03 Cocaine Flashcards
what plant does cocaine come from?
found in the leaves of the coca shrub
cocaine is (almost) the only local anesthetic that…
causes constriction rather than dilation of the blood vessels
-“nerve conduction blocks” thus it doesn’t need any epi to keep the anesthetic localized
duration of cocaine anesthetic
very short duration of action
toxic above what dosage?
30 mg, and addictive if consume systemically
what are the different routes of administering cocaine?
IV, smoking, snorting, chewing (in order of effectiveness), it does have good transmucosal absortion
how is it made?
coca leaves–> chemical extraction–> cocaine paste (not water soluble)–>oxidation, acids–> cocaine HCL (this is what is snorted or IV)—>baking soda—>”crack cocaine”, cocaine free base precipitates, Evaporation, broken into rocks for resale
why is cocaine smoked?
all the blood passes thru the lungs
- 15% of cardiac output from left ventricle goes to the brain
- peak brain concentrations within 6-8 seconds
cocaine is broken down where and how
in the liver by cholinesterase, broken down into Benzoylecgonine (BEG) which is the major urinary metabolite, this is still present for up to 10 days
- the second metabolite is Ecgonine or methylecgonine (MEG) and Benzoic acid
what does MEG do?
depresses the heart by muscarinic receptor activation
cocaine does what to neurotransmitters?
blocks neuronal transporter for NE, DA, and 5-HT (serotonin)
-it blocks reuptake
mechanisms of Cocaine: ANS
- Indirect agonist: blocks uptake-1 protein on noradrenergic terminal, leads to higher NE levels in the synaptic cleft
- local anesthetic: blocks Na+ channels
what does cocaine do to the heart?
- tachycardia and increase cardiac output (Beta-1)
- arrhythmias in some individuals (beta-1)
- local anesthetic effect (depresses heart)
- MEG from “crack” also depresses cardiac fn
effect of cocaine on organ systems/vasculature
- vasoconstriction (alpha-1)=hypertension
- myocardial infarction: vasospasm of coronary arteries, may occur in minutes or up to 18 hours later
cocaine effect in CNS
- indirect agonist
- blocks uptake-1 protein on NE, DA, and serotonergic terminals
- leads to higher NE, DA, and 5-HT levels in synaptic cleft - local anesthetic
- blocks Na+ channels
- may cause seizures
death from cocaine use can come from:
- cerebral infarction or vasospasm
- intracranial hemorrhage