to snoo-finity ... and beyond!
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I think they are talking about the GHRH receptor on somatotrophs, which works through the cAMP pathway.
I don’t know how it relates to GH/IGF-1 in particular, but the question said there was a mutation in the alpha subunit of Gs, which activates adenylyl cyclase.
I agree the patient does have Acromegaly, but in the question it talked about how the patient had a mutation that prevented the GTPase activity of Gas. So Gs would be overactive --> excess adenylyl cyclase
ugh i was so excited too bc i thought i remembered jak stat epicfail
I think it’s because meningiomas are able to calcify (aka sometimes they have psamomma bodies). I got this question wrong too but I totally did not completely register that the tumor was in the dura (interhemispheric fissure + central sulcus). Hope that helps!
the only reason I got this right was because they described the tumour as being near the falx cerebri.
Other hints include being described as round and seen in a female. Both indicative of Meningioma
also meningiomas typically present with seizures or focal neurological signs
yeah, i’ve never heard of antiphospholipids increasing PT time ...
Not sure if that little detail was to throw us off. I think the point of the question was to ID antiphospholipid syndrome based on the clinical criteria (spontaneous abortion + thrombosis)
I actually went down a rabbit hole with this one recently - essentially in vitro findings =/= in vivo findings, clot-wise with anti-phospholipid antibodies.
No mention of lupus anticoagulant, anticardiolipin, or anti Beta 2 antibodies. FA mentios prolonged PTT but nothing on PT. What a piece of shit question. But thanks to the dudes above who explained it
UWorld mentioned "prolong aPTT (and sometimes PT)" in APS
@yb_26 Can u please tell the QID because the one I have seen it says, "Although patients often have prolonged ptt (because the antiphospholipid interferes with ptt test), pt is normal."