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eTh msot omtapirnt nshit ot hte itsueqon aer sa wslof,lo thwi #2 eigbn eth tsom cp:eifsci

)1 pttaine ertosrp anip wthi veoherad minoot nda tesprro trrrneceu heoevdar iomton rgndiu .okwr hdaOeerv onitom acn agdmea the aisausnspptur smecul edu to imimnpgeent yb eht iorcno.am

)2 aiPn is srowt iwht nltneiar irtoanot fo eht sludroeh - sith is tsintnecso hwti eht fdiinsgn fo eth acetn-ymp tst,e ichwh aetsndcii a pisuprssuatan rnijy.u

mousie  I was thinking along the lines of overhead motion - damage to the subacromial bursa which is between the acromion and the supraspinatus ... also its the most commonly injured rotator cuff m. so could have guessed this one right +1  
sympathetikey  Thanks for the explanation. I was scratching my head as to why this is correct, since supraspinatus only does 15 degrees of abduction, but you make a lot of sense. +1  
charcot_bouchard  IDK WTF i picked Trapezius +34  
ls3076  why would injury to supraspinatus cause weakness with internal rotation though? +6  
targetusmle  yeah coz of that i picked subscapularis +2  
maddy1994  ya the whole question pointed to supraspinatus ...but last line internal rotation made me pick subscapularis +3  
darthskywalker306  I went for Trapezius. That shoulder flexion thing was a big distraction. Silly me. +1  
lowyield  saw someone post this on one of the other questions about shoulder... and it works pretty good for this https://www.amboss.com/us/knowledge/Soft_tissue_lesions_of_the_shoulder there's some videos in it, this specific one for the question is the neer test +  
psay1  FA2019 pg. 438 +1  


submitted by usmile1(105),
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does oeanny onkw hwat eht rrucsttue E is itnopngi ot?

thomasburton  Not sure looks like it might be free ribosomes or other such small cytosolic structure (I picked E too, thought B looked way too big!) +  
targetusmle  same here!! marked e thinking of it as a mitochondria +1  
msyrett  Glycogen Granules! They are not membrane bound and float freely in the cytoplasm. +4  


submitted by hello(302),
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ateis'Ptn soyspmmt gnbea 03 nim erfat igwnmo lnaw e(.i. ftera ngdoi ihyasplc yci)vta.it eH has veseer echst naip and is oc,lo mcy,alm c.oitiahrpde eH hsa rideaesnc loumparyn taryer reerssup nda aecsndrei tlfe tliara e.esprrus aekTn hrlgte,oeat iths si cgiocrdenia sk.ohc

anoeidiCcgr ocskh is a htaer uppm eprboml -- het LV ts'ni .ikngwor

nhWe teh L,V it'ns ikgorn,w ti aucsse a bkca pu in eht ctnirieod optospie to who dbloo rlalmyno lsof.w roheTfee,r lobdo llwi kbac up in eth slnu.g

ihsT scesau ceseranid alliprcya ohatytcrsid srrpuees -&;tg- isth ivrdes rmeo liudf itno het ttiniemsiurt tg&--; hits esucas secanidre anrtslittiei sotyihrtadc spuersre -t&-g; tereh is own orem iufld nhat rlonma in hte rettsiiinumt -&g-t; hsti fcafets het tponrei toari whinit eht itettniurms &g-;t- tish sscuae dacsderee alisetitnitr ncoicot espuerrs.

targetusmle  awesomely explained :) +  
lilyo  This was amazingly explained Thank you @Hello! +  
pseudopseudopth  For edema to occur shouldn't interstitial oncotic pressure be increased?(when proteins are there, they can pull the fluid) +1  
pseudopseudopth  And when increased interstitial hydrostatic pressure is pressure, shouldn't it oppose the edema by pushing against it? +1  
pseudopseudopth  *when interstitial hydrostatic pressure is increased +2  
pmofmalasia  You don't necessarily need to have increased oncotic pressure, you're correct in that decreased oncotic pressure would act against causing edema but as long as the net change in forces still acts "for" edema it will still occur. For example in this scenario, if the capillary hydrostatic pressure is greater than the change in interstitial hydrostatic and oncotic pressures. Also, the change in interstital hydrostatic and oncotic pressures is a direct result of the edema in this scenario, so it's more like they're responsible for setting the new equilibrium - if they didn't counteract it, you'd never come to a point where the leakage of fluid stops. +  


submitted by alexb(46),
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I csoefudn oyeldpstmyciasl ordynmes hwti yrmirpa yorislfmbiseo uabseec I utohhtg 32- fo thsoe CsRB lekdoo leik drertpao l.lces stJu ilke hnew ehty sowh na eaigm rfo olbuusl odgipemphi adn eh'tsre esmo driwe scdeon pri grhutho eth dmr/sabareeulldm erlya kiagnm me ntikh is't nto BP eevn tuhgho I ondt' know ahwt slee it lwoud e.b lmf

whoissaad  Made the same mistake +7  
targetusmle  i thought exactly the same!! 2 cells looked like tear drop cells :/ +2  
ilovemypuppies2295  I thought there were tear drop cells too. Seemed like it should be a metaplasia then. Oh well +  
lynn  I did the same, but looking at FA19 pg 423 it says "ineffective hematopoiesis --> defects in cell maturation of nonlymphoid lineage." You can get bilobed neutrophils, or if it progressed to AML you'd see auer rods. Nothing about tear drop cells. Then on pg 406 tear drop cells would be seen in myelofibrosis, and possibly thalassemias +  
waterloo  I thought the same, but I think that would be myelofibrosis, not myelodysplastic. Hb is really high here too. Pretty tricky for them to put that there, easy knee jerk. +1  
jawnmeechell  Interestingly enough, agnogenic myeloid metaplasia is the old name for myelofibrosis, with "agnogenic" being synonymous with "idiopathic." (or did everyone already know this) +