The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
This document discusses pharmacological aspects of pain management. It provides definitions of pain, describes the different types of pain (nociceptive and neuropathic), and outlines the normal pain pathways and sites where analgesics can act in the body. It then categorizes and discusses various classes of analgesics including opioids, NSAIDs, local anesthetics, anticonvulsants, antidepressants, and others. Specific opioid drugs like morphine, fentanyl, oxycodone, and others are also summarized in terms of their pharmacology, mechanisms of action, and use in pain management.
This document discusses various classes of opioid and nonopioid analgesics, including strong opioids like morphine and fentanyl, moderate opioids like codeine, and mixed agonist-antagonists like buprenorphine. It also covers nonopioid classes such as NSAIDs, TCAs, and antiepileptics used for pain treatment. Key points include the three opioid receptor families, uses of naloxone and naltrexone, signs of opioid overdose and withdrawal, and treatment of acute and chronic pain with different classes of analgesics.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
The document discusses various classes of analgesics including opioids, adjuvant analgesics, and NSAIDs that are used to treat different levels of pain. It describes different opioid medications including natural and synthetic opioids, how they work on opioid receptors in the body, and their uses, benefits, risks, and nursing considerations for administration and monitoring. The goal of pain management is to effectively treat pain while minimizing risks and improving patient quality of life.
The document discusses various opioid analgesics including their mechanisms of action, effects, and therapeutic uses. It describes how opioids like morphine and pethidine work in the central nervous system to provide analgesia and other effects through binding to mu, kappa, and delta opioid receptors. It also covers the pharmacokinetics, indications, adverse effects and classifications of different opioid drugs.
Opioid analgesic.pptx by dr.nadira sultanaainnasultana
This document discusses various opioid analgesic drugs, including both natural and synthetic opioids. It describes how opioids act through mu, kappa, and delta opioid receptors in the central nervous system and peripheral tissues to produce analgesia, respiratory depression, and other effects. The document categorizes common opioids like morphine, codeine, heroin, pethidine, fentanyl, methadone, and tramadol. For each opioid, it provides details on pharmacological effects, metabolism, excretion, preparations, doses, uses, and adverse drug reactions.
The document discusses opioid analgesics and their mechanisms of action, receptors, endogenous opioids, and examples like morphine, codeine, pethidine. It summarizes their pharmacokinetics, pharmacodynamics, uses, adverse effects, interactions, and contraindications. The three major classes of opioid receptors are mu, kappa, and delta, which are G-protein coupled receptors located in the CNS and peripheral nerves. Opioids can act as agonists, antagonists, or mixed agonist-antagonists at these receptors. Tolerance and dependence develop with repeated use of opioids.
This document summarizes key information about opioid analgesics including:
1. It classifies opioids based on their strength from strong to weak and lists examples in each category.
2. It outlines several clinical uses of opioids such as for analgesia, cough suppression, and treatment of opioid dependence.
3. It describes the pharmacokinetics of opioids including absorption, metabolism, and ability to cross the placental barrier and affect fetuses.
4. It explains the mechanism of action of opioids including their binding to μ, δ, and κ receptors in the brain and spinal cord to produce effects like analgesia and respiratory depression.
This document discusses pharmacological aspects of pain management. It provides definitions of pain, describes the different types of pain (nociceptive and neuropathic), and outlines the normal pain pathways and sites where analgesics can act in the body. It then categorizes and discusses various classes of analgesics including opioids, NSAIDs, local anesthetics, anticonvulsants, antidepressants, and others. Specific opioid drugs like morphine, fentanyl, oxycodone, and others are also summarized in terms of their pharmacology, mechanisms of action, and use in pain management.
This document discusses various classes of opioid and nonopioid analgesics, including strong opioids like morphine and fentanyl, moderate opioids like codeine, and mixed agonist-antagonists like buprenorphine. It also covers nonopioid classes such as NSAIDs, TCAs, and antiepileptics used for pain treatment. Key points include the three opioid receptor families, uses of naloxone and naltrexone, signs of opioid overdose and withdrawal, and treatment of acute and chronic pain with different classes of analgesics.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
The document discusses various classes of analgesics including opioids, adjuvant analgesics, and NSAIDs that are used to treat different levels of pain. It describes different opioid medications including natural and synthetic opioids, how they work on opioid receptors in the body, and their uses, benefits, risks, and nursing considerations for administration and monitoring. The goal of pain management is to effectively treat pain while minimizing risks and improving patient quality of life.
The document discusses various opioid analgesics including their mechanisms of action, effects, and therapeutic uses. It describes how opioids like morphine and pethidine work in the central nervous system to provide analgesia and other effects through binding to mu, kappa, and delta opioid receptors. It also covers the pharmacokinetics, indications, adverse effects and classifications of different opioid drugs.
Opioid analgesic.pptx by dr.nadira sultanaainnasultana
This document discusses various opioid analgesic drugs, including both natural and synthetic opioids. It describes how opioids act through mu, kappa, and delta opioid receptors in the central nervous system and peripheral tissues to produce analgesia, respiratory depression, and other effects. The document categorizes common opioids like morphine, codeine, heroin, pethidine, fentanyl, methadone, and tramadol. For each opioid, it provides details on pharmacological effects, metabolism, excretion, preparations, doses, uses, and adverse drug reactions.
The document discusses opioid analgesics and their mechanisms of action, receptors, endogenous opioids, and examples like morphine, codeine, pethidine. It summarizes their pharmacokinetics, pharmacodynamics, uses, adverse effects, interactions, and contraindications. The three major classes of opioid receptors are mu, kappa, and delta, which are G-protein coupled receptors located in the CNS and peripheral nerves. Opioids can act as agonists, antagonists, or mixed agonist-antagonists at these receptors. Tolerance and dependence develop with repeated use of opioids.
This document summarizes key information about opioid analgesics including:
1. It classifies opioids based on their strength from strong to weak and lists examples in each category.
2. It outlines several clinical uses of opioids such as for analgesia, cough suppression, and treatment of opioid dependence.
3. It describes the pharmacokinetics of opioids including absorption, metabolism, and ability to cross the placental barrier and affect fetuses.
4. It explains the mechanism of action of opioids including their binding to μ, δ, and κ receptors in the brain and spinal cord to produce effects like analgesia and respiratory depression.
Opioids are drugs that bind to opioid receptors in the brain and body to produce analgesic, sedative, and euphoric effects. They have been used for thousands of years to relieve pain and induce euphoria. Natural opioids are found in opium from the poppy plant, while semi-synthetic and synthetic opioids are derived from morphine or synthesized. The three main opioid receptor types are mu, kappa, and delta, with mu receptors primarily responsible for analgesia, respiratory depression, and euphoria. Common opioids include morphine, codeine, oxycodone, fentanyl, methadone, and heroin. Tolerance and dependence develop with prolonged use.
Opioids are drugs that bind to opioid receptors in the central nervous system to relieve pain. This document discusses the clinical pharmacology of opioids including their mechanisms of action, types, and effects. It describes natural opioids like morphine and codeine derived from opium, semi-synthetic opioids created from modifications to natural opioids, and fully synthetic opioids like fentanyl. The document outlines how different opioids act on mu, kappa, and delta receptors to produce analgesia and other effects. It also covers the pharmacokinetics, indications, and side effects of various opioids.
opioid analgesics with detailed description of introduction, mechanism of action, adverse effect, uses and contraindication along with examples for under graduates.
This slide deck give detail presentation on Analgesic, Anti-inflammatory & Anti-pyretic drugs |Narcotic analgesics | Non-steroidal anti-inflammatory drugs (NSAID'S)
For all Five video lecture series of this topic click:
https://youtube.com/playlist?list=PLBVbJ9HCa1BZtDY4oTVu7zPXlvY2gqiZY
- For More Such Learning You Can Subscribe to My YouTube Channel.
https://www.youtube.com/channel/UC5o-WkzmDJaF7udyAP2jtgw/featured?sub_confirmation=1
Facebook Page: https://www.facebook.com/asacademylearningforever
Website Blog: https://itasacademy.blogspot.com/
The document discusses opium and its derivatives that are used as pain medications. It begins by explaining that opium is obtained from the poppy plant and describes the basic process of pain signaling in the nervous system. It then focuses on opioids like morphine, codeine, heroin, and other synthetic opioids. It covers topics like how opioids work in the body by binding to opioid receptors, their uses as analgesics, side effects, dependence and withdrawal, important terminology, and interactions with other drugs.
Opioids are analgesics that relieve pain by stimulating mu, kappa, and delta opioid receptors in the brain and spinal cord. Morphine is a naturally occurring opioid that is commonly used to treat severe acute pain such as that from burns, fractures, cancer, or myocardial infarction. Morphine acts by producing analgesia, sedation, respiratory depression, constipation, and can lead to physical and psychological dependence with long term use. Adverse effects of morphine include vomiting, respiratory depression, constipation, itching, and the development of tolerance. Naloxone is used as an antidote for morphine overdose.
This document summarizes opioids and their use as analgesics. It discusses:
1. The classification of opioids including natural alkaloids like morphine and codeine, semi-synthetic opioids like heroin, and synthetic opioids like fentanyl and methadone.
2. The mechanism of action of opioids, which involves binding to mu, kappa, and delta opioid receptors in the central nervous system.
3. Important opioids like morphine, codeine, fentanyl, methadone, and tramadol as well as mixed agonist-antagonists and opioid antagonists.
Opioids and opiates act on mu, kappa, and delta opioid receptors throughout the body and brain. Mu receptors are responsible for analgesia, respiratory depression, and euphoria, making overdose dangerous. Chronic use can increase tolerance and risk of overdose. While prescription opioids started the current crisis, many users transition to highly dangerous illegal opioids like fentanyl and fentanyl analogs. Naloxone is used to treat overdoses but very potent synthetic opioids require high doses or continuous infusion.
Opioid analgesics work by binding to opioid receptors in the brain and spinal cord to reduce pain. There are several types of opioid receptors that endogenous opioid peptides and exogenous opioids can bind to, including mu, delta, and kappa receptors. Opioids are well absorbed orally or parenterally and distributed widely throughout the body. They are metabolized in the liver mainly by conjugation with glucuronic acid and excreted in urine. Opioids produce analgesia, sedation, respiratory depression, nausea, vomiting, and constipation by acting on central and peripheral opioid receptors. Tolerance and physical dependence may develop with repeated use.
The document discusses drug treatment of pain, outlining the goals of understanding pain pathways and classifications of analgesics like narcotic and non-narcotic drugs. It covers topics like peripheral and central pain mechanisms in the body, the role of the brain in pain perception, types of acute and chronic pain, and mechanisms of pain relief through drugs that act on opioid receptors in the nervous system. The document provides details on classification and examples of opioid analgesics, including their actions on mu, delta, and kappa opioid receptors in the body.
Opiod analgesics used in Dentistry by Dr. Amit T. Suryawanshi
(MDS) Facial Cosmetic Surgeon
Oral & Maxillofacial Surgeon
Dental Surgeon & Implantologist
Hair Transplant Surgeon (Germany)
Consulting Surgeon in Kolhapur, Sangli, Pune & Mumbai (India)
&
founder of
Face Art International Super speciality
at Kolhapur (India)
Opioid use disorder is classified in the DSM-5 and involves misuse or addiction to natural or synthetic opioids. Opioid use disorder has high rates of psychiatric and medical comorbidity. Treatment involves detoxification through tapering or rapid methods, followed by maintenance therapies like methadone or buprenorphine. Psychosocial treatments help prevent relapse and include support groups, cognitive behavioral therapy, and vocational programs. Carefully monitored medical maintenance with opioid agonists is effective long-term management for opioid use disorder.
This document discusses different types of pain medications, including opioids. It describes various opioid drugs like morphine, codeine, heroin, methadone, fentanyl, and others. It explains how opioids work by binding to mu, delta, and kappa receptors in the central nervous system and periphery. Tolerance and dependence are noted as issues with long-term opioid use. Guidelines are provided for using different opioids to treat mild, moderate, and severe acute and chronic pain according to the World Health Organization.
The document discusses several newer narcotics including their origin, pharmacological properties, medical uses, and risks of abuse. Opium is obtained from the opium poppy and contains morphine along with other alkaloids. Morphine can be processed chemically to produce semi-synthetic opioids like levorphanol, an potent analgesic also used to reduce anaesthetic doses. Meperidine is a synthetic opioid analgesic with a toxic metabolite that can accumulate and cause seizures. Fentanyl is a very potent synthetic opioid related to phenylpiperidines. Sufentanil and remifentanil are even more potent synthetic opioids used in anesthesia. Methadone is an orally active opioid used to treat opioid
Opioid analgesics are the important group of medications used in pain management. The present seminar has been prepared by referring to standard textbooks of pharmacology and presented point wise for easy understanding.
The document discusses various aspects of opioid drugs including their classification, mechanisms of action, effects, and uses. It describes the different opioid receptor types (mu, kappa, delta) and their endogenous ligands. It provides details on natural and synthetic opioid agonists, partial agonists, and antagonists; their pharmacokinetics, metabolism, and indications. The document also covers opioid tolerance, dependence, withdrawal, intoxication and effects on various body systems.
This document summarizes opioids and their classification, mechanisms of action, and effects. Opioids are compounds that bind to opioid receptors in the central nervous system to produce morphine-like analgesic effects. The three main opioid receptor types are mu, kappa, and delta, which have different selectivities for opioids. Opioids relieve pain by altering pain perception in the brain and spinal cord. Common side effects include respiratory depression, constipation, and euphoria. Opioid antagonists like naloxone can reverse the effects of opioid overdose.
This document provides information on opioids and their use as analgesics. It begins by defining analgesics as any drug used to relieve pain and classifies them as opioids, NSAIDs, or paracetamol. Opioids act on opioid receptors in the brain and nervous system to produce morphine-like pain relief effects. Both natural and synthetic opioids are discussed. The document outlines the historical use of opium from the opium poppy and how semi-synthetic and synthetic opioids are derived from natural opiates. It also discusses how opioids work by binding to opioid receptors in the brain and nervous system to reduce pain transmission. Different classifications of opioids are presented including source, chemical structure, strength, and effects on opioid receptor subtypes. Common
This document summarizes the history and classification of opioids. It discusses how opioids were first extracted from poppy seeds in ancient times and used medicinally. In the 19th century, morphine was isolated and the hypodermic needle was invented, leading to increased drug abuse. Opioids are classified as natural alkaloids like morphine and codeine, semisynthetic drugs derived from morphine like heroin, and fully synthetic drugs like fentanyl. The document describes several common opioids, their mechanisms of action via opioid receptors, and their therapeutic uses and side effects.
This document discusses emerging trend drugs according to reports from 2015. It notes that the National Institute on Drug Abuse and Community Epidemiology Work Group monitor drug trends across cities. Their 2015 report found that the most popular drugs included fentanyl, heroin, synthetic marijuana ("Spice" and "K2"), suboxone, and bath salts. Each drug is described, including its intended medical use versus popular street use. A quote from a police sergeant questions why new pain medications are developed when existing drugs are already overprescribed and fueling addiction.
K2, also known as synthetic cannabis, is a dangerous drug that mimics the effects of THC. It is made from man-made chemicals sprayed onto plant material. While it is marketed as a safe alternative to cannabis, K2 can cause unpredictable and severe side effects like hallucinations, anxiety, seizures, and even death. Usage of K2 has risen in recent years among young people due to its cheap price and inability to be detected in drug tests. However, health experts warn that K2 is not safe and can lead to serious short- and long-term health problems.
Opioids are drugs that bind to opioid receptors in the brain and body to produce analgesic, sedative, and euphoric effects. They have been used for thousands of years to relieve pain and induce euphoria. Natural opioids are found in opium from the poppy plant, while semi-synthetic and synthetic opioids are derived from morphine or synthesized. The three main opioid receptor types are mu, kappa, and delta, with mu receptors primarily responsible for analgesia, respiratory depression, and euphoria. Common opioids include morphine, codeine, oxycodone, fentanyl, methadone, and heroin. Tolerance and dependence develop with prolonged use.
Opioids are drugs that bind to opioid receptors in the central nervous system to relieve pain. This document discusses the clinical pharmacology of opioids including their mechanisms of action, types, and effects. It describes natural opioids like morphine and codeine derived from opium, semi-synthetic opioids created from modifications to natural opioids, and fully synthetic opioids like fentanyl. The document outlines how different opioids act on mu, kappa, and delta receptors to produce analgesia and other effects. It also covers the pharmacokinetics, indications, and side effects of various opioids.
opioid analgesics with detailed description of introduction, mechanism of action, adverse effect, uses and contraindication along with examples for under graduates.
This slide deck give detail presentation on Analgesic, Anti-inflammatory & Anti-pyretic drugs |Narcotic analgesics | Non-steroidal anti-inflammatory drugs (NSAID'S)
For all Five video lecture series of this topic click:
https://youtube.com/playlist?list=PLBVbJ9HCa1BZtDY4oTVu7zPXlvY2gqiZY
- For More Such Learning You Can Subscribe to My YouTube Channel.
https://www.youtube.com/channel/UC5o-WkzmDJaF7udyAP2jtgw/featured?sub_confirmation=1
Facebook Page: https://www.facebook.com/asacademylearningforever
Website Blog: https://itasacademy.blogspot.com/
The document discusses opium and its derivatives that are used as pain medications. It begins by explaining that opium is obtained from the poppy plant and describes the basic process of pain signaling in the nervous system. It then focuses on opioids like morphine, codeine, heroin, and other synthetic opioids. It covers topics like how opioids work in the body by binding to opioid receptors, their uses as analgesics, side effects, dependence and withdrawal, important terminology, and interactions with other drugs.
Opioids are analgesics that relieve pain by stimulating mu, kappa, and delta opioid receptors in the brain and spinal cord. Morphine is a naturally occurring opioid that is commonly used to treat severe acute pain such as that from burns, fractures, cancer, or myocardial infarction. Morphine acts by producing analgesia, sedation, respiratory depression, constipation, and can lead to physical and psychological dependence with long term use. Adverse effects of morphine include vomiting, respiratory depression, constipation, itching, and the development of tolerance. Naloxone is used as an antidote for morphine overdose.
This document summarizes opioids and their use as analgesics. It discusses:
1. The classification of opioids including natural alkaloids like morphine and codeine, semi-synthetic opioids like heroin, and synthetic opioids like fentanyl and methadone.
2. The mechanism of action of opioids, which involves binding to mu, kappa, and delta opioid receptors in the central nervous system.
3. Important opioids like morphine, codeine, fentanyl, methadone, and tramadol as well as mixed agonist-antagonists and opioid antagonists.
Opioids and opiates act on mu, kappa, and delta opioid receptors throughout the body and brain. Mu receptors are responsible for analgesia, respiratory depression, and euphoria, making overdose dangerous. Chronic use can increase tolerance and risk of overdose. While prescription opioids started the current crisis, many users transition to highly dangerous illegal opioids like fentanyl and fentanyl analogs. Naloxone is used to treat overdoses but very potent synthetic opioids require high doses or continuous infusion.
Opioid analgesics work by binding to opioid receptors in the brain and spinal cord to reduce pain. There are several types of opioid receptors that endogenous opioid peptides and exogenous opioids can bind to, including mu, delta, and kappa receptors. Opioids are well absorbed orally or parenterally and distributed widely throughout the body. They are metabolized in the liver mainly by conjugation with glucuronic acid and excreted in urine. Opioids produce analgesia, sedation, respiratory depression, nausea, vomiting, and constipation by acting on central and peripheral opioid receptors. Tolerance and physical dependence may develop with repeated use.
The document discusses drug treatment of pain, outlining the goals of understanding pain pathways and classifications of analgesics like narcotic and non-narcotic drugs. It covers topics like peripheral and central pain mechanisms in the body, the role of the brain in pain perception, types of acute and chronic pain, and mechanisms of pain relief through drugs that act on opioid receptors in the nervous system. The document provides details on classification and examples of opioid analgesics, including their actions on mu, delta, and kappa opioid receptors in the body.
Opiod analgesics used in Dentistry by Dr. Amit T. Suryawanshi
(MDS) Facial Cosmetic Surgeon
Oral & Maxillofacial Surgeon
Dental Surgeon & Implantologist
Hair Transplant Surgeon (Germany)
Consulting Surgeon in Kolhapur, Sangli, Pune & Mumbai (India)
&
founder of
Face Art International Super speciality
at Kolhapur (India)
Opioid use disorder is classified in the DSM-5 and involves misuse or addiction to natural or synthetic opioids. Opioid use disorder has high rates of psychiatric and medical comorbidity. Treatment involves detoxification through tapering or rapid methods, followed by maintenance therapies like methadone or buprenorphine. Psychosocial treatments help prevent relapse and include support groups, cognitive behavioral therapy, and vocational programs. Carefully monitored medical maintenance with opioid agonists is effective long-term management for opioid use disorder.
This document discusses different types of pain medications, including opioids. It describes various opioid drugs like morphine, codeine, heroin, methadone, fentanyl, and others. It explains how opioids work by binding to mu, delta, and kappa receptors in the central nervous system and periphery. Tolerance and dependence are noted as issues with long-term opioid use. Guidelines are provided for using different opioids to treat mild, moderate, and severe acute and chronic pain according to the World Health Organization.
The document discusses several newer narcotics including their origin, pharmacological properties, medical uses, and risks of abuse. Opium is obtained from the opium poppy and contains morphine along with other alkaloids. Morphine can be processed chemically to produce semi-synthetic opioids like levorphanol, an potent analgesic also used to reduce anaesthetic doses. Meperidine is a synthetic opioid analgesic with a toxic metabolite that can accumulate and cause seizures. Fentanyl is a very potent synthetic opioid related to phenylpiperidines. Sufentanil and remifentanil are even more potent synthetic opioids used in anesthesia. Methadone is an orally active opioid used to treat opioid
Opioid analgesics are the important group of medications used in pain management. The present seminar has been prepared by referring to standard textbooks of pharmacology and presented point wise for easy understanding.
The document discusses various aspects of opioid drugs including their classification, mechanisms of action, effects, and uses. It describes the different opioid receptor types (mu, kappa, delta) and their endogenous ligands. It provides details on natural and synthetic opioid agonists, partial agonists, and antagonists; their pharmacokinetics, metabolism, and indications. The document also covers opioid tolerance, dependence, withdrawal, intoxication and effects on various body systems.
This document summarizes opioids and their classification, mechanisms of action, and effects. Opioids are compounds that bind to opioid receptors in the central nervous system to produce morphine-like analgesic effects. The three main opioid receptor types are mu, kappa, and delta, which have different selectivities for opioids. Opioids relieve pain by altering pain perception in the brain and spinal cord. Common side effects include respiratory depression, constipation, and euphoria. Opioid antagonists like naloxone can reverse the effects of opioid overdose.
This document provides information on opioids and their use as analgesics. It begins by defining analgesics as any drug used to relieve pain and classifies them as opioids, NSAIDs, or paracetamol. Opioids act on opioid receptors in the brain and nervous system to produce morphine-like pain relief effects. Both natural and synthetic opioids are discussed. The document outlines the historical use of opium from the opium poppy and how semi-synthetic and synthetic opioids are derived from natural opiates. It also discusses how opioids work by binding to opioid receptors in the brain and nervous system to reduce pain transmission. Different classifications of opioids are presented including source, chemical structure, strength, and effects on opioid receptor subtypes. Common
This document summarizes the history and classification of opioids. It discusses how opioids were first extracted from poppy seeds in ancient times and used medicinally. In the 19th century, morphine was isolated and the hypodermic needle was invented, leading to increased drug abuse. Opioids are classified as natural alkaloids like morphine and codeine, semisynthetic drugs derived from morphine like heroin, and fully synthetic drugs like fentanyl. The document describes several common opioids, their mechanisms of action via opioid receptors, and their therapeutic uses and side effects.
This document discusses emerging trend drugs according to reports from 2015. It notes that the National Institute on Drug Abuse and Community Epidemiology Work Group monitor drug trends across cities. Their 2015 report found that the most popular drugs included fentanyl, heroin, synthetic marijuana ("Spice" and "K2"), suboxone, and bath salts. Each drug is described, including its intended medical use versus popular street use. A quote from a police sergeant questions why new pain medications are developed when existing drugs are already overprescribed and fueling addiction.
K2, also known as synthetic cannabis, is a dangerous drug that mimics the effects of THC. It is made from man-made chemicals sprayed onto plant material. While it is marketed as a safe alternative to cannabis, K2 can cause unpredictable and severe side effects like hallucinations, anxiety, seizures, and even death. Usage of K2 has risen in recent years among young people due to its cheap price and inability to be detected in drug tests. However, health experts warn that K2 is not safe and can lead to serious short- and long-term health problems.
Jay Lance Kovar, MD discusses new synthetic substances like "bath salts" and synthetic marijuana (K2/Spice) that are being abused. These products contain chemicals that mimic drugs like cocaine, ecstasy, and marijuana but their effects are unpredictable and sometimes dangerous, causing issues like psychosis, elevated heart rate and blood pressure, seizures and suicidal behavior. While some states and the DEA have taken steps to ban specific chemicals and products, new versions continue to be produced making them challenging to regulate. Emergency treatment focuses on supportive care for agitation and psychosis until the effects subside.
NMS Labs offers drug testing and analysis services relevant to DRE investigations of synthetic cannabinoids like K2 and Salvia divinorum. Their tests can identify compounds in K2 blends like JWH-018 and metabolites in biological samples. A Missouri study found K2 impaired subjects similarly to cannabis. A Pennsylvania case identified JWH-018 in a driver's blood after smoking "Space". NMS Labs provides sensitive and specific analysis of salvinorin A and B to support DRE examinations involving Salvia.
K2 or Spice is a mixture of herbs and spices sprayed with synthetic compounds similar to THC, the active ingredient in marijuana. It is commonly sold in stores and online as incense or "fake weed" and can be smoked to produce effects similar to marijuana like increased heart rate and feelings of paranoia or giddiness. While no overdoses have been reported, the long-term health effects are unknown. Several synthetic cannabinoids found in K2 were placed in Schedule I of the Controlled Substances Act in 2011, banning their manufacture and sale in the United States. K2 products often originate from China and are sold via websites, with little regulation of ingredients or dosage.
K2 is a synthetic marijuana that causes dangerous health effects like seizures, elevated blood pressure, paranoia, and psychotic behavior when smoked. Reports of K2 overdoses in teens have increased dramatically from 119 calls to poison control in 2009 to over 2,200 calls in 2012. The inventor of K2 warns that using the drug is like "Russian roulette" because very little is known about its effects. The document concludes that K2 is a risky drug and teens should avoid it to prevent potential health problems.
K2, also known as "spice", is a mixture of herbs sprayed with synthetic cannabinoids that is smoked to produce psychoactive effects similar to marijuana. It is often contaminated with toxic and unknown substances which have led to numerous adverse health effects such as seizures, elevated blood pressure, and addiction. While currently legal in most states, there is a push to ban K2 and its chemicals due to growing evidence of its dangers and rising emergency room admissions. The DEA has temporarily scheduled five chemicals found in K2 to curb its use and study whether permanent controls are needed.
Synthetic marijuana, also known as K2 or Spice, is created by spraying synthetic cannabinoids onto legal herbs and sold to mimic the effects of marijuana. The document discusses the chemicals involved like JWH-018, how they were created by researchers to study cannabinoid receptors, unintended consequences of their recreational use, associated health risks, and debates around regulation.
Stereotype Threats’ Influence on Elementary Pre-service Teachers\' Attitude T...lilsnickr
I, along with Dr. Vincent of WSU, researched the stereotype threats pre-service math teachers encountered throughout their education. Through qualitative research we analyzed the testimonials of the students and identified factors that contributed to their attitudes toward mathematics.
This presentation aims to describe and compare the new designer drugs, #KratomEffects or sometimes referred to as "legal highs" (kratom, bath salts and k2, among others) to the opiates and cocaine from the good old days.
Pharmacodynamics and Pharmacokinetics of Synthetic CannabinoidsNMS Labs
Presented on February 21, 2012 at the AAFS 64th Annual Scientific Meeting by Barry K. Logan, PhD, DABFT, NMS Labs National Director of Forensic Services and Wendy R. Adams, Ph.D., DABFT, Forensic Toxicologist
K2 and the Synthetic Cannabinoids: Pharmacology, Effects and Chemical AnalysisNMS Labs
The document discusses K2 and synthetic cannabinoids like JWH-018 and JWH-073. It summarizes their origins, effects, and challenges in analyzing them. Studies found synthetic cannabinoids can cause effects like tachycardia, dry mouth, impaired coordination and concentration. They are difficult to detect but studies found metabolites in blood and urine for hours after use, requiring targeted analysis to identify them in overdose or DUI cases.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
Opioid Analgesics by : Ali ghalib MTU college of Iraqnoipali123
This document discusses opioids and their classification, mechanisms of action, effects, uses, and side effects. It covers the following key points:
1. Opioids are chemical drugs derived from opium that bind to opioid receptors in the human body to relieve and reduce pain. They include morphine, codeine, fentanyl, oxycodone, and others.
2. Opioids are classified based on their receptor binding properties as strong agonists, weak agonists, mixed agonists/antagonists, and antagonists. Agonists activate opioid receptors to relieve pain while antagonists block receptor activation and are used to treat overdoses.
3. Common opioids like morphine,
This document discusses opioid receptors and opioid analgesics. It begins by introducing opioids and their interaction with opioid receptors in the central nervous system and gastrointestinal tract. It then describes the three main types of opioid receptors - mu, kappa, and delta - and their locations in the brain and spinal cord. The document outlines various classes of opioid analgesics and antagonists based on their receptor interactions. It explains the mechanisms of action of opioids like morphine at opioid receptors, including their analgesic, sedative, and other effects. The pharmacokinetics, uses, and adverse effects of representative opioids like morphine and semi-synthetic derivatives are summarized. Finally, the mechanisms and applications of opioid antagonists such as naloxone and naltrexone
This document discusses opioid analgesics and antagonists. It summarizes their mechanisms of action, pharmacology, uses, and side effects. The main points are:
1. Opioid analgesics like morphine act on central and peripheral opioid receptors to provide analgesia, euphoria, sedation, and other effects. They can cause respiratory depression, constipation, and dependence with chronic use.
2. Opioid antagonists like naloxone reverse the effects of opioids by competitively binding opioid receptors. Naloxone is used to treat opioid overdose and neonatal depression from maternal opioid use.
3. Other opioid analgesics discussed include codeine, pethidine, methadone, tra
Analgesics are drugs that relieve pain by acting in the central nervous system or on peripheral pain mechanisms without altering consciousness. There are several types of pain including nociceptive pain caused by tissue damage activating pain receptors, neuropathic pain caused by nerve damage, and idiopathic pain of unknown origin. Analgesics can be classified based on their mechanism of action, source, and receptor activity. Opioids like morphine are potent narcotic analgesics that act centrally while nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen and aspirin reduce inflammation and pain peripherally by inhibiting prostaglandin synthesis.
This document discusses analgesic drugs used in anesthesia, focusing on opioids. It describes how opioids act in the central and peripheral nervous systems to reduce the perception and reaction to pain. Various opioids are classified and their mechanisms of action, pharmacokinetics, clinical uses, and adverse effects are outlined. Morphine, meperidine, and fentanyl are discussed as examples to illustrate differences between opioids commonly used for analgesia.
This document discusses opioid analgesics, also known as narcotic analgesics, which are pain relievers that act on the central nervous system. It defines different types of pain and describes various opioids including their history, pharmacological actions, pharmacokinetics, therapeutic uses, and classification. Opioids such as morphine, codeine, pethidine, methadone, and tramadol are discussed in detail along with endogenous opioid peptides and opioid antagonists such as naloxone, naltrexone, nalorphine, and pentazocine. The document provides an overview of the mechanisms and effects of different opioid receptor stimulation.
clinical pharmacology of opioid analgesics .pptNorhanKhaled15
This document discusses opioids and their use for pain management. It begins by introducing opioids and their mechanisms of action, binding to opioid receptors in the central nervous system. It then discusses the different types of opioid receptors and their distributions in the body. The remainder of the document focuses on specific opioid drugs, including morphine, meperidine, and methadone. It provides details on the pharmacological properties, therapeutic uses, pharmacokinetics, adverse effects, and dependencies associated with each drug.
This document provides an overview of neuropharmacology and various central nervous system agents that act on the brain and spinal cord. It discusses the two main branches of neuropharmacology - behavioural and molecular neuropharmacology. It then covers various drug classes that act on the central nervous system including sedatives/hypnotics like benzodiazepines, barbiturates, and cholinergic drugs. Specific drugs are discussed in terms of their mechanisms of action, indications, dosages, and side effects. The document concludes with nursing responsibilities when administering these central nervous system agents.
Major Neurotransmitters are divided into two types - small rapid acting molecules like acetylcholine, norepinephrine, glutamate, and aspartate that are excitatory, and larger slower acting molecules like GABA, glycine, and dopamine that are inhibitory. Neurotransmitters are involved in various functions in both the central and peripheral nervous systems, and imbalances can lead to conditions like depression, Alzheimer's disease, and Parkinson's disease.
The document discusses opioid analgesics, which are derived from the opium seed and relieve deep seated pain without causing loss of consciousness. It describes the endogenous opioid peptides and their receptors in the brain and spinal cord that regulate pain responsiveness. It provides details on the classification, mechanisms of action, effects and therapeutic uses of various opioid analgesics, including morphine, codeine, heroin, pethidine, fentanyl, and tramadol. It also discusses the treatment of opioid dependence and the use of opioid antagonists like naloxone and naltrexone.
This document discusses various opioid analgesics and antagonists used for pain management. It describes how opioids work by binding to receptors in the central nervous system and periphery to reduce pain transmission. The major opioid receptor types are μ, κ, and δ, with μ receptors mainly responsible for analgesia. Common opioid agonists discussed include morphine, codeine, meperidine, methadone, fentanyl, and heroin. Their mechanisms of action, therapeutic uses, pharmacokinetics, and adverse effects are summarized.
Opioids are medications prescribed to treat severe pain. They work in the brain to reduce pain signals and include drugs derived from opium poppy plants like morphine and heroin. This document discusses the classification, mechanisms of action, indications, and side effects of various opioids and opioid antagonists. It provides details on how different opioid drugs target receptor types in the brain and body to produce analgesic and other effects. The document also summarizes guidelines for using opioids to treat acute and chronic pain conditions.
The document discusses opioid analgesics, including their uses, actions, adverse reactions, contraindications, and precautions. It explains that opioids are used to treat moderate to severe pain according to the WHO pain ladder. Their main action is binding to mu and kappa receptors in the central nervous system to reduce pain perception and cause side effects like respiratory depression. Common adverse reactions include nausea, constipation, sedation, and respiratory issues. Opioids are contraindicated in conditions like asthma, increased intracranial pressure, or pregnancy. Precautions must be taken with opioid-naive patients and older adults due to risk of respiratory depression.
This document provides an overview of opioids and opioid analgesics. It discusses how opioids act in the central nervous system and peripheral tissues to relieve pain. It describes the endogenous opioid system and three families of opioid peptides: endorphins, enkephalins, and dynorphins. It also discusses the three main types of opioid receptors: mu, kappa, and delta. The rest of the document details specific opioid analgesics including natural alkaloids like morphine and codeine, semi-synthetic opioids like heroin and oxycodone, and synthetic opioids like methadone and tramadol. It provides information on their mechanisms of action, therapeutic uses, and adverse effects.
Music TherapyL.Amoia-Watters, Ed.D. MSN, CRNP, RNkarenahmanny4c
Music Therapy
L.Amoia-Watters, Ed.D. MSN, CRNP, RN
*
Music TherapyDefinition – the controlled use of music & its influence on the human being to aid in physiologic, psychological, & emotional integration of the individual during treatment of an illness or disease
https://youtu.be/ZbZSe6N_BXs
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Music TherapyWho can do it?Graduates of colleges or universities from more than 70 approved music therapy programs are eligible to take a national examination administered by the Certification Board for Music Therapists (CBMT), an independent, non-profit certifying agency fully accredited by the National Commission for Certifying Agencies. Evidence based and research based practiceNon therapists-music medicine
https://youtu.be/LGnWyS2Y4r8
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Music Therapy-OverviewMusic therapy interventions can be designed to:Promote WellnessManage StressAlleviate PainExpress FeelingsEnhance MemoryImprove Communication (Autism)Promote Physical RehabilitationLessen effects of dementia
*
Music Therapy-BenefitsBrain WavesStrong Beat-sharp concentration, alertnessSlow Tempo-Calm, meditative state
Heart Rate\Respiratory RateSlower HR, slower RR=Decrease stress!
*
Music Therapy-BenefitsMindUplifting music\uplifting lyrics-decrease depression
https://youtu.be/tiJ9X_wLSWM
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Continue
https://youtu.be/DfUKOBlZXdw
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Music TherapyFound that the volume, pitch, melody, rhythm & type of music all affect BP.Fast music – Increase BPSlow music- Decrease BPRandom introduction of pause in the music lowers BP even more
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Close your eyes…what do you feel?Indian raga (Introduction from Debabrata Chaudhuri's "Raga Maru Behag") https://youtu.be/5809nggUoc0Slow classical (Adagio from Beethoven's "9th Symphony") https://youtu.be/VTvkA0Msfs0Fast classical (Presto from Vivaldi's "L'estate")
https://youtu.be/YeQTl8nyVyMDodecaphonic ("Zart bewegt" from Webern's "6 Pieces for Orchestra”)
https://youtu.be/Z2imIFkkBJsRap (Red Hot Chili Peppers: "The Power of Equality") https://youtu.be/V2bh1feOjZkTechno (Gigi D'Agostino: "You Spin Me Round")
https://youtu.be/pCREs85oIws
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Music TherapyMusic & Aging – dementia
Music is a form of sensory stimulation, which provokes responses due to the familiarity, predictability, and feelings of security associated with it.
https://youtu.be/Hbd9wQCZQ-g
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Music TherapyEffects of Music & SurgeonsMeasures of stress lower surgeon-selected musicSpeed & accuracy higherMusic effects during surgical & treatment proceduresDecrease anxiety pre op, decreased pain post op
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Music TherapyMusic & premature infantsMost benefits with :Live music, entrained (aligned w\ RR and heart beat sounds), parent preferred lullaby or musicIncrease capacity to feed, eat, sleep, and self regulate
https://youtu.be/4qjx2BrrQJg
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Music TherapyEntrainment music, shifts from tension to relaxation, negative to positive and effective for reducing painMatch music of current mood then shift to positive one
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Music Therapy(Bell ...
This document summarizes the classification, mechanisms of action, and therapeutic uses of opioid analgesic drugs. It discusses:
1) The classification of opioids into strong agonists like morphine and weak agonists like codeine.
2) The sites of action of opioids in the central nervous system and peripheral tissues to reduce pain transmission.
3) The therapeutic indications of opioids for moderate to severe acute and chronic pain.
4) The adverse effects of opioids including respiratory depression, nausea, constipation, and development of tolerance and physical dependence with chronic use.
This document provides an overview of non-narcotic analgesics and anti-inflammatory agents. It begins by classifying analgesics as either opioid or non-opioid. It then discusses the mechanisms of action of various opioid analgesics like morphine, codeine, and meperidine. It provides details on their uses, pharmacology, and mechanisms of binding to opioid receptors in the central nervous system. The document also covers opioid antagonists like nalorphine and levallorphane that are used to reverse the effects of opioid overdose.
Similar to Analgesics / dental implant courses (20)
Opportunity for Dentists (BDS/MDS )to relocate to United kingdom -Register as a DENTAL HYGIENIST/ DENTAL THERAPIST without Board exams and after approval you can register in GDC as a DH/DT and start working as a DH/DT Immediately and get paid.
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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Use of modified tooth forms in complete denture occlusion / dental implant...Indian dental academy
This document discusses dental occlusion concepts and philosophies for complete dentures. It introduces key terms like physiologic occlusion and defines different occlusion schemes like balanced articulation and monoplane articulation. The document discusses advantages and disadvantages of using anatomic versus non-anatomic teeth for complete dentures. It also outlines requirements for maintaining denture stability, such as balanced occlusal contacts and control of horizontal forces. The goal of occlusion for complete dentures is to re-establish the homeostasis of the masticatory system disrupted by edentulism.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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This document discusses dental casting investment materials. It describes the three main types of investments - gypsum bonded, phosphate bonded, and ethyl silicate bonded investments. For gypsum bonded investments specifically, it details their classification, composition including the roles of gypsum, silica, and modifiers, setting time, normal and hygroscopic setting expansion, and thermal expansion. It provides information on how the properties of gypsum bonded investments are affected by their composition. The document serves as a comprehensive overview of dental casting investment materials.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UPRAHUL
This Dissertation explores the particular circumstances of Mirzapur, a region located in the
core of India. Mirzapur, with its varied terrains and abundant biodiversity, offers an optimal
environment for investigating the changes in vegetation cover dynamics. Our study utilizes
advanced technologies such as GIS (Geographic Information Systems) and Remote sensing to
analyze the transformations that have taken place over the course of a decade.
The complex relationship between human activities and the environment has been the focus
of extensive research and worry. As the global community grapples with swift urbanization,
population expansion, and economic progress, the effects on natural ecosystems are becoming
more evident. A crucial element of this impact is the alteration of vegetation cover, which plays a
significant role in maintaining the ecological equilibrium of our planet.Land serves as the foundation for all human activities and provides the necessary materials for
these activities. As the most crucial natural resource, its utilization by humans results in different
'Land uses,' which are determined by both human activities and the physical characteristics of the
land.
The utilization of land is impacted by human needs and environmental factors. In countries
like India, rapid population growth and the emphasis on extensive resource exploitation can lead
to significant land degradation, adversely affecting the region's land cover.
Therefore, human intervention has significantly influenced land use patterns over many
centuries, evolving its structure over time and space. In the present era, these changes have
accelerated due to factors such as agriculture and urbanization. Information regarding land use and
cover is essential for various planning and management tasks related to the Earth's surface,
providing crucial environmental data for scientific, resource management, policy purposes, and
diverse human activities.
Accurate understanding of land use and cover is imperative for the development planning
of any area. Consequently, a wide range of professionals, including earth system scientists, land
and water managers, and urban planners, are interested in obtaining data on land use and cover
changes, conversion trends, and other related patterns. The spatial dimensions of land use and
cover support policymakers and scientists in making well-informed decisions, as alterations in
these patterns indicate shifts in economic and social conditions. Monitoring such changes with the
help of Advanced technologies like Remote Sensing and Geographic Information Systems is
crucial for coordinated efforts across different administrative levels. Advanced technologies like
Remote Sensing and Geographic Information Systems
9
Changes in vegetation cover refer to variations in the distribution, composition, and overall
structure of plant communities across different temporal and spatial scales. These changes can
occur natural.
Leveraging Generative AI to Drive Nonprofit InnovationTechSoup
In this webinar, participants learned how to utilize Generative AI to streamline operations and elevate member engagement. Amazon Web Service experts provided a customer specific use cases and dived into low/no-code tools that are quick and easy to deploy through Amazon Web Service (AWS.)
This document provides an overview of wound healing, its functions, stages, mechanisms, factors affecting it, and complications.
A wound is a break in the integrity of the skin or tissues, which may be associated with disruption of the structure and function.
Healing is the body’s response to injury in an attempt to restore normal structure and functions.
Healing can occur in two ways: Regeneration and Repair
There are 4 phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. This document also describes the mechanism of wound healing. Factors that affect healing include infection, uncontrolled diabetes, poor nutrition, age, anemia, the presence of foreign bodies, etc.
Complications of wound healing like infection, hyperpigmentation of scar, contractures, and keloid formation.
2. PAIN- IS A SUBJECTIVE EXPERIENCE WHICH CAN NOT
BE OBJECTIVELY DEFINED OR QUANTIFIED
SATISFACTORILY.
ALGESIA (pain) is an ill-defined, unpleasant sensation, usually
evoked by an external or internal noxious stimulus.
Classification-
1. Supeficial/ cutaneous pain.
2. Deep non-visceral pain
3. Visceral pain
4. Reffered pain
5. Psychogenic or functional pain
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5. Somatic pain arises from stimulation of receptors in the skin, in
which case it is called superficial somatic pain.
From stimulation of receptors in skeletal muscles, joints, tendons
and fascia it is called deep somatic pain.
In most cases of visceral pain, sensation is not projected back to point of
stimulation. Pain may be felt in a surface area far from stimulated organ. This
phenomenon is called referred pain.
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6. ANALGESICS are drugs which relieve pain without loss of
consciousness.
ANALGESICS selectively relives pain by acting in the CNS or on
peripheral pain mechanisms with out significantly altering
consciousness.
Classification:
OPIOIDS
NON-OPIOIDS (NSAID’s)
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7. OPIOID ANALGESICS / NARCOTID /
MORPHINE LIKE ANALGESICS:
The word opiates refers to the products from the opium
poppy.
The term opioid (opoiate – like) is used to denote all
naturally occurring, semi synthetic and synthetic drugs
which have a morphine like action viz relief from pain
and depression of the CNS, both of which are reversed by
naloxone.
These drug formerly called ‘narcotic’ analgesics because
some of them induce sleep. The word ‘narcotic’ is derived
from the greek prefix ‘Narco’ which means to deaden.
Opioids are capable of producing drug dependencies.
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8. Sub classification of opioid
analgesics1. AGONISTS : such as morphine and compounds
which resemble it in most of their actions, viz,
derivatives of morphine, codeine and its
derivatives, synthetic compounds such as
pethidine, methadone, propoxyphine,
levorphonol and tramadol.
2. PARTIAL AGONISTS: Ex:Buprenorphine and
meptazinol They have partial agonist action only
on the mu receptors.
3. MIXED AGONIST – ANTAGONISTS: which act
as agonists at one type of opioid receptors and
as competitive antagonists at another type of
receptors. Eg: Nalburphine,
pentazocine and butorphanol.
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9. Peptides with strong opiate-like analgesic &
mu receptor binding activity are now known
to present in CNS & other tissues. In CNS,
they act as endogenous analgesics, as NTs
& behaviour modulators. They are:
1.Beta-endorphin
2.Enkephalins
3.Dynorphins
4.Nociceptin/orphanin
5.Endomorphins 1 & 2
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10. Opioids – Mechanism of action:
1. The opioid drugs produce their effects by binding to opioid receptors which
are widely distributed in the CNS and other tissues.
2. Opioid receptors are part of the family of G-protein complex receptors and
act to open K+ channels and prevent opening of voltage- grated Ca++
channels.
3. They their by inhibit the release of other neurotransmitters. The opioid
receptors have been classified into
i. Mu
ii. Delta
iii. Kappa(k1 and k2) and
iv. Nociceptin (orphanin ) types.
Apart from the 4 major classes, several other sub types have been
identified. The pharmacological effects associated with these receptors
subtypes and the selectivity of the various opioid drugs for these
receptors are as follows.
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11. PHARMACOLOGICAL EFFECTS ASSOC WITH OPIOID RECEPTOR TYPES:
RECEPTOR EFFECTS
Mu • Supraspinal/ spinal A
• Euphoria, resp dep, sedation, miosis, decreased
GI motility, Sm mus spasm.
• Physical dependece, release of prolactin & GH, N
& V, feeding.
Kappa • Supraspinal/ spinal A, euphoria, resp dep,
sedation, miosis,
• Decreased GI motility,less phy dep,
dysphoria,psychomimetic effects, diuresis,
Delta • Supraspinal/ spinal A, less resp depn, dec GI motility, realese
GH, feeding.
Nocciceptin/orph
hanin FQ
• Drug reward & reinforcement
• Stress responsiveness
• learning & memory
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12. Selectivity of common opioid analgesic drugs 3 for
different receptors
Compounds Receptor type
Mu Kappa Delta
1. Pure agonists
morphine
methadone
codeine
+++
+++
+
+
0
+
+
0
0
2. Partial agonists
buprenorphine
butorphanol
propinam
(+++)
(++)
(++)
-
+++
0
0
0
3. Agonist/ anatagonists
pentazocine
nalbuphine
-
-
++
(++)
+
+
+ agonist (++) partial agonist - antogonist 0 no action
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13. Opium alkaloids:
Divided in to:
1. Phenanthrene group
-morphine, codeine, thebaine
2. Benzyl iroquinoline group
- papaverine, noscapine, narcine
(it is devoid of Analgesic activity, but act as smooth m relaxants)
MORPHINE: is the most important alkaloid of opium & is used as sulphate or
hydrochloride; both salts are soluble in water.
Pharmacological actions-
- periaqueductal gray matter of the brain stem & thalamus: high opioid
receptor density.
- Analgesic actions- seletive action on mu receptors situated both in higher
centers & in S.C
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14. - Opiate receptors are also found in the area postrema which contains
the CTZ & the solitary nuclei which receive visceral sensory fibers
from the vagus & the 9 th C.N
- Opiate receptors have also been identified in the amygdala & it is
possible that they are assoc with influences of opiates on emotional
reaction.
- Within the spinal cord, opiate receptors are localized in the substantia
gelatinosa, which is the first site in the CNS for the integration of
sensory information.
- Opioids & endogenous opioid like peptides have been shows to
modify the release of acetylcholine, noradrenaline, dopamine & sub-
p.
On CNS:
1) analgesia: M produces relief of pain in a dose that usually does not
cause motor incoordination.
-in subanaesthetic doses-has little effect on pinprick sensation &
withdrawal reflex, though pain arising from tissues is well suppresed.
- in moderate doses- releaves cont dull pain.
- In largr doses- releaves sharp intemittant pain & visceral pain.
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15. -Dose just short of causing toxicity- in treatment of terminal cancer.
-M raises the pain theshold, there by reducing the perception of pain.
2) Euphoria, sedation & hypnosis:
-in therapeutic doses, M produces a sense of emotional well being
termed euphoria( this makes this drug one of the worst drugs of abuse)
- rarely, it may produce a sense of anxiety/fear termed dysphoria
particularly in pain free individuals.
- Causes sedation
- larger doses induce sleep with EEG changes similar to those
observed during natural sleep.
- psychological effects of M lasts longer than its analgesic effect.
3) Respiration- depresses the respiratory center. Therapeutic doses
acts by * direct depression action on the respiratory center &
* reducing its sensitivity to increased plasma CO2 conc.
-causes broncho constriction as a result of histamine release.
-Toxic doses – breathing maintained by hypoxic drive mediated through
carotid and aortic body chemo receptors – chyne stokes resp.
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16. 4. Pupils- M stimulates occulomotor centre
5. Nausea and emesis – M stimulates CTZ and produces vomitting
-this is abolished by Nalorphin and Prochlorperazine (5-10mg 4-8
hrly), metoclopramide)10mg 4-8 hrly), haloperidol(1-2mg daily) but
not by antihistamines.
-In larger doses- depresses the vomiting centre.
6. Cough supression
7. Vagal stimulation
8. Spinal cord: M increases the reflex excitability of SC.
-this is masked by depression of higher centres in CNS.
-therapeutic doses produce significant increase in CSF pressure.
9. GIT – induces vigorous spasm of smooth muscle of gut, ileocolic
and anal spinchters while at same time it reduces peristaltic
movements.
-spasmogenic actoin in duodenum of large intestine
-Reduces salivary, gastric and intestinal secretions
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17. -Dessication of feaces , abolision of peristaltic movements, spasm of
sphinctres and in attention to normal sensory stimuli from a loaded
rectum as a result of psychololgical effect of M, all lead to constipation
-Atropine antagonists spasmodic action of M
-M increases the intrabililary pressure
10. Smooth muscles – M produces increased in the tone of uterus and
deturus muscle of bladder – reults in urinary retention.
-produces increase in the tone of bronchi and bronchioles.
-larger doses has effect on human uterus at full term.
11. CVS - therapeutic doses of M have negligible effect on
myocardium ,BP, HR.
-Produces dilatation of B.V, this may reduce the pre load on the heart.
-pruritis , sweating and flushing often accompany cutaneous cappilary
dilatation.
-toxic doses of M may produce hypotension.
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18. 12.Neuro endocrine system- M acts in the hypothalamus and
inhibits the release of GnRH & CHR.It thus decreases plasma
concentration of FSH, LH & ACTH.
-Plasma conc of prolactin increases .
13.Immune system – opioid suppresses various immune functions
and increses the susceptibility to infections.
14. Metabolism- M decreases the metabolic rate resulting in slight
fall in body temp , reduced RR ,reduced muscular activity and
peripheral vasodilatation.
ABSORPTION, FATE AND EXCERTION-
-adequately absorbed when given orally, but extensively
metabolised during first pass through the liver ( oral bioavailability
20 to 40%)
-Sustained release prep have longer duration of action
- can also be given rectally
-Given subcutaneously it prouces analgecic effect within 15 to 20
mins with peak effect at 60 to 90 mins , persisting for 3-5 hrs
-Given IV, produces immediate effect
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19. -M circulates in plasma partly bound to plasma proteins and partly in
free form.
-crosses placental barrier readily
-metabolised by liver and kidney readily
-M is congugated with glucouronic acid to form M-6-glucoronide
(more potent than M)
-in adults plasma half life of M is 2 hrs
-small amounts of free M and large amounts of congugted M are
excreted in urine (90% within 24hrs)
-biliary excretion of congugated form – 7-10%
PREPARATIONS & DOSAGE-
1.Tincture opium- is a hydro alcoholic solution of 10% opium and 1%
M . Dose – 0.3 – 2ml
2.Chlorodyne- is a cloroform and M tincture containing 0.22gm % of
morphine hydrocholride.Dose 0.3 – 0.6ml
3.M solution(2 to 20 mg/ml for oral use)-
10-30mg for adults , upto 200 mg in terminal cancer
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20. 4.M hydrochloride and sulphate injection-
Dose – 10-20mg SC/IM
2.5- 5mg IV slowly over 5 mins
5.Controlled release tablets (10,30 and 60mg) of morphine sulphate
ADVERSE REACTIONS-
1.Intolerence
2.effects on CNS
3.Resp depression
4.Constipation
5.hypotension
6.urinary retention
7.A/E on foetus
8.Tolerence
9.Drug dependence
10.Acute M poisoning
11.Drug interactinons
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21. TOLERANCE: Repeated admn of M results in the development of
tolerance. With intermittant use of M, however, it is possible to obtain the
desired analgesic effect & sedative effects.
-tolerance develops to the resp depressant, analgesic, sedative &
euphoriant effects of M as well as to urinary retention, but the pupils &
GIT do not share the tolerance.
-A morphine addict thus has chaly
pin-point pupil & is habitually
constipated.
-Tolerance to M is attributed primarily to the ability of the cells of the
CNS to withstand the larger doses of the drug.
-Persons tolerant to M exhibits cross tolerance to other opioid drugs &
even to compounds like barbiturates & alcohol.
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22. DRUG DEPENDENCE-
-is a major drawback of M therapy.
-Mainly due to its euphoriant effects.
-Morphine addicts are usually malnourished & debilitated.
-A/E of self injections
-Depression of libido
-withdrawal syndrome manifestations are as follows
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23. ABSTINENCE PERIOD MANIFESTATIONS
6-12 hrs Intense craving for the drug,
lethargy & weakness
12 hrs Yawning, lacrimation,
perspiration, rhinorrhoea,
tremors ,anorexia
48 hrs Peak of withdrawal S, fever,
increase in BP, inc in HR,
dilatation of previously
constricted pupils,intestinal
cramps.
7-10 days Symptoms clear up but pt
c/o restlessness, insomnia,
weakness, back & leg pain
for several weaks
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24. - Prevention of morphine dependence
-Treatment for morphine dependence
Principles of treatment of drug dependence
1. Hospitalization of pt.
2. Gradual or sudden withdrawal of drug
3. Substitution therapy- methadone
4. Psychotherapy & occupational therapy
5. Specific drug therapy
6. Correction of nutritional deficiency
7. Community treatment & rehabilitation.
- in acute opiate withdrawal symptoms & signs drugs like
chlorpromazine, propranolal & clonidine are given(which counter the
nor-adr over activity).
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25. ACUTE MORPHIN POISONING
-may occur from clinical overdose , accidental over ingestion in an
addict or suicidal or homicidal intention
-a dose of 60mg is usually toxic but rarely fatal in a normal adult who
is not in pain.A dose of 250mg is usually fatal.
-In addicts the toxic as well as fatal doses are much higher.
-M poisoning is charecterised by resp dep, pin point pupils,
cyanosis ,reduced body temp and urinary output, hypotension, shock
and coma.Convulsions may occur in infants.death is usually due to
resp dep or shock , pulmonary edema & secondary infection.
-Naloxone & Nalorphine are the specific M antagonist.
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26. THERAPEUTIC USES OF MORPHINE:
1.For relief of pain – in acute MI , fracture of long bones, burns,
terminal stage of cancer, pulmonary embolism, acute pericarditis,
pleurisy and spontaneos pneumothorax
-in sudden excruciating pain – IV M given, this also minimises shock
-SC administration of M is not advocated in the presence of shock.
-used for relief of pain in renal and biliary colic
-Post operatively parenteral M is given
-intrathecal and epidural M has also used to produce analgesia.
-deafferentiation pain is relatively resistant to M gp of drugs
2.In acute left ventricular failure and pulmonary edema
3.As sedative
4.As pre anesthetic medication
5.To produce constipation
6.As an anesthetic
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27. Precautions with M therapy
1.COPD
2.Myxoedema
3.old people and infants
4.head injuries
5.acute abdomen
6.IV M may produce hypotension if administered during hypovolumeic
shock.
7.In sever impairment of kidney or liver infection
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28. Other Phenantherin alkaloids of opium
1.Codine
-is a weak agonist, less potent than M.
-does not produce significant dep of respiration & has a low
dependence liability.
-in toxic doses, may produce excitement convulsions.
-It enhances the analgesic effect of aspirin.
-Better absorbed when given orally, oral bio-avl is 50%
-About 10% codeine is converted to M in liver
-Used as antitussive.
-Available as codeine phosphate(for oral & I.m use)
-Main disadv is constipation, used as antidiarrhoeal
-Dihydrocodiene & oxycodone.
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29. 2.Tramadol:it is weak synthetic opioid, acts seletively on mu receptors.
-absorbed & metabolized in liver.
-t1/2 is 6hrs.
-actions are similar to those of codiene & it has low addiction potential.
-causes less resp dep.
-causes dizziness, sedation & nausea.
-it is expensive.
BENZYLISOQUINOLINE ALKALOIDS OF OPIUM
1. Papaverine
2. Noscapine
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30. SEMISYNTHETIC DERIVATIVES OF NATURAL OPIUM ALKALOIDS
-the M derivatives are
1.Heroin(diacetyl morphine, diamorphine):
-more potent analgesic than M, produces greater euphoria & has
higher dependence liability.
-Rarely employed therapeutically, (cos- drug abuse)
-Withdrawal syndrome in newborns- mothers who are heroin addicts.
-Treatment for addiction is simillar to that of M- 1mg of methadone.
-Their toxicity is similar to that of Morphine.
2. Apomorphine-
-It is a stimulant of CTZ, acts as a potent emitic
-effect is blocked by cholorpromazine
-Steriotyped behaviour syndrome
- acts both on pre & post synaptic DA receptors & thus produces a
variety of behavioural, neuropharmacological & endocrine effects.
-A/E- N,V, dizziness, hypotension & bradycardia.
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31. SYNTHETIC MORPHINE SUBSTITUTES
1. PETHIDINE & ITS CONGENERS
2. METHADONE & ITS CONGENERS
3. MORPHINAN COMPOUNDS & CONGENERS. Eg: LEVOPHANOL
& BUTORPHANOL
4. BENZOMORPHAN DERIVATIVES.Eg: PENTAZOCINE
5. MISCELLANEOUS- NABBUPHINE,BUPRENORPHINE
PETHIDINE( Meperidine, Demerol)
-ph actions are similar to morphine.
-devoid of significant antitussive activity.
-the incidence of N & V is higher.
-has vagolytic action.
- may occasionally produce hypotension & syncope due to peripheral
vasodilatation.
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32. ABSORPTION, FATE & EXCRETION:
-50% bio-avai on oral administration, the analgesic effects appears
with in 10-15 min.
- on parental admn the action lasts for 2-4 hrs
- Crosses placental barrier & also secreted in milk
- Metabolized by liver, norpethidine possesses significant excitatory
action on the CNS.
- norpethidine tends to accumulate during chronic use.
- Small portion of pethidine is excreted unchanged in urine, the
urinary excreation is enhanced when urine is acidic.
PREPARATION & DOSAGES:
1. Pethidine hydrochloride tablets
dose- 25-100mg
2. Pethidine hydrochloride inj 2ml amp containing 50mg/ml of the salt.
Dose- im/sc 25-100mg
iv- 25-50mg to be repeated, if necessary after 4 hrs.
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33. A/E-
-local irritation on parenteral admn,sweating, euphoria, dizziness,
drymouth, vomiting,dysphoria, visual disturbances, weakness
&palpitation.
-Anaphylactoid reaction
- admn to mothers produces significant depression of foetal respiration.
-Causes bronchospasm,Decreases secretion
-Pethidine overdosage causes resp depn, coma or tremors myoclonus
& convulsions.
-Drug tolerance & dependence
DRUG INTERACTIONS: with
-Phenytoin
-cimitidine
-imipramine or an MAOI
C/I ARE SIMILAR TO MORPHINE
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34. THERAPEUTIC USES:
1.as analgesic
2.preanaesthetic medication
3.obsterical analgesia
4.epidural & intrathecal analgesia
PETHEDINE CONGENERS:
Eg Priminodine,
Phenopridine,Fentanyl,Aifentanil,Remifentanyl,Anileridine &
Alphaprodine.
-used mainly as anesthetic adjuncts
-Alphaprodine has shorter duration of action , used for relief of pain in
first stage of labour
-Diphenoxylate is used in treatment of diarrhoea.
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35. Methadone(Physeptone)
-Analgesic potency >/= to M.
-Pharmocological actions similar to M but less hypnotic
-Resp dep is same degree as M , and has marked anti- tussive
effect
-Methadone inhibits the reuptake of nor adrenaline and 5-HT and
blocks the action of NMDA receptors
ABSORPTION FATE AND EXCRETION
-80% Oral bio availability
-analgesic effect occurs within 10-15 mins following parenteral and
20-30 mins following oral medication
-highly bound to plasma & tissue proteins
-plasma half life is 24 – 36 hrs
-crosses placental barrier
-metabolized in liver
-< 10% is excreted unchanged in kidneys
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36. PREPARATIONS AND DOSAGE
1.Methadone hydrochloride tablet 5 – 10 mg
2.Methadone hydrochloride inj , 5-10mg IM/SC
ADVERSE EFFECTS
-Similar to those of morphine
-acute intoxication responds to naloxone
-tolerance and withdrawal syndrome develops more slowly
-codeine is often used as substitute during treatment of methadone
addiction
USES
1.In chronic pain, visceral pain
2.Drug of choice in treatment of opioid withdrawal sydrome
3.Anti-tussive
METHADONE CONGENERS-levomethadyl acetate and propoxane
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37. MORPHINIAN COMPOUNDS
Levorphanol-
-More potent analgesic than M
-better absorbed on oral administration
-produces less constipation
-can cause drug dependence
-can be given orally or IM/SC in the dose of 2-3 mg
Pentazocine(Fortral, Fortvin, Talwin)
-is a benzo morphine derivative
-acts on kappa receptors in S.C
-weak opiod antagonist at mu receptors
-less analgesic activity, shorter duration of action , do not cause
euphoria.
-has lower dependence liability, constipation is uncommon, less
resp dep, raises systemic and pulmonary artetrial BP(not
recommended in MI).
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38. Absorption fate and excretion
-well absorbed when given orally
-metabolised in liver
-excreted as glucornide
-Smokers metabolise 40% > than non smokers
Dose-
25mg tab &30mg (lactate) per ml inj
-oral dose 25mg –100mg every 3-4 hrs
-SC or IM or IV –30-60mg every 3-4 hrs
Adverse effects-
1.CNS- sedation sweating dizziness and nausea
2.Psychomimetic reactions, hallucinations and unpleasent dreams
3.precipitation of acute withdrawal syndrome in a morphine addict
4.tolerence and physical dependence (low)
-Naloxone -antidote
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40. NON ANALGESIC USES OF OPIODS
1.Anti diarrheal eg; diphenoxylate, loperamide
2.central cough suppresant eg: codiene
3.emetic eg: apomorphine
4. In acute LVF eg;morphine
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41. OPIOD ANTAGONISTS
-Acts mainly by competitive antagonism
Classification-
1.Pure antagonists eg: naloxone ,naltrexone
2.Partial agonists of Nalorphine type eg: nalorphine, levallorphan and
cyclazocine
3.Partial agonists of morphine type eg: propiran , profadil
NALOXONE(Narcan)- N-allyl analogue of oxymorphone, a pure
antagonist, selectively antagonizes the resp depressant action of
morphine & other opioids.
-when given orally, only 1/50 as potent as when given parenterally
cos of its metabolism in liver.
-1mg given I.v completely blocks the action of 25mg of heroin. Its
duration of action is 3-4hrs.
-it is almost completely metabolized in liver.
- tolerance to the opioid antagonist properties does not occur.
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42. -available in 1 ml vials containing 0.4mg/ml & is the antagonist of choice
in treatment of opioid poisoning.
-it is administered as iv bolous in the dose of 0.8-2mg every 2-3min to a
total max of 10mg.
-in children iv 10mg/kg, if no response then inject 100mcg/kg(bolous)
-it is used to reverse the residual resp dep effect of opioid at the end of
op. procedure.
NALTREXONE(Nalorex):Orally administered, long acting, opioid
antagonist.
-well tolerated & has no euphoric effect
-available as 50mg scored tablets
-For treating heroin addiction, small doses 25mg/day is used initially,
followed by 50mg/day.
- it is given in former opioid addicts to prevent re-addiction.
-Also used in alcohol addiction.
-A/E; GI dist, nervousness, sleeping difficulty & muscular pains. Rarely
thrombocytopenia & liver function abnormalities may occur.
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43. NALORPHINE(N-allyl-normorphine)
-semisyntetic congener of morphine.
-for treatment of acute M poisoning.
Actions-
1. When administered without prior medication with morphine
2. When administered after morphine
3. When administered to a morphine addict
Absorption fate and excretion
-oral-poor absorption
-subcutaneous- rapid a
- metabolized in liver by conjugation
Dose-10mg/ml-sc or iv in dose of 3-10mg(total of 40mg)
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44. Uses-
1. Acute poisoning due to M & related compounds.
2. Diagnosis of M addiction.
3. Used in M addicts along with M.
LEVALLORPHAN-
CYCLOZOCINE-
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49. MECHANISM OF ACTION:
- During inflammation, pain & fever, arachidonic acid is
liberated from phospholipid fraction of the cell membrane.
- AA is then converted via cyclo-oxygenase(COX-1&2)
pathways to PGs. The steps are
1. Oxidation of AA to the endoperoxide PGG2 &
2. Its subsequent reduction to hydroxy endoperoxide PGH2- this
is transformed in to the primary prostanoids PGE2, PGF2,
PGD2, PGI2 & TXA2
- COX-1 activity is constitutively present in nearly all cell types
at a constant level & is involved in tissue homeostasis
- COX-2 activity is normally absent from cells(except those of
kidney & brain) but is induceble by bacterial liposaccharides
IL2 & TNF in activated leucocytes & other inflammatory cells
- Thus, COX-1 is physiological & COX-2 is usually pathological
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50. - Actions of PGs
- most NSAIDs inhibit COX-1 & COX-2 nonselectively, but
now some selective COX-2 inhibitors have been produced
- aspirin inhibits COX irreversibly by acetylating one of its
serine residues, return of COX activity depends on synthesis
of fresh enzyme.
- others- competative & reversible inhibition of COX
BENIFICIAL ACTIONS DUE TO PG SYN INHIBITION:
1. Analgesia, Antipyresis, Anti-inflammatory
2. Antithrombotic
3. Closure of ductus arteriosus
SHARED TOXICITIES:
1. Gastric mucosal bleeding, inh of platelet function
2. Limitation of renal blood flow- Na & water retention
3. Asthma & anaphylactoid reactions in suceptible individuals
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51. SALICYLATES(esters of salicylic acid)
Eg: methyl S& sodium S & aspirin(acetyl S acid)
Pharmcological action-
1. Local actions:
- salicylic acid & methyl S are irritants, salicylic acid also
has keratolytic,antiseptic & fugistatic action.
- Salts of salicylic acid do not irritate unbroken skin but
when ingested, may release free salicylic acid in
stomach causing local irritation.
2. CNS-
• Analgesia-act predominantly peripheral.
• Can be combined with codeine
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52. •Aspirin Inhibits the biosynthesis of PG’s by irreversible
acetylation & consequent inactivation of COX in contrast to
other NSAID’s which cause its revesible inhibition.
• not usefull in deaffrenation & visceral pain.
• in smaller dose-only analgesic action, larger doses- anti
inflammatory activity, releive vascular congestion & edema.
Antipyretic action-
•By inhibiting brain PG synthesis & release.
• do not reduce heat production but increase dissipation of
heat by producing cutaneous vasodilatation.
Respiration-
•Stimulate resp as a result of direct & indirect actions.
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53. Acid base balance & electrolytes-
•Compensated resp alkalosis
• hypokalemia
• dehydration & hypernatremia
• in a.toxic doses-metabolic acidosis.
3. GIT- salicylates may produce
•dyspepsia, N & V- gastric irritation
• peptic ulceration, GI bleeding, hematemisis, malena.
•decrease in PGE2 & PGI2-loss of protective effect of PGon
stomach
• also reduce motility of stomach & increase gastric emptying
time.
• alkalies reduce gastric irritation & absorption of salicylates.
•To avoid gastric irritation:
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54. 4. Anti inflammatory & anti rheumatic effect-
•By inhibiting PG synthesis
• by reducing capillary permiability
• by inhibition of neutrophil aggregation & activation
• inhibit the formation of activated kallikerin from inactive
plasma & leucocyte kallikerin
• inhibit mucopolysac bio-synthesis
5. Immunologic phenomenon-
•Prevent release of histamine as a result of Ag-Ab reaction.
• do not significantly interfere with the development of
agglutinins following typhoid inoculation
• may reduce CMI.
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55. 6. Blood & Platelets:
•Does not affect normal leucocyte count
• reduce leucocytosis & reduce the high ESR in acute rh fever
• inhibit platelet aggregation(suppersion of TXA2 in platelets)-
irreversible, other NSAID’s- reversible
•non acetylated salicylates such as sodium S do not posses
antiplatelet action.
7. Hepatic & renal effects
8. Uricosuric effects
9. On CVS
10. Endocrine effects
11. Metabolic effects- uncoupling of oxidative phosphorylation
- on sugar level
- reduce lipogenisis
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56. INR values and its importance in dentistry
Absorption, fate & excretion-
• absorbed from intact skin, given orally, absorbed in stomach & upper
small intestine.
• plasma ½ life- 2-8 hrs
• after absorption, 80% of salicylate is bound to P.P(aspirin-50%)
• aspirin ½ life 15 min
• Dose dependent pharmacokinetics
1. Lower dose- 300-600mg- Ist order kinetics.
2. Higher dose- 1-2g- zero order kinetics
• Mainly excreted in urine
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57. Adverse effects-
1. Intolerance
2. On GIT
3. On hemopoietic system
4. On kidneys
5. Rey’s syndrome
6. Pregnant women & infants
7. Salicylism
8. Acute salicylate intoxication
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58. S
s
a
SALICYLISM
-High doses of salicylates may produce a condition of mild salicylate
intoxication termed salicylism.
-syndrome usually developes when the plasma salicylate levels
>25mg%
-charecterised by headcahe, dizziness, vertigo, tinitus, difficulty in
hearing n sight, drowsiness, lethargy, mental confusion, nausea,
vomitting & diarrhoea may occur
-may also be associated with tachypneoa & resp alkalosis
-signs & symptoms are reversible on cessation of drug.
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59. ACUTE SALICYLATE INTOXICATION
-overzealous therapy in infants or accidental ingestion
-50mg% mild toxicity & > 75mg% potentially fatal
-charecterised by acid base electrolyte disturbances, hypoglycemia,
hyperpyrexia, GI irritation, restlessness, vertigo, tremors ,
convulsions ,coma
-moderate doses cause resp alkalosis, with higher doses the resp
centre is depressed leading to metabolic acidosis
-treatment : correction of acidosis & urinary alkalinization using 2%
dextrose & 2% sodium bicarbonate, at the rate of 2 lt/hr with frequent
determination of blood ph & plasma bicarbonate to prevent metabolic
alkalosis.
-sedatives like barbiturates are dangerous in these cases
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60. Principles of management of salicylate poisoning
1. Hopitalization
2. Gastric lavage
3. Correct hyperthermia, de/overhydration, hypokalemia, acid-base
disturbances, ketosis.
4. Increase elimination by alkalinization, potential dialysis &
hemoperfusion.
5. Vit-K, blood transfusion.
6. Exchange transfusion in very small children.
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62. Uses-
1. Local application
2. As analgesic antipyretic
3. As anti-inflammatory
4. As anti-rheumatic
5. As anti platelet agent
6. Miscellaneous- Indomethacin in persistant patent ductus, barters
syndrome, food intolerence , diarrhoea, sun burns , ocular
inflammation etc…
DIFLUNISAL-
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63. PARA AMINOPHENOL DERIVATIVES-
Eg- Paracetamol, Acetanilid, Phenacetin
PARACETAMOL-
-Aanlgesic & antipyrectic
-less antiinflammatory effects
-< GI irritation, acid base imbalance , electrolyte disturbances
as compared to salicylates
ABSORPTION , FATE & EXCRETION-
-Oral administration rapidly absp
-reaches plasma levels in ½ to 1 hr
-metabolised in liver and excreted in urine as conjugate
products of glucuronic & sulfuric acid
-Infants have poor ability for glucuronidation thus causes
enhanced toxicity of drugs in neonates
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64. ADVERSE EFFECTS
-Hepatic & renal toxicity (7-10gm)
-liver toxicity due to N-acetyl-p-benzoquinoneimine
-may cause fever , neutropenia, thrombocytopenia, nephropathy &
skin reaction
-rarely produces anemia as a result of hemolysis &
methhemoglobinaemia
PREPARATION AND DOSAGE
1.250-500MG TAB analgesic & antipyrectic(adult 2.5g)
2.liquid dosage form in children
3.inj Febrinil- 150mg/ml
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65. PYRAZOLONE DERIVATIVES
-Aminopyrine & antipyrine (not well tolerated no longer used)
-phenylbutazone & oxyphenbutazone
-others phenyl dimethyl pyrazalone(analgin, dipyrone)
PHENYLBUTAZONE
-Potent antiinflammatory drug
-poorly tolerated as it causes various GI ,hepatic , renal ,
fetal, heamatologic toxic effects
-gives rise to various drug interactions
-hence rarely used
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66. OXYPHENABUTAZONE(Phenabid,Oxyin)
-metabolic degradation product of Phenylbutazone
-claimed to cause less gastric irritation
ANALGIN (Dipylone, Novalgin)
-potent analgesic & antipyretic but no uricosuric effect
-has no advantage over aspirin except that it can be injected
-toxic effect are similar to those of phenylbutazone & include fatal blood
dyscrasias
INDOLES & RELATED DRUGS
Indomethacin(Indocid)
-anti inflammatory, analgesic , antipyretic
-used in Rheumatoid Arthritis
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67. -used in treatment of acute attack of gout
-acts as an analgesic even in the absence of obvious inflammation
eg- osteoarhtritis, ankylosing spondylitis
ABSORPTION ,FATE ,EXCRETION
-oral admist completely absorbed reaching a peak plasma con. In
1-2hrs
-metabolised in liver & excreted in kidneys as glucuronide
-t1/2 is 2hrs
ADVERSE EFFECTS
-Headache, mental confusion, giddiness, blurring of vision,
depression & psychotic disturbances
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68. -neuropsychiatric adverse effects are common
-less common adverse effects are nausea, vomitting,
dyspepsia, diarrhoea , skin rashes and rarely blood
dyscariasis.
-peptic ulceration associated with bleeding & liver damage is
reported
-may cause sodium retention , oedema
-may aggrevate renal disease
PREPARATION AND DOSAGE
25mg CAP : 50-150mg/day in divided doses
USES
-acute gout attacks,ankylosing spondylitis
-it does not interfere with the uricosuric effect of probenecid
-not a drug of choice in rheumatoid a, due to side effects.
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69. HETROCYCLIC ARYLACETIC ACID DERIVATIVES:
DICLOFENAC(Voveran):
-has greater activity than other NSAIDs.
-50% of sodium salt is metabolised during first pass through the
liver.
-It is extensively bound to plasm proteins, t1/2 is 1-2 hrs.
-It accumulates in the synovial fluid, which probably is
responsible for its longer duration of action than its plasma half
life.
A/E:
- 20% incidence
-similar to propionic acid derivatives.
-GI symptoms & elevation of liver enzymes occur more
frequently
- other side effects include CNS effects & fluid retention
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70. USES:
-Rheumatoid arthritis, severe osteoarthritis, ankylosing spondalitis
-75-100mg/day in divided doses, im/oral
-also used as 0.1% eye drops for inhibition of intraoperative
miosis & to prevent postop inflammation in cataract surgery.
-for postop analgesia,75-100mg in divided doses, intrarectal
route.
KETOROLAC:
-Moderately effective analgesia
-Dose: 20-30mg(single dose)
-T1/2 is 5hrs
-Like other NSAIDs, it also has antiplatelet activity
-Initial dose of 20-30mg I.m may be followed by 10-15mg by the
same route 6-8hrly(max-80-120mg)
- I.V doses is simillar to im dose
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71. TOLMETIN(Tolectin):
-pyrrole acetic acid derivative
- resembles ibuprofen in its action & toxicity
-Less potent than indomethacin.
PROPIONIC ACID DERIVATIVE:
Eg- ibuprofen, naproxen, fenoprofen, flurbiprofen & ketoprofen
-have analgesic-antipyretic & anti-inflammatory properties similar
to aspirin
-Better tolerated orally
-Highly bound to plasma albumin(92-99%) & like aspirin, can
displace drugs such as hydantoins, sulfonylureas &
waraferin.They, however, differ in their Pharmacokinetics &
hence, in their duration of action following single dose.
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72. A/E:
-GI disturbances such as epigastric pain, nausea, sensation of
fullness in the stomach & heartburn.
-Occult blood loss is less common.
-Less frequently, they may cause CNS symptoms such as
headache, dizziness, blurred vission & tinitus.
-In a few cases, fluid retntion & edema may occur
-Jaundice, impairment of renal function, thrombocytopenia are
rare
USES:
-Rheumatoid arthritis, osteoarthritis, ankylosing spondalitis
-flurbiprofen eye drops for eye inflammation.
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73. FENAMATES:
Eg: Mefenamic acid( meftal,pontstan)
-anthranilic acid derivative
-used in chronic & dull aching pains.
-Mefenamic acid is a weaker analgesic than aspirin
-A/E- D, gastric upset, dizziness, headache, skin rashes,
hemolytic anemia & blood dyscrasias
-Dose: 500mg 2-3 times a day
-USES:in dysmennorhoea
-Flufenamic acid has similar properties.
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74. OXICAMS:Eg- piroxicam(feldene, pirox)
-this is structurally different from other agents
-well absorbed when given orally
-longer half life(38-45hrs)-hence administred once a day
-doses- 10-20mg(antipyretic & analgesic)
20-40(anti-inflammatory)
-causes GI & CNS disturbances
-USES: Rheumatoid arthritis,osteoarthritis, ankylosing
spondalitis, acute gout
-has no advantage except a longer duration of action
- other oxicams are tenoxicam, meloxicam & lornoxicam
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75. SELECTIVE COX-2 INHIBITOR NSAID’S:
- Selectively block COX-2 activity more than COX-1 activity, thus
interfering less with the protective action of COX-1 in the
stomach, BV & kidneys.
-Eg: nimesulide, meloxicam, nabumetone, celecoxib, rofecoxid &
valdecoxib.
- given orally, their absorption is complete.
- effective analgesic-anti inflmmatory action(single dose)
- effective in treatment of osteoarthritis & rheumatoid arthritis.
ADVANTAGES:
-fewer gastric ulcers
- do not inhibit platelet aggregation
DISADVANTAGES:
- have prothrombotic effect, leading to a higher incidence of
cardiovascular events.
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76. A/E:-N, V, dyspepsia, abdominal pain, diarrhoea & edema of
lower extrimities
- renal A/Es like decrease renal blood flow
- edema & dose releated worsening of hypertension
- studies in animals suggest that inhibiting COX-2 may interfere
with wound(ulcer) healing, bone remodeling, ovulaton & prenatal
renal development.
C/I:
-children, pregnant women, lactating mothers
-Celecoxib is contraindicated in pts allergic to sulfonamides.
- nimesulide causes nephrotoxicity & hepatotoxicity. So drug
should be avoided in children & old people.
- recently, the use of rofecoxib & valdecoxib has been reported
to be associated with icrease incidence of MI & stroke. Hence,
COX-2 inhibitors are under suspicion regarding their long term
toxicity.
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77. DRUG ½ LIFE(Hrs) DOSE-mg
NABUMETONE(
RELIFEX)
24 500-1000 OD
NIMUSULIDE
(NIMULID, NISE)
<5 100 TID
MELOXICAM(M
UVERA, MOBIC)
20 7.5-15 OD
CELECOXIB
(CELEBREX)
11 200-400 OD/BID
ROFECOXIB
(VIOXX)
17 12.5-15 OD
VALDECOXIB
(BEXTVA)
8 10 OD
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78. NSAID & RENAL DAMAGE:
- All NSAIDs can cause acute or chronic renal damage
following repeated use, sometimes as short as 2 wks.
- drugs with a long half life(naproxan & piroxicam) are more
likely to cause renal damage than those with shorter half
life(ibuprofen)
- clinically the renal injury can present it self in several forms
1. Acute renal failure
2. Mild asymptomatic renal impairment
3. Chronic renal impairment due to papillary necrosis/interstitial
fibrosis
4. Serious hyperkalemia
- first 3 are releated to the action of NSAIDs to inhibit
intrarenal PG synthesis by blocking COX-1
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79. - Locally produced PGE act as intrarenal vasodilators to
counter act the vasoconstriction effect of Angiotensin II & nor
adrenaline(as in shock), they also influence the tubular
transport of ions & water.
- in normal young individuals the renal perfusion is not
dependent upon the locally produced PGs, in old people & in
individuals with diseases such as DM, it is.
- effects of inhibition of PG synthesis within kidney are:
1. The protective intrarenal vasodilator effect is lost
2. Renal blood flow & GFR are reduced in people with pre-
existing renal impairment
3. The natriuretic effect of PFE2 on renal medulla is lost with
consequent sodium retension
- hyperkalemia is due to diminished aldosterone synthesis
secondary to inhibition of renin synthesis by NSAID-
hyporeninimic hypoaldosteronism
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80. - hyperkalemia is particularly likely to occur in pts with DM,
renal disease & in those on potassium sparing diuretics
- mechanism of NSAID induced renal damage include
1. Analgesic Nephropathy
2. Allergic type of intestitial nephritis &
3. Urate nephropathy.
- increased risk for this is seen in- pts of old age, cirrhosis of
liver, diabetic nephropathy, gout, renal & renovascular
disease & salt or volume depletion.
- NSAID enhance the effects of vasopressin on the kidneys &
can diminish excretion of free water
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