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Comments ...

 +2  (nbme22#40)
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kTea a kool ta atht eiasvsm ttlpleae octun -- evor a omlnili pre mm3! Ttha olshud point yuo drtaosw a orerilaompflevtiey srdoider of meos rots eisnc hsit alfle ts'in dliebegn out as rfa as ew nca ltel frmo eht doolb aepln hcw(ih ldwuo utp ecvreita otbsyshroicotm on the .dd)x

oNw 'ltse kloo at sheto eyecyrtsrhot. alrNmo -- so 'tsi tno ampioytlceyh r,vae dan iridcnognse eht kacl of yt,okiuscleso borlpbay not CLM or liyeomd eapmlstia.a

So ruo wserna msut be ateenliss bhctieoomrh!atmy


 +4  (nbme22#23)
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Can omnsoee naxlipe eprlrpoy who we kwno htta tshi trait oslwofl eMinnelad gensitec nad si mausotaol eeisescvr nad oerfuertrhm ohw teh tasenpr eerw ugr?oehtoszye

I ssgdeeu a lto no hsti ounsqeti adn got lyuck (:

niboonsh  Autosomal Dominant disorders usually present as defects in structural genes, where as Autosomal Recessive disorders usually present as enzyme deficiencies. P450 is an enzyme, so we are probably dealing with an autosomal recessive disorder. furthermore, the question states there was a "homozygous presence of p450.....". In autosomal recessive problemos, parents are usually heterozygous, meaning that 1/4 of their kiddos will be affected (aka homozygous), 1/2 of the kids will be carriers, and 1/4 of their kids will be unaffected. +36
nwinkelmann  Is this how we should attack this probelm?: First clue stating endoxifen is active metabolite of Tamoxifen should make us recognize this undering first pass hepatic CYP450 metabolism? Once we know that, the fact that the metabolite is decrease suggests an enzyme defect, which is supported by patient's homozygous enzyme alleles. Then use the general rule that enzyme defects are AR whereas structural protein defects are AD inheritance patters. Once we know the pattern, think that most common transmission of AR comes from two carrier parents. So offspring alleles = 25% homozygous normal, 50% heterozygous carrier, and 25% homozygous affected, thus sister has a 25% of having the same alleles as patient (i.e. homozygous CYP450 2D6*4)? +6
impostersyndromel1000  we had the exact same thought process, so i too am hoping this is the correct way to approach it get reasoning friend +
ajss  thanks for this explanation, I totally forgot about AR patterns are most likely enzymes deficiencies, this kind of make the question easier if you approach it that way, thanks +

 +0  (nbme22#2)
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Juts sa iacr,fiitnocal cpilryaal ahstdorycti suesrpre udlow eecedrsa acueesb fo ictsmsye nrvsooacctitions in sosrpene ot tiraco myec/utretpiruss pothnne?oyis

lolmedlol  i believe you get peripheral vasoconstriction and central vasodilation in the first stages of shock, which would cause stasis in the capillary beds, which would mean decreased capillary hydrostatic pressure, despite interstital hydrostatic pressure going down as well. https://www.sciencedirect.com/topics/medicine-and-dentistry/vasoconstriction and amboss shock description +1
trichotillomaniac  ^ this type of question is really hard for me to conceptualize. the link above walks you through it step by step with pictures. Theres not much of an explanation in FA. +
trichotillomaniac  Overall is has to do with osmotic vs hydrostatic pressure. osmotic pressure stays the same and hydrostatic decreases. Hydrostatic pressure is the pressure pushing fluid out of the capillary and in the setting of blood loss this would decrease in efforts to keep as much fluid in the intravascular compartment as possible +2

 +15  (nbme22#42)
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oncrhCi nlare fncucfi:yisnie

1) oorp ahppsheot rcncleaea &t;g-- ighh muesr icoaingrn rupoohoshps

2) hhgi meusr eoppthahs tg;&-- sxmclpoee thiw ieavlntd acntoi Ca -&;-tg aC lfals

3) Ca lafsl -g&t;- getrsirg PTH sxia

)4 kidyen erlufia &-t;g- eeedrcdas tyaciivt of hasy-eodx1lry at hte yniekd ;-t&-g sesl trcolcliia

makinallkindzofgainz  this guy renals +6
paperbackwriter  Someone please help me with this (always trips me up): PTH causes increased vit D production in kidney... are we assuming the increased PTH can't catch up with the kidney failure? Is it the level prior to PTH compensation that they want? D: +
miriamp3  @paperbackwriter what it works for me ;;;; is find the first abnormality so CKD low calcitriol (no D vit) ---> is gonna increase PTH ---> the kidney are not working (chronic, they don't tell u recently- you can;t revert a CKD so the kidney never going to catch up) --> increase inorganic phosphorus.--> always start with the problem. I also use this for celiac and types of shocks. start with the problem, and trust yourself. +2
paperbackwriter  @miriamp3 thank you! I will try out your strategy next time!! :) +1
snripper  I thought renal insufficiency -> inability to reabsorb phosphate at PCT -> decreased phosphate? +2

 +3  (nbme22#1)
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sTih quieonst cfnseoud me a olt cesuaeb so mayn ieqtnossu eavh lddeirl me no teh ipearomctn of hte ANP ecspae mnsehmaic in eismt fo fluid avdleoor sa( in )HFC.

I ohughtt APN saw a eguh rlypea ni the olss fo Na in ecnsaicrumtsc fo olvemu ovoeardl as ni shti atipetn which( si hwy you ees veioemluc ymahiOtnpear in enitsatp thiw AIHSD or raiytocvvtei of eth ARSA sa ni C)F.H

hWy is DAH now ingeb dnema sa teh prseonilebs ena?tg

jooceman739  My thinking is that ANP causes natriuresis, so you're losing salt and water at the same time (isoosmotic fluid?). Meanwhile, ADH absorbs only free water, so it would dilute the serum. Correct me if i'm wrong. +10
bubbles  Ohhh you are right. Thank you for the explanation! I got so fixated on that one mechanism haha. +3

 +13  (nbme22#47)
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emesnaBt emenmabr rientigty si the nrienmttdea fo full gnul eeocryvr fwlnloiog lryopaumn sltinu.

yummaSr:

1)( ssol fo ebtesnma emrnmbea rgtiinety si altcrcii ni ditgnmeerni hte “tonip fo no rtn,uer” dna ubrsoienttc to teh ynaitliib to arhbeltessi mlaron lgnu irauctetchre iwht tonrpmooi of f;isrbios

2)( slos of lletpeaihi llsce, ehonlatedil s,clel dna ensamebt mmeaebrn titrgeyin in uausl nrtsiiettail oenuipmna dtaieaossc htwi iadctiihop ymoplaunr sbsifroi dseal ot teddeysor gnul thrtueicacre nda lpeurepta rs;iiosbf

3() ntnsrigoramf otwrhg βcort-af si ancres,sye tbu nto neilyetr ns,iiuetffc ot pmtoreo pmnarnete sfsibrio;

4() tnretiepss nrjineyirtai/rnnutat/gi is tircilac rfo the prtapaingoo of ;forissib

(5) idpiohiact roluamypn bsfoirsi si an eeaplxm of a cpsesro eedltar ot eht ssetenercip fo na (ng”s)net,a“i onhrcic atnmaomi,filn dan sisfri;bo adn

6() nuqiue eclsl rae iitccrla rllceaul ayslpre in teh uanitgelro fo ir.sofbis

tt:oiic na.o./nl.4hvmsnb2wt:/i6s5gpic/4wnpc1rMmiaeP./lct/w/2htC

endochondral1  any FA or pathoma or uworld correlation? +
endochondral1  or was this a random? +
taediggity  Type II pneumocytes serve as the stem cell precursors, w/out those you're more or less fucked: FA 2020 pg 661 +4

 +0  (nbme22#41)
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'oludtWn inconitostrc of leearipphr ssvlees laso rtgrieg ipahlnscnc nsn,savcioocoitrt wchhi slumtsaei anerl ismacehi and ucases encsreida ARAS aitct?yiv

drdoom  Constriction of peripheral (cutaneous) arterioles/capillaries in response to cold surroundings is an attempt to reduce heat loss & maintain internal body temp; it is not at all coupled with splanchnic vasoconstriction. In fact, the peripheral vasoconstriction is trying to “re-route” blood to more internal/visceral compartments; simultaneous splanchnic vasoconstriction would impede that very process! +54
bubbles  Ah, okay! I got led off track because I had a bunch of super hard practice questions asking about hepatorenal syndrome and how the constriction of sphlancnic vessels might trigger renal ischemia. Do you know if there would ever be a time when sphlancnic vasoconstriction occur outside of hepatorenal syndrome? +
drdoom  @bubbles i would think only in cases of catastrophic shock (when the body is doing everything it can to maintain central tension; pressure to vital organs like heart,kidneys); in those cases, i could see the body sacrificing visceral flow as an "option of last resort" +

 +0  (nbme22#50)
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Can seooemn ldouc lenixpa to em how tshi is lyquievcuaoln ureuotbs srilsceos tdsieep -1FN nad tW-Sreeegubr loas nsteirgepn tihw iksn nsesol,i egpienmpothdy ,eusaclm and re?uizess

dAn esndinocigr teh egtvneia amlyfi hsyroi,t I owlud vhea ssumdea thta a aposrdic oitnmuat iekl( WS) duolw eb mero yk..ell.i

cocoxaurus  This question was tricky! Tuberous sclerosis= Hypopigmented= Ash leaf spot (The skin lesion in NF is Hyperpigmented- Cafe au lait and in Sturge Weber it's a port wine stain (also not hypopigmented). I'm assuming that the SINGLE raised flesh colored lesion is a Hamartoma (The angiofibromas in NF1 are typically multiple). Although both Tuberous Sclerosis and Sturge Weber are both associated with seizures, I used all the other stuff to narrow it down to the correct answer. Also, don't forget that there is Incomplete penetrance and variable expressivity in Tuberous Sclerosis. So I think the lack of family history of "seizure or major medical illness" was there to throw us off. +18
bubbles  Thank you! :) I thought I really knew my congenital disorders, so I was a little annoyed when they trotted this question out +7
pg32  @cocoxaurus I believe the single raised flesh-colored lesion is actually a Shagreen patch, which helps you arrive at TSC as the diagnosis. +1

 +1  (nbme22#33)
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sJut ot eb rtsaycl arlce sc(eaebu veI' egotnt rome royithd iaxs niequssot ognrw anht I lduh:)so

4T -g;&-t 3T is liesbosp utb 3T ;&-tg- 4T isn?t'

meningitis  Exactly. I know there are papers saying there is some conversion of T3 to T4 but I try to keep it simple and think of it as once you break it apart (T4->T3), you cant put it back together. Only thyroglobin etc can put another I on it, so any T3 cant become T4 because you need it to be done in thyroid. +8
angelaq11  I honestly don't know about this, but the way I reasoned this was: she is taking a whole lot of T3, so on top of already having hypothyroidism, she is just making things worse, so TSH is going to be decreased because of feedback inhibition, and hence T4 (Which is the main one produced by the thyroid) is also going to be decreased. I think the high T3 is the exogenous T3. +

 +23  (nbme22#13)
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orF the epesp how gto sdfouenc on iths iutqneso cb fo 'sroUlWd rdewi isutenqo no HVI avlri d:lao

uctae V-IH1 in:ncietof HIHG rlaiv a,ldo wlo HVAI-b2 intc:nifeo LWO lvira oal,d low Ab (bc dnsdarat IVH syasas detcte p24, whihc is not spreent no 2-HVI)

iKdna nyeodan I msidse na aeys lugmnoyoim nepccot qituneos /:

eacv  I feel you my friend! same stupid mistake over here -.- +3
step1soon  FA 2019 pg 176 +2

 -8  (nbme22#3)
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yrorS if m'I eigbn ehed.yw.s.n eosd thsi nowam ahve iraeardh deu to ,stianst t,edi dan ?xsiercee I iddt'n yllear rtedansdun wtha hyet were igsnka for rhee ot be hson.et

.ooo.   I believe they were asking what the most common effect of statins, which is GI upset (including diarrhea). Rarely you can have hepatotoxicity and myopathy but neither of these are a side effect in the answer choices. Hopefully this helps! +2
niboonsh  Theyre asking about the most common side effect of Orlistat - which is really fatty diarrhea +3
asharm10  Orlistat is not a statin drug, it basically inhibits pancreatic lipase so that you absorb less fatm drug is used for weight loss. So when you are not absorbing fat you are inviting diarrhea. +2

 +2  (nbme22#33)
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aHs nyybaod oufdn a gdoo aoxeniaptln rof tihs yit?lgshoo I uylgeenin ahev no iead waht 'mI gloonki ta.

meningitis  This is common in Klinefelter.. think of the equivalent of Streaked ovaries seen in Turners. White streaks, red/pink material of hyaline, and hyperplasia of Leydig cells. Just remember: It doesn't look like normal structured testicle histology (No organized seminiferous tubules with Sertoli cells around) +11

 -1  (nbme22#34)
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oa.r.snl.Scco-eto suidtse eapmroc a ogpur fo eolepp iwth teh ssieeda dna a uoprg fo olppee otiwuth eth eaeisd.s Im' ton seur I nuetsddrna hwy uoy cna lalc eploep rdyomnal nda lalc tath a cotnrlo ogu.rp htWa fi ongma htoes dllace dlnramy,o eosm of thme ehav sola dha mhoaegrihrc os?esrkt

impostersyndromel1000  this is one of those Qs where you just dont over think it and focus on your first point, that they are comparing a group with the disease vs (potentially) one without it. Thats what i took from it at least (sorry fi this is too late) +3
tiagob  Why is not Cohort ? since it compares groups exposed to drug X? +
djinn  Cohort studies determines end of disease and CC determines begins +3




Subcomments ...

submitted by mcl(599),
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oT nepxad on sthi, lolyotptahogeisnu cbeeissdr teh ogholytis of pwiokas rmascoa sa dilnep"s scell fiomrng tliss whti tsdvataexera erd olobd lels"c

mcl  lul i don't know why i spell kaposi like that, my b +10  
bubbles  This site is super helpful. Thanks for sharing :) +  
mcl  yesssssss ofc <3 I love path outlines +  
usmleuser007  Just realize that spindle cells are similar to the endothelial cells of blood vessels. Anything that have vessel association might have spindle-shaped cells. a. NF-1 b. NF-2 ~ Schwannoma (Antoni A) = Cutaneous neurofibroma ~ high cellularity (w/ palisading patterns with interspersing nuclear-free zones called Verocay bodies c. Leiomyoma (uterus & esophagus) d. Mesothelioma (cytokeratin positive) e. Anaplastic Thyroid cancer (biphasic & along with giant cells) f. Medullary Thyroid cancer (can also have polygonal cells) g. Primary cardiac angiosarcoma (malignant vascular spindle cells) h. Osteosarcoma (bone cancer) (pleomorphic cells) i. Meningioma j. Kaposi's Sarcoma (HHV-8) = Slit-like vascular spaces with plump spindle-shaped stromal cells +5  


submitted by bubbles(69),
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ihsT ensuotqi deucfsno em a tol sebauce os naym qensusito ehav edlrlid em no the tporaicmen fo the APN ecseap hcaemimns in simte of fdilu vladeroo (as ni .F)HC

I uhttgoh ANP aws a geuh lreapy ni het loss fo Na ni saneimccrsuct fo ulvmeo elaordvo sa in ihst tetnpia (hiwch is yhw uoy ees lvmeceoiu eanraOmphyit ni tpsaneit with AHSID ro eyacvortiitv fo eht ASAR sa ni CH).F

yhW is ADH wno begin emdan sa het pbsenreosli tgnae?

jooceman739  My thinking is that ANP causes natriuresis, so you're losing salt and water at the same time (isoosmotic fluid?). Meanwhile, ADH absorbs only free water, so it would dilute the serum. Correct me if i'm wrong. +10  
bubbles  Ohhh you are right. Thank you for the explanation! I got so fixated on that one mechanism haha. +3  


submitted by bubbles(69),
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tu'onldW csoocnnrtiit of lpeierraph ssvseel sloa tireggr spainhcnlc sotnviairon,ctcos ihwhc mealsisut arnel ahemscii nda seuacs cisreeadn SRAA v?ttiicya

drdoom  Constriction of peripheral (cutaneous) arterioles/capillaries in response to cold surroundings is an attempt to reduce heat loss & maintain internal body temp; it is not at all coupled with splanchnic vasoconstriction. In fact, the peripheral vasoconstriction is trying to “re-route” blood to more internal/visceral compartments; simultaneous splanchnic vasoconstriction would impede that very process! +54  
bubbles  Ah, okay! I got led off track because I had a bunch of super hard practice questions asking about hepatorenal syndrome and how the constriction of sphlancnic vessels might trigger renal ischemia. Do you know if there would ever be a time when sphlancnic vasoconstriction occur outside of hepatorenal syndrome? +  
drdoom  @bubbles i would think only in cases of catastrophic shock (when the body is doing everything it can to maintain central tension; pressure to vital organs like heart,kidneys); in those cases, i could see the body sacrificing visceral flow as an "option of last resort" +  


submitted by bubbles(69),
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naC osemoen uolcd elxpian to me woh ihts si iqyelvaucuoln uutebros ssorsciel petsedi -N1F dna bSueeW-grtre olsa tgpeernsin tiwh iksn eosnlsi, ghpmitenopdey ul,amecs and eizss?eru

dnA nicgsonedri eth egtnavei ialfmy so,ihyrt I wudlo heav messdua ahtt a apsriocd oaumntti kli(e )SW wuold eb orme ekil.ly..

cocoxaurus  This question was tricky! Tuberous sclerosis= Hypopigmented= Ash leaf spot (The skin lesion in NF is Hyperpigmented- Cafe au lait and in Sturge Weber it's a port wine stain (also not hypopigmented). I'm assuming that the SINGLE raised flesh colored lesion is a Hamartoma (The angiofibromas in NF1 are typically multiple). Although both Tuberous Sclerosis and Sturge Weber are both associated with seizures, I used all the other stuff to narrow it down to the correct answer. Also, don't forget that there is Incomplete penetrance and variable expressivity in Tuberous Sclerosis. So I think the lack of family history of "seizure or major medical illness" was there to throw us off. +18  
bubbles  Thank you! :) I thought I really knew my congenital disorders, so I was a little annoyed when they trotted this question out +7  
pg32  @cocoxaurus I believe the single raised flesh-colored lesion is actually a Shagreen patch, which helps you arrive at TSC as the diagnosis. +1  


submitted by shaydawn88(8),
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I lduow tkinh itnseoourl voelvisn eth stem llcse pyt(e II sy)eputmeo.cn sI hte ctaitn abtmesne enbmarme hte esrwna esbceua it similt ?dpreas

aesalmon  I would also like to know if anyone can answer this question - I saw it as a Sattar "one day, one week, one month" kind of question. Its probably very simple but I still don't get it +  
bubbles  I posted a new comment explaining: basement membrane integrity is the strongest determinant of full fx recovery following pulmonary insult :) +5  
drdoom  You have to think about it this way: the basement membrane is the “scaffolding” on which [restorative] healing occurs. So, yes, stem cells (type II pneumocytes) would be involved in that healing process but they couldn’t restore the *normal* architecture (“no abnormalities”) without the ‘skeleton’ of the basement membrane telling them where to go, in what direction to grow, which way is “up”, etc. If the basement membrane is destroyed, you can still get healing, but it won’t be organized healing -- it’ll be *disorganized* healing, which does not appear as normal tissue. (Disorganized healing is better than no healing, but without a BM, the regenerating cells don’t have any “direction” and therefore can’t restore the normal architecture.) +8  
nwinkelmann  Yes, this a great summary to the post by @bubbles and the article he posted! Another way to think of the question is not, what causes repair, but what causes irreversible injury/fibrosis. That article explained an experiment that showed TGF-beta was necessary to initiate fibrosis, but if BM was intact and TGF-beta was removed, the fibrosis didn't persist, i.e. intact BM is protective against TGF-beta. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/ +  


submitted by keycompany(310),
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m2nscstai8whp6w5..l0Cnt/gM.vPih/np9/m:wt/i0.erc/bloc/

lersO gniS si a yvnio,itsiset-wl lypccfoi-ewits difning fo grMkbeeonc oriAcrsrtlseleioso ()MA rairccehzatde yb a" bpelplaa lutoahhg elsspul,se aalird aerryt whlei teh PB ffuc si nfdlaeti aoebv scsiylot erup"rses.

It is isspeblo hatt )eae:rhit The tciwfoecispy-il of tsih stte ensam ti is saol balppealic ot lsortricohsseae tn(o tsju b) A)M heT NEMB tclrcriyone pesliim ttha AM is hnntreicgebala htiw s.trerlcoeshisoa

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 skraniotis(10),
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zeyaldUndi ranel lfiaure dslea to tobceiaml cdaiss,io nda as a utresl icrabb sget ddltpeee as it tsrei to bffrue the aotuuicnaclm fo nrgocia d.iasc

bubbles  Thanks for the explanation! Do you know why Mg would not be a potential answer? Phosphate also accumulates in those with undialyzed renal failure, so I was thinking that maybe magnesium as a divalent cation would complex with PO3 (in a mechanism similar to Ca). +  
nwinkelmann  From the little bit of research I just did (because I didn't learn anything about dialysis at my medical school), ESRD can be associated with either low or high Mg levels, so the dialysate can cause either increased or decreased Mg levels depending on the patient's serum content, therefore I don't think based on this question, would could determine if removal of dialysis would lead to elevated or decreased magnesium. The end of the first article seems to favor ESRD leading to hypermagnesemia, so if that's the case, then removal of dialysis would cause Mg to increase as well. https://www.karger.com/Article/FullText/452725 and https://www.karger.com/Article/FullText/485212 +1  
hyperfukus  why is it that we aren't learning this stuff and they r just throwing it on step there's barely a blurb in FA about ckd/eskd +1  
hyperfukus  does uremia potentially have to do with this? +  
medulla  ESRD and not getting dialysis -> he is uremic -> met acidosis -> dec bic +11  
angelaq11  @medulla this is the best and simplest explanation. I got it wrong and chose Mg, wish I had made that connection. +