Primary Care of the Psychiatric Mental Health Client II

Substance Use Disorder Video Transcript

Michelle Gibson: Hi, everyone. This is Professor Gibson. Today, I'm going to go over the fundamentals of substance use disorders. So the topics I'll cover are stigma, the epidemiology of addiction, followed by the neurobiology. We'll talk about screening and assessment of substance use disorders. And lastly, we'll talk about the treatments.

[video with music playing]

Blind Man: What did you do to my sign?

Woman: I wrote the same but in different words.

Blind Man: Thanks, love.

[end video & music playback]

Michelle Gibson: So there is a vicious cycle of stigma, and it is the biggest barrier to treatment. It does affect the public perception. So when discussing or documenting about patients with substance use disorder, do not use stigmatizing language. Always use a person-first language. So it's a person with substance use disorder. Because remember, a diagnosis doesn't define who someone is.

Addiction is a lot like other diseases such as diabetes, as in they both disrupt the normal healthy functioning of an organ. They have serious harmful effects, and in many cases, are preventable and treatable. Although, genetics account for an estimated 40% to 60% of the risk of developing addiction, societal and environmental factors do play key roles.

According to the National Institute on Drug Abuse, over 20 million people were diagnosed with substance use disorder in the last year, but only 10% received treatment. And so this leaves a significant treatment gap. Men are more likely to use illicit drugs than women. We know that overdose deaths are on the rise. In fact, in 2021, overdose deaths reached over 100,000. And synthetic opioids were the main driver of overdose deaths with nearly a 7 1/2 fold increase from 2015 to 2021. However, overdose deaths involving stimulants increased significantly during that same time.

So, the reward pathway produces pleasure from all of the activities that we find rewarding. This particular pathway is activated when a person receives a positive reinforcement for certain behaviors or rewards. The pathway in the brain for these pleasurable activities includes the neurotransmitter dopamine. And this figure shows the reward pathway going from the ventral tegmental area through the nucleus accumbens and out to the prefrontal cortex.

So what happens in addiction? Well, addiction happens through reoccurring cycles that worsen over time and have multiple neuroadaptations in three corresponding domains. First is increased incentive salience, decreased brain reward and increased stress, and a compromised executive function. And this happens in three major neurocircuits in the basal ganglia, the extended amygdala, and the prefrontal cortex. So feedback from the prefrontal cortex to the VTA helps us to overcome drives to obtain pleasure through actions that may be unsafe or unwise. But this feedback is compromised in individuals who become addicted to drugs.

So, some screening tools that we can use, the first being AUDIT-C. This consists of three questions related to drinking frequency and quantity. And the higher the score, the more likely alcohol is affecting that individual's health. The SASQ asks how many times in the past year have you had a certain number or more of drinks in a day? Four drinks for women and five drinks for men. This is helpful in helping to identify binge drinking. TAPS is a validated tool for use in adults to generate a risk level for each substance class.

And then adults— or adolescents, excuse me— 12 through 17, the BSTAD or the S2BI can be used. So when taking a substance use history, there are several questions that must be asked. Some of the most key ones being the type of substance used, the time, and the amount of last use. This is really helpful for indicating if there is likely to be any intoxication or predicting when withdrawal symptoms might start. We also want to know the routes of use and any past history of withdrawal states. So for example, have they had withdrawal seizures or have they had DTs?

When looking at the DSM criteria to diagnose substance use disorder, those criteria fit into four domains, being impaired control, social impairment, risky use, and psychological adaptation.

So we do use drug screening in substance use treatment, and it is sometimes referred to as the technology of addiction treatment. But like other technology, its reliability is due to valid testing procedures. And so that would include sample collection, the analysis, and then your interpretation of those results.

Essentially, drug screening answers a very narrow question. Is sample x detected in sample y? Depending on the biological matrices used is when substances can be detected. So saliva can reveal drug use earlier than urine. And while hair and nail provide evidence of drug use over an extended period of time, clinically we don't use those.

There are some disadvantages to using both orals fluid and urine. So in oral fluid, you can have contamination from smoking or eating. It may be hard to collect a sample due to the patient having a dry mouth. Urine samples are very easy to tamper with. So the patient could use substitution, dilution, adulteration. Also, if you are doing witnessed collection, there's also the resources that that takes, and you may not have those resources readily available.

So the detection period of the drug depends on many variables, including dosage, comorbidities, genetic variability, pathophysiology, as well as the limitations and detection threshold of the assay itself. Typically, most substances can be detected within a one- to three-day time period. Others can be detected for longer periods of time. And for those who are chronically exposed to fentanyl, as it is highly lipophilic, we do see a slow dissipation. And the mean time for fentanyl clearance from urine is about one week. And norfentanyl clearance was nearly two weeks. So this is similar to THC found in cannabis use.

So, we're going to switch gears here and talk about treatment options. And for the purpose of this lecture, we're just going to focus on alcohol use disorder and opioid use disorder.

So in alcohol use disorder, our FDA approved medications include disulfiram or Antabuse, acamprosate or Campral, and naltrexone or Vivitrol.

And so with disulfiram, there are many risks to this medication. There's also compliance issues. So utilization of this medication is limited. But if you do use it, we recommend a written informed consent because of the risks of this medication. In Campral, it is more effective in achieving and maintaining abstinence, as opposed to preventing return to use, if drinking occurs.

In naltrexone, it reduces the subjective pleasurable effects of alcohol. It reduces the cravings. It reduces the drinks per day. And then it also helps in the rates of return to use. But of course, you cannot use this in patients who are taking opioid analgesics. And you may see off-label use of topiramate in alcohol use disorder, in helping to prevent return to use.

For opioid use disorder, we have methadone, which is a full agonist. It is probably one of the oldest and most thoroughly studied drugs. Methadone maintenance began in the 1960s. It is very highly regulated. And it is regulated by 42 CFR part 8 from the federal government. It does have a long half life, and it takes about five days to reach steady state. But half of each day's dose remains in the body, and it's added to the next day's dose. So it produces a rising serum level even without an increase in the dose. And so this is why it takes close monitoring during the induction phase because there have been reports of patients dying during that phase.

It is metabolized in the liver by the CYP3A4, 2D6, a smaller extent of 1A2. And so it does have numerous interactions with other medications. And so you have to be cognizant of that. The average dose for methadone is 80 to 120 milligrams. You do need at least 80 milligrams to achieve the opioid blockade.

Next, we have buprenorphine, which is a partial mu agonist. It activates the mu opioid receptors, producing the same results. So you get the analgesia, the euphoria, the constipation, the respiratory depression. But it does so to a certain limit, and that's called the ceiling effect. So even if you raise the dose of buprenorphine, those effects do not go above that theoretical ceiling limit. So in comparison to methadone, it is a highly safe medication because it doesn't have as many risks that come with methadone treatment.

So in talking about buprenorphine, we do have to talk about the receptor effects. So affinity is the strength, which a drug physically binds to a receptor. And buprenorphine's affinity is very strong, and it will displace full agonists like heroin and methadone. And this is the reason that you get precipitated withdrawal, if the patient is not in a mild to moderate withdrawal state.

Dissociation is the speed of disengagement or uncoupling of that drug from the receptor. And buprenorphine's is slow. So therefore, the buprenorphine stays on the receptor for a long time and it blocks heroin or methadone from binding to that receptor.

So there are a number of formulations that buprenorphine come in. Being sublingual, there's an implant, and also an injection. The sublingual formulation also comes in two forms-- one being the combo product, which is a combination of buprenorphine and naloxone, or the mono product, which is just buprenorphine alone.

So, naloxone has a limited bioavailability orally or sublingually. However, if that product is crushed and dissolved and then the patient injects it, the naloxone will cause an initial withdrawal if that person is opioid dependent. So this helps to decrease diversion and misuse of the medication. Typically, the mono product is used more so with pregnant patients. The implant and the injection formulations, they are expected to have a significant impact on improving adherence and also decreasing diversion. And although they have shown efficacy in the clinical trials, there's been really no demonstrated superiority of the long-acting formulations over the sublingual formulation.

So for the sublingual formulation, the usual dosage is between 8 and 32 milligrams per day. And so as I mentioned before, when you induct buprenorphine, the patient should be in mild to moderate withdrawal. There are some challenges surrounding induction, and the first being that you may precipitate withdrawal, which potentially could interfere with treatment retention or abstinence. Second is that the high potency synthetic opioids, such as fentanyl and the analogs that really have flooded the market, are not only highly potent, but they're highly lipophilic. And so the precipitated withdrawal during induction has become more frequent because of that.

So, some providers will also provide supportive medications for patients when doing buprenorphine inductions. In anticipation, if there are any precipitated withdrawal symptoms, they can use the supportive medications to help them.

Another approach is buprenorphine microdosing. So what happens in microdosing is that the patient will continue on the full agonist, whether that's illicit or prescribed. And then they'll induce Bup very slowly and gently. And then as Bup is slowly increased, the full agonist is slowly displaced. So this helps mitigate the potential for anticipated withdrawal. And then eventually, the Bup completely outcompetes the full agonist for the mu receptor. And so then the receptor is saturated, and at that point the full agonist can either be rapidly tapered off or just simply discontinued.

So there are many methods and protocols for microdosing, one of them being the Bernese method. The one displayed here is a modified Bernese. But these methods are only published in case reports and case studies, so there's really no randomized controlled trials of them. However, there are benefits to these protocols, and likely that outweighs the risk of the patient going without care and this life-saving treatment.

So, some principles for effective treatment, of course, is that no single treatment is appropriate for everyone. The treatment should include the multiple needs of the patient and really individualized to that patient. It is critical that they remain in treatment. Of course, if they stop treatment, then this will increase their risk for overdose deaths because their tolerance has been decreased during treatment.

Medications are an important element in treating substance use disorders, but it's not the only element. And so we have lots of behavioral interventions, which I have a worksheet that covers that should be used in combination with medications. And also these patients should be screened for HIV/AIDS, hepatitis B and hepatitis C, and potentially TB, and be provided any risk reduction counseling.

And so these are some references used to compile this lecture. And let me know if you have questions. Thank you.