Management of op poisoning-definitive treatment
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This document discusses the treatment of organophosphate poisoning with atropine and cholinesterase reactivators (oximes). It notes that atropine is used as an anticholinergic drug to block muscarinic receptors until the organophosphate is metabolized, while oximes like pralidoxime (2-PAM) can restore neuromuscular transmission by reactivating inhibited cholinesterase enzymes within 24 hours before they become resistant to reactivation through aging. The document provides dosing guidelines for atropine and oximes and notes that oxime treatment is secondary to atropine for organophosphate poisoning.
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Organophosphate Poisoning - Update on Management
Organophosphorus compounds are widely used as pesticides and were also developed as nerve agents. They work by inhibiting the enzyme acetylcholinesterase, leading to excess acetylcholine in the body and cholinergic toxicity. Management of organophosphate poisoning involves atropinization to counteract effects, with incremental atropine dosing shown to be better than bolus dosing. While pralidoxime is recommended to reactivate acetylcholinesterase, clinical trials show no clear benefit and potential for harm. Three types of paralysis can occur - acute cholinergic crisis, intermediate syndrome, and organophosphate-induced delayed polyneuropathy. Further research is still needed on many aspects of management
5. organophosphate poisoning
Organophosphate poisoning occurs when a person is exposed to organophosphate pesticides or nerve agents, which inhibit the enzyme acetylcholinesterase. This causes acetylcholine to accumulate at nerve synapses, resulting in overstimulation of the nervous system. Signs and symptoms include excessive sweating, vomiting, diarrhea, increased urination, blurred vision, slow heart rate, low blood pressure, and muscle weakness or paralysis. Diagnosis involves testing for low acetylcholinesterase levels in red blood cells or plasma. Treatment focuses on atropine administration to block acetylcholine receptors, pralidoxime to reactivate acetylcholinesterase, oxygen supplementation, and supportive care. Complications can include
OP poisoning
Organophosphorus compounds were first synthesized in the early 1800s and later introduced as insecticides in the 1940s. They work by inhibiting acetylcholinesterase enzymes, leading to accumulation of acetylcholine and overstimulation of receptors. Clinical features of organophosphorus poisoning include nicotinic effects like muscle weakness and adrenaline release, as well as muscarinic effects like excessive salivation and tearing. More severe poisoning can cause intermediate syndrome, delayed polyneuropathy, or death from respiratory failure. Prompt treatment is needed to prevent these potentially fatal outcomes.
Acute poisoning of antidepressants
Tricyclic antidepressants have been used since the 1950s and include compounds with three rings. They are the largest group of drugs used to treat depression. Overdoses can be life-threatening due to their rapid absorption and effects on the central nervous system, cardiovascular system, and respiratory system. Treatment for overdoses involves stabilizing the patient, reducing drug absorption, increasing elimination, treating seizures and arrhythmias, and observing the patient for at least 6 hours if symptoms resolve before discharge.
Organophosphate poisoning
This document discusses organophosphate poisoning. It begins by introducing organophosphates as a group of chemicals used in domestic and industrial settings that act as acetylcholinesterase inhibitors. It then describes the chemical structure and mechanisms of organophosphates, their routes of entry into the body, and how they cause toxicity by inhibiting acetylcholinesterase. The document goes on to describe the clinical features, phases, and syndromes of organophosphate poisoning as well as their treatment, which involves stabilization, decontamination, administration of the antidotes atropine and pralidoxime, and supportive care.
Organophosphate poisoning
The patient presented with seizures, altered sensorium, and respiratory failure. Low serum cholinesterase levels and response to atropine treatment suggested organophosphate poisoning. He was treated with atropine, pralidoxime, antibiotics, and supportive care and showed gradual improvement over 5 days, though fluctuating sensorium was seen initially.
Organophosphate poisoning and its management (Clinical Toxicology)
This presentation includes: Introduction, usual fatal dose, mechanism of action, clinical (toxic) symptoms, diagnosis and management of organophosphate poisoning (Clinical Toxicology).
Organophosphate poisoning and its management
Please find the power point on Organophosphate poisoning and its management. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Recommended
Organophosphate Poisoning - Update on Management
Organophosphorus compounds are widely used as pesticides and were also developed as nerve agents. They work by inhibiting the enzyme acetylcholinesterase, leading to excess acetylcholine in the body and cholinergic toxicity. Management of organophosphate poisoning involves atropinization to counteract effects, with incremental atropine dosing shown to be better than bolus dosing. While pralidoxime is recommended to reactivate acetylcholinesterase, clinical trials show no clear benefit and potential for harm. Three types of paralysis can occur - acute cholinergic crisis, intermediate syndrome, and organophosphate-induced delayed polyneuropathy. Further research is still needed on many aspects of management
5. organophosphate poisoning
Organophosphate poisoning occurs when a person is exposed to organophosphate pesticides or nerve agents, which inhibit the enzyme acetylcholinesterase. This causes acetylcholine to accumulate at nerve synapses, resulting in overstimulation of the nervous system. Signs and symptoms include excessive sweating, vomiting, diarrhea, increased urination, blurred vision, slow heart rate, low blood pressure, and muscle weakness or paralysis. Diagnosis involves testing for low acetylcholinesterase levels in red blood cells or plasma. Treatment focuses on atropine administration to block acetylcholine receptors, pralidoxime to reactivate acetylcholinesterase, oxygen supplementation, and supportive care. Complications can include
OP poisoning
Organophosphorus compounds were first synthesized in the early 1800s and later introduced as insecticides in the 1940s. They work by inhibiting acetylcholinesterase enzymes, leading to accumulation of acetylcholine and overstimulation of receptors. Clinical features of organophosphorus poisoning include nicotinic effects like muscle weakness and adrenaline release, as well as muscarinic effects like excessive salivation and tearing. More severe poisoning can cause intermediate syndrome, delayed polyneuropathy, or death from respiratory failure. Prompt treatment is needed to prevent these potentially fatal outcomes.
Acute poisoning of antidepressants
Tricyclic antidepressants have been used since the 1950s and include compounds with three rings. They are the largest group of drugs used to treat depression. Overdoses can be life-threatening due to their rapid absorption and effects on the central nervous system, cardiovascular system, and respiratory system. Treatment for overdoses involves stabilizing the patient, reducing drug absorption, increasing elimination, treating seizures and arrhythmias, and observing the patient for at least 6 hours if symptoms resolve before discharge.
Organophosphate poisoning
This document discusses organophosphate poisoning. It begins by introducing organophosphates as a group of chemicals used in domestic and industrial settings that act as acetylcholinesterase inhibitors. It then describes the chemical structure and mechanisms of organophosphates, their routes of entry into the body, and how they cause toxicity by inhibiting acetylcholinesterase. The document goes on to describe the clinical features, phases, and syndromes of organophosphate poisoning as well as their treatment, which involves stabilization, decontamination, administration of the antidotes atropine and pralidoxime, and supportive care.
Organophosphate poisoning
The patient presented with seizures, altered sensorium, and respiratory failure. Low serum cholinesterase levels and response to atropine treatment suggested organophosphate poisoning. He was treated with atropine, pralidoxime, antibiotics, and supportive care and showed gradual improvement over 5 days, though fluctuating sensorium was seen initially.
Organophosphate poisoning and its management (Clinical Toxicology)
This presentation includes: Introduction, usual fatal dose, mechanism of action, clinical (toxic) symptoms, diagnosis and management of organophosphate poisoning (Clinical Toxicology).
Organophosphate poisoning and its management
Please find the power point on Organophosphate poisoning and its management. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
ORGANOPHOSPHATE COMPOUND POISONING
This document summarizes organophosphate poisoning. It discusses various organophosphate compounds used as insecticides and their relative toxicities. It describes the mechanisms of toxicity involving inhibition of acetylcholinesterase and excess acetylcholine accumulation. Signs and symptoms are outlined for both muscarinic and nicotinic effects. Diagnosis and various aspects of treatment are covered including decontamination, atropine administration, pralidoxime use, and management of complications such as intermediate syndrome and delayed polyneuropathy.
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This document summarizes different classes of drugs used to treat respiratory conditions like asthma and COPD. It discusses bronchodilators including xanthine derivatives, beta agonists, and anticholinergics. It also covers anti-leukotrienes, corticosteroids, and mast cell stabilizers. For each class, it describes the mechanism of action, effects, uses, and important nursing considerations.
Organophosphorus poisoning
This document discusses the case of a 27-year-old male who was brought to the emergency department unconscious after having an argument at home. On examination, he was found to have pinpoint pupils, increased muscle tone, and other signs suggestive of organophosphate or carbamate poisoning. The document then goes on to discuss in detail the management of organophosphate poisoning, including decontamination, use of atropine and pralidoxime, and monitoring for intermediate syndrome. Common organophosphate compounds and their mechanism of action via acetylcholinesterase inhibition is also explained.
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Aspirin is widely consumed as a pain reliever but can be toxic in high doses, especially for children. Symptoms of aspirin poisoning range from mild like ringing in the ears to more severe signs such as confusion, breathing difficulties, and coma. Treatment aims to prevent further aspirin absorption, correct dehydration and acidosis, and enhance aspirin removal through activated charcoal, IV fluids, and alkaline diuresis such as sodium bicarbonate which makes urine less acidic and helps flush aspirin from the body through the kidneys. Patients are monitored and may require supportive care like intubation and dialysis for dangerous overdoses.
Skeletal muscle relaxant
This document summarizes skeletal muscle relaxants. It describes both peripherally-acting and centrally-acting muscle relaxants. Peripherally-acting muscle relaxants include neuromuscular blocking agents like nondepolarizing (competitive) blockers and depolarizing blockers, which act at the neuromuscular junction. Centrally-acting muscle relaxants like baclofen, tizanidine and mephenesin derivatives act in the central nervous system to decrease muscle tone. The document discusses the mechanisms, uses and side effects of various muscle relaxant drugs.
Neostigmine - Mechanism of action, indications and side effects
Neostigmine is a medication used to treat myasthenia gravis and other conditions by inhibiting the enzyme acetylcholinesterase. This allows more acetylcholine to attach to receptors and improve muscle strength. It works by slowing the breakdown of acetylcholine at nerve endings. Common side effects include nausea, vomiting, and reduced heart rate. It is often given with atropine to prevent side effects from excess acetylcholine build up.
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Organophosphorus poisoning final
Organophosphorus compounds are widely used as pesticides and chemical weapons. They work by inhibiting acetylcholinesterase, leading to accumulation of acetylcholine and overstimulation of nicotinic and muscarinic receptors. Clinical features include excessive secretions, nausea, vomiting, diarrhea, weakness and respiratory failure. Treatment involves decontamination, atropine to block muscarinic effects, pralidoxime to reactivate acetylcholinesterase, and supportive care. Prognosis depends on prompt diagnosis and treatment, with mortality risks highest within 24 hours from respiratory or cardiac failure.
ORGANOPHOSPHATE POISONING AND MANAGEMENT
its all about organophosphate poisoning management in sri lanka. here this is most commonest poisoning.
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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.
Organophosphorus poisoning
Organophosphate poisoning occurs when organophosphate compounds such as insecticides and nerve agents inhibit the enzyme acetylcholinesterase. Symptoms range from mild effects like blurred vision and excess saliva to severe effects like respiratory failure and death. Treatment involves atropine to block acetylcholine effects and pralidoxime or obidoxime to reactivate acetylcholinesterase. Nursing care focuses on maintaining airway, breathing, circulation and preventing infection while the toxic substances are metabolized and excreted from the body. Organophosphate poisoning is a significant global health problem causing millions of hospitalizations annually.
Atropine
Atropine is a naturally occurring alkaloid extracted from deadly nightshade, Jimson weed, and mandrake. It has a wide variety of medical uses including as a cycloplegic and mydriatic in ophthalmology to dilate the pupils. It is also used to treat bradycardia and various types of heart block by increasing the heart rate. Additionally, atropine inhibits secretions and acts as a bronchodilator. It is used to treat organophosphate and nerve agent poisoning by blocking acetylcholine receptors. Common side effects include vision changes, dry mouth, fast heart rate, and confusion. Atropine is contraindicated in conditions like glaucoma and myast
Anti-cholinergic Drugs
Anticholinergic drugs work by blocking the actions of acetylcholine in the parasympathetic nervous system. They are competitive antagonists that bind to muscarinic receptors, reversibly blocking acetylcholine transmission. Atropine is a prototypical anticholinergic derived from deadly nightshade. It causes dilation of the pupils, increased heart rate, decreased secretions, and relaxed smooth muscles. Anticholinergics are used to treat Parkinson's disease, motion sickness, asthma, peptic ulcers, overactive bladder, and other conditions. Side effects include dry mouth, blurred vision, constipation, urinary retention, and excitement or delirium in overdose.
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Diuretics act at different sites along the nephron to promote the excretion of sodium, chloride, and water. The main classes are carbonic anhydrase inhibitors, loop diuretics, thiazides, potassium-sparing diuretics, and osmotic diuretics. They are used to treat conditions like edema, hypertension, and liver cirrhosis. Each class has a distinct mechanism of action and side effect profile. For example, loop diuretics inhibit sodium reabsorption in the loop of Henle but can cause ototoxicity, while thiazides target the distal tubule and cause hypokalemia. The site and mechanism of the drug determines its clinical applications and adverse effects
Phenol
Phenol is a toxic compound discovered in 1834 that has a variety of industrial and medical uses. It is absorbed through the skin, lungs, and gastrointestinal tract, distributing widely in the body before being metabolized and excreted in urine. Acute exposure can cause rapid nervous system effects like seizures and coma, while chronic exposure is associated with damage to the kidneys, liver, heart and skin. Phenol was also used by Nazis during World War II for individual executions by injection.
Bronchodilators
Bronchodilators are drugs used to relieve bronchospasms associated with respiratory disorders. The main classes of bronchodilators include adrenoceptor agonists like selective beta2 agonists, antimuscarinic bronchodilators, xanthine derivatives, and leukotriene antagonists. Beta2 agonists work by stimulating beta2 receptors in the lungs to promote bronchodilation. Antimuscarinics block acetylcholine's bronchoconstrictive effects. Xanthines like theophylline inhibit phosphodiesterase to increase cAMP and cause bronchodilation. Leukotriene receptor antagonists suppress the bronchoconstrictive effects of leukotrienes. Corticosteroids
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Op Poisoning
This document summarizes organophosphorus insecticides and nerve gas agents poisoning. It discusses the mechanisms, clinical manifestations and management of organophosphorus poisoning, which can cause acute cholinergic crisis, intermediate syndrome and organophosphate-induced delayed polyneuropathy. Treatment involves decontamination, atropine to block muscarinic effects, oximes like pralidoxime to reactivate acetylcholinesterase, and ventilatory support for respiratory failure and intermediate syndrome. Prognosis depends on dose, toxicity of agent and timeliness of treatment.
Op poisoning and its management
1) The document describes several cases of poisoning including organophosphorus, Cleistanthus collinus (Oduvanthalai), and oleander.
2) For the organophosphorus case, the patient presented with pinpoint pupils and muscle weakness. Atropine and pralidoxime were used for treatment.
3) The Cleistanthus collinus case involved hypokalemia, metabolic acidosis, and ARDS. Treatment included sodium bicarbonate and potassium supplementation.
4) Oleander poisoning can cause cardiac glycoside toxicity leading to arrhythmias. Management focuses on supportive care and treating arrhythmias.
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ORGANOPHOSPHATE COMPOUND POISONING
This document summarizes organophosphate poisoning. It discusses various organophosphate compounds used as insecticides and their relative toxicities. It describes the mechanisms of toxicity involving inhibition of acetylcholinesterase and excess acetylcholine accumulation. Signs and symptoms are outlined for both muscarinic and nicotinic effects. Diagnosis and various aspects of treatment are covered including decontamination, atropine administration, pralidoxime use, and management of complications such as intermediate syndrome and delayed polyneuropathy.
Bronchodilators
This document summarizes different classes of drugs used to treat respiratory conditions like asthma and COPD. It discusses bronchodilators including xanthine derivatives, beta agonists, and anticholinergics. It also covers anti-leukotrienes, corticosteroids, and mast cell stabilizers. For each class, it describes the mechanism of action, effects, uses, and important nursing considerations.
Organophosphorus poisoning
This document discusses the case of a 27-year-old male who was brought to the emergency department unconscious after having an argument at home. On examination, he was found to have pinpoint pupils, increased muscle tone, and other signs suggestive of organophosphate or carbamate poisoning. The document then goes on to discuss in detail the management of organophosphate poisoning, including decontamination, use of atropine and pralidoxime, and monitoring for intermediate syndrome. Common organophosphate compounds and their mechanism of action via acetylcholinesterase inhibition is also explained.
Aspirin poisoning
Aspirin is widely consumed as a pain reliever but can be toxic in high doses, especially for children. Symptoms of aspirin poisoning range from mild like ringing in the ears to more severe signs such as confusion, breathing difficulties, and coma. Treatment aims to prevent further aspirin absorption, correct dehydration and acidosis, and enhance aspirin removal through activated charcoal, IV fluids, and alkaline diuresis such as sodium bicarbonate which makes urine less acidic and helps flush aspirin from the body through the kidneys. Patients are monitored and may require supportive care like intubation and dialysis for dangerous overdoses.
Skeletal muscle relaxant
This document summarizes skeletal muscle relaxants. It describes both peripherally-acting and centrally-acting muscle relaxants. Peripherally-acting muscle relaxants include neuromuscular blocking agents like nondepolarizing (competitive) blockers and depolarizing blockers, which act at the neuromuscular junction. Centrally-acting muscle relaxants like baclofen, tizanidine and mephenesin derivatives act in the central nervous system to decrease muscle tone. The document discusses the mechanisms, uses and side effects of various muscle relaxant drugs.
Neostigmine - Mechanism of action, indications and side effects
Neostigmine is a medication used to treat myasthenia gravis and other conditions by inhibiting the enzyme acetylcholinesterase. This allows more acetylcholine to attach to receptors and improve muscle strength. It works by slowing the breakdown of acetylcholine at nerve endings. Common side effects include nausea, vomiting, and reduced heart rate. It is often given with atropine to prevent side effects from excess acetylcholine build up.
general anaesthesia
General Anaesthesia produces reversible loss of sensation and consciousness through the use of drugs. There are two main classifications of anaesthetics - inhalational and intravenous. Inhalational includes gases like nitrous oxide and liquid anaesthetics administered using a vaporizer. Intravenous anaesthetics include inducing agents like thiopentone sodium and propofol, as well as slower acting drugs like ketamine and benzodiazepines. Anaesthesia involves three stages - induction, maintenance, and recovery. The ideal stage for surgery is stage III, where there is loss of muscle tone and reflexes. Careful monitoring is needed to prevent progression to stage IV, which can cause respiratory and circulatory depression.
Skeletal muscle relaxants, Neuromuscular blocking agents, Neuromuscular blockers
This document discusses neuromuscular blocking agents. It begins by defining neuromuscular blocking drugs as agents that act at the neuromuscular junction to block neuromuscular transmission, facilitating muscle relaxation for surgery or ventilation. It then categorizes these drugs as either depolarizing or non-depolarizing. Succinylcholine is discussed as the primary depolarizing agent, causing initial muscle fasciculations before paralysis through prolonged depolarization. Non-depolarizing agents like pancuronium and vecuronium are competitive antagonists that block acetylcholine receptors. The document covers the mechanisms, uses, and side effects of various neuromuscular blocking drugs.
Management of Opioid Analgesic Overdose
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
Organophosphorus poisoning final
Organophosphorus compounds are widely used as pesticides and chemical weapons. They work by inhibiting acetylcholinesterase, leading to accumulation of acetylcholine and overstimulation of nicotinic and muscarinic receptors. Clinical features include excessive secretions, nausea, vomiting, diarrhea, weakness and respiratory failure. Treatment involves decontamination, atropine to block muscarinic effects, pralidoxime to reactivate acetylcholinesterase, and supportive care. Prognosis depends on prompt diagnosis and treatment, with mortality risks highest within 24 hours from respiratory or cardiac failure.
ORGANOPHOSPHATE POISONING AND MANAGEMENT
its all about organophosphate poisoning management in sri lanka. here this is most commonest poisoning.
Benzodiazepines toxicity
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.
Organophosphorus poisoning
Organophosphate poisoning occurs when organophosphate compounds such as insecticides and nerve agents inhibit the enzyme acetylcholinesterase. Symptoms range from mild effects like blurred vision and excess saliva to severe effects like respiratory failure and death. Treatment involves atropine to block acetylcholine effects and pralidoxime or obidoxime to reactivate acetylcholinesterase. Nursing care focuses on maintaining airway, breathing, circulation and preventing infection while the toxic substances are metabolized and excreted from the body. Organophosphate poisoning is a significant global health problem causing millions of hospitalizations annually.
Atropine
Atropine is a naturally occurring alkaloid extracted from deadly nightshade, Jimson weed, and mandrake. It has a wide variety of medical uses including as a cycloplegic and mydriatic in ophthalmology to dilate the pupils. It is also used to treat bradycardia and various types of heart block by increasing the heart rate. Additionally, atropine inhibits secretions and acts as a bronchodilator. It is used to treat organophosphate and nerve agent poisoning by blocking acetylcholine receptors. Common side effects include vision changes, dry mouth, fast heart rate, and confusion. Atropine is contraindicated in conditions like glaucoma and myast
Anti-cholinergic Drugs
Anticholinergic drugs work by blocking the actions of acetylcholine in the parasympathetic nervous system. They are competitive antagonists that bind to muscarinic receptors, reversibly blocking acetylcholine transmission. Atropine is a prototypical anticholinergic derived from deadly nightshade. It causes dilation of the pupils, increased heart rate, decreased secretions, and relaxed smooth muscles. Anticholinergics are used to treat Parkinson's disease, motion sickness, asthma, peptic ulcers, overactive bladder, and other conditions. Side effects include dry mouth, blurred vision, constipation, urinary retention, and excitement or delirium in overdose.
Diuretics
Diuretics act at different sites along the nephron to promote the excretion of sodium, chloride, and water. The main classes are carbonic anhydrase inhibitors, loop diuretics, thiazides, potassium-sparing diuretics, and osmotic diuretics. They are used to treat conditions like edema, hypertension, and liver cirrhosis. Each class has a distinct mechanism of action and side effect profile. For example, loop diuretics inhibit sodium reabsorption in the loop of Henle but can cause ototoxicity, while thiazides target the distal tubule and cause hypokalemia. The site and mechanism of the drug determines its clinical applications and adverse effects
Phenol
Phenol is a toxic compound discovered in 1834 that has a variety of industrial and medical uses. It is absorbed through the skin, lungs, and gastrointestinal tract, distributing widely in the body before being metabolized and excreted in urine. Acute exposure can cause rapid nervous system effects like seizures and coma, while chronic exposure is associated with damage to the kidneys, liver, heart and skin. Phenol was also used by Nazis during World War II for individual executions by injection.
Bronchodilators
Bronchodilators are drugs used to relieve bronchospasms associated with respiratory disorders. The main classes of bronchodilators include adrenoceptor agonists like selective beta2 agonists, antimuscarinic bronchodilators, xanthine derivatives, and leukotriene antagonists. Beta2 agonists work by stimulating beta2 receptors in the lungs to promote bronchodilation. Antimuscarinics block acetylcholine's bronchoconstrictive effects. Xanthines like theophylline inhibit phosphodiesterase to increase cAMP and cause bronchodilation. Leukotriene receptor antagonists suppress the bronchoconstrictive effects of leukotrienes. Corticosteroids
Adrenaline & Noradrenaline
Catecholamine, sympatho-mimetic monoamine, derived -phenylalanine and tyrosine.
C9H13NO3
MOL WT:183.20442 g/mol
Classification of Adrenergic Hormone Receptors
ADRENALINE PREPARATIONS
Adrenaline - DOC -cardiac arrest.
ADR IN ACLS
Phenytoin Toxicity
Phenytoin is a commonly used anticonvulsant with a narrow therapeutic window, making toxicity a risk. Acute toxicity from overdose causes neurological symptoms like nystagmus and ataxia in a concentration-dependent manner, while chronic use risks side effects like gingival enlargement. Factors like changes in dose, medications, albumin levels and disease states can affect phenytoin levels. Evaluation includes phenytoin levels and albumin. Treatment focuses on supportive care, with activated charcoal for acute overdoses and hemodialysis in severe cases. Prognosis is generally good but deaths can occur at very high concentrations.
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Op Poisoning
This document summarizes organophosphorus insecticides and nerve gas agents poisoning. It discusses the mechanisms, clinical manifestations and management of organophosphorus poisoning, which can cause acute cholinergic crisis, intermediate syndrome and organophosphate-induced delayed polyneuropathy. Treatment involves decontamination, atropine to block muscarinic effects, oximes like pralidoxime to reactivate acetylcholinesterase, and ventilatory support for respiratory failure and intermediate syndrome. Prognosis depends on dose, toxicity of agent and timeliness of treatment.
Op poisoning and its management
1) The document describes several cases of poisoning including organophosphorus, Cleistanthus collinus (Oduvanthalai), and oleander.
2) For the organophosphorus case, the patient presented with pinpoint pupils and muscle weakness. Atropine and pralidoxime were used for treatment.
3) The Cleistanthus collinus case involved hypokalemia, metabolic acidosis, and ARDS. Treatment included sodium bicarbonate and potassium supplementation.
4) Oleander poisoning can cause cardiac glycoside toxicity leading to arrhythmias. Management focuses on supportive care and treating arrhythmias.
Organophosphorous poisoning
This document summarizes organophosphorous (OP) poisoning. OP compounds are commonly used as agricultural insecticides and were historically developed as chemical warfare agents. They work by inhibiting the enzyme acetylcholinesterase, leading to excess acetylcholine in the body. Clinical effects range from acute cholinergic crisis to intermediate muscle weakness to delayed neuropathy. Diagnosis is based on history of exposure and clinical features. Treatment involves atropine to control muscarinic effects, pralidoxime to reactivate acetylcholinesterase, benzodiazepines for seizures, and supportive care. Prognosis depends on prompt diagnosis and treatment to prevent respiratory failure, intermediate syndrome, or delayed neuropathy.
Organophosphate poisoning
Organophosphate poisoning occurs when organophosphate compounds inhibit acetylcholinesterase in the nervous system, causing overstimulation of muscarinic and nicotinic receptors. Examples of organophosphates include nerve gases and insecticides. Symptoms include excessive salivation, urination, diarrhea, nausea, and pinpoint pupils. Treatment involves atropine to block parasympathetic effects and pralidoxime as an antidote to reactivate acetylcholinesterase. Exposure can occur through ingestion, inhalation or skin contact of pesticides and chemical weapons.
Organophosphorous poisoning
Organophosphorus (OP) compounds are a large family of chemicals that are widely used as pesticides and were developed as nerve agents. Exposure to OPs can cause acute poisoning by inhibiting acetylcholinesterase and overstimulating the parasympathetic nervous system. This can result in muscle weakness, seizures, respiratory failure and death. Several cases of accidental and intentional OP poisoning in India are described, including an incident where school children were poisoned by contaminated food, resulting in many deaths. Chronic low-level exposure to OP pesticides also poses health risks and is a major cause of poisoning in developing nations.
Oppoisoning
Organophosphate poisoning occurs when someone is exposed to organophosphate compounds, which are commonly found in insecticides, nerve agents, and other chemicals. These compounds work by inhibiting acetylcholinesterase, leading to excess acetylcholine in the body and stimulation of muscarinic and nicotinic receptors. Symptoms include bronchospasm, vomiting, diarrhea, muscle weakness and paralysis. Diagnosis is made through history, physical exam, checking acetylcholinesterase levels in blood and urine. Treatment involves atropine to counteract excess acetylcholine, pralidoxime to reactivate acetylcholinesterase, benzodiazepines for seizures, and supportive care. Prognosis depends on
Organophosphorous compounds toxicity
Organophosphorous compounds work by inhibiting acetylcholinesterase, leading to overstimulation of muscarinic and nicotinic receptors. Signs and symptoms include muscarinic effects like excessive sweating, urination, and salivation ("DUMBELS") and nicotinic effects like muscle weakness. Treatment involves atropine to reverse muscarinic effects, pralidoxime to reactivate acetylcholinesterase within 48 hours, benzodiazepines for seizures, and supportive care like ventilation and fluid management. Measuring red blood cell acetylcholinesterase levels can help confirm exposure.
ORGANOPHOSPHOROUS POISONING NEUROVIEW
Organophosphate (OP) compounds irreversibly inhibit acetylcholinesterase (AChE), leading to accumulation of acetylcholine and overstimulation of muscarinic and nicotinic receptors. Clinical features include muscarinic, nicotinic, and central nervous system effects. Diagnosis is based on exposure history and low AChE levels. Treatment involves atropine for muscarinic effects, pralidoxime for reactivation of AChE, supportive care, and monitoring for intermediate syndrome or delayed neuropathy. Prevention focuses on safe use of pesticides and other OP sources.
Organophosphorus and organoochlorine poisoning clinical features
This document summarizes the clinical manifestations of organophosphorus and organochlorine poisoning. It describes how organophosphates work by inhibiting acetylcholinesterase, leading to increased acetylcholine levels and overstimulation of muscarinic and nicotinic receptors. Signs and symptoms are divided into muscarinic effects (SLUDGE), nicotinic effects, and CNS effects. Organochlorines are strongly lipid soluble and sequester in tissues, causing prolonged systemic effects. The document also outlines routes of absorption, presentations of acute and chronic toxicity, and introduces the Peradeniya Organophosphorus Poisoning scale for assessing severity without laboratory tests.
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ANRI COLLEGE OF NURSING
VISAKHAPATNAM
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Organophosphorus and organoochlorine poisoning clinical features
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Similar to Management of op poisoning-definitive treatment
Anticholinesterases
CONTENTS:
INTRO to Anticholinesterases
MECHANISM OF ACTION
THERAPEUTIC USES
ADVERSE DRUG REACTIONS
OP POISONING- TREATMENT
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Op poisoing.pdf
Organophosphate poisoning is caused by exposure to pesticides, herbicides, and nerve gases. It results in the inhibition of acetylcholinesterase, leading to accumulation of acetylcholine and overstimulation of muscarinic and nicotinic receptors. Symptoms range from mild like nausea to severe like respiratory failure. Treatment involves atropine to block acetylcholine receptors, oximes like pralidoxime to reactivate inhibited acetylcholinesterase, diazepam for seizures, supportive care, and monitoring for complications like pneumonia. Prognosis depends on prompt treatment and severity of exposure.
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Organophosphate poisoning - a brief toxicological study
this is a brief study on organophosphate poisoning , as it being more common problem in the health sector and emergency medicine now a days , this will be much helpful among health professionals .........text me for more topics
martinsuaj369@gmail.com
thank you
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preclinical screening method of antiemetic drugs.pptx
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This document summarizes information about cholinergic transmission and drugs that act on the cholinergic system. It discusses acetylcholine as a neurotransmitter and its roles. It describes the distribution of muscarinic and nicotinic receptors and the effects of cholinergic drugs. Specifically, it covers direct and indirect cholinergic agonists as well as anticholinesterases and antimuscarinic drugs. It also provides information on myasthenia gravis and organophosphate poisoning, including associated signs/symptoms and treatment approaches.
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Management of op poisoning-definitive treatment
- 3. (a)ATROPINE Anti cholinergic drug. Objective : To block the muscarinic receptors until the organophosphate is metabolised away from the body. Atropine : Adult dose : 2-5mg i.v. repeated every 5 min doubling the initial dose. Children : 0.05-0.1mg/kg Given till signs of atropinization appear. Continued treatment: maintenance dose (30% of atropinization dose) for 1-2 weeks.
- 4. (b)CHOLINESTERASE REACTIVATORS Oximes are used to restore neuromuscular transmission. If more reactive OH groups in the form of oximes (Generic formula R-CH=N-OH) are provided reactivation occurs more faster. Eg: Pralidoxime ( 2-PAM)
- 5. Action of Pralidoxime (2-PAM) Attaches to the anionic site of the enzyme. Oxime end reacts with the phosphorus atom attached to the esteratic site. Oxime-phosphonate form and diffuse away. Reactivated ChE remain. Treatment should be started within 24 hours before the phosphorylated enzyme undergoes ‘Aging’ and become resistant to hydrolysis.
- 6. It is ineffective to carbamate poisoning as in that case the anionic site of the enzyme is not free. It is rather contraindicated because it has weak anti-ChE activity of its own.
- 7. Injected Doses Use i.v. slowly in a dose of 1-2g. may be repeated according to need. of oximes in OP poisoning is secondary to that of Atropine.
- 8. OTHER OXIMES: Obidoxime: more potent than pralidoxime Diacetyl-monoxime (DAM): Lipophilic; so if the OP poisoning symptoms are more central DAM is used as it can cross the blood brain barrier.