PS452 Unit 4 Alcohol and Withdrawal Paper Example

Day Two Tremor, Day Three Danger: A PS452 Unit 4 Alcohol Paper

[Student Name]

Purdue University Global

PS452: Psychopharmacology of Alcohol and Drugs

Unit 4 Alcohol Paper

[Instructor Name]

[Date]

The writer, the unit, the patient and every detail are composite and illustrative; the articles cited are real.

Gilbert's First Three Days

Gilbert, fifty-eight, arrived at our Albuquerque withdrawal unit with a breath alcohol level of 0.22 after ten years of drinking most of a large bottle of vodka every day. On his first evening, as his level fell, he was restless and could not sleep. By the second morning, his hands shook so badly that he spilled his coffee, his heart rate was 112 and he was sweating. On the third day, he told me the shadows in the corner of his room looked like they were moving. The nurse scored his withdrawal on a standard scale every few hours, and the physician's protocol guided his medication.

Each of those changes has a pharmacological explanation.

A Brain in Balance Against Alcohol

Alcohol acts on several systems at once, but two matter most for withdrawal. It enhances inhibitory signaling at GABA-A receptors and reduces excitatory signaling at glutamate NMDA receptors. Over months and years of heavy drinking, the brain adapts to keep functioning: GABA-A receptors become less responsive, and glutamate systems become more active, including an increase in NMDA receptors. Koob and Volkow (2016) describe related adaptations in the brain's stress systems, which shift toward heightened activity whenever alcohol is absent.

These adaptations are how Gilbert could function at a blood level that would sedate most people. They are also what makes stopping dangerous.

When the Alcohol Is Gone

When drinking stops, the adapted brain is left with weakened inhibition and strengthened excitation and no alcohol to balance them. The result is a hyperexcitable nervous system. Mild withdrawal, beginning within hours, brings anxiety, insomnia, tremor, sweating and a rapid pulse. In more severe cases, seizures can occur, usually within the first two days, and some patients develop hallucinations. The most severe form, delirium tremens, usually appears forty-eight to ninety-six hours after drinking stops and brings confusion, agitation, fever and unstable blood pressure and heart rate; without treatment, it can be fatal.

The same adaptations that let Gilbert function at 0.22 left his brain with no brakes when the alcohol was gone.

Why Benzodiazepines

Mayo-Smith (1997) reviewed the evidence on pharmacological management of alcohol withdrawal for a national practice guideline. Benzodiazepines were found effective in reducing withdrawal severity and in reducing the incidence of seizures and delirium, and the review supported them as the treatment of choice. It also supported dosing guided by symptoms, using a standard rating scale, which can reduce the total amount of medication given compared with fixed schedules.

The rationale follows from the mechanism. Benzodiazepines enhance GABA-A receptor function, partly substituting for the inhibition alcohol had provided, and they are then tapered as the brain readjusts. Gilbert received a benzodiazepine whenever his scores crossed the protocol threshold, and the dose fell over five days.

What Glial Cells Add

Most explanations of addiction focus on neurons, but the brain also contains glial cells, including astrocytes and microglia, which outnumber neurons in many regions. Linker et al. (2019) reviewed evidence that glia contribute to substance use disorders. Astrocytes help regulate glutamate in the synapse by clearing it through transporters, and changes in that clearance have been linked to drug seeking. Microglia, the brain's immune cells, become activated by alcohol and other drugs, releasing inflammatory signals that may affect neuronal function, mood and drinking. The authors stressed that rodent work supplies most of this evidence and that human studies are still catching up.

For a patient like Gilbert, the glial findings suggest that long-term heavy drinking may change the brain's support and immune systems as well as its neurons, which could help explain why some effects outlast withdrawal. The research also points toward possible treatments aimed at inflammation or glutamate regulation, though none is yet standard.

Why Past Withdrawals Matter

Gilbert told the admitting nurse that he had stopped drinking on his own twice before, once for a week after a hospital stay and once for three days during a family crisis, and that the second time had been much worse than the first. That history matters. Clinicians have long observed that people who go through repeated withdrawals tend to have more severe episodes over time, a pattern often called kindling, by analogy with experiments in which repeated small electrical stimulation of the brain gradually lowers the threshold for seizures. The idea is that each withdrawal leaves the nervous system a little more excitable. Whatever the exact mechanism, a history of previous withdrawals, and especially of withdrawal seizures, raises the risk of a dangerous course. It is one of the questions our admission form asks, and Gilbert's answer moved him to more frequent monitoring from the first night.

My Part in Monitoring

As a technician, I do not dose medication, but I am often the person who notices change first. I take vital signs every four hours, or more often when a patient is scoring high, and I tell the nurse right away about a heart rate over 110, a temperature above normal, new confusion or a patient who reports seeing or hearing things. On Gilbert's third day, it was my note about the moving shadows that prompted the nurse to rescore him early.

Other Effects of Heavy Drinking

Withdrawal is not the only concern. Heavy drinking depletes thiamine, a B vitamin the brain needs; a severe shortage can produce Wernicke's encephalopathy, marked by confusion, abnormal eye movements and a staggering walk. Our protocol gives thiamine to every patient withdrawing from alcohol. Gilbert's liver tests were also elevated.

Gilbert's Course

Gilbert's tremor peaked on the second day. On the third day, his visual disturbances prompted the nurse to score him more often and the physician to adjust his medication, and they faded by evening. He did not have a seizure or develop delirium. By day five, his vital signs were normal and his benzodiazepine had been tapered off. He left with a referral to outpatient treatment and a discussion of medications that could help him stay sober.

Conclusion

Gilbert's withdrawal followed the timeline his brain's adaptations predicted: tremor on day two, perceptual disturbances on day three and a gradual return to balance with treatment. GABA and glutamate adaptations explain why, Koob and Volkow describe the stress systems involved, Mayo-Smith's review supports benzodiazepines guided by symptoms, and Linker and colleagues show that glial cells may play a part researchers are still mapping.

References

Koob, G. F., & Volkow, N. D. (2016). Neurobiology of addiction: A neurocircuitry analysis. The Lancet Psychiatry, 3(8), 760-773. https://doi.org/10.1016/S2215-0366(16)00104-8

Linker, K. E., Cross, S. J., & Leslie, F. M. (2019). Glial mechanisms underlying substance use disorders. European Journal of Neuroscience, 50(3), 2574-2589. https://doi.org/10.1111/ejn.14163

Mayo-Smith, M. F. (1997). Pharmacological management of alcohol withdrawal: A meta-analysis and evidence-based practice guideline. JAMA, 278(2), 144-151. https://doi.org/10.1001/jama.1997.03550020076042