PSYC 3011 Week 2 – Assignment: Prepare a Lecture on Models of Substance Use Disorder
PSYC 3011 Week 2 – Assignment: Prepare a Lecture on Models of Substance Use Disorder
Introduction
A substance use disorder (SUD) is a mental illness that affects a person’s brain and behavior and makes it difficult for them to regulate their use of drugs, alcohol, or other substances, whether they are legal or illicit (Julian et al., 2018). Addiction is the most severe form of SUDs, with symptoms ranging from mild to severe. Those who have a substance use disorder (SUD) may also have a co-occurring mental disorder, and the opposite is also true. Anxiety disorders, attention-deficit hyperactivity disorder (ADHD), depression, personality disorders, bipolar disorder, and schizophrenia are just a few examples of co-occurring disorders.
Even if they wish to stop and attempt, those who are addicted to substances or behaviors may not be able to do so (Hironaka, 2019). In addition to interpersonal issues with coworkers and friends, family members, and friends, addiction can lead to physical and psychological issues as well. One of the major national contributors to preventable illness and early mortality is the use of alcohol and other drugs. This lecture will focus on the pharmacological effects of alcohol as a drug of abuse.
Alcohol Use Disorder
In the United States, alcohol is among the most widely consumed drugs. According to statistics on alcohol addiction from the 2019 National Survey on Drug Use and Health (NSDUH), 86.6% of persons ages 18 and older report having consumed alcohol at any point in their lives, with 69.5% reporting doing so in the previous year and 54.9% in the previous month (Yang et al., 2022). Heavy drinking is defined as engaging in binge drinking 5 or many days in the previous month. Binge drinking is defined as consuming at least 5 bottles for a man or 4 glasses for a woman in about 2 hours. The NSDUH found that 25.8% of adults (18 and older) reported binge drinking within the previous month. In this age group, 22.2% of women and 29.7% of males reported binge drinking. In addition, 6.3% of people (8.3% of men and 4.5% of women) said they had had a lot of alcohol in the previous month (Hironaka, 2019). This habit increases a person’s likelihood of going to the ER for alcohol-related issues by 70%. The likelihood of visiting the ER for identical problems increased by 93% for those who drank three times the gender-specific threshold.
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Alcohol Use Economic Burden
The Centers for Disease Control and Prevention (CDC) have estimated the entire monetary cost of alcohol use disorder to be $249 billion, with $27 billion going toward medical expenses (Carvalho et al., 2019). According to the CDC, each person’s annual economic impact on society is estimated to be $807. Alcohol use disorder also has an influence on the economy through the disruption of the workforce brought on by absenteeism, tardiness, employee turnover, and workplace conflict. Potential employee, customer, and taxpayer bases are reduced as a result. The CDC reports that, between 2011 and 2015, alcohol use was directly linked to 95,000 fatalities annually (Hironaka, 2019). This exceeded the total amount of illegal substances. According to the CDC, for the same period, alcohol-related illnesses cost nearly 685,000 years of potential life. More than 200 diseases and injuries have been linked to alcohol as a contributing factor. It has been demonstrated that an average volume of alcohol use has a causal relationship with several diseases. The three conditions that account for the bulk of alcohol-related deaths among a long list of other conditions are cancer, liver cirrhosis, and injury.
Pharmacology of Alcohol
Background:
Alcohol (ethanol) is a flammable, volatile fluid produced by the fermentation of carbohydrates by several Saccharomyces species. It is a colorless, transparent liquid that enters the body through the gastrointestinal system and is quickly disseminated throughout (Yang et al., 2022). It possesses bactericidal properties and is frequently used as a topical sterilant. It is frequently utilized in medicinal preparations as a preservative and solvent in addition to being the main component of alcoholic drinks.
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Ethanol’s primary effects are on the CNS. The well-known hallmarks of intoxication, from moderate inebriation through drunken behavior and the subsequent hangover, to profound coma, demonstrate that alcohol has typical and severe effects on men (Whalen et al., 2019). The first alterations influence emotional and autonomic processes; as intoxication advances, a variety of cognitive phenomena are negatively affected. It should be remembered that alcohol is always a depressive from the start of its activity in man.
Routes of Administration
Although dermal absorption of ethanol is a possibility, it is a relatively ineffective way to deliver alcohol, especially to adults. Little children are even more vulnerable to ingesting alcohol this way since they have less keratin in their skin. Alcohol administration by inhalation is also ineffective. The argument that a person “accidentally breathed alcohol through their employment or the environment in which they were before driving” has been the subject of several investigations to better understand this route of administration (Pereverzev et al., 2021). It has been demonstrated that only trace quantities of alcohol may be absorbed by the nose, and typically, extremely stressful circumstances must exist for this to happen. The best way to get alcohol into your blood is by intravenous injection. Intravenous injections of ethanol do happen occasionally—usually in “junkie” situations where the demand for a quick dose via a needle is the main factor—but they are uncommon since they cause excruciating agony. Given the rarity of intravenous alcohol injection and the ineffectiveness of topical or inhalational alcohol delivery, it should come as no surprise that oral intake is the most popular method of alcohol administration in humans.
Pharmacokinetics of Alcohol
The drinking pattern (bolus or repeated drinking), the concentration of alcohol in the drink, and the presence of food in the stomach all have a role in the rate of alcohol absorption into the blood (Jones, 2019). The absorption of ingested alcohol begins in the stomach via the mucous membranes of the lumen. Because of the substantially increased surface area offered by the villi and microvilli, absorption into the blood happens faster from the duodenum and small intestine (Whalen et al., 2019). Gastric emptying is a fundamental regulator of ethanol absorption speed and has a significant impact on the tmax and Cmax of blood-alcohol curves.
After absorption from the gastrointestinal system, ethanol is circulated throughout the body’s organs and tissues (Yang et al., 2022). Without attaching to plasma proteins, ethanol flows freely across cellular membranes and spreads into the overall body water area. Yet, a concentration gradient occurs between arterial (A) and venous (V) blood concentrations, with A > V during absorption and V > A during the post-absorptive interval.
Alcohol is mostly metabolized by enzymatic mechanisms, with only trace quantities exhaled as vapor through the lungs. Since it is impacted by contaminants in alcoholic beverages, the odor of the mouth is not a reliable indicator of alcohol intake. Alcohol is broken down in the liver by ADH and mixed-function oxidases like P450IIE1 (CYP2E1) (Hironaka, 2019). Chronic drinkers may have higher CYP2E1 levels (Jones, 2019). ADH turns alcohol into acetaldehyde, which can then be transformed into acetate by acetaldehyde dehydrogenase. Because the enzyme is saturated at fairly low blood alcohol levels, the rate of alcohol metabolism by ADH is largely constant, exhibiting zero-order kinetics. In adults, alcohol metabolism is related to body weight and averages around 1 oz of pure alcohol every 3 hours. As a result, the time required for a person to get sober after even modest alcohol consumption might be significant. Although stimulants are frequently employed to mask the depressive effects of alcohol, no effective “alcohol antagonists” that may fast counteract the intoxicating effects caused by alcohol appear to exist.
Pharmacodynamics of Alcohol
Alcohol has a short-term depressive effect on the central nervous system (CNS). A time of disinhibition frequently happens during the first stage, when alcohol content levels are rising, and behavioral arousal indications are frequent. They include reduced anxiety, a rise in talkativeness, euphoric and confident sentiments, and improve assertiveness. Drinking more causes ataxia, higher emotional outbursts, and a decrease in judgment and reaction time. Alcohol works as a sedative and hypnotic at higher blood levels, albeit the quality of sleep is frequently compromised after drinking (Ray et al., 2020). Alcohol heightens the severity and frequency of apneic episodes in people with sleep apnea, as well as the subsequent hypoxia. Barbiturates and benzodiazepines both have sedative-hypnotic effects that are amplified by alcohol, possibly indicating that both drugs have similar mechanisms of action. Rapid alcohol intoxication is not usually accompanied by sleepiness or coma; in fact, some drunk people exhibit aggressive behavior that necessitates the prescription of further sedatives or antipsychotic medications.
Acute alcohol consumption typically results in a warm sensation due to an increase in cutaneous blood flow, which is followed by a drop in core body temperature. Although the amount of alcohol consumed impacts this reaction, large concentrations (>20%) of alcohol limit gastric secretions. Gastric secretions are often enhanced (Pereverzev et al., 2021). Long-term consumption of large amounts of alcohol can cause several gastrointestinal tract diseases, such as esophageal varices and bleeding, diarrhea, and vitamin and nutrient malabsorption. Also, drinking alcohol is linked to a higher chance of developing cancers in the GI tract as well as other organs including the lung and breast. Alcohol use, whether acute or chronic, often reduces sexual performance across both men and women, yet sexual activity may be intensified due to a loss of judgment and inhibitory control (Whalen et al., 2019). Alcohol has a variety of impacts on the circulatory system, and both acute and chronic alcohol use can result in alterations in contractility and function. Little doses of alcohol’s beneficial effects on cardiovascular tissue counteract alcohol’s harmful effects on the heart as well as other organ systems. Hence, moderate to low alcohol use is linked to a lower risk of coronary disease, which may be brought on by alcohol-induced alterations in plasma lipoproteins and modifications to cell defense mechanisms.
Drug-Drug Interactions
Alcohol depresses the central nervous system (CNS) in a manner comparable to other centrally acting medications such as barbiturates, general anesthetics, benzodiazepines, solvents, and anti-convulsants (Papaseit et al., 2019). Antihistamines, which are frequently employed in the management of nasal congestion, also have sedative effects that are enhanced by alcohol. Some drugs might cause substantial CNS depression when combined with alcohol, which can make it more difficult to perform daily tasks safely, including driving a car. The hepatotoxic consequences of paracetamol (Tylenol) and the stomach irritant effects of NSAIDs can both be enhanced by alcohol, which raises the risk of gastritis and upper gastrointestinal bleeding. Persistent alcohol consumption can cause increased levels of liver enzymes, which can affect how some medicines are metabolized.
Neurobiology (Mechanisms of Addiction)
According to a generally acknowledged premise of addiction research, addictive drugs by definition result in pleasant effects that encourage behaviors that encourage continued drug use and desire. According to this theory, addictive substances like alcohol must at least initially give some kind of positive reinforcement that serves as a powerful incentive to use the substance again (Julian et al., 2018). When drug usage continues, the intensity of immediate reinforcement or reward may diminish, and drinking may increase as unpleasant withdrawal symptoms manifest. Drug use is repeated, which activates learning mechanisms and can result in ingrained behaviors that can take on the characteristics of rituals and habits. According to study findings, drug and alcohol addiction is a sort of dysfunctional, deviant learning that, once developed, is hard to eradicate (Elvig et al., 2021). Recent findings indicate a significant link between midbrain dopamine-based reward systems and cortical processes of brain plasticity and learning many of which are mediated by the neurotransmitter glutamate in terms of the brain systems that underpin the development of addiction.
Mechanisms of Addiction
All addictive substances, including alcohol, have an impact on the dopaminergic projections in the midbrain that control neurotransmission in the limbic and cortical circuits that control motivated behavior (Whalen et al., 2019). The midbrain ventral tegmental area (VTA) is home to the dopamine (DA) neurons implicated in this function, which project to specific regions of the brain, such as the nucleus accumbens, amygdala, olfactory tubercle, frontal cortex, and septal/hippocampal areas. These areas may be crucial in starting and maintaining drug-seeking behavior because they are considered to be involved in converting emotion and perception into action by activating motor pathways. In experimental animals, lesions or inactivation of these distinct brain regions might lessen the development of drug-seeking as well as its reemergence after protracted abstinence.
Drug Toxicity
Drug toxicity is described as an unpleasant response or fatal occurrence induced by taking the incorrect dose of a medicine (Elvig et al., 2021). A dosage can be classified as either lethal (LD), which results in the death of animals or cells, or effective (ED), which results in another observable consequence. The therapeutic index is the ratio of the ED50 for therapeutic effectiveness and substantial deleterious effects.
Ethanol concentration in alcoholic drinks ranges from 4% to 9% by volume in beer, 16% in wine, 20% to 40% in liqueurs and infusions, and 40% in liquor (Julian et al., 2018). Moreover, ethanol is utilized as a home or industrial solvent, as well as an antiseptic (70%), in cosmetics, food flavorings, mouthwash, and medications. A blood ethanol concentration of 0.1 g/dL is produced by approximately 0.8 g/kg of pure ethanol (or three to four drinks) (Gagnon et al., 2022). Those who consume 1 to 1.5 mL/kg of pure ethanol may have clinical manifestations of ethanol intoxication. Mortality is often linked with levels in the range of 80 to 90 mmol/L, although for chronic ethanol users, the deadly dose may be much higher.
Alcohol Tolerance (Neuroadaptation)
Alcohol tolerance is a complicated phenomenon that distinguishes AUD in which more alcohol must be consumed to produce a particular effect, such as the sensation of intoxication (Ray et al., 2020). In other words, tolerance lessens the impact of a recommended alcohol intake. The population’s levels of alcohol sensitivity and tolerance vary as per the individual’s age, sex, prior alcohol exposure, drinking environment, and genetics (Elvig et al., 2021).
Tolerance’s physiological makeup has been categorized as either functional or metabolic. The term “metabolic tolerance” refers to changes in ethanol metabolism that cause the blood alcohol level to drop after consuming a specific amount of alcohol (Gagnon et al., 2022). Functional tolerance is a diminished sensitivity to alcohol that is unrelated to how quickly it is metabolized. While many of the chemicals that the liver uses to process alcohol are also expressed in the nervous system, little is known about the interaction between functional and metabolic tolerance.
Treatment of Alcohol Use Disorder
Alcohol addiction is a challenging socio-medical condition with a high recurrence rate. Drugs that lessen the desire for alcohol appear to target several CNS neurotransmitter systems. In certain individuals, naltrexone (opioid receptor antagonist) has shown promise, perhaps due to its capacity to lessen the effects of endogenous opioid peptides on the brain (Carvalho et al., 2019). For once-monthly administration, a long-acting depot formulation of naltrexone is authorized. Although they are not licensed for this use, some antidepressants have been observed to lessen alcohol appetite in limited trials. The FDA has also authorized the NMDA glutamate receptor antagonist acamprosate for the treatment of alcoholism (Ray et al., 2020). Disulfiram, an aldehyde dehydrogenase inhibitor, is a supplement included in various treatment plans. A patient who has taken disulfiram may experience nausea, headaches, flushing, and hypotension if they ingest ethanol.
PSYC 3011 Week 2 – Assignment: Prepare a Lecture on Models of Substance Use Disorder References
•Carvalho, A. F., Heilig, M., Perez, A., Probst, C., & Rehm, J. (2019). Alcohol use disorders. The Lancet, 394(10200), 781–792. https://doi.org/10.1016/s0140-6736(19)31775-1
•Elvig, S. K., McGinn, M. A., Smith, C., Arends, M. A., Koob, G. F., & Vendruscolo, L. F. (2021). Tolerance to alcohol: A critical yet understudied factor in alcohol addiction. Pharmacology Biochemistry and Behavior, 204, 173155. https://doi.org/10.1016/j.pbb.2021.173155
•Gagnon, L. R., Sadasivan, C., Perera, K., & Oudit, G. Y. (2022). Cardiac Complications of Common Drugs of Abuse: Pharmacology, Toxicology, and Management. Canadian Journal of Cardiology, 38(9), 1331–1341. https://doi.org/10.1016/j.cjca.2021.10.008
•Hironaka, N. (2019). Pharmacology of Alcohol and Alcohol Use Disorder. NeuroPsychopharmacotherapy, 1–20. https://doi.org/10.1007/978-3-319-56015-1_340-1
•Jones, A. W. (2019). Alcohol, its absorption, distribution, metabolism, and excretion in the body, and pharmacokinetic calculations. Wiley Interdisciplinary Reviews: Forensic Science, 1(5). https://doi.org/10.1002/wfs2.1340
•Julian, T., Glascow, N., Syeed, R., & Zis, P. (2018). Alcohol-related peripheral neuropathy: a systematic review and meta-analysis. Journal of Neurology. https://doi.org/10.1007/s00415-018-9123-1
•Papaseit, E., Pérez-Mañá, C., de Sousa Fernandes Perna, E. B., Olesti, E., Mateus, J., Kuypers, K. P., Theunissen, E. L., Fonseca, F., Torrens, M., Ramaekers, J. G., de la Torre, R., & Farré, M. (2019). Mephedrone and Alcohol Interactions in Humans. Frontiers in Pharmacology, 10, 1588. https://doi.org/10.3389/fphar.2019.01588
•Pereverzev, A. P. P., Ostroumova, O. D. O., & Sychev, D. A. S. (2021). Drug-alcohol interactions: focus on central-acting drugs and analgesics. Pharmateca, 13_2021, 9–15. https://doi.org/10.18565/pharmateca.2021.13.9-15
•Ray, L. A., Du, H., Green, R., Roche, D. J. O., & Bujarski, S. (2020). Do behavioral pharmacology findings predict clinical trial outcomes? A proof-of-concept in medication development for alcohol use disorder. Neuropsychopharmacology. https://doi.org/10.1038/s41386-020-00913-3
•Whalen, K., Feild, C., & Radhakrishnan, R. (2019). Pharmacology (7th ed.). Wolters Kluwer.
•Yang, W., Singla, R., Maheshwari, O., Fontaine, C. J., & Gil-Mohapel, J. (2022). Alcohol Use Disorder: Neurobiology and Therapeutics. Biomedicines, 10(5), 1192. https://doi.org/10.3390/biomedicines10051192
For this task, you will prepare a lecture suitable for a community college course on the pharmacological effects of a particular drug of abuse. This will be a PowerPoint or Emaze.
Be sure to include the following in your lecture:
Provide an opening statement regarding substance and the number of people affected by the substance, as well as statistics related to health and societal costs.
Present information on the drug’s pharmacology.
Discuss how the drug is typically administered, absorbed, and distributed throughout the body.
Include the concept of biotransformation, explain where it occurs, and then identify the pharmacological processes involved.
Explain the difference between effective dose and lethal dose and how these concepts relate to the therapeutic index of the drug you are presenting.
Discuss how this drug affects the process of neurotransmission and include in your discussion the impact this drug has on specific neurotransmitters.
Be sure to include information on tolerance (neuroadaptation) with this drug and the different types of tolerance experienced with this drug.
Length: 10-15 slides, including a slide for the resources; and a note section of 150-250 words
Resources: In addition to information found in the course text, find at least 3 research articles relevant to the pharmacology of the drug you are presenting (published within the past 5 years) to support your lecture.
Your lecture should demonstrate thoughtful consideration of the ideas and concepts presented in the course by providing new thoughts and insights relating directly to this topic. Your response should reflect scholarly writing and current APA standards. Be sure to adhere to Northcentral University’s Academic Integrity Policy.
