Welcome to goldenwakosu’s page.
Contributor score: 7
Comments ...
pug_sheen
I think they are talking about the GHRH receptor on somatotrophs, which works through the cAMP pathway.
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staygoodpupper
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.
+3
kash1f
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
+31
hyperfukus
ugh i was so excited too bc i thought i remembered jak stat epicfail
+3
skonys
Doesn't GHRH act through an IP3 seconary messanger?
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xmen
the tumor secretes GH. GH act via a JAK/STAT Pathway.
But the GH secretion is stimulated via a GHRH through a Gs.
This Gs in this tumor's cells is mutated and is permanently actif. so cAMP will increase.
+1
kcyanide101
GnRH is IP3 --- Remember GOAT HAG? GHRH is CAMP remember FLAT ChAMP
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Subcomments ...
goldenwakosu
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!
+2
pipter
the only reason I got this right was because they described the tumour as being near the falx cerebri.
+2
fcambridge
Other hints include being described as round and seen in a female. Both indicative of Meningioma
+17
niboonsh
also meningiomas typically present with seizures or focal neurological signs
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suckitnbme
I thought enhancing meant it uptakes contrast. Meningiomas are commonly enhancing lesions per Radiopaedia.
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monoloco
yeah, i’ve never heard of antiphospholipids increasing PT time ...
+26
goldenwakosu
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)
+5
johnthurtjr
I actually went down a rabbit hole with this one recently - essentially in vitro findings =/= in vivo findings, clot-wise with anti-phospholipid antibodies.
+4
link981
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
+9
yb_26
UWorld mentioned "prolong aPTT (and sometimes PT)" in APS
+5
oslerweberrendu
@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."
QID: 1298
+1
kevin
just to clarify, lupus anticoag is in antiphospholipid and presents with paradoxical increased ptt +/- pt despite increase risk thrombosis
+2
Why is the answer adenylyl cyclase? I looked in FA and I saw that GH uses the JAK2/STAT pathway and that IGF-1 uses the MAP Kinase pathway. Not sure how adenylyl cyclase plays into this.