ANXIOLYTICS (1).pptx
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Sedatives and hypnotics act on the GABA receptor to produce calming and sleep effects. Sedatives relieve anxiety with little effect on other functions, while hypnotics produce drowsiness and promote sleep. Both show dose-dependent central nervous system depression. Major groups include barbiturates and benzodiazepines. These drugs bind to GABA receptors and enhance the effects of the inhibitory neurotransmitter GABA, resulting in sedation, hypnosis, anesthesia, anticonvulsant, and other effects. However, they also carry risks of tolerance, dependence, and side effects like drowsiness if misused.
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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 Barbiturates were previously widely used as sedatives, hypnotics and anticonvulsants but have been replaced by benzodiazepines due to their lower risk of overdose, dependence and withdrawal symptoms.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
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Sedatives and hypnotics are central nervous system depressants that can calm or soothe the nervous system. Sedatives reduce nervousness and irritability without causing sleep, while hypnotics cause sleep. Sedative-hypnotics can have sedative effects at low doses and hypnotic effects at high doses. Barbiturates were commonly used as sedative-hypnotics but have been replaced in large part by benzodiazepines due to safety and efficacy concerns. Both classes work by inhibiting activity in the brain stem and cerebral cortex.
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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
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Central nervous system (CNS) depressants are drugs that reduce nervousness, excitability, and irritability without causing sleep at low doses, or that cause sleep at high doses. There are two main types: sedatives, which calm the CNS, and hypnotics, which induce sleep. Common sedative-hypnotics are barbiturates and benzodiazepines. Barbiturates have a narrow therapeutic index and can cause respiratory depression in overdose. Benzodiazepines are more commonly prescribed due to their favorable side effects, efficacy, and safety compared to barbiturates. Nursing implications for CNS depressants include monitoring for side effects and ensuring patient safety.
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Central nervous system (CNS) depressants are drugs that reduce nervousness, excitability, and irritability without causing sleep. They include sedatives and hypnotics. Sedatives calm the CNS without inducing sleep, while hypnotics calm the CNS enough to cause sleep. Barbiturates were commonly used as sedative-hypnotics but have been replaced by benzodiazepines, which have more favorable side effects and safety profiles. Both can cause drowsiness, respiratory depression, and interactions with other CNS depressants like alcohol. Nurses must monitor patients taking these drugs for therapeutic effects and side effects.
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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.
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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).
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Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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- 2. Anxiolytic/Sedative: Agent that relieves anxiety and exert a calming effect with little or no effect on motor or mental functions. Hypnotics: It produce drowsiness and encourage the onset and maintenance of state of sleep. Hypnotics have more CNS depressant actions than Sedatives.
- 3. All sedatives/hypnotics show graded dose dependent CNS depression Barbiturates have linear relationship. Benzodiazepines have nonlinear relationship.
- 4. Antipsychotics Antihistamines Antidepressants They are sedatives but have marked effects on autonomic system Didnot produce General Anesthesia No Abuse liability.
- 5. Two Major Groups Barbiturates(Older) Benzodiazepines(Newer) Others: Zolpidem,Buspirone,Zalepion,Meprobamat e,chloral hydrate,glutethimide,alcohols
- 6. Benzodiazepines: Barbiturates: Diazepam Pentobarbital Chlordiazepoxide Phenobarbital Flurazepam Secobarbital Lorazepam Triazolam Alprazolam
- 7. Benzodiazepines: Oral absorption Hepatic Metabolism Renal excretion Slow Redistribution Can form Active Metabolites Like: Chlordiazepoxide,diazepam,prazepam,Cloraze pate,Flurazepam……………Cumulative effects
- 8. Barbiturates: No Active Metabolites Fast Redistribution Elimination half lives of some are longer Cause enzyme induction in Liver
- 9. All sedatives and hypnotics Cross the Placental Barrier.
- 10. They bind to GABA A receptor It is a ionotropic transmembrane protein that functions as chloride channel, is activated by the inhibitory neurotransmittter GABA. Receptor is a Pentameric structure Three subunits are important: Alpha, Beta and Gamma
- 11. Benzodiazepines potentiate GABAergic inhibition via membrane hyperpolarization, They enhance Gabaergic effects without directly activating GABA receptor. They increase the frequency of chloride channel opening whereas the barbiturates increase the duration of channel opening. Barbiturates also effect other excitatory neurotansmitters so induce surgical Anesthesia and have greater adverse effects.
- 13. Sedation Hypnosis General Anesthesia Anticonvulsant Muscle Relaxation Respiratory and Cardiovascular Depression
- 14. REM:25% dreams NREM:70-75% four stages 50% sleep in stage two Fourth stage;night terror Hypnotics decrease onset of sleep Decrease REM sleep Increase stage 2 of NREM Decrease 4 stage of NREM
- 15. Barbiturates cause Surgical Anesthesia e.g., Thiopental,Methohexital Benzodiazepines are used as Preanesthetic medications but cannot cause surgical Anesthesia
- 16. Tolerance Psychologic Dependance Physiologic Dependence
- 17. Anxiety states Sleep disorders As Pre-anesthetic Medication Pre procedure(Endoscopy,Bronchoscopy) Mania(Initial Management) Drug induced hyper excitability Major Depressive Episode(Alprazolam)
- 18. CNS depression Drowsiness Impaired judgement Impaired driving Anterograde Amnesia(inability to remember the events during drug’s action) Hangover Confusion Teratogenic effects Hypersensitivity
- 19. Antagonists: Flumazenil Inverse Agonist:Negative allosteric modulator of GABA receptor e,g: Beta Carboline
- 20. Only available benzodiazepine receptor antagonist Indication: Benzodiazepine overdose Anesthesia speedy recovery Blocks only actions of benzodiazepines and imidazopyridine Can cause Precipitated Abstinence Syndrome