PS452 Unit 2 Basic Pharmacology Paper Example

One Drink an Hour and a Liver That Cannot Hurry: A PS452 Unit 2 Basic Pharmacology Paper

[Student Name]

Purdue University Global

PS452: Psychopharmacology of Alcohol and Drugs

Unit 2 Basic Pharmacology Paper

[Instructor Name]

[Date]

The writer, the unit, the patient and every figure are composite and illustrative; the sources cited are real.

An Admission That Did Not Match the Number

My job on an Albuquerque withdrawal unit, where doctors and nurses supervise detox around the clock, is to take vital signs, record withdrawal symptoms on standard scales and support patients through the first days without alcohol or drugs. On a Tuesday in January, Gilbert, fifty-eight, arrived from the emergency department. His breath alcohol was 0.22, nearly three times the legal driving limit, but he signed his own forms, joked with the nurse and walked to his room without help.

Understanding why requires the two halves of basic pharmacology: how the body handles a drug over time, and how the drug acts on the body's cells.

What the Body Does to Alcohol

Pharmacokinetics describes how a drug is absorbed, distributed, metabolized and eliminated (Meyer & Quenzer, 2019).

Absorption: alcohol is a small molecule that passes easily through membranes. Some is absorbed in the stomach and most in the small intestine. Food in the stomach slows the passage of alcohol into the intestine and lowers the peak blood level, which is why drinking on an empty stomach produces faster, higher peaks.

Distribution: once in the blood, alcohol spreads through the body's water. Because it mixes freely with water and crosses the blood-brain barrier, it reaches the brain within minutes. People with more body water, often those with more muscle, reach lower concentrations from the same amount.

Metabolism: the liver breaks down most alcohol, mainly through the enzyme alcohol dehydrogenase, which converts it to acetaldehyde, a toxic compound, which another enzyme then converts to acetate. A key feature is that these enzymes become saturated at fairly low blood levels, so the liver removes alcohol at a roughly constant rate, about one standard drink per hour in many adults, regardless of how much is in the blood. Heavy long-term drinking can increase this rate somewhat by inducing other liver enzymes.

Elimination: most alcohol leaves the body after metabolism, with small amounts excreted unchanged in breath, urine and sweat. The breath portion is what a breathalyzer measures.

Gilbert's liver could not hurry: at roughly one drink an hour, his 0.22 would take most of a day to clear.

Enzymes, Genes and Heavy Drinkers

Cederbaum (2012) reviewed how the body metabolizes alcohol and why the process differs between people. Alcohol dehydrogenase does most of the work at ordinary levels, but a second pathway, built around a liver enzyme known as CYP2E1, becomes more active with chronic heavy drinking. Induction of that enzyme helps explain why long-term drinkers like Gilbert clear alcohol somewhat faster than occasional drinkers, and it has a cost: the pathway produces reactive molecules that contribute to liver damage. Genes matter too. Some people inherit a less active form of aldehyde dehydrogenase, the enzyme that clears acetaldehyde, and they flush, feel nauseated and develop a rapid heartbeat after small amounts of alcohol. That reaction is uncomfortable enough to protect many of them from heavy drinking, and the same principle underlies an older medication, disulfiram, which blocks the enzyme on purpose.

For Gilbert, faster metabolism did not mean safety. His liver tests on admission showed elevated enzymes, and the physician ordered further evaluation, including an ultrasound before discharge.

What Alcohol Does to the Body

Pharmacodynamics describes what a drug does at its targets and how its effects change with dose (Meyer & Quenzer, 2019). Alcohol does not act on a single receptor the way many drugs do. It enhances the inhibitory effects of GABA at GABA-A receptors, reduces excitatory signaling at glutamate NMDA receptors, and affects other systems, including those involving dopamine, serotonin and endogenous opioids. The net effect at low doses is relaxation and disinhibition, and at higher doses sedation, poor coordination, memory blackouts and, at very high doses, suppression of breathing.

Effects depend on dose, which for alcohol means blood concentration. In a person without tolerance, 0.08 impairs driving, 0.15 to 0.20 produces obvious intoxication, and 0.30 and above can cause stupor.

Tolerance

Gilbert's near-normal behavior at 0.22 reflects tolerance, a reduced response to the same dose after repeated exposure. Two kinds were likely at work. Metabolic tolerance, from enzyme changes in the liver, clears alcohol somewhat faster. Functional, or pharmacodynamic, tolerance is the larger effect: after years of daily drinking, his brain had adapted by reducing GABA-A receptor sensitivity and increasing glutamate activity, pushing back against alcohol's effects so that he could function. Learned tolerance also plays a part; people who drink regularly in the same settings learn to compensate for some impairments.

Koob and Volkow (2016) describe how such adaptations, especially in stress systems, persist and shift the brain toward a state in which the absence of the drug is uncomfortable. That shift links tolerance to dependence.

Dependence and Withdrawal

Tolerance and dependence are related but not identical. Dependence means that the body has adapted so that stopping the drug produces withdrawal. For Gilbert, the same adaptations that let him function at 0.22 meant that, as his level fell, his brain would be left with reduced inhibition and increased excitation. On his second day, as expected, his hands shook, his heart rate rose and he sweated through his sheets. The nurse used a standard withdrawal scale every few hours and gave medication on the physician's protocol, and I recorded his vital signs between her checks.

Neither tolerance nor dependence is the same as addiction, which involves compulsive use despite harm. Many patients on long-term pain medication have tolerance and dependence without addiction. Gilbert's history of continued drinking despite losing his job suggested all three.

Why This Matters on the Unit

Pharmacology explains what I see each shift. A patient's blood level tells us little about how intoxicated he will look; tolerance changes the picture. Constant-rate metabolism means we can estimate when alcohol will clear and when withdrawal may begin. And the brain's adaptations explain why withdrawal can be dangerous, the subject of a later paper.

Conclusion

Gilbert's admission level and his behavior did not match because years of drinking had produced tolerance. Meyer and Quenzer's account of pharmacokinetics explains why his liver cleared alcohol at a fixed rate, and their account of pharmacodynamics explains alcohol's effects on GABA and glutamate. Koob and Volkow explain how those adaptations become dependence, which arrived on his second day.

References

Cederbaum, A. I. (2012). Alcohol metabolism. Clinics in Liver Disease, 16(4), 667-685. https://doi.org/10.1016/j.cld.2012.08.002

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

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