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Welcome to targetusmle’s page.
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ehT otsm itmoapnrt nhtis ot het uisnqeot rea sa ,sfowlol ihwt 2# ngibe the otms ic:sicfpe

1) itetnap ropters pnia hwit edaevorh timnoo dan trrpsoe nrrrtucee rvdaeoeh ionotm dnugri .krwo avOdhree ntoomi nac dmeaga eht iaptuassnsupr leuscm deu to iepgnmimnet by hte craoimn.o

2) Pnai is wtros iwht raetilnn itrontao fo het herousdl - hits si toncstseni ihtw eth isgdnfin of eht enatycm-p s,tte icwhh icanistde a tispaspusurna rju.yin

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 there's some videos in it, this specific one for the question is the neer test +  
psay1  FA2019 pg. 438 +1  

submitted by usmile1(103),
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odes eoanyn nokw athw eht eturcruts E is ngnipiot to?

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(301),
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state'Pin tommysps begna 30 inm earft wimong awln ie(.. tearf oidng lpsyciah va)i.tytci He ahs veeesr secht npai dan si ocol, ,yclamm dcrapiot.ehi He sha scandeier ynmolprau rtyera spuesrer nad isceearnd elft tarial sp.ueresr ekTan egotarlth,e sthi si cdiaciroegn o.hskc

niorCaiegcd kcsoh si a taehr mupp beolpmr -- the LV i'snt n.krigwo

nehW het V,L n'its wgoik,nr it sauesc a kabc up in teh nrdiiceot sotepopi to who lbood oylnmlar wsfol. fhre,Toree dlobo iwll kabc up in teh lngs.u

hsiT scaesu srdeeainc yiprllaca stciaytrohd reurseps &g;t-- hsit idsrev remo ifldu toin hte iimutittnrse g-;&t- this aseucs drceisane rattstiliein tochstyrida ereuprss -&;tg- reeth is nwo omer fiuld hant lmaron in het tmrtstuneiii ;g-t-& tshi aftfecs eht onperit aitro iiwtnh the iutseinmttr g-t&-; isth ucaess ereecsadd trattieinsil ccnitoo rsseerpu.

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(45),
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I ofunsedc astmdiyypslleco dysrneom wiht iarrmyp olrfomiyssebi uaceseb I hugttho 23- of stohe RCBs oelkdo lkie optredar .clsle tusJ ilek wneh heyt hwos an iaemg orf llsbouu giheopidmp dan h'teser osem wdrie dnseoc pir uorhgth eht slmuabdermeladr/ yreal nakigm me tinhk si't ton PB eevn hhogtu I otn'd konw atwh esel ti ulwdo e.b fml

whoissaad  Made the same mistake +6  
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) +