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RE: Student question [HAPP-L]



Here's my two cents (and two more cents from one of our medicinal chemists)

The autonomic nervous system effects of cocaine are due to its alpha-2
adrenergic receptor agonism. Alpha-2 receptors are inhibitory and block
catecholamine reuptake. The resultant excess of neurotransmitter at the post
synaptic receptor site leads to increased activation of the sympathetic
nervous system in a dose dependent manner. Accordingly, patients with
cocaine toxicity manifest a prototypic sympathomimetic toxidrome as a
hyperadrenergic state with elevated blood pressure, tachycardia,
nervousness, tremors, fever, tachypnea and agitation.


Cocaine intoxications can lead to either acidemia or alkalemia. In the
emergent setting, acidemia is observed more frequently, and is predominantly
due to metabolic acidosis (lactic acidosis) due to seizures or other violent
muscle activity. In patients who collapse and hypoventilate, acidemia may
also be aggravated by a respiratory acidosis. Less commonly, alkalemia may
be present which is typically a respiratory alkalosis. Continuing lactate
elevation may also result from perfusion failure.

D. Ford

-----Original Message-----
From: Mike Postula [mailto:mpostula@parkland.cc.il.us]
Sent: Thursday, June 28, 2001 11:54 AM
To: HAPP-L@scimath.imperial.cc.ca.us
Subject: Student question [HAPP-L] 


A student in my A & P class is an EMT.  He indicated that, in the case of a
cocaine overdose, a patient goes into acidosis.  They administer bicarb for
this.  His question is why does a cocaine overdose result in acidosis if
cocaine is an alkaloid ?

My guess is that the cocaine represents a minor addition of an alkaline
substance in the body  in relation to the increased metabolism that results.

Can someone please clarify ?

Thanks.


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