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Comments ...

 +3  (nbme21#8)

Question is asking what part of the kidney secreted renin.

order of thinking:

  1. Renin is made by the JG cells
  2. JG cells are "juxtaglomerular" to the glomeruls aka right next to the glomeruli (furthermore, they actually are modified smooth muscle cells of the AFFERENT arteriole FA pg 577)
  3. Glomerulus is in the renal corpuscle. "renal corpuscle is the blood-filtering component of the nephron of the kidney. It consists of a glomerulus - a tuft of capillaries composed of endothelial cells, and a glomerular capsule known as Bowman's capsule"-wikipedia
  4. Renal cortex "contains the renal corpuscles and the renal tubules except for parts of the loop of Henle which descend into the renal medulla" -wikipedia

TLDR; if renin is secreted by JG cells and JG cells are in the glomeruli which is in the renal corpuscle which is in the renal cortex, then JG cells are in the renal cortex so RENIN WILL BE HIGHEST IN CORTEX

djeffs1  I think I overthought this one. I initially thought all of the above, but then I thought, blood that isnt filtered goes in peritubular capillaries down into the medulla (where it becomes most concentrated -hence papillary necrosis in sickle cell) and therefore renin will be most concentrated there... +1




Subcomments ...

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illwwSonga iotncmai uildf is a crlticai nctpeoomn fo nlug oedpvetemnl. euseFts whit resvee nyirolasoohmgdi rea pldague by pumyrnola ilsayohap,p chiwh is hte ausce of ehtda ni tusseef robn tihw oettPr nsdeymro n(lrea gsnia).see

mambaforstep  this is the second explanation that makes sense to me that I see downvoted. if you see something wrong and downvote, please explain! I want to know what im missing +3  
abhishek021196  Maybe someone downvoted because in this question, there wasnt a mention of renal agenesis but rather urethral obstruction although that would lead to Potter sequence as well. +  


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nzaamrbeaCpei is a oturnosio Y54P0C ceud,rni so you sulohd be uggeinss iosematlbm on ttmrea wha.t 4PC50Y pyasl na mrintotap leor ni hotb mvniait D vciintboataio nda irdanoaetdg in eht elriv.

mambaforstep  ahhhh i didnt know CYP450 played a role in vit D bioactivation/degradation. thanks! +5  


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shiT si a abd sitnoqu.e lettlaPe rtnoiagegag eimt inbge n,aolrm ok efni I anc ese hatt. tuB WFV iazessibtl rcfato 8 dna 'oudy see na esainrce ni PTT strf(i ilen xnte to FVW in rsFit Ad).i hWy si tiehr TPT ?amorln

a1_antitrypsin  Totally agree, and they give you a slight increase in PT instead +  
mambaforstep  yeah but if they gave you an increase in PTT then Hemophilia A could have been a valid answer choice. so they prob showed a nl PTT to differentiate vWF dz from hemophlia A +  
drpee  VWD only sometimes presents with a slightly increased PTT. Don't let those anki facts steer you wrong... Plus all the other answers make no sense. Afibrinogenemia? That means literally no fibrinogin (PT and PTT would be infinitely increased). Hemophelia? Or vitamin K deficiency? Those are coagulation factor disorders so they would present with deep bleeding and large bruising. (Unlike platelet disorders, including VWD, which present with mucosal bleeding, petechiae, and heavy menses). VWD is actually the ONLY one that makes sense. +5  
cbreland  I get why it's not afibrinogenemia (which is what I picked), but still don't understand how VWD is right. You have normal PTT and normal platelet aggregation (both of which should be abnormal). Is the only thing leading us to VWD is it being a primary bleeding issue? Again, my answer made no sense, but VWD in this context, seems way out there +  
osteopathnproud  I agree with you @cbreland once I noticed I had to bend lab values for any answer choice then in my head most of them were possible. I took a step back and answer with the most common bleeding disorder, vW disease. Funny thing is when I retook it to check my answers, I had time to overthink and got it wrong. +  
aakb  the anki facts never steer you wrong! my zanki cards say "Low vWF in von Willebrand disease impairs platelet {{c1::adhesion}}" (Gp1B binds to vWF) not platelet aggregation (GpIIbIIIa binds to fibrinogen). additionally it says you can have either a normal or increase PTT. in this case the PT is not increased. It is decreased a little, which I assume is fine esp w an INR of 1.0 +  
lebabs  Shut up +  


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olhhAgtu heter aer no ipseficc eesrhp rtcdoni,sia a FCS nealp htwi omytsl csueeolkty incdtaeis a lvari inetofinc (as lewl sa eht lnroam u.lgoec)s oS you nac ulre uot ,TB rcosiooneirdsasu and lra.beatic rndg/zkneuiBiksir gisn rea eraeldt to iie,tmsginn ubt nvee fi you ondt' nokw twah teohs ea,r hte eqtisnou ayss ttha ehrte si an tolybnriama in hte PLRMTEAO eolb iisgt(nnmei = en)me.igsn sechtEialnpi uwdlo eb hte sbte srwane, laeplyisce beacesu rsHepe Ehipctnaeisl ctfsefa hte mrteapol .oelb

taediggity  Also look for Kluver-Bucy like symptoms in the stem +1  
mambaforstep  why? +  
b1ackcoffee  I agree with everything but normal glucose. Glucose here is NOT normal. to quote wiki "The glucose level in CSF is proportional to the blood glucose level and corresponds to 60-70% of the concentration in blood. Therefore, normal CSF glucose levels lie between 2.5 and 4.4 mmol/L (45–80 mg/dL)." +  
baja_blast  NBME reference table gives normal CSF glucose to be 40-70 mg/dL. As far as I'm concerned, for the purposes of the exam the reference table is probably a better source than wiki. +4  


submitted by joha961(43),
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eanaitnnMec oeds = Css( * CL * )t / F

... rhwee t is pdseale itme ebenetw odses tno( taevernl reeh scine st’i tnncouiuso ufsnii)no nad F is aiilbltvbioiyaa (ichhw si 00%1 ro 1.0 eher ecbeuas i’st nvgei .)VI

​srCoattn wthi inagold e:dos

sCs( * V)d / F

... erewh dV si muoelv of rstii.niutdob

yotsubato  So do we just have to memorize this... +9  
gh889  yep +14  
drschmoctor  @yotsubato Not necessarily. I can't remember a formula to save my life. The Css is the amount you want in the blood. The clearance is the fraction removed per unit time. Since we want to maintain a steady state, we only need to replace what is removed. Thus, maintenance dose = amount present * fraction removed. +9  
mambaforstep  https://www.youtube.com/watch?v=gnqOUmNhmdg good & short explanation +1  
castlblack  I remember CLoCk Time as in check the clock time to give the next dose Cl = clearance, C = concentration and T = half life. I have never had to use F. +22  
baja_blast  This is on p. 233 in FA 2019. +  


submitted by alexp1101(2),
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hTese aiyatlpc ycsoetyhlp,m aak eDnyow leslc (eDowny 23,19) rea ualclaty ceaidvatt D8C T eymophcylts, tsmo fo wichh era ngodspinre to VdeniEecBft- lcls.e

+CD8 -T esllc erianesc ni umnrsbe in the odobl amrest nda rea vetaadcit a(ka Doenwy csle,l raitecve emoclsyhtpy ro ailtyapc ocsymytphel esaecub of htrie yplacita recepesn in pripleeahr dloob) to eaitmnlei VBE tdefceni B- estyylcophm.

mambaforstep  if you watched sketchy, the guy on the bottom right corner was representing a downey cell aka a reactive T lymphocyte +1  
mambaforstep  also FA 2019 says "atypical lymphocytes on peripheral blood smear- not infected B cells but reactive cytotoxic T cells." pg 165 +  
mambaforstep  also ^ i meant bottom left for the sketchy sketch sorrryy +  


submitted by alexp1101(2),
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sTeeh citpayal slechpmtyy,o aak owyneD ecsll neDy(ow ,3)192 ear lyaacult idvcaeatt DC8 T ptcmleoys,yh ostm fo hiwhc ear ornngidspe ot edB-nfietcVE ls.cel

+8CD -T lscel ereacisn ni semnubr in the odobl satmre nad are taditceav aak( neoDwy scell, aetvcier pycseohytlm ro aptcyail cehlotpsyym sacbeue fo eihtr aitcylpa erscpnee in rlpierepah d)bool ot enmeiialt BVE edtfinec -B lethmpsyoyc.

mambaforstep  if you watched sketchy, the guy on the bottom right corner was representing a downey cell aka a reactive T lymphocyte +1  
mambaforstep  also FA 2019 says "atypical lymphocytes on peripheral blood smear- not infected B cells but reactive cytotoxic T cells." pg 165 +  
mambaforstep  also ^ i meant bottom left for the sketchy sketch sorrryy +  


submitted by alexp1101(2),
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hseeT typaiacl lmyhecsto,yp aka wyDone clsel Dywn(oe 193),2 era yatlcalu ticeavatd DC8 T ytsmohpleyc, somt fo icwhh rea ognnrdesip to Etn-BiVdeefc ell.sc

C+D8 T- cesll ercaisne in sbreunm in eth dbloo rmaets and rae vtctieaad kaa( wDeyon lce,ls tecrieav motyclspeyh or cyaaltip tsyylmophec ebesauc of htire itcpyala renpeecs in ilprheeapr )dobol to etmiliena VEB icdnfeet -B ycmphlsoety.

mambaforstep  if you watched sketchy, the guy on the bottom right corner was representing a downey cell aka a reactive T lymphocyte +1  
mambaforstep  also FA 2019 says "atypical lymphocytes on peripheral blood smear- not infected B cells but reactive cytotoxic T cells." pg 165 +  
mambaforstep  also ^ i meant bottom left for the sketchy sketch sorrryy +  


submitted by hayayah(1074),
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tyorphA is aecersed in seiuts amss edu to seeeardc in eszi ernaesdi(c ttoelnskecyo gadoinaetdr via ttomsuapebirqouiein- wpthyaa and ht;gyuopaa  daeceesdr npieort yhss)eints n/aodr nmbure fo lscel staoi.(osp)p uaCses nluecdi u,eisds edav,tinoenr lsos of bdloo psu,ylp ssol of hoarmonl ltumio,iatsn oorp .tnuironti

mambaforstep  FA 2019 pg 206 +1  


submitted by hayayah(1074),
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entscbuSa P S)(P is an puetpdidcnaee peesrnt in eth NCS dna teh hlarpipeer ourevsn y.tsesm A umcpdono uthogth to be lneiodvv in het tnycpasi amsotnirissn fo nipa and theor ernve ispsl.meu

mambaforstep  also, apparently enkephalins attenuate substance p... so it would be dec her pain. +1  


submitted by lianallado(2),
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odihcSzi ayipstoelrn desiodrr si decihaezrartc by vuoyalnrt soaicl wrdlw,ahati ldtiiem olentoima sxeirsepon adn ascloi ilotoan.si

step1soon  Answer is not avoidant personality because these people actually desire relationships whereas schizoid personalities do not (they are content with being loners-like this pt) +2  
mambaforstep  i think i saw this on a @DirtyMedicine youtube video but i always think schiZOOOOid wants to be/is happy to be a lOOOOOOner +  
jawnmeechell  Or perhaps schizoid wants to avoid :) +2  


submitted by step420(34),
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rethO nkyedi eyresHrtpiohp ued ot snreedaic srtess &g-t;- otn apyiphlsear bc ont crcesnauo

masonkingcobra  Above answer is incorrect because hyperplasia can be either physiological or pathological. Prolonged hyperplasia can set the seed for cancerous growth however. Robbins: Stated another way, in pure hypertrophy there are no new cells, just bigger cells containing increased amounts of structural proteins and organelles. Hyperplasia is an adaptive response in cells capable of replication, whereas hypertrophy occurs when cells have a limited capacity to divide. Hypertrophy and hyperplasia also can occur together, and obviously both result in an enlarged (hypertrophic) organ. +43  
johnthurtjr  FTR Pathoma Ch 1 Dr. Sattar mentions hyperplasia is generally the pathway to cancer, with some exceptions like the prostate and BPH. +4  
sympathetikey  Tubular hypertrophy is the natural compensation post renal transplant. Just one of those things you have to know, unfortunately. +2  
charcot_bouchard  Isnt Kidney a labile a tissue & thus should undergo both. This ques is dipshit +  
brbwhat  Dr Sattar says, kidney is a stable tissue, at least pct is as seen in ATN. But I read, basically kidneys are mostly formed whatever number of nephrons have to be formed by birth, after that they can only undergo hyperplasia aka increase in size/or regenerate if need be in case of atn. We cant have more number of nephrons. +1  
mambaforstep  @brbwhat , do you mean kidneys can only undergo hyperTROPHY? +2  
j44n  .... you're not making more cells..... so it cant be hyperplasia +  


submitted by neonem(568),
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nheropMi is a mu ipoido aiostng - noe vdaeres efctfe fo idooips si tams cell ldngeoautiarn ahtt is -nneepdItdEegin. eeleaRs of itehnisam si nkia to na hynaiacptlac rtenciao t&--;g ritr,spui .ect

sympathetikey  Never had heard of that one. Just a good guess. Thanks! +  
yb_26  IgE-independent mast cell degranulation can also be caused by radiocontrast agents, some antibiotics (vancomycin) +7  
temmy  it was a u world question +  
mambaforstep  FA 2019 pg 400 +  
mannywillsee  i'm in FA 2019 and pg 400 is blood groups and hemolytic diseases of the newborn. I found this info in page 535 +  
mannywillsee  i'm in FA 2019 and pg 400 is blood groups and hemolytic diseases of the newborn. I found this info in page 535 +1  
mambaforstep  under mast cells "IgE-independent mast cell degran"! FA 2019 pg 400 +  
mumenrider4ever  Uworld QID 11852 talks about this Also FA 2020 pg. 408 (under mast cells) +  


submitted by ergogenic22(320),
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+C3inaaHC-nO-ol=()-N gap = 11(0514+0)0- = 25 /mELq

lrnmao regan ofr ianno apg si 8 to 61 Le.qrE.Tree.,fmo/h oipsteiv ianon .agp

pH = 275,. lmaorn gaenr 75..7...34-5 freehTeor cissodia

morlNa raeoanticbb 2,2-28 qinoetuss wssho cabibr of 10. erTehfero lcoabtemi iodcisas

oAdnytadllii 2COP nrymoall -5343 mm ,gH snteiquo hsswo OPC2 of 32 hiwt rlmnao ,PO2 reetoerhf yeortriprsa neoascntomip

mambaforstep  why did the stem say she had a drinking problem... is that just a distractor? +  
castlblack  I think alcohol uses up all the NAD+ in its metabolism leading to increased NADH/NAD ratio. After that, TCA cannot progress and the cell is forced to use anaerobic metabolism, which increases lactate. lactate causes anion gap metabolic acidosis (L in MUDPILES from first aid) +1  
nafilnaf  She may also have ingested methanol if she couldn't get her hands on regular ethanol which causes an anion gap metabolic acidosis (M in mudpiles). +1  


submitted by hayayah(1074),
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LHLEP enmory:sd vsyoEsidHeeelm alt reLvi nwseo yzLme seaetlPt.l

A naimaoentfits of eersev apasilr.eempc Bdloo mrsea hwsso ssh.tcoysitce nCa ldae to ICD nda etcphia cteauas sbamhmupasrol Ž euptrur Ž eeesrv ento.inopsyh

mambaforstep  FA 2019 pg 629 +2  
qball  One thing I find odd with this question is HELLP is a manifestation of severe preeclampsia but she has had an otherwise unremarkable pregnancy. Shouldn't she have hypertension/edema in regards to her pregnancy beforehand? +  
demihesmisome  Pre-eclampsia, if not severe, can be entirely asymptomatic. +1  
misterdoctor69  Her blood pressure is 164/102, which qualifies her as having preeclampsia. +  


submitted by temmy(129),
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I egrae whit hwta has eebn sdai btu saol oten htta eht npaitet lealcd erh etsriintn to elhp ehr esdarsd hte ocntlcif ebwenet eth owt iciyhspnsa hwich ahs gtonet her w.drieor Ttah is reh i.ersed dAn mfro hatw i evah rde,ahteg herwe spsile,ob eht psttenia ewhiss suodlh eb .met

mambaforstep  true... i totally missed the part "pt CALLS HER PRIMARY CARE INTERNIST TO HELP ADDRESS THIS CONFLICT BTW THE 2 PHYSICIANS" smh +1  


submitted by cantaloupe5(76),
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saCrulap aohriaeslycdcp ceicsnva rea fteno onagtjudec to orepisnt to ioprevm imien.numgoctyi alngFllie si eth nloy asnwre eiochc ths'ta a n.oterip

mambaforstep  both MHC 1 and 2 are present antigens that are PROTEINS (FA 2019 pg 100). so in order to elicit a T cell response, you need a protein (CANT BE A POLYSACC). that is why vaccines for polysaccaride antigens are often conjugated to PROTEINs--> so that we can elicit a T-cell response (FA 2019 pg 127). +6  
lovebug  Flagellum = Protein, (FA19, pg.124) +  


FA 2020, page 127:

Encapsulated bacteria are opsonized and then cleared by spleen. Asplenic patients have decreased opsonizing ability and an increased risk for severe infections.

They need vaccines to protect against Neisseria meningitidis, Streptococcus Pneumoniae, Haemophilus influenza

mnemonic: "No Spleen Here"

regardless I got this one wrong because of a 50/50 guess between strep and e. coli. I guess they wanted you to recognize that he was at risk for S. pneumonia sepsis and therefore needed to be vaccinated, whereas there's not much you can do to protect him from E. coli other than wash your hands lol

drdoom  ^ voted best username +  
mambaforstep  ^^what he/she said. FA 2019 pg 127 +  
meryen13  its not e coli not because you couldn't vaccinate the pt but because he was in an accident and the chances of infection with s. pneumo is higher. page 186 FA 2020: splenic pt: s.pneumo >> H. influenza b> N meningitidis +  


submitted by neonem(568),
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ponMhrie is a um oipdio angsoti - oen edesvra etefcf fo idipsoo is tmsa llec nteniogarldau tath si eEeI-egtdnnidnp. sleReea fo shtieimna is nkia to na aylpatnccahi aietronc -;-g&t p,riisutr .cte

sympathetikey  Never had heard of that one. Just a good guess. Thanks! +  
yb_26  IgE-independent mast cell degranulation can also be caused by radiocontrast agents, some antibiotics (vancomycin) +7  
temmy  it was a u world question +  
mambaforstep  FA 2019 pg 400 +  
mannywillsee  i'm in FA 2019 and pg 400 is blood groups and hemolytic diseases of the newborn. I found this info in page 535 +  
mannywillsee  i'm in FA 2019 and pg 400 is blood groups and hemolytic diseases of the newborn. I found this info in page 535 +1  
mambaforstep  under mast cells "IgE-independent mast cell degran"! FA 2019 pg 400 +  
mumenrider4ever  Uworld QID 11852 talks about this Also FA 2020 pg. 408 (under mast cells) +