Chose a medication discussed from the Anti-psychotic or Mood Stabilizer Power Points
NSG 502 # 2 Discussion Board
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Chose a medication discussed from the Anti-psychotic or Mood Stabilizer Power Points.
In your initial post discuss the following:
-Describe pharmacodynamics, pharmacokinetics, neurotransmitters and receptor sites involved. (Be sure to discuss to if your medication is an agonist, antagonist etc and how it will affect the receptors involved) In your discussion of pharmacokinetics be sure to include the CYP 450 system.
– Discuss side effects, be sure to explain why the side effects may be occurring (remember to use neuroscience and your knowledge of receptor sites).
-Include FDA approval and off label use for this medications.
-Lastly, include a thorough discussion of lab monitoring including if levels are needed, labs that should be drawn to monitor for side effects, or complications. Discuss any other testing indicated, such as EKG
It is expected that you will have sources for this discussion.
Response Post:
You must respond to two other students’ initial post. Your responses are due 48 hours after the initial post’s due date. Please respond to different medications so you will be exposed to three different medications. Your response post should be substantive, adding to the discussion of the initial post you are responding to. This will requires a minimum of 250 words as well as use APA citations and references.
At the psychiatric facility I work at, I have seen an increase in patients being treated with Lamotrigine (generically commonly known as Lamictal). I have heard prescribers discussing it’s effectiveness in specifically treating the depressive aspect of bipolar. Our lecture mentioned that Lamictal “treats from below” (depression) as opposed to “treating from above” (mania). I have learned about the risk of throwing a patient into a manic episode if using an antidepressant as monotherapy to treat the depression associated with bipolar, therefore I was curious about whether Lamictal could be an alternative to combination therapy for bipolar depression and decided to investigate this drug further.
The kindling of neurons in the frontal lobe is theorized to be the cause of seizures. Similarly, the excess firing of neurons in the limbic system is theorized to cause mood disorders. Lamotrigine is a mood stabilizer and anticonvulsant with FDA approval for maintenance treatment of bipolar 1 disorder. Lamotrigine is also FDA approved to treat partial seizures, generalized seizures of lennox-gastaut syndrome, and primary tonic-clonic seizures. Off label it is used for bipolar depression, and although it is considered and prescribed by many providers, it is not yet FDA approved for bipolar depression. It is also used off label for bipolar mania, psychosis, schizophrenia, neuropathic pain, and major depressive disorder (Stahl, 2017). Lamotrigine is thought to prevent seizures and stabilize mood by blocking voltage-sensitive sodium channels and by inhibiting the release of glutamate and asparate. It is a Glu-CB or glutamate, voltage-gated sodium channel blocker, and is considered an antagonist of voltage sensitive sodium channels (Stahl, 2017).
Lamotrigine is absorbed rapidly and completely and its distribution is not affected by food. It has 100% bioavailability, and is 55% protein bound. It is metabolized in the liver primarily through conjugation, rather than through the CYP450 enzyme system, however there is some UGT1A4 & 2B7 enzyme involvement (Procyshyn & Butler, 2017). It has an inactive metabolite and induces it’s own metabolism. In acute use lamotrigine has a 33 hour half life, while it’s half like is 26 hours with chronic use. Lamotrigine is renally excreted (Procyshyn & Butler, 2017).
Lamotrigine has a uniquely high tolerability profile in comparison to other antidepressant mood stabilizers. Side effects include dizziness, ataxia, blurred or double vision, sedation, headache, tremor, insomnia, poor coordination, and fatigue. Nausea, vomiting, dyspepsia, and rhinitis may also occur. The majority of side effects are considered central nervous system side effects and are caused by the excessive actions occurring at voltage-sensitive sodium channels (Stahl, 2017).
Lab tests are not typically utilized during Lamotrigine therapy as the value of monitoring plasma concentrations has not been established. Lamotrigine binds to melanin containing tissues, therefore ophthalmological checks may be advised (Stahl, 2017). The most important aspect of patient monitoring and education is that of toxic epidermal necrolysis described below.
Lamotrigine comes with a black box warning for a severe life threatening rash called Stevens Johnson syndrome (toxic epidermal necrolysis). This side effect is considered an allergic reaction and can be minimized by very slow titration upon initiation, educating and monitoring for symptoms, and avoiding drug interactions that raise levels such as valproate (Stahl, 2013). In order to safely monitor for this life threatening rash and respond appropriately, providers must educate patients to immediately contact them should a rash appear. Rashes that are widespread with involvement of neck, upper trunk, and involvement of lips, eyes and mouth with associated symptoms of fever, malaise, pharyngitis, anorexia or lymphadenopathy are most concerning. Laboratory tests for complete blood count, liver function, urea, and creatinine should be collected if there is concern of Stevens Johnson syndrome. Lamictal should be discontinued in this event, and hospitalization may be required (Stahl, 2017).
References:
Ric Procyshyn, Kalyna Bzchlibnyk-Butler, J. Joel Jeffries. (2017). Clinical Handbook of Psychotropic Drugs; 22nd edition. Ashland: Hogrefe Publishing.
Stahl, S. M. (2017). Stahl’s essential Psychopharmacology, Prescriber’s guide (6th ed.). Cambridge University Press.
Stephen M. Stahl, (2013). Stahl’s Essential Psychopharmacology Neuroscientific Basis and Practical Applications; 4th Edition. New York: Cambridge University Press.
I see lamotrigine prescribed quite frequently as well for bipolar maintenance due to tolerability and less risk of weight gain. I have seen a lamotrigine rash before in a patient who was on 25mg per day for two weeks, then appeared at the 50mg dose two days after initiating. Her rash was systemic and pruritic, but fortunately did not progress to Steven Johnson syndrome (SJS) or toxic epidermal necrolysis as the medication was stopped. Her rash resolved within two weeks of discontinuation of lamotrigine.
According to Kverno, Beauvois, and Dudley-Brown (2018), lamotrigine rashes can occur as soon as five days and as late as eight weeks after starting treatment. Interestingly, the aromatic ring of some anti-epileptics, including lamotrigine and carbamazepine, is thought to contribute to hypersensitivity skin reactions (Kverno et al., 2018). It is important to note that if adding Depakote to lamotrigine, it can increase lamotrigine levels and therefore increase the risk of rash (Stahl, 2020). According to Stahl (2020), a slow titration can reduce the risk of rash by starting at 25mg per day for two weeks, then increasing to 50 mg per day at week three, increasing to 100mg per day at week five, and at week six an increase to 200 mg (Stahl, 2020). Finally, if a patient stops lamotrigine, the provider must evaluate for how long they have been off the medication (Stahl, 2020). According to Stahl (2020), lamotrigine should be restarted at an initial titration dose of 25mg per day if the patient has been off the medication for longer five days. Kverno et al. (2018) note the importance of stopping lamotrigine for a rash due to risks of progression to more life-threatening rashes such as SJS. Although the percentage of individuals who develop a rash with lamotrigine are low, careful titration and knowledge of drug interactions can reduce this risk (Stahl, 2020).
Kverno, K., Beauvois, L., & Dudley-Brown, S. (2018). Lamotrigine rash: benign allergy or severe adverse reaction? Nurse Practitioner, 43(3), 48–51. https://doi-org.rivier.idm.oclc.org/10.1097/01.NPR.0000530211.32278.96.
Stahl, S.M. (2020). Stahl’s Essential Psychopharmacology Prescriber’s Guide (7th Ed.). Cambridge University Press: New York, NY. ISBN-10: 1108926010.
Perphenazine (Trilafon)
Perphenazine is a high-potency, first generational antipsychotic, also referred to as a neuroleptic or typical antipsychotic. It is FDA approved for the treatment of schizophrenia and nausea/vomiting with off-label uses for other psychotic disorders as well as bipolar disorder (Stahl, 2021). The key pharmacological property of typical antipsychotics is their ability to block dopamine D2 receptors, a mechanism that is responsible for drug efficacy as well as undesirable side effects.
Theoretically, perphenazine’s therapeutic action in reducing positive symptoms of psychosis is due to the blockage of postsynaptic D2 receptors in the mesolimbic dopamine pathway, thus reducing hyperactivity (National Center for Biotechnology Information, 2021; Stahl, 2013). Furthermore, perphenazine appears to block the histamine-1 and cholinergic M1 receptors which may reduce nausea and vomiting; it is therefore a dopamine antagonist with both antiemetic and antipsychotic traits (National Center for Biotechnology Information, 2021; Stahl, 2021). Because D2 receptors in the mesolimbic dopamine pathway are postulated to mediate the reward system of the brain and positive symptoms associated with schizophrenia simultaneously, blockage of this pathway often leaves patients apathetic and anhedonic (Stahl, 2013). Additionally, and unfortunately so, typical antipsychotics are associated with greater risk for extrapyramidal symptoms (EPS) due to prolonged D2 blockage, and severe cases may result in tardive dyskinesia. They may also increase prolactin levels in individuals taking this medication (Stahl, 2021).
Absolute bioavailability of perphenazine is 40% following oral administration. The medication is extensively metabolized in the liver by CYP 2D6, CYP 1A2, CYP 3A4, and CYP 2C19 to several metabolites via sulfoxidation, hydroxylation, dealkylation and glucuronidation (National Center for Biotechnology Information, 2021). Perphenazine is highly protein bound with a peak plasma level between one and four hours and a half-life of 9-21 hours. The primary route of excretion is through the kidneys (Stahl, 2021).
Typical antipsychotics are associated with weight gain due to the blockage of H1 receptors and therefore place patients at risk for metabolic syndrome. H1 receptor antagonism may also cause sedation but this is often transient. Baseline values such as weight, BMI, fasting triglycerides and A1C should be taken prior to pharmacological initiating and periodically throughout treatment. Prolactin levels should also be monitored for early identification of galactorrhea and amenorrhea due to prolonged D2 receptor blockage in the pituitary, as well as emerging symptoms of EPS or abnormal movements of tardive dyskinesia (Stahl, 2021). If EPS is present, an anticholinergic can be added to the patient’s medication regimen. Rarely, neuroleptic malignant syndrome (NMS) can occur. Symptoms include hyperpyrexia, muscle rigidity, autonomic instability, and delirium with elevated creatine phosphokinase, myoglobinuria, and acute renal failure (Stahl, 2021). Perphenazine, as with other typical antipsychotics, is associated with an increased risk of death and cerebrovascular events in elderly patients with dementia (Stahl, 2021).
Dosing begins at 4-8mg three times daily. The drug must be titrated, especially when switching antipsychotics and to avoid rebound psychosis and worsening of symptoms (Stahl, 2021). Treatment should be immediately stopped if patients develop NMS, and the medication should be used cautiously in anyone with respiratory disorders. Patient teaching should include avoiding undue exposure to sunlight and extreme heat exposure. Caution should be used in patients with renal, hepatic, and cardiac impairment, and this medication is not recommended for use in children under 12 years of age (Stahl, 2021).
References
National Center for Biotechnology Information (2021). PubChem Compound Summary for CID4748, Perphenazine. Retrieved September 29, 2021 from https://pubchem.ncbi.nlm.nih.gov/compound/Perphenazine (Links to an external site.).
Stahl, S. M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications. Cambridge University Press.
Stahl, S. M., Grady, M. M., & Muntner, N. (2021). Stahl’s essential psychopharmacology: Prescriber’s Guide. Cambridge University Press.
Thank you for providing all this information, It was interesting reading your response and learning more about this typical antipsychotic, perphenazine. I remember being really confused when a patient at my work was experiencing nausea and one of the providers prescribed an antipsychotic to treat it. It is interesting that sometimes the side effects of a medication that we typically consider to be undesirable or problematic can work to our advantage such as the mechanism that you mentioned. Most antipsychotics (and many other neuropsych medications) block cholinergic receptors resulting in side effects such as dry mouth, blurred vision, and constipation. Blocking this receptor can also reduce nausea and vomiting for patients. Another example is utilizing the blockage of histamine receptors to our advantage. The bothersome side effects of sedation and weight gain are typically extremely problematic and lead to intolerability and noncompliance. However, occasionally these mechanisms can be utilized to help patients sleep (such as with Seroquel) or to increase appetite in cancer patients (such as with Remeron).
As you mentione dopamine effects the symptoms and medication side effects associated with schizophrenia and other forms of psychosis. Blocking dopamine in the nigrostriatal pathway causes side effects related to movement disorders such as parkinsonianism and tardive dyskinesia (Stahl, 2017). One disadvantage of using a typical antipsychotic over an atypical antipsychotic are the higher risk of these extrapyramidal symptoms, and their inability to treat the cognitive/negative symptoms of schizophrenia related to dopamine and serotonin in the mesocortical pathway. Since the typical antipsychotics have potent dopamine blocking properties, hyperprolactemia can result from decreased dopamine in the tuberoinfundibular pathway. That being said the dopamine bloackade in the mesolimbic pathway is strong and therefore positive symptoms of schizophrenia such as hallucinations and delusions can be appropriately and effectively treated with the typical antipsychotics.
Due to their lower side effect profile, atypical antipsychotics have become the antipsychotics of choice. That being said. Patients with inadequare responses to the atypicals may benefit from a trial of either augmentation or switch to a typical antipsychotic (Stahl, 2013). Perphenazine primarily targets the positive symptoms of psychosis, motor and autonomic hyperactivity, and violent or aggressive behavior. There is an intramuscular formulation available for emergency use (Stahl, 2013).
Great job on your post, very informative.
References:
Stahl, S. M. (2017). Stahl’s essential Psychopharmacology, Prescriber’s guide (6th ed.). Cambridge University Press.
Stephen M. Stahl, (2013). Stahl’s Essential Psychopharmacology Neuroscientific Basis and Practical Applications; 4th Edition. New York: Cambridge University Press.
i enjoyed reading your in-depth analysis of Perphenazine. You made it easy to understand the drug’s key pharmacological properties, metabolism, and side effects, among other crucial elements. As an FDA-approved drug for treating schizophrenia, it is important to understand how Perphenazine functions as a first-generation antipsychotic medication.
Regarding Perphenazine’s therapeutic action, you have mentioned that it reduces positive symptoms of psychosis by blocking postsynaptic D2 receptors in the mesolimbic dopamine pathway. To elaborate its action, Keshavan and Eack (2019) mentioned that despite the exact mechanism of antipsychotics being unclear, Perphenazine has been proven to work by blocking the dopamine in the brain. For patients with schizophrenia, neurotransmission is adversely affected, and Perphenazine is more effective than other antipsychotics. It is the most recommended option, particularly when patients fail to respond to other antipsychotics.
You have further highlighted how typical antipsychotics are associated with weight gain due to the blockage of H1 receptors. With H1 receptor antagonism likely to cause sedation, albeit transient, it is crucial to highlight how Perphenazine reacts to the body under different conditions. Irtelli and Vincenti (2018) found that Perphenazine may cause abnormal muscle contractions, neck spasms, and blood pressure problems. As a result, the patient’s health status regarding muscle strength, blood pressure, and breathing difficulties should be evaluated before recommending Perphenazine. The medication also interacts with other drugs and supplements, which may affect its overall effectiveness and reaction. For instance, combining Perphenazine with sotalol or dofetilide is associated with abnormal heartbeats (Keshavan & Eack, 2019). Also, many patients with psychiatric problems usually consider taking antidepressants along with other medications. Unfortunately, antidepressants such as Prozac and Zoloft may inhibit Perphenazine’s breakdown, which, in most cases, increase blood levels.
References
Irtelli, F., & Vincenti, E. (Eds.). (2018). Psychosis: Biopsychosocial and relational perspectives. BoD–Books on Demand.
Keshavan, M., & Eack, S. (2019). Cognitive enhancement in schizophrenia and related disorders. Cambridge University Press.
Lamotrigine (Lamictal)
Lamotrigine (Lamictal) is an anticonvulsant which was the second drug approved in 2003 for the maintenance treatment of bipolar I disorder (Schatzberg, 2015). It is FDA approved for maintenance treatment of bipolar I disorder, partial seizures, generalized seizures, and primary generalized tonic-clonic seizures. It is used off label to treat bipolar depression, bipolar mania, psychosis, neuropathic pain and chronic pain, adjunctive treatment for MDD, and other seizure types. The drug blocks voltage-sensitive sodium channels and inhibits release of glutamate and asparate (Stahl, 2013). It also seems to modulate reuptake of serotonin and blocks reuptake of dopamine (Schatzberg, 2005). It has a half-life of 33 hours, which can either increase or decrease depending on the other medication the patient is currently taking. Although Lamotrigine is not metabolized by the CYP450 system in the liver, dosages should be reduced 25% in patients with moderate to severe liver impairment, and 50% if they have more severe impairment. It is absorbed throughout the entire gastrointestinal tract, but absorption is not affected by food intake (Mufson, 2018). It is renally excreted so those with renal impairment may need a decreased maintenance dose. If patients are also taking Valproate, the Lamotrigine dose should be reduced by 50% as it inhibits the metabolism of Lamotrigine. If individuals are also taking carbamazepine, phenytoin, phenobarbital, oral contraceptives, or they are pregnant, the dosage needs to be increased due to decreased plasma concentration (Mufson, 2018). In general, pregnant patients with bipolar disorder would benefit from an atypical antipsychotic, due to increased risk of fetus harm during pregnancy and lack of safety with breastfeeding while taking Lamotrigine as well (Stahl, 2013).
Lamotrigine is prescribed as monotherapy for bipolar disorder at 100-200mg/day and is prescribed as adjunctive treatment for bipolar disorder in combination with antiepileptic drugs up to 400mg/day. For bipolar disorder, it should be started off at 25mg/day for 2 weeks and slowly titrated up by 25-50mg every 2 weeks to avoid skin rash. The drug should not be abruptly stopped and should be tapered slowly over at least 2 weeks to avoid risk of relapse in bipolar disorder. If it is discontinued and restarted, the provider should begin slow titration again (Stahl, 2013). While it may take several weeks to notice benefit from this medication to improve bipolar depression and stabilize mood, it can take as little as 2 weeks to reduce seizures (Stahl, 2013).
Lamotrigine may be superior to other mood stabilizers as it does not have a negative impact on cognition (Zavodnick & Ali, 2012). It is also one of the best tolerated mood stabilizers as there is low risk of weight gain or sedation. It is best prescribed for those with depressive stages of bipolar disorder or depressive recurrence as it delays the onset of depression episodes but is not as helpful with managing manic stage (Schatzberg, 2015). It can be prescribed with an atypical antipsychotic and/or lithium to help manage acute mania if necessary (Stahl, 2013). It is often used as augmentation therapy for those with unipolar depression or comorbid anxiety (GAD, PTSD), as well as individuals with treatment resistant depression, especially if they have a family history of bipolar depression. It can be safely augmented with lithium, atypical antipsychotics, and SSRIs/SNRIs, and bupropion. Lamotrigine has been shown to accelerate the response of SSRI in patients with depression. In addition to psychiatric treatment, it may also help patients who have comorbid migraine or seizure disorder (Zavodnick & Ali, 2012). Some studies have shown the potential for Lamotrigine with treating schizophrenia. Due to its different mechanism of action on glutamate vs. dopamine, it differs from other antipsychotics. Further studies are needed to determine the implication for treating bipolar depression with lamotrigine given there were a few reports of side effects of psychosis and hallucinations (Kajiya et al., 2017).
The most common side effects of Lamotrigine are a benign rash (10%), headache, dizziness, sedation, tremor, insomnia, and poor coordination. A few side effects are dose dependent and include blurry vision and nausea. A serious adverse effect is Stevens-Johnson Syndrome, which can cause multi-organ failure, and toxic epidermal necrolysis. This presents as a widespread, itchy, or tender, confluent rash located on the neck or upper trunk, which can also present with systemic symptoms such as a fever, sore throat, anorexia, and lymphadenopathy. If this develops, patients should be instructed to immediately stop the medication and should be monitored closely in the hospital. Alternatively, a benign skin rash would present as nonconfluent without systemic features but can be difficult to differentiate from a more severe skin rash as it can look similar during the initial phase. Elderly and pediatric patients less than 12, especially if they are also taking valproate, may be more at risk for developing a rash. The highest risk of developing a rash is during the first 6 weeks of treatment (Mufson, 2018). Another rare but serious adverse event is a reaction called hemophagocytic lymphohistiocytosis. The FDA safety alert was released in 2018 and this immune system reaction presents with fever, rash, tenderness in abdomen, lymphadenopathy (Stahl, 2013). It is commonly triggered by viral illnesses, or rheumatologic disease, and presents within the first few weeks of treatment (Mufson, 2018). Patients should be educated on both the common and rare adverse effects of the medication and try to avoid any new skin products, fabric softeners, or sun exposure during the first few months of treatments to prevent skin irritation and rashes. Patients should discontinue the medication if they develop a rash or fever and should be monitored in a hospital setting. No routine labs or imaging is necessary for patients prescribed Lamotrigine (Schatzberg, 2015).
References
Kajiya, T., Sugawara, H., & Kajio, Y. (2017). Effect of lamotrigine in the treatment of bipolar depression with psychotic features: a case report. Ann Gen Psychiatry 16, 31. https://doi.org/10.1186/s12991-017-0154-2 (Links to an external site.)
Mufson, J. M. (2018). Lamotrigine: Pharmacology, Clinical Utility, and New Safety Concerns. The American Journal of Psyhchiatry, 3(12), 2-4. https://doi.org/10.1176/appi.ajp-rj.2018.131201 (Links to an external site.)
Schatzberg, A. F., & DeBattista, C. (2015). Manual of clinical psychopharmacology. American Psychiatric Publishing.
Stahl, S. M., Grady, M. M., & Muntner, N. (2021). Stahl’s essential psychopharmacology: Prescriber’s guide. Cambridge University Press.
Zavodnick, A., & Ali, R. (2012). Lamotrigine in the Treatment of Unipolar Depression with and Without Comorbidities: A Literature Review. Psychiatric Quarterly, 83(3), 371–383. https://doi-org/10.1007/s11126-012-9208-4
Thanks for your brilliant post on Lamictal. Lamictal is an anticonvulsant that stabilizes mood from below. Its Antiglutamatergic and neuroprotective actions are important candidate mechanisms for lamotrigine psychotropic effects, (Ketter,2003).
Lamictal maximizes the impact of depressive symptoms in bipolar disorder. I do strongly agree with you on lamotrigine as monotherapy for bipolar disorder at 100-200mg/day as this will help minimize medication side effects. According to Hurley, (2002), adverse effects are infrequent when the drug is used alone, but become more frequent when lamotrigine is combined with other anticonvulsants. And as such caution needs to be taken to ensure that adjunct medications to be prescribed will not affect the effectiveness of Lamictal. In monitoring, labs should include pertinent serum levels of concurrent anticonvulsants and liver function testing and renal function assessments. Clinical team staff should spend ample time educating patients on monitoring themselves for hypersensitivity, particularly rashes or other skin changes occurring near or on the mucosa. Patient education should also include discussing how to monitor for changes in seizures and their frequency and duration. Patients should also monitor for changes in suicidality, including suicidal thoughts and increased desire to commit suicide. Finally, patients should learn how to watch for signs/symptoms of aseptic meningitis. Slow upward dose titration is recommended to reduce the incidence of serious rash. In addition, it is recommended to educate the patient that Lamictal is expensive but that insurance could cover the cost and it is worth the try. Lamotrigine costs 2-4 times more than lithium, carbamazepine, and generic valproic acid (Hurley, 2002).
References
Hurley, S.C., (2002). Lamotrigine update and its use in mood disorders. Ann Pharmacother. 36(5):860-73. DOI: 10.1345/aph.1A102. PMID: 11978166.
https://pubmed.ncbi.nlm.nih.gov/11978166/ (Links to an external site.)
Ketter, T.A., Manji, H.K, Post, R.M.,(2003). Potential mechanisms of action of lamotrigine in the treatment of bipolar disorders. J Clin Psychopharmacol. 484-95. DOI: 10.1097/01.jcp.0000088915.02635.e8. PMID: 14520126. https://pubmed.ncbi.nlm.nih.gov/14520126/
Lithium Brands: Eskalith, Eskalith CR, Lithobid slow-release tablets, Lithostat tablets, Lithium carbonate tablets, Lithium citrate syrup
Lithium is a mood stabilizer; it is used in the treatment of bipolar disorder I and II. According to Stahl 2017, Lithium is FDA approved for manic episodes of manic-depressive illness, maintenance treatment for manic-depressive patients with a history of mania. It is used off label for the treatment of bipolar depression, major depressive disorder (adjunctive), vascular headache and neutropenia. Lithium dosing range for mania, recommended 1.0-1.5 mEq/L. Depression: 0.6-1.0 mEq/L. Maintenance: 0.7-1.0 mEq/L. Liquid: 10 ml, 3 times a day acute mania; 5 ml 3-4 times a day long-term. dosage forms: 300 mg tablets slow release and 450 mg controlled-release. Capsule can be use 150mg, 300 mg and 600 mg. liquid form 8 mEq/5 ml (Stahl, 2017).
The biochemical mechanism of Lithium is unknown. It alters sodium transport across cell membranes in nerve and muscle cells. It alters metabolism of neurotransmitters including catecholamines and serotonin. It may alter intracellular signaling through actions on second messenger systems. It specifically inhibits inositol monophosphatase, possibly affecting neurotransmission via phosphatidyl inositol second messenger system. It reduces protein kinase C activity, possibly affecting genomic expression associated with neurotransmission. Lithium inhibits excitatory neurotransmitters such as dopamine and glutamate and promotes GABA-mediated neurotransmission. One mechanism is Lithium modulates synaptic transmission mediated by monoamine neurotransmitters, accelerates presynaptic destruction of catecholamines, inhibits transmitter release at the synapses and decreased post synaptic receptor sensitivity (Ayano, 2016).
Lithium is given by mouth, either solid or liquid form. It is absorbed from the GI tract, rapid and completely. Patients can take lithium with food or without. Its bioavailability is 95-100% absorbed in conventional, 60-90% in extended release. Lithium peak plasma levels are 1-2 hours, its slow release is 4-5 hours. The elimination half-life of Lithium is 18-24 hours, it is longer in the elderly, because of age. It is not plasma protein bound. Lithium is purely renally excreted, it has no hepatic metabolic component. It lacks any inhibitory or inductive capabilities. Therefore, Lithium is not metabolized by CYP2D6. It is primarily unchanged by the kidneys, saliva sweat, and feces (Schatzberg & DeBattista, 2015).
According to Stahl 2017, the cause of side effects is unknow and complex. In theory, CNS side effects are due to excessive actions at the same or affiliated sites that mediate its therapeutic actions. Some renal side effects might be due to Lithium actions on ion transport. Lithium side effects are nausea, diarrhea, dry mouth, or metallic taste in the mouth, feeling thirsty and need to drink more and urinate more, mild hand tremor, feeling tired or sleepy and gradually gain weight. Patients need to stop taking Lithium or call 911 immediately if they have these symptoms. It could be Lithium toxicity, loss of appetite, vomiting, blurred vision, feeling thirsty, lack of control over bladder or bowel, lightheaded or drowsy, confusion, blackouts, shaky, muscle weakness, muscle twitches, jerks or spasms and difficulty speaking. Signs of serious allergic reactions are skin rash, wheezing, tightness in chest or throat, trouble breathing or talking, mouth/face/lips/tongue or throat start to swell. Patients need to call 911 and get immediate treatment in the hospital.
Providers need to obtain baseline lab work on patients before starting them on Lithium. They also need to obtain personal or family history of thyroid function, cardiac and renal disease. Baseline labs are FBS, TSH, CBC with diff, thyroid function, BUN and creatinine, calcium level, urinalysis, ECG for ages greater than 40 years, and pregnancy test in females. Lithium plasma levels need to be checked 5 days after first initiation, then checked on a weekly basis until therapeutic levels are reached. If patient is stable check Lithium level every 3-6 months unless they are elderly or has unstable renal or physical illness. Through level is measured 9-13 hours after taken last dose (Schatzberg & DeBattista, 2015).
References
Ayano, G. (2016). Bipolar Disorders and Lithium: Pharmacokinetics, Pharmacodynamics, Therapeutic Effects, and Indications of Lithium: Review of Articles. Journal of Psychiatry and Behavioral Sciences.
Schatzberg, A. F. & DeBattista, C. D. M. (2015). Manual of Clinical Psychopharmacology (8th Ed.). American Psychiatric Publishing: Arlington, VA.
Stahl, S.M. (2017). Stahl’s Essential Psychopharmacology Prescriber’s Guide. (6th Ed.). Cambridge University Press: New York, NY. ISBN 978-1-316-61813-4
Stahl, S.M. (2013). Stahl’s Essential Psychopharmacology: Neuroscientific Basis and Practical Applications (4th Ed.). Cambridge University Press: New York, NY. ISBN 10: 9781107686465
Thank you for a comprehensive overview of lithium utilized as a medication approved for bipolar disorder. A noted limitation of lithium is a delayed onset of action of for mania, of one to two weeks (Schzatberg & De-Battista, 2015). Lithium is sometimes utilized off label as an adjunct for major depressive disorder (
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