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Welcome to sars’s page.
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submitted by imgdoc(132),
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I tuthogh taubo it lkei h:tis tnteaPi is vghina hcnpoyecisg ED - tsi lal in his hdea, lidboi si namlor dan roualnnct enoticrse era .amonlr

fI ihs onTtsresotee eelvl wsa owl - idbLoi cers.eaded fI shi svnuroe mesyst rytepst(ysaemhmipptic)achtaa/ wsa dadmgea - ctrolanun tceerniso .cdeerdeas

eoHp isht e.hspl

sars  Idk about this. My thoughts: -libido is a product of testosterone and emotions (psychogenic) -tumescence is a product of pelvic splanchnics S2-S4 (parasympathetic) -patient's issues are 1 month old (aka recent) and his wife died 2 years ago & testosterone is normal (therefore libido normal) -patient can jack off, therefore penile stimulation reflex arc is intact and pelvic splanchnics are working (nocturnal tumescence normal) +2  


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saBecue you era upse,ni tsh’eer desrcaein oarpedl igogn cbka to ruyo earht on( nede to kwor inagsta ayvgri,t ruyo odbol n’sit opnloig ni oury sleg as chum teerhi). sA a suelr,t NAP si etrdecse ued ot AR etrshc,t adegnil to irdussie dan a oneudticr fo odlob oe.mvul

urachus  When the person is lying down (supine position), gravitational forces are similar on the thorax, abdomen and legs because these compartments lie in the same horizontal plane. In this position, venous blood volumes and pressures are distributed evenly throughout the body. https://www.cvphysiology.com/Cardiac%20Function/CF017 +  
thelupuswolf  RAAS trumps ANP though, so the dec. in RAAS as said by colonelred_ is likely going to have more of an effect than ANP. +1  
lola915  If you have an increase in ANP wouldn't natriuresis occur and cause a decrease in blood sodium? +2  
mynamejeff  Because you are suprine, there's increased preload going back to your heart (no need to work against gravity, your blood isn't pooling in your legs as much). As a result, ANP is secreted due to RA stretch, leading to diuresis and a reduction of blood volume. +  
sars  This is a "read my mind" question and complete it in 1.5 minutes. Thanks +2  
faus305  @sars that is every question +  


submitted by lsmarshall(395),
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I uhtoght this asw a ktcri ueqionst icens kins sacecnr era het stom omomcn epyt of neccsar lla.over utB aultlayc gnmoa VIH s,eatintp VIaldHre-te ecncras are uhmc emor nommco athn HateeInn-olVd-r aecrscn (neve ksin a)rncce.s edcBn-VEdui mairrpy CSN lmomhpya si eth ynol pnooit ahtt si figIsnDiAned- l.rcnsseeac/nli

medskool123  why not hep B? i guess another whats the better answer ones... Just rem reading that it was more common with aids pts.. anyone have an idea about this? +1  
haliburton  Yes, I think CNS lymphoma as an AIDS defining illness wins the day. My thought was since SHE has AIDS it is most likely from IVDA, which has a high risk of HBV that could go undiagnosed for a long time. at 32, that might not be long enough to have HBV and get HCC (but with no immune system...?) +3  
yotsubato  God damn this is such BULLSHIT... +13  
trichotillomaniac  Why you gotta do me dirty like this NBME +2  
sars  My thought process, usually wrong all the time, was that HBV (IVDU) can occur to anyone. Acute hepatitis to Chronic occurs when HBV incorporates its DNA into host and releases mutagenic proteins. This is regardless of immunosuppresion. Primary CNS Lymphoma reappears primarily when you are immunosuppressed (organ transplant, immunodeficiency, HIV/AIDS). +  
syoung07  Hep C is far more likely to become HCC than hep B +1  
jurrutia  Even if you were thinking skin cancer is more common, that's only true for basal cell and squamous. Melanoma is rare. EBV much more likely in aids patient. Even H pylori was a better answer. +  


submitted by m-ice(325),
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lAl XOH eensg rae rtsioiantncrp rscofta ttah help guetealr boyd uoaylt nda eerfnftdi iopexrsens of egsne rof haec obyd etn.mgse

sunshinesweetheart  I got this one right but wasn't exactly sure how to rule out 'translation'. I guess just because we're talking about a gene i.e. trasncription and not miRNA i.e. post-translational modifiers? +  
sars  Hox (homeodomain) genes code for homeodomain proteins which are specific transcription factors (bind to enhancers, making these activators). They promote transcription of certain genes involved in development. Thanks so much +  


submitted by lm4(9),
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in eth ecnxoeri srcna,pea ddeallr,balg nda ievrl paooyhltg oenctsi of oaapt,mh tstraa smteonni atht het tpliehuiem lngiin byaliir ttcra ash lklanaie stpphehoaas so ehnw ehyt rea adagmed it reassele ihs,t anreinscgi umers alk .opsh

lilyo  Cholestasis will present with elevated conjugated bilirubin, Alkaline phosphatase, GGT. Depending on the cause for cholestasis it can present with pale stools and dark urine. This patient has cholestasis due to choledocolithiasis. Look at FA 2019 page 390. +  
sars  From what I understand, this could be acute cholangitis (inflammation of the bile duct-charcot triad-hypotension, RUQ pain, jaundice). Biggest risk factor for this is choledocholithiasis. Damage to bile ducts releases ALP and GGT. Thanks +1  


submitted by nwinkelmann(285),
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sDoe onneay heav a oogd nptixolaane orf why deeesdrac lsevle of ihibnin is ?owgrn ormF my rnnsidntgu,ade innhiib adn atviinc kwor rteg,hteo in ttha biiinhn nsdib and bsclko ainvcit nldagie to adreecsde feacdbke no uyahhtmspoal and cnaitiv ncrieesas HFS adn HGRn tpd.uconir.o hts,u fi yuo cresdeae inbnihi ehnt ouy oudwl aehv aiceensrd vitcani cwhhi dluwo lade ot asndiecre nHRG dan FH,S ith?rg I undfo eno aetlcri nlgaitk aubot ti ni agerdrs to tpb,uyre but ti meess ot be a otteoh/nyphsis mirdofenc at itsh o.ti.pn. si that hwy? tuB t.lli..s ohw do I rleu ti otu no a e?stt

yb_26  I also picked decreased inhibin. may be it was one of the "experimental questions", which are not even counted on the real exam +1  
artist90  Inceased FSH will lead to spermatogenesis and spermiogenesis NOT Increase in Testosterone which is causing increased Height of this pt +6  
artist90  Inhibin B only has negative feeback on FSH not GnRH. see the diagram on the topic of semineferous tubules in FA. Testosterone has a negative feedback on BOTH LH and GnRH +1  
usmile1  Kind of like how nocturnal pulsatile GNRH release occurs during sleep to stimulate growth (FA page327), the same thing happens for puberty. Pg 325 in FA, "pulsatile GnRH leads to puberty and fertility." It doesn't explicitly state during sleep, but pulsatile release of GnRH leading to pulsatile release of LH and FSH will lead to puberty. Puberty starts in the brain, its onset really has nothing to do with decreased inhibin levels which happens in the testes. hope that makes sense! +3  
sars  From what I understand, inhibin is only released by granulosa cells when FSH levels are high. This is a boy. Next off, this question is about puberty, which is due to pulsatile GnRH leading to large amounts of LH and FSH, leading to large amounts of dihydrotestosterone (males) and estradiol (females), and eventually secondary characteristics of puberty. The increased pulse of estrogen and testosterone leads to GH release, which is metabolized into IGF-1 in the liver. This leads to long bone growth from what I understand, which is not much. +  
cassdawg  @sars inhibin B is also released by sertoli cells in males and will feedback to inhibit FSH release, its not just a female thing. Also, there is actually an inhibin B pubertal surge in both females and males that corresponds to maturation of the granulosa and sertoli cells, respectively. Hormones are wack. https://pubmed.ncbi.nlm.nih.gov/15319819/ +  
j44n  I think youre just supposed to see that he's starting puberty and know that the nocturnal pulses are involved +  


submitted by neonem(552),
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lFnglia on rehttedcouts h:and osahcipd si mots nmomco eno ot be ,rutceadrf eunlta si smto moocmn to eb ctdsoe.ladi tnaLeu odcitilnosa nca saeuc uetca raaclp ntenul dsnmroe.y

nThik fo teh emmncnio gratSit"h eiLn To ykPni, reeH Csoem hTe "hTbmu for eht bneos fo hte la,mp gnrwadi a lboofalt aeshp tagstrni bleow the hbumt PMC ijton ctejanad ot het su,rida hetn mnivog to ruyo lemida sr,wit dna hnet bcka to eth bhmu.t

adSohpc,i lenua,t trerut,imuq ropi,smfi ,ataemh aape,ttci rept,idoza im.prtuaze The netual lkoso kiel tsi' ryrilsoepot itdecsdoal .rhee

sympathetikey  Yep. I didn't even look at the X-ray. +9  
dr.xx  loonies love lunate +2  
wes79  she landed on her "right hand", but the X-ray is showing a left hand?? +1  
wes79  i legit have no idea whats going on in that xray lol +9  
nbme4unme  X-ray confused the hell out of me, I was going to put lunate based on Q stem but ended up putting Pisiform because it looks like that's what's messed up in the photo? Should have ignored the picture haha. +1  
nwinkelmann  for @dr.xx, love your mnemonic. I added to it, or at least found an explanation on why it works. "loonies love lunate" and "loonies" are "dislocated" from reality. +3  
niboonsh  Some Lovers Try Positions That They Cant Handle +9  
vsn001  ngl if scaphoid was an option - would've sprung at that real quick -> thanks for teaching me the importance of knowing to look for dislocation vs fracture :D +  
regularstudent  Ahh, the classic "left hand" x-ray but actual fracture of "right hand" NBME tactic +  
sars  I think the x-ray is showing the lunate protruding out of the palmar side. Imagine the situation where you are falling and using your hand to stop the fall. Your lunate will dislocate forward as the rest of the carpal bones recoil back, hence why it protrudes through the palmar side. Thats why it causes an acute carpal tunnel syndrome. +  


submitted by monoloco(132),
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If oaenny u’tndowl n:dmi How ma I deposspu to ownk htta DTM1 has a malisir ideegrpe ot rhpzhocsa?iein caThe em ohw ot thnki, l.esp

ankistruggles  I think they were getting at how developing T1DM and schizophrenia are both multifactorial. I don’t remember what the other choices were off the top of my head, but they had clear inheritance patterns. +9  
pathogen7  Just as a slight tangent, is there a difference between "multifactorial" and "polygenic" inheritance? +  
ac3  polygenic = multiple genes affect phenotype while multifactorial = genes, environmental factors, etc that can affect phenotype +1  
sars  Multifactorial: cleft lip, cleft palate, type 1 diabetes mellitus, sjogren syndrome, pyloric stenosis, congenital heart disease, neural tube defects +1  


submitted by greentea733(17),

Why wouldn't the body down-regulate the conversion of FT4 into FT3? Is that conversion just constitutively activated? Since FT3 is more potent than T4, it would make sense for the body to turn that conversion down...that was my reasoning...obviously not correct, but idk why that wouldn't be the case. Anyone have insight?

maria_danieli  i thought the same... i remember that T3 conversion is somehow regulated but evidently not in this case +  
sars  Peripheral conversion of free T4 to T3 is done by 5-deiodinase. From what I know, only way to decrease this conversion is via b-blockers, glucocorticoids, propylthiouracil, and potassium iodide (lugols). I believe this was mentioned in the sketchy pharm vid as well. +1  
sars  Peripheral conversion of free T4 to T3 is done by 5-deiodinase. From what I know, only way to decrease this conversion is via b-blockers, glucocorticoids, propylthiouracil, and potassium iodide (lugols). I believe this was mentioned in the sketchy pharm vid as well. +  
sars  4th blocking agent isn't lugols, its iodinated radiocontrast dye! Sorry for that mistake. +  
cassdawg  "T3 is derived from peripheral conversion of T4... normal plasma T3 levels are obtained in athyreotic patients treated with sufficient T4 to achieve high-normal plasma (F)T4 levels. Administration of T4 to hypothyroid rats to achieve normal plasma T4 levels results in subnormal plasma T3 levels not only because of the lack of T3 secretion but also because of a decreased T3 production by D1 in peripheral tissues, since this enzyme is under positive control of T3 itself". (https://www.ncbi.nlm.nih.gov/books/NBK285545/) i.e. because he is taking SUPRATHERAPEUTIC T4 his T3 is NORMAL. If he was taking NORMAL T4 then he would have DECREASED T3. Pretty sure the normal T4/decreased T3 thing is in another NBME test or UWorld somewhere. +  
cassdawg  ^Sorry to add, her is suprasupratherapeutic so his T3 is elevated. Essentially in a normal hypothyroid patient they are given supratherapeutic T4 to get normal T3 since T3 is the hormone with the action. Apologies if anything is confusing. +  


submitted by greentea733(17),

Why wouldn't the body down-regulate the conversion of FT4 into FT3? Is that conversion just constitutively activated? Since FT3 is more potent than T4, it would make sense for the body to turn that conversion down...that was my reasoning...obviously not correct, but idk why that wouldn't be the case. Anyone have insight?

maria_danieli  i thought the same... i remember that T3 conversion is somehow regulated but evidently not in this case +  
sars  Peripheral conversion of free T4 to T3 is done by 5-deiodinase. From what I know, only way to decrease this conversion is via b-blockers, glucocorticoids, propylthiouracil, and potassium iodide (lugols). I believe this was mentioned in the sketchy pharm vid as well. +1  
sars  Peripheral conversion of free T4 to T3 is done by 5-deiodinase. From what I know, only way to decrease this conversion is via b-blockers, glucocorticoids, propylthiouracil, and potassium iodide (lugols). I believe this was mentioned in the sketchy pharm vid as well. +  
sars  4th blocking agent isn't lugols, its iodinated radiocontrast dye! Sorry for that mistake. +  
cassdawg  "T3 is derived from peripheral conversion of T4... normal plasma T3 levels are obtained in athyreotic patients treated with sufficient T4 to achieve high-normal plasma (F)T4 levels. Administration of T4 to hypothyroid rats to achieve normal plasma T4 levels results in subnormal plasma T3 levels not only because of the lack of T3 secretion but also because of a decreased T3 production by D1 in peripheral tissues, since this enzyme is under positive control of T3 itself". (https://www.ncbi.nlm.nih.gov/books/NBK285545/) i.e. because he is taking SUPRATHERAPEUTIC T4 his T3 is NORMAL. If he was taking NORMAL T4 then he would have DECREASED T3. Pretty sure the normal T4/decreased T3 thing is in another NBME test or UWorld somewhere. +  
cassdawg  ^Sorry to add, her is suprasupratherapeutic so his T3 is elevated. Essentially in a normal hypothyroid patient they are given supratherapeutic T4 to get normal T3 since T3 is the hormone with the action. Apologies if anything is confusing. +  


submitted by greentea733(17),

Why wouldn't the body down-regulate the conversion of FT4 into FT3? Is that conversion just constitutively activated? Since FT3 is more potent than T4, it would make sense for the body to turn that conversion down...that was my reasoning...obviously not correct, but idk why that wouldn't be the case. Anyone have insight?

maria_danieli  i thought the same... i remember that T3 conversion is somehow regulated but evidently not in this case +  
sars  Peripheral conversion of free T4 to T3 is done by 5-deiodinase. From what I know, only way to decrease this conversion is via b-blockers, glucocorticoids, propylthiouracil, and potassium iodide (lugols). I believe this was mentioned in the sketchy pharm vid as well. +1  
sars  Peripheral conversion of free T4 to T3 is done by 5-deiodinase. From what I know, only way to decrease this conversion is via b-blockers, glucocorticoids, propylthiouracil, and potassium iodide (lugols). I believe this was mentioned in the sketchy pharm vid as well. +  
sars  4th blocking agent isn't lugols, its iodinated radiocontrast dye! Sorry for that mistake. +  
cassdawg  "T3 is derived from peripheral conversion of T4... normal plasma T3 levels are obtained in athyreotic patients treated with sufficient T4 to achieve high-normal plasma (F)T4 levels. Administration of T4 to hypothyroid rats to achieve normal plasma T4 levels results in subnormal plasma T3 levels not only because of the lack of T3 secretion but also because of a decreased T3 production by D1 in peripheral tissues, since this enzyme is under positive control of T3 itself". (https://www.ncbi.nlm.nih.gov/books/NBK285545/) i.e. because he is taking SUPRATHERAPEUTIC T4 his T3 is NORMAL. If he was taking NORMAL T4 then he would have DECREASED T3. Pretty sure the normal T4/decreased T3 thing is in another NBME test or UWorld somewhere. +  
cassdawg  ^Sorry to add, her is suprasupratherapeutic so his T3 is elevated. Essentially in a normal hypothyroid patient they are given supratherapeutic T4 to get normal T3 since T3 is the hormone with the action. Apologies if anything is confusing. +  


submitted by m-ice(325),
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hTe tapneti neesd idamcel netotanti meietalimy,d hwhci aenmsitlei tagninoib a orcut ,orred ro rfarneginrts .ehr A eunrs dseo tno ehav eht smae gtninira nda aloicstnquiafi sa a hciyanpis, so it wlduo be otrapriaieppn to ska hmet to xmeeani the .tnpiaet igAsnk teh iaphlsot apnclhai ianag doclu be peptrraiapino, adn lwodu atek erom .eimt Tfeeohrer, hte sbet ntipoo goamn setoh gvein is to ska eht nateipt if hes wlil loawl tihw ehr abhdsnu rte.pnse

sympathetikey  Garbage question. +56  
masonkingcobra  So two men is better than one apparently +28  
zoggybiscuits  GarBAGE! ? +1  
bigjimbo  gárbágé +4  
fulminant_life  this question is garbage. She doesnt want to be examined by a male how would the presence of her husband make any difference in that respect? +12  
dr.xx  I guess this is a garbage question because what hospital, even small and rural, does not have a female physician on staff. NBME take notice -- this is the 2010s not 1970s. https://images.app.goo.gl/xBL4cK31ta7nG4L39 +9  
medpsychosis  The question here focuses on a specific issue which is the patient's religious conservative beliefs vs. urgency of the situation. A physician is required to respect the patient's autonomy while also balancing between beneficence and non-maleficence. The answer choice where the physician asks the patient if it would be ok to perform the exam with the husband present is an attempt to respect the conservative religious belief of the patient (not being exposed or alone with another man in the absence of her husband) while also allowing the physician to provide necessary medical treatment that could be life saving for her and or the child. Again, this allows for the patient to practice autonomy as she has the right to say no. +15  
sahusema  I showed this question to my parents and they said "this is the kind of stuff you study all day?" smh +25  
sherry  I totally agree this is a garbage question. I personally think there is more garbage question on new NBME forms than the previous ones...they can argue in any way. I feel like they were just trying to make people struggle on bad options when everybody knows what they were trying to ask. +  
niboonsh  This question is a3othobillah +5  
sunshinesweetheart  this question is really not that garbage....actually easy points I was grateful for... yall are just clearly ignorant about Islam. educate yourselves, brethren, just as this exam is trying to get you to do. but yeah I agree there should be an option for female physician lol +5  
drmohandes  I think this NBME24 is a waste of $60. On one hand we have these types of questions, that have 0 connection to our week-month-year-long studying. On the other hand we have "Synaptobrevin" instead of SNARE, because f*ck coming up with good questions. +11  
myoclonictonicbionic  @sunshinesweetheart I actually have studied the religion tremendously and there a clear consensus among all Muslims that in the case of an emergency, it is completely allowed to have someone from the opposite gender examine you. I think this actually represents how ignorant the exam writers are of Islam. +10  
korahelqadam  All it takes is one NBME question concerning muslims for the Islamophobia to jump out I guess +  
sars  This is a very fair question. I agree with sunshinesweetheart above. That is all. +  
wrongcareer69  Garbage question +  
alimd  well we should wait for the question "if a man shouts I CANT BREATHE with a police knee on his neck, what is your next step? Ans- wait 8 minutes." +1  


submitted by m-ice(325),
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rctineVsnii si a htecpuetmohrciae urgd htat zsebsliait ctsulberomui adn tevsrepn hemt rmof ssseli.aimnbgd ehT elcl ni teh turcpei si scktu in npaaah,se iwht emorcltuusbi hattcaed to sti ohorsmecmso, enuabl ot upll etmh atrpa ecuseab ti tcanno sssbmlaidee tis umilsbru.coet

vshummy  So I get that by process of elimination cyclophosphamide, cyclosporine, doxorubicin, and 5-fluorouracil are not related to microtubules but vincristine in First Aid 2019 says it prevents microtubule formation, doesn’t stabilize it because the one that stabilizes microtubules is paclitaxel. +  
vshummy  Okay, I realize now- the picture is stuck in metaphase, not anaphase. Both paclitaxel and vincristine stop the cell in metaphase but by two different mechanisms. Vincristine prevents mitotic *spindle* formation while paclitaxel prevents mitotic spindle *breakdown*. Mitotic spindle is needed to pull the chromosomes apart before anaphase begins. +14  
azibird  No, I think you were right to begin with. Without spindle formation the cell should be stuck in prophase (vincristine). Without breakdown it should be stuck in metaphase (paclitaxel). Metaphase is shown here with spindle fully formed, so it should be paclitaxel. +  
sars  I agree with the logic stated above. It could also be that the researchers added Drug X later on in M-phase, so therefore maybe the microtubules aren't even fully formed to fully reach metaphase. I think they're harping on "pick the best answer" +  
sars  I agree with the logic stated above. It could also be that the researchers added Drug X later on in M-phase, so therefore maybe the microtubules aren't even fully formed to fully reach metaphase. I think they're harping on "pick the best answer" +  


submitted by m-ice(325),
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nniireVtsci si a hrctheacemiuoept rdgu ahtt zbitseslai suiembclutro adn pvtrsene etmh frmo isgdsemsnlbia. hTe llce in teh ruipetc is kusct in pnah,aeas ihtw otelbmcrsuiu catdateh to sti cosehomosm,r neablu to llup htem tarap aucsbee it cnatno aslsbdsmeie tis ilrumes.buoct

vshummy  So I get that by process of elimination cyclophosphamide, cyclosporine, doxorubicin, and 5-fluorouracil are not related to microtubules but vincristine in First Aid 2019 says it prevents microtubule formation, doesn’t stabilize it because the one that stabilizes microtubules is paclitaxel. +  
vshummy  Okay, I realize now- the picture is stuck in metaphase, not anaphase. Both paclitaxel and vincristine stop the cell in metaphase but by two different mechanisms. Vincristine prevents mitotic *spindle* formation while paclitaxel prevents mitotic spindle *breakdown*. Mitotic spindle is needed to pull the chromosomes apart before anaphase begins. +14  
azibird  No, I think you were right to begin with. Without spindle formation the cell should be stuck in prophase (vincristine). Without breakdown it should be stuck in metaphase (paclitaxel). Metaphase is shown here with spindle fully formed, so it should be paclitaxel. +  
sars  I agree with the logic stated above. It could also be that the researchers added Drug X later on in M-phase, so therefore maybe the microtubules aren't even fully formed to fully reach metaphase. I think they're harping on "pick the best answer" +  
sars  I agree with the logic stated above. It could also be that the researchers added Drug X later on in M-phase, so therefore maybe the microtubules aren't even fully formed to fully reach metaphase. I think they're harping on "pick the best answer" +  


submitted by sympathetikey(1258),
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rDtcei Aonilntbglui = etriDc ooCmsb stTe

seettcD seoitnabid uobnd icltdery ot RBs.C yomiHslse stmo kyeill deu to hogimsent in teh snuedsftar dolbo n(ot rsue why ti tkoo 4 esewk ehwn pyeT 2 SH si ssupeodp to be riqcuek but )w.e/

ergogenic22  there is a delayed onset hemolytic transfusion reaction which should be evaluated with direct cooms test. https://www.ncbi.nlm.nih.gov/books/NBK448158/ +5  
hungrybox  such a dumb question wtf +25  
sonichedgehog  takess longer due to slow destruction by RES +  
baja_blast  Dang, I didn't know that was the same thing as a direct Coombs test. I guess it makes sense in hindsight. Thanks! +  
sars  Theres a UWORLD question with a table displaying the different types of hemolytic reactions. Don't know the question ID. Agree with delayed hemolytic transfusion reaction due to formation of antibodies against donor non ABO antigens. Typically presents as an asymptomatic patient or mild symptoms (jaundice, anemia). Different from an acute hemolytic transfusion reaction, which is against ABO antigens. +1  
tomatoesandmoraxella  The Uworld table is in question 17780 +1  


submitted by drdoom(812),
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sA ebcdredsi ni eht uoiqsnte stme, this matuotin sucroc twhnii na nitonr a( ngee tgsemen whihc si encrstbadri -g]ARtN&DA;N[ ubt ton a.ldseatrt)n ANR ipcsinlg ensz)eym( agrb ARN dna op“lo ”i;t na otnrni is tcu uot dan teh exosn on ehiter esid fo teh ronnti era jae,dinod klie sih:t

ooorntixxen2n—e1—n t&=;g exo—12nenxo

llciypyT,a itsh slpginci oscrcu at teh reyv gedse of hte rtinon ahwt( I etdoden thiw eht ”—“ t.carearch) tuB in oru e,asc a mnuoitta within the rntoni is sgnaciu NAR pcnislig ezenmy to rcezinego a new :iets the spreicl sctu twihni eht innrot insat(de of ta the yrev ,gede sa it )dul.ohs ,So we teg msonegiht atht loosk ekil hsti:

nn1nexioxto—re—2

T’stha a lylttao feetnfird ARNm ml,ulecoe nad t'is iongg to akem ruo b-lβgnoi penitro kool n(ad e)bvhea lwyufal n.tgares

drdanielr  I remember that in the pre-mRNA, the splicing sites of the intron where the spliceosome attaches are surrounded by "GU---AG" like "guac", so here the homologous DNA to this strand would be transcribed into "gu............ag......" and this would create a 3' slice site too soon +4  
vivarin  if this is supposed to be pre-mRNA, why are there T's in the sequence? I'm so confused by this for some reason +8  
sars  This is the gene (DNA), not heterogenous mRNA. +  


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nac sonmoee ixepaln hwy ti sysa eh sah an tnicta'' TPH tce.intsi.nca.noor ti ot elt su onkw atth teh TPH nicrtetnnaoco is a etlurs of yopa?a lhtogdn wtsa'h ish ?xd sa!thnk

yotsubato  I swear they make up some of this stuff. Like whats up with the thirst, urination, and peptic ulcer diseases. +6  
redvelvet  hypercalcemia can cause nephrogenic diabetes inspidus; so thirst, urination. hypercalcemia can also cause peptic ulcer disease. His symptoms are all about hypercalcemia due to hyperparathyroidism. +2  
namira  "Hypercalcemia can cause renal dysfunction such as nephrogenic diabetes insipidus (NDI), but the mechanisms underlying hypercalcemia-induced NDI are not well understood." https://www.kidney-international.org/article/S0085-2538(16)30704-9/fulltext +  
dulxy071  Why can't the correct answer be C) which points towards renal failure, which may lead to secondary hyperparathyroidism having the same results I believe +1  
pmofmalasia  The secondary hyperparathyroidism in renal failure is due to loss of calcium in the non-functioning kidney. In this question the calcium was elevated, so you can rule out renal failure. +  
sars  Hyper-calcemia causes stones (calcium stones), groans (constipation), thrones (increased urination), bones (increased osteoclast activation), and psychiatric overtones (depression). +  


According to Goljan, men have boobs three times in their lives: when they're babies, when they're going through puberty, and when they're old. It's physiological/normal.

sars  I agree, babies-estrogen transfer through placenta from mother puberty-testosterone conversion via aromatase to estrogen elderly-increased fat content with androstenedione conversion to estrone read this somewhere and it sticks LOL +