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The most important hints to the question are as follows, with #2 being the most specific:

1) patient reports pain with overhead motion and reports recurrent overhead motion during work. Overhead motion can damage the supraspinatus muscle due to impingement by the acromion.

2) Pain is worst with internal rotation of the shoulder - this is consistent with the findings of the empty-can test, which indicates a supraspinatus injury.

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 +14  
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 +2  
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 +  


submitted by usmile1(55),

does anyone know what the structure E is pointing 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. +1  


submitted by hello(184),

Patient's symptoms began 30 min after mowing lawn (i.e. after doing physical activity). He has severe chest pain and is cool, clammy, diaphoretic. He has increased pulmonary artery pressure and increased left atrial pressure. Taken altogether, this is cardiogenic shock.

Cardiogenic shock is a heart pump problem -- the LV isn't working.

When the LV, isn't working, it causes a back up in the direction opposite to how blood normally flows. Therefore, blood will back up in the lungs.

This causes increased capillary hydrostatic pressure --> this drives more fluid into the interstitium --> this causes increased interstitial hydrostatic pressure --> there is now more fluid than normal in the interstitium --> this affects the protein ratio within the interstitum --> this causes decreased interstitial oncotic pressure.

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 +1  
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(38),

I confused myelodysplastic syndrome with primary myelofibrosis because I thought 2-3 of those RBCs looked like teardrop cells. Just like when they show an image for bullous pemphigoid and there's some weird second rip through the dermal/subdermal layer making me think it's not BP even though I don't know what else it would be. fml

whoissaad  Made the same mistake +3  
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. +  
jawnmeechell  Interestingly enough, agnogenic myeloid metaplasia is the old name for myelofibrosis, with "agnogenic" being synonymous with "idiopathic." (or did everyone already know this) +  


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