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submitted by beeip(124),
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You nca see the eotfdneoemnair certuutsr ni stih adrg.ami

lsmarshall  Rectal prolapse through posterior vagina ("rectocele"). +8  
famylife  "When a rectocele becomes large, stool can become trapped within it, making it difficult to have a bowel movement or creating a sensation of incomplete evacuation. Symptoms are usually due to stool trapping, difficulty passing stool, and protrusion of the back of the vagina through the vaginal opening. During bowel movements, women with large, symptomatic rectoceles may describe the need to put their fingers into their vagina and push back toward the rectum to allow the stool to pass (“splinting”). Rectoceles are more common in women who have delivered children vaginally." +17  
usmleuser007  really like the pubic hair.... +4  
nnp  why not spasm of external anal sphincter? +  
vulcania  After looking it up I think that external anal sphincter spasm would be more associated with rectal pain and maybe fecal incontinence. I chose the same answer because I figured if there was a problem with the rectovaginal septum it would have been noted on physical exam... +1  
ajss  I did the same, put sphincter spasm because I thought a rectocele would be found on a physical exam. +  
thisshouldbefree  this is the map ive been looking for +1  
mnunez187  I didn't choose spasm because the stem says there the rectal tone is normal +1  

submitted by lsmarshall(417),
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nA neeiaemxrtlp gsedni or aemptelnrxie ytsud umst heav an trnineveotin, by fndte.iioni nolCe-tsraoc esstidu rae tornslaoeviba usiedts, ton nlpetiem.aexr Thsi esnqotiu si tclhacnelyi econirrtc. ehyT tawend to ekam a ptnio taht caeos-ltorcn sedsiut aer iemt nda tocs nfcteiefi sneci tehy ntdo' rieeurq ooglwlfni tseiptna orve tiem ro yan uosserecr ebessid ggvwihineirtgn/raee .airintmofno saCe erssei docul nto sett htis y.sthihpeos

os,Al eth widrgno tdcsaeioas" wit an aiesrcend rs"ik shmewaot usdlael to lraotosnc-ec ustdesi ynlo nhigav the itaylib to dnif odsd of an siaansociots tenbeew eepsrxuo adn ,ouomtec tbu not ilebhssat aaculs ra.ihoseiltnp

bigjimbo  classic nbme +1  
poisonivy  totally agree, I dont understand why the right answer is Case control since that is not experimental +1  
howdywhat  am I subject to this kind of poor wording for the day of the exam? +  
ajss  I bieleve so +1  

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aMts cells autnaredleg, copnrugid snimheait hhicw arsttcat iilhosno.sep eTh aelry eagst fo na ierallgc oinrecat si tasm llce ,admtedie but het ltea asegt dligin(cun suumc o)indproutc is mteddaei yb e.ohlonissip

atstillisafraud  Thanks for a good answer. This question made me feel like I was taking T21 pills +17  
medguru2295  Thank you- I was really thinking this question had 2 correct answers... of course my dumbass picked Mast cells. +5  
ajss  where do i find this info?? +  
paperbackwriter  @ajss pg 112 of first aid 2019, under type I hypersensitivity. Immediate --> mast cells releasing histamine and tryptase, late--> eosinophils and leukotrienes recruited via chemokines +2  
graciewacie9  Wow, i missed the fact that the question is asking for the RESULT of the reaction, NOT the cause of the reaction. Mast cells cause the initial reaction, eosinophils would be the result of the eosinophils. *facepalm +6  
greentea733  @graciewacie9 SAME UGH +  
lba9587  Pathophys (as far as I understand it)...Mast cell degranulates, thus the phospholipid bilayer et. Al are left behind and needs to be degraded. Who comes in? Our good friend eosinophils, as they contain Major Basic Protein (responsible from breakdown of expired mast cell). Note, you can tie this in to the delayed Leukotriene effects of an allergic rxn, as the bilayer is also broken down by arach. Acid. (See this link to support my credibility +  
mutteringly  who else looked up what T21 pills were +3  

submitted by bubbles(70),
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naC oenmoes lixnape ryoepprl ohw ew nwok atth ihts rtati owslfol Menlndeia ctsgeien nad is aslotamou sceseeirv dan rmehtrfreuo ohw eth prsnate were r?egtzoseyuoh

I desusge a lto on htis uistonqe nda gto yukcl :(

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 +  

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arfnWiar biitnshi iVt K pdteeednn tnsihesys of ofrsatc a&;mp ost.enirp

tiV K is cysensera fro eth maairtnuot of tingotlc rscofat ,II VII, IX, X nda tnpoier C pa;m& S

oS a durg tath acn hbntiii teh ocaityrxanblo of uperrocrs responti ro ni treho sowrd bniitih eth nmrtouiaat fo eth ctlotnig tascrof iwll eesacrde eth rski fo obomtirssh ni hsti ptiant.e

ajss  this is why warfarin is given as prophylaxis after this type of surgeries +  

submitted by sacredazn(81),
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ehT ptccnoe is a uvnlctedoo awy fo nkigsa if ouy wekn how JVD tcninmrbeoaio s,wrok chwhi si taht ti is lalcayut an pmaxele fo ergitaln eht DNA of eht BT/ ytpceh.ymol

ruSehtno tblo inhecu:teq So hnew ythe eus a rpbeo tgnsaai smeo ienog,r dna itttupnuog a iesz fo 1.5 kb ro 6 k,b isth si litgnel uyo teh iesz of eth DNA antrmgef in echa cell (sen’tdo atetrm fi ythe say J bpoer ro ontnacts eiogrn pe,orb eyhret’ juts nisyag ehtyr’e gnatregti moes ntoldeeicu ecueenqs dnofu ni eth Ig uTCo/lRcs eatb hnaci lsuoc ipyteevsrcel rfo /BT ll).ecs

I itnhk the onfnscgui rapt ldouc eb gwnidenor owh yuo kwno eehhrtw ’oyreu rplyat grohuht rrnaneeemtgar (nrwsae escciho B uthr D) or fi ti hns’ta oureccrd at lla tey rrtcec(o asrnew). eHre, eht tpenocc is ahtt B slecl ueodngr DJV)( nrgrtraeeeanm in eth eonb aowrrm, hielw T sclle do ti in eth uh,ysmt nda ti lla paesnhp at .eocn So a smlapa lecl ni het bodol ilke in ilpltueM yomaeMl douwl vahe lylfu deunonegr ,toicomeanirnb lwieh a T cell ni eht boodl culdo hetier eb fllyu etadeduc dn(a heav dfinhesi DJV rn)onciitmbeoa or tmmuiear ah(’tns dtrates V)DJ.

nSeic the T lcle nege asw 6 kb dan fieinyeldt ibeggr hnta teh 5.1 kb ,enge eht T lcle n’tash ogurednen mntiobronaice eyt.

trichotillomaniac  very nice explanation! +28  
nwinkelmann  This was awesome! Made so much sense and hopefully I will be able to think that critically about questions in the future (because I NEVER would have come up with this on my own, hah). +4  
eacv  OMG! THANK YOU. I DIDNT KNOW ANYTHING about this!! Hope this is not testesd on real examen :p +4  
ajss  wow! this explanation was awesome! thanks! +  
mrglass  Also the T-cell V-D-J segments are not the same as the B-cell V-D-J segments. Therefore a B-cell J segment southern blot would look for whether the B-cell site VDJ segment in a T-cell, which would always non-rearranged. +6  
mynamejeff  Thank you! So is this because multiple myeloma produces excessive monoclonal light chain Ig? Is this the 1.5 kb gene? Whereas, T-cells that have not gone through differentiation yet and their J region includes everything (VDJ) vs. just VJ in the light chain? (FA 2020 pg 104) +  
peridot  This explanation is amazing! However, to fully understand another step of what the question is getting at, please take a look at @highyieldboardswards's and/or @mrglass' explanation as well - a very important addition!! +1