Published Nov 4, 2002
You are reading page 2 of Q & A
direct and indirect actions of ephedrine at receptor, how does it cause the release of norepi? Then what?
The clinical instructor drove us crazy with this question when we first started clinicals.
Not to break the Q and A, but is everyone using Memory master for school?
Do you find it helpful in your day to day progress?
Are you then attending the review courses for the cert.exam as well?
Thx in advance
What a bummer, I missed more Q & A.
Although, I know very little about SSEP. We call it EMG in ICU.
I am not a neuro expert, but in regards to SAH and increased ICP, I was under the impression that the blood in the subarachnoid space prevents the reabsorption of CSF resulting in hydrocephalus and increased ICP.
but in regards to SAH and increased ICP, I was under the impression that the blood in the subarachnoid space prevents the reabsorption of CSF resulting in hydrocephalus and increased ICP.
True B-Dad. BTW, some answers are school specific. I had a hard time until I just went with the answer tah incorperated what was taught in class, not what I knew from before or found in other texts. You'll see.
OK, I give on the ephedrine question, all I could find is that norepi is realeased from the pre synaptic terminal. I'm guessing it is due to an influx of calcium but I do'nt know if that's related. Give it up.
BTW, it is 0615 on a sunday and I'm heading off to study physics for those of you wanting to know about time issues.
Next question, (for the juniors here) less subjective, What compound from what neuromuscular blocker is considered a CNS stimulant?
Direct action at the beta 1&2 receptors and alpha 1 receptor, (like epinephrine) the presynaptic beta 2 receptor promotes release of norepinephrine (via calcium) The indirect effects are on beta 1, alpha 1 & 2,(from norepinephrine) the presynaptic alpha 2 receptor then decreases the release of norepinephrine.
CNS stimulant: ACh
let me restate the question, I think Quiigley misunderstood. There is a metabolite from a certain non depolarizing neuromuscular blocker that has CNS effects, I'm looking for the drug and the metabolite.
Yep, I misunderstood. Ok, gonna guess this answer... Drug: atracurium. Extensively metabolized. One way is by ester hydrolysis and the second is Hofmann elimination which breaks down into laudanosine. I think it causes CNS excitation and seizures. Am I close?
Perfect, that's what I was looking for.
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