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Contributor score: 17
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ht3
you're definitely not alone lol
+
yotsubato
And its not in FA, so fuck it IMO
+1
link981
I guessed it because the names sounded similar :D
+18
yb_26
I also guessed because both words start with "glu")))
+30
impostersyndromel1000
same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle.
+1
jaxx
Not a clue. This was so random.
+
mkreamy
this made me feel a lot better.
also, no fucking clue
+1
amirmullick3
My immediate thought after reading this was "why would i know this and how does this make me a better doctor?"
+10
mrglass
Generally speaking Glutamine is often used to aminate things. Think brain nitrogen metabolism. You know that F-6-P isn't an amine, and that Glucosamine is, so Glutamine isn't an unrealistic guess.
+6
taediggity
I literally shouted wtf in quiet library at this question.
+2
bend_nbme_over
Lol def didn't know it. Looks like I'm not going to be a competent doctor because I don't know the hexosamine pathway lol
+25
drschmoctor
Is it biochemistry? Then I do not know it.
+5
jesusisking
I Ctrl+F'd glucosamine in FA and it's not even there lol
+
batmane
i definitely guessed, for some reason got it down to arginine and glutamine
+3
baja_blast
Narrowed it down to Arginine and Glutamine figuring the Nitrogen would have to come from one of these two but of course I picked the wrong one. Classic.
+2
feeeeeever
Ahhh yes the classic Glucosamine from fructose 6-phosphate question....Missed this question harder than the Misoprostol missed swing
+1
schep
no idea. i could only safely eliminate carbamoyl phosphate because that's urea cycle
+
flvent2120
Lol I didn't either. I think this is just critical thinking though. The amine has to come from somewhere. Glutamine/glutamate is known to transfer amines at the least
+1
temmy
Me it was so weird
+
peridot
I do want to add, that while PGE2 is the right answer, FA19 p.213 says that IL-1 and TNF are involved as well. However, because the question asks about what is going on in the hypothalamus, the answer is PGE2. If the question had been asking about what the macrophages were releasing to influence the hypothalamus, then the answer would have been IL-1 or TNF (FA didn't specify if it was TNF-a though...).
+4
magneto
To add to @peridot, IL-1 acts on the anterior hypothalamus to increase local production of PGE2, which in turn will induce fever (PGE2 increase the set-point temperature)
+2
194orbust
per UWorld, "cortisol exerts a permissive effect on many hormones to help improve the response to a variety of stressors. For example, cortisol increases vascular and bronchial smooth muscle reactivity to catecholamines". FA also uses the effect of cortisol on catecholamine responsiveness as the lone example for a permissive drug interaction (FA2018 pg 229). The difference here is that we're talking about exogenous glucocorticoid and adrenergic agonist. I guess it was expected for us to assume that the mechanism is analogous for the analogous drugs
+16
maxillarythirdmolar
I'm sure it's related to the activating effect of Cortisol on phenylethanolamine-N-methyltransferase, converting NE to Epi. Sounds like a synergistic thing to me. (FA.83)
+4
feeeeeever
My logic is probably flawed, but I also thought that if cortisol has the ability inhibit COX, LOX, and NFKB you can reduce inflammation and bronchoconstrictive mediators. Therefore, the B2 agonists would have a greater effect since things like LTB4 will be reduced.
+2
feeeeeever
*LTC4, LTD4, LTE4 for bronchoconstriction, my bad
+1
194orbust
per UWorld, "cortisol exerts a permissive effect on many hormones to help improve the response to a variety of stressors. For example, cortisol increases vascular and bronchial smooth muscle reactivity to catecholamines". FA also uses the effect of cortisol on catecholamine responsiveness as the lone example for a permissive drug interaction (FA2018 pg 229). The difference here is that we're talking about exogenous glucocorticoid and adrenergic agonist. I guess it was expected for us to assume that the mechanism is analogous for the analogous drugs
+16
maxillarythirdmolar
I'm sure it's related to the activating effect of Cortisol on phenylethanolamine-N-methyltransferase, converting NE to Epi. Sounds like a synergistic thing to me. (FA.83)
+4
feeeeeever
My logic is probably flawed, but I also thought that if cortisol has the ability inhibit COX, LOX, and NFKB you can reduce inflammation and bronchoconstrictive mediators. Therefore, the B2 agonists would have a greater effect since things like LTB4 will be reduced.
+2
feeeeeever
*LTC4, LTD4, LTE4 for bronchoconstriction, my bad
+1
This patient has pulmonary fibrosis, which causes a restrictive (not obstructive)-type disease. Since there was no occupational exposure, I'm assuming this is idiopathic pulmonary fibrosis. This causes thickened alveolar membranes, limiting gas diffusion. Therefore, eventually O2 won't be able to diffuse quickly enough into the blood across the alveolar-arterial membrane, resulting in a larger A-a difference. (I think there's normally a small A-a gradient, from 2-14 mm Hg, but when this gets too big, you get hypoxic)