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Medical Student 8 Hour Buprenorphine Training
Session 3: Pharmacology
Session 3: Pharmacology
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Video Transcription
Hello again, this is your friendly guide, Dr. Pracken. In this module, we will review the pharmacology of medications used for the treatment of opiate use disorder. Before we get started, let's consider what you have already learned about the pharmacology and medication-assisted treatment. Take a moment and consider what you've already learned about methadone, buprenorphine, and naltrexone. Methadone is the oldest medication for treatment of opiate use disorder used in the United States. It is a synthetic opioid with two different forms, however. Our methadone is the only one with therapeutic activity. Methadone was first formulated in 1937 and approved by the FDA in 1947. It was approved initially for the treatment of pain, for which it is still very effective. During the 1960s, there was ongoing research around the use of this medication for both supervised withdrawal and maintenance treatment of patients with opioid use disorders. It was approved for the treatment of medically supervised withdrawal in 1970. It was then the first opioid medication in the United States to be approved for the treatment of patients with opioid use disorders. That was in 1973. There were and still are very clear guidelines and licensing associated with the establishment of opiate treatment programs and how the medication will be administered. The waiver that you're going to be eligible for in the completion of this training is actually a waiver to that original law in 1973. As stated, methadone is a very effective pain medication with active metabolites, but can be lethal when used inappropriately. Therefore, it is important that the administration of this medication be started at a low dose and titrated up slowly. Methadone is metabolized in the liver by cytochrome P450 3A4. It is ultimately excreted through the biliary tract with only small amounts in the urine. It is therefore detectable in the urine drug screens, however, not as an opiate. Remember, this is a synthetic opioid. There is significant oral bioavailability of this medication, though there is variability of that between 36% and 100%. One feature which makes methadone an effective medication in the treatment of opiate use disorders is its long half-life between 15 and 60 hours, allowing for once-a-day dosing. Another feature of methadone contributing to its effectiveness in treating opiate use disorder is its interaction with other opioids. If you think back in the Module 2 and the effect of opioids and the brain, especially how Bruce's brain was affected, here we can see how methadone works applying those principles. Though it has a weaker affinity for the opioid receptor at higher doses, it still interferes with the euphoric effect of other opioids. Thus, it not only will reduce cravings secondary to the satiation of the mu receptor, but also reduce any positive reinforcing effect of the concurrent opioid use. It is important to understand, however, that methadone will result in significant respiratory suppression and interfere with the normal response to rising CO2 levels in the medullary respiratory center, and this may result in respiratory arrest. Methadone is also associated with QT prolongation and the potential for tossade point, particularly at high doses and with patients with a particular predisposition. Consequently, one should be cautious in using this medication at doses greater than 120 milligrams and with those having a predisposition to cardiac instability or family history of the same. There are specific guidelines on obtaining an EKG for patients being initiated or in maintenance treatment with methadone. Buprenorphine is a semi-synthetic analog of Thebane, which is a precursor to codeine. Buprenorphine, a Schedule 3 medication, was approved by the FDA in 2002 as a medication for the treatment of opioid use disorders. The brands that were approved at that time were Suboxone, a combination of buprenorphine and naloxone, and Subutex, the buprenorphine monoproduct. There are now a variety of other buprenorphine-approved medications for the treatment of an opioid use disorder. Buprenorphine is metabolized in the liver by cytochrome P450 3A4. There is a less active metabolite called norbuprenorphine. Most buprenorphine, close to 70%, is excreted in the biliary tract prior to metabolism. Again, there's a small fraction that is excreted in the urine, making it detectable in urine drug screens. Because of the extensive first-pass metabolism of buprenorphine, it is a poor oral bioavailability agent when swallowed. Consequently, it is only administered by injection, transdermally or sublingually. Sublingual administration bypasses this first-pass metabolism and allows for the bioavailability to be up to the range of 30%. The features of buprenorphine that make it a very effective medication for the treatment of opioid use disorder include the fact that it can be used quite safely in the outpatient setting due to its comparatively less effects on the respiratory system. Though tragically, there have been some infant deaths when exposed to buprenorphine alone, there have been no reported overdose deaths in adults from buprenorphine alone. Buprenorphine will slow the respiratory rate, but it does not have the effect on the medullary respiratory index of disrupting normal response to rising levels of CO2. And that is seen in full opioid agonists. However, buprenorphine, when mixed with other sedatives, can be lethal. It also has a long half-life, allowing for a once-a-day administration. Due in part to the long half-life, it has even been administered on-site three times a week. Though this is not a typical protocol, it is prescribed on an outpatient basis. Buprenorphine also has a very high affinity to the mu receptor. As we have talked about, this has to do with the strength of the bond to the receptor, but not associated with the intrinsic activity of the molecule. Consequently, when buprenorphine is currently in the patient's system, it will block the euphoric activation of other opioids. We'll be talking about the treatment of pain when the patient is currently taking buprenorphine at a later module. But to be clear, there is some increased analgesic activity in the co-administration of full opiate agonists when prescribed for pain. This high affinity to the opioid receptor by buprenorphine will result in displacement of other full opiate agonists from the receptor, which can result in an experience of withdrawal. This is the reason patients need to be in mild to moderate withdrawal from their full opiate agonist prior to the administration of buprenorphine. The other aspect of buprenorphine that makes it a good medication for the treatment of an opioid use disorder is a slow disassociation of this medication from the receptor. This means the receptor is blocked for a considerable period of time, resulting in decreased cravings and allowing the patient to get on with their life without frequent re-administration. So now that you know more about the pharmacology, let's review how buprenorphine actually works. As stated, buprenorphine has a high affinity for and a slow disassociation from the mu receptor. This results in a prevention from withdrawal symptoms if taken in an adequate dose at least every 36 to 48 hours. It decreases cravings by stimulation of the opioid receptor. Secondary to its high affinity, it blocks the opioid receptor from activation by other opioids that may produce a euphoric effect. But interestingly, it does not block all the effects of other opioids. This may be in part because of some opioid receptors still being available and the dynamic interaction between buprenorphine and those receptors. For this reason, there is some improvement of pain when a full opioid agonist is administered while buprenorphine is still present. Buprenorphine comes in a variety of formulations and there are various considerations in determining which formulation would be best for a particular patient. There should be consideration as per patient preference, what their insurance will provide, safety considerations, particularly whether there are children in the home, and what formulation might have the potential of reducing the patient's risk for diversion and to injection drug use as for sales. The primary way in which it's used is sublingually, either as a sublingual film or tablet. Subdermal implants have been available for a couple of years, though the uptake of this medication has not been good. These are six-month implants applied subdermally in the forearm. More recently, there has been availability of a one-month subcutaneous injection. And this is a new and innovative opportunity for the treatment of patients with opioid use disorders. And there will likely be other shorter duration injections available in the near future. All of these formulations have shown similar efficacy in the treatment of opioid use disorders. Please be clear, only buprenorphine products approved by the FDA for the treatment of opioid use disorder can be used to treat these patients. Therefore, medications like the transdermal patch of buprenorphine called Butrans, and some buccal products like Belbuca are only available for the treatment of pain. They are not approved and consequently cannot be used for the treatment of an opioid use disorder. Why would combining buprenorphine and naloxone be a good idea? The most common and safest formulation of buprenorphine used for the outpatient treatment of opioid use disorder is the combination product. First of all, note that when this product is used as prescribed sublingually, there is a negligible bioavailability of naloxone. The naloxone is present in this formulation to reduce the diversion of this product to injection drug use. This is because though there is negligible naloxone with sublingual administration, there is significant activity of this medication when injected. So when compared to the model product, buprenorphine alone, there is clearly a reduction in injection drug misuse. This is for two reasons. There's potential for the naloxone in this combination product to precipitate withdrawal symptoms when injected. The other important aspect is that naloxone will compete with buprenorphine when injected together, resulting in a mildly uncomfortable experience, but more importantly, a slow onset of the effect of the injected buprenorphine. When patients inject a drug, they are doing it primarily to get a very immediate effect of the drug. In fact, it is the speed in which a drug gets to the brain that increases the addictive potential of that drug. Because of this competition between buprenorphine and naloxone when injected, there is a significant reduction in the injection drug use of this product. This was most clearly identified in a long naturalistic study in France where the model product had been available for nearly 10 years before the introduction of the combination product. During the period of time when the model product was only available, there were significant problems with diversion to injection drug use and associated HIV and hepatitis C infections. Following the availability of the combination product, injection drug use dropped off significantly and morbidity improved. Other evidence of the increased diversion of the model product is the evidence identifying a greater diversion for prescription and street value of the model product. Thus, the combination is highly encouraged. Here are the current available products of buprenorphine for the treatment of opioid use disorder. Notice that the combination products are typically in a four to one buprenorphine to naloxone ratio. Naltrexone is a long acting, high affinity, competitive opioid antagonist. Very small plasma concentration, as low as two nanograms per mil, can successfully block all opioid activity. Naloxone tablets have been available for the treatment of opioid use disorder since the mid 1980s. They are very effective in blocking exogenous opioids. However, the oral product has not been successful in treatment of opioid use disorder, secondary to poor daily adherence to treatment. Naltrexone long acting injectable medication was actually first approved for the treatment of alcohol use disorders. It is very effective in reducing cravings for alcohol, which are in part associated with endorphin release when one is experiencing cravings. This medication was approved for the treatment of opioid use disorder in 2010. It is a once a month injection that results from circumventing the problems with daily adherence of the tablet. It has been shown to be equally effective as buprenorphine. The difficulty is establishing the seven to 10 days free of any opioid prior to the administration of this medicine. Here you see the major features of naltrexone. It is a full antagonist at the immune receptor. It has a long half-life. It has a high affinity to the opioid receptor, blocking other opioids or displacing them when they are currently in the patient's system. This will result in a significant and sometimes severe precipitated withdrawal. Again, it is available both as a tablet and as an injectable medication. Naltrexone works in the treatment of opiate use disorders a couple of different ways. Clearly having injectable product on board means the patient cannot use an opioid allowing for neurobiologic and behavioral healing to take place without the stimulation of an opioid. There are decreased cravings secondary to the fact that the patient knows they will not experience an opioid-like effect if they use an opioid while currently taking naltrexone. Interestingly, when we know we cannot have something, we have a reduction in the recurrent thought of wanting it. For example, an opioid use disorder patient that is incarcerated or in another controlled setting, they will, after a relatively short period of time, have a significant reduction of that recurrent thought and behavioral drive of using an opioid. This is because it literally is not available to them. It is similar to removing ourselves from an environment where we are continually stimulated to consider using a substance, like food for example, or behaving in a particular way. If we don't bring those foods into our home, we have less frequent thoughts of eating them. This is associated with psychological theory of extinction. The other mechanism by which it works is pharmacologic. This is associated with a reduction in the endorphin release associated with cravings similar to the way this medication works for alcohol craving reduction. Because this is not an opioid, one does not need a waiver to their DEA license to use it. Having this medication available for patients can consequently attract this subset of patients increasing overall availability of treatment. This slide shows you a table comparing the three products that we have talked about. Methadone, full agonist, buprenorphine, partial agonist, and naltrexone, an antagonist. You see that both full and partial agonists activate the mereceptor and thus satiate some of the drive to use other opioids. Naltrexone occupies a receptor without activation, blocking other opioid use and decreasing the drive to use other opioids. Methadone, a full opioid agonist, has significant reinforcement. Buprenorphine is also reinforcing, but somewhat less than methadone. Naltrexone has no reinforcing properties, and thus can be more difficult for the patient to establish engagement in treatment. Given the efficacy of buprenorphine and the availability to use this agonist medication in an office-based setting, there is significant increase in overall availability of treatment. It is available in the office because of increased safety profile of this medication compared to methadone as a full opiate agonist. Naltrexone has the advantage of not being an opioid medication, thus without potential for misuse or diversion. Patients are not physically dependent on this medication as they are on both methadone and buprenorphine. Naltrexone is available to be prescribed by any provider without a waiver. The long-term injectable product is now available through many commercial and public insurances. Other considerations between these medications include, methadone has multiple drug-drug interactions that can affect the efficacy of other medications and methadone. It also, as previously pointed out, will result in QT prolongation at higher doses. This is a concern for the diversion of buprenorphine, primarily in its distribution on the street. Naltrexone is difficult to use because the patient needs to be completely off opioids before it can be administered. Patients also need to be clear that on discontinuation of this medication, they have completely lost their tolerance and that they once had opioids and thus they are at risk for overdose if they're not extremely careful. Patients also need to clearly understand that while taking Naltrexone, there can be difficulty in using standard opiate therapy for the treatment of pain secondary to other issues due to the blockade. We will talk about this more in the discussion of co-occurring pain with an opiate use disorder. In looking at the efficacy of methadone compared to buprenorphine, we see that there is some improvement in retention and treatment of methadone over buprenorphine. However, this can be in part dose related. Both these medications are very effective in improving treatment retention, which is highly correlated with successful treatment. In a Cochrane review of 31 trials involving over 5,400 patients, it was found that buprenorphine is an effective medication for retaining people and treatment at doses greater than two milligrams and suppressing illicit opioid use at doses 16 milligrams or above. However, buprenorphine appeared to be less effective than methadone and retaining patients in treatment in doses two to six milligrams per day. On the other hand, in comparing buprenorphine at fixed doses greater than seven milligrams per day, it was equally as effective as methadone, prescribed at 40 milligrams and above on a daily basis and retaining people in treatment and suppressing their opioid use. The bottom line is that both these medications have been shown to be very effective in retention and treatment and suppression of opioid misuse. What does this graph tell you? In looking at buprenorphine dosing, this graph points out that one milligram was not very successful in establishing an opioid-free state for these patients. But as one goes up on the dose, there is an increasing efficacy in reducing opioid use. This graph again identifies that one milligram is not effective in establishing a therapeutic regimen that is successful in decreasing cravings of a patient with an opioid use disorder. It is also interesting, though, to look at how 16 milligrams is able to drop that craving rapidly compared to either four or eight milligrams. But over time, if the patient is maintained in treatment, four or eight milligrams are nearly equal as effective in reducing cravings as 16. This is an important consideration in establishing treatment with the patient. We will talk about this more when we look at the clinical use of buprenorphine, but I would point out here that close contact with the patient and allowing the patient to reach a steady state in the first couple of weeks of treatment can mean that you can use a lower dose initially, allowing for there to be increases in dose later because of craving or opioid use over time if needed. Remember, craving is a primary reason for dosage change. Patients will sometimes ask to go up on their dose because of withdrawal symptoms, but if given an adequate time to reach a steady state, the withdrawal symptoms will stabilize. So increases in doses are used to reduce craving only. One of the most common questions people have concerns how long a patient should be on medication. This study was of patients both initiated on buprenorphine, but one treatment arm was tapered from the buprenorphine between four and seven weeks while the other arm continued maintenance to administration of buprenorphine. As you can see, there was significant retention and treatment of that cohort of patients that were maintained on buprenorphine compared to those that were tapered off. Again, it is the retention and treatment that is most clearly identified with patient success over time. There is no specific time period in which patients should be taken off this medication. It is primarily patient-driven and associated with their experience of success and stability that determines when the patient is ready to discontinue this medication. This multi-center study identified the efficacy of the treatment of prescription opioid use disorders with buprenorphine. It also reiterated the importance of continuation of treatment with medication over time. It should also be pointed out that though some patients will have greater improvement with the addition of counseling, this is not universal. It is always important to listen to the patient and identify their individual biopsychosocial problems that may be associated with their opioid use disorder and tailor their treatment to those needs. There can be adverse effects to the use of buprenorphine. The most common are headache and constipation. Patients will occasionally describe some nausea also. We'll be talking about the administration of buprenorphine in the clinical module. But I would point out now that when buprenorphine with naloxone is taken sublingually, one pill or film is completely dissolved and allowed to be absorbed over the next couple of minutes. It can then be either swallowed or spit out where there will be no further significant absorption of the medication that's swallowed. However, there can be reduction in nausea and sometimes the headache when it is spit out instead of swallowed. This is worth reviewing with the patient. The headache typically only lasts for a short period of time and patients can control it if need be with acetaminophen. This however may be a reason to change the product because constipation is a problem. However, most patients will talk about an improvement in their constipation over what it was while using a full opiate agonist like heroin. Dry mouth can also be a problem. It is however often remedied if the patient increases their fluid intake and maintains good oral hygiene. This slide points out something that we talked about a few times already and that is the safety profile of buprenorphine. As you see, with increasing dose of buprenorphine, there is a slowing of respirations but that it stabilizes in the range of 12 breaths per minute. There is no further reduction in oxygen saturation at that point. One should be careful however in educating patients on the potential for increasing respiratory risk on the co-administration of other sedatives including alcohol. There should also be consideration in patients with concurrent significant respiratory illness. Here we see a dosing study for injectable naltrexone and retention and treatment. Of course if the patient believes they have an opiate antagonist on board, they may have some reduction in their use of opioids. However, as previously pointed out, there is some reduction in cravings secondary to the medication itself as opposed to purely the understanding of the blockade to the euphoric effects of an opioid. This is nicely demonstrated in the increased efficacy of 384 milligrams of Depo injection compared to the 192 milligram injection. The current available product is sold as a 380 milligram product. These graphs point out three important aspects associated with the efficacy of naltrexone over placebo in the treatment of an opiate use disorder. In the first graph, points out the difference in number of opiate-free urines between the red line which is injectable naltrexone and placebo, the blue line. In the middle graph, you see the efficacy in reducing cravings which is most dramatic between naltrexone and placebo. In the third graph, you see the potential of injectable naltrexone in improving retention and treatment over placebo. There are two well-done studies looking at efficacy of buprenorphine compared to injectable naltrexone reported in the literature. The studies indicate that both medications were comparable in efficacy although there was some concern associated with the dosing protocol of buprenorphine that may have skewed this data. It was also clear that one of the variables that was important was the fact that there was a significant drop off in patients completing the study in the naltrexone arm because of the difficulty of establishing sufficient abstinence prior to the administration of the drug. However, when the drug was administered, there was very similar outcomes between these two medications. Methadone has some significant drug-drug interactions which must be considered. When methadone is used with a serotonin reuptake inhibitor which can result in inhibition of metabolism, this can result in a slowing of the metabolism of methadone and thus potential for higher blood levels. This can be monitored clinically though one may want to get blood levels of methadone to confirm this. Fluoxetine is known to have the greatest potential for enzyme inhibition. Carbamazepine induces enzymes associated with the metabolism of methadone and consequently there have been reports of the patient experiencing withdrawal symptoms after the initiation of carbamazepine. As a result of this, there should be greater consideration for the use of valproate, Depakote, over the use of carbamazepine when the patient is taking methadone. Methadone should not be used in conjunction with monoamine oxidase inhibitors. Alternative antidepressants should be used instead. Buprenorphine is metabolized in the liver by cytochrome P450-3A4. Drugs that may either induce or inhibit this enzyme may change the efficacy of buprenorphine though this is rare. Typically, this would be monitored clinically. It is important to monitor the pharmacodynamic interactions of buprenorphine particularly with other sedatives. This has been mentioned in all other areas of this training. There can be synergistic effects and the use of centrifugation There can be synergistic effects and the use of central nervous system depressants such as benzodiazepines and alcohol that can be dangerous to the patient. As has also been pointed out, the interaction between buprenorphine and other opioids will have varying effects and should be monitored clinically in a patient with pain. Compared to methadone, buprenorphine has no significant association with the prolongation of QT interval that sets patients up for risk of torsades de pommes. This slide reviews the interaction of buprenorphine with other opioids. Of course, when buprenorphine is used alone, it will be the only medication occupying the opioid receptor. However, when a full opiate agonist is occupying the receptor and buprenorphine is administered, buprenorphine will displace the full opiate agonist. This can result in precipitated withdrawal depending on the degree of current opioid activation by the full agonist. Next, when buprenorphine is currently occupying the opioid receptor and a full agonist is introduced, buprenorphine will remain dominant due to its higher affinity. So consequently, there is a reduction in the efficacy of the full opioid agonist. Finally, when buprenorphine is on board and an antagonist is introduced, there is a competitive response between these medications due to the high affinity of both. In this competition, naltrexone will dominate, leading to full withdrawal, thus buprenorphine needs to be stopped seven days before initiating naltrexone treatment. There have been reports of fatalities associated with the concurrent use of a benzodiazepine and buprenorphine. However, this has been associated with the use of these medications outside of appropriate medical management. In both animal and human studies, there was evidence of an increased safety profile of buprenorphine co-administered with benzodiazepines compared to the full agonist opiate combination. What is important to understand in the use of benzodiazepines with buprenorphine is the greater potential for disinhibition and accidental injuries when combining these medications. There is also evidence that it is an indicator of polysubstance and erratic drug use. The FDA has put forth recommendations concerning the co-administration of buprenorphine and benzodiazepines. Initially in 2016, there was a black box warning of the risk for slowed and difficult breathing, sedation, and death. This, however, was tempered in 2017 due to the desire to make clear that a person taking benzodiazepines therapeutically should not be restricted from treatment for their opiate use disorder, which is much more dangerous with buprenorphine or methadone. Though in this note, they continue to make clear the potential serious side effects of combining these medications. They encourage careful medication management by a healthcare professional in reducing these risks. The FDA guidance outlines the actions and precautions that should be part of the treatment plan of patients that are being prescribed benzodiazepines or other central nervous system depressants along with buprenorphine or methadone. Patients should be educated about the serious side effects and the importance of using these medications only as prescribed. Whenever possible, benzodiazepines or other CNS depressants should be tapered or discontinued. It is important that other medication options be considered prior to the use of benzodiazepines for anxiety or insomnia. This is in light of the fact patients with an opiate use disorder may require medications such as buprenorphine and methadone indefinitely for the treatment and it should be not stopped in patients that have co-occurring anxiety or insomnia disorder. They also point out the importance of coordinating care with other prescribers and continued monitoring of other drug use through urine or blood screening. Keep in mind, alcohol is also a central nervous system depressant that can have a similar pharmacodynamic effect when used in combination with agonist treatments for an opiate use disorder. There has been some limited evidence that buprenorphine will reduce cravings for alcohol, but more importantly, it is the retention and treatment and continued discussion with the patient concerning their use of alcohol and other drugs in association with their treatment with buprenorphine that can be most beneficial. There is evidence that continued use of alcohol, particularly in those in the alcohol use disorder, will increase the rate of relapse in an opiate use disorder patient. Lastly, in looking at problems associated with the use of buprenorphine, we need to again understand clearly the potential for diversion to injection drug use. There has been some evidence that higher dose tablets of the generic product compared to film have a higher diversion to injection drug use. Clearly, monoproduct tablets are more likely to be diverted to injection drug use than the combination product. This is secondary to a mild adverse effect that can take place because the naloxone is more available in this delivery than when used sublingually. It also will cross the blood-brain barrier more rapidly than buprenorphine. However, as we have reviewed, they both have a very strong affinity to the opiate receptor so consequently, there is more of a slowing of onset of the buprenorphine, which is not what the patient is looking for. They're injecting the drug in order to get a rapid response. This increased potential for injection drug use of one product over the other has been identified by rates of diversion. The buprenorphine naloxone tablet has a little over two times the rate of diversion to the film, but the monoproduct is greater than six times more frequently diverted to injection drug use than the film. The combination product is the standard of care for general use in treating a patient for an opiate use disorder with buprenorphine. The protocol for initiating long-acting injectable naltrexone in a patient with an opiate use disorder recommends an abstinent period from all opioids of seven to 10 days to avoid potential precipitated withdrawal. This can be challenging as has previously been pointed out. This may be easier by using non-opiate medications for withdrawal, thereby including the time the patient is in medication-assisted withdrawal in the seven to 10 days line. This is particularly true if the patient is in residential or inpatient treatment programs. There are protocols for attempting to shorten this period of time using smaller doses of naltrexone earlier. However, there's only limited literature available outlining the efficacy of these protocols. Treatment adherence can be challenging in patients on long-acting injectable naltrexone. As stated, oral naltrexone is not recommended because of the poor compliance and greater risk of relapse. Remember, the patient will have complete loss of tolerance to opioids and be at greater risk of overdose if they relapse. Therefore, the long-acting injectable naltrexone is the preferred formulation. While patients are being treated for their opiate use disorder with naltrexone, there should be consideration for continued counseling, motivational techniques to emphasize adherence to relapse prevention, and anticipatory guidance associated with the need for repeat injections over no shorter than a six-month period of time. The involvement of collaterals, including, potentially, a significant other, may be helpful in supporting adherence with these monthly injections. This can be concurrent with contingency management, such as a young person might be able to continue living in the parent's home if they continue to get their monthly injections. Side effects to this medication can include some subacute withdrawal symptoms in the first couple of weeks following the first injection of naltrexone. This is associated with a slow but complete withdrawal from previous opioids. The most common complaint associated with the use of this medication is soreness at the injection site. This can be overcome with good technique surrounding the injection and making sure that the medication is delivered deep intramuscularly in the gluteus maximus muscle. Very important, patients should clearly understand the risk of relapse and potential overdose on discontinuation of this medication. From all that we have discussed, what is the most important information to remember? Think for a moment or two before reading the summary on your own.
Video Summary
In this video, Dr. Pracken discusses the pharmacology of medications used for the treatment of opiate use disorder. He starts by providing an overview of methadone, the oldest medication used for this purpose. Methadone is a synthetic opioid that has been used since the 1940s for pain management and later for opioid use disorder treatment. Dr. Pracken explains that methadone is metabolized in the liver and has a long half-life, allowing for once-a-day dosing. Methadone works by satiating the mu opioid receptor and interfering with the euphoric effects of other opioids.<br /><br />Next, he discusses buprenorphine, a semi-synthetic opioid that was approved by the FDA in 2002 for the treatment of opioid use disorder. Buprenorphine has a high affinity for the mu receptor and a slow dissociation, making it effective in reducing cravings and blocking the euphoric effects of other opioids. Buprenorphine has a favorable safety profile compared to methadone and is often used in outpatient settings.<br /><br />Lastly, Dr. Pracken talks about naltrexone, a long-acting opioid antagonist that blocks the effects of opioids. Naltrexone can be administered orally or via injection and requires patients to be completely free of opioids before starting treatment. Naltrexone can reduce cravings and prevent relapse but has a lower adherence rate than other medications.<br /><br />Overall, the video emphasizes the importance of medication-assisted treatment for opioid use disorder and highlights the key features and considerations of methadone, buprenorphine, and naltrexone. The information provided aims to support healthcare professionals in their understanding and management of these pharmacological interventions.
Keywords
opiate use disorder
medications
pharmacology
methadone
buprenorphine
naltrexone
medication-assisted treatment
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Funding for this initiative was made possible by cooperative agreement no. 1H79TI086770 and grant no. 1H79TI085588 from SAMHSA. The views expressed in written conference materials or publications and by speakers and moderators do not necessarily reflect the official policies of the Department of Health and Human Services; nor does mention of trade names, commercial practices, or organizations imply endorsement by the U.S. Government.
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