- India has an opioid dependence problem, with approximately 4 million people using opioids and 1 million dependent. Punjab has around 232,000 people dependent on opioids alone.
- Opioids are classified as natural, semi-synthetic, synthetic, and endogenous. Common opioids used in India include morphine, heroin, methadone, buprenorphine, and tramadol.
- Opioid dependence is treated through pharmacological therapies like opioid substitution therapy (OST) using methadone and buprenorphine, and symptomatic treatments. Non-pharmacological therapies include individual therapy, family therapy, and support groups.
Quetiapine (brand name Seroquel) is an antipsychotic medication used to treat schizophrenia, bipolar disorder, depression, and other mental health conditions. It works by affecting dopamine and serotonin levels in the brain. Generic versions have been found to be equivalent to the brand name when rated by the FDA. Common side effects include drowsiness, dizziness, and dry mouth. It is important to take quetiapine as prescribed by your doctor and notify them immediately of any severe side effects. Community support workers should follow care plans, monitor for side effects, and ensure clients stay hydrated when taking quetiapine.
Dopamine receptor agonists are important in the treatment of Parkinson's disease as they have fewer side effects than levodopa therapy. Key points:
- Dopamine agonists work directly on dopamine receptors and do not require metabolic conversion like levodopa. This avoids toxic metabolites.
- They are effective as initial therapy for mild Parkinson's and can be used alongside levodopa to smooth fluctuations and reduce dyskinesias in advanced disease.
- Common side effects include nausea, hypotension, hallucinations, impulse control disorders and sleep attacks. Ergot derivatives like bromocriptine and pergolide also carry risks of fibrosis and cardiac side effects.
- Apomorphine injections provide temporary
Insomnia is defined as difficulty falling asleep, staying asleep, or early awakening despite opportunities for sleep, associated with impaired daytime functioning for at least 3 nights per week for over a month. It can be acute (under 3 months) or chronic. Assessment involves medical history, sleep history, and screening for sleep apnea, depression/anxiety, and other medical issues. Treatment goals are to improve sleep quality and quantity and daytime functioning. Non-pharmacological treatments like CBT, sleep hygiene, and sleep restriction are recommended initially. Hypnotics may be used short-term but have risks and should be avoided for chronic insomnia when possible.
Quetiapine is a first-line atypical antipsychotic that has been used since 1998 for schizophrenia, bipolar disorder, depression, and other conditions. It is absorbed quickly in the body and metabolized in the liver. Quetiapine acts as an antagonist at serotonin, histamine, alpha-1, and dopamine receptors, with varying degrees of affinity. Common side effects include sedation, dizziness, hypotension, weight gain, and metabolic changes. Overdoses may cause lethargy, tachycardia, respiratory issues, and other symptoms, but are typically not fatal.
This document summarizes the pharmacology of the antidepressant fluoxetine. It begins by defining depression and antidepressants. It then discusses fluoxetine specifically, including that it is a selective serotonin reuptake inhibitor (SSRI) introduced in 1987. The document covers fluoxetine's mechanism of action, pharmacokinetics, pharmacodynamics, therapeutic uses, side effects, toxicity, drug interactions, contraindications, dosing, administration, and market preparations. It provides details on fluoxetine's absorption, distribution, metabolism, and excretion. The summary focuses on key information about fluoxetine's pharmacology and use as an antidepressant.
The document compares the serotonergic antidepressants currently available in the US on variables such as indications, efficacy, structure, pharmacodynamics, pharmacokinetics, side effects, dosing preparations, and cost considerations. It discusses that while the drugs are structurally unrelated, they all inhibit neuronal reuptake of serotonin. Their potency and selectivity at the serotonin transporter varies, which may account for some differences seen between individual patient responses. Overall, all drugs are considered similarly effective compared to placebo and TCAs for treating conditions like depression and anxiety.
This document discusses the history, pathophysiology, diagnosis, and treatment of insomnia. It begins with definitions of insomnia and provides a historical overview of insomnia pharmacotherapy. It then covers the epidemiology of insomnia, describing prevalence rates and risk factors. The pathophysiology section explains the physiological mechanisms involved in sleep-wake regulation. Diagnosis and classification of insomnia subtypes are outlined. Treatment approaches discussed include pharmacological management with benzodiazepines, non-benzodiazepine hypnotics, melatonin agonists, and other drugs. Non-pharmacological therapies are also mentioned. New drug targets for insomnia are briefly noted.
Quetiapine (brand name Seroquel) is an antipsychotic medication used to treat schizophrenia, bipolar disorder, depression, and other mental health conditions. It works by affecting dopamine and serotonin levels in the brain. Generic versions have been found to be equivalent to the brand name when rated by the FDA. Common side effects include drowsiness, dizziness, and dry mouth. It is important to take quetiapine as prescribed by your doctor and notify them immediately of any severe side effects. Community support workers should follow care plans, monitor for side effects, and ensure clients stay hydrated when taking quetiapine.
Dopamine receptor agonists are important in the treatment of Parkinson's disease as they have fewer side effects than levodopa therapy. Key points:
- Dopamine agonists work directly on dopamine receptors and do not require metabolic conversion like levodopa. This avoids toxic metabolites.
- They are effective as initial therapy for mild Parkinson's and can be used alongside levodopa to smooth fluctuations and reduce dyskinesias in advanced disease.
- Common side effects include nausea, hypotension, hallucinations, impulse control disorders and sleep attacks. Ergot derivatives like bromocriptine and pergolide also carry risks of fibrosis and cardiac side effects.
- Apomorphine injections provide temporary
Insomnia is defined as difficulty falling asleep, staying asleep, or early awakening despite opportunities for sleep, associated with impaired daytime functioning for at least 3 nights per week for over a month. It can be acute (under 3 months) or chronic. Assessment involves medical history, sleep history, and screening for sleep apnea, depression/anxiety, and other medical issues. Treatment goals are to improve sleep quality and quantity and daytime functioning. Non-pharmacological treatments like CBT, sleep hygiene, and sleep restriction are recommended initially. Hypnotics may be used short-term but have risks and should be avoided for chronic insomnia when possible.
Quetiapine is a first-line atypical antipsychotic that has been used since 1998 for schizophrenia, bipolar disorder, depression, and other conditions. It is absorbed quickly in the body and metabolized in the liver. Quetiapine acts as an antagonist at serotonin, histamine, alpha-1, and dopamine receptors, with varying degrees of affinity. Common side effects include sedation, dizziness, hypotension, weight gain, and metabolic changes. Overdoses may cause lethargy, tachycardia, respiratory issues, and other symptoms, but are typically not fatal.
This document summarizes the pharmacology of the antidepressant fluoxetine. It begins by defining depression and antidepressants. It then discusses fluoxetine specifically, including that it is a selective serotonin reuptake inhibitor (SSRI) introduced in 1987. The document covers fluoxetine's mechanism of action, pharmacokinetics, pharmacodynamics, therapeutic uses, side effects, toxicity, drug interactions, contraindications, dosing, administration, and market preparations. It provides details on fluoxetine's absorption, distribution, metabolism, and excretion. The summary focuses on key information about fluoxetine's pharmacology and use as an antidepressant.
The document compares the serotonergic antidepressants currently available in the US on variables such as indications, efficacy, structure, pharmacodynamics, pharmacokinetics, side effects, dosing preparations, and cost considerations. It discusses that while the drugs are structurally unrelated, they all inhibit neuronal reuptake of serotonin. Their potency and selectivity at the serotonin transporter varies, which may account for some differences seen between individual patient responses. Overall, all drugs are considered similarly effective compared to placebo and TCAs for treating conditions like depression and anxiety.
This document discusses the history, pathophysiology, diagnosis, and treatment of insomnia. It begins with definitions of insomnia and provides a historical overview of insomnia pharmacotherapy. It then covers the epidemiology of insomnia, describing prevalence rates and risk factors. The pathophysiology section explains the physiological mechanisms involved in sleep-wake regulation. Diagnosis and classification of insomnia subtypes are outlined. Treatment approaches discussed include pharmacological management with benzodiazepines, non-benzodiazepine hypnotics, melatonin agonists, and other drugs. Non-pharmacological therapies are also mentioned. New drug targets for insomnia are briefly noted.
This document summarizes various psych drugs including antidepressants, mood stabilizers, antipsychotics, and anxiolytics/hypnotics. It describes how antidepressants like SSRIs work to increase serotonin and norepinephrine levels. It also discusses the mechanisms and side effects of different classes of antidepressants and mood stabilizers. The summary outlines conventional and atypical antipsychotics indicating their uses and side effects. Finally, it reviews anxiolytic benzodiazepines and their therapeutic indications as well as risks like dependence.
Migraine pathophysiology, diagnosis and treatmentsYung-Tsai Chu
Introduction of migraine, including symptoms, epidemiology, pathophysiology(neurotransmitter, neural network, channel, CGRP), diagnostic criteria and treatment (oral, intravenous therapy at ED and long-term prevention)
This document summarizes the pharmacokinetics of various classes of antidepressants. It discusses their absorption, metabolism, protein binding, and elimination profiles. The main classes covered are SSRIs, SNRIs, TCAs, 5-HT2 antagonists, tetracyclic/unicyclic agents, and MAOIs. Key points include that most are well absorbed orally, undergo hepatic metabolism primarily through the CYP system, and have half-lives ranging from a few hours to over 24 hours, necessitating different dosing schedules.
classification , mechanism of actions, pharmacokinetics, adverse effects, uses and contra indications of antiparkinsonian drugs. with a note on other movement diorders and treatment
The document discusses the management of migraines. Key points include:
- Migraines are a common cause of recurrent headaches affecting 10-20% of the population. They are often underdiagnosed and undertreated.
- Treatment involves both abortive and preventive therapies. Common abortive medications include NSAIDs, triptans, and ergot alkaloids. Preventive options include beta-blockers like propranolol, antidepressants, anti-seizure medications, and calcium channel blockers.
- Propranolol, especially the extended release formulation, is an effective and well-tolerated option for migraine prevention and reduces attack frequency, severity, and analgesic use
Aripiprazole is an atypical antipsychotic drug that acts as a partial agonist at dopamine D2 and serotonin 5-HT1A receptors and as an antagonist at serotonin 5-HT2A, 5-HT2C, and 5-HT7 receptors. It is FDA approved to treat schizophrenia, bipolar disorder, major depressive disorder, irritability associated with autism, and acute agitation related to schizophrenia or bipolar disorder. Common side effects include weight gain, extrapyramidal symptoms, hyperglycemia, and sedation. It is metabolized by CYP3A4 and CYP2D6 enzymes and can have interactions with drugs that inhibit these pathways such as ritonavir and
Vortioxetine was approved by the FDA in 2013 under the brand name Brintellix for the treatment of major depressive disorder. However, it was later renamed Trintellix due to brand name confusion with the antiplatelet drug Brilinta. Trintellix is a multimodal antidepressant that works by inhibiting the serotonin transporter, antagonizing various serotonin receptors, and indirectly increasing release of other neurotransmitters. Clinical trials showed Trintellix to be effective at reducing depressive symptoms and may have benefits for cognitive function compared to placebo. It has a favorable side effect and safety profile, making it a treatment option when other antidepressants cannot be tolerated or are ineffective.
This document presents a case study of a 31-year-old female patient diagnosed with systemic lupus erythematosus (SLE) and depression. She presented with symptoms of sadness, fever, malar rash, and headache over the past few months. Laboratory tests confirmed elevated ESR and ANA levels. She was treated with intravenous methylprednisolone and oral prednisone, azathioprine, and clonazepam. Her symptoms improved with treatment. The goals of treatment were outlined as preventing recurrence, eliminating depression symptoms, and managing acute and chronic aspects of SLE to prevent organ damage and complications.
Migraine is a neurological disorder characterized by recurrent headaches that can last from 4 to 72 hours. It is often accompanied by nausea, vomiting, sensitivity to light and sound. There are two main types - migraine with aura and migraine without aura. Treatment involves using over-the-counter pain relievers for mild migraines, prescription triptans or ergotamines for moderate migraines, and preventative medications for severe or frequent migraines. Preventative medications taken daily include beta blockers, antidepressants, anticonvulsants, and calcium channel blockers, and aim to reduce migraine frequency within 2-6 months.
Mr. X, a 25-year-old male, presented with a high fever for one week and one episode of vomiting. His medical history included diabetes and hypertension. On examination, his temperature was 104 F, pulse was 102 beats/min, and blood pressure was 110/80 mm Hg. Laboratory tests confirmed paratyphoid A fever. He was diagnosed with paratyphoid A fever and treated intravenously with cefoperazone, sulbactam, pantoprazole, ondansetron, and ofloxacin. Upon discharge, he was advised to take paracetamol and pantoprazole tablets.
SSRIs and SNRIs are commonly used to treat depression. SSRIs work by blocking the reuptake of serotonin, increasing levels of the neurotransmitter in the brain. Common SSRIs include fluoxetine, paroxetine, sertraline, and citalopram. SNRIs like venlafaxine also block the reuptake of serotonin and norepinephrine. These drugs are generally well-tolerated but side effects may include nausea, insomnia, sexual dysfunction, and agitation. Guidelines recommend SSRIs as first-line treatment for moderate to severe depression.
Obesity is defined as excess body fat and is measured using body mass index (BMI). Anti-obesity drugs work by decreasing fat absorption, increasing satiety hormones, or altering brain pathways regulating appetite. Common anti-obesity drugs include Orlistat, Sibutramine, Lorcaserin, Qsymia, Contrave, and Liraglutide. These drugs work through various mechanisms like inhibiting lipase, reuptake of serotonin/norepinephrine, activating serotonin receptors, or being GLP-1 receptor agonists. All have potential adverse effects ranging from gastrointestinal issues to psychiatric problems. Bariatric surgery remains the most effective long-term treatment for obesity but also carries postoperative risks.
This document discusses antidepressant drugs and their mechanisms of action. It begins by describing how antidepressants work by altering neurotransmitter systems like serotonin and norepinephrine in the brain. Several classes of antidepressants are then discussed, including MAOIs, TCAs, SSRIs, SNRIs, and NDRIs. Each works differently but generally aims to increase neurotransmitter activity in the brain. The document examines specific drugs in each class, their history, mechanisms, and common side effects. Mood disorders like depression and bipolar disorder are also briefly overviewed.
Valproic acid is an anticonvulsant used to treat epilepsy, bipolar disorder, and migraines. It exists in multiple preparations and salt forms. Dosing is initially 10-15 mg/kg/day divided every 8-12 hours, up to a maximum of 60 mg/kg/day. Therapeutic drug monitoring aims for serum concentrations of 50-100 mcg/mL. Valproic acid has nearly complete bioavailability and is highly protein bound. It undergoes hepatic metabolism and renal excretion. Dose adjustments may be necessary in renal or hepatic impairment due to altered protein binding and clearance.
This document discusses mood stabilizers used to treat bipolar disorder. It describes the symptoms of mania and depression in bipolar disorder. Lithium, valproic acid, carbamazepine, lamotrigine and various antipsychotics are described as first-line mood stabilizing agents. The mechanisms of action of these drugs involve inhibition of inositol monophosphatase and other enzymes, decreasing intracellular inositol levels. Novel targets for treating bipolar disorder discussed include inhibition of glycogen synthase kinase-3, protein kinase C, modulation of brain-derived neurotrophic factor, enhanced Bcl2 expression, effects on oxidative stress, and modulation of glutamatergic transmission.
Lithium was first introduced as a treatment for mania in 1949 and approved by the FDA for this purpose in 1970. It is effective for treating manic episodes and preventing recurrent manic/depressive episodes in bipolar patients. Lithium is readily absorbed and distributed throughout extracellular fluid, reaching peak plasma levels within 2-4 hours. It is excreted primarily through the kidneys, with an elimination half-life of around 24 hours. Therapeutic lithium levels range from 0.6-1.2 mEq/L, depending on whether it is being used to treat an acute episode or for long-term maintenance. Adverse effects are generally dose-related and include nausea, tremors, and
Depression is a treatable mental illness characterized by changes in mood and loss of interest. Antidepressants work by increasing levels of neurotransmitters like serotonin, dopamine, and norepinephrine in the brain. There are several classes of antidepressants including tricyclic antidepressants, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, and atypical antidepressants. Each class has different mechanisms of action, side effects, and prescribing considerations. Antidepressants generally take 4-6 weeks to take effect and should be tapered gradually rather than stopped abruptly.
This document discusses the case of a 45-year-old male patient brought to the emergency department in an agitated state. His symptoms meet the diagnostic criteria for schizophrenia. He is initially treated with haloperidol to control his agitation. After 2 weeks, his symptoms improve and he is started on an atypical antipsychotic for long-term stabilization. The document then discusses various first and second generation antipsychotics, their mechanisms of action, indications, side effects, and monitoring considerations.
Gabapentin is an anticonvulsant used to treat partial seizures in adults and children over 12 years old. It is also used to treat postherpetic neuralgia and pain associated with diabetic neuropathy. Common side effects include somnolence, dizziness, and fatigue. Special populations like those with renal impairment require dosage adjustments. Abrupt withdrawal may cause increased seizure frequency so gabapentin should be tapered off slowly over at least a week.
This document discusses opioid dependence and addiction. It begins with an overview of opioids and their mechanism of action in the body. It then defines addiction, dependence, and tolerance. The mechanisms of dependence and addiction involve both negative reinforcement from withdrawal and positive reinforcement from rewarding effects. Physical dependence theory and positive incentive theory are described as models of addiction. The document outlines treatment options including drug substitution therapy with methadone or buprenorphine, abstinence-based treatment, and psychosocial treatments. It discusses opioid withdrawal and post-acute withdrawal syndrome. The six stages of recovery are defined. Special considerations for treating opioid addicts are noted.
Schizophrenia is a thought disorder characterized by positive, negative, cognitive, and mood symptoms. While the true cause is unknown, there are several theories involving dopamine and glutamate imbalances. Diagnosis requires symptoms for over 6 months and significant impairment in functioning. Treatment involves first-generation antipsychotics like chlorpromazine or second-generation antipsychotics like clozapine, risperidone, and olanzapine. Two major studies, CATIE and CUtLASS, found few differences in effectiveness between first and second-generation drugs, though second-generation drugs had fewer side effects in some cases.
This document summarizes various psych drugs including antidepressants, mood stabilizers, antipsychotics, and anxiolytics/hypnotics. It describes how antidepressants like SSRIs work to increase serotonin and norepinephrine levels. It also discusses the mechanisms and side effects of different classes of antidepressants and mood stabilizers. The summary outlines conventional and atypical antipsychotics indicating their uses and side effects. Finally, it reviews anxiolytic benzodiazepines and their therapeutic indications as well as risks like dependence.
Migraine pathophysiology, diagnosis and treatmentsYung-Tsai Chu
Introduction of migraine, including symptoms, epidemiology, pathophysiology(neurotransmitter, neural network, channel, CGRP), diagnostic criteria and treatment (oral, intravenous therapy at ED and long-term prevention)
This document summarizes the pharmacokinetics of various classes of antidepressants. It discusses their absorption, metabolism, protein binding, and elimination profiles. The main classes covered are SSRIs, SNRIs, TCAs, 5-HT2 antagonists, tetracyclic/unicyclic agents, and MAOIs. Key points include that most are well absorbed orally, undergo hepatic metabolism primarily through the CYP system, and have half-lives ranging from a few hours to over 24 hours, necessitating different dosing schedules.
classification , mechanism of actions, pharmacokinetics, adverse effects, uses and contra indications of antiparkinsonian drugs. with a note on other movement diorders and treatment
The document discusses the management of migraines. Key points include:
- Migraines are a common cause of recurrent headaches affecting 10-20% of the population. They are often underdiagnosed and undertreated.
- Treatment involves both abortive and preventive therapies. Common abortive medications include NSAIDs, triptans, and ergot alkaloids. Preventive options include beta-blockers like propranolol, antidepressants, anti-seizure medications, and calcium channel blockers.
- Propranolol, especially the extended release formulation, is an effective and well-tolerated option for migraine prevention and reduces attack frequency, severity, and analgesic use
Aripiprazole is an atypical antipsychotic drug that acts as a partial agonist at dopamine D2 and serotonin 5-HT1A receptors and as an antagonist at serotonin 5-HT2A, 5-HT2C, and 5-HT7 receptors. It is FDA approved to treat schizophrenia, bipolar disorder, major depressive disorder, irritability associated with autism, and acute agitation related to schizophrenia or bipolar disorder. Common side effects include weight gain, extrapyramidal symptoms, hyperglycemia, and sedation. It is metabolized by CYP3A4 and CYP2D6 enzymes and can have interactions with drugs that inhibit these pathways such as ritonavir and
Vortioxetine was approved by the FDA in 2013 under the brand name Brintellix for the treatment of major depressive disorder. However, it was later renamed Trintellix due to brand name confusion with the antiplatelet drug Brilinta. Trintellix is a multimodal antidepressant that works by inhibiting the serotonin transporter, antagonizing various serotonin receptors, and indirectly increasing release of other neurotransmitters. Clinical trials showed Trintellix to be effective at reducing depressive symptoms and may have benefits for cognitive function compared to placebo. It has a favorable side effect and safety profile, making it a treatment option when other antidepressants cannot be tolerated or are ineffective.
This document presents a case study of a 31-year-old female patient diagnosed with systemic lupus erythematosus (SLE) and depression. She presented with symptoms of sadness, fever, malar rash, and headache over the past few months. Laboratory tests confirmed elevated ESR and ANA levels. She was treated with intravenous methylprednisolone and oral prednisone, azathioprine, and clonazepam. Her symptoms improved with treatment. The goals of treatment were outlined as preventing recurrence, eliminating depression symptoms, and managing acute and chronic aspects of SLE to prevent organ damage and complications.
Migraine is a neurological disorder characterized by recurrent headaches that can last from 4 to 72 hours. It is often accompanied by nausea, vomiting, sensitivity to light and sound. There are two main types - migraine with aura and migraine without aura. Treatment involves using over-the-counter pain relievers for mild migraines, prescription triptans or ergotamines for moderate migraines, and preventative medications for severe or frequent migraines. Preventative medications taken daily include beta blockers, antidepressants, anticonvulsants, and calcium channel blockers, and aim to reduce migraine frequency within 2-6 months.
Mr. X, a 25-year-old male, presented with a high fever for one week and one episode of vomiting. His medical history included diabetes and hypertension. On examination, his temperature was 104 F, pulse was 102 beats/min, and blood pressure was 110/80 mm Hg. Laboratory tests confirmed paratyphoid A fever. He was diagnosed with paratyphoid A fever and treated intravenously with cefoperazone, sulbactam, pantoprazole, ondansetron, and ofloxacin. Upon discharge, he was advised to take paracetamol and pantoprazole tablets.
SSRIs and SNRIs are commonly used to treat depression. SSRIs work by blocking the reuptake of serotonin, increasing levels of the neurotransmitter in the brain. Common SSRIs include fluoxetine, paroxetine, sertraline, and citalopram. SNRIs like venlafaxine also block the reuptake of serotonin and norepinephrine. These drugs are generally well-tolerated but side effects may include nausea, insomnia, sexual dysfunction, and agitation. Guidelines recommend SSRIs as first-line treatment for moderate to severe depression.
Obesity is defined as excess body fat and is measured using body mass index (BMI). Anti-obesity drugs work by decreasing fat absorption, increasing satiety hormones, or altering brain pathways regulating appetite. Common anti-obesity drugs include Orlistat, Sibutramine, Lorcaserin, Qsymia, Contrave, and Liraglutide. These drugs work through various mechanisms like inhibiting lipase, reuptake of serotonin/norepinephrine, activating serotonin receptors, or being GLP-1 receptor agonists. All have potential adverse effects ranging from gastrointestinal issues to psychiatric problems. Bariatric surgery remains the most effective long-term treatment for obesity but also carries postoperative risks.
This document discusses antidepressant drugs and their mechanisms of action. It begins by describing how antidepressants work by altering neurotransmitter systems like serotonin and norepinephrine in the brain. Several classes of antidepressants are then discussed, including MAOIs, TCAs, SSRIs, SNRIs, and NDRIs. Each works differently but generally aims to increase neurotransmitter activity in the brain. The document examines specific drugs in each class, their history, mechanisms, and common side effects. Mood disorders like depression and bipolar disorder are also briefly overviewed.
Valproic acid is an anticonvulsant used to treat epilepsy, bipolar disorder, and migraines. It exists in multiple preparations and salt forms. Dosing is initially 10-15 mg/kg/day divided every 8-12 hours, up to a maximum of 60 mg/kg/day. Therapeutic drug monitoring aims for serum concentrations of 50-100 mcg/mL. Valproic acid has nearly complete bioavailability and is highly protein bound. It undergoes hepatic metabolism and renal excretion. Dose adjustments may be necessary in renal or hepatic impairment due to altered protein binding and clearance.
This document discusses mood stabilizers used to treat bipolar disorder. It describes the symptoms of mania and depression in bipolar disorder. Lithium, valproic acid, carbamazepine, lamotrigine and various antipsychotics are described as first-line mood stabilizing agents. The mechanisms of action of these drugs involve inhibition of inositol monophosphatase and other enzymes, decreasing intracellular inositol levels. Novel targets for treating bipolar disorder discussed include inhibition of glycogen synthase kinase-3, protein kinase C, modulation of brain-derived neurotrophic factor, enhanced Bcl2 expression, effects on oxidative stress, and modulation of glutamatergic transmission.
Lithium was first introduced as a treatment for mania in 1949 and approved by the FDA for this purpose in 1970. It is effective for treating manic episodes and preventing recurrent manic/depressive episodes in bipolar patients. Lithium is readily absorbed and distributed throughout extracellular fluid, reaching peak plasma levels within 2-4 hours. It is excreted primarily through the kidneys, with an elimination half-life of around 24 hours. Therapeutic lithium levels range from 0.6-1.2 mEq/L, depending on whether it is being used to treat an acute episode or for long-term maintenance. Adverse effects are generally dose-related and include nausea, tremors, and
Depression is a treatable mental illness characterized by changes in mood and loss of interest. Antidepressants work by increasing levels of neurotransmitters like serotonin, dopamine, and norepinephrine in the brain. There are several classes of antidepressants including tricyclic antidepressants, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, and atypical antidepressants. Each class has different mechanisms of action, side effects, and prescribing considerations. Antidepressants generally take 4-6 weeks to take effect and should be tapered gradually rather than stopped abruptly.
This document discusses the case of a 45-year-old male patient brought to the emergency department in an agitated state. His symptoms meet the diagnostic criteria for schizophrenia. He is initially treated with haloperidol to control his agitation. After 2 weeks, his symptoms improve and he is started on an atypical antipsychotic for long-term stabilization. The document then discusses various first and second generation antipsychotics, their mechanisms of action, indications, side effects, and monitoring considerations.
Gabapentin is an anticonvulsant used to treat partial seizures in adults and children over 12 years old. It is also used to treat postherpetic neuralgia and pain associated with diabetic neuropathy. Common side effects include somnolence, dizziness, and fatigue. Special populations like those with renal impairment require dosage adjustments. Abrupt withdrawal may cause increased seizure frequency so gabapentin should be tapered off slowly over at least a week.
This document discusses opioid dependence and addiction. It begins with an overview of opioids and their mechanism of action in the body. It then defines addiction, dependence, and tolerance. The mechanisms of dependence and addiction involve both negative reinforcement from withdrawal and positive reinforcement from rewarding effects. Physical dependence theory and positive incentive theory are described as models of addiction. The document outlines treatment options including drug substitution therapy with methadone or buprenorphine, abstinence-based treatment, and psychosocial treatments. It discusses opioid withdrawal and post-acute withdrawal syndrome. The six stages of recovery are defined. Special considerations for treating opioid addicts are noted.
Schizophrenia is a thought disorder characterized by positive, negative, cognitive, and mood symptoms. While the true cause is unknown, there are several theories involving dopamine and glutamate imbalances. Diagnosis requires symptoms for over 6 months and significant impairment in functioning. Treatment involves first-generation antipsychotics like chlorpromazine or second-generation antipsychotics like clozapine, risperidone, and olanzapine. Two major studies, CATIE and CUtLASS, found few differences in effectiveness between first and second-generation drugs, though second-generation drugs had fewer side effects in some cases.
Diarrhea and constipation are common gastrointestinal issues. For diarrhea, treatment focuses on rehydration and managing symptoms. Oral rehydration salts are the first line treatment for rehydration. Antimotility and antisecretory agents can relieve symptoms. For constipation, treatments include bulk laxatives, stool softeners, saline and osmotic laxatives, and stimulant laxatives. Selection of treatment depends on the individual patient and condition.
This document summarizes different types of antiemetic drugs. It discusses emetics that induce vomiting such as apomorphine and ipecacuanha. It then covers various classes of antiemetics including anticholinergics, H1 antihistamines, neuroleptics, prokinetic drugs, 5-HT3 antagonists, and NK1 receptor antagonists. For each class, it provides examples of drugs, their mechanisms of action, dosages, and trade names. The document aims to comprehensively review pharmacology of both emetic and antiemetic medications.
The document discusses drugs used to treat diarrhea and constipation. It describes the epidemiology of diarrhea and constipation and provides an overview of treatment approaches. It then focuses on specific drug classes used to treat diarrhea, including oral rehydration salts, antimotility agents, antisecretory agents, adsorbents, bacteria replacements, and antibiotics. It also briefly discusses drugs used to treat constipation, including bulk laxatives, stool softeners, saline/osmotic laxatives, stimulant laxatives, and lubricant laxatives.
The document discusses barbiturate and morphine/opioid poisoning. It provides details on the classification, mechanism of action, signs and symptoms, and management of barbiturate poisoning. It describes how barbiturates bind to GABA receptors and prolong opening of chloride channels, inhibiting the central nervous system. Signs of acute poisoning include depression, amnesia, respiratory issues and death from respiratory arrest. Management involves cardio-respiratory support, preventing drug absorption, and removing barbiturates from the body through charcoal, diuresis or dialysis. For morphine/opioid poisoning, it notes respiratory depression as a major risk and describes treatment with naloxone to reverse effects or intubation to ensure
PHARMACOLOGICAL MANAGEMENT OF OPIOID USE DISORDER.pptxSoumen Karmakar
This document summarizes the pharmacological management of opioid use disorder. It discusses the types of opioid receptors and their effects. It then covers the physiological and harmful effects of opioid use, as well as the goals and modalities of treatment, including opioid overdose management with naloxone, opioid withdrawal management with methadone, buprenorphine, and other agents, and relapse prevention with naltrexone. Recommendations are provided on initial dosing, maintenance dosing, dose tapering, and treatment duration for various pharmacological agents used to treat opioid use disorder.
Opioids and opiates act on mu, kappa, and delta opioid receptors throughout the body and brain. Mu receptors are responsible for analgesia, respiratory depression, and euphoria, making overdose dangerous. Chronic use can increase tolerance and risk of overdose. While prescription opioids started the current crisis, many users transition to highly dangerous illegal opioids like fentanyl and fentanyl analogs. Naloxone is used to treat overdoses but very potent synthetic opioids require high doses or continuous infusion.
The document discusses opioid analgesics, including their uses, actions, adverse reactions, contraindications, and precautions. It explains that opioids are used to treat moderate to severe pain according to the WHO pain ladder. Their main action is binding to mu and kappa receptors in the central nervous system to reduce pain perception and cause side effects like respiratory depression. Common adverse reactions include nausea, constipation, sedation, and respiratory issues. Opioids are contraindicated in conditions like asthma, increased intracranial pressure, or pregnancy. Precautions must be taken with opioid-naive patients and older adults due to risk of respiratory depression.
Dopamine agonists in advanced Parkinson’s disease.pptxPramod Krishnan
This document summarizes information about dopamine receptor agonists for the treatment of advanced Parkinson's disease. It discusses various dopamine agonists including pramipexole, ropinirole, rotigotine, cabergoline, pergolide, and apomorphine. It reviews their dosages, adverse effects, role in reducing motor fluctuations, and evidence from clinical studies showing benefits of extended release preparations in improving motor symptoms and reducing off time in advanced Parkinson's disease. It highlights the advantages of continuous dopamine replacement therapy for providing more consistent dopamine levels.
This document provides an overview of steroids and opioids. It defines steroids and classifies them into glucocorticoids, mineralocorticoids, androgens, and others. It discusses the dosing, mode of action, clinical uses and side effects of steroids. The document also defines opioids and classifies them into endogenous, exogenous, and synthetic opioids. It describes the mechanisms of action, tolerance, clinical uses and examples of commonly used opioids like morphine, pethidine, tramadol, heroin, and fentanyl. The document concludes by discussing opioid antagonists like naloxone.
Drugs used in pregnancy, labor and puerperiumAnamika Ramawat
The document discusses drugs used during pregnancy, labor, and the postpartum period. It provides information on folic acid, iron, calcium, antihypertensive drugs, diuretics, tocolytic agents, oxytocics, analgesics, and anticoagulants. For each drug, it describes preparations, mode of action, indications, contraindications, adverse effects, dosage, and important nursing considerations. The document is intended to give nurses thorough knowledge of medications commonly administered during obstetric care.
1. There are 5 classes of antidepressants: tricyclic and tetracyclic antidepressants, selective serotonin reuptake inhibitors, monoamine oxidase inhibitors, selective serotonin-norepinephrine reuptake inhibitors, and dopamine norepinephrine reuptake inhibitors.
2. Tricyclic and tetracyclic antidepressants work by blocking the reuptake of serotonin and norepinephrine and have indications for major depressive disorder, panic disorder, and others but can cause anticholinergic side effects.
3. Selective serotonin reuptake inhibitors like fluoxetine, sertraline selectively inhibit serotonin reuptake, have fewer side effects than tricyclics, and are widely used for conditions like
This document discusses the management of diarrhea through rehydration and drug therapy. It defines diarrhea and describes oral rehydration solutions for acute diarrhea treatment. Loperamide is recommended for acute diarrhea while opioids like codeine, diphenoxylate, and tincture of opium can be used for chronic diarrhea. Antimicrobial agents may be given if an infectious cause is known. Other drugs discussed for chronic diarrhea include clonidine, octreotide, cholestyramine, bulk forming agents, and certain plant alkaloids, calcium channel blockers, and chloride channel blockers.
Many semisynthetic derivatives of belladonna
alkaloids and a large number of synthetic compounds have been introduced with the aim of
producing more selective action on certain
functions. Most of these differ only marginally
from the natural alkaloids, but some recent ones
appear promising.
Ondansetron
Class
• Seratonin ( 5-HT3) antagonist.
Uses
1. The management of nausea and vomiting induced by chemotherapy and
radiotherapy .
2. In the prevention and treatment of PONV
Main action
• Antiemetic.
- Addiction involves psychological and physiological dependence on drugs that affect the central nervous system, causing withdrawal symptoms when discontinued. Commonly abused substances include alcohol, opioids, cannabis, cocaine, and amphetamines.
- Drugs used in deaddiction work by interfering with neurotransmitters like dopamine, serotonin, GABA, and endorphins. Medications are used to manage acute withdrawal symptoms from alcohol and opioids, and to prevent relapse for alcohol, opioids, nicotine, and other substances.
- Pharmacotherapies for specific substances include disulfiram, acamprosate, and naltrexone for alcohol; methadone and buprenorphine for opioids; nicotine replacement therapy and v
Schizophrenia is a complex psychiatric disorder characterized by disorganized thoughts, delusions, hallucinations, inappropriate affect, and impaired social functioning. The exact causes are unknown but likely involve genetic, brain chemical, environmental, and family history factors. Brain imaging shows enlarged ventricles and decreased cortical size, particularly in the left temporal lobe. Symptoms include positive symptoms like hallucinations, negative symptoms like loss of interest, and mood symptoms. Treatment involves pharmacological therapy with antipsychotics and non-pharmacological approaches like therapy, social skills training, and vocational rehabilitation.
Opioids and opiates act on opioid receptors in the brain, spinal cord and gut to reduce pain perception. They can cause respiratory depression, physical dependence and euphoria. Opioid overdose deaths have increased significantly in recent decades. Common signs of overdose include pinpoint pupils, decreased breathing and unconsciousness. History and examination may reveal signs of drug use as well as depressed breathing and mental status. Naloxone is used to reverse effects in an overdose.
This document discusses insecticide and opioid poisoning and treatment. It covers the following main points:
1) It describes the main groups of insecticides (organophosphorus, carbamates, chlorinated, naphthalene) and their modes of action as acetylcholinesterase inhibitors or through other mechanisms.
2) The symptoms, diagnosis, and treatment of poisoning from each group is outlined, including use of atropine as an antidote for organophosphorus and carbamates.
3) It also discusses opioids like morphine, their pharmacological effects, and treatment of overdose with opioid antagonists like naloxone, naltrexone, and nalmef
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
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Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
2. • India is situated between the two largest illicit opium-
producing regions of the world – “Golden Crescent” and
“Golden Triangle,” which makes it vulnerable for being
both a destination and transit route for opioids.
• It is estimated that currently, India has about 4 million
people who use opioids and around 1 million people
who are opioid dependent.
• A recent study reported that around 232,000 people
were opioid dependent in Punjab alone.
3.
4. Opioids are the class of drugs derived from poppy plant; papaver
somniferum.
CLASSIFICATION TYPE DRUG
A) NATURAL MORPHINE, CODEINE.
B) SEMI SYNTHETIC HEROIN, HYDROCODONE, OXYCODONE.
C) SYNTHETIC FENTANYL, MEPERIDINE, PENTAZOCINE,
METHADONE, LOPERAMIDE
D) ENDOGENOUS ENDORPHINS, ENKEPHALINS AND
DYNORPHINS.
11. MORPHINE AND HEROIN: Withdrawal begins after 4-6 hours of
last dose, usually after 1-2 week of continuous use reaches
peak after 2-3 day and subsides after 7-10 days.
METHADONE: Begin after 1-3 days, peak between 4-5 days and
end in 10-14 days.
Untreated buprenorphine lasts for about 10 days.
12. ASSESSMENT OF WITHDRAWL:
CLINICAL OIPOID WITHDRAWL SCALE(COWS)
Score: 5-12 = mild; 13-24 = moderate; 25-36 = moderately severe; more
than 36 = severe withdrawal
16. GOALS of OST are:
a) To reduce or prevent withdrawal.
b) To reduce or eliminate non prescribe drug use.
c) To stabilize drug intake of lifestyle.
d) To reduce drug related harm.
OPIOID SUBSTITUTION THERAPY
18. Peak plasma conc. Is achieved in 1.5-2 hrs.
Dose range: 300–400 mg/day.
• Because of the short half-life of tramadol, it should be
prescribed in 3–4 divided doses per day.
• Available in the form of tablets (SR) 50mg and 100mg.
S/E: Light-headedness, sedation, nausea, constipation, weight gain,
decreased libido, insomnia, perspiration, fatigue, vomiting, dry
mouth.
19. TAPENTADOL
MOA Mu -opioid receptor agonist and norepinephrine
reuptake inhibitor.
DOA Analgesia occurs within 32 minutes of oral
administration, and lasts for 4–6 hours.
DOSE 100-500 mg/day.
S/E: Nausea, vomiting, dizziness, sleepiness, itchiness, dry
mouth, headache, and fatigue, hypotension.
C/I: In people prone to seizures.
20. NOTE:
*Combination with SSRIs/SNRIs, SRAs, serotonin receptor
agonists may lead to potentially lethal serotonin syndrome.
*Tapentadol was invented at the German pharmaceutical
company Grünenthal in the late 1980s.
21. BUPRENORPHINE
MOA: Synthetic partial opioid agonist
with low intrinsic activity and high
affinity at mu receptors, also weak
antagonist at kappa receptors.
It has a ceiling effect, therefore high
clinical safety.
Pk: s/l, takes 5-10 min to disintegrate
and absorb.
SIDE EFFECTS:
Headache, nausea, constipation,
orthostatic hypotension.
22.
23. DOSING RANGE:
• Start from 2-16mg/day
• Maximum dose is 32mg/day
FORMS:
• S/L tablet: 0.2, 2mg/8mg alone.
• Plus naloxone: 2/0.5mg and 8/2mg.
INSTRUCTION:
Patient should be asked to place it under the tongue until it is
completely absorbed not to swallow or chew it.
Note: 4mg of buprenorphine = 40mg of methadone.
* Precipitated withdrawal.
24. PATIENT STATUS DOSE OF BUPRENORPHINE
IN WITHDRAWAL AND NO RISK FACTORS 8MG
NO WITHDRAWAL AND NO RISK FACTORS 4MG
RISK FACTORS (MEDICAL CO MORBIDITY,
POLY DRUG USE OR PSYCHIATRIC DISORDER)
2-4MG
According to Maudsley guidelines.
• No more than 8mg on day 1.
• Maximum to 32mg/day.
• Recommended maintenance dose: 12-16mg/day.
25. RECOMMENDED DOSE REDUCTON SCHEDULE
DAILY BUPRENORPHINE DOSE REDUCTION RATE
ABOVE 16 MG 4 MG EVERY 1-2 WEEKS
8-16 MG 2-4 MG EVERY 1-2 WEEKS
2-8 MG 2 MG PER WEEK OR FORTNIGHT
BELOW 2 MG REDUCE 0.4-0.8 MG PER WEEK
26. METHADONE:
• Synthetic opioid.
• Schedule 2 drug.
• MOA: acts as a pure agonist at mu-
receptor and negligible activity on any
other receptor.
• DOA: >24hrs; od dose is adequate.
• Adv; in c/o injectable , no drowsiness,
minimal euphoria.
• Disadv; high dependency potential and
low lethal dose.
27. USED FOR:
• Short term detoxification(7-30 days)
• Long term detoxification(up to 180 days)
• Maintenance (>180 days)
DOSAGE:
Initial dose of 15-20mg, increased to 70mg over weeks, maximum
dosage is 120mg.
*Daily supervised consumption is recommended. Cumulative
toxicity may develop (3-10 days) because of long half life,
therefore reviewed regularly.
28. Five institutions/hospitals were chosen for feasibility assessment
through site visits where methadone was made available. These
include:
• National Drug Dependence Treatment Centre, AIIMS
(including its community centres), New Delhi.
• Department of Psychiatry and Drug De-addiction Centre,
King Edward Memorial Hospital, Mumbai, Maharashtra.
• Department of Psychiatry and Drug De-addiction Centre,
Regional Institute of Medical Sciences, Imphal, Manipur.
• Drug De-addiction Centre, Civil Hospital, Bathinda, Punjab.
• Drug De-addiction Centre, Civil Hospital, Kapurthala, Punjab.
29.
30. OPIOID ANTAGONIST
Naloxone:
Highest affinity for mu receptors , but
competitive antagonist of all receptors.
Half- life is 15-30 minutes.
Naltrexone: Active metabolite is 6 beta
naltrexol, half life of naltrexone is 1-3hrs and
active metabolite is 13hrs.
Potent mu antagonist and weak kappa
antagonist.
Nalmefene: Half life is 8-10hrs.
31. NALOXONE CHALLENGE TEST
0.8mg of naloxone is drawn
into a needle, out of which
0.2 is injected.
Observe for 20 seconds for
withdrawal signs , if no
evidence, inject rest 0.6mg.
Observe for next 20 minutes,
if no signs can start with
naltrexone.
IV CHALLENGE
33. DOSAGE AND GUIDELINES
INITIATING TREATMENT
• Wash out period is required.
• Informing the patient.
• Negative urine drug screen test
• Naloxone challenge test should be
negative.
DOSE:
• Initial dose of 25mg is given,
monitored for 4hrs.
• If tolerated a dose is increased to
50mg daily as a maintenance dose or
100mg every alternate day, 150 mg
every third day.
34. RAPID DETOXIFICATION
• 0.2mg orally every 2 hours for 9 doses to
maximum of 1.8mg.
• BP monitoring every 30-60 minutes for first
8 hours.
CLONIDINE
• 12.5 mg, 1-3 hours after first dose of
clonidine, increased to 25mg on 2nd day and
to 50mg on 3rd day.
NALTREXONE
• To reduce muscle cramps 30-60mg is given
with the first dose of clonidine and half of the
initial dose is given after every 4-6 hours.
• Maximum is 180mg.
OXAZEPAM
Benzodiazepines and clonidine are tapered off over next 5-10 days.
36. MOA: Alpha-2 agonistic action.
Half life is 12-16hours.
DOSAGE: 0.1mg three times
daily.
*Next dose withheld if BP falls
<90/60mmHg.
*Tapering required, abrupt
stoppage leads to rebound
hypertension.
SIDE EFFECTS: Dry mouth,
dizziness, constipation, sedation,
hypotension.
CLONIDINE
43. INDIVIDUAL THERAPY
A) COGNITIVE BEHAVIOUR THERAPY
This is a short list of the types of negative thinking that are
obstacles to recovery and are topics for cognitive therapy:
1)My problem is because of other people;
2) I don’t think I can handle life without using;
3) Maybe I can just use occasionally;
4) Life won’t be fun — I won’t be fun — without using;
5) I’m worried I will turn into someone I don’t like;
6) I can’t make all the necessary changes; I can’t change my
friends;
44. 7) I don’t want to abandon my family;
8) Recovery is too much work;
9) My cravings will be overwhelming; I won’t be able to resist
them;
10) If I stop, I’ll only start up again; I have never finished
anything;
11) No one has to know if I relapse; and
12) I’m worried I have been so damaged by my addiction that I
won’t be able to recover.
WHAT WE HAVE TO DO??
• FEAR.
• REDEFINING FUN.
• LEARNING FROM SETBACKS.
• BECOMING COMFORTABLE WITH BEING UNCOMFORTABLE
45.
46.
47. B) MOTIVATIONAL ENHANCEMANT THERAPY
The need or desire to change from using to quitting a substance.
BASIC PRINCIPLES:
• Express empathy.
• Develop discrepancy.
• Avoid argumentation.
• Role with resistance.
• Support self-efficacy.
48. OUR ROLE:
• Eliciting self motivational statements.
• Listening with empathy.
• Questioning.
• Presenting personal feedback.
• Affirming the client
• Handing resistance.
• Reframing
• Summarizing.
• Discussing the plan.
• Communicating free choice.
• List of consequences of action and inaction.
• Information and advice.
• The change plan worksheet.
49. GROUP THERAPY
• Groups provide positive peer support and pressure to abstain
from substances of abuse.
• Groups reduce the sense of isolation that most people who have
substance abuse disorders experience.
• Groups enable people who abuse substances to witness the
recovery of others.
• Groups help members learn to cope with their substance abuse
and other problems by allowing them to see how others deal
with similar problems.
• Groups provide feedback concerning the values and abilities of
other group members.
• Groups allow a single treatment professional to help a number
of clients at the same time.
• Groups can effectively confront individual members about
substance abuse and other harmful behaviors with each other.
50. TYPES OF RELAPSE:
a) EMOTIONAL:
Signs of emotional relapse:
1) bottling up emotions;
2) isolating;
3) not going to meetings;
4) going to meetings but not sharing;
5) focusing on others (focusing on other people’s problems or
focusing on how other people affect them);
6) poor eating and sleeping habits.
The common cause for emotional relapse is *poor self-care.
HALT: hungry, angry, lonely, and tired.
RELAPSE
51. b) MENTAL RELAPSE:
Signs of mental relapse:
1) craving for drugs or alcohol;
2) thinking about people, places, and
things associated with past use;
3) minimizing consequences of past use or
glamorizing past use;
4) bargaining;
5) lying;
6) thinking of schemes to better control
using;
7) looking for relapse opportunities; and
8) planning a relapse.
52. c) PHYSICAL RELAPSE:
• Either lapse or relapse.
Educating clients in these rules can help them focus on what is
important:
1) change your life (recovery involves creating a new life where it
is easier to not use);
2) be completely honest;
3) ask for help;
4) practice self-care; and
5) don’t bend the rules.
55. 1. M Raga J, Sabater A, Perez-GB, Castellano M, Cervera G. Add-on gabapentin in the treatment of opiate
withdrawal. Prog Neuropsychopharmacol Biol Psychiatry. 2004; 28(3): 599-601.
2. Steigerwald I, Müller M, Davies A, Samper D, Sabatowski R, Baron R et.al. Effectiveness and safety of
tapentadol prolonged release for severe, chronic low back pain with or without a neuropathic pain
component: results of an open-label, phase 3b study. Curr Med Res Opin. 2012; 28(6): 911-36.
3. Alekseev VV. [Flupirtin (katadolon): a nonstandard action on pain transmission]. Zh Nevrol Psikhiatr Im S S
Korsakova. 2011; 111(4): 101-4.
4. Freynhagen R, Backonja M, Schug S. Pregabalin for the Treatment of Drug and Alcohol Withdrawal
Symptoms: A Comprehensive Review. CNS Drugs. 2016; 30(12): 1191-200.
5. Larimer ME, Palmer RS, Marlatt GA. Relapse prevention. An overview of Marlatt's cognitive-behavioral
model. Alcohol Res Health. 1999; 23(2): 151-60.
6. Melemis SM. Relapse Prevention and the Five Rules of Recovery. Yale J Biol Med. 2015; 88(3): 325-32.
7. Tamaskar R, Parran TV Jr, Heggi A, Brateanu A, Rabb M, Yu J. Tramadol versus buprenorphine for the
treatment of opiate withdrawal: a retrospective cohort control study. J Addict Dis. 2003; 22(4): 5-12
8. Bell J. Pharmacological maintenance treatments of opiate addiction. Br J Clin Pharmacol. 2014; 77(2): 253-
63.
REFFERENCES
56. 9. Bart G. Maintenance medication for opiate addiction: the foundation of recovery. J Addict Dis. 2012; 31(3): 207-
25.
10. Kleber HD. Pharmacologic treatments for opioid dependence: detoxification and maintenance options. Dialogues
Clin Neurosci. 2007; 9(4): 455-70.
11. Center for Substance Abuse Treatment. Substance Abuse Treatment: Group Therapy. Rockville (MD): Substance
Abuse and Mental Health Services Administration (US); 2005; 41(1): 1-8.