epi q. re: step 1

[HiddenTruth]

does boards go crazy on epi graphs--i.e, all the variabilty in it's action based on low dose, med dose, high dose? or, is it pretty straight forward, lose dose = beta activ. high dose = alpha >>>beta? med dose = will take me more than 72 seconds to figure out what's going on.

also, why is there no to minimum reflex tachy with alpha 1 selective blockers (doxazosin), contrary to nonselective alpha blockers (phentolamine/phenoxybenzamine)?
It has something to do with NE feedback mech intact with alpha selective blockers, but i don't quite get that in this context.

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[HiddenTruth]

also, why is there no to minimum reflex tachy with alpha 1 selective blockers (doxazosin), contrary to nonselective alpha blockers (phentolamine/phenoxybenzamine)?
It has something to do with NE feedback mech intact with alpha selective blockers, but i don't quite get that in this context.

alrite, i wasn't thinking. But, it's pretty obvious based on my last sentence. For those that are interested, with aplha 1 block will result in decrs TPR and consequently decrs BP. Compensatory mechanisms, including NE release mediate reflexive tachy and reflexive RAA activ. With phentolamine, however, alpha 2 rec are also blocked, thus preventing the feedback inhibition of NE release (that should occur in response to compensatory release), so you end up with reflex tachycardia and perhaps, even water and salt retention (real life, probably not...usmle, probably yes).

So, accordingly, with doxazosin, you don't lose the alpha 2 mediated feedback inhibition--> decreases NE release---> dereased to almost none reflex tachy. Regulator (NE at alpha 2 rec) is present, so compensation to decrs BP doesn't really occur.

Alrite now that i've just answered and explained myself, I am still curious about my first question.