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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
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.
why would injury to supraspinatus cause weakness with internal rotation though?
yeah coz of that i picked subscapularis
ya the whole question pointed to supraspinatus ...but last line internal rotation made me pick subscapularis
I went for Trapezius. That shoulder flexion thing was a big distraction. Silly me.
FA2019 pg. 438
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!)
same here!! marked e thinking of it as a mitochondria
Glycogen Granules! They are not membrane bound and float freely in the cytoplasm.
This was amazingly explained Thank you @Hello!
For edema to occur shouldn't interstitial oncotic pressure be increased?(when proteins are there, they can pull the fluid)
And when increased interstitial hydrostatic pressure is pressure, shouldn't it oppose the edema by pushing against it?
*when interstitial hydrostatic pressure is increased
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.
Made the same mistake
i thought exactly the same!! 2 cells looked like tear drop cells :/
I thought there were tear drop cells too. Seemed like it should be a metaplasia then. Oh well
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
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.
Interestingly enough, agnogenic myeloid metaplasia is the old name for myelofibrosis, with "agnogenic" being synonymous with "idiopathic." (or did everyone already know this)