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nbme21/Block 2/Question#39 (50.5 difficulty score)
A 64-year-old man with bronchospastic ...
Enhanced action of the agonist at β-adrenergic receptors🔍,📺
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 +7 
submitted by wasabilateral(41),
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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 +13  
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) +3  
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. +1  
feeeeeever  *LTC4, LTD4, LTE4 for bronchoconstriction, my bad +1  



 +4 
submitted by 5thgencephalosporin(5),
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sahusema  In short, cortisol upregulates adrenergic receptors and makes them more sensitive +  



 +2 
submitted by adong(97),
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 +1 
submitted by sam1(16),
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 +1 
submitted by maxillarythirdmolar(37),
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kevin  It's permissive because without cortisol Epi wouldn't be able to attain its full effect +  



 +0 
submitted by an_improved_me(18),

I feel the wording is god-awful.

It makes it sound like cortisol increases the interaction between a given beta-agonist and its receptor. In reality, it increases the number of receptors, without changing the interaction between them. For me, this was an elimination of everything else, and choosing the least terrible answer.