Acute Cocaine Toxicity

Cocaine is a highly addictive recreational drug, traditionally extracted from the coca plant grown in south America and more recently Columbia.  This drug was commonly used throughout the United States during the 19th century to remove pain as an anesthetic, increase labor as a stimulant, and as a food additive until the Jones-Miller Act of 1920 and the Controlled Substances Act of 1970 restricted the capacity to manufacture, import, or possess cocaine(Das, 1993).  Modern cocaine consumption skyrocketed during the 1980s and early 2000s, with North America holding the largest per capita consumption of cocaine.  Furthermore a steady increase of both cocaine use and cocaine induced seizures in developing nations demonstrates a need for further research treating the effects of cocaine use, namely addiction and acute toxicity (United Nations Publications, 2013).


Fig 1. Coco plants cultivated in Peru (Google Images)

Cocaine gives its user a ‘high’ due to its capacity to turn off the re-uptake of ‘feel good’ molecules which regulate reward-motivation systems within the brain.  Usually a neurotransmitter such as Dopamine is release from a Dopaminergic cell and interacts with its neighboring cell for a short period of time until it is either destroyed or brought back to the first cell; however, Cocaine stops the reuptake of molecules such as Dopamine causing a longer, more intense high(Schindler, 1996).  Since cocaine doesn’t specifically target the dopamine pathway, neurons which use neurotransmitters such as epinephrine and norepinephrine and ion channels for controlling sodium concentrations are also effected.  The heart for example is excessively stimulated causing the surrounding cardiovascular blood network to be tightened (vasoconstriction), causing an increase in heart rate and blood flow.  Large amounts of cocaine can sustain this constricted state for long periods of time, causing a decrease in the oxygen supply for the heart (ischemia) resulting in a heart attack (myocardial infarction) (O’Leary and Hancox, 2008).


Fig 2. Cocaine acts by inhibiting the proper reuptake of neuropeptides like Dopamine, Serotonin, and Norepinephrine. (Google Images)

Cocaine usually has a short period of activity and resulting high, after which it is broken down in the liver to two non-toxic metabolites.  Since cocaine is associated with short highs, multiple doses are often taken resulting in two increased risks.  First, as a party drug cocaine is often taken alongside alcohol, which when metabolized at the same time results in a new molecule cocaethylene.  This molecule is able to react almost identically to cocaine, while taking a lot longer to metabolize.  Taking several doses of cocaine alongside ethanol increases the cocaethylene concentrations and can lead to acute cocaine toxicity, resulting in seizures and heart failure(Hayase, 1999).  Secondly due to its role as a dopamine reuptake inhibitor the increased use of cocaine has a higher capacity to cause addiction, increasing cravings for cocaine when addicted users are exposed to places or people associated with cocaine(Carey, 2008).  It is the combination of increased risk and capacity to become addicted that makes cocaine such a potent toxin.


Fig 3. Cocaine represents one of the most dangerous chemicals due to its high capacity to both become dependent and have physical harm due to one’s dependance. (Google Images)

10 Replies to “Acute Cocaine Toxicity”

  1. The title of this page could definitely be more than it is now. Perhaps you could reference the addictive nature of cocaine, or the way in which people tend to use it to their detriment. I liked the background information that was given on the history of the drug, as many people assume that a “bad drug” has always been that way. The chart is very helpful in relaying the mechanism that produces pleasure when cocaine is taken.

    1. Hmm, I definitely agree that the title is a bit vague. I’ll be changing it to Acute Cocaine Toxicity. Thanks for your comment and kind words! I definitely agree that the creation of a term “bad drug” becomes so weighed, particularly when we’re attempting to contextualize its use. Half the sources talk about how the Incans were addicted and only nobility used it, and they were animals…

  2. Very interesting title page and extremely well outlined. The flow was great beginning with the background of where cocaine comes from, then how it affects the body, and then ending with the more clinical side effects of those biochemical interactions. The only thing I could think of that may be beneficial might be to have a figure with the structure of cocaine but that may be not very well understood by non-scientific audiences. Overall, great job!

    1. Thanks, I definitely was also debating having the structure there as well. I’m currently feeling that the title page won’t have it, to make sure it doesn’t seem to bad, and that I’ll definitely include a picture in some of the pages.

  3. What is the disease being studied? From the title I inferred that the drug was the main aspect of the research not the addictive qualities of said drug. The cover page however was easy to follow and I am curious how this pertains to similar drugs that are still used medically.

    1. The title page will be acute toxicity of cocaine, so you’re definitely right. I’m taking the approach that a disease is “a particular quality, habit, or disposition regarded as adversely affecting a person or group of people.” So the capacity for cocaine to adversely harm a group through their own choice or the choice of others, could probably constitute a disease. I don’t know how many other medical drugs went through a similar process…I’d be interested though.

  4. This was a very interesting discussion of the background and reason why cocaine must be studied. I feel like the second paragraph in regards to discussion of the reuptake mechanism could be clarified slightly, maybe talk about it in respect to the figure below it, which was extremely helpful. I find that your discussion of cocaine’s affect on neurons can be expanded upon. How does cocaine affect the neurons? Since we are discussing diseases for our project. I feel like it would be helpful to discuss more how cocaine can be seen in that context as a form of addiction which is a disease. I feel like it can be very helpful to discuss more of treatment in regards to addiction and if there are any known treatments of acute cocaine toxicity in the body, to protect against overdose. An explanation of how the actual chemistry might lead to the heart attack might be helpful. Maybe I am getting a head of myself and this will be explained later in the other sections. The pictures were extremely helpful and aid the reader through the paper. Overall this summary was very well written.

    1. I love the direction you’re going! A good portion of your questions will be included in the pages; however, I do agree that some concepts such as “why is this a disease” need to be explained better. Also I’m a bit shy about going into too much depth…I’m not sure people would like me throwing around the world Benzodiazepam without too much preface.

  5. This topic is particularly interesting to me because I’ve always been curious about how addictions work in someone’s brain. Is this generally how most work or is this specific to cocaine? It wasn’t 100% clear that addiction was the topic given the title so maybe consider adding something to highlight that it is about the addiction related to cocaine, not just cocaine itself.

    1. Ahh unfortunately I’ve decided to take my project towards Acute cocaine toxicity, so while addiction is an interesting and extremely relevant topic in cocaine studies; I will be keeping it to the side and giving more time to cocaine toxicity.

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