Carbon Monoxide is one of the most common causes of inhalation poisoning worldwide and can result in significant morbidity due to persistent neuropathology and cognitive sequelae. The manifestation of carbon monoxide poisoning are non specific and severity of symptoms range from mild such as headache, confusion, lack of energy to severe, such as coma, respiratory depression, cardiac dysfunction and even death. Hyperbaric oxygen therapy has been used for decades in the treatment of acute and delayed effects of carbon monoxide poisoning. Hyperbaric Oxygen is the only treatment for acute CO poisoning where it competes with CarboxyHemoglobin preventing the resultant damage and in delayed neuropsychological sequelae. This case report is of a young lady from rural Haryana presented after 48 hours of CO Poisoning with acute confusion, partial retrograde and complete anterograde memory loss. Following 15 days of hyperbaric oxygen she showed near complete recovery and her Mini Mental Scale Examination (MMSE) score which was 12/30 on the first day went up to 29/30. This case demonstrates that HBO therapy is efficacious in recovery of delayed neuropsychiatric sequelae of Carbon Monoxide poisoning.
Effects of yoga on the control of dopaminenaveen a
This document discusses the role of yoga in treating nicotine addiction. It begins by outlining the harmful toxins in cigarette smoke like nicotine, carbon monoxide, and tar. Nicotine is highlighted as the primary addictive substance, stimulating the brain's reward system. Repeated nicotine exposure leads to tolerance and dependence through changes in neurotransmitters like dopamine, glutamate, and GABA. The document then proposes that yoga can aid in deaddiction by disrupting genes related to nicotine metabolism and sensitization. Specifically, yoga is suggested to decrease nicotine and cotinine levels by reducing liver enzymes and increasing monoamine oxidase. This helps normalize neurotransmitter activity and prevents withdrawal symptoms. The conclusion restates that
This document provides information about tobacco cessation and the harms of smoking. It discusses how smoking harms smokers' health, causing various cancers and respiratory diseases. It also outlines the negative health effects of secondhand smoke exposure. The document covers nicotine addiction and reasons for tobacco use, as well as the significant health and economic costs of smoking. Finally, it discusses strategies and health benefits for quitting smoking.
Smoking is a major public health problem. Cigarette smoking acts as a nicotine delivery in humans, has found to produce profound changes in physiological architecture. Smoking’s as well as chronic pain are one of the major challenging health concerns faced in day to day life. During smoking nicotine is quickly absorbed into the blood stream within a time gap of 30 seconds it reaches the brain. It stimulates the brain to release various chemicals namely epinephrine which will give a pleasurable euphoric effect. It is a proven fact that smoking of tobacco will cause the production of Rheumatoid factors or anti-cyclic citrullinated peptide autoantibodies which is a risk factor for the development of Rheumatoid arthritis. There is a positive relation between smoking and depression and it has been seen smokers use more number of cigarettes when depressed and smoking also caused the individual who is depressed more prone to pain than a normal smoker. Quitting of smoking is quite difficult because of unpleasant withdrawal syndrome that consists of frustration, depression, anxiety, reduced heart rate, increased weight, depressed mood, difficulty in concentration. Because of all these withdrawal symptoms individuals who try to quit start up again very soon. Smoking is a health hazard, this is a well-known fact and the noxious effects are multiple so in management of pain in theseindividual’s, necessary steps has to be put forward in order to quit the habit. Cognitive behavioural therapy or antidepressant therapy in the management of pain of depressed patients who are smokers has shown good results in a rehabilitation centre on the course of the management of pain.
Introductory Psychology: Neuropharmacology II (Stimulants)Brian Piper
1) Stimulants are drugs that excite neural activity and speed up body functions, including nicotine, caffeine, amphetamines, and ecstasy.
2) Nicotine is the active ingredient in tobacco and has effects on acetylcholine receptors in the brain. Smoking increases nicotine and receptor levels in brain areas involved in movement and cognition.
3) Quitting smoking provides significant health benefits and reduces risks of cancer, heart disease, and other conditions, according to statistical studies of doctors and other populations, though the psychology of decision making makes continuing smoking seem less risky.
This Cochrane review summarizes evidence on interventions for smoking cessation and reduction in individuals with schizophrenia. The review finds that bupropion is effective for smoking cessation in patients with schizophrenia based on available evidence. No significant deterioration of mental state or increased seizure risk was found from bupropion use. Evidence for bupropion's effect on smoking reduction is inconclusive. The review also found some evidence supporting varenicline for smoking cessation in this population, though the evidence is limited compared to studies of bupropion.
This document provides an overview of the pharmacologic treatment of opiate dependence, including:
- A historical perspective on approaches to treatment such as methadone maintenance and more recent developments like buprenorphine.
- An explanation of how opioid agonists like methadone and buprenorphine work in the brain and body to reduce withdrawal symptoms and cravings while blocking the effects of other opioids.
- Guidance on patient selection criteria for buprenorphine treatment and considerations around its use as a replacement therapy in office-based settings to expand treatment access.
The importance of treating tobacco dependenceSimon Thornley
1) Smoking is a major risk factor for cardiovascular disease. Stopping smoking significantly reduces this risk and provides both short-term and long-term health benefits.
2) Healthcare providers should identify smokers and ensure they receive evidence-based cessation treatments including behavioral support and pharmacotherapy to maximize chances of long-term abstinence.
3) Physicians play a key role by advising patients to quit smoking and offering cessation support through brief counseling and recommending combinations of behavioral support and medication.
Smoking cessation should be a priority for all smokers and healthcare providers should routinely evaluate smoking status and offer treatments. The document outlines smoking as an addiction that requires both brief interventions and more intensive behavioral and pharmacological treatments to increase chances of long term abstinence. It emphasizes treating tobacco dependence as a primary disorder and implementing systems to ensure all smokers are identified and receive evidence-based cessation support.
Effects of yoga on the control of dopaminenaveen a
This document discusses the role of yoga in treating nicotine addiction. It begins by outlining the harmful toxins in cigarette smoke like nicotine, carbon monoxide, and tar. Nicotine is highlighted as the primary addictive substance, stimulating the brain's reward system. Repeated nicotine exposure leads to tolerance and dependence through changes in neurotransmitters like dopamine, glutamate, and GABA. The document then proposes that yoga can aid in deaddiction by disrupting genes related to nicotine metabolism and sensitization. Specifically, yoga is suggested to decrease nicotine and cotinine levels by reducing liver enzymes and increasing monoamine oxidase. This helps normalize neurotransmitter activity and prevents withdrawal symptoms. The conclusion restates that
This document provides information about tobacco cessation and the harms of smoking. It discusses how smoking harms smokers' health, causing various cancers and respiratory diseases. It also outlines the negative health effects of secondhand smoke exposure. The document covers nicotine addiction and reasons for tobacco use, as well as the significant health and economic costs of smoking. Finally, it discusses strategies and health benefits for quitting smoking.
Smoking is a major public health problem. Cigarette smoking acts as a nicotine delivery in humans, has found to produce profound changes in physiological architecture. Smoking’s as well as chronic pain are one of the major challenging health concerns faced in day to day life. During smoking nicotine is quickly absorbed into the blood stream within a time gap of 30 seconds it reaches the brain. It stimulates the brain to release various chemicals namely epinephrine which will give a pleasurable euphoric effect. It is a proven fact that smoking of tobacco will cause the production of Rheumatoid factors or anti-cyclic citrullinated peptide autoantibodies which is a risk factor for the development of Rheumatoid arthritis. There is a positive relation between smoking and depression and it has been seen smokers use more number of cigarettes when depressed and smoking also caused the individual who is depressed more prone to pain than a normal smoker. Quitting of smoking is quite difficult because of unpleasant withdrawal syndrome that consists of frustration, depression, anxiety, reduced heart rate, increased weight, depressed mood, difficulty in concentration. Because of all these withdrawal symptoms individuals who try to quit start up again very soon. Smoking is a health hazard, this is a well-known fact and the noxious effects are multiple so in management of pain in theseindividual’s, necessary steps has to be put forward in order to quit the habit. Cognitive behavioural therapy or antidepressant therapy in the management of pain of depressed patients who are smokers has shown good results in a rehabilitation centre on the course of the management of pain.
Introductory Psychology: Neuropharmacology II (Stimulants)Brian Piper
1) Stimulants are drugs that excite neural activity and speed up body functions, including nicotine, caffeine, amphetamines, and ecstasy.
2) Nicotine is the active ingredient in tobacco and has effects on acetylcholine receptors in the brain. Smoking increases nicotine and receptor levels in brain areas involved in movement and cognition.
3) Quitting smoking provides significant health benefits and reduces risks of cancer, heart disease, and other conditions, according to statistical studies of doctors and other populations, though the psychology of decision making makes continuing smoking seem less risky.
This Cochrane review summarizes evidence on interventions for smoking cessation and reduction in individuals with schizophrenia. The review finds that bupropion is effective for smoking cessation in patients with schizophrenia based on available evidence. No significant deterioration of mental state or increased seizure risk was found from bupropion use. Evidence for bupropion's effect on smoking reduction is inconclusive. The review also found some evidence supporting varenicline for smoking cessation in this population, though the evidence is limited compared to studies of bupropion.
This document provides an overview of the pharmacologic treatment of opiate dependence, including:
- A historical perspective on approaches to treatment such as methadone maintenance and more recent developments like buprenorphine.
- An explanation of how opioid agonists like methadone and buprenorphine work in the brain and body to reduce withdrawal symptoms and cravings while blocking the effects of other opioids.
- Guidance on patient selection criteria for buprenorphine treatment and considerations around its use as a replacement therapy in office-based settings to expand treatment access.
The importance of treating tobacco dependenceSimon Thornley
1) Smoking is a major risk factor for cardiovascular disease. Stopping smoking significantly reduces this risk and provides both short-term and long-term health benefits.
2) Healthcare providers should identify smokers and ensure they receive evidence-based cessation treatments including behavioral support and pharmacotherapy to maximize chances of long-term abstinence.
3) Physicians play a key role by advising patients to quit smoking and offering cessation support through brief counseling and recommending combinations of behavioral support and medication.
Smoking cessation should be a priority for all smokers and healthcare providers should routinely evaluate smoking status and offer treatments. The document outlines smoking as an addiction that requires both brief interventions and more intensive behavioral and pharmacological treatments to increase chances of long term abstinence. It emphasizes treating tobacco dependence as a primary disorder and implementing systems to ensure all smokers are identified and receive evidence-based cessation support.
Lecture 12 from a college level neuropharmacology course taught in the spring 2012 semester by Brian J. Piper, Ph.D. (psy391@gmail.com) at Willamette University. Focus is on pharmacokinetics, pharmacodynamics, epidemiology, and health risks
Nicotine replacement therapy uses various dosage forms to deliver nicotine in a controlled manner and reduce withdrawal symptoms when quitting smoking. These include transdermal patches, sublingual tablets, nasal sprays, lozenges, and gum. Newer electronic cigarettes resemble smoking but deliver nicotine without smoke. Vaccines are also in development that could provide long-term protection from nicotine by interacting with it in the bloodstream rather than brain receptors. Nicotine replacement aims to substitute nicotine intake from safer sources to support smoking cessation efforts.
The document discusses nicotine addiction and pharmacotherapy options for smoking cessation. It begins by explaining how nicotine acts on the brain's reward pathway similarly to drugs like heroin and cocaine. Nicotine rapidly increases dopamine release in the nucleus accumbens, reinforcing the behavior. Pharmacotherapies like nicotine replacement therapy, bupropion, and varenicline can help relieve withdrawal symptoms and cravings by interacting with nicotinic receptors. NRT is considered low risk and safer than smoking, delivering nicotine without other harmful chemicals. Combining medication with behavioral counseling improves quit rates.
Nicotine is highly addictive and the primary reason for tobacco addiction worldwide. Quitting smoking can be challenging due to nicotine withdrawal symptoms and cravings. This article discusses nicotine addiction, statistics on smoking worldwide, methods for quitting smoking such as nicotine replacement therapy and non-nicotine medications, and the long term health benefits of quitting such as reduced risk of cancer, heart disease, and other smoking-related illnesses. Overcoming nicotine addiction requires commitment to treatment and lifestyle changes but can significantly improve health outcomes.
This presentation describes the Effect of smoking on response to periodontal therapy
1. Non surgical periodontal therapy 2. Antimicrobial therapy
3. Conventional surgical therapy 4. Regenerative procedures
5. Mucogingival surgeries
This document is a biology report on drug addiction by Sourabh Meena. It includes an introduction, classification of drugs, descriptions of harmful drugs like heroin, cannabis and cocaine. It discusses how drug addiction begins, the social and health impacts of drug abuse. It also covers the harms of tobacco, nicotine, alcohol and provides news clippings about drug abuse issues. The report was completed to fulfill biology course requirements and obtain a certificate.
This document provides information on tobacco dependence treatment. It begins with objectives and an introduction noting the global impact of tobacco use. It then describes various types of tobacco products and their significant health side effects. Signs and symptoms of nicotine dependence are outlined using the Fagerstrom Test. The benefits of quitting and roles of medical staff in treatment are discussed. Treatment methods covered include counseling, nicotine replacement therapy, medications, and support groups. Nicotine withdrawal symptoms and specifics of nicotine patches, gum, and other replacement products are also summarized.
Nicotine Replacement Therapy (NRT) can help with the withdrawal symptoms in patients who find it difficult to quit tobacco. It is available in the form of - gums, patches, sprays, inhalers or lozenges.
This document provides information and instructions for responding to an opioid overdose emergency using naloxone. It begins with an overview of the REVIVE program and training objectives. It then discusses opioid overdoses, how to recognize one, and risk factors. Myths about reversing overdoses are dispelled. The document emphasizes that naloxone is the only effective response and provides step-by-step instructions: check responsiveness and give rescue breaths if needed, call 911, administer naloxone, continue rescue breathing, and give a second dose of naloxone if needed. Proper positioning and calling for emergency help are also described.
Nicotine is highly addictive and found in tobacco. When tobacco is smoked, nicotine reaches the brain within seconds and is distributed throughout the body rapidly, causing stimulation and increased heart rate and blood pressure. Long-term smoking is associated with many serious health issues like cancer, heart disease, and emphysema. While smoking rates have declined due to public health campaigns, tobacco use prevention and treatment programs could be expanded further.
COPD; a chronic, progressive airway obstruction; is directly linked with persistent inflammation and high oxidative stress. Airway obstruction is added on by plugging of airways with thick mucus. Role and efficacy of N-acetyl cysteine is reviewed with clinical cases.
Carbon monoxide is an odorless, colorless gas that is produced as a byproduct of combustion from various sources like vehicles, furnaces, generators and stoves. It can be lethal even in small amounts by preventing red blood cells from carrying oxygen. The document provides information about carbon monoxide's chemical structure and properties, sources of CO in homes, symptoms of CO poisoning like headaches and dizziness, safety tips to prevent CO exposure and the importance of installing CO detectors. It also lists a website for more resources on protecting against carbon monoxide poisoning.
Carbon Monoxide is also known as silent killer because it has no taste, odor and smell. Carbon Monoxide Kills (http://www.carbonmonoxidekills.com/) helps you to recover from carbon monoxide poisoning.
Facts you should know about Carbon MonoxideEthan Jacob
Carbonmonoxidekills (http://www.carbonmonoxidekills.com/) helps you to know about CO poisoning and how to protect your self and your family from CO poisoning.
This document discusses carbon monoxide poisoning, including its structure, pathophysiology, effects on the human body, sources, prevention, and treatment strategies. Carbon monoxide is an odorless, colorless gas that binds to hemoglobin over 200 times more than oxygen, preventing oxygen from being transported throughout the body and causing hypoxia. Symptoms range from headaches and dizziness at low levels to seizures, loss of consciousness, and death at high levels. Common sources include vehicles, heaters, and cooking equipment. Treatment focuses on high-flow oxygen therapy and hyperbaric oxygen chambers.
Management of op poisoning-definitive treatmentNuwani Kodi
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.
Carbon monoxide poisoning by dr Yasser DiabYasser Diab
This document describes two cases of carbon monoxide poisoning. In the first case, a 67-year-old man was admitted to the hospital multiple times with symptoms before being diagnosed with carbon monoxide poisoning from a faulty furnace. His wife also had carbon monoxide poisoning. In the second case, a 69-year-old man was admitted to the hospital with confusion and other symptoms, and his sister and daughter-in-law later came to the emergency room with carbon monoxide poisoning from his faulty water heater. The document then provides details on carbon monoxide, sources, effects on the body, signs and symptoms, treatment, and differential diagnosis.
Carbon monoxide poisoning results in over 50,000 emergency department visits per year in the US. While normobaric oxygen is the standard treatment, hyperbaric oxygen therapy may provide benefits for certain high-risk patients. One randomized trial found hyperbaric oxygen reduced cognitive sequelae rates at both 6 weeks and 12 months post-poisoning compared to normobaric oxygen alone in patients treated within 24 hours. Guidelines recommend considering hyperbaric oxygen for patients with serious poisoning symptoms or those over 36, exposed over 24 hours, or with CO-Hb over 25%. Patients should be informed of potential for long-term effects even after treatment.
This document provides information on carbon monoxide poisoning, including pathophysiology, signs and symptoms, diagnosis, treatment and prognosis. It notes that CO binds to hemoglobin over 200 times more than oxygen, resulting in hypoxia. Symptoms range from headaches and nausea to confusion, loss of consciousness and death. Treatment involves high-flow oxygen and potentially hyperbaric oxygen therapy. Prognosis can vary from full recovery to neurological deficits or death depending on severity and treatment.
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.
The document summarizes a case report of a 18-year-old female patient admitted for organophosphorus pesticide poisoning. She initially presented with excessive salivation, constricted pupils, tachycardia and decreased oxygen levels. She later developed intermediate syndrome with altered sensorium and difficulty breathing. Further examination showed signs of delayed neuropathy with weakness and sensory deficits. Treatment with atropine, pralidoxime and steroids improved her condition. The document then discusses organophosphorus poisoning, its mechanisms, clinical syndromes and delayed complications including intermediate syndrome and organophosphorus-induced delayed neuropathy.
Lecture 12 from a college level neuropharmacology course taught in the spring 2012 semester by Brian J. Piper, Ph.D. (psy391@gmail.com) at Willamette University. Focus is on pharmacokinetics, pharmacodynamics, epidemiology, and health risks
Nicotine replacement therapy uses various dosage forms to deliver nicotine in a controlled manner and reduce withdrawal symptoms when quitting smoking. These include transdermal patches, sublingual tablets, nasal sprays, lozenges, and gum. Newer electronic cigarettes resemble smoking but deliver nicotine without smoke. Vaccines are also in development that could provide long-term protection from nicotine by interacting with it in the bloodstream rather than brain receptors. Nicotine replacement aims to substitute nicotine intake from safer sources to support smoking cessation efforts.
The document discusses nicotine addiction and pharmacotherapy options for smoking cessation. It begins by explaining how nicotine acts on the brain's reward pathway similarly to drugs like heroin and cocaine. Nicotine rapidly increases dopamine release in the nucleus accumbens, reinforcing the behavior. Pharmacotherapies like nicotine replacement therapy, bupropion, and varenicline can help relieve withdrawal symptoms and cravings by interacting with nicotinic receptors. NRT is considered low risk and safer than smoking, delivering nicotine without other harmful chemicals. Combining medication with behavioral counseling improves quit rates.
Nicotine is highly addictive and the primary reason for tobacco addiction worldwide. Quitting smoking can be challenging due to nicotine withdrawal symptoms and cravings. This article discusses nicotine addiction, statistics on smoking worldwide, methods for quitting smoking such as nicotine replacement therapy and non-nicotine medications, and the long term health benefits of quitting such as reduced risk of cancer, heart disease, and other smoking-related illnesses. Overcoming nicotine addiction requires commitment to treatment and lifestyle changes but can significantly improve health outcomes.
This presentation describes the Effect of smoking on response to periodontal therapy
1. Non surgical periodontal therapy 2. Antimicrobial therapy
3. Conventional surgical therapy 4. Regenerative procedures
5. Mucogingival surgeries
This document is a biology report on drug addiction by Sourabh Meena. It includes an introduction, classification of drugs, descriptions of harmful drugs like heroin, cannabis and cocaine. It discusses how drug addiction begins, the social and health impacts of drug abuse. It also covers the harms of tobacco, nicotine, alcohol and provides news clippings about drug abuse issues. The report was completed to fulfill biology course requirements and obtain a certificate.
This document provides information on tobacco dependence treatment. It begins with objectives and an introduction noting the global impact of tobacco use. It then describes various types of tobacco products and their significant health side effects. Signs and symptoms of nicotine dependence are outlined using the Fagerstrom Test. The benefits of quitting and roles of medical staff in treatment are discussed. Treatment methods covered include counseling, nicotine replacement therapy, medications, and support groups. Nicotine withdrawal symptoms and specifics of nicotine patches, gum, and other replacement products are also summarized.
Nicotine Replacement Therapy (NRT) can help with the withdrawal symptoms in patients who find it difficult to quit tobacco. It is available in the form of - gums, patches, sprays, inhalers or lozenges.
This document provides information and instructions for responding to an opioid overdose emergency using naloxone. It begins with an overview of the REVIVE program and training objectives. It then discusses opioid overdoses, how to recognize one, and risk factors. Myths about reversing overdoses are dispelled. The document emphasizes that naloxone is the only effective response and provides step-by-step instructions: check responsiveness and give rescue breaths if needed, call 911, administer naloxone, continue rescue breathing, and give a second dose of naloxone if needed. Proper positioning and calling for emergency help are also described.
Nicotine is highly addictive and found in tobacco. When tobacco is smoked, nicotine reaches the brain within seconds and is distributed throughout the body rapidly, causing stimulation and increased heart rate and blood pressure. Long-term smoking is associated with many serious health issues like cancer, heart disease, and emphysema. While smoking rates have declined due to public health campaigns, tobacco use prevention and treatment programs could be expanded further.
COPD; a chronic, progressive airway obstruction; is directly linked with persistent inflammation and high oxidative stress. Airway obstruction is added on by plugging of airways with thick mucus. Role and efficacy of N-acetyl cysteine is reviewed with clinical cases.
Carbon monoxide is an odorless, colorless gas that is produced as a byproduct of combustion from various sources like vehicles, furnaces, generators and stoves. It can be lethal even in small amounts by preventing red blood cells from carrying oxygen. The document provides information about carbon monoxide's chemical structure and properties, sources of CO in homes, symptoms of CO poisoning like headaches and dizziness, safety tips to prevent CO exposure and the importance of installing CO detectors. It also lists a website for more resources on protecting against carbon monoxide poisoning.
Carbon Monoxide is also known as silent killer because it has no taste, odor and smell. Carbon Monoxide Kills (http://www.carbonmonoxidekills.com/) helps you to recover from carbon monoxide poisoning.
Facts you should know about Carbon MonoxideEthan Jacob
Carbonmonoxidekills (http://www.carbonmonoxidekills.com/) helps you to know about CO poisoning and how to protect your self and your family from CO poisoning.
This document discusses carbon monoxide poisoning, including its structure, pathophysiology, effects on the human body, sources, prevention, and treatment strategies. Carbon monoxide is an odorless, colorless gas that binds to hemoglobin over 200 times more than oxygen, preventing oxygen from being transported throughout the body and causing hypoxia. Symptoms range from headaches and dizziness at low levels to seizures, loss of consciousness, and death at high levels. Common sources include vehicles, heaters, and cooking equipment. Treatment focuses on high-flow oxygen therapy and hyperbaric oxygen chambers.
Management of op poisoning-definitive treatmentNuwani Kodi
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.
Carbon monoxide poisoning by dr Yasser DiabYasser Diab
This document describes two cases of carbon monoxide poisoning. In the first case, a 67-year-old man was admitted to the hospital multiple times with symptoms before being diagnosed with carbon monoxide poisoning from a faulty furnace. His wife also had carbon monoxide poisoning. In the second case, a 69-year-old man was admitted to the hospital with confusion and other symptoms, and his sister and daughter-in-law later came to the emergency room with carbon monoxide poisoning from his faulty water heater. The document then provides details on carbon monoxide, sources, effects on the body, signs and symptoms, treatment, and differential diagnosis.
Carbon monoxide poisoning results in over 50,000 emergency department visits per year in the US. While normobaric oxygen is the standard treatment, hyperbaric oxygen therapy may provide benefits for certain high-risk patients. One randomized trial found hyperbaric oxygen reduced cognitive sequelae rates at both 6 weeks and 12 months post-poisoning compared to normobaric oxygen alone in patients treated within 24 hours. Guidelines recommend considering hyperbaric oxygen for patients with serious poisoning symptoms or those over 36, exposed over 24 hours, or with CO-Hb over 25%. Patients should be informed of potential for long-term effects even after treatment.
This document provides information on carbon monoxide poisoning, including pathophysiology, signs and symptoms, diagnosis, treatment and prognosis. It notes that CO binds to hemoglobin over 200 times more than oxygen, resulting in hypoxia. Symptoms range from headaches and nausea to confusion, loss of consciousness and death. Treatment involves high-flow oxygen and potentially hyperbaric oxygen therapy. Prognosis can vary from full recovery to neurological deficits or death depending on severity and treatment.
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.
The document summarizes a case report of a 18-year-old female patient admitted for organophosphorus pesticide poisoning. She initially presented with excessive salivation, constricted pupils, tachycardia and decreased oxygen levels. She later developed intermediate syndrome with altered sensorium and difficulty breathing. Further examination showed signs of delayed neuropathy with weakness and sensory deficits. Treatment with atropine, pralidoxime and steroids improved her condition. The document then discusses organophosphorus poisoning, its mechanisms, clinical syndromes and delayed complications including intermediate syndrome and organophosphorus-induced delayed neuropathy.
The document provides guidelines for the diagnosis and treatment of chronic obstructive pulmonary disease (COPD) from the European Respiratory Society and American Thoracic Society. It aims to improve COPD patient care, promote a disease-oriented approach, and be updated based on new evidence. The guidelines cover defining COPD, epidemiology, pathogenesis, diagnosis, management of stable COPD including pharmacological therapies, pulmonary rehabilitation, and smoking cessation.
This document discusses various types of poisons and their effects. It describes 6 major groups of poisons including corrosives, irritants, neurotoxins, cardiovascular poisons, asphyxiants, and miscellaneous poisons. It also discusses factors that determine a poison's effects such as quantity ingested, form, route of administration, and individual susceptibility. Methods for assessing and treating poisoned patients are outlined, including airway management, evaluation of breathing and circulation, treatment of coma, and various decontamination procedures.
1. The child has relapsed acute lymphoblastic leukemia (ALL) and underwent reinduction chemotherapy.
2. Following the first cycle of reinduction therapy, laboratory tests show: a white blood cell count of 21,900, uric acid level of 9, and LDH level elevated.
3. These laboratory abnormalities indicate tumor lysis syndrome, a potential complication of effective chemotherapy in patients with high tumor burden. Urgent intervention is needed to prevent renal failure and other complications.
Mindfulness aplicada a la EPOC - Dr. Jordi Roig CutillasJordi Roig
Qué es el Mindfulness y cómo puede ayudar a los pacientes con enfermedades respiratorias como la EPOC.
Presentación del Dr. Jordi Roig Cutillas, doctor en medicina y especialista en neumología, durante el XVI Simposio sobre EPOC, dónde introduce el Mindfulness, la evidencia científica y su uso como complemento en la terapia de pacientes con enfermedades respiratorias crónicas.
Vídeo de la presentación: https://youtu.be/ivkwhxV2vVs?t=1362
This document summarizes information about carbon monoxide (CO) gas, including its common sources of exposure, mechanisms of toxicity, effects on the body, diagnosis, and treatment. It notes that CO is a colorless, odorless gas that is readily absorbed through the lungs and skin. It binds to hemoglobin in the blood over 200 times more strongly than oxygen, interfering with oxygen delivery to tissues. High levels of CO exposure can cause headaches, dizziness, and loss of consciousness. Diagnosis is made through measurement of carboxyhemoglobin levels in the blood. Treatment involves administration of 100% oxygen or hyperbaric oxygen therapy to accelerate CO elimination from the body. Long term neurological effects are also described.
IOSR Journal of Pharmacy (IOSRPHR), www.iosrphr.org, call for paper, research...iosrphr_editor
This article reviews the use of naloxone for treating opioid overdose. Naloxone is an opioid antagonist that reverses the effects of opioid intoxication. The preferred route of administration is intravenous, though intramuscular and intranasal are alternatives. Recommended dosing ranges from 0.05-2mg depending on the opioid and severity of overdose. Patients must be monitored after naloxone administration due to its shorter half-life compared to opioids. For short-acting opioids, observation for 2 hours is sufficient, while long-acting opioids require 4-6 hours of monitoring or continuous naloxone infusion to prevent recurrence of toxicity.
Risk of pulmonary aspiration with the outpatient electroconvulsive therapy: C...Ahmed Elaghoury
A case study presented at the 2nd International Brain Stimulation in Barcelona.
Cite as: Gad, M., & Elaghoury, A. (2017). Risk of pulmonary aspiration with the outpatient electroconvulsive therapy: Case report. Brain Stimulation: Basic, Translational, and Clinical Research in Neuromodulation, 10(2), 419.
http://dx.doi.org/10.1016/j.brs.2017.01.244
Understanding Physiological Mechanisms of Opioid Addiction: Advancements in C...InsideScientific
The opioid crisis can be traced back to the 1990s. Amid rising demand for pain relief, pharmaceutical companies assured doctors that their drugs carried little risk of addiction, and doctors began prescribing them at a higher rate. Since then, prescription, production and misuse of opioids have risen dramatically. In 2017 alone, an estimated 1.7 million Americans suffered from substance abuse disorders involving prescription or illegal opioids, with some 47,000 deaths due to overdose. Clearly, more research is required to better understand and prevent opioid misuse.
In this webinar sponsored by Data Sciences International, Dr. Ralph Lydic and Dr. Tally Largent-Milnes discuss the role of respiratory and neuroscience research in addressing the opioid epidemic. Dr. Ralph Lydic, professor of neuroscience and co-director of anesthesiology research at the University of Tennessee, presents data demonstrating the systemic and neurological effects of opioids on breathing and sleep in rodent models. Following, Dr. Tally Largent-Milnes, assistant professor of pharmacology at the University of Arizona, presents research investigating how cannabinoid receptors modulate opioid-induced respiratory depression in rodent models.
Key discussion topics include:
- How opiates induce changes in sleep and breathing
- Animal model selection: which mouse lines are most suitable for preclinical respiratory research?
- The scientific insight gained from simultaneously collecting plethysmography and telemetry signals in a single study
- Brain chemistry as the basis of physiology and behavior
- How opioids induce respiratory depression
- Which cannabinoids, if any, induce respiratory depression in preclinical models
- How the site of action determines how cannabinoid targeting agents interact with opioid-induced respiratory depression
This document discusses the management of breathlessness, which is a common and distressing symptom. It begins by defining breathlessness and describing how patients experience it. Various scales for measuring breathlessness are then outlined. The document notes that breathlessness is a major cause of emergency department visits and ambulance calls but is under-reported in primary care. Non-pharmacological interventions like breathing techniques and pulmonary rehabilitation are discussed as ways to reduce breathlessness. Pulmonary rehabilitation in particular is highlighted as an effective program. The role of pharmacological interventions is also summarized.
OP Poisoning routes, pathophysiology, diagnosis, sludge syndrome, effects on different systems, symptoms and severity, goals of treatment, decontamination and treatment
This document discusses general anesthetics, including their stages of anesthesia, characteristics of an ideal anesthetic, mechanisms of action, classifications, and specific anesthetics like halothane, barbiturates, ketamine, cyclopropane, ethyl chloride, and nitrous oxide. It describes the four stages of general anesthesia from analgesia to medullary depression. An ideal anesthetic should be potent, non-irritating, produce smooth anesthesia with muscle relaxation but no side effects. Mechanisms of action include lipid and protein theories. Anesthetics are classified as volatile or non-volatile, with examples like halothane, thiopental, ketamine, cyclopropane, ethyl chloride and nitrous oxide discussed
Pharmacology Lecture Slides on COPD - Chronic obstructive pulmonary disease by Sanjaya Mani Dixit Assistant Professor of Pharmacology at Kathmandu Medical College
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A Case of Neuropsychological Sequelae of Carbon Monoxide Poisoning Treated with Hyperbaric Oxygen Therapy
1. A Case of Neuropsychological Sequelae of Carbon Monoxide
Poisoning Treated with Hyperbaric Oxygen Therapy
2. Case Report
INTRODUCTION
Carbon monoxide (CO) is a colourless, odourless,
tasteless, non irritating, but significantly toxic gas. CO is
one of the leading causes of accidental poisonings
worldwide and also in India both in rural and urban areas.
However there is improper reporting of morbidity and
mortality attributable to suspected CO poisoning. The
sources of exogenous carbon monoxide that causes
poisoning include motor vehicle fumes, poorly functioning
heating systems (gas heaters, ovens, stoves),improper use of
coal or wood stoves and inhaled smoke [1-3]. It often results
in residual and persistent neuropathologic and cognitive
sequel [1-3]. Carbon monoxide’s affinity for haemoglobin
is more than 200 times that of oxygen resulting in the
formation of carboxyhemoglobin causing hypoxia and
shifting the oxyhemoglobin dissociation curve to the left
[2-4]. The acute injuries caused by CO are due to a hypoxic
stress mediated by an elevated carboxyhemoglobin (COHb)
level [3-6]. In acute phase, the level of carboxyhemoglobin
is directly proportional to the severity of poisoning and the
long term effects (Table1). Experts agree that it is difficult to
estimate the incidence of CO poisoning cases, because the
symptoms resemble many other common ailments [1,2].
High index of suspicion, and a careful history taking, helps
in making the diagnosis (Fig.1).
A CASE OF NEUROPSYCHOLOGICAL SEQUELAE OF CARBON MONOXIDE
POISONING TREATED WITH HYPERBARIC OXYGEN THERAPY
Tarun Sahni*, Madhur Jain** and Gurudatta#
*Senior Consultant, Internal & Hyperbaric Medicine, ** Associate Consultant, Hyperbaric Medicine,
#
DNB Internal Medicine, Indraprastha Apollo Hospitals, Sarita Vihar, New Delhi 110 076, India.
Correspondence to: Dr Tarun Sahni, Senior Consultant, Internal & Hyperbaric Medicine, Indraprastha Apollo Hospitals,
Sarita Vihar, New Delhi 110 076, India.
Carbon Monoxide is one of the most common causes of inhalation poisoning worldwide and can result in
significant morbidity due to persistent neuropathology and cognitive sequelae. The manifestation of carbon
monoxide poisoning are non specific and severity of symptoms range from mild such as headache, confusion,
lack of energy to severe, such as coma, respiratory depression, cardiac dysfunction and even death.
Hyperbaric oxygen therapy has been used for decades in the treatment of acute and delayed effects of carbon
monoxide poisoning. Hyperbaric Oxygen is the only treatment for acute CO poisoning where it competes with
CarboxyHemoglobin preventing the resultant damage and in delayed neuropsychological sequelae. This case
report is of a young lady from rural Haryana presented after 48 hours of CO Poisoning with acute confusion,
partial retrograde and complete anterograde memory loss. Following 15 days of hyperbaric oxygen she
showed near complete recovery and her Mini Mental Scale Examination (MMSE) score which was 12/30 on
the first day went up to 29/30. This case demonstrates that HBO therapy is efficacious in recovery of delayed
neuropsychiatric sequelae of Carbon Monoxide poisoning.
Key words: Carbon monoxide, Hyperbaric oxygen therapy, Cognitive sequelae.
The delayed neuropsychological sequelae are a result
of inflammatory mediated residual injury to the brain and
may manifest many years later. Administration of
supplemental oxygen is the cornerstone of treatment of
CO poisoning. Hyperbaric Oxygen inhalation will hasten
disassociation of CO from haemoglobin to occur at rate
greater than that achievable by breathing pure oxygen at
sea-level pressure and is better than normobaric oxygen
[4,6,7].
CASE REPORT
A 31 year old lady from Sirsa, Haryana presented with
Table 1. Symptoms associated with a given
concentration of COHb
Level of COHb (%) Symptoms
0-10 No symptoms
15 Mild headache
25 Nausea and serious
headache
30 Symptoms intensify
45 Unconsciousness
>50 Death
57 Apollo Medicine, Vol. 8, No. 1, March 2011
3. Apollo Medicine, Vol. 8, No. 1, March 2011 58
Case Report
a history of acute confusion and partial retrograde and
total anterograde memory loss of approx 48 hours
duration following exposure to leakage from a gas heater
for about 45 minutes. She was lying unconscious on the
floor after 12 hours and on regaining consciousness, she
was in a confused state and unable to recognize her family
members.
When examined, she was alert but not oriented to
person, place or time. Mood was inappropriate; speech
was spontaneous with normal rate but of high tone. She
denied any perceptual disturbances. The patient displayed
impaired short term and long term recall memory. There
was no history of any psychiatric illnesses, abnormal
behavior, seizures or head trauma.
Assessment of neuropsychological parameters by
MMSE gave her a score of 12/30 indicating severe
impairment in orientation, attention, anterograde and
retrograde memory, calculation, language and
construction (Table 2 & 3). She required constant
reorientation by family members to place, time and
person. The patient showed no ability to recall events
spontaneously that had occurred the day before.
Patient underwent MRI Brain scan and EEG which
were normal. The level of carboxyhemoglobin was not
measured at the rural hospital since this facility was not
available and since more than 48 hours has elapsed, it was
not considered relevant at this hospital. As a part of
medical treatment she was prescribed an anti oxidant,
Clonazepam (1mg), Aspirin (75mg) for 10 days. The
patient was referred to this centre 48 hours after the event
for Hyperbaric Oxygen Therapy for possible resolution of
her cognitive symptoms. The patient underwent fifteen,
ninety minute treatment with hyperbaric oxygen at 2.4
ATA.
On completion of hyperbaric treatment the patient was
alert and oriented to person, place, month, and year her
mini mental state examination score was 29/30. Her short
term memory was normal (ability to recall three objects at
3 minutes and three of three with prompting). There was
Fig 1. Spectrum of symptoms of exposure to Carbon Monoxide, on the basis of duration of exposure.
Table 2. Assessment of patient using MMSE during
different phases of treatment
Assessment Patient’s Maximum
score score
Day 1 Day 10 Day 15
Orientation to time 0 5 5 5
Orientation to place 0 5 5 5
Immediate recall 3 3 3 3
Delayed verbal recall 2 3 3 3
Attention 0 2 5 5
Naming 2 2 2 2
Repetition 1 1 1 1
3 Stage command 3 3 3 3
Reading 1 1 1 1
Writing 0 0 1 1
Copying 0 0 0 1
Total 12 25 29 30
4. Case Report
59 Apollo Medicine, Vol. 8, No. 1, March 2011
also an increased ability to recall recent events. She
showed improvement in her recall and remembered the
event and was aware of why she was undergoing
treatment. There was also a remarkable improvement in
her ability to care for herself and was able to perform
activities of daily living without assistance.
Neuropsychological testing (MMSE Score) obtained two
weeks after hyperbaric oxygen treatment disclosed a
further improvement with score of 29/30 from score of
12/30 at her initial testing. The patient had improved
memory for events, but was unable to reproduce the
designs after a delay. An additional set of five hyperbaric
treatments for residual cognitive losses were given,
however this did not improve her MMSE score further.
DISCUSSION
Carbon monoxide poisoning is resulting in more than
50,000 emergency department visits per year globally.
Sources of carbon monoxide include faulty furnaces,
inadequate ventilation of heating sources, and exposure to
engine exhaust. Spectrum of CO Poisoning symptoms
may be wide and variable, most common symptoms are
mild headache, nausea, malaise, dizziness, syncope,
altered mental state and loss of consciousness [3-6]. The
symptoms of carbon monoxide poisoning occur with
many other types of poisonings and infections. The
diagnosis is often difficult and hence high level of
suspicion is essential [1,2]. If CO poisoning is suspected,
the carboxyhemoglobin level is measured if available and
determines the severity of the poisoning [7-9]as explained
in Table 1.
No specific therapy for neuropsychological sequelae
after carbon monoxide poisoning is well established, but
clinical experience has shown that patients with sequelae
should be treated with hyperbaric oxygen therapy [10].
Substantial improvement in memory, concentration,
attention, and activities of daily living were seen in this
patient when treated with hyperbaric oxygen. Several
animal studies show that treatment with hyperbaric
oxygen is effective in reducing carbon monoxide
associated brain injury and suggests that hyperbaric
oxygen acts possibly by inhibiting cellular processes such
as oxidative injury and brain lipid peroxidation [11-14].
Weaver, et al [3] reported that treatment of patients with
acute symptomatic CO poisoning with HBOT sessions
appeared to reduce rate of cognitive sequelae and support
the use of HBO. It has been reported that HBOT has
provided a prominent improvement in the early and late
effects of CO poisoning and improvement is more
effective when applied in acute phase. Hyperbaric-oxygen
therapy elevates arterial and tissue oxygen tensions,
promoting carbon monoxide elimination and also
increases adenosine triphosphate production and reduces
oxidative stress and inflammation [12, 13]. Thom, et al [4]
showed in their study that hyperbaric oxygen leads to
improvement of neuropsychological consequences similar
to response in our patient. HBOT is a life saving procedure
in acute carbon monoxide poisoning as it speeds removal
of CO from tissues and counters a number of its
deleterious effects. Further research is needed to examine
the exact mechanism by which hyperbaric oxygen acts. In
this case report, the patient continued to have some degree
of neurological sequelae despite the treatment given.
CONCLUSION
Acute carbon monoxide poisoning continues to be an
important health problem. The spectrum of CO poisoning
symptoms may be wide and variable, therefore high index
of suspicion, detailed history and examination is required.
Hyperbaric oxygen therapy has not only a well defined
role in acute but also in the delayed effects of CO
poisoning and the same has been demonstrated in this case
report.
ACKNOWLEDGEMENT
We would like to thank Dr G S Shergill from Mediciti
Hospital, Haryana for his timely referral of this patient and
research coordinators in hyperbaric team Ms Shweta &
Ms Sapna who helped us gather the necessary data and
information needed for this compilation.
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Table 3. Interpretation of MMSE
Score Interpretation
24-30 No cognitive impairment
18-23 Mild cognitive impairment
0-17 Severe cognitive impairment
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Case Report
6. Amitai Y, Zlotogorski Z, Golan-Katzav V, Wexler A, Gross
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