Cocaine dependence

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Cocaine dependence

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A 29-year-old primigravid woman at 34 weeks gestation comes to the clinic for a routine prenatal examination. She has noticed regular fetal movements and does not have complaints of vaginal bleeding, leaking or abdominal pain. She had an upper respiratory infection and hyperemesis in the first trimester that have since resolved. The patient uses illicit drugs including heroin, cocaine and marijuana. She does not use tobacco. Prior to conceiving, she would consume alcohol with her friends on the weekends. Temperature is 98°F (36.6°C), pulse is 110 bpm, blood pressure is 100/70 mmHg. Ultrasound reveals a biparietal diameter of 32 weeks and abdominal circumference of 28 weeks. Which of the following complications should be anticipated at the time of delivery? 

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Cocaine, sometimes called coke, is a powerful psychoactive stimulant that alters how the brain functions—specifically, how we perceive our surroundings.

Cocaine comes from the leaves of the South American coca plant, and has been used for over a thousand years.

In modern times, it’s become a popular “party drug” because cocaine reduces inhibitions and creates a feeling of euphoria or pleasure; this feeling lasts between fifteen and ninety minutes, depending on how the drug’s it’s administered.

Around 18 million people worldwide use cocaine, and because of its strong potential for addiction and overdose, the drug is heavily regulated in many countries.

To understand how cocaine works, let’s zoom into one of the synapses of the brain.

Normally, electrical signals, or action potentials, travel down the axon to the axon terminal, where they trigger the release of chemical messengers called neurotransmitters from synaptic vesicles into the synapse.

The neurotransmitters travel across the synapse and bind to receptors on the postsynaptic neuron, where they give the cell a message.

After the neurotransmitters have done their job, they unbind from the receptors, and can just diffuse away, get degraded by enzymes, or get picked up by proteins and returned to their release site in a process called reuptake.

Cocaine increases the release of certain neurotransmitters, but it’s biggest effect is blocking reuptake receptors on presynaptic axon terminals.

Both of these actions keep neurotransmitters like dopamine, norepinephrine, and serotonin in the synapse longer, increasing their effects.

For example, increased concentrations of dopamine in the brain’s reward pathway (which includes the nucleus accumbens, ventral tegmentum, and prefrontal cortex) produce intense feelings of euphoria, pleasure, and the emotional “high” associated with cocaine.

This physical “high” or feeling of hyper-stimulation is caused by increased norepinephrine concentrations throughout the brain, which produces a variety of effects throughout the body like increased energy, constricted blood vessels, dilated pupils, increased body temperature, increased heart rate, and increased blood pressure. Finally, these higher levels of serotonin are associated with greater confidence.

Cocaine can get into the blood and to the brain via a few different methods.

One way is by simply ingesting it, but the drug is often inactivated by stomach acid unless it’s mixed with something alkaline.

Cocaine is also metabolized by the liver, and it causes capillaries in the mouth and esophagus to constrict, which makes it harder for the body to absorb.

A more direct route is insufflation—snorting it—because the drug is easily and rapidly absorbed through the mucous membranes of the nasal passages, or smoking it so the drug can be absorbed through the lungs.

The fastest route, though, is direct injection into the blood.

Typically, the faster cocaine reaches the brain, the stronger the relationship between the behavior and the reward, which ultimately leads to addiction.

This huge potential for addiction is the reason many individuals keep coming back to use cocaine.

Now, your brain is constantly striving for balance, and if you use cocaine regularly, your brain starts to notice that it’s constantly flooded with dopamine.

As a result, it down-regulates dopamine receptors, which means that the receptor is no longer active and that dopamine can’t give its message as easily to the postsynaptic neuron.

This decreases the effect that a particular amount of dopamine can have on your brain, so if you want to continue to feel euphoric when taking cocaine, you have to take more and more to make up for the down-regulated receptors—and by this point, you’ve probably developed a physiological tolerance to cocaine’s effects.

More cocaine use means more down-regulation, but if the cocaine use stops, then the receptors slowly up-regulate once more.

Alright, so now let’s say that you’re at rest, there aren’t any drugs or anything stimulating your reward pathway.

In this situation, your brain keeps your heart rate, your blood pressure, and wakefulness in a normal state, called homeostasis.

Now, let’s say that your secret crush sends you a text.

All of a sudden you may feel sweaty and flushed, your heart rate may jump a bit.

You’re now above your normal level of homeostasis, because something has changed, right?

But it doesn’t stay that way for long, and after the text message, your brain brings things back down to this baseline.

With repeated cocaine use, a few things start to happen.

Let’s say you take cocaine at a specific time and setting, like 3:00 P.M. in the bedroom. Because it’s a stimulant, it makes everything speed up, including heart rate, blood pressure, and wakefulness.

Your brain, being the smart brain that it is, will pick up on the pattern. Now, next time at 3:00 P.M. in the bedroom, the brain preemptively decreases everything, since it knows that when you take cocaine, it’s all going to increase again.

Now, let’s say 3:00 P.M. in the bedroom rolls around again, but there’s no cocaine… In that situation, the brain still decreases everything, but the changes aren’t countered with the effects of the drug, and the person ends up feeling awful.

These awful feelings are called withdrawal symptoms, and they can persist to the point where a person may need drugs just to feel normal. If that’s the case, they are considered to be dependent on that drug.

Now, on the flip side, let’s say that you use the drug in an unfamiliar setting, like at 11pm at a party.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  3. "The Anti-Addiction Drug Ibogaine and the Heart: A Delicate Relation" Molecules (2015)
  4. "Cocaine pharmacokinetics in humans" Journal of Ethnopharmacology (1981)
  5. "Cocaine Dependence" Annual Review of Medicine (1989)
  6. "Harrison’s principles of internal medicine" McGraw Hill Education/ Medical (2018)
  7. "Diagnostic and Statistical Manual of Mental Disorders: DSM-5" American Psychiatric Assoc Pub (2013)
  8. "Diagnostic and Statistical Manual of Mental Disorders: DSM-5" American Psychiatric Assoc Pub (2013)