This document provides an overview of antidepressant medications. It begins with a brief history noting the accidental discovery of antidepressant effects from tuberculosis medications in the 1950s. It then covers the therapeutic uses and classifications of antidepressants, including tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and others. The mechanisms of action, uses, side effects, and drug interactions are described for different classes of antidepressants like monoamine oxidase inhibitors, tricyclics, and selective serotonin reuptake inhibitors.
The document provides information about various hallucinogenic drugs like PCP, LSD, and ecstasy. It discusses the pharmacological effects of these drugs on the brain and body. It also covers the potential symptoms of toxicity and overdose from hallucinogen use as well as myths and rumors surrounding these drugs. The goal is to educate students about hallucinogens and their consequences in order to help students make informed choices.
The document provides an overview of antipsychotic drugs. It discusses the history and classification of antipsychotics and their mechanisms of action. First generation antipsychotics act primarily as dopamine antagonists, while second generation drugs also act as serotonin antagonists. Common side effects include extrapyramidal symptoms, weight gain, metabolic issues, and tardive dyskinesia. Newer treatments target glutamate receptors or have novel mechanisms of action like partial dopamine agonism to provide antipsychotic effects with fewer side effects.
Lithium is used to treat mania and gout. Its exact mechanism of action is unclear but it affects intracellular signaling pathways related to mood stabilization and energy metabolism. It is rapidly absorbed orally and excreted by the kidneys. Toxicity symptoms vary depending on lithium levels and can include nausea, arrhythmias, neurological effects, and renal issues. Diagnosis is based on history, exam, and serum lithium concentration. Treatment involves hydration, gastrointestinal decontamination, and hemodialysis in severe cases.
This document discusses various types of antidepressant drugs, their mechanisms of action, and side effects. It begins by defining depression and its symptoms. It then explains two major theories for the pathophysiology of depression - the monoamine theory and neurotrophic hypothesis. The document categorizes and describes different classes of antidepressants including TCAs, SSRIs, SNRIs, MAOIs, and atypical antidepressants. It provides details on the mechanism of action, pharmacokinetics, indications, interactions and side effects of these drug classes.
This document discusses depression, mania, and various antidepressant medications. It covers the symptoms of depression and mania. It then discusses various classes of antidepressants including SSRIs, SNRIs, TCAs, MAOIs, and atypical antidepressants. For each class, it describes the mechanisms of action, therapeutic uses, adverse effects, and examples of medications within the class.
Khedezla is the brand name for the drug desvenlafaxine, which is a selective serotonin and norepinephrine reuptake inhibitor used to treat major depressive disorder. It was approved by the FDA in July 2013 and is manufactured by Osmotica Pharmaceutical. Desvenlafaxine works by increasing serotonin and norepinephrine levels in the central nervous system. Common side effects include dizziness, nausea, insomnia, and sexual dysfunction. Special precautions are needed if the patient has taken MAO inhibitors recently or is pregnant or breastfeeding.
Benzodiazepines are commonly prescribed sedative-hypnotic agents that were introduced in 1960. They are used for conditions like anxiety, insomnia, alcohol withdrawal, and seizures by enhancing the effects of the inhibitory neurotransmitter GABA. While generally safe, benzodiazepines can cause side effects with prolonged use or overdose like dependence, withdrawal symptoms, and respiratory depression. The effects of different benzodiazepines vary based on their ability to cross the blood-brain barrier and metabolism, with short-acting agents having faster onsets but shorter durations of action.
This document discusses the development and properties of various atypical antipsychotic drugs. It provides chemical structures and names for common atypical antipsychotics like clozapine, risperidone, olanzapine, quetiapine and ziprasidone. It summarizes the pharmacokinetics, therapeutic indications, side effects and dosing for these drugs. The document also discusses differences between first and second generation antipsychotics and adverse effects of antipsychotic treatment.
The document provides information about various hallucinogenic drugs like PCP, LSD, and ecstasy. It discusses the pharmacological effects of these drugs on the brain and body. It also covers the potential symptoms of toxicity and overdose from hallucinogen use as well as myths and rumors surrounding these drugs. The goal is to educate students about hallucinogens and their consequences in order to help students make informed choices.
The document provides an overview of antipsychotic drugs. It discusses the history and classification of antipsychotics and their mechanisms of action. First generation antipsychotics act primarily as dopamine antagonists, while second generation drugs also act as serotonin antagonists. Common side effects include extrapyramidal symptoms, weight gain, metabolic issues, and tardive dyskinesia. Newer treatments target glutamate receptors or have novel mechanisms of action like partial dopamine agonism to provide antipsychotic effects with fewer side effects.
Lithium is used to treat mania and gout. Its exact mechanism of action is unclear but it affects intracellular signaling pathways related to mood stabilization and energy metabolism. It is rapidly absorbed orally and excreted by the kidneys. Toxicity symptoms vary depending on lithium levels and can include nausea, arrhythmias, neurological effects, and renal issues. Diagnosis is based on history, exam, and serum lithium concentration. Treatment involves hydration, gastrointestinal decontamination, and hemodialysis in severe cases.
This document discusses various types of antidepressant drugs, their mechanisms of action, and side effects. It begins by defining depression and its symptoms. It then explains two major theories for the pathophysiology of depression - the monoamine theory and neurotrophic hypothesis. The document categorizes and describes different classes of antidepressants including TCAs, SSRIs, SNRIs, MAOIs, and atypical antidepressants. It provides details on the mechanism of action, pharmacokinetics, indications, interactions and side effects of these drug classes.
This document discusses depression, mania, and various antidepressant medications. It covers the symptoms of depression and mania. It then discusses various classes of antidepressants including SSRIs, SNRIs, TCAs, MAOIs, and atypical antidepressants. For each class, it describes the mechanisms of action, therapeutic uses, adverse effects, and examples of medications within the class.
Khedezla is the brand name for the drug desvenlafaxine, which is a selective serotonin and norepinephrine reuptake inhibitor used to treat major depressive disorder. It was approved by the FDA in July 2013 and is manufactured by Osmotica Pharmaceutical. Desvenlafaxine works by increasing serotonin and norepinephrine levels in the central nervous system. Common side effects include dizziness, nausea, insomnia, and sexual dysfunction. Special precautions are needed if the patient has taken MAO inhibitors recently or is pregnant or breastfeeding.
Benzodiazepines are commonly prescribed sedative-hypnotic agents that were introduced in 1960. They are used for conditions like anxiety, insomnia, alcohol withdrawal, and seizures by enhancing the effects of the inhibitory neurotransmitter GABA. While generally safe, benzodiazepines can cause side effects with prolonged use or overdose like dependence, withdrawal symptoms, and respiratory depression. The effects of different benzodiazepines vary based on their ability to cross the blood-brain barrier and metabolism, with short-acting agents having faster onsets but shorter durations of action.
This document discusses the development and properties of various atypical antipsychotic drugs. It provides chemical structures and names for common atypical antipsychotics like clozapine, risperidone, olanzapine, quetiapine and ziprasidone. It summarizes the pharmacokinetics, therapeutic indications, side effects and dosing for these drugs. The document also discusses differences between first and second generation antipsychotics and adverse effects of antipsychotic treatment.
The document provides an overview of the four main classes of hallucinogenic drugs: serotonergic hallucinogens like LSD and psilocybin; methylated amphetamines like MDMA; anticholinergic hallucinogens found in plants; and dissociative anesthetics like PCP. It discusses the history of hallucinogen use from the 1960s counterculture movement to current trends, physiological and psychological effects of different classes of drugs, risks and adverse effects, and mechanisms of action in the brain.
Aspirin toxicity remains an important clinical problem due to aspirin's widespread availability and use. Aspirin is rapidly absorbed in the stomach and metabolized in the liver. Toxicity can cause a wide range of symptoms affecting multiple organ systems. Diagnosis is based on history of ingestion and characteristic laboratory abnormalities. Management involves gastric decontamination, fluid replacement, urine alkalinization, and hemodialysis in severe cases.
This document discusses the classification and properties of various antidepressants and anxiolytics. It covers the mechanisms and classifications of major antidepressant drug classes including MAOIs, TCAs, SSRIs, SNRIs, and atypical antidepressants. It also discusses the classification and properties of common anxiolytic drugs like benzodiazepines, buspirone, hydroxyzine, and beta blockers. Treatment approaches for anxiety are outlined, emphasizing using the lowest effective dose of benzodiazepines and gradual withdrawal when larger doses have been used long-term.
This document discusses dopamine receptors and their subtypes. It describes the five subtypes of dopamine receptors (D1, D2, D3, D4, D5), their classification into D1-like and D2-like families based on their mechanisms of action, and their roles and expression in different brain regions. It also briefly outlines some therapeutic uses of drugs that target specific dopamine receptor subtypes, such as antipsychotics that bind to D2 receptors.
This document discusses drugs used to treat heart failure. It defines heart failure and provides global statistics on prevalence. The goals of pharmacotherapy are to relieve symptoms, improve cardiac function, prevent disease progression and prolong survival. Drugs discussed include ACE inhibitors, ARBs, beta-blockers, aldosterone antagonists, ARNIs, diuretics, digoxin, ivabradine, and omega-3 fatty acids. Recommendations are provided on use of these drugs for heart failure with reduced ejection fraction based on guidelines. The document also briefly discusses treatment of heart failure with preserved ejection fraction.
Effective treatment in depression and anxietyHarsh shaH
The document discusses mechanisms, types, symptoms, and treatment approaches for anxiety and depression. It provides details on specific medications including SSRIs (fluoxetine, fluvoxamine, paroxetine, sertaline, citalopram, escitalopram), paroxetine, escitalopram, desvenlafaxine, dosages, indications, mechanisms of action, efficacy, adverse effects, and warnings/precautions for safe use. Combination therapy with escitalopram and L-methylfolate is also rationale given their complementary mechanisms for enhancing neurotransmitter production and treatment response.
This document discusses poison management. It begins by defining poison and sources of poisoning such as chemicals, toxins, and venoms. It then lists common agents involved in poisoning and signs and symptoms. The document outlines supportive treatment including monitoring, controlling symptoms, and considering specific treatments. It discusses various decontamination and enhanced elimination methods. It also explains the mechanisms and examples of specific antidotes. The document provides details on managing several specific poisonings including paracetamol, barbiturates, benzodiazepines, cyanide, iron, methanol, and organophosphates. It concludes by thanking the reader.
This document provides information on bronchial asthma including its definition, triggers, pathophysiology, classification, airway inflammation, and treatment options. Bronchial asthma is characterized by reversible airway obstruction due to hyperresponsiveness of the tracheobronchial smooth muscles. Common triggers include allergens, infections, exercise, and environmental factors. Treatment includes bronchodilators like beta-2 agonists, methylxanthines, anticholinergics, mast cell stabilizers, leukotriene antagonists, and corticosteroids.
This document provides an overview of the pharmacology of antidepressants. It discusses the history of antidepressant development beginning in the 1950s. It then classifies antidepressants and describes the mechanisms of action, pharmacokinetics, pharmacological actions, adverse effects and recent advances for various classes including tricyclic antidepressants, SSRIs, SNRIs, atypical antidepressants. It provides details on specific drugs within each class.
This presentation provides information about parkinsonism or Parkinson disease and pathophysiology, classification, pharmacological action and side effects of Anti Parkinson drugs.
Congestive Heart Failure and Drugs used in CCF by Dr. PawanDr. Pawan Kumar B
Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs or receive blood returning to the heart. It is classified as left or right, chronic or acute, and low or high output failure. Common causes include hypertension, heart attacks, congenital heart disease, and cardiomyopathy. Treatment involves reducing the workload on the heart through medications like diuretics, ACE inhibitors, beta-blockers, and vasodilators to decrease preload and afterload and manage fluid retention and edema. The goal is to improve symptoms and prolong life for patients with congestive heart failure.
Dopamine is a neurotransmitter that binds to dopamine receptors and influences movement, memory, reward, behavior and other functions. It is synthesized from tyrosine and transported through dopaminergic pathways in the brain. There are two families of dopamine receptors, D1-like and D2-like, which are G protein-coupled receptors that either activate or inhibit the enzyme adenylyl cyclase. Dopamine receptor dysfunction is implicated in diseases like Parkinson's, schizophrenia and addiction. Dopamine agonists mimic dopamine while antagonists block dopamine receptors.
This document discusses the mechanisms of action of benzodiazepines. It notes that benzodiazepines augment the effects of the inhibitory neurotransmitter GABA at GABA-A receptors. They can be selective for different GABA receptor subunits involved in sleep, anxiety, or addiction. The hypnotic and anxiolytic effects of benzodiazepines are explained by their actions on GABA receptors in the amygdala, hippocampus, and hypothalamic regions involved in sleep/wake regulation. Adverse effects and issues with dependence and withdrawal are also covered. Novel approaches to anxiolytic drugs targeting GABA receptors without addiction liability are mentioned.
This document provides information on the pharmacology of second generation antipsychotics. It discusses the history and development of antipsychotic drugs from chlorpromazine to clozapine. It describes the mechanisms of action of atypical antipsychotics including their effects on serotonin and dopamine receptors. The document classifies antipsychotics and examines the pharmacology of individual drugs like clozapine, risperidone, and olanzapine, covering their indications, mechanisms, side effects and interactions.
This document discusses antiepileptic drugs used to treat epilepsy. It begins by defining epilepsy as a chronic medical condition caused by sudden changes in brain electrical function, characterized by recurrent seizures. It then discusses the etiology, or causes, of epilepsy including congenital defects, injuries, infections, tumors and drug withdrawal. It provides details on commonly prescribed antiepileptic drugs like phenytoin, carbamazepine, valproate, phenobarbital and newer drugs. The treatment section covers guidelines for monotherapy versus polytherapy, monitoring drug levels, managing status epilepticus, and tapering off treatment.
The video for this presentation is available on our Youtube channel:
https://youtube.com/allceuseducation A continuing education course for this presentation can be found at https://www.allceus.com/member/cart/index/index?c=
Unlimited Counseling CEUs for $59 https://www.allceus.com/
Specialty Certificate tracks starting at $89 https://www.allceus.com/certificate-tracks/
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Patreon: https://www.patreon.com/CounselorToolbox
Pinterest: drsnipes
Identify the signs and symptoms of intoxication and withdrawal as well as the neurobiological effects of stimulants, depressants and hallucinogens.
INTRODUCTION
DISEASE SPOTLIGHT
CLASSIFICATION OF CONVULSION
MACHANISM OF ANTICONVULSANT
CLASSIFICATION OF ANTICONVULSANT DRUGS
CONTRAINDICATIONS
ADVERSE EFFECTS OF CONVULSANTS
DOSAGE AND DILUTION
NURSES PRECAUTION AND RESPONSIBILITIES
CONCLUSION
1. Antidepressants work by increasing levels of neurotransmitters like serotonin and norepinephrine in the brain. They are divided into several classes including SSRIs, SNRIs, TCAs, and MAOIs.
2. SSRIs are now the most commonly prescribed due to their safer side effect profile. They work by inhibiting reuptake of serotonin. TCAs affect serotonin and norepinephrine but have more side effects.
3. Antidepressants take 2-3 weeks to start working and should be taken long term to prevent relapse of depression. Side effects are usually mild and transient but can include nausea, sexual dysfunction, and dry mouth depending on the drug class.
1. The document discusses different classes of antidepressant medications, including their mechanisms of action and pharmacology. The main classes covered are tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and monoamine oxidase inhibitors (MAOIs).
2. TCAs work by inhibiting the reuptake of norepinephrine and serotonin, while SSRIs and SNRIs are more selective in inhibiting reuptake. MAOIs work by inhibiting the monoamine oxidase enzyme and preventing breakdown of neurotransmitters.
3. The document reviews the practical applications of antidepressants in treatment of depression and other disorders
The document provides an overview of the four main classes of hallucinogenic drugs: serotonergic hallucinogens like LSD and psilocybin; methylated amphetamines like MDMA; anticholinergic hallucinogens found in plants; and dissociative anesthetics like PCP. It discusses the history of hallucinogen use from the 1960s counterculture movement to current trends, physiological and psychological effects of different classes of drugs, risks and adverse effects, and mechanisms of action in the brain.
Aspirin toxicity remains an important clinical problem due to aspirin's widespread availability and use. Aspirin is rapidly absorbed in the stomach and metabolized in the liver. Toxicity can cause a wide range of symptoms affecting multiple organ systems. Diagnosis is based on history of ingestion and characteristic laboratory abnormalities. Management involves gastric decontamination, fluid replacement, urine alkalinization, and hemodialysis in severe cases.
This document discusses the classification and properties of various antidepressants and anxiolytics. It covers the mechanisms and classifications of major antidepressant drug classes including MAOIs, TCAs, SSRIs, SNRIs, and atypical antidepressants. It also discusses the classification and properties of common anxiolytic drugs like benzodiazepines, buspirone, hydroxyzine, and beta blockers. Treatment approaches for anxiety are outlined, emphasizing using the lowest effective dose of benzodiazepines and gradual withdrawal when larger doses have been used long-term.
This document discusses dopamine receptors and their subtypes. It describes the five subtypes of dopamine receptors (D1, D2, D3, D4, D5), their classification into D1-like and D2-like families based on their mechanisms of action, and their roles and expression in different brain regions. It also briefly outlines some therapeutic uses of drugs that target specific dopamine receptor subtypes, such as antipsychotics that bind to D2 receptors.
This document discusses drugs used to treat heart failure. It defines heart failure and provides global statistics on prevalence. The goals of pharmacotherapy are to relieve symptoms, improve cardiac function, prevent disease progression and prolong survival. Drugs discussed include ACE inhibitors, ARBs, beta-blockers, aldosterone antagonists, ARNIs, diuretics, digoxin, ivabradine, and omega-3 fatty acids. Recommendations are provided on use of these drugs for heart failure with reduced ejection fraction based on guidelines. The document also briefly discusses treatment of heart failure with preserved ejection fraction.
Effective treatment in depression and anxietyHarsh shaH
The document discusses mechanisms, types, symptoms, and treatment approaches for anxiety and depression. It provides details on specific medications including SSRIs (fluoxetine, fluvoxamine, paroxetine, sertaline, citalopram, escitalopram), paroxetine, escitalopram, desvenlafaxine, dosages, indications, mechanisms of action, efficacy, adverse effects, and warnings/precautions for safe use. Combination therapy with escitalopram and L-methylfolate is also rationale given their complementary mechanisms for enhancing neurotransmitter production and treatment response.
This document discusses poison management. It begins by defining poison and sources of poisoning such as chemicals, toxins, and venoms. It then lists common agents involved in poisoning and signs and symptoms. The document outlines supportive treatment including monitoring, controlling symptoms, and considering specific treatments. It discusses various decontamination and enhanced elimination methods. It also explains the mechanisms and examples of specific antidotes. The document provides details on managing several specific poisonings including paracetamol, barbiturates, benzodiazepines, cyanide, iron, methanol, and organophosphates. It concludes by thanking the reader.
This document provides information on bronchial asthma including its definition, triggers, pathophysiology, classification, airway inflammation, and treatment options. Bronchial asthma is characterized by reversible airway obstruction due to hyperresponsiveness of the tracheobronchial smooth muscles. Common triggers include allergens, infections, exercise, and environmental factors. Treatment includes bronchodilators like beta-2 agonists, methylxanthines, anticholinergics, mast cell stabilizers, leukotriene antagonists, and corticosteroids.
This document provides an overview of the pharmacology of antidepressants. It discusses the history of antidepressant development beginning in the 1950s. It then classifies antidepressants and describes the mechanisms of action, pharmacokinetics, pharmacological actions, adverse effects and recent advances for various classes including tricyclic antidepressants, SSRIs, SNRIs, atypical antidepressants. It provides details on specific drugs within each class.
This presentation provides information about parkinsonism or Parkinson disease and pathophysiology, classification, pharmacological action and side effects of Anti Parkinson drugs.
Congestive Heart Failure and Drugs used in CCF by Dr. PawanDr. Pawan Kumar B
Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs or receive blood returning to the heart. It is classified as left or right, chronic or acute, and low or high output failure. Common causes include hypertension, heart attacks, congenital heart disease, and cardiomyopathy. Treatment involves reducing the workload on the heart through medications like diuretics, ACE inhibitors, beta-blockers, and vasodilators to decrease preload and afterload and manage fluid retention and edema. The goal is to improve symptoms and prolong life for patients with congestive heart failure.
Dopamine is a neurotransmitter that binds to dopamine receptors and influences movement, memory, reward, behavior and other functions. It is synthesized from tyrosine and transported through dopaminergic pathways in the brain. There are two families of dopamine receptors, D1-like and D2-like, which are G protein-coupled receptors that either activate or inhibit the enzyme adenylyl cyclase. Dopamine receptor dysfunction is implicated in diseases like Parkinson's, schizophrenia and addiction. Dopamine agonists mimic dopamine while antagonists block dopamine receptors.
This document discusses the mechanisms of action of benzodiazepines. It notes that benzodiazepines augment the effects of the inhibitory neurotransmitter GABA at GABA-A receptors. They can be selective for different GABA receptor subunits involved in sleep, anxiety, or addiction. The hypnotic and anxiolytic effects of benzodiazepines are explained by their actions on GABA receptors in the amygdala, hippocampus, and hypothalamic regions involved in sleep/wake regulation. Adverse effects and issues with dependence and withdrawal are also covered. Novel approaches to anxiolytic drugs targeting GABA receptors without addiction liability are mentioned.
This document provides information on the pharmacology of second generation antipsychotics. It discusses the history and development of antipsychotic drugs from chlorpromazine to clozapine. It describes the mechanisms of action of atypical antipsychotics including their effects on serotonin and dopamine receptors. The document classifies antipsychotics and examines the pharmacology of individual drugs like clozapine, risperidone, and olanzapine, covering their indications, mechanisms, side effects and interactions.
This document discusses antiepileptic drugs used to treat epilepsy. It begins by defining epilepsy as a chronic medical condition caused by sudden changes in brain electrical function, characterized by recurrent seizures. It then discusses the etiology, or causes, of epilepsy including congenital defects, injuries, infections, tumors and drug withdrawal. It provides details on commonly prescribed antiepileptic drugs like phenytoin, carbamazepine, valproate, phenobarbital and newer drugs. The treatment section covers guidelines for monotherapy versus polytherapy, monitoring drug levels, managing status epilepticus, and tapering off treatment.
The video for this presentation is available on our Youtube channel:
https://youtube.com/allceuseducation A continuing education course for this presentation can be found at https://www.allceus.com/member/cart/index/index?c=
Unlimited Counseling CEUs for $59 https://www.allceus.com/
Specialty Certificate tracks starting at $89 https://www.allceus.com/certificate-tracks/
Live Webinars $5/hour https://www.allceus.com/live-interactive-webinars/
Patreon: https://www.patreon.com/CounselorToolbox
Pinterest: drsnipes
Identify the signs and symptoms of intoxication and withdrawal as well as the neurobiological effects of stimulants, depressants and hallucinogens.
INTRODUCTION
DISEASE SPOTLIGHT
CLASSIFICATION OF CONVULSION
MACHANISM OF ANTICONVULSANT
CLASSIFICATION OF ANTICONVULSANT DRUGS
CONTRAINDICATIONS
ADVERSE EFFECTS OF CONVULSANTS
DOSAGE AND DILUTION
NURSES PRECAUTION AND RESPONSIBILITIES
CONCLUSION
1. Antidepressants work by increasing levels of neurotransmitters like serotonin and norepinephrine in the brain. They are divided into several classes including SSRIs, SNRIs, TCAs, and MAOIs.
2. SSRIs are now the most commonly prescribed due to their safer side effect profile. They work by inhibiting reuptake of serotonin. TCAs affect serotonin and norepinephrine but have more side effects.
3. Antidepressants take 2-3 weeks to start working and should be taken long term to prevent relapse of depression. Side effects are usually mild and transient but can include nausea, sexual dysfunction, and dry mouth depending on the drug class.
1. The document discusses different classes of antidepressant medications, including their mechanisms of action and pharmacology. The main classes covered are tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and monoamine oxidase inhibitors (MAOIs).
2. TCAs work by inhibiting the reuptake of norepinephrine and serotonin, while SSRIs and SNRIs are more selective in inhibiting reuptake. MAOIs work by inhibiting the monoamine oxidase enzyme and preventing breakdown of neurotransmitters.
3. The document reviews the practical applications of antidepressants in treatment of depression and other disorders
This document discusses depression and its treatment with antidepressants. It first defines depression as a mood disorder causing persistent sadness and loss of interest. It then discusses several theories of depression's causes. Symptoms include changes in sleep, appetite, and thoughts of suicide. Depression is diagnosed based on symptoms lasting over a month and may be caused by medical or psychiatric conditions. Treatment involves psychotherapy, antidepressant medications like SSRIs and SNRIs, or older medications like TCAs and MAOIs. The document focuses on the mechanisms and side effects of various classes of antidepressants.
The document describes various classes of antidepressant drugs, including:
1. Tricyclic antidepressants (TCAs) like amitriptyline
2. Monoamine oxidase inhibitors (MAOIs) like phenelzine that irreversibly inhibit the MAO enzyme
3. Selective serotonin reuptake inhibitors (SSRIs) like fluoxetine that selectively inhibit reuptake of serotonin
It also discusses the biological factors and mechanisms of depression, such as genetic and biochemical influences on neurotransmitter systems in the brain.
This document discusses various classes of antidepressant drugs, including their mechanisms of action, classifications, and side effects. It describes how tricyclic antidepressants and selective serotonin reuptake inhibitors work by inhibiting the reuptake of neurotransmitters like serotonin and norepinephrine. Monoamine oxidase inhibitors are also covered, noting how they work by inhibiting the enzyme MAO. The summary provides an overview of the major classes of antidepressants and their clinical applications and risks.
Antidepressants are a class of medication used to treat major depressive disorder, anxiety disorders, chronic pain conditions and to help manage addictions. Common side-effects of antidepressants include dry mouth, weight gain, dizziness, headaches, sexual dysfunction, and emotional blunting
Antidepressants work by modifying neurotransmitter levels in the brain. The most common theory is that depression is caused by low levels of serotonin, norepinephrine, and/or dopamine. Antidepressants increase the levels of these neurotransmitters through mechanisms like inhibiting reuptake by transporter proteins. Common classes include SSRIs, SNRIs, SARIs, TCAs, TeCAs, and MAOIs. While effective for many people, antidepressants can cause side effects like weight gain, sexual dysfunction, headaches, and fatigue. New research also questions whether the serotonin theory fully explains how depression develops or how antidepressants work.
Pharmacological management of depressionPriyash Jain
This document provides an overview of the pharmacological management of depression. It discusses general considerations for antidepressant treatment, types of antidepressants including SSRIs, SNRIs, TCAs and others. It covers treating refractory depression, antidepressant use in special populations like children/adolescents and during pregnancy, and a symptom-based approach. Key points include recommending SSRIs as first-line treatment for moderate-severe depression and continuing medication for 6-9 months after symptom resolution to prevent relapse.
Major depression and mania are two extremes of affective disorders which refer to a pathological change in mood state
Major depressions characterized by symptoms like sad mood, loss of interest and pleasure, low energy, worthlessness, guilt, psychomotor retardation or agitation, change in appetite and/or sleep, melancholia, suicidal thoughts, etc
3. The mood change may have a psychotic basis with delusional thinking or occur in isolation and induce anxiety. On the other hand, pathological anxiety may lead to depression.
The document discusses various classes of antidepressant drugs, including their mechanisms of action, pharmacological profiles, and clinical uses. It describes tricyclic antidepressants which inhibit the reuptake of serotonin and norepinephrine. Selective serotonin reuptake inhibitors like fluoxetine selectively block the reuptake of serotonin. Serotonin-norepinephrine reuptake inhibitors block the reabsorption of both neurotransmitters. Monoamine oxidase inhibitors prevent the breakdown of monoamines by inhibiting monoamine oxidase.
Depression is caused by a deficit of neurotransmitters like norepinephrine and serotonin in the brain. Antidepressants work by inhibiting the reuptake of these neurotransmitters, increasing their availability. Tricyclic antidepressants like imipramine were the first developed but have more side effects. Selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) are now preferred as they are more tolerable while still effective. Antidepressants are used to treat major depression, obsessive-compulsive disorder, anxiety disorders, neuropathic pain, premature ejaculation, and other conditions. The choice of antidepressant depends on individual factors and side effect profiles.
This document summarizes information about antidepressant and anti-anxiety drugs. It discusses the classification of major affective disorders like episodal depression and mania. It describes the mechanisms and side effects of different classes of antidepressants including tricyclic antidepressants, selective serotonin reuptake inhibitors, atypical antidepressants, and monoamine oxidase inhibitors. It also discusses anti-anxiety drugs like benzodiazepines and their mechanisms and side effects. The precise causes of affective disorders are still unclear but evidence implicates alterations in neurotransmitter systems like norepinephrine and serotonin.
1) Antidepressants work by increasing levels of neurotransmitters like serotonin and norepinephrine in the brain. Selective serotonin reuptake inhibitors (SSRIs) specifically inhibit the reabsorption of serotonin while serotonin-norepinephrine reuptake inhibitors (SNRIs) inhibit both serotonin and norepinephrine reabsorption.
2) Tricyclic antidepressants non-selectively inhibit the reuptake of serotonin, norepinephrine, and other neurotransmitters. They also block various receptors which can cause side effects.
3) All antidepressants take 2-4 weeks to have an effect and maximum benefits may take 12 weeks. They are used to treat depression and other conditions like anxiety disorders.
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.
Trazodone is a serotonin antagonist and reuptake inhibitor (SARI) antidepressant. The document discusses various classes of antidepressants including their mechanisms of action, indications, side effects and classifications such as SSRIs, SNRIs, TCAs, MAOIs and others. It provides an overview of the neurobiology of depression and genetics as well as guidelines on treatment duration.
Clozapine is an atypical antipsychotic that was the first to be developed. It was introduced in Europe in 1971 but withdrawn in 1975 due to fatal agranulocytosis in some patients. In 1989, studies showed it was more effective than other antipsychotics for schizophrenia, and the FDA approved its use for treatment-resistant schizophrenia with mandatory blood monitoring. Clozapine has a black box warning for agranulocytosis and requires monitoring of white blood cell and absolute neutrophil counts before each prescription. It is initiated at a low dose and gradually titrated up to achieve therapeutic effects while minimizing side effects.
This document outlines bone and joint infections, including:
- The main causes are bacteria such as Staph. aureus and Strep. pyogenes entering through the bloodstream, direct inoculation, or contiguous spread.
- Infection progresses through stages of invasion, suppuration, necrosis, and new bone formation over weeks.
- Risk factors include local trauma or foreign bodies and systemic factors like diabetes or immunosuppression.
- Treatment involves identifying the bacteria, analgesia, draining pus, removing dead tissue, stabilizing fractures, and long-term antibiotics. Complications can include metastatic infection or chronic osteomyelitis if not properly treated.
Medical student lecture Obstetric anaesthesia_074208.pptxXavier875943
1) The document provides an outline for a lecture on obstetric anaesthesia and analgesia, covering topics such as physiological changes in pregnancy, labour analgesia options, indications for anaesthesia in obstetrics, and types of anaesthesia techniques.
2) It discusses various pharmacological and regional techniques for labour analgesia, including epidurals, intrathecal opioids, and inhalational agents.
3) The risks and complications of regional anaesthesia techniques are reviewed, as well as general anaesthesia concerns for caesarean sections.
1. Acute kidney injury (AKI) is the sudden deterioration of renal function that can range from mild to severe. It is a global problem associated with high morbidity and mortality.
2. AKI is classified based on location of injury (pre-renal, intrinsic, post-renal), urine output, and severity of decline in renal function. Common causes include sepsis, nephrotoxins, and decreased renal perfusion.
3. Management involves treating the underlying cause, maintaining fluid/electrolyte balance, and potentially renal replacement therapy for complications like fluid overload or severe electrolyte imbalances. Outcomes depend on factors like age, cause, and need for dialysis.
Urinary tract infection in children.pptxXavier875943
UTI is a common bacterial infection in children that can lead to renal scarring and other long term issues if not properly treated. It is more common in girls than boys, especially around the time of toilet training. The most common causative organism is E. coli. Diagnosis involves urine culture and microscopy showing bacteria and white blood cells. Treatment consists of a course of oral antibiotics. For recurrent UTIs or those indicating renal involvement, further imaging may be needed to identify issues like vesicoureteral reflux that require prophylactic treatment or surgery. Complications can include recurrent infections, renal scarring, hypertension, and even end stage renal failure if not adequately managed.
Renal replacement therapy (RRT) replaces some or most of the functions of the normal kidney when renal function is less than 10-15%. It includes dialysis and renal transplantation. The two main forms of dialysis are hemodialysis, which filters waste through an artificial kidney, and peritoneal dialysis, which uses the peritoneal membrane for filtration. Renal transplantation is the preferred therapy for children with end-stage renal disease as it allows them to live a near-normal life.
This document discusses short stature in children. It defines short stature as a height more than 2 standard deviations below the mean for a child's age and gender. The causes of short stature are classified as chronic disease, familial short stature, or constitutional delay of growth. Evaluating a child for short stature involves comparing their height to parental heights and assessing bone age. If an endocrine cause is suspected, further investigations may include hormone levels and imaging. Treatment depends on the underlying cause but can include growth hormone therapy, surgery, or addressing underlying illnesses or malnutrition.
Central precocious puberty (CPP) is the early activation of the hypothalamic-pituitary-gonadal axis, leading to premature sexual maturation. Peripheral precocious puberty (PPP) involves the appearance of secondary sex characteristics without activation of the HPG axis, instead caused by direct sex steroid production. Evaluation of precocious puberty involves determining which pubertal changes are present to classify it as CPP or PPP, followed by laboratory tests and imaging studies to identify potential underlying causes.
This document discusses enuresis (bedwetting) in children. It covers the epidemiology, etiology, pathophysiology, clinical features, diagnosis and treatment of the condition. Enuresis is defined as repeated bedwetting in children over 5 years old. It occurs most commonly in boys and prevalence decreases with age. Treatment involves behavioral modifications like fluid restrictions and alarm therapy, as well as medications like desmopressin if needed. A positive attitude from parents and motivation from the child are important for treatment success.
Jaundice is caused by elevated bilirubin levels which turn the skin and eyes yellow. It is common in newborns and the elderly. Bilirubin is produced from the breakdown of red blood cells and is normally conjugated in the liver before being excreted. Jaundice can be pre-hepatic from excessive breakdown, intrahepatic from liver damage impairing conjugation, or post-hepatic/obstructive from bile duct blockage. Evaluation involves history, exam, liver tests, imaging and considering causes like viral hepatitis, drugs, tumors or gallstones. Treatment focuses on the underlying cause, rehydration, antibiotics and monitoring for complications.
Burkitt Lymphoma GROUP A BATCH 2 PRESENTATION (1).pptxXavier875943
Burkitt lymphoma is a type of non-Hodgkin's lymphoma first described in 1958 by Denis Burkitt in Uganda. It is caused by a translocation of the MYC gene which leads to uncontrolled B-cell proliferation. The disease is associated with areas that have high rates of malaria and early Epstein-Barr virus infection, which are thought to contribute to B-cell hyperplasia and increase the chances of a MYC translocation occurring. AIDS-associated Burkitt lymphoma has also been reported and its incidence increased with the HIV epidemic.
This document provides background information on childhood immunization. It defines key terms like immunity, vaccines, vaccination, and immunization. It describes Edward Jenner's discovery of vaccination by injecting cowpox into a boy in 1796. It also outlines the types of vaccines including live attenuated, inactivated, fractional, recombinant, and discusses herd immunity. The document discusses immunization in special circumstances and provides an overview of Nigeria's National Programme on Immunization.
The document provides an outline on paediatric HIV/AIDS covering epidemiology, biology, pathogenesis, natural history, clinical manifestations, and treatment. It notes that children account for 5-10% of global HIV cases, with over 90% in sub-Saharan Africa. HIV targets and destroys CD4+ cells, causing progressive immunosuppression and increased risk of opportunistic infections. Clinical stages range from asymptomatic to severe disease and death, with faster progression in children than adults.
CONGENITAL RENAL ABNORMALITIES By Dr. Enobong Runcie(0).pptxXavier875943
This document provides an overview of congenital renal abnormalities, including their embryology, classification, and clinical presentation. It describes anomalies of kidney number, structure, and location. It also discusses anomalies of the urinary tract, including duplication of the ureters, posterior urethral valves, and bladder abnormalities. Specific conditions covered in detail include bilateral and unilateral renal agenesis, horseshoe kidney, polycystic kidney disease, prune belly syndrome, and posterior urethral valves. The overview of embryology provides background on the development of the pronephros, mesonephros, and metanephros.
RENAL and ALIMENTARY CHANGES IN PREGNANCY.pptxXavier875943
The document discusses changes to the renal and gastrointestinal systems during pregnancy. Key changes include increased kidney size and blood flow leading to higher glomerular filtration rate. Hormonal changes cause fluid retention and lower blood pressure. In the GI system, hormones cause increased reflux and salivation while relaxing the esophageal sphincter. The liver produces more bile and enzymes while the gallbladder's motility decreases, raising gallstone risk. Pregnancy displaces the organs which affects testing and symptoms.
Chronic liver disease (CLD) can present with signs of liver failure like jaundice, ascites, and encephalopathy. Common causes include alcohol, viral hepatitis, autoimmune conditions, and metabolic diseases. Investigating CLD involves liver function tests (LFTs), which measure hepatic (ALT, AST), cholestatic (ALP, bilirubin), and synthetic (albumin, INR) function, as well as imaging, endoscopy, and biopsy. Managing CLD addresses complications like infection, ascites, bleeding, and malnutrition through conservative measures, medications, procedures, and transplantation if needed. The case study demonstrates applying this knowledge to diagnose and treat a patient with suspected alcoholic cirrhosis.
GENERAL INTRODUCTION TO CHEMICAL PATHOLOGY-SPECIMENS COLLECTION BY DR ABUDU...Xavier875943
This document provides an overview of chemical pathology and clinical chemistry laboratory testing. It discusses common terminology used in chemical pathology, such as reference values and units of measurement. It describes the collection, handling, and preservation of specimens in chemical pathology laboratories. The document outlines the purpose and types of clinical chemistry tests, including tests that measure substances involved in biological functions, waste products, substances indicating cell damage or disease, and drugs or toxins. It discusses the types of specimens used in chemical analysis, including whole blood, serum, plasma, urine, and other fluids. The document provides details on patient preparation, phlebotomy procedures, and factors that can affect test results such as fasting, lipemia, and hemolysis.
This document discusses water and electrolyte balance, focusing on sodium balance. It covers:
- Body fluid compartments and volumes, with two thirds of total body water located intracellularly.
- Factors regulating fluid movement between compartments, including osmolality and oncotic pressure.
- Mechanisms maintaining water and sodium balance, such as thirst, ADH release, and renal reabsorption.
- Common disorders of water and sodium balance like dehydration, edema, hyponatremia, and hypernatremia.
This document provides an overview of urinalysis including its indications, methods of collection and preservation, physical and chemical examination, and microscopic examination. A urinalysis is a common medical test that can screen for and diagnose diseases of the kidneys, urinary tract, and other bodily systems by analyzing the physical characteristics, chemical components, and cellular contents of a urine sample. Key aspects covered include normal versus abnormal physical findings, chemical testing using dipsticks, and microscopic evaluation of urine sediment.
Acute dystonic reactions and tardive dyskinesia are medication-induced movement disorders. Acute dystonic reactions typically develop within hours of a trigger like medication and involve involuntary muscle contractions. Tardive dyskinesia results from prolonged use of dopamine-blocking medications and causes abnormal movements in the face and limbs. Risk factors include prolonged antipsychotic use, older age, and female sex. Treatment focuses on minimizing triggering medications and using anticholinergic drugs or VMAT2 inhibitors.
Classification of psychiatric disorders by Dr. Fatima.pptXavier875943
This document discusses the classification of psychiatric disorders. It explains that psychiatric disorders are mainly diagnosed based on symptoms, unlike physical conditions which are often classified by etiology or structural pathology. The purposes of psychiatric classification include making agreed-upon diagnoses, facilitating communication between professionals, and establishing frameworks for research. There are three main types of psychiatric classification: categorical, dimensional, and multiaxial. Categorical classification groups disorders into separate categories based on symptoms, course, and outcome. Dimensional classification diagnoses patients on separate dimensions like psychoticism. Multiaxial classification uses multiple sets of information, as seen in systems like the DSM and ICD. The document also discusses organic vs. non-organic disorders, psychosis vs. neuro
- 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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Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
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.
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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.
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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).
2. OUTLINE
• INTRODUCTION
• BRIEF HISTORY OF ANTIDEPRESSANT USE
• THERAPEUTICS OF ANTIDEPRESSANT USE
• GOOD AND BAD NEWS OF ANTIDEPRESSANT TREATMENT
• USE OF ANTIDEPRESSANTS ACROSS LIFE CYCLES
• BIOLOGICAL BASIS OF DEPRESSION
• CLASSIFICATION OF ANTIDEPRESSANTS
• MECHANISM OF ACTION, USES AND SIDE EFFECTS OF EACH
ANTIDEPRESSANT
• SUMMARY OF THE GENERAL USES OF ANTIDEPRESSANTS
3. INTRODUCTION
• These are varied groups of therapeutic agent that significantly elevate the
mood of depressed patients. Despite the duration of the discovery of
these agents, the precise pharmacological activity of some of them remain
unexplained.
• The first group of antidepressants to be used were the tricyclic
antidepressants which were closely followed by the monoamine oxidase
inhibitors.
• Recently, a series of highly successful innovative agents have been
introduced. These include, selective serotonin reuptake inhibitors (SSRI),
Selective Noradrenalin reuptake inhibitors (SNRIS), dual SSRI and SNRI,
dual 5HT2 antagonist/5HT reuptake inhibitors, NE/DA reuptake inhibitors.
4. BRIEF HISTORY OF ANTIDEPRESSANT USE
• The history of antidepressants began, by chance, in the 1950s.
Chemists developing a new treatment for tuberculosis tested the drug
iproniazid on patients at Seaview Hospital on Staten Island. It was a
crucial step in the history of depression treatment, as these patients
experienced a dramatic change in well-being. Formerly lethargic and
sad, they now reported better mood, increased appetite, and
improved sleep.
5. THERAPEUTICS OF ANTIDEPRESSANT USE
The Five R’s of Antidepressant Treatment
3 R’s use to describe improvement
Response
(At least 50% Reduction in symptom)
Remission
(All symptoms disappear for 6-12 months)
Recovery
(Symptoms disappear for over 12 months)
6. • 2 R’s used to describe worsening
• Relapse
• (Worsening before remission)
• Reoccurrence
• (Worsening after recovery)
7. Good news/Bad news about Antidepressant
treatment
• Good news
• All antidepressants show about the same response (getting
better) after 8 weeks (50 - 75% of patients)
• Bad news
• Raising the bar of “getting better” dims the success rate; 50%
may show remission in 6 months; 75% in 12 months.
• All antidepressants significantly reduce relapse rates during the
first 6-12 months after initial response to the medication.
8. Use of antidepressants across life cycle
• Children: currently no antidepressant has been expressly approved
for treatment of depression in children (used in OCD)
• Adolescents: Better than children as in adults. Synaptic restructuring
generally occurs after the age of 6 years.
9. Biological Basis of Depression
• 1. Monoamine Hypothesis:
1st major theory about biological etiology of depression. It
predicts that the underlying pathophysiologic basis of depression
is a depletion in the levels of serotonin, norepinephrine, and/or
dopamine in the central nervous system.
10. • 2. Neurotransmitter Receptor Hypothesis.
Problem with receptors for the key monoamine neurotransmitters
11. • 3. Monoamine Hypothesis of Gene Expression.
BASED ON:
• Lack of clear and convincing evidence of absolute monoamine
deficiency
• No clear and convincing evidence of that excess or deficiencies of
mono amines account for depression
• Clear evidence that systems do not respond normally.
12. • POSSIBILITIES:
• Pseudo monoamine deficiency due to a deficiency in signal transduction
from neurotransmitter to receptor (molecular functioning)
• Abnormal molecular activity; post receptor (2nd messenger) problems with
intracellular transcription factors that control gene regulation.
• Abnormality in signal transduction from monoamine receptors.
• Brain Derived Neurotrophic Factor (BDNF) may be responsible for repeated
depressive episodes and poor response to treatment (supported by
decrease in size of hippocampal neurons and impaired function in
depression).
13. • 4. Neurokinin Hypothesis of Emotional Dysfunction
• Presence of neurokinins in amygdala
• Presence of neurokinins in areas where mono amines are in
abundance.
•
14. CLASSIFICATION OF ANTIDEPRESSANTS
1. MONOAMINEOXIDASE INHIBITORS
A. REVERSIBLE INHIBITORS OF MAO-A (RIMAS)
• Moclobemide,
• Clorgyline
B. IRREVERSIBLE INHIBITIORS OF MAO-A
• Selegiline (Emsam),
• phenelzine (Nardil),
• tranylcypromine (Parnate),
• isocarboxazid (Marplan).
19. IRREVERSIBLE INHIBITIORS OF MAO-A
MECHANISM OF ACTION
• Uniquely among antidepressants, MAOI’s increase synaptic levels of
all three catecholamines (serotonin, norepinephrine, and dopamine).
• Because of this, MAOI’s are among the most effective of all
antidepressants, especially in the subtype of depression known as
atypical depression .
• Atypical depression is characterized by mood reactivity, interpersonal
rejection sensitivity, increased appetite, hypersomnia, and leaden
paralysis (the sensation that one’s arms are too heavy to lift).
20. • Selegiline is unique, however, in that it is sele ctive for the B-subtype
of MAO, whereas the other three are non-selective and hit both
MAO-A and MAO-B.
21. SIDE EFFECTS
• anticholinergic and
• antihistaminic effects discussed with the tricyclics,
• multiple drug-drug interactions,
• withdrawal symptoms, and potentially
• fatal hypertensive events.
• Because of these considerations, MAOI’s are not prescribed very
often in modern psychiatry and are typically used as a “last resort”
after a patient has failed multiple other medications from several
different classes first.
22. INTERACTIONS
• (i) Cheese reaction Certain varieties of cheese, beer, wines, pickled
meat and fish, yeast extract contain large quantities of tyramine,
dopa, etc. In MAO inhibited patients these indirectly acting
sympathomimetic amines escape degradation in the intestinal wall
and liver → reaching into systemic circulation they displace and
release large amounts of NA from transmitter loaded adrenergic
nerve endings → hypertensive crisis, cerebrovascular accidents.
When such a reaction occurs, it can be treated by i.v. injection of a
rapidly acting α blocker, e.g. phentolamine. Prazosin or
chlorpromazine are alternatives.
23. • (ii) Cold and cough remedies They contain ephedrine or other
sympathomimetics—hypertensive reaction can occur.
• (iii) Reserpine, guanethidine, tricyclic antidepressants Excitement, rise in BP and
body temperature can occur when these drugs are given to a patient on MAO
inhibitors. This is due to their initial NA releasing or uptake blocking action.
• (iv) Levodopa Excitement and hypertension occur due to increase in biological
t½ of DA and NA that are produced from levodopa.
• (v) Antiparkinsonian anticholinergics Hallucinations and symptoms similar to
those of atropine poisoning occur.
• (vi) Barbiturates, alcohol, opioids, antihistamines Action of these drugs is
intensified and prolonged. Respiration may fail.
• (vii) Pethidine High fever, sweating, excitation, delirium, convulsions and severe
respiratory depression have occurred. The most accepted explanation is— MAO
inhibitors retard hydrolysis of pethidine but not its demethylation. Thus, excess
of norpethidine (normally a minor metabolite—see p. 475) is produced which
has excitatory actions.
24. REVERSIBLE INHIBITORS OF MAO-A
(MOCLOBEMIDE)
• MECHANISM OF ACTION
• It is a reversible and selective MAO-A inhibitor with short duration of
action; full MAO activity is restored within 1–2 days of stopping the drug.
Because of competitive enzyme inhibition, tyramine is able to displace it
from the enzyme, so that potentiation of pressor response to ingested
amines is minor, and dietary restrictions are not required. Clinical trials
have shown moclobemide to be an efficacious antidepressant, comparable
to TCAs, except in severe cases. and is safer in overdose.
• This makes it a particularly good option in elderly patients and in those
with heart disease.
• Dose: 150 mg BD–TDS (max 600 mg/day)
• RIMAREX, TRIMA 150, 300 mg tabs.
25. SIDE EFFECTS
• Nausea,
• dizziness,
• headache,
• insomnia,
• rarely excitement and
• liver damage.
26. INTERACTIONS
• Chances of interaction with other drugs and alcohol are remote, but
caution is advised while coprescribing pethidine, SSRIs and TCAs.
• NOTE: It has emerged as well tolerated alternative to mild and
moderate depression and for social phobia
27.
28. TRICYCLIC ANTIDEPRESSANTS
• Now we come to the oldest class of antidepressants, and some of the
first drugs to be officially prescribed for that purpose: the tricyclic
antidepressants (often shortened to just “tricyclics” or “TCA’s”). You
can generally recognize TCA’s by their name, as they usually have the
suffixes–triptyline (as in amitriptyline and nortriptyline) or
–ipramine (as in clomipramine and imipramine).
29. MECHANISM OF ACTION OF TCA
• First, TCA’s inhibit the reuptake of both serotonin and norepinephrine
(similar to SNRI’s). This is the action that is primarily responsible for
their antidepressant effects.
• Second, TCA’s antagonize acetylcholine and histamine , which
accounts more for their side effect profile than their antidepressant
efficacy.
• Third, TCA’s are known to work as sodium and calcium channel
inhibitors as well. Clinically, this property may account for some of
their analgesic properties (like duloxetine, they are helpful for some
chronic pain conditions).
30. SIDE EFFECTS OF TCA
• Anticholinergic side effects, including dry mouth, itchy eyes, blurry
vision, constipation, urinary retention, memory impairment, and
increased body temperature.
• Antagonism of histamine results in a diphenhydramine-like effect,
with drowsiness and sedation being common complaints while on a
tricyclic.
31. • TOXICITY OF TCA OVERDOSE
• They have a therapeutic index of 7, (meaning that taking just 7 times
the normal amount of the drug could cause death). Slowing these ion
channels affects both cardiac and neuronal conduction, leading to
arrhythmias and altered mental status or coma.
NOTE:
A wide QRS in the context of suspected overdose is likely TCA
overdose . Treatment is sodium bicarbonate .
32. • In summary
• TCA’s act as agonists at two neurotransmitters, antagonists at another
two, and inhibitors of two ion channels.
PNEUMONIC
TCA’s increase serotonin and norepinephrine , block acetylcholine and
histamine , and inhibit sodium and calcium ion channels.
TCA’s affect T rans, C hans, and A ns.
33. INTERACTIONS
• 1. TCAs potentiate directly acting sympathomi-metic amines (present
in cold/asthma remedies). Adrenaline containing local anaesthetic
should be avoided. However, TCAs attenuate the action of indirect
sympathomi-metics (ephedrine, tyramine).
• 2. TCAs abolish the antihypertensive action of guanethidine and
clonidine by preventing their transport into adrenergic neurones.
• 3. TCAs potentiate CNS depressants, including alcohol and
antihistaminics.
• 4. Phenytoin, phenylbutazone, aspirin and
Chlopromazine(antipsychotic) can displace TCAs from protein binding
sites and cause transient overdose symptoms.
34. • 5. Phenobarbitone competitively inhibits as well as induces imipramine
metabolism.
• Carbamazepine and other enzyme inducers enhance metabolism of
TCAs.
• 6. SSRIs inhibit metabolism of several drugs (see later) including TCAs—
dangerous toxi-city can occur if the two are given concur-rently.
• 7. By their anticholinergic property, TCAs delay gastric emptying and
retard their own as well as other drug’s absorption. However, digoxin
and tetracyclines may be more completely absorbed. When used
together, the anticho-linergic action of neuroleptics and TCAs may add
up.
• 8. MAO inhibitors—dangerous hypertensive crisis with excitement and
hallucinations has occurred when given with TCAs.
35. IMIPRAMINE
The first antidepressant ever developed! Imipramine is a
prototypical TCA, so everything we’ve talked about thus far applies.
One thing that sets imipramine apart is that it is sometimes used for
management of nocturnal enuresis, or bed wetting, in children.
The anticholinergic effect of imipramine prevents the bladder from
contracting, thus holding the urine. Because of its side effects, it is not
used as a first-line agent but can be useful in refractory cases
36. CLOMIPRAMINE
• Clomipramine (Anafranil) is another TCA that can be used to treat
depression. However, clomipramine is unique in that it is considered
to be the gold-standard for medication treatment of obsessive-
compulsive disorder (OCD) , as it was found in several randomized
controlled trials to be more effective than SSRI’s. Due to its higher
side effect burden, however, clomipramine should be reserved for
more severe or refractory cases of OCD, with SSRI’s as the first-line
option.
37. AMITRIPTYLINE AND NORTRIPTYLINE
• Two other commonly prescribed TCA’s are amitriptyline (Elavil) and
nortriptyline (Pamelor). Both are prototypical TCA’s, but in addition to
depression, you will also see them prescribed for chronic pain issues,
such as diabetic peripheral neuropathy, chronic low back pain, or
pelvic pain.
• Compared to amitriptyline, nortriptyline tends to be much less
associated with sedation, orthostatic hypotension, and falls (owing to
less antihistaminergic and anticholinergic effects). For this reason, it is
preferred for elderly patients for whom sedation and falls can be very
big deals.
38. • Amoxapine
• This tetracyclic compound is unusual in that it blocks dopamine D2
receptors in addition to inhibiting NA reuptake. It is chemically related
to the antipsychotic drug loxapine and has mixed antidepressant +
neuroleptic properties—offers advantage for patients with psychotic
depression. Risk of extrapyramidal side effects is also there. Seizures
(including status epilepticus) occur in its overdose.
39. • Reboxetine
• This is a newer selective NA reuptake blocker with weak effect on 5-
HT reuptake. Antimuscarinic and sedative actions are minimal. It
appears to produce fewer side effects and may be safer in overdose
than the older TCAs.
• Side effects are insomnia, palpitation, dry mouth, constipation,
sexual distress and urinary symptoms.
Dose: NAREBOX 4, 8 mg tab.
4 mg BD or 8 mg OD
40.
41.
42. SELECTIVE SEROTONIN REUPTAKE INHIBITORS
(SSRIs)
• These drugs work by inhibiting the reuptake of serotonin, effectively
increasing the amount of serotonin active and available in the
synaptic cleft
• One thing to counsel patients on before starting an SSRI is how long
they can take to work. In multiple studies, it has been shown that full
treatment efficacy is often not reached until 4 to 6 weeks (although
typically some benefit is noticed within the first 2 weeks). Patients
can sometimes feel like stopping the drug early, as the side effects
(like diarrhea) are immediate, while the desired effects can take
several weeks.
43. Antidepressant Profile of SSRI
• Starting dose usually the same as the maintenance dose.
• Response is frequently complete with remission of symptoms.
• Target symptoms do not worsen when treatment initiated.
44. SIDE EFFECTS
• Commonly cause;
• nausea and GI upset,
• headache,
• restlessness, and insomnia;
• may be less effective for severe depressive episodes;
45. • Contraindications: manic episode, concomitant use of MAOIs
• Interactions: alcohol, anticoagulants, anticonvulsants, antipsychotics,
BDZs, B-blockers
46.
47. Fluoxetine
• A bicyclic compound, is the first SSRI to be introduced, and the longest
acting.
• Its plasma t½ is 2 days and that of its active demethylated metabolite is 7–
10 days. It has been approved for use in children 7 years or older for
depression and OCD on the basis of similar efficacy and side effect profile
as in adults, but should be given to children only when psychotherapy fails.
• Agitation and dermatological reactions are more frequent than other SSRIs
Because of slower onset of antidepressant effect, it is considered less
suitable for patients needing rapid effect, but is more appropriate for
poorly compliant patients. Its stimulant effect could worsen patients
showing agitation.
• Fluoxetine has a very long half-life, lasting 1 to 2 weeks
48. Sertraline
• This SSRI has gained popularity, because in clinical trials fewer
patients stopped sertraline due to side effects.
• Efficacy in juvenile depression has been demonstrated, and it is
recommended for anxiety and post-traumatic stress disorder (PTSD)
as well.
• Drug interactions due to inhibition of CYP isoenzymes are less likely
to occur with this SSRI. Its plasma t½ is 26 hours and it produces a still
longer-lasting active metabolite.
• NOTE: Sertraline has more GI side effects but is safe when pregnant
or breastfeeding .
49. Citalopram
• This SSRI shares with sertraline a lower propensity to cause drug
interactions.Its t½ is 33 hours and no active metabolite is known.
However, few deaths due to overdose of citalopram are on record,
because of which it is to be avoided in patients likely to attempt
suicide. Citalopram is the preferred SSRI for mood disorders in
premenstrual syndrome.
50. Escitalopram
• It is the active S(+) enantiomer of citalopram, effective at half the
dose, with similar properties. Side effects are milder and safety is
improved.
51. Dapoxetine
• A SSRI which has been developed and is being promoted for delaying
premature ejaculation, a property common to many SSRIs and some
TCAs.
• Dapoxetine acts rapidly and can be taken 1 hour before sexual
intercourse.
• Combined with behavioural therapies, it has been found to help many
sufferers.
• Side effects are nausea, vomiting, loose motions, headache, dizziness
and occasionally insomnia.
• Dose: 60 mg taken 1 hour before intercourse; older patients 30 mg.
52. • Mode of action: 5-HT and NE reuptake inhibition.
• • Common adverse effects: nausea, GI upset, constipation, loss of
appetite, dry mouth, dizziness, agitation, insomnia, sexual
dysfunction, headache, nervousness, sweating, weakness
SEROTONIN AND NORADRENALINE REUPTAKE
INHIBITORS (SNRIs)
53. • 1. Venlafaxine
• A novel antidepressant referred to as SNRI, because it inhibits uptake of both NA
and 5-HT but, in contrast to older TCAs, it does not interact with cholinergic,
adrenergic or histaminergic receptors or have sedative property. Trials have
shown it to be as effective antidepressant as TCAs and may work in some
resistant cases. A faster onset of action is claimed. Mood changes and hot flushes
in menopausal syndrome, some anxiety and eating disorders are also benefited
by venlafaxine. It does not produce the usual side effects of TCAs;
• tends to raise rather than depress BP and is safer in overdose.
• Prominent side effects are nausea, sweating, anxiety, dizziness, impotence and
withdrawal reactions on discontinuation
• Venlafaxine can cause hypertension .
• Venlafaxine is a rapidly metabolized antidepressant with unpleasant
discontinuation effects .
54. • 2. Duloxetine
• A newer SNRI similar to venla-faxine. It is neither sedative, nor
anticholinergic, nor antihistaminic, nor α blocker.
• SIDE EFFECTS: including g.i. and sexual problems are milder, but some
agitation, insomnia and rise in BP can occur. /Antidepressant efficacy
is comparable to TCAs. Duloxetine is also indicated in panic attacks,
diabetic neuropathic pain, fibromyalgia and stress urinary
incontinence in women (because it increases urethral tone).
• Duloxetine is a dual mechanism antidepressant used for chronic
pain conditions.
55. ATYPICAL ANTIDEPRESSANTS
• 1. Trazodone
• It is the first atypical anti-depressant; less efficiently blocks 5-HT uptake and has
prominent α adrenergic and weak 5-HT2 antagonistic actions. The latter may
contribute to its antidepressant effect, which nevertheless is modest. It is
sedative but not anticholinergic, causes bradycardia rather than tachycardia, does
not interfere with intracardiac conduction—less prone to cause arrhythmia and
better suited for the elderly. Nausea is felt, especially in the beginning. Mild
anxiolytic effect has been noted and it has benefited cases of OCD.
• Inappropriate, prolonged and painful penile erection (priapism) occurs in few
recipients resulting in impotence in a fraction of these.
• The α1 adrenergic blocking property has been held responsible for this effect as
well as for postural hypotension. In general, trazodone is infrequently used now
in depression.
56. 2. BUPROPION
This inhibitor of DA and NA uptake has excitant rather than sedative
property.
It is metabolized into an amphetamine like compound which can cause
presynaptic release of DA and NA
It can cause insomnia, agitation, dry mouth and nausea, but not sexual side
effects. Seizures occur in over dose and in predisposed patients due to
lowering of seizure threshold.
The dose of 150 mg BD should not be exceeded. It is contraindicated in
eating disorders and in bipolar illness.
Bupropion is infrequently used to treat depression; may be added to a SSRI.
57. SUMMARY OF THE GENERAL USES OF
ANTIDEPRESSANTS
• 1. Endogenous (major) depression:
• The aim is to relieve symptoms of depression and restore normal
social behaviour.
• The SSRIs are currently used as first choice for their better tolerability,
safety and may be higher efficacy as well.
• The SNRIs and newer atypical agents also offer some advantages.
• The only antidepressants clearly shown to be effective in juvenile
depression are fluoxetine and sertraline
58. • The TCAs are mostly used as alternatives in non-responsive cases or in
those not tolerating the second generation antidepressants.
• Moclobemide is a well tolerated option for mild to moderate
depression, especially suited for elderly and cardiac patients.
• After a depressive episode has been controlled, continued treatment
at maintenance doses (about 100 mg imipramine/day or equi-valent)
for months is recommended to prevent relapse.
• Discontinuation of the antidepressant may be attempted after 6–12
months. Long-term therapy may be needed in patients who tend to
relapse.
59. • ECT may be given in the severely depressed, especially initially while
the effect of antidepressants is developing, because no
antidepressant has been clearly demonstrated to act fast enough to
prevent suicide.
• The TCAs or SSRIs must be combined with lithium/
valproate/lamotrigine for bipolar depression, and not used alone due
to risk of switching over to mania.
• Combination of one of the SSRIs with an atypical antipsychotic (such
as olanzapine, aripiprazole or quetiapine) is also accepted as a
treatment option for bipolar depression.
60. • 2. Obsessive-compulsive and phobic states:
• The SSRIs, particularly fluoxamine, are the drugs of choice due to
better patient acceptability.
• TCAs, especially clomipramine, are highly effective in OCD and panic
disorders: more than 25% improvement occurs in OCD rating scale
and panic attacks are reduced in >75% patients.
• SSRIs and TCAs also reduce compulsive eating in bulimia, and help
patients with body dysmorphic disorder, compulsive buying and
kleptomania, though these habits may not completely die.
61. • 3. Anxiety disorders:
• Antidepressants, especially SSRIs, exert a delayed but sustained
beneficial effect in many patients of generalized anxiety disorder; may
be used along with a short course of BZDs to cover exacerbations.
SSRIs have also proven helpful in phobic disorders, sustained
treatment of panic attacks and in post-traumatic stress disorder.
62. • 4. Neuropathic pain:
• Amitriptyline and other TCAs afford considerable relief in diabetic
and some other types of chronic pain. Amitriptyline reduces intensity
of post-herpetic neuralgia, approximately 50% patients.
• The SSRIs are less effective in these conditions. Duloxetine, a SNRI, is
now a first line drug for diabetic neuropathy, fibro-myalgia, etc. Other
drugs useful in neuropathic pain are pregabalin or gabapentin.
Combination of duloxetine + pregabalin may work if monotherapy is
not satisfactory.
63. • 5. Attention deficit-hyperactivity disorder (ADHD) in children:
• TCAs with less depressant properties like imipramine, nortriptyline
and amoxapine are now first line drugs in this dis-order, comparable
in efficacy to amphetamine-like drugs, with the advantage of less
fluctuating action and fewer behavioural side effects.
• Atomoxetine is a NA reuptake inhibitor unrelated to both TCAs as well
as amphetamine, which is used specifically in ADHD.
64. • 6. Premature ejaculation
• Most SSRIs and some TCAs, especially clomipramine have the
common property of delaying and in some cases inhibiting ejaculation
(this itself can cause sexual distress). The primary treatment of
premature ejaculation is counselling and behavioural therapy, but this
can be supplemented by drugs. Dapoxetine is a SSRI which has been
specifically introduced for this purpose. It acts rapidly; 60 mg taken 1
hour before intercourse has helped many subjects.
65. • Clomipramine 10–25 mg three times a day is a slow acting drug which
needs to be taken regularly for maximum benefit. For on demand use,
25 mg may be taken 6 hours before sex.
66. • 7. Enuresis:
• In children above 5 years, imipramine 25 mg at bedtime is effective,
but bed wetting may again start when the drug is stopped.
• Eldery subjects with bed wetting have also benefited.
67. • 8. Migraine:
• Amitriptyline has some prophy-lactic value, especially in patients with
mixed headaches.
• 9. Pruritus: Some tricyclics have antipruritic action. Topical doxepin
has been used to relieve itching in atopic dermatitis, lichen simplex,
etc.
• NOCTADERM 5% cream.