofrm body rsaae lewob het elelv of 6T si ecdrria yb lcrisaig dan inoifmarton fomr yodb resaa baoev eth elvle of T6 si ceirrad by cnaesuut.

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 +4  
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(1567),
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g.brieion//i)kthg_i/d.igwPoao/kfopeeyswado:rlnii(ptr

eerH is a elittl ibt on peroporeafig.dHno ti selhp

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(34),
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nRraitovi sithbiin 40Y!5CP So uyo nca eus ti to otosb eht etooiarnnncct of eht hreto ereotaPs nrbsioiiht by ritnegenvp irhte etmabmisol by C4!50YP

mousie  who knew +6  
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 +4  
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(533),
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Teh sinegl tsom ptorantmi gnhti atuob hsit rgsos gthyopola is atht the sesaedi is dominluu.trla ihTs dtscnieia aatmeessts rmof tsinadt is.ets

rvLie csssebesa rea asyuul lgarni,us lildfe whti cayemr eylwlo sup, adn may oswh a irbfosu .upaelsc rhisCrosi otefn hswso a lolyew roloc ude to atfty ehnacg sa lwle sa vrtneegeiera eus,dlon ichhw rea ton ertsnpe eher. A oflca dlonrua ayelppirsah si a graslnui mrtuo of het ,ilevr dna hsti is rdtoul.ianmul iiaestHpt B si a etitll darrhe to ghinissitdu eceusba ofmr athw I nac tlel ti can be alnrlouutdmi in omse cssae, utb siht velri alos swosh nneo of eth srislosec from ncohcri mmtaonlnafii ahtt uwold liekyl myacoanpc Hpe B. i,laynlF ew see on kadr orolsnditoaci to cnidaeti fintorn.aci

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! +  
sophia  UW QId: 59 +  


submitted by sugaplum(376),
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slwaay reembrem ehtm in rdero ihtw rfa,umlo SSTEEIA=I
dan teh wto no teh NED aer ICNADOUT-D

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(1358),
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Pre FA (pg. 63:)6 cienoCnrgn trseba .ncea.rc.

"oAitainicpfmlovn/rperisexseo of rgnrrepsoeo/tsete noge pcetrerso or c2br-eB HR(,2E G aEnF coet)erpr si coom;mn RE ,⊝ PR ⊝, e2Hdnun aE/R ⊝ mfro emro vrgg"ses.eai

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(218),
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wyh seod mertteant fo roophyhtyid (wiht tvneehoyxrloi mI' ss)unigam ceirneas rski fro poy?taymh I ochse it pmylis bc sit a nmcoom vresaed fcfete fo itnsast utb I o'tdn rlyeal rutndansde woh argneitt dopytymrishhoi at teh amse miet wduol heav hyigtnan ot do htiw it ??? lphe epsea!l

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(80),

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(533),
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nI an dleyelr nitatpe twhi eidlotsa etvedlae enklaial phhtspeasoa n(loram sremu aucciml dna e)stpphaoh Pe'gsat sesidea of enbo ludsho eb at hte pto fo hte tinea.dlffeir hTis saeidse si due ot sulieordnyatg fo aocstltoesci nda eatcistoobsl iyttvica; rftis an italini slstoateoc reciytthvaiyp eph,sa nhte renecdias tsetsolaob ativiytc rof a ,xturime hnet eotsatloscs noburt"u" edaling to ntlvreaiiozn-omraie dna sceocrlti neob qel.asup nI oiidta,nd isht nac aeetcr svrrnetaoueoi thussn ni eth soebn iwhch eacesdesr nreeastsci, gaeidnl ot ighh ttupuo cadicar ulrefia (a iiaslrm mlberop acn eisra ni reoaoetnrusiv susiaflt mfor oobdl dyia.)issl nO ohlistyog it wlil haev a oa""cims e.trtpna

-A) lemynAsrau onbe ctys- llgryea a pudroct of ytcvaiheriytp of tlosae,csots sthi ccsruo reom ontef in eht s,iblm nad ssohw a cticsy aespc htiw klinolba-elo lniota.di B) g-iaorAsocmna osrocgnamiaa of eth oenb si n asoltm elpury ictly s.oinel yheT rccuo orme lnfqetyuer in eonuryg pol.epe )C cNinia ifieyce-cdn I nca dnfi hnnitgo utboa nvaitibm B3 ccfyeneidi gniliovnv obs.en 3B ictfniedce urssetl ni ,ageapllr ithw hte lcacssi hTree 'Ds- aemtirdits ahs(r cecaenlk on 43/CC m,emtodea)r ,deaetimn dan erdiraah. E) reaaOcsoms-to duFon tmaslo ixevucslely ni orneygu ,opelep itsh ebon gwrhto srcuco at het htwrgo et,lpa ruclrpitaaly ta eht liprmaxo nde fo teh aiti,b dtails den fo eth mfrue, or milorxpa den fo teh umurhse i(n eht ngol nbose donaur royu sekne or at uroy .o)lsrheuds It wohss a g,erla sodil ggonrwi smsa hatt amy eiasr eht omsteiepru ni a tnsbusru toed/rnn'Csmapat ilnrteag. F) torctsPia mar-occina rera ofr inbeg noe o,f fi otn hte loyn aactmtstie oebn aenrcc ahtt si puyrle sio.aoblesttc

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. +2  
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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eht tepatin sah sosbstea ihcwh is ittricevesr ce(ul aws palurle l squ)CpeaDLO si derecdeas in hoaitcrcnir-ta nonctoidsi isttilen(itra lnug zd )cte and lomran on ratacihocex-tr itdsoincon surmal(cu s)eissu

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. +1  
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(376),
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meoopirphllnnypnaea si an phaal nogista that ausmslitte herualrt tmhoos eulmcs ctni.tnraoco - mrfo upeotda,t he,eorvw it lsao yass ti si otn ncdmmeorede tetermnta mearoyn

ugalaxy  α1 stimulation (via α1 agonist) constricts the bladder sphincter thereby, preventing sudden bouts of micturition during coughing/sneezing (abdominal stress). +7  
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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nneArdsog seauc ea.cn reoetsTetons si a bterte sanerw htan drdoinoansAlet b/c hte seTrtontesoe si asdosctaei wthi ptrybu,e dAstoailnrodne si eomr astedoacis htiw het ardnlae da.glsn

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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riFst athre nosdu S1() si etnedager yb wot rheta va:selv teh atlmri elvva dan psdcriuti vv.eal Nealyr siuulmstnoae glosnci of seeth vavesl layrmlon tgrnseeea a isnegl 1S snod.u Slgtintip fo teh 1S sdoun is hread nehw trmlai adn tudscirip vesvla esclo ta litghsyl nidfertfe te,smi twhi saluuyl the lritam lgscion efebor pcridtusi

yotsubato  Then why the fuck is it describing a mitral valve sound in the tricuspid area +25  
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. +36  
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. +10  
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 nssrpeet wthi na rnaamlbo essotnnia fo hsi ltfe dhan atth searspd to btho his lfte mar nad f.ace A eosnil of eht eosntaptlcr uyrsg uolwd seuca iths sa ti it nsrsbpeileo fro tneoassni.

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(59),
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i tdno' tihnk you ened to knhti lal atth u.hcm olko ta lal eht nopoits nda hknit of hawt pspnahe whne hyte ,eeAsc. iarn B, ,C D adn F lla can aseuc irlttsiinate Bua e.emdt aigcrinnse paipeylrrcal ensricates yildtefien .dsotn'e

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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ePnatti hsa aclphmtioyye re,va sa eeidvnced yb orhtytrs,osieyc acolysorisu,gtn nda haehcasde am;p& inezd.ssi POE is adsecdree ude ot yysrhstciroot.e Dardcesee APL dowlu niedtaci CM,L nto V.P

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(134),
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To be cpelmloyet clera!

Thsi ptniaet sha iintsosysC a rare sltuomoaa sreeceivs oolmsslya stgaoer isordred and msot monmoc auesc of nnicoFa mrdenyso ni cein.lrdh Cntoiysiss is eyicsstm nad adels ot itycnes aclystr osdptesi in cesll and ssuesit hrhouogttu het byo.d

lhtAghou slWinos seaised can adle ot F,S hte lstyrcas ni eth nroasce sode ton treoalecr wthi lisnsoW dsiaes.e
e Mor :onfi .vo8/n.ts4arwcitbC./1/p4smM.geh0/1it/pwwmicncn6:/hlPl

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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Of eshte isopnto aa,eilvlba nSwchan sllec owldu be teh lony eclls epesnrt ni the SN.P , tesrtcsoAy amilocirg nda olgsio aer all NCS clles leetat liS secll are in the semclu dan rvees to dia in cumles paerri and rnirganeeteo

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 +16  
drzed  Myosatellite cells are also called satellite cells so it is not clear which definition they were using. +2  


submitted by iviax94(7),
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erThe vaeh eneb a epuocl of usstoiqen touba isth tocip no het ernew msea.x e’Iv bene aswrgnien yb tngquaei lioibd to oseeonttrtes lselev dna lcornautn tsenrieoc ot thleha of vatluuerasc eetsrsi(crhooals or .)not sI isth cctero?r

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. +28  
_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. +1  
drzed  @pg32 bro spoilers +2  


submitted by mguan1993(9),
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anc oeenmso xinlpae yhw teh rsaenw si not arlndae dn?lag I efle iek fi nealrad dlgan wsa the uises eehrt udlwo soal eb raesecedd oranttccnsonie fo S,FH HL, nda gsrenteo tr?ghi

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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wnoD seydmnor n2d tsrmiteer rncsee sa(uuyll dauonr )6ws-1k81 hssow rescdadee FPA, teoislr nda iercednas CGh adn biihnni .A

fO otsyimr 18,3/2/11 wnDo rneoSdmy si eth yoln to heav na leeetevd hGC

makinallkindzofgainz  "Down Syndrome has high HI (hCg and inhibin)" the relationship between the words down/high really stuck for me +2  
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) +3  


submitted by pppro(23),
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etniatP ahs B.HP ievG hpala eno inagottsna to eecrud ohmtso cesmul iartnoocnct dan eeelriv lfiicyufdt i.nnigutar

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) +4  
pathogen7  @drzed tI mean techinically alpha-1 blockers are on the Criteria too ... +1  


submitted by pparalpha(84),
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Cna enoesom pelsae xanilpe wyh ti lwudo otn eb ocyngleg ?doieetnpl I hghtout het seqtuion wsa iaknltg oubta eht rabWrgu .enn.h.moepon os hyw ont wnekodbra fo lygcgneo ot ugelcso?

I gessu ti oludw ont enlaxip hte ?deame

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(293),
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hsiT arelcit aslpexin hte tsogiplypyaohoh lle:w .:b/./Nvgknt.oosoim3/hlwb/cpK4/in8wt410.Bshwn.

eTh hgrit leirntevc si arripliym pdiselup yb eth ACR hichw osal sueplisp hte AS oden dan AV dneo 90%( fo sretha eucabes etyh era rghti dn)ma,toni denliag to lsso of titinraotyccl of hte higtr side, adn uhts dlifu bilpudu acusngi vltaeede terlanc osvneu ps.sreeur aEetvedl rpsseresu in hte revil dna alotrp ysestm oludw eadl ot elhyatemapog nad fere idulf uouctimlacan ni the .tempronieu

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. +10  
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(113),
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ingfLti daeh lwieh nope:r 1 mtc hoaoinSl mlsie: 2 so:mnoCionthg 2 thmnso

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  


submitted by fallot4logy(10),
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ywh otn tioiscoie1mdoadsurh?r.as arristthi keli y.ytu eo dp2.mnismskione.svs.t 3y.il osietssir is a ibt nesritoarvlco

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(227),
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So I hitkn htat isseu of wsitr xtosienne dora/n frigne pdro dwuol eb eorm ladari .envre rHevoe,w etrhe aws emor moxilrap e,nakesws os ti wdolu eb C7.

"78- yla hmte r,ts"ihtag eth pt loutdnc' la"y tmhe ar"tthigs os it wodul be 7C toro

welpdedelp  *As an addition, median nerve involvement would have leaned more toward C8 than C7. +6  
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(23),

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(1567),
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isTH squoeitn is utsj itcriacl hnniti.kg The lenrasda aer laitalreybl nda iemslmlrytacy lalms. llA rheto nsrwae icoehcs aer ont ylklei to eb vnee ellarai.blyt enracC twno' quylale eaprsd ni fetrecp rmtmeysy rno ceniftoisu cuessa hwlie gaiinantnim teh ealrand raceethrc.tiu

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(1567),
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TsiH eiusotnq is tjsu tiailcrc ig.iknnht The dreasaln ear ralllyibeta dna cemytrmilsyal lmasl. All heotr wanres eciochs era nto yiekll ot eb vene lati.brelyla nceraC ntow' laulqey rapeds in reetfcp yysrmemt rno uonistcfei esaucs hwile ngaitininma teh naedrla crreeiutcta.h

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(33),

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(1032),
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ahtW do oyu eus ot ratet ctipHae holeany?pcptaEh tasLcl.oeu hatW esdo ahtt ,od ti iescfadii N3H in eht IG actrt oint N+H4 adn mtpeoors slso of eth ogoeusnirnt upcstrod thta aseuc .hcnypaapehloet sihT si who ouy beemrmer hsti e.rsopcs

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. +1  


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stOrtail rkwos by tbininihig rtagcis adn aictaprenc i,lpeass hte yesnezm taht erkab ondw csdretlirygei ni teh snteit.eni

n'toD rebak ihgnst wndo ni eth &es--tnin-s-egt;it csotiom ahaeirdr

lptanAprey peolpe esu it to elos thegiw. hWo w.nek otN em

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


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o'nWdlut tignell the entapit tuabo teh lrefarer od rmeo rhma htna ?odog

  1. tP orssndeci it a brieb and valsee
  2. uRsni dtsyu edu ot olpcab tfcfese
  3. Ptsu aolpihsdto/c ta kris ofr aeltiontp geall hlass.e

I ssuge myeba I erad it as a udsty whne ti rllyae si jtsu a frrrlaee btu sti nto taht hucm of a leap ot hinkt htat shit ""nxa"lpmereeit atetmnter is ratp fo a utyds

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(76),
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sola ni csea etyh ask mrebreem htat eshet era Pvh'FaeUsA( bueold n)dsob dna eyth aer erttbe ahnt tuteaSdra nos(fta lueodb s)nr+bscbdoa

drzed  PUFA = poly-unsaturated fatty acids in case anyone didn't know the acronym. +5  


submitted by suckitnbme(176),

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(43),
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(oFmr WU 8)1521 eSom cnaditoseim giuincldn s,dioipo ioadstntarorc ,dyes nad meos bciatsniiot .e.(g )moavyinccn nac undcei dan DDNIEgENIPETNE- tams ellc tengiolraduna yb atnatocivi fo nipotre kneais A dna P3I ei,sakn wchih steuslr in aeeresl fo nhsitme,ia niinrbky,ad dan toehr eticcocamth rsfacto -;&tg seuiffd h,itngci n,ipa a,shobnrcopms dan oziacdlle inll=sewge it.cia(ruar)

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(60),
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lla het roeht insoopt tp oudwl vhea sretu,u v.eioars ernutsr ehty dtlouwn lkoo loamnr dan hyte uwdol heva prtaiohc v.sroiea

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(99),
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cnrhbosu iooscnurbtt stp ar ongeyx in oivlael no oeninrgt ebla to nerte hpcre(mtaiso air ngrnitee boyd 87%( rnineogt nad %12 exn,ogy etignonr is os nmrtoitpa ritnogne cb it is a ylproo rdsboabe sga adn thsu si in egchdra fo gepkeni ilealov xlt)dnoefeanygi ni teh vaeloli is rboeabsd niot the oolgecbdin rdu het oulmve of eth loielvl aoaelrav eslocpla bnpsoaro ti tsetaacsile

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(65),
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eyvr udstpi tsiqouen. ehT usriv asw iehdaln -- tbas hnag sdipue wnhe tyeh lspee nad od.rol oS it drseasp to hte airbn ylerdcti form eth cfrtaoloy ssmtye aiv odetrgaerr nrastropt hghurot e.rsnev

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 +  


submitted by sympathetikey(1358),
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eTh holew ck"psi at teh nsil.ceuesa.o.s semo bn"dg,ilee dmea me knhti iPrsoais.s ouhSdl haev gneo wtih tniAcic tKasoisre dasbe no the teinatp yirosht (lsto of sun euopxsr)e.

Aiicntc saeitsrKo

lngaetmnirPa ssnoeil scadeu yb nus espoeux.r lmal,S orghu, hmtsoueeatyr ro irhwbson eualpsp erslqaop.u sRik of qsuoamus ellc cnoacamir si nplioroporat ot greeed fo lpetlheiia .spdlaasyi

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),
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yhW is si nto edpsuo ra?usymen

tci"orA srusueenydoamsp ltiycylap ucroc sa a ultser of uamrta /+- onintten,vrei a enodrsicde esbtus of riatmcaut itroca nujiyr ni het yijtaorm fo sacse. yehT nac be ceuta ro "cohincr.

nu/i?aaipgerrhuy/ogndstmor.sacaoetple=sdpotslaar:dtaiiu/cre/-s

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(47),
  • 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(1077),
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ardncyeSo aphiprhosdmaeityyrr u(slyaul /dt onccrhi lnera rai).felu

Lba fgidnins udnleci ↑ THP sneo(pser to wol a)m,lccui ↓ smeur iaucmcl ner(al el)ifuar, ↑ suerm oethaphsp (ernal )irf,ulae and ↑ eklianal tpeshpohaas TH(P cviinatgta )ott.oseaslBs

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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reiarDah sauecs slos fo ,eratw aN nda c.rBabi merbeRme ahtt rdiraahe is a escua of non noian apg abmltoice iaisdcso ucaseeb eht osls of raoebiacbtn si stendeomacp by aenrgiincs dloiehCr pn.teioarobsr So hes cna eavh pyheliorcahmre or yaieprtaomhn due ot itneka of nyol eref twrea for 42 rhso.u uBt hse hsa IESSZREU so inmapeyraoht is tmos yiklel

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. +1  


submitted by hayayah(1077),
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rSttche ro taiidoln fo eth icxrev dna anvaig rea trgnso uitilsm orf yocniotx rsocetien, middaeet by lraenu htypaaws lldace the sogFrneu exfle.r

ctA:reli nuti-wnc/sehcocc.refx/ceriitcslstefw.eeonduecroose//sni:g/ptmeprw

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!). +1  


submitted by hayayah(1077),
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eitNo,c het mest yssa orocprs"res in the ksin"

D3 c(llcloehir)oaefc romf rexpseou of nisk asr(umtt eabal)s ot sun, itnoiegsn of fish, ik,lm .altnsp

2D allccroorg(fe)ie fmro iistegnon of als,tpn ginf,u .seysat

oBht rtednoecv to 2-O5H 3D rta(soeg )mfro in rivle nda to het aviect orfm ,H(1O52-2) 3D loirctlci)a( in y.kendi

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! +5  
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(79),
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I kitnh htat if yteh adh ingmohtse lkie ntitsa" patehr"y as na resnwa ,cicoeh ew udlow veah an anrmtgeu fro hatt as it wuodl csareeed ytorlmait by heplgni nvprete ANROHTE rhtea ttakac. vwr,Heoe I ntihk that aestdeiprt-nans prteayh lwli do a OTL to eptrven cieds,iu liewh m-3egoa tafty adsci lh(aythe sa tyhe ae)r lutwond' do AS HCMU ot retpvne a reaht kctaat.

hTe isuentoq si blsaacliy ka,igsn o"uY cna nlyo briesprce eon fo ehset ot pkee tihs dude evali sa nlog sa .ssboepil Wichh one illw aehv teh ebts cnceah ta iomclsphngaic tt"h?a

erereTfh,o eth ranswe lshduo eb ee-apnsstrdntai ptyrh.ea

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(165),
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soMt of teh stp vsaule wree loa.rnm Diirknng ntswa' uog,atseour LLD saw dli,m IBM ahs en.fi eH ddi avhe NTH gt.houh eTh gesgitb srki fotcasr era hte cfat ttah eh adh erusffde an IM nda taedtrs gruensffi seevre ipsdeeonrs (ighetw sio./tlsaneyx) h,sTu he si reom at risk rfo .idisuec

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 +20  
doodimoodi  Yeah, recommended LDL in people with previous heart problem is < 100 jeez +1  
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(136),
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tEleucpnasad nssgaoimr rnu tnmrapa in ntipetsa how avhe on lens,ep erwhhte lplyiaychs or laouifc.ynnlt l(aeRlc eht -iyredaraw fo euleqaas lcsiek ellc antisept reeipexenc natshk ot irhte ntoufialnc .m)aoyntotslupcee

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? +26  
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(1032),
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iTsh uteinqso si u.ihlblts eTh omnwa dwlou smto lyikle eb tiaacnvecd to erptS uempno, csyiellape if esh hda a empelst.cnoy

E lico si also na epdaaetuncsl mauecritb that scesau ,emunpoian so ahtt is reom yiklel OIM.

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(376),
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eeThs aasywl ppdeitr em p:u
+ lsdpiyaoPi= esnopdsr ot reatw ritep,oaidvn wol rsume Na
+ aln=rteC sdposrne ot r,sonasepvsi gihh usrem Na
hp+Nngieroce = dnspsreo to t,ninohg anorml murse Na

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(136),
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Tish si a hypspalaio fo hte nlpterolparoeiue nme.merba eTh tsug eiaethrn tnio eht a,trxho llsyuau on het flte ,isde and esultr in yoalasipph fo het gnlsu ucsbaee( eehrt'y bloyirrh rme.oes)cdps

johnthurtjr  Usually on the left because the liver prevents herniation through the right hemidiaphragm +9  
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. +