PS452 Unit 3 Stimulant Pharmacology Paper Example

Blocked Doors and Opened Floodgates: A PS452 Unit 3 Stimulants Paper

[Student Name]

Purdue University Global

PS452: Psychopharmacology of Alcohol and Drugs

Unit 3 Stimulants Paper

[Instructor Name]

[Date]

The writer, the unit, the patients and every detail are composite and illustrative; the sources cited are real.

Two Patients

In the same week in February, our Albuquerque withdrawal unit admitted Andre, twenty-nine, after a car crash at the end of a three-day methamphetamine binge, and Lena, forty-four, who had used cocaine, mostly smoked as crack, for about twenty years. Both described the same early effects: energy, confidence, alertness and a rush of pleasure. Both slept for most of their first two days with us. Yet the drugs that brought them in work differently, and the differences help explain why methamphetamine binges last longer and why each drug's long-term effects differ.

The Monoamine Synapse

Dopamine, norepinephrine and serotonin, the monoamines, are released from neurons into the synapse, where they act on receptors of the next neuron. Their signal ends mainly through reuptake: transporter proteins in the releasing neuron's membrane pull the neurotransmitter back inside, where it is repackaged into storage vesicles for reuse (Meyer & Quenzer, 2019). Stimulants act on this system, especially on dopamine in the brain's reward pathways.

Cocaine Blocks the Door

Cocaine binds to the dopamine, norepinephrine and serotonin transporters and blocks them. Meyer and Quenzer (2019) describe this reuptake blockade as cocaine's central mechanism: neurotransmitter that would normally be cleared stays in the synapse longer and at higher levels, intensifying signaling. Cocaine also blocks sodium channels, which is why it numbs tissue as a local anesthetic and why large doses can disturb heart rhythm.

Its effects are short. Smoked or injected cocaine reaches the brain within seconds, and its high fades within half an hour or so, which drives repeated dosing in binges. Lena described using every twenty minutes through a night.

Methamphetamine Opens the Floodgates

Methamphetamine does more than block the door. It enters dopamine neurons through the transporter itself, disrupts the vesicles that store dopamine and causes the transporter to run in reverse, pushing large amounts of dopamine out into the synapse regardless of normal firing (Fleckenstein et al., 2007). It also has a much longer duration of action than cocaine, lasting many hours. The result is a larger and longer surge of dopamine, which helps explain multi-day binges like Andre's.

Cocaine keeps dopamine from leaving the synapse; methamphetamine pours more of it in.

Route, Speed and Craving

How a stimulant enters the body changes its effects as much as which stimulant it is. Smoked crack cocaine and smoked or injected methamphetamine reach the brain within seconds, producing a sharp spike in dopamine and an intense rush. Snorted cocaine takes minutes and peaks lower, and oral amphetamines prescribed for attention-deficit/hyperactivity disorder are absorbed slowly over an hour or more, producing much smaller, steadier increases. Meyer and Quenzer (2019) note that the speed of a drug's rise in the brain is closely tied to its reinforcing power: the faster the rise, the stronger the pull to repeat it. Lena switched from snorting to smoking cocaine in her twenties, and she dated her loss of control to that change. Andre smoked methamphetamine from the start. Both patterns fit the principle that fast routes make binges more likely.

Treatment Without a Medication

Unlike opioid and alcohol use disorders, stimulant use disorders still lack a federally approved medication, although many have been tested. Treatment relies mainly on behavioral approaches, especially contingency management, which rewards verified abstinence. Our unit refers stimulant patients to outpatient programs that offer it, and both Andre and Lena left with an intake appointment already scheduled. Lena's was at a program that also treats the depression she described, which her counselor thought might be driving part of her use.

What Happens When the Drug Wears Off

Both drugs deplete monoamine stores and push the brain's reward systems out of balance. The crash that follows, which we saw in both patients, includes exhaustion, long sleep, increased appetite, low mood and intense craving. For most people, stimulant withdrawal is not medically dangerous in the way alcohol withdrawal can be, but the low mood can be severe, and we monitor for suicidal thoughts during the first week.

Long-Term Brain Changes

Ersche et al. (2013) compared brain scans of people dependent on cocaine with those of healthy volunteers across a range of ages. Gray matter volume declines with age in everyone, but in the cocaine-dependent group, the age-related loss was steeper, nearly twice the rate seen in controls, particularly in prefrontal and temporal regions. The authors suggested that chronic cocaine use may accelerate brain aging.

The finding is concerning for patients like Lena, who has used for twenty years. But it needs careful reading. The study was cross-sectional, comparing different people at different ages rather than following the same people over time, so it cannot show that cocaine caused the difference. People who become dependent on cocaine may differ in other ways, such as alcohol use, smoking, stress or prior brain differences. The finding is a warning worth taking seriously, not proof of cause.

Methamphetamine raises different concerns. At high doses, its effects on dopamine terminals and its production of oxidative stress can damage neurons, and imaging studies have found reduced dopamine transporter levels in heavy users, some of which recover partially with long abstinence.

What This Means on the Unit

Mechanisms shape care. Methamphetamine's long action means intoxication and agitation last longer, and patients may arrive after days without sleep. Cocaine's short action means rapid binges and quick crashes. Both drugs' effects on the heart mean we take vital signs carefully on admission. And both crashes call for close attention to mood.

Explaining It to Patients

Lena asked me why she could not stop after "just one." I explained, in plain words and with the nurse's approval, that cocaine makes the brain's reward chemical linger and then leaves the system drained, so the next use feels urgent. She said that made more sense than being told she lacked willpower, and she asked me to write it down so she could show her sister.

Conclusion

Andre and Lena felt similar highs from drugs that act differently. Cocaine blocks monoamine transporters, while methamphetamine reverses them and releases stored dopamine, producing a larger and longer surge, as Meyer and Quenzer and Fleckenstein and colleagues describe. Ersche and colleagues' finding of faster gray matter loss with long-term cocaine use is a serious warning, read with the caution its design requires.

References

Ersche, K. D., Jones, P. S., Williams, G. B., Robbins, T. W., & Bullmore, E. T. (2013). Cocaine dependence: A fast-track for brain ageing? Molecular Psychiatry, 18(2), 134-135. https://doi.org/10.1038/mp.2012.31

Fleckenstein, A. E., Volz, T. J., Riddle, E. L., Gibb, J. W., & Hanson, G. R. (2007). New insights into the mechanism of action of amphetamines. Annual Review of Pharmacology and Toxicology, 47, 681-698. https://doi.org/10.1146/annurev.pharmtox.47.120505.105140

Meyer, J. S., & Quenzer, L. F. (2019). Psychopharmacology: Drugs, the brain, and behavior (3rd ed.). Oxford University Press.