Benzodiazepines like diazepam act as sedative-hypnotics by potentiating the effects of the inhibitory neurotransmitter GABA at GABA-A receptors in the brain. This enhances chloride influx which hyperpolarizes neurons and has sedative, anxiolytic, and muscle relaxing effects. Common side effects include drowsiness, dizziness, and impaired coordination. Long-term use can cause tolerance, dependence, and withdrawal symptoms.
This document discusses sedative-hypnotic drugs. It defines sedatives as drugs that decrease excitement and cause drowsiness without sleep, while hypnotics induce and maintain sleep. Different stages of sleep are described, along with the effects of sedative-hypnotics on sleep architecture. Benzodiazepines and barbiturates are provided as examples of sedative-hypnotic drugs and their mechanisms of action, effects, uses, and adverse effects are summarized. Non-benzodiazepine hypnotics such as zolpidem and zopiclone are also mentioned.
This document summarizes treatments for Parkinson's disease. It begins by describing the symptoms and pathogenesis of the disease. The main treatments discussed are levodopa, dopamine agonists like bromocriptine and pramipexole, MAO-B inhibitors like selegiline, and COMT inhibitors like entacapone. These work to restore the dopamine/acetylcholine balance in the basal ganglia. Levodopa is most effective initially but causes dyskinesias long term. Dopamine agonists have less motor effect but fewer dyskinesias. Combination therapy aims to control symptoms and delay adverse effects.
General anesthetics provide amnesia, analgesia, muscle relaxation and sedation, placing the patient in a reversible state of unconsciousness. There are inhalational agents like nitrous oxide, halothane, enflurane and isoflurane, and intravenous agents like propofol, ketamine and thiopental. They work mainly by enhancing the effect of the inhibitory neurotransmitter GABA at GABAA receptors. Different agents have advantages and disadvantages related to their potency, metabolism, effects on vital organs and side effects. Careful selection of agents and monitoring is required for safe anesthesia.
Parkinson's disease is a progressive nervous system disorder that causes a loss of dopamine-producing brain cells, leading to motor symptoms like tremors and rigidity. It occurs due to degeneration of the substantia nigra, decreasing dopamine levels in the basal ganglia. The document discusses the causes, symptoms, diagnosis, treatment and management of Parkinson's disease with a focus on increasing dopamine levels through drugs like L-DOPA, COMT inhibitors, and dopamine receptor agonists.
This document discusses narcolepsy, a chronic sleep disorder characterized by excessive daytime sleepiness. It defines narcolepsy and explains its symptoms like cataplexy, sleep paralysis, and hallucinations. The document also covers how narcolepsy is diagnosed through polysomnograms and multiple sleep latency tests. While there is no cure, treatment focuses on controlling symptoms through stimulant drugs, antidepressants, and lifestyle changes. The document provides statistics on narcolepsy's prevalence and potential complications.
This document provides an overview of Parkinson's disease, including its etiology, incidence, pathophysiology, clinical presentation, diagnosis, prognosis, and treatment. Some key points:
- Parkinson's disease is a chronic neurodegenerative disorder that affects the basal ganglia and is characterized by bradykinesia, rigidity, tremor, and postural instability.
- It has an annual incidence of 0.2 per 1000 people and prevalence of 1.5 per 1000. Risk increases with age.
- Pathologically it involves the loss of dopamine-producing neurons in the substantia nigra and formation of Lewy bodies.
- Clinical diagnosis is based on the presence of cardinal motor symptoms
This document discusses Parkinson's disease. It begins by defining neurodegenerative diseases and listing Parkinson's disease as a disorder caused by the loss of nigrostriatal dopamine neurons. It then provides more details on Parkinson's disease, noting that it was first defined in 1817 and typically affects those over 65 years old. The document outlines the clinical findings and symptoms of Parkinson's disease including tremors, rigidity, bradykinesia, and other motor impairments. It discusses the pathology of Parkinson's disease including degeneration of dopamine neurons in the substantia nigra and loss of dopamine in the striatum. The document also briefly covers dopamine metabolism and different therapies used to treat Parkinsonism, including levodopa,
Parkinson's disease is a degenerative disorder of the central nervous system that affects movement. It occurs when nerve cells in the brain do not produce enough dopamine. The document outlines the symptoms, stages, causes, treatment, and animal models of Parkinson's disease. The main symptoms are motor symptoms like tremors and rigidity as well as non-motor symptoms like mood changes. Treatment focuses on replacing dopamine and managing symptoms, primarily using levodopa and dopamine agonists. Animal models aim to reproduce the features of Parkinson's through pharmacological or genetic means to better understand and research the disease.
This document discusses sedative-hypnotic drugs. It defines sedatives as drugs that decrease excitement and cause drowsiness without sleep, while hypnotics induce and maintain sleep. Different stages of sleep are described, along with the effects of sedative-hypnotics on sleep architecture. Benzodiazepines and barbiturates are provided as examples of sedative-hypnotic drugs and their mechanisms of action, effects, uses, and adverse effects are summarized. Non-benzodiazepine hypnotics such as zolpidem and zopiclone are also mentioned.
This document summarizes treatments for Parkinson's disease. It begins by describing the symptoms and pathogenesis of the disease. The main treatments discussed are levodopa, dopamine agonists like bromocriptine and pramipexole, MAO-B inhibitors like selegiline, and COMT inhibitors like entacapone. These work to restore the dopamine/acetylcholine balance in the basal ganglia. Levodopa is most effective initially but causes dyskinesias long term. Dopamine agonists have less motor effect but fewer dyskinesias. Combination therapy aims to control symptoms and delay adverse effects.
General anesthetics provide amnesia, analgesia, muscle relaxation and sedation, placing the patient in a reversible state of unconsciousness. There are inhalational agents like nitrous oxide, halothane, enflurane and isoflurane, and intravenous agents like propofol, ketamine and thiopental. They work mainly by enhancing the effect of the inhibitory neurotransmitter GABA at GABAA receptors. Different agents have advantages and disadvantages related to their potency, metabolism, effects on vital organs and side effects. Careful selection of agents and monitoring is required for safe anesthesia.
Parkinson's disease is a progressive nervous system disorder that causes a loss of dopamine-producing brain cells, leading to motor symptoms like tremors and rigidity. It occurs due to degeneration of the substantia nigra, decreasing dopamine levels in the basal ganglia. The document discusses the causes, symptoms, diagnosis, treatment and management of Parkinson's disease with a focus on increasing dopamine levels through drugs like L-DOPA, COMT inhibitors, and dopamine receptor agonists.
This document discusses narcolepsy, a chronic sleep disorder characterized by excessive daytime sleepiness. It defines narcolepsy and explains its symptoms like cataplexy, sleep paralysis, and hallucinations. The document also covers how narcolepsy is diagnosed through polysomnograms and multiple sleep latency tests. While there is no cure, treatment focuses on controlling symptoms through stimulant drugs, antidepressants, and lifestyle changes. The document provides statistics on narcolepsy's prevalence and potential complications.
This document provides an overview of Parkinson's disease, including its etiology, incidence, pathophysiology, clinical presentation, diagnosis, prognosis, and treatment. Some key points:
- Parkinson's disease is a chronic neurodegenerative disorder that affects the basal ganglia and is characterized by bradykinesia, rigidity, tremor, and postural instability.
- It has an annual incidence of 0.2 per 1000 people and prevalence of 1.5 per 1000. Risk increases with age.
- Pathologically it involves the loss of dopamine-producing neurons in the substantia nigra and formation of Lewy bodies.
- Clinical diagnosis is based on the presence of cardinal motor symptoms
This document discusses Parkinson's disease. It begins by defining neurodegenerative diseases and listing Parkinson's disease as a disorder caused by the loss of nigrostriatal dopamine neurons. It then provides more details on Parkinson's disease, noting that it was first defined in 1817 and typically affects those over 65 years old. The document outlines the clinical findings and symptoms of Parkinson's disease including tremors, rigidity, bradykinesia, and other motor impairments. It discusses the pathology of Parkinson's disease including degeneration of dopamine neurons in the substantia nigra and loss of dopamine in the striatum. The document also briefly covers dopamine metabolism and different therapies used to treat Parkinsonism, including levodopa,
Parkinson's disease is a degenerative disorder of the central nervous system that affects movement. It occurs when nerve cells in the brain do not produce enough dopamine. The document outlines the symptoms, stages, causes, treatment, and animal models of Parkinson's disease. The main symptoms are motor symptoms like tremors and rigidity as well as non-motor symptoms like mood changes. Treatment focuses on replacing dopamine and managing symptoms, primarily using levodopa and dopamine agonists. Animal models aim to reproduce the features of Parkinson's through pharmacological or genetic means to better understand and research the disease.
parkinson's disease by me ..........prakash mahala p.g. medical surgical nursing at himalayan college of nursing dehradun.......prakashjpmmahala@gmail.com
This document discusses opioids, their classification, pharmacological actions, routes of administration, metabolism, toxicity, and withdrawal. It describes how opioids work on mu, kappa, and delta receptors to produce analgesia, sedation, respiratory depression and other effects. It outlines the treatment for opioid overdose including naloxone administration and activated charcoal. Symptoms and management of opioid withdrawal are also reviewed.
The document discusses various classes of sedative and hypnotic drugs including benzodiazepines, barbiturates, and newer agents. It describes how these drugs work in the central nervous system by facilitating the action of the inhibitory neurotransmitter GABA. The document also covers the pharmacokinetics, uses, adverse effects, and treatment of overdose for different sedative and hypnotic medications.
Gonorrhea is a sexually transmitted disease caused by Neisseria gonorrhoea that mainly affects the genitals, rectum, and throat. It is estimated that 98 million new cases occur annually worldwide. Risk factors include having multiple sex partners or a new sex partner. Symptoms vary depending on the infected area but may include painful urination, increased discharge, or bleeding. It is treated with antibiotics like ceftrioxone or cefotaxime. Prevention involves safe sex practices and testing of partners.
This document discusses drugs used to treat constipation and diarrhea. For constipation, it describes laxatives that promote bowel evacuation, including bulk formers, stool softeners, and stimulant purgatives. For diarrhea, it outlines rehydration therapy and maintaining nutrition. Drug treatment includes specific antimicrobials, probiotics, drugs for inflammatory bowel disease, and nonspecific antidiarrheal drugs that are absorbents, antisecretory, or antimotility agents.
Parkinson's disease is a chronic neurological disorder that affects movement. It is caused by the loss of dopamine-producing neurons in the brain. The main symptoms are tremors, rigidity, bradykinesia, and impaired balance. While the exact cause is unknown, risk factors include genetics, drugs, toxins, and head injuries. There is no cure, but treatment aims to manage symptoms and improve quality of life through medications and sometimes surgery.
Parkinsonism is a progressive neurological disorder characterized by bradykinesia, muscular rigidity, resting tremor, and impaired balance. It can be caused by idiopathic Parkinson's disease, vascular issues, certain drugs that block dopamine, or dementia with Lewy bodies. Treatment aims to increase dopamine in the brain and involves levodopa, dopamine agonists, MAO inhibitors, COMT inhibitors, amantadine, and anticholinergic drugs.
This document discusses sedative, hypnotic, and anxiolytic drugs. It describes barbiturates and benzodiazepines, which are commonly used as sedative-hypnotics. Barbiturates act by potentiating the inhibitory neurotransmitter GABA, while benzodiazepines facilitate GABA effects by binding to GABAA receptors. The document outlines the mechanisms, effects on sleep, and adverse effects of these drug classes. It also discusses newer nonbenzodiazepine hypnotics and the benzodiazepine antagonist flumazenil.
Parkinson's disease is a progressive neurodegenerative disorder characterized by tremors, rigidity, akinesia, and postural instability. It results from the loss of dopamine-producing neurons in the substantia nigra. Drug therapy aims to increase dopamine levels through L-Dopa, dopamine agonists, MAO-B inhibitors, COMT inhibitors, or dopamine reuptake inhibitors. Anticholinergics may also be used. L-Dopa is very effective but side effects include dyskinesia and fluctuations. Later stages may require additional drugs or surgical interventions like deep brain stimulation. Management involves both drug therapy and non-pharmacological measures tailored to each patient's age, symptoms, and disease progression
Parkinson's disease is a progressive neurodegenerative disorder caused by the deterioration of neurons in the basal ganglia. It results in symptoms like tremors, rigidity, bradykinesia, and impaired balance. The average age of onset is 60 years, though 5-10% of cases occur before age 40. While the cause is largely unknown, risk factors include family history, male gender, head injuries, and pesticide exposure. Treatment involves drug therapy with levodopa and other medications, as well as surgical procedures like deep brain stimulation for advanced cases. Research is ongoing into treatments like neural grafting and gene therapy.
This document summarizes information about seizures and epilepsy. It defines a seizure as abnormal excessive neuronal discharge and epilepsy as a chronic seizure disorder. Seizures are classified as partial or generalized. Common causes of epilepsy include family history, head injuries, infections, and tumors. Diagnosis involves EEG and brain imaging. Treatment depends on seizure type but may include carbamazepine, lamotrigine, valproic acid, and other anticonvulsants. The majority of people with epilepsy live normal lives, as epilepsy is not contagious or a mental illness.
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.
This document provides information about antimuscarinic agents. It discusses their classification, sources, examples like atropine and scopolamine, mechanisms of action, therapeutic uses, and side effects. Antimuscarinic agents work by blocking the effects of acetylcholine, especially at muscarinic receptors. They have various applications like as antisecretory agents, to treat peptic ulcer, asthma, and Parkinson's disease. However, common side effects include constipation, blurred vision, dry mouth, urinary retention and confusion in elderly.
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.
Parkinson's disease is a progressive nervous system disorder that causes motor symptoms like rigidity, bradykinesia, tremors, and impaired balance. It is caused by degeneration of dopamine-producing neurons in the brain. Physical therapy focuses on improving motor skills through exercises to enhance flexibility, strength, balance, gait, and cardiovascular fitness. Treatment involves both pharmacological interventions and physical therapy techniques like cueing, relaxation exercises, and functional training. The goals are to reduce symptoms, improve mobility and quality of life, and help patients better manage their condition.
Sedatives calm without sleep, hypnotics induce sleep. Benzodiazepines like diazepam are commonly used sedative-hypnotics with high safety indices. They act by enhancing GABA inhibition. Newer drugs like zolpidem act similarly but with less residual effects. Barbiturates were widely used previously but are no longer preferred due to risks of overdose and dependence. The goal of treatment is to reduce anxiety, induce sleep, and have minimal daytime effects.
Reviews the uses for benzodiazepines and barbiturates, the signs of intoxication and withdrawal, impact on sports performance. Continuing Education for mental health and substance abuse counselors and therapists.
Corticosteroids are a class of steroid hormones produced in the adrenal cortex that are involved in stress response, immune response, inflammation, metabolism, and other physiological systems. They include glucocorticoids like cortisol which control carbohydrate, fat and protein metabolism and are anti-inflammatory, and mineralocorticoids like aldosterone which control electrolyte and water levels. Corticosteroids have various medical uses but also carry risks of side effects if not taken correctly.
This document discusses sedative, hypnotic, and anxiolytic drugs. It describes barbiturates and benzodiazepines. Barbiturates were popular hypnotics and sedatives until the 1960s but are no longer used due to risks of overdose, dependence, and withdrawal effects. Benzodiazepines replaced barbiturates as they have a higher therapeutic index and are less likely to cause respiratory depression even at high doses. The document outlines the mechanisms, effects on sleep, and pharmacological properties of barbiturates and benzodiazepines.
Sedative-hypnotics are central nervous system depressants that reduce excitement and induce sleep. Common classes include barbiturates, benzodiazepines, and newer nonbenzodiazepine drugs. Barbiturates such as phenobarbital are no longer primarily used due to risk of dependence and withdrawal symptoms. Benzodiazepines like diazepam are now preferred for treatment of insomnia and anxiety. Sleep involves different stages including REM sleep, which is important for dreaming. Classification, mechanisms of action, uses, and adverse effects of sedative-hypnotics are described.
parkinson's disease by me ..........prakash mahala p.g. medical surgical nursing at himalayan college of nursing dehradun.......prakashjpmmahala@gmail.com
This document discusses opioids, their classification, pharmacological actions, routes of administration, metabolism, toxicity, and withdrawal. It describes how opioids work on mu, kappa, and delta receptors to produce analgesia, sedation, respiratory depression and other effects. It outlines the treatment for opioid overdose including naloxone administration and activated charcoal. Symptoms and management of opioid withdrawal are also reviewed.
The document discusses various classes of sedative and hypnotic drugs including benzodiazepines, barbiturates, and newer agents. It describes how these drugs work in the central nervous system by facilitating the action of the inhibitory neurotransmitter GABA. The document also covers the pharmacokinetics, uses, adverse effects, and treatment of overdose for different sedative and hypnotic medications.
Gonorrhea is a sexually transmitted disease caused by Neisseria gonorrhoea that mainly affects the genitals, rectum, and throat. It is estimated that 98 million new cases occur annually worldwide. Risk factors include having multiple sex partners or a new sex partner. Symptoms vary depending on the infected area but may include painful urination, increased discharge, or bleeding. It is treated with antibiotics like ceftrioxone or cefotaxime. Prevention involves safe sex practices and testing of partners.
This document discusses drugs used to treat constipation and diarrhea. For constipation, it describes laxatives that promote bowel evacuation, including bulk formers, stool softeners, and stimulant purgatives. For diarrhea, it outlines rehydration therapy and maintaining nutrition. Drug treatment includes specific antimicrobials, probiotics, drugs for inflammatory bowel disease, and nonspecific antidiarrheal drugs that are absorbents, antisecretory, or antimotility agents.
Parkinson's disease is a chronic neurological disorder that affects movement. It is caused by the loss of dopamine-producing neurons in the brain. The main symptoms are tremors, rigidity, bradykinesia, and impaired balance. While the exact cause is unknown, risk factors include genetics, drugs, toxins, and head injuries. There is no cure, but treatment aims to manage symptoms and improve quality of life through medications and sometimes surgery.
Parkinsonism is a progressive neurological disorder characterized by bradykinesia, muscular rigidity, resting tremor, and impaired balance. It can be caused by idiopathic Parkinson's disease, vascular issues, certain drugs that block dopamine, or dementia with Lewy bodies. Treatment aims to increase dopamine in the brain and involves levodopa, dopamine agonists, MAO inhibitors, COMT inhibitors, amantadine, and anticholinergic drugs.
This document discusses sedative, hypnotic, and anxiolytic drugs. It describes barbiturates and benzodiazepines, which are commonly used as sedative-hypnotics. Barbiturates act by potentiating the inhibitory neurotransmitter GABA, while benzodiazepines facilitate GABA effects by binding to GABAA receptors. The document outlines the mechanisms, effects on sleep, and adverse effects of these drug classes. It also discusses newer nonbenzodiazepine hypnotics and the benzodiazepine antagonist flumazenil.
Parkinson's disease is a progressive neurodegenerative disorder characterized by tremors, rigidity, akinesia, and postural instability. It results from the loss of dopamine-producing neurons in the substantia nigra. Drug therapy aims to increase dopamine levels through L-Dopa, dopamine agonists, MAO-B inhibitors, COMT inhibitors, or dopamine reuptake inhibitors. Anticholinergics may also be used. L-Dopa is very effective but side effects include dyskinesia and fluctuations. Later stages may require additional drugs or surgical interventions like deep brain stimulation. Management involves both drug therapy and non-pharmacological measures tailored to each patient's age, symptoms, and disease progression
Parkinson's disease is a progressive neurodegenerative disorder caused by the deterioration of neurons in the basal ganglia. It results in symptoms like tremors, rigidity, bradykinesia, and impaired balance. The average age of onset is 60 years, though 5-10% of cases occur before age 40. While the cause is largely unknown, risk factors include family history, male gender, head injuries, and pesticide exposure. Treatment involves drug therapy with levodopa and other medications, as well as surgical procedures like deep brain stimulation for advanced cases. Research is ongoing into treatments like neural grafting and gene therapy.
This document summarizes information about seizures and epilepsy. It defines a seizure as abnormal excessive neuronal discharge and epilepsy as a chronic seizure disorder. Seizures are classified as partial or generalized. Common causes of epilepsy include family history, head injuries, infections, and tumors. Diagnosis involves EEG and brain imaging. Treatment depends on seizure type but may include carbamazepine, lamotrigine, valproic acid, and other anticonvulsants. The majority of people with epilepsy live normal lives, as epilepsy is not contagious or a mental illness.
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.
This document provides information about antimuscarinic agents. It discusses their classification, sources, examples like atropine and scopolamine, mechanisms of action, therapeutic uses, and side effects. Antimuscarinic agents work by blocking the effects of acetylcholine, especially at muscarinic receptors. They have various applications like as antisecretory agents, to treat peptic ulcer, asthma, and Parkinson's disease. However, common side effects include constipation, blurred vision, dry mouth, urinary retention and confusion in elderly.
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.
Parkinson's disease is a progressive nervous system disorder that causes motor symptoms like rigidity, bradykinesia, tremors, and impaired balance. It is caused by degeneration of dopamine-producing neurons in the brain. Physical therapy focuses on improving motor skills through exercises to enhance flexibility, strength, balance, gait, and cardiovascular fitness. Treatment involves both pharmacological interventions and physical therapy techniques like cueing, relaxation exercises, and functional training. The goals are to reduce symptoms, improve mobility and quality of life, and help patients better manage their condition.
Sedatives calm without sleep, hypnotics induce sleep. Benzodiazepines like diazepam are commonly used sedative-hypnotics with high safety indices. They act by enhancing GABA inhibition. Newer drugs like zolpidem act similarly but with less residual effects. Barbiturates were widely used previously but are no longer preferred due to risks of overdose and dependence. The goal of treatment is to reduce anxiety, induce sleep, and have minimal daytime effects.
Reviews the uses for benzodiazepines and barbiturates, the signs of intoxication and withdrawal, impact on sports performance. Continuing Education for mental health and substance abuse counselors and therapists.
Corticosteroids are a class of steroid hormones produced in the adrenal cortex that are involved in stress response, immune response, inflammation, metabolism, and other physiological systems. They include glucocorticoids like cortisol which control carbohydrate, fat and protein metabolism and are anti-inflammatory, and mineralocorticoids like aldosterone which control electrolyte and water levels. Corticosteroids have various medical uses but also carry risks of side effects if not taken correctly.
This document discusses sedative, hypnotic, and anxiolytic drugs. It describes barbiturates and benzodiazepines. Barbiturates were popular hypnotics and sedatives until the 1960s but are no longer used due to risks of overdose, dependence, and withdrawal effects. Benzodiazepines replaced barbiturates as they have a higher therapeutic index and are less likely to cause respiratory depression even at high doses. The document outlines the mechanisms, effects on sleep, and pharmacological properties of barbiturates and benzodiazepines.
Sedative-hypnotics are central nervous system depressants that reduce excitement and induce sleep. Common classes include barbiturates, benzodiazepines, and newer nonbenzodiazepine drugs. Barbiturates such as phenobarbital are no longer primarily used due to risk of dependence and withdrawal symptoms. Benzodiazepines like diazepam are now preferred for treatment of insomnia and anxiety. Sleep involves different stages including REM sleep, which is important for dreaming. Classification, mechanisms of action, uses, and adverse effects of sedative-hypnotics are described.
This document defines sedatives and hypnotics, and classifies common drugs used as such. It describes the mechanisms, pharmacokinetics, uses and side effects of barbiturates, benzodiazepines, zolpidem, and zaleplon. Barbiturates act by facilitating GABA activity and directly activating chloride channels, while benzodiazepines facilitate GABA activity at receptor sites. Both are metabolized in the liver and have risks of tolerance, dependence and withdrawal. Benzodiazepines generally have fewer side effects and less abuse potential than barbiturates. Zolpidem and zaleplon are shorter acting hypnotics that also facilitate G
This document summarizes sedatives and hypnotics, including their mechanisms of action and classifications. It discusses that sedatives calm without inducing sleep while hypnotics induce and maintain sleep. The main classes covered are barbiturates and benzodiazepines. Barbiturates act by potentiating GABA receptors but are no longer commonly used due to side effects like tolerance and dependence. Benzodiazepines also act through GABA receptors with fewer side effects and are still frequently prescribed as hypnotics, anxiolytics, anticonvulsants, and muscle relaxants.
Sedatives and hypnotics are drugs that decrease activity and induce sleep. Benzodiazepines are commonly used psychoactive drugs for treating anxiety, seizures, muscle relaxation and insomnia. They work by enhancing the effects of the inhibitory neurotransmitter GABA at GABA-A receptors. While generally safe and effective for short-term use, long-term use can lead to tolerance, dependence and adverse effects. Barbiturates were previously widely used as sedatives, hypnotics and anticonvulsants but have been replaced by benzodiazepines due to their lower risk of overdose, dependence and withdrawal symptoms. Both classes of drugs produce their effects by modulating GABA receptors to hyperpolar
This document discusses different classes of sedative and hypnotic drugs, including their mechanisms of action, pharmacokinetics and therapeutic uses. It covers barbiturates, benzodiazepines, zolpidem, and buspirone. Barbiturates and benzodiazepines enhance the effects of the inhibitory neurotransmitter GABA, whereas zolpidem selectively binds to GABA receptors. These drugs have varying onset and duration of action and are used to treat conditions like anxiety, insomnia and seizures. Adverse effects include respiratory depression, dependence and withdrawal symptoms.
The document discusses sedative/hypnotic and anxiolytic drugs. It describes their mechanisms of action, which primarily involve enhancing GABAergic transmission in the brain. Benzodiazepines and barbiturates act as agonists at GABA-A receptors. These drugs can relieve anxiety and induce sleep, but have side effects like sedation, respiratory depression, and dependence with long-term use. Newer non-benzodiazepine drugs like zolpidem are also discussed.
This document summarizes information on sedative and hypnotic drugs. It discusses the mechanisms and effects of benzodiazepines, barbiturates, and other drugs such as zolpidem, zaleplon, zopiclone, melatonin, and buspirone. It provides details on the pharmacokinetics, therapeutic uses, and side effects of these classes of drugs. The document also covers topics like tolerance, dependence and withdrawal symptoms, overdose treatment, and newer non-benzodiazepine hypnotics.
This document discusses sedatives and hypnotics, including their classification, mechanisms of action, pharmacokinetics, uses, and adverse effects. It covers barbiturates, benzodiazepines, and newer non-benzodiazepine hypnotics. Barbiturates and benzodiazepines act as depressants in the central nervous system by enhancing GABA activity. They are used as hypnotics to induce and maintain sleep, but have risks of tolerance, dependence, and withdrawal symptoms with chronic use. Newer non-benzodiazepine hypnotics like zolpidem, zopiclone, and zaleplon selectively target GABA receptors to
Sedatives and hypnotics drugs ppt by kashikant yadavKashikant Yadav
Sedatives and hypnotics are central nervous system depressants that are used to induce sleep or reduce anxiety. Barbiturates were previously commonly used but have largely been replaced by benzodiazepines due to lower risks of dependence and overdose. Both classes of drugs work by enhancing the effects of the inhibitory neurotransmitter GABA. Sedatives primarily reduce anxiety and excitement while hypnotics are used to induce sleep. Common side effects include drowsiness, dizziness, and impaired coordination. Tolerance can develop with repeated use of both barbiturates and benzodiazepines.
This document summarizes information about sedatives and hypnotics. It defines sedatives as drugs that reduce excitement and calm patients without inducing sleep, while hypnotics produce sleep resembling natural sleep. Both act by facilitating GABAergic transmission. Common classes discussed are benzodiazepines, barbiturates, antihistamines, and other sedative-hypnotics. Their mechanisms, clinical uses, and side effects are compared. Sedatives are used to relieve anxiety, while hypnotics induce sleep. Toxic doses can depress respiration and blood pressure, potentially causing death.
This document provides information about sedatives and hypnotics. It defines sedatives as drugs that reduce excitement and calm patients without inducing sleep, while hypnotics produce sleep resembling natural sleep. Both act through facilitating GABA neurotransmission. Common classes discussed are benzodiazepines, barbiturates, antihistamines, and other newer non-benzodiazepine drugs. Their mechanisms, clinical uses, and side effects are explained. Sedatives are used to relieve anxiety and cause sedation, while hypnotics are used for sleep initiation or maintenance.
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This document discusses various sedative-hypnotic drugs that act on the central nervous system. It begins by distinguishing drugs that produce sedation from those that induce sleep. It then describes normal sleep cycles and the stages of sleep. The rest of the document details different classes of sedative-hypnotic drugs including benzodiazepines, barbiturates, antihistamines, and others. It provides information on their mechanisms of action, pharmacological effects, clinical uses, and important considerations regarding administration and withdrawal.
This document summarizes sedative hypnotic drugs, including their mechanisms of action, pharmacokinetics, and clinical uses. It discusses how these drugs act on GABA receptors in the central nervous system to produce sedation, hypnosis, and anesthesia. Specific drug classes covered include benzodiazepines, barbiturates, buspirone, zolpidem, zaleplon, and ramelteon. Ideal properties of hypnotic drugs and their unwanted effects such as tolerance and dependence are also summarized.
This document discusses sedatives and hypnotics, including their mechanisms of action, classifications, and examples. It focuses on barbiturates and benzodiazepines. Barbiturates act by enhancing GABA activity in the brain, leading to CNS depression. They are classified based on duration of action and therapeutic use. Common side effects include dependence and withdrawal. Benzodiazepines also enhance GABA activity and are used as anxiolytics, for seizures, and to treat sleep disorders. They are classified based on duration of action from long to short acting.
Pharmacology document discusses central nervous system (CNS) depressants like alcohols, barbiturates, benzodiazepines, and newer non-benzodiazepine hypnotics. It describes their mechanisms of action, pharmacological effects on various body systems, classifications, and examples. Key points include ethanol and methanol acting as CNS depressants; barbiturates formerly used as hypnotics and sedatives but now replaced due to side effects; benzodiazepines having lower CNS depression than barbiturates; and newer non-benzodiazepine hypnotics like zolpidem and zaleplon acting on GABA receptors with improved
The document discusses psychoactive drugs and the synthesis of barbiturates and phenobarbital. It defines psychoactive drugs as chemicals that alter mood, behavior, and perceptions. It describes the four main types - stimulants, depressants, narcotics, and hallucinogens. It then focuses on barbiturates, describing their synthesis, mechanism of action by enhancing the GABA neurotransmitter, and uses including epilepsy treatment. Finally, it discusses phenobarbital as a long-acting barbiturate used for seizures, its synthesis, mechanism of action, uses, and disadvantages like withdrawal risks.
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LGBTQ+ Adults: Unique Opportunities and Inclusive Approaches to CareVITASAuthor
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2. The duration and pattern of
sleep varies considerably
among individuals. Age has
an important effect on
quantity and depth of
sleep.
It has been recognized that
sleep is an architectured
cyclic process. The different
phases of sleep and their
characteristics are—
3. From lying down to falling asleep and occasional
nocturnal awakenings; constitutes 1–2% of sleep
time.
Eye movements are irregular or slowly rolling.
4. Eye movements are reduced but there may be bursts
of rolling.
Neck muscles relax. Occupies 3–6% of sleep time.
5. (unequivocal sleep) θ waves with interspersed
spindles, K complexes can be evoked on sensory
stimulation; little eye movement; subjects are easily
arousable. This comprises 40–50% of sleep time.
Stage 3 (deep sleep transition)
Eye movements are few; subjects are not easily
arousable; comprises 5–8% of sleep time.
6. (cerebral sleep) δ activity predominates in EEG, K
complexes cannot be evoked. Eyes are practically
fixed , subjects are difficult to arouse. Night terror
may occur at this time. It comprises 10–20% of sleep
time.
During stage 2, 3 and 4 heart rate, BP and respiration
are steady and muscles are relaxed. Stages 3 and 4
together are called slow wave sleep (SWS).
7. REM sleep (paradoxical sleep)
EEG has waves of all frequency, K
complexes cannot be elicited.
There are marked, irregular and
darting eye movements; dreams
and nightmares occur, which may
be recalled if the subject is aroused.
Heart rate and BP fluctuate;
respiration is irregular. Muscles are
fully relaxed, but irregular body
movements occur occasionally.
8. A drug that subdues excitement and calms the subject
without inducing sleep, though drowsiness may be
produced.
Sedation refers to decreased responsiveness to any
level of stimulation; is associated with some decrease
in motor activity and ideation.
9. A drug that induces and/or maintains sleep, similar to
normal arousable sleep.
This is not to be confused with ‘hypnosis’ meaning a
trans-like state in which the subject becomes passive
and highly suggestible.
13. Barbiturates are a group of drugs in the class
of drugs known as sedative-hypnotics, which
generally describes their sleep-inducing and
anxiety-decreasing effects.
14. Barbiturates are general depressants for all
excitable cells, the CNS is most sensitive
where the effect is almost global, but certain
areas are more susceptible.
CNS Barbiturates produce dose-dependent
effects:
sedation → sleep → anaesthesia → coma.
15. Hypnotic dose (100–200 mg of a short acting
barbiturate) shortens the time taken to fall asleep and
increases sleep duration.
The sleep is arousable, but the subject may feel
confused and unsteady if waken early. Night
awakenings are reduced.
REM and stage 3, 4 sleep are decreased; REM-
NREM sleep cycle is disrupted. The effects on sleep
become progressively less marked if the drug is taken
every night consecutively
16. Sedative dose (smaller dose of a longer acting
barbiturate) given at daytime can produce
drowsiness, reduction in anxiety and
excitability
Barbiturates can impair learning, short-term
memory and judgement. Barbiturates have
anticonvulsant property
17. Barbiturates appear to act primarily at the GABA :
BZD receptor–Cl¯ channel complex and potentiate
GABA ergic inhibition by increasing the lifetime of
Cl¯ channel opening induced by GABA.
At high concentrations, barbiturates directly increase
Cl¯ conductance and inhibit Ca2+ dependent release
of neurotransmitters. In addition they depress
glutamate induced neuronal depolarization through
AMPA receptors(is a non-NMDA-type ionotropic
transmembrane receptor for glutamate that mediates
fast synaptic transmission in the central nervous
system (CNS).)
18. Respiration is depressed by relatively higher doses.
hypercapneic and hypoxic oocurs.
CVS Hypnotic doses of barbiturates produce a slight
decrease in BP and heart rate, Reflex tachycardia can
occur, though pressor reflexes are depressed.
Even the dose producing cardiac arrest is about 3 times
larger than that causing respiratory failure.
Skeletal muscle- Hypnotic doses have little effect but
anaesthetic doses reduce muscle contraction by
depressing excitability of neuromuscular junction.
19. Smooth muscles Tone and motility of bowel is
decreased slightly by hypnotic doses; more
profoundly during intoxication. Action on bronchial,
ureteric, vesical and uterine muscles is not
significant.
Kidney Barbiturates tend to reduce urine flow by
decreasing BP and increasing ADH release. Oliguria
attends barbiturate intoxication.
20. Phenobarbital, the longest-acting barbiturate,
is used for its anticonvulsant and sedative-
hypnotic properties in the management of all
seizure disorders except absence (petit mal)
21. Phenobarbital acts on GABAa receptors, increasing
synaptic inhibition. This has the effect of elevating
seizure threshold and reducing the spread of seizure
activity from a seizure focus.
Phenobarbital may also inhibit calcium channels,
resulting in a decrease in excitatory transmitter
release. The sedative-hypnotic effects of
phenobarbital are likely the result of its effect on the
polysynaptic midbrain reticular formation, which
controls CNS arousal.
22. Central nervous system effects,
such as dizziness, nystagmus
and ataxia, are also common.
In elderly patients, it may cause
excitement and confusion,
while in children, it may result
in paradoxical hyperactivity.
Another rare side effect is
amelogenesis imperfecta
23. Hypersensitivity to any barbiturates
Prior dependence on barbiturates
Severe respiratory insufficiency
Hyperkinesia in children
24. Butobarbital (BAN), also called
butobarbitone or butethal, Soneryl, and
Neonal, is a hypnotic drug which is a
barbiturate derivative.
Butobarital is a barbiturate and is used as a hypnotic.
Although it is no longer recommended due to the risk
of dependence, tolerance and adverse effects, its
continued use may be necessary in severe intractable
insomnia in patients already on it
25. Oral
Severe intractable insomnia
Adult: 100-200 mg at bedtime.
26. Children, young adults, elderly and debilitated
patients.
Patients with depression or with a history of drug or
alcohol abuse or addiction. Insomnia caused by pain.
Acute porphyria.
Severe hepatic impairment. History of CNS
depression or coma, pulmonary insufficiency and
sleep apnoea.
Pregnancy & lactation.
29. Site and mechanism of action
Benzodiazepines act preferentially on
midbrain ascending reticular formation
(which maintains wakefulness) and on limbic
system (thought and mental functions).
Muscle relaxation is produced by a primary
medullary site of action and ataxia is due to
action on cerebellum.
30. BZDs act by enhancing presynaptic/postsynaptic
inhibition through a specific BZD receptor which
is an integral part of the GABAA receptor–Cl¯
channel complex.
31. The most common side-effects of benzodiazepines
are related to their sedating and muscle-relaxing
action.
drowsiness, dizziness, and decreased alertness and
concentration.
Lack of coordination may result in falls and injuries.
Hypotension and suppressed breathing.
changes in appetite, blurred vision, confusion,
euphoria, depersonalization and nightmares
irritability and suicidal behavior sometimes occur
32. Pregnancy-
risk of cleft palate.
The symptoms include tremors, hypertonia,
hyperreflexia, hyperactivity, and vomiting and may
last for up to three to six months.
Elderly-
Effects such as memory problems
daytime sedation
impaired motor coordination
and increased risk of motor vehicle accidents and
falls
and an increased risk of hip fractures.
33. Diazepam, a benzodiazepine, generates the same active
metabolite as chlordiazepoxide and clorazepate.
Diazepam appears to act on parts of the limbic system,
the thalamus and hypothalamus, and induces calming
effects.
VALIUM 2, 5, 10 mg tab., 10 mg/2 ml inj.
CALMPOSE 5, 10 mg tab, 2 mg/5 ml syr, 10 mg/2 ml
inj.
34. Benzodiazepines bind nonspecifically to
benzodiazepine receptors which mediate sleep,
affects muscle relaxation, anticonvulsant activity,
motor coordination, and memory.
As benzodiazepine receptors are thought to be
coupled to gamma-aminobutyric acid-A (GABAA)
receptors, this enhances the effects of GABA by
increasing GABA affinity for the GABA receptor.
Binding of GABA to the site opens the chloride
channel, resulting in a hyperpolarized cell membrane
that prevents further excitation of the cell.
35. It Produces an active metabolite which has a long t½,
residual effects are likely next morning; cumulation
occurs on daily ingestion peaking after 3–5 days;
suitable for patients who have frequent nocturnal
awakenings.
NINDRAL, FLURAZ 15 mg cap.
36. Nitrazepam is a type of benzodiazepine drug. It is
a powerful hypnotic drug which possesses strong
sedative, anxiolytic, amnestic, anticonvulsant, and
skeletal muscle relaxant properties. Nitrazepam
shortens the time required to fall asleep and
lengthens the duration of sleep. It is also useful
for the management of myoclonic seizures.
SEDAMON, HYPNOTEX, NITRAVET 5 mg tab.,
5, 10 mg cap.
37. Nitrazepam belongs to a group of medicines called
benzodiazepines. It acts on benzodiazepine receptors
in the brain which are associated with the GABA
receptors causing an enhanced binding of GABA
(gamma amino butyric acid) to GABAA receptors.
GABA is a major inhibitory neurotransmitter in the
brain, involved in inducing sleepiness, muscular
relaxation and control of anxiety and fits, and slows
down the central nervous system.
38. The anticonvulsant properties of nitrazepam and
other benzodiazepines may be in part or entirely due
to binding to voltage-dependent sodium channels
rather than benzodiazepine receptors. Sustained
repetitive firing seems to be limited by
benzodiazepines effect of slowing recovery of
sodium channels from inactivation
39. Alprazolam, a benzodiazepine, is used to treat panic
disorder and anxiety disorder. Unlike chlordiazepoxide,
clorazepate, and prazepam, alprazolam has a shorter
half-life and metabolites with minimal activity.
DOSAGE
0.25 to 0.5 mg orally administered 3 times a day
Maximum dose: 4 mg orally administered in divided
doses
40. It is an intermediate acting BZD.
Absorption is slow in case of tablet but fast when
used in soft gelatin capsule. Good for sleep onset
difficulty, free of residual effects. Accumulation can
occur on daily ingestion.
DOSAGE
7.5 to 30 mg orally once a day at bedtime
-In transient insomnia, a 7.5 mg dose may be
sufficient to improve sleep latency.
-In elderly or debilitated patients, therapy should
be initiated at 7.5 mg until individual responses are
determined.
41. Temazepam produces CNS
depression at limbic, thalamic,
and hypothalamic levels of the
CNS. Temazepam increases the
affinity of the neurotransmitter
gamma-aminobutyric acid
(GABA) for GABA receptors by
binding to benzodiazepine
receptors. Results are sedation,
hypnosis, skeletal muscle
relaxation, anticonvulsant activity,
and anxiolytic action.
42. Chlordiazepoxide-
Chlordiazepoxide has antianxiety, sedative,
appetite-stimulating and weak analgesic
actions. The drug seems to block EEG
arousal from stimulation in the brain stem
reticular formation. The drug has been
studied extensively in many species of
animals and these studies are suggestive of
action on the limbic system of the brain,
which recent evidence indicates is involved
in emotional responses.
43. Mild to moderate anxiety: 5 or 10 mg orally, 3 or 4
times per day
Severe anxiety: 20 or 25 mg orally, 3 or 4 times per
day
44. Chlordiazepoxide binds to stereospecific
benzodiazepine (BZD) binding sites on GABA
receptor complexes at several sites within the central
nervous system, including the limbic system and
reticular formation. This results in an increased
binding of the inhibitory neurotransmitter GABA to
the GABA receptor.
BZDs, therefore, enhance GABA-mediated chloride
influx through GABA receptor channels, causing
membrane hyperpolarization. The net neuro-
inhibitory effects result in the observed sedative,
hypnotic, anxiolytic, and muscle relaxant properties
45. Oxazepam is believed to stimulate GABA receptors
in the ascending reticular activating system. Since
GABA is inhibitory, receptor stimulation increases
inhibition and blocks both cortical and limbic arousal
following stimulation of the brain stem reticular
formation.
DOSAGE
10 to 15 mg, 3 or 4 times daily
46. Similar to other benzodiazepines, oxazepam exerts its
anxiolytic effects by potentiating the effect of
gamma-aminobutyric acid (GABA) on GABA-A
receptors through a cooperative mechanism of action.
Benzodiazepine binding increases chloride
conductance in the presence of GABA by increasing
the frequency at which the channel opens. In contrast,
barbiturates increase chloride conductance in the
presence of GABA by prolonging the time in which
the channel remains open.
47. The α2 subunit of the α2β3γ2 receptor complex is
thought to mediate anxiolytic effects while the α1
subunit of the α1β2γ2 receptor complex is thought to
mediate sedative, anticonvulsant and anterograde
amnesia effects
48. Lorazepam, a benzodiazepine not transformed to
active metabolites, is used to treat anxiety, status
epilepticus, and for sedation induction and
anterograde amnesia.
DOSAGE
Initial dose: 2 to 3 mg orally per day administered 2
to 3 times per day
Maintenance dose: 1 to 2 mg orally 2 to 3 times a day
Parenteral:
IV: 2 mg total, or 0.044 mg/kg, whichever is smaller
49. Clonazepamam
Clonazepam, a benzodiazepine, is used primarily as
an anticonvulsant in the treatment of absence
seizures, petit mal variant seizures akinetic and
myoclonic seizures, and nocturnal myoclonus
50. 1.5 mg orally per day divided into 3 doses; this may be
increased in increments of 0.5 mg to 1 mg every 3 days
until seizures are adequately controlled or until side
effects preclude any further increase.
Maximum dose: 20 mg orally per day
51. Zopiclone
This newer cyclopyrrolone hypnotic is an agonist at a
subtype of BZD receptor involved in the hypnotic
action. The effect on sleep resemble those of BZDs,
but it does not alter REM sleep and tends to prolong
stages 3 and 4.
DOSAGE
ZOPITRAN, ZOPICON, ZOLIUM, 7.5 mg tab, one
tab at bedtime for not more than 2–4 weeks (elderly
3.75 mg).
52. Zopiclone exerts its action by binding on the
benzodiazepine receptor complex and
modulation of the GABABZ receptor chloride
channel macromolecular complex.
53. Zolpidem is a sedative or hypnotic agent
zolpidem in vitro binds the (alpha1) receptor
preferentially. The (alpha1) receptor is found
primarily on the Lamina IV of the sensorimotor
cortical regions, substantia nigra (pars reticulata),
cerebellum molecular layer, olfactory bulb, ventral
thalamic complex, pons, inferior colliculus, and
globus pallidus.
DOSAGE
NITREST, ZOLDEM, DEM 5, 10 mg tabs.
54. This is the shortest acting of the newer non-BZD
hypnotics
It interacts with the gamma-aminobutyric acid-
benzodiazepine (GABABZ) receptor complex.
Subunit modulation of the GABABZ receptor
chloride channel macromolecular complex is
hypothesized to be responsible for some of the
pharmacological properties of benzodiazepines,
which include sedative, anxiolytic, muscle relaxant,
and anticonvulsive effects in animal models.
DOSAGE
Dose: 5–10 mg (max 20 mg) at bed time.
ZAPLON, ZALEP, ZASO 5, 10 mg tabs.
55. Do not mix intravenous drugs in solution with any
other drugs to avoid potential drug-drug interactions.
Taper dose as ordered because abrupt withdrawal can
precipitate seizure attacks.
Provide comfort measures (e.g. small, frequent meals,
access to bathroom facilities, orientation, etc.) to help
patient tolerate drug effects Provide safety measures
(e.g. adequate lighting, raised side rails, etc.) to
prevent injuries.
Educate client on drug therapy to promote
compliance.
56. Monitor patient response to therapy (e.g. controlled
anxiety, sleep, etc).
Monitor for adverse effects (e.g. hypotension,
dependence, hepatorenal dysfunction, etc).
Evaluate patient understanding on drug therapy by
asking patient to name the drug, its indication, and
adverse effects to watch for.
Monitor patient compliance to drug therapy.