Barbiturates were first synthesized in 1864 and were widely used as sedative-hypnotic drugs. They have largely been replaced by safer benzodiazepines due to side effects like respiratory depression. Barbiturates enhance the effects of the inhibitory neurotransmitter GABA. They are classified based on duration of action and can be used for anesthesia, anticonvulsant, and sedative purposes. Toxicity is treated through airway management, hemodynamic support, activated charcoal, urine alkalinization, and hemodialysis if needed. A case example described a woman who overdosed on phenobarbital after childbirth and postpartum depression, requiring intubation, ICU care, and
Gut decontamination or methods of poison removal in clinical toxicology Soujanya Pharm.D
Gastrointestinal decontamination refers to removing toxins from the gastrointestinal tract. Methods include inducing vomiting, gastric lavage, cathartics, activated charcoal, and whole bowel irrigation. Inducing vomiting with ipecac or apomorphine is only recommended for alert patients within 4-6 hours of ingestion. Gastric lavage may be considered for life-threatening ingestions within 1-2 hours but has risks. Cathartics like sorbitol and magnesium can help purge the bowels. Activated charcoal binds toxins and is most effective within 1 hour. Whole bowel irrigation with solutions like PEG-ELS may help for late presentations over 4 hours after ingestion. These methods aim to reduce toxin
The document summarizes various methods for decontaminating the gastrointestinal tract after poison ingestion, including induced vomiting, gastric lavage, catharsis, activated charcoal, and whole bowel irrigation. It describes the mechanism of action, dosing, contraindications, and complications for each method. Emesis involves administering ipecac syrup to induce vomiting. Gastric lavage uses an orogastric tube to sequentially administer and aspirate fluid to empty the stomach. Catharsis purges the gastrointestinal tract using saline or saccharide laxatives. Activated charcoal adsorbs poisons in the gastrointestinal tract. Whole bowel irrigation empties the entire gastrointestinal tract using large volumes of irrigating solution
The document outlines the definitions, regulatory bodies, and provisions around the import, manufacture, and sale of Ayurvedic drugs and cosmetics under the Drugs and Cosmetics Act of India. It describes the roles of organizations like the Drugs Technical Advisory Board and Drug Consultative Committees in advising the government on these matters. It also summarizes the rules for licensing, inspection, sampling, and testing of imported, manufactured, and sold drugs and cosmetics to ensure quality standards are maintained.
1) Antidotes work by forming inert complexes with poisons, accelerating detoxification, reducing toxic conversion, competing at receptor sites, blocking receptor sites, or bypassing toxic effects.
2) Common antidotes are activated charcoal, acetylcysteine, atropine, calcium gluconate, dimercaprol, digoxin immune fab, fomepizole, hydroxocobalamin, methylene blue, naloxone, pralidoxime, and sodium bicarbonate.
3) While supportive care is often sufficient, antidotes can be life-saving in acute poisoning by quickly counteracting toxic effects and reducing burden on the healthcare
General principles involved in management of poisoning- by rxvichu!!RxVichuZ
Hellow friends!!! I am back....with my 13th ppt!!
This ppt is regarding TOXICOLOGY,which happens to be my 1st....and i am happy to release the same on INDEPENDENCE DAY!!
Wishing a very happy and blissful Independence Day to all....i release my toxicology ppt regarding GENERAL PRINCIPLES IN POISONING MANAGEMENT.....
Since its my 1st attempt in Toxicology, i would love to hear ur reviews, and comments....so that i can improve in upcoming editions......
Keep reading...thanks for ur support!!!
With love and regards,
Vishnu.R.Nair (rxvichu-alwz4uh!!)
:) :)
Management of Opioid Analgesic OverdoseSun Yai-Cheng
This document summarizes the management of opioid analgesic overdoses. It notes that opioid overdoses can have life-threatening effects on multiple organ systems. The duration of action varies between opioid formulations and an overdose can prolong intoxication. Prescriptions for opioid analgesics in the US increased 700% from 1997-2007. Opioid overdoses lead to over 27,500 health care facility admissions in 2010. Clinical signs of overdose include respiratory depression, apnea, miosis, and stupor. Naloxone is the antidote and works by reversing opioid receptor activity but has a shorter duration than many opioids. Higher and repeated naloxone doses may be needed for long-acting opioids like
Gut decontamination or methods of poison removal in clinical toxicology Soujanya Pharm.D
Gastrointestinal decontamination refers to removing toxins from the gastrointestinal tract. Methods include inducing vomiting, gastric lavage, cathartics, activated charcoal, and whole bowel irrigation. Inducing vomiting with ipecac or apomorphine is only recommended for alert patients within 4-6 hours of ingestion. Gastric lavage may be considered for life-threatening ingestions within 1-2 hours but has risks. Cathartics like sorbitol and magnesium can help purge the bowels. Activated charcoal binds toxins and is most effective within 1 hour. Whole bowel irrigation with solutions like PEG-ELS may help for late presentations over 4 hours after ingestion. These methods aim to reduce toxin
The document summarizes various methods for decontaminating the gastrointestinal tract after poison ingestion, including induced vomiting, gastric lavage, catharsis, activated charcoal, and whole bowel irrigation. It describes the mechanism of action, dosing, contraindications, and complications for each method. Emesis involves administering ipecac syrup to induce vomiting. Gastric lavage uses an orogastric tube to sequentially administer and aspirate fluid to empty the stomach. Catharsis purges the gastrointestinal tract using saline or saccharide laxatives. Activated charcoal adsorbs poisons in the gastrointestinal tract. Whole bowel irrigation empties the entire gastrointestinal tract using large volumes of irrigating solution
The document outlines the definitions, regulatory bodies, and provisions around the import, manufacture, and sale of Ayurvedic drugs and cosmetics under the Drugs and Cosmetics Act of India. It describes the roles of organizations like the Drugs Technical Advisory Board and Drug Consultative Committees in advising the government on these matters. It also summarizes the rules for licensing, inspection, sampling, and testing of imported, manufactured, and sold drugs and cosmetics to ensure quality standards are maintained.
1) Antidotes work by forming inert complexes with poisons, accelerating detoxification, reducing toxic conversion, competing at receptor sites, blocking receptor sites, or bypassing toxic effects.
2) Common antidotes are activated charcoal, acetylcysteine, atropine, calcium gluconate, dimercaprol, digoxin immune fab, fomepizole, hydroxocobalamin, methylene blue, naloxone, pralidoxime, and sodium bicarbonate.
3) While supportive care is often sufficient, antidotes can be life-saving in acute poisoning by quickly counteracting toxic effects and reducing burden on the healthcare
General principles involved in management of poisoning- by rxvichu!!RxVichuZ
Hellow friends!!! I am back....with my 13th ppt!!
This ppt is regarding TOXICOLOGY,which happens to be my 1st....and i am happy to release the same on INDEPENDENCE DAY!!
Wishing a very happy and blissful Independence Day to all....i release my toxicology ppt regarding GENERAL PRINCIPLES IN POISONING MANAGEMENT.....
Since its my 1st attempt in Toxicology, i would love to hear ur reviews, and comments....so that i can improve in upcoming editions......
Keep reading...thanks for ur support!!!
With love and regards,
Vishnu.R.Nair (rxvichu-alwz4uh!!)
:) :)
Management of Opioid Analgesic OverdoseSun Yai-Cheng
This document summarizes the management of opioid analgesic overdoses. It notes that opioid overdoses can have life-threatening effects on multiple organ systems. The duration of action varies between opioid formulations and an overdose can prolong intoxication. Prescriptions for opioid analgesics in the US increased 700% from 1997-2007. Opioid overdoses lead to over 27,500 health care facility admissions in 2010. Clinical signs of overdose include respiratory depression, apnea, miosis, and stupor. Naloxone is the antidote and works by reversing opioid receptor activity but has a shorter duration than many opioids. Higher and repeated naloxone doses may be needed for long-acting opioids like
Cocaine is derived from the coca plant and can be administered via smoking, insufflation, or injection. It acts by inhibiting the reuptake of dopamine, serotonin, and norepinephrine. Initial effects include euphoria and increased energy, but overdose can cause seizures, cardiac issues, and death. Regular use is associated with nasal damage, weight loss, dependence, and psychological issues. Treatment focuses on managing the acute effects of overdose and providing therapies for addiction.
The document summarizes the key aspects of the Narcotic Drugs and Psychotropic Substances Act of 1985 in India. It provides definitions of important terms related to narcotic drugs and psychotropic substances. It outlines the objectives of the act to consolidate and amend laws around the control of narcotic drugs. It describes various offenses related to illicit trafficking and penalties associated with contravening provisions of the act. The document also discusses the roles and powers of central government officers in administering the act.
Narcotic Drugs and Psychotropic Substances Act, 1985Ganesh Shevalkar
The Narcotic Drugs and Psychotropic Substances Act, 1985, commonly referred to as the NDPS Act, is an Act of the Parliament of India that prohibits a person to produce/manufacture/cultivate, possess, sell, purchase, transport, store, and/or consume any narcotic drug or psychotropic substance.
1. Tobacco refers to plants in the Nicotiana genus and products prepared from cured tobacco leaves.
2. The most common commercial tobacco is Nicotiana tabacum, while Turkish tobacco comes from Nicotiana rustica which is more potent.
3. Nicotine is the main active alkaloid in tobacco. It is a stimulant but can also cause nausea, increased heart rate and blood pressure, and addiction.
Drugs and cosmetics act 1940 and rules 1945Anoop Singh
Secretary - Drugs Controller, India
30
Functions of DTAB:
1. Advise the Central Government and the State Governments on technical
matters arising out of the administration of this Act.
2. Advise on any matter referred to it by the Central Government.
3. Carry out the functions assigned to it by or under this Act.
4. Perform such other functions as may be prescribed.
31
Drugs Consultative Committee(DCC)
1. The Central Government may constitute one or more Drugs Consultative
Committees to advise it, inter alia, on technical matters arising out of the
administration of this Act and to carry out the functions assigned to
1) Ms. ABC experienced brief episodes of seizures and loss of consciousness. Testing found abnormal brain activity in her left temporal lobe, leading to a diagnosis of epilepsy.
2) Epilepsy is caused by excessive electrical discharges in the brain that cause seizures. The patient was prescribed phenytoin to prevent further seizures.
3) The patient was counseled to take her medication as prescribed, avoid high risk activities, seek medical help for prolonged or repeated seizures, and make lifestyle changes to manage her condition.
Opioid overdose is a leading cause of death worldwide, killing an estimated 69,000 people per year. Opioids depress the respiratory drive, leading to apnea, reduced breathing rate, hypoxemia, cerebral hypoxia, and cardiac arrest. Prolonged cerebral hypoxia from impaired breathing is the main mechanism of brain injury and death in opioid overdoses. Naloxone is an opioid antagonist that can reverse the effects of opioid overdose when administered promptly through various routes such as IV, IM, SC, or intranasally. It displaces opioids from receptors and restores normal breathing without abuse potential.
Morphine toxicity was presented as a case of multidrug toxicity involving morphine, diazepam and methamphetamine. Morphine can cause coma, respiratory depression, hypotension and pinpoint pupils while diazepam and methamphetamine interactions were also discussed. Naloxone is used to reverse morphine toxicity by competitively binding opioid receptors. Proper administration of naloxone and monitoring for withdrawal symptoms after reversal are important for management of morphine overdoses.
Benzodiazepines are commonly prescribed sedative-hypnotic agents that were introduced in 1960. They are used for conditions like anxiety, insomnia, alcohol withdrawal, and seizures by enhancing the effects of the inhibitory neurotransmitter GABA. While generally safe, benzodiazepines can cause side effects with prolonged use or overdose like dependence, withdrawal symptoms, and respiratory depression. The effects of different benzodiazepines vary based on their ability to cross the blood-brain barrier and metabolism, with short-acting agents having faster onsets but shorter durations of action.
Narcotic Drugs and Psychotropic Substances Act (NDPS)SHUBHAM MANTRI
The document discusses the Narcotic Drugs and Psychotropic Substances Act of 1985 in India. Some key points:
- The Act consolidated and amended existing laws regarding narcotic drugs and introduced controls on psychotropic substances. It aimed to strengthen penalties for drug trafficking offenses.
- It defines various narcotic and psychotropic substances including cannabis, cocaine, opium, poppy straw, and manufactured drugs.
- The Act establishes authorities for drug control like the Narcotics Commissioner and outlines offenses and penalties related to drug production, possession, sale, and use. It also addresses procedures for investigation and prosecution of drug crimes.
This document provides an overview of stroke, including its definition, types, risk factors, pathophysiology, clinical presentation, diagnosis, treatment both initially and long-term, and management considerations. The two main types of stroke are ischemic (87%) and hemorrhagic (13%). Risk factors include modifiable factors like hypertension and non-modifiable factors like age. Treatment involves stabilizing the patient, diagnosing with imaging, treating the cause, preventing complications, and long-term prevention with medications like aspirin, statins, and anticoagulants depending on the cause of stroke.
The document discusses drug information centers and poison information centers. It provides details on:
- The history and development of the first drug information centers (DICs) and poison control centers (PCCs) in the 1960s in the US and other countries.
- The aims of DICs and PCCs, which include providing drug and poison information to health professionals, developing treatment guidelines, conducting research and education.
- The staffing of DICs and PCCs, which typically includes pharmacists, pharmacy technicians, toxicologists and other professionals.
- The services provided by DICs and PCCs, such as answering drug and poison inquiries via phone/email, publishing
Opioid intoxication can cause altered mental status, low heart rate and breathing, and pinpoint pupils. The effects are due to activation of mu opioid receptors in the brain. Treatment involves ensuring adequate breathing and administering the opioid antagonist naloxone. However, naloxone may have limited effectiveness for long-acting opioids due to their slow metabolism. Careful monitoring is needed given the potential lethal effects of opioid overdose.
Methanol poisoning causes signs and symptoms within an hour of ingestion, including nausea, vomiting, abdominal cramps, headache, confusion and visual disturbances. Post-mortem findings include cyanosis, congestion of the lungs, liver and kidneys, and hemorrhages in the brain and GI tract. Treatment involves gastric lavage, activated charcoal, ethanol administration to compete for metabolism, hemodialysis for severe cases, and correcting acidosis and electrolyte abnormalities. Prognosis depends on prompt diagnosis and treatment to prevent metabolic acidosis and optic nerve damage from methanol and its toxic byproducts.
Opioid Poisoning and treatment-By Prafull JainPrafull Jain
This document discusses opioids, opioid overdoses, and the treatment of opioid poisoning. It defines opioids and describes their therapeutic effects and adverse effects. An opioid overdose occurs when the body ingests more opioids than it can handle, attacking receptors that control breathing. Treatment for an opioid overdose includes administering the opioid antagonist naloxone, which competitively binds to opioid receptors to rapidly reverse the effects of respiratory depression.
Digitalis toxicity is caused by the cardiac glycoside digoxin, which is commonly used to treat heart conditions but has a narrow therapeutic window. Digoxin toxicity can cause various cardiac arrhythmias by inhibiting the sodium-potassium pump in cardiac cells. Management of digoxin toxicity involves supportive care, treating arrhythmias, correcting electrolyte abnormalities, and administering digoxin antibody fragments for severe cases. Symptoms and signs of digoxin toxicity can affect the heart, gastrointestinal system, central nervous system, and vision.
This document provides an introduction to the field of toxicology. It discusses the history of toxicology, including famous historical poisonings. It describes toxicology as the study of the harmful effects of chemicals on living organisms. The document outlines some key concepts in toxicology including dose-response relationships, types of poisoning, factors affecting toxicity, classification of poisons, routes of administration, diagnosis of poisoning, and medico-legal aspects of toxicology. It provides an overview of the general considerations and approaches in the study of toxicology.
Opiate overdose is a major public health issue, as over half of all drug-related deaths in the UK involve opiates like heroin. Opiate overdoses often affect older male drug users who are no longer in contact with treatment services. While naloxone is an effective antidote for opiate overdoses, those experiencing an overdose are often not taken to hospital due to fears of police involvement. Education programs teach signs of overdose and encourage calling emergency services, as naloxone can reverse an overdose if administered quickly.
1. The document discusses types, classification, and treatment of poisons. It defines poison and how they enter the body. Poisons are classified based on their action (e.g. corrosive, irritants) and medicolegal purpose (e.g. suicidal, homicidal).
2. General treatment of poisoning aims to remove unabsorbed poison through induction of vomiting or gastric lavage. Absorbed poison is treated and eliminated through use of antidotes, symptomatic treatment, and general patient care.
3. Specific methods for removing unabsorbed poison are discussed depending on route of exposure. Induction of vomiting and gastric lavage must be done carefully and with consideration of various contraindications
All about barbiturate poisoning , causes , clinical symptoms , types of poisoning , barbiturates classification , adverse effects and toxic effects of barbiturate poisoning , Management of barbiturate poisoning , Scandinavian method , support vital function , prevention and further absorption .
This document discusses various substances that can cause coma through exogenous intoxication, including their mechanisms of action, signs and symptoms, diagnosis, and treatment. It covers ethylene glycol, which is metabolized to toxic acids responsible for metabolic acidosis and tissue injury. It also discusses barbiturates as CNS depressants, methanol which is metabolized to the toxic compound formic acid, benzodiazepines which act as GABA agonists, and opioids which act through mu, kappa, and other receptors to cause respiratory depression, analgesia, and sedation. Signs of overdose include coma, seizures, and respiratory failure. Treatment focuses on supportive care, decontamination, and use of ant
Cocaine is derived from the coca plant and can be administered via smoking, insufflation, or injection. It acts by inhibiting the reuptake of dopamine, serotonin, and norepinephrine. Initial effects include euphoria and increased energy, but overdose can cause seizures, cardiac issues, and death. Regular use is associated with nasal damage, weight loss, dependence, and psychological issues. Treatment focuses on managing the acute effects of overdose and providing therapies for addiction.
The document summarizes the key aspects of the Narcotic Drugs and Psychotropic Substances Act of 1985 in India. It provides definitions of important terms related to narcotic drugs and psychotropic substances. It outlines the objectives of the act to consolidate and amend laws around the control of narcotic drugs. It describes various offenses related to illicit trafficking and penalties associated with contravening provisions of the act. The document also discusses the roles and powers of central government officers in administering the act.
Narcotic Drugs and Psychotropic Substances Act, 1985Ganesh Shevalkar
The Narcotic Drugs and Psychotropic Substances Act, 1985, commonly referred to as the NDPS Act, is an Act of the Parliament of India that prohibits a person to produce/manufacture/cultivate, possess, sell, purchase, transport, store, and/or consume any narcotic drug or psychotropic substance.
1. Tobacco refers to plants in the Nicotiana genus and products prepared from cured tobacco leaves.
2. The most common commercial tobacco is Nicotiana tabacum, while Turkish tobacco comes from Nicotiana rustica which is more potent.
3. Nicotine is the main active alkaloid in tobacco. It is a stimulant but can also cause nausea, increased heart rate and blood pressure, and addiction.
Drugs and cosmetics act 1940 and rules 1945Anoop Singh
Secretary - Drugs Controller, India
30
Functions of DTAB:
1. Advise the Central Government and the State Governments on technical
matters arising out of the administration of this Act.
2. Advise on any matter referred to it by the Central Government.
3. Carry out the functions assigned to it by or under this Act.
4. Perform such other functions as may be prescribed.
31
Drugs Consultative Committee(DCC)
1. The Central Government may constitute one or more Drugs Consultative
Committees to advise it, inter alia, on technical matters arising out of the
administration of this Act and to carry out the functions assigned to
1) Ms. ABC experienced brief episodes of seizures and loss of consciousness. Testing found abnormal brain activity in her left temporal lobe, leading to a diagnosis of epilepsy.
2) Epilepsy is caused by excessive electrical discharges in the brain that cause seizures. The patient was prescribed phenytoin to prevent further seizures.
3) The patient was counseled to take her medication as prescribed, avoid high risk activities, seek medical help for prolonged or repeated seizures, and make lifestyle changes to manage her condition.
Opioid overdose is a leading cause of death worldwide, killing an estimated 69,000 people per year. Opioids depress the respiratory drive, leading to apnea, reduced breathing rate, hypoxemia, cerebral hypoxia, and cardiac arrest. Prolonged cerebral hypoxia from impaired breathing is the main mechanism of brain injury and death in opioid overdoses. Naloxone is an opioid antagonist that can reverse the effects of opioid overdose when administered promptly through various routes such as IV, IM, SC, or intranasally. It displaces opioids from receptors and restores normal breathing without abuse potential.
Morphine toxicity was presented as a case of multidrug toxicity involving morphine, diazepam and methamphetamine. Morphine can cause coma, respiratory depression, hypotension and pinpoint pupils while diazepam and methamphetamine interactions were also discussed. Naloxone is used to reverse morphine toxicity by competitively binding opioid receptors. Proper administration of naloxone and monitoring for withdrawal symptoms after reversal are important for management of morphine overdoses.
Benzodiazepines are commonly prescribed sedative-hypnotic agents that were introduced in 1960. They are used for conditions like anxiety, insomnia, alcohol withdrawal, and seizures by enhancing the effects of the inhibitory neurotransmitter GABA. While generally safe, benzodiazepines can cause side effects with prolonged use or overdose like dependence, withdrawal symptoms, and respiratory depression. The effects of different benzodiazepines vary based on their ability to cross the blood-brain barrier and metabolism, with short-acting agents having faster onsets but shorter durations of action.
Narcotic Drugs and Psychotropic Substances Act (NDPS)SHUBHAM MANTRI
The document discusses the Narcotic Drugs and Psychotropic Substances Act of 1985 in India. Some key points:
- The Act consolidated and amended existing laws regarding narcotic drugs and introduced controls on psychotropic substances. It aimed to strengthen penalties for drug trafficking offenses.
- It defines various narcotic and psychotropic substances including cannabis, cocaine, opium, poppy straw, and manufactured drugs.
- The Act establishes authorities for drug control like the Narcotics Commissioner and outlines offenses and penalties related to drug production, possession, sale, and use. It also addresses procedures for investigation and prosecution of drug crimes.
This document provides an overview of stroke, including its definition, types, risk factors, pathophysiology, clinical presentation, diagnosis, treatment both initially and long-term, and management considerations. The two main types of stroke are ischemic (87%) and hemorrhagic (13%). Risk factors include modifiable factors like hypertension and non-modifiable factors like age. Treatment involves stabilizing the patient, diagnosing with imaging, treating the cause, preventing complications, and long-term prevention with medications like aspirin, statins, and anticoagulants depending on the cause of stroke.
The document discusses drug information centers and poison information centers. It provides details on:
- The history and development of the first drug information centers (DICs) and poison control centers (PCCs) in the 1960s in the US and other countries.
- The aims of DICs and PCCs, which include providing drug and poison information to health professionals, developing treatment guidelines, conducting research and education.
- The staffing of DICs and PCCs, which typically includes pharmacists, pharmacy technicians, toxicologists and other professionals.
- The services provided by DICs and PCCs, such as answering drug and poison inquiries via phone/email, publishing
Opioid intoxication can cause altered mental status, low heart rate and breathing, and pinpoint pupils. The effects are due to activation of mu opioid receptors in the brain. Treatment involves ensuring adequate breathing and administering the opioid antagonist naloxone. However, naloxone may have limited effectiveness for long-acting opioids due to their slow metabolism. Careful monitoring is needed given the potential lethal effects of opioid overdose.
Methanol poisoning causes signs and symptoms within an hour of ingestion, including nausea, vomiting, abdominal cramps, headache, confusion and visual disturbances. Post-mortem findings include cyanosis, congestion of the lungs, liver and kidneys, and hemorrhages in the brain and GI tract. Treatment involves gastric lavage, activated charcoal, ethanol administration to compete for metabolism, hemodialysis for severe cases, and correcting acidosis and electrolyte abnormalities. Prognosis depends on prompt diagnosis and treatment to prevent metabolic acidosis and optic nerve damage from methanol and its toxic byproducts.
Opioid Poisoning and treatment-By Prafull JainPrafull Jain
This document discusses opioids, opioid overdoses, and the treatment of opioid poisoning. It defines opioids and describes their therapeutic effects and adverse effects. An opioid overdose occurs when the body ingests more opioids than it can handle, attacking receptors that control breathing. Treatment for an opioid overdose includes administering the opioid antagonist naloxone, which competitively binds to opioid receptors to rapidly reverse the effects of respiratory depression.
Digitalis toxicity is caused by the cardiac glycoside digoxin, which is commonly used to treat heart conditions but has a narrow therapeutic window. Digoxin toxicity can cause various cardiac arrhythmias by inhibiting the sodium-potassium pump in cardiac cells. Management of digoxin toxicity involves supportive care, treating arrhythmias, correcting electrolyte abnormalities, and administering digoxin antibody fragments for severe cases. Symptoms and signs of digoxin toxicity can affect the heart, gastrointestinal system, central nervous system, and vision.
This document provides an introduction to the field of toxicology. It discusses the history of toxicology, including famous historical poisonings. It describes toxicology as the study of the harmful effects of chemicals on living organisms. The document outlines some key concepts in toxicology including dose-response relationships, types of poisoning, factors affecting toxicity, classification of poisons, routes of administration, diagnosis of poisoning, and medico-legal aspects of toxicology. It provides an overview of the general considerations and approaches in the study of toxicology.
Opiate overdose is a major public health issue, as over half of all drug-related deaths in the UK involve opiates like heroin. Opiate overdoses often affect older male drug users who are no longer in contact with treatment services. While naloxone is an effective antidote for opiate overdoses, those experiencing an overdose are often not taken to hospital due to fears of police involvement. Education programs teach signs of overdose and encourage calling emergency services, as naloxone can reverse an overdose if administered quickly.
1. The document discusses types, classification, and treatment of poisons. It defines poison and how they enter the body. Poisons are classified based on their action (e.g. corrosive, irritants) and medicolegal purpose (e.g. suicidal, homicidal).
2. General treatment of poisoning aims to remove unabsorbed poison through induction of vomiting or gastric lavage. Absorbed poison is treated and eliminated through use of antidotes, symptomatic treatment, and general patient care.
3. Specific methods for removing unabsorbed poison are discussed depending on route of exposure. Induction of vomiting and gastric lavage must be done carefully and with consideration of various contraindications
All about barbiturate poisoning , causes , clinical symptoms , types of poisoning , barbiturates classification , adverse effects and toxic effects of barbiturate poisoning , Management of barbiturate poisoning , Scandinavian method , support vital function , prevention and further absorption .
This document discusses various substances that can cause coma through exogenous intoxication, including their mechanisms of action, signs and symptoms, diagnosis, and treatment. It covers ethylene glycol, which is metabolized to toxic acids responsible for metabolic acidosis and tissue injury. It also discusses barbiturates as CNS depressants, methanol which is metabolized to the toxic compound formic acid, benzodiazepines which act as GABA agonists, and opioids which act through mu, kappa, and other receptors to cause respiratory depression, analgesia, and sedation. Signs of overdose include coma, seizures, and respiratory failure. Treatment focuses on supportive care, decontamination, and use of ant
- The document discusses the history and development of barbiturates, which were originally synthesized in the 19th century as hypnotic compounds. Barbiturates were widely prescribed as sedatives until being displaced by benzodiazepines in the 1960s due to issues with abuse and overdose.
- Barbiturates are classified based on duration of action and examples are provided. Their pharmacological properties and mechanisms of action in the central nervous system, respiratory system, and elsewhere are described. Adverse effects, signs of toxicity, and treatment approaches for barbiturate poisoning are outlined.
This document discusses the poisoning and treatment of several substances:
1. Barbiturate poisoning can cause lethargy, slurred speech, coma and respiratory arrest. Treatment involves protecting the airway, treating coma/hypotension, and no specific antidote exists.
2. Morphine poisoning presents as stupor, flaccidity, shallow breathing, and pinpoint pupils. Treatment is respiratory support, naloxone antidote, and gastric lavage.
3. Organophosphate poisoning impacts the muscarinic, nicotinic and central nervous systems. Treatment includes atropine antidote, pralidoxime to restore nerve function, and supportive care.
Barbiturates and benzodiazepines are CNS depressants that can cause poisoning when taken in toxic doses. Barbiturates act on GABA receptors to inhibit neurotransmission, while benzodiazepines stimulate GABA receptors. Toxic signs of both include slurred speech, confusion, coma and respiratory depression. Treatment involves supportive care, activated charcoal, flumazenil to reverse benzodiazepine effects, and managing withdrawal symptoms by substituting long-acting drugs and gradually tapering doses.
Barbiturates are sedative-hypnotic agents that were first used in medicine in the early 1900s. They act by potentiating the effects of the neurotransmitter GABA at GABA receptors. Commonly abused barbiturates include secobarbital, pentobarbital, and amobarbital. While their use has decreased due to less toxic alternatives like benzodiazepines, barbiturates continue to be used as anticonvulsants, anesthetics, and tranquilizers. Signs of barbiturate poisoning include stupor, coma, respiratory depression, and hypotension. Treatment involves maintaining airway, breathing, and circulation. Gastric lavage and activated char
This document discusses the diagnosis and management of uncommon poisonings, including pesticides, herbicides, carbon monoxide, cyanide, and various toxins. It focuses on organophosphate and carbamate poisoning, providing details on the mechanisms of toxicity, clinical features including acute cholinergic syndrome, intermediate syndrome and delayed sequelae. Treatment involves resuscitation, anticholinergic agents like atropine, cholinesterase reactivators like pralidoxime, and other supportive therapies. Paraquat poisoning is also discussed, noting the progression to pulmonary fibrosis and respiratory failure as the main cause of death.
This document discusses several potential drug-drug interactions involving various medications:
1. A woman taking simvastatin, diltiazem, aspirin is prescribed clarithromycin. Clarithromycin is a strong CYP3A4 inhibitor and may significantly increase simvastatin levels, increasing risk of side effects like rhabdomyolysis. The patient's simvastatin dose should not exceed 40 mg daily while taking clarithromycin.
2. Minocycline is unlikely to reduce the effectiveness of a low-dose combined oral contraceptive. Any interaction would be due to suppressed gut bacteria and is considered very rare.
3. A man's phenytoin levels increased after starting flu
Drug Monograph and Literature Review: "Arcapta Neohaler"Joy Awoniyi
This document provides a drug monograph and literature review for Arcapta Neohaler, which contains indacaterol maleate. It is approved for the treatment of chronic obstructive pulmonary disease (COPD) as a once-daily long-acting beta agonist. The monograph details the drug's indications, dosage forms, mechanism of action, pharmacokinetics, contraindications, warnings, adverse effects, drug interactions, and dosing. It concludes with a review of the literature on indacaterol maleate and COPD treatment.
This chapter discusses pharmacologic management of stable COPD. It identifies the main drug classes used: bronchodilators including beta-2 agonists and anticholinergics, corticosteroids, and antibiotics. The chapter reviews the benefits and side effects of these drugs and notes guidelines have differing recommendations due to a lack of scientific evidence. Noncompliance with drug therapy is also addressed.
Hepatic encephalopathy, short review & updateRushdanZakariah
This document provides an overview of hepatic encephalopathy. It describes hepatic encephalopathy as a complex neuropsychiatric syndrome characterized by disturbances in consciousness and personality changes. Acute episodes can be reversible while chronic cases may progress to coma or death. Precipitating factors include constipation, surgery, and progressive liver disease. Ammonia plays a central role in pathogenesis, as the liver is unable to metabolize and excrete nitrogenous waste products, leading to accumulation of ammonia in the blood and brain. Treatment aims to remove precipitating factors, reduce nitrogenous load from the gut, and manage symptoms. Options include nutritional management, laxatives, antibiotics like rifaximin, and lactulose to produce
This document summarizes various classes of antihypertensive drugs including their mechanisms of action, pharmacokinetics, adverse effects and uses. It discusses diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, alpha blockers, beta+alpha blockers and central sympatholytics. Key drugs discussed include captopril, losartan, verapamil, propranolol, prazosin, carvedilol and clonidine. The document provides classifications of hypertension and details the pharmacology of several individual antihypertensive drugs.
7. d.) Barbiturates and Benzodiazepine.pptxAnusha Are
This document discusses barbiturates and benzodiazepines. It covers their clinical uses, effects of overdose, diagnosis, and management. Barbiturates were widely used as sedative-hypnotics but have been replaced by benzodiazepines due to fewer adverse effects and dependence issues. Overdose of both can cause CNS and respiratory depression leading to coma. Diagnosis is based on history and symptoms. Management involves airway support, gastric decontamination, monitoring for complications, and symptomatic treatment.
1. The document describes an experiment investigating drug interactions and the effects of the liver on drug action in mice. Various groups of mice were administered different combinations of drugs including thiopentone, pentobarbitone, phenobarbitone, and carbon tetrachloride.
2. The duration of drug effects were measured and recorded for each mouse. Preliminary results show that starvation prior to drug administration increased the duration of drug effects for some groups. Pretreatment with other drugs also increased duration of effects for some groups.
3. Further analysis of the results is needed to fully understand the interactions between the different drugs and effects of liver function and pretreatments. The study aims to provide insights into how multiple drug use
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- Bronchodilators like epinephrine, salbutamol, and terbutaline work by binding to beta-2 receptors in the lungs, relaxing smooth muscle and dilating airways. They have been used for thousands of years to treat respiratory conditions.
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- Inhalation is the preferred route of administration as it delivers drugs directly to the lungs, but oral and intravenous routes can also be used. Common side effects include
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These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
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2. Barbituric acid
Barbiturates were synthesized in 1864 by Adolf von Baeyer, though
the synthetic process was developed and perfected by the French
chemist Edouard Grimaux in 1879, making possible the subsequent
widespread development of barbiturate derivatives.
The first of the barbiturates to come onto the market was diethyl-
barbituric acid, also known as barbital, since then barbiturates were
used extensively as sedative-hypnotic drugs.
Except for a few specialized uses, they have been largely replaced
by the much safer benzodiazepines and non-benzodiazepine sedative
compounds.
Barbituric acid is 2,4,6-trioxohexahydropyrimidine, In general,
structural changes that increase lipid solubility decrease duration of
action, decrease latency to onset of activity, accelerate metabolic
degradation, and increase hypnotic potency.
Introduction
3. Classification
They often are divided into four major groups according to
their pharmacologic activity and clinical use:
o ultra–short-acting
o short-acting
o intermediate- acting
o long-acting
4.
5. Therapeutic uses
1. Anesthesia: The ultra–short-acting barbiturates, such as
thiopental.
2. Anticonvulsant: Phenobarbital is used in long-term
management of tonic–clonic seizures. Similarly, phenobarbital
may be used for the treatment of refractory status epilepticus.
3. Sedative/hypnotic:. When used as hypnotics, they suppress
REM sleep more than other stages, Butalbital is commonly used
in combination products (with acetaminophen and caffeine or
aspirin and caffeine) as a sedative to assist in the management of
tension-type or migraine headaches
Surgery Sleep Epilepsy
Short-acting Intermediate-acting Long-acting
6. Mechanism of action
Enhancement of inhibition occurs primarily at
synapses where neurotransmission is mediated by
GABA acting at GABA-A receptors.
Barbiturates bind to a distinct allosteric site on the
GABA-A receptor; binding leads to an increase in the
mean open time of the GABA-activated Cl- channel,
with no effect on frequency. At higher concentrations,
barbiturates directly activate channel opening, even
in the absence of GABA
7. Side effect
Profound sedation, mental dulling, memory impairment, mood
changes and respiratory depression. With chronic therapy, tolerance
can develop within weeks, The effects on CYP450 vary with the
duration of exposure to the barbiturate.
- Acute exposure: barbiturates interact with several CYPs and
inhibit the biotransformation of a number of other drugs and
endogenous substrates, such as steroids; other substrates may
reciprocally inhibit barbiturate biotransformations.
- Chronic administration markedly increases the protein and lipid
content of the hepatic smooth endoplasmic reticulum, as well as
the activities of glucuronyl transferase and CYPs 1A2, 2C9, 2C19,
and 3A4. leading to increases in the metabolism of a number of
drugs and endogenous substances.
8. Route of exposure
Typically, the route of exposure is oral through ingesting
tablets unintentionally or even intentionally in suicidal
attempts, other routes include intravenous and
intramuscular injections.
9. Toxic dose
The toxic dose of barbiturates varies widely and depends on the
drug, the route and rate of administration, and individual patient
tolerance. In general, toxicity is likely when the dose exceeds 5–
10 times the hypnotic dose.
Chronic users or abusers may have striking tolerance to
depressant effects.
A. The potentially fatal oral dose of the shorter-acting agents
such as pentobarbital is 2–3 g, compared with 6–10 g for
phenobarbital.
B. Several deaths were reported in young women undergoing
therapeutic abortion after they received rapid IV injections of as
little as 1–3 mg of methohexital per kilogram.
10. Diagnosis
o History of ingestion
o Skin bullae (sometimes and non-specific)
o Exclusion of other sedative-hypnotic agents, narcotics, alcohol
intoxication or overdose of TCAs, trazodone and antipsychotics,
o Carbon monoxide poisoning, head trauma, CNS infections, sepsis,
hypoglycemia, electrolyte abnormalities, and hypothermia may
present similarly to barbiturate overdose and must be excluded.
o Specific plasma levels concentrations greater than 60–80 mg/L are
usually associated with coma, and those greater than 150–200 mg/L
with severe hypotension. For short- and intermediate-acting
barbiturates, coma is likely when the serum concentration exceeds
20–30 mg/L.
o Other useful laboratory studies include electrolytes, glucose, BUN,
creatinine, arterial blood gases or pulse oximetry, and chest
radiography.
11. Mechanism of toxicity
All barbiturates cause generalized depression of neuronal
activity in the brain. Interaction with a barbiturate receptor
leads to enhanced gamma aminobutyric acid (GABA)–mediated
chloride currents and results in synaptic inhibition.
Hypotension that occurs with large doses is caused by
depression of central sympathetic tone as well as by direct
depression of cardiac contractility.
This also leads to depression in both the respiratory drive
and the mechanisms responsible for the rhythmic character of
respiration. The oxybarbiturates tend to decrease the tone of
the GI musculature and the amplitude of rhythmic
contractions.
12. Toxicokinetics
Vary by agent and group; depending on the lipid solubility and rate of
metabolic inactivations; the onset of action ranges from 20 to 60
minutes if taken orally, and 5 minutes if taken intravenously.
1. Ultra–short-acting barbiturates are highly lipid soluble and rapidly
penetrate the brain to induce anesthesia, then are quickly redistributed
to other tissues. For this reason, the duration of effect is much shorter
than the elimination half-life for these compounds.
2. Long-acting barbiturates like phenobarbital: phenobarbital is only
partially converted and can be found unchanged in the urine. It is a long-
acting, polar drug that is slowly absorbed and slowly redistributed,
contributing to its longer duration of action. they easily cross the
placenta and are excreted into breast milk, and abrupt cessation of
these barbiturates while taking a beta blocker could increase the effect
of the beta blocker or cause frank toxicity.
13. Clinical manifestations (1)
Significant ingestion of barbiturates is life threatening and
typically presents as a depressed level of consciousness ranging
from lethargy to deep coma. Patients may also have respiratory
depression, which is responsible for most deaths that occur.
With the short- and intermediate-acting barbiturates,
symptoms usually begin within 1 hour of ingestion, and peak
effects are seen within 4 to 6 hours. Patients with chronic lung
disease are more susceptible to respiratory depression, even at
therapeutic doses.
Other clinical findings in overdose include hypothermia,
sluggish papillary light reflex, nystagmus, and diminished bowel
sounds. Bullous skin lesions, occasionally referred to as “coma
blisters,” may appear on shoulders, hands, buttocks, and knees.
About 40% of patients who present with severe toxicity develop
aspiration pneumonia.
14. Clinical manifestations (2)
Cardiovascular collapse may be manifested by bradycardia or
tachycardia, hypotension, and shock. Drug-induced dilatation of
capacitance vessels (venous circulation) with consequent
pooling of blood and reduction in effective vascular volume can
lead to shock. Other complications include rhabdomyolysis and
acute tubular necrosis secondary to shock and a mixed
respiratory and metabolic acidosis.
Ethanol and barbiturates have synergistic effects, and there is
increased toxicity even when lesser amounts are ingested.
Chronic use of barbiturates leads to tolerance and physical
dependence as well as withdrawal symptoms when the drug is
discontinued. Tolerance can develop with prolonged use and
abuse, the withdrawal state is similar to ethanol withdrawal.
15. Management (1)
Treatment of barbiturate toxicity remains supportive as
there is no specific antidote for overdose. Patients with
depressed respirations and altered mental status require
airway management and intubation to support breathing and
protect the airway. Blood pressure should be supported
initially with intravenous crystalloid, administering 500- to
1,000 mL boluses, and with close monitoring of response.
The core temperature should be checked and rewarming
instituted if needed.
For serious phenobarbital overdose, multiple-dose
activated charcoal (MDAC) leads to more rapid recovery and
a significant reduction in elimination half-life. The usual dose
is 1 g/kg initially in sorbitol, followed in 2 to 4 hours by 0.5
g/kg in aqueous solution without sorbitol and alternating for
24 hours.
16. Management (2)
Since barbiturates are weak acids with pKas ranging from
7.2 to 8.5. Increasing the urine pH increases the fraction of
ionized drug in the urine and thus decreases the amount of
unionized drug available for passive tubular reabsorption.
Urine alkalinization can increase the renal clearance of
phenobarbital up to 10-fold and can shorten the half-life by
one-half to two-thirds.
Hemodialysis may be used in life-threatening barbiturate
overdose. Both charcoal hemoperfusion and high-flux
hemodialysis enhance the elimination of all barbiturates,
Sustained low efficiency dialysis might be taken under
consideration as an extracorporeal treatment modality in
severe phenobarbital poisoning with hemodynamic instability
where conventional hemodialysis may be difficult to initiate.
17. Example ( case )
A 30-year-old female who was a known case of chronic depression aggravated by
postpartum status (history of child-birth 6 months back) and on venlafaxine therapy was
found unconscious, 4 h after a suspected overdosage of 54 g of phenobarbital (90 tablets of
60 mg each), Being healthcare personnel, she had access to phenobarbital tablets.
In the emergency department, she was intubated and ventilated. Toxicology screen came
back positive for barbiturate, and she was shifted to the Intensive Care Unit (ICU). In the ICU,
she was further resuscitated with fluids. She developed severe hypoxia due to large
aspiration of gastric contents, possibly during transport. It was opted for initial treatment in
the form of forced alkaline diuresis with sodium bicarbonate, ventilator support and gastric
decontamination with activated charcoal every six hourly for 48 h.
The first measured phenobarbital level (about 20 h from time of ingestion) was 198
mcg/ml. After 2 days of therapy, the phenobarbital level came down only to 153.8 mcg/ml.
18. Example ( case )
A trial of 4 h sustained low-efficiency dialysis (SLED) with dialysate-flow rate 300
ml/min was opted, blood-flow rate 150 ml/min and no fluid removal, since she was
hypotensive and requiring noradrenaline support.
Following the first dialysis her phenobarbital level dropped from 153.8 mcg/ml to 92.5
mcg/ml, hemodynamics improved and vasopressors were tapered off. Following the next
dialysis, the drug level further dropped to 40.7 mcg/ml, patient started having
spontaneous eye opening and became restless for which mild sedative in the form of
dexmedetomidine in a low dose had to be started. Phenobarbital level continued to fall
subsequently and in the next day with a drug level of 27.8 mcg/ml, the patient was
extubated. Within the following 6 h, she started communicating verbally and started
taking oral feeds. A full psychiatric assessment was carried out and she was started on
appropriate medication. She was shifted out of the ICU the next day and went on to
make a full recovery.
19. References
- Poisoning and drug overdose 7th edition, Edited by: Kent R. Oslon, Lange
Mcgraw Hill education, 2018.
- Lippincott’s manual of toxicology, Lippincott Williams and Wilkins, 2012.
- Goodman and Gilman’s the pharmacological Basis of therapeutics, 13th
edition, Laurence L. Brunton Mc Graw Hill education.
- Basic and clinical pharmacology, Bertram G. Katzung, 13th edition, Mc
Graw Hill, 2018.
- Successful use of sustained low efficiency dialysis in a case of severe
phenobarbital poisoning, Sayandeep Jana, Chandrashish Chakravarty,
Abhijit Taraphder, and Suresh Ramasubban Indian J Crit Care Med,
v.18(8); 2014 Aug.