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.
Carbon monoxide is a byproduct of combustion that can be emitted from gasoline engines, heating systems, and other fuels when burned. It binds to hemoglobin in red blood cells, preventing oxygen from binding and being transported through the body. Symptoms of carbon monoxide poisoning range from mild headaches and nausea at lower levels to confusion, loss of consciousness, and even death at higher levels. Treatment involves removing the victim from the source of carbon monoxide and providing 100% oxygen therapy to allow the carbon monoxide to clear from the body.
This document discusses carbon monoxide (CO) poisoning, its pathophysiology, effects on fetuses, and management. CO poisoning occurs when endogenous or exogenous CO levels in the air rise. It binds to hemoglobin, reducing oxygen delivery. Fetuses are particularly susceptible due to higher CO-hemoglobin levels and slower CO elimination. Acute exposure can cause death from anoxia, while chronic exposure increases CO-hemoglobin levels. Effects on fetuses depend on gestational age and can include neurological and skeletal abnormalities as well as growth restriction. Management involves removal from the source, high-flow oxygen therapy, and hyperbaric oxygen in severe cases or when the fetus is compromised.
Carbon monoxide poisoning kills over 5,000 people per year in the US, mostly from suicide. CO is a colorless, odorless gas produced by incomplete combustion of carbon-containing fuels like gasoline. It is deadly because it binds to hemoglobin in red blood cells over 200 times more strongly than oxygen, preventing oxygen from being delivered to tissues. Symptoms range from headache and nausea at low levels to confusion, coma and death at high levels. Treatment focuses on removing the victim from the source of CO and administering high-concentration oxygen therapy to accelerate removal of CO from the bloodstream.
1. Asphyxia is a condition caused by a severely deficient supply of oxygen to the body due to abnormal breathing or other reasons. Carbon monoxide is a colorless, odorless gas that can cause asphyxiation by displacing oxygen from hemoglobin in the blood.
2. Carbon monoxide poisoning causes symptoms ranging from mild headache at low levels of saturation to coma and death at very high levels. Symptoms progress as the level of carbon monoxide in the blood increases.
3. At autopsy, tissues of victims of carbon monoxide poisoning exhibit a characteristic cherry red discoloration due to the formation of carboxyhemoglobin in the blood. Spectroscopy and chemical tests can also be used
This document outlines the dangers of alcohol consumption. It defines alcohol as a depressant and lists its percentage in different drinks. Heavy drinking can lead to cirrhosis of the liver and death. Alcohol impairs bodily functions and reaction time at different blood alcohol content levels. Factors like body weight and food intake influence how alcohol affects individuals. The document warns of risks like alcohol poisoning, drunk driving, and fetal alcohol syndrome. It provides alternatives to drinking and defines terms like binge drinking, tolerance, and alcoholism.
1. Carbon monoxide (CO) and hydrogen cyanide (HCN) are chemical asphyxiants that interfere with cellular respiration.
2. CO binds to hemoglobin with greater affinity than oxygen, forming carboxyhemoglobin and preventing oxygen delivery to tissues. Above 40% carboxyhemoglobin can be fatal. HCN directly inhibits cytochrome c oxidase in the electron transport chain.
3. Treatment for CO poisoning includes 100% oxygen administration and hyperbaric oxygen therapy when COHb levels are high or neurological symptoms are present. Treatment for HCN poisoning uses amyl nitrite to convert hemoglobin to methemoglobin, which then binds cyanide, followed by sodium thiosulfate or
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.
Carbon monoxide is a byproduct of combustion that can be emitted from gasoline engines, heating systems, and other fuels when burned. It binds to hemoglobin in red blood cells, preventing oxygen from binding and being transported through the body. Symptoms of carbon monoxide poisoning range from mild headaches and nausea at lower levels to confusion, loss of consciousness, and even death at higher levels. Treatment involves removing the victim from the source of carbon monoxide and providing 100% oxygen therapy to allow the carbon monoxide to clear from the body.
This document discusses carbon monoxide (CO) poisoning, its pathophysiology, effects on fetuses, and management. CO poisoning occurs when endogenous or exogenous CO levels in the air rise. It binds to hemoglobin, reducing oxygen delivery. Fetuses are particularly susceptible due to higher CO-hemoglobin levels and slower CO elimination. Acute exposure can cause death from anoxia, while chronic exposure increases CO-hemoglobin levels. Effects on fetuses depend on gestational age and can include neurological and skeletal abnormalities as well as growth restriction. Management involves removal from the source, high-flow oxygen therapy, and hyperbaric oxygen in severe cases or when the fetus is compromised.
Carbon monoxide poisoning kills over 5,000 people per year in the US, mostly from suicide. CO is a colorless, odorless gas produced by incomplete combustion of carbon-containing fuels like gasoline. It is deadly because it binds to hemoglobin in red blood cells over 200 times more strongly than oxygen, preventing oxygen from being delivered to tissues. Symptoms range from headache and nausea at low levels to confusion, coma and death at high levels. Treatment focuses on removing the victim from the source of CO and administering high-concentration oxygen therapy to accelerate removal of CO from the bloodstream.
1. Asphyxia is a condition caused by a severely deficient supply of oxygen to the body due to abnormal breathing or other reasons. Carbon monoxide is a colorless, odorless gas that can cause asphyxiation by displacing oxygen from hemoglobin in the blood.
2. Carbon monoxide poisoning causes symptoms ranging from mild headache at low levels of saturation to coma and death at very high levels. Symptoms progress as the level of carbon monoxide in the blood increases.
3. At autopsy, tissues of victims of carbon monoxide poisoning exhibit a characteristic cherry red discoloration due to the formation of carboxyhemoglobin in the blood. Spectroscopy and chemical tests can also be used
This document outlines the dangers of alcohol consumption. It defines alcohol as a depressant and lists its percentage in different drinks. Heavy drinking can lead to cirrhosis of the liver and death. Alcohol impairs bodily functions and reaction time at different blood alcohol content levels. Factors like body weight and food intake influence how alcohol affects individuals. The document warns of risks like alcohol poisoning, drunk driving, and fetal alcohol syndrome. It provides alternatives to drinking and defines terms like binge drinking, tolerance, and alcoholism.
1. Carbon monoxide (CO) and hydrogen cyanide (HCN) are chemical asphyxiants that interfere with cellular respiration.
2. CO binds to hemoglobin with greater affinity than oxygen, forming carboxyhemoglobin and preventing oxygen delivery to tissues. Above 40% carboxyhemoglobin can be fatal. HCN directly inhibits cytochrome c oxidase in the electron transport chain.
3. Treatment for CO poisoning includes 100% oxygen administration and hyperbaric oxygen therapy when COHb levels are high or neurological symptoms are present. Treatment for HCN poisoning uses amyl nitrite to convert hemoglobin to methemoglobin, which then binds cyanide, followed by sodium thiosulfate or
Carbon monoxide poisoning can occur from sources like space heaters, wood-burning stoves, and generators without adequate ventilation. CO binds to hemoglobin over 200 times more than oxygen, forming carboxyhemoglobin which impairs oxygen delivery. Clinical features include headache, confusion, vomiting, and loss of consciousness. Diagnosis is made through elevated carboxyhemoglobin levels and treatment involves high-flow supplemental oxygen and possibly hyperbaric oxygen therapy for more severe cases involving symptoms like syncope, seizures, or focal neurologic deficits.
This document provides information on carbon monoxide (CO) poisoning, including its sources, effects on the body, signs and symptoms, and treatment. CO is an odorless, colorless gas produced by incomplete combustion of carbon-containing fuels. It binds to hemoglobin in the blood, reducing oxygen delivery to tissues. Early symptoms of low-level exposure include headache, dizziness, and nausea. Higher levels can cause confusion, loss of consciousness, organ damage, and death. Treatment involves removing the person from the source of CO and administering high-concentration oxygen.
This document provides information on various types of asphyxiants including irritant gases, chemical asphyxiants, simple asphyxiants, and volatile agents. It then focuses on carbon monoxide, describing its formation, mode of action, signs and symptoms, treatment, and post-mortem findings. Finally, it briefly discusses carbon dioxide, hydrogen sulfide, and chemical weapons gases used in warfare.
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.
The document discusses different types of asphyxiants including irritants, chemical asphyxiants, simple asphyxiants, and volatile drugs. Irritants such as smoke and tear gas injure the air passages while chemical asphyxiants like carbon monoxide and hydrogen sulfide prevent oxygen utilization. Simple asphyxiants like carbon dioxide act by excluding oxygen. Volatile drugs can act as anesthetics or toxins to organs. Specific asphyxiants are then discussed in more detail including their properties, mechanisms of action, signs and symptoms, and treatment approaches.
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 the clinical features and management of methanol, aluminium phosphide, benzodiazepine, and cocaine poisoning. It describes the mechanisms of toxicity, signs and symptoms, toxic dose thresholds, diagnostic tests, and treatment approaches for each type of poisoning including gastric lavage, activated charcoal, antidotes like ethanol, flumazenil and supportive care. Complications involve the central nervous system, eyes, gastrointestinal tract, cardiovascular system and mortality is high for aluminium phosphide poisoning.
This document discusses various types of asphyxiants including irritants, chemical asphyxiants, simple asphyxiants, and volatile and systemic asphyxiants. It provides detailed information about specific asphyxiants such as carbon monoxide, hydrogen cyanide, hydrogen sulfide, carbon dioxide, and methyl isocyanate. For each one, it describes properties, sources, mechanisms of action, signs and symptoms, treatment, and post-mortem findings. Common features of asphyxiation and approaches to management are also outlined.
The woman and her family have symptoms consistent with carbon monoxide poisoning, as their symptoms began when it started getting cold and they likely had increased use of gas appliances. A COHb level would be the most appropriate test to confirm this suspicion.
The man was exposed to paint remover fumes in an enclosed space and is presenting with symptoms of CO poisoning. A COHb level would be helpful in this case to diagnose CO poisoning and guide management. Treatment for exposures from paint removers may need to continue longer than other sources due to longer half-life of carboxyhemoglobin formation. Severe metabolic acidosis is a potential complication of CO poisoning.
This document discusses inhalation poisoning from asphyxiants. It classifies asphyxiants as simple asphyxiants like carbon dioxide and nitrogen that displace oxygen, or chemical asphyxiants like carbon monoxide and cyanide that interfere with cellular oxygen transport or utilization. Carbon dioxide causes respiratory distress and symptoms like headaches and vomiting above certain concentrations. Carbon monoxide binds to hemoglobin over 200 times more than oxygen, impairing oxygen delivery. Cyanide poisoning is rapidly lethal by inhibiting mitochondrial cytochrome oxidase. Treatments include removal from exposure, oxygen therapy, and possibly hyperbaric oxygen therapy.
Carbon monoxide poisoning can occur from incomplete combustion of carbon-containing materials like smoke or vehicle exhaust. CO binds to hemoglobin in blood over 200 times more than oxygen, reducing oxygen delivery to tissues. Symptoms range from headache and dizziness at low levels to organ damage, coma and death at high levels. Diagnosis involves exposure history and measuring carboxyhemoglobin levels. Treatment focuses on removing the patient from exposure and administering high-flow oxygen or hyperbaric oxygen to accelerate CO elimination from blood.
Carbon monoxide poisoning occurs when carbon monoxide gas is inhaled from incomplete combustion sources. It binds to hemoglobin in the blood over 200 times more than oxygen, reducing oxygen delivery to tissues. Primary assessment involves airway and breathing evaluation along with 100% oxygen therapy to accelerate carbon monoxide elimination from the blood. Secondary assessment includes monitoring for symptoms of hypoxia, vital signs, and carboxyhemoglobin blood levels to determine severity and guide hyperbaric oxygen treatment if needed.
Carbon monoxide (CO) is a colorless, odorless gas produced by incomplete combustion that binds strongly to hemoglobin. CO poisoning presents variably from headache to coma and death. Diagnosis is based on exposure history and elevated COHb levels on oximetry. Treatment involves high-flow oxygen via mask or hyperbaric oxygen therapy to accelerate CO removal from hemoglobin. Common causes of CO toxicity are fires, heaters, engines, and cigarette smoke.
Ammonia is corrosive and irritating to the eyes, skin, respiratory tract, and gastrointestinal tract upon contact. Acute exposure can cause burns, while chronic inhalation has been associated with increased coughing, phlegm production, wheezing, and asthma. Ammonia is metabolized in the liver and excreted in urine as urea. It is not considered carcinogenic or toxic to reproduction based on animal studies.
Ammonia Colorless gas with a pungent ammoniacal smell
Extremely soluble in water forming a caustic alkaline solution of ammonium hydroxide (NH4OH)
Used as a refrigerant, fertilizer
Gas leak.
Fertilizers.
The spillage of Household and industrial cleaners
Ammonia is produced by decaying manure.
Increased ammonia levels of 25–30 ppm can damage the mucociliary apparatus of the upper respiratory tract, and higher levels (50–75 ppm) can cause decreased feed intake as well as caustic burns to the cornea, which can result in blindness.
Urea, also called carbamide, is an organic compound with the chemical formula CO(NH2)2.
Diamide of carbonic acid
Easily soluble in water
White crystalline powder and odourless
Liberates ammonia smell
MECHANISM OF ACTION
Toxicity of urea and non-protein nitrogen is due to ammonia absorbed from the stomach.
When the level of ammonia is high, the animal cannot detoxify ammonia fast because the urea and glutamine synthesizing mechanisms are saturated.
Increased ammonia leads to inhibition of citric acid cycle.
There is an increase in anaerobic glycolysis, blood glucose and blood lactate.
A decreased energy production and cellular respiration leads to convulsions.
In animals that are not too ill, cold water-acetic acid treatment can be given. 19-38 litres of water and 3.8litres of 5% acetic acid can be administered to an adult cow
Intravenous fluids should be administered.
Toxicity of hydrocarbons can affect many organs but most commonly the lungs due to aspiration. Hydrocarbons are a diverse group of organic compounds including gasoline, oils, and solvents. Their physical properties like viscosity and volatility determine toxicity risk. Inhalation can cause pneumonitis while ingestion risks aspiration pneumonia. Symptoms include respiratory, CNS, cardiac, and GI issues. Treatment is supportive with monitoring for pulmonary or cardiac complications.
Ammonia is commonly used in household cleaners but also has many industrial uses including fertilizers, pharmaceuticals, and refrigeration. It is a colorless gas with a strong odor, molecular weight of 17.0, and boiling point of -28°F. Exposure to ammonia can occur through inhalation, skin contact, or eye contact and can cause burns, respiratory issues, and blindness. Proper precautions like PPE, ventilation, and training are needed when handling ammonia to prevent health hazards.
This document discusses drugs acting on the respiratory system. It begins by defining cough and its types. It then discusses common respiratory conditions like asthma and COPD in detail. The causes, symptoms and treatment options for cough, asthma and COPD are explained. Finally, it discusses various classes of drugs used for cough like expectorants, suppressants and adjuvents. Specific drugs like codeine, dextromethorphan, ammonium chloride, guaifenesin, bromhexine and bronchodilators are also explained in terms of their mechanisms, indications, doses and side effects.
Clinical symptoms and management of poisoningschiragmarwah1
The document discusses lead poisoning, including its causes, clinical features, diagnosis, and treatment. Lead poisoning occurs when lead is absorbed into the body, such as from lead-based paint, contaminated dust, or water. Symptoms depend on the amount of lead absorbed but can include abdominal pain, constipation, fatigue, and in more severe cases, damage to the nervous system. Diagnosis involves testing blood and urine samples to check for elevated lead levels. Treatment focuses on removing lead from the body through chelation therapy or other means while also preventing further exposure.
Ammonia is produced from urea in horse urine and feces and can cause respiratory issues in horses when present at high levels. The document discusses how ammonia levels vary in stables and can exceed recommended limits for humans. Prolonged exposure to ammonia can lead to inflammatory airway disease in horses and cause coughing, decreased stamina, and difficulty breathing. Preventing the buildup of ammonia through frequent mucking, adequate ventilation, and the use of ammonia-reducing products can help improve horse respiratory health.
This document discusses the toxicity of ethanol and methanol. Ethanol is commonly used as an alcohol ingredient but can cause intoxication in high amounts by depressing the central nervous system. Methanol is toxic and can cause blindness or death when metabolized into formic acid. Both ethanol and methanol are absorbed quickly and metabolized in the liver, with their toxicity resulting from metabolic byproducts. Proper diagnosis and treatment is needed for methanol poisoning due to its delayed onset and serious complications.
Carbon monoxide poisoning can occur from sources like space heaters, wood-burning stoves, and generators without adequate ventilation. CO binds to hemoglobin over 200 times more than oxygen, forming carboxyhemoglobin which impairs oxygen delivery. Clinical features include headache, confusion, vomiting, and loss of consciousness. Diagnosis is made through elevated carboxyhemoglobin levels and treatment involves high-flow supplemental oxygen and possibly hyperbaric oxygen therapy for more severe cases involving symptoms like syncope, seizures, or focal neurologic deficits.
This document provides information on carbon monoxide (CO) poisoning, including its sources, effects on the body, signs and symptoms, and treatment. CO is an odorless, colorless gas produced by incomplete combustion of carbon-containing fuels. It binds to hemoglobin in the blood, reducing oxygen delivery to tissues. Early symptoms of low-level exposure include headache, dizziness, and nausea. Higher levels can cause confusion, loss of consciousness, organ damage, and death. Treatment involves removing the person from the source of CO and administering high-concentration oxygen.
This document provides information on various types of asphyxiants including irritant gases, chemical asphyxiants, simple asphyxiants, and volatile agents. It then focuses on carbon monoxide, describing its formation, mode of action, signs and symptoms, treatment, and post-mortem findings. Finally, it briefly discusses carbon dioxide, hydrogen sulfide, and chemical weapons gases used in warfare.
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.
The document discusses different types of asphyxiants including irritants, chemical asphyxiants, simple asphyxiants, and volatile drugs. Irritants such as smoke and tear gas injure the air passages while chemical asphyxiants like carbon monoxide and hydrogen sulfide prevent oxygen utilization. Simple asphyxiants like carbon dioxide act by excluding oxygen. Volatile drugs can act as anesthetics or toxins to organs. Specific asphyxiants are then discussed in more detail including their properties, mechanisms of action, signs and symptoms, and treatment approaches.
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 the clinical features and management of methanol, aluminium phosphide, benzodiazepine, and cocaine poisoning. It describes the mechanisms of toxicity, signs and symptoms, toxic dose thresholds, diagnostic tests, and treatment approaches for each type of poisoning including gastric lavage, activated charcoal, antidotes like ethanol, flumazenil and supportive care. Complications involve the central nervous system, eyes, gastrointestinal tract, cardiovascular system and mortality is high for aluminium phosphide poisoning.
This document discusses various types of asphyxiants including irritants, chemical asphyxiants, simple asphyxiants, and volatile and systemic asphyxiants. It provides detailed information about specific asphyxiants such as carbon monoxide, hydrogen cyanide, hydrogen sulfide, carbon dioxide, and methyl isocyanate. For each one, it describes properties, sources, mechanisms of action, signs and symptoms, treatment, and post-mortem findings. Common features of asphyxiation and approaches to management are also outlined.
The woman and her family have symptoms consistent with carbon monoxide poisoning, as their symptoms began when it started getting cold and they likely had increased use of gas appliances. A COHb level would be the most appropriate test to confirm this suspicion.
The man was exposed to paint remover fumes in an enclosed space and is presenting with symptoms of CO poisoning. A COHb level would be helpful in this case to diagnose CO poisoning and guide management. Treatment for exposures from paint removers may need to continue longer than other sources due to longer half-life of carboxyhemoglobin formation. Severe metabolic acidosis is a potential complication of CO poisoning.
This document discusses inhalation poisoning from asphyxiants. It classifies asphyxiants as simple asphyxiants like carbon dioxide and nitrogen that displace oxygen, or chemical asphyxiants like carbon monoxide and cyanide that interfere with cellular oxygen transport or utilization. Carbon dioxide causes respiratory distress and symptoms like headaches and vomiting above certain concentrations. Carbon monoxide binds to hemoglobin over 200 times more than oxygen, impairing oxygen delivery. Cyanide poisoning is rapidly lethal by inhibiting mitochondrial cytochrome oxidase. Treatments include removal from exposure, oxygen therapy, and possibly hyperbaric oxygen therapy.
Carbon monoxide poisoning can occur from incomplete combustion of carbon-containing materials like smoke or vehicle exhaust. CO binds to hemoglobin in blood over 200 times more than oxygen, reducing oxygen delivery to tissues. Symptoms range from headache and dizziness at low levels to organ damage, coma and death at high levels. Diagnosis involves exposure history and measuring carboxyhemoglobin levels. Treatment focuses on removing the patient from exposure and administering high-flow oxygen or hyperbaric oxygen to accelerate CO elimination from blood.
Carbon monoxide poisoning occurs when carbon monoxide gas is inhaled from incomplete combustion sources. It binds to hemoglobin in the blood over 200 times more than oxygen, reducing oxygen delivery to tissues. Primary assessment involves airway and breathing evaluation along with 100% oxygen therapy to accelerate carbon monoxide elimination from the blood. Secondary assessment includes monitoring for symptoms of hypoxia, vital signs, and carboxyhemoglobin blood levels to determine severity and guide hyperbaric oxygen treatment if needed.
Carbon monoxide (CO) is a colorless, odorless gas produced by incomplete combustion that binds strongly to hemoglobin. CO poisoning presents variably from headache to coma and death. Diagnosis is based on exposure history and elevated COHb levels on oximetry. Treatment involves high-flow oxygen via mask or hyperbaric oxygen therapy to accelerate CO removal from hemoglobin. Common causes of CO toxicity are fires, heaters, engines, and cigarette smoke.
Ammonia is corrosive and irritating to the eyes, skin, respiratory tract, and gastrointestinal tract upon contact. Acute exposure can cause burns, while chronic inhalation has been associated with increased coughing, phlegm production, wheezing, and asthma. Ammonia is metabolized in the liver and excreted in urine as urea. It is not considered carcinogenic or toxic to reproduction based on animal studies.
Ammonia Colorless gas with a pungent ammoniacal smell
Extremely soluble in water forming a caustic alkaline solution of ammonium hydroxide (NH4OH)
Used as a refrigerant, fertilizer
Gas leak.
Fertilizers.
The spillage of Household and industrial cleaners
Ammonia is produced by decaying manure.
Increased ammonia levels of 25–30 ppm can damage the mucociliary apparatus of the upper respiratory tract, and higher levels (50–75 ppm) can cause decreased feed intake as well as caustic burns to the cornea, which can result in blindness.
Urea, also called carbamide, is an organic compound with the chemical formula CO(NH2)2.
Diamide of carbonic acid
Easily soluble in water
White crystalline powder and odourless
Liberates ammonia smell
MECHANISM OF ACTION
Toxicity of urea and non-protein nitrogen is due to ammonia absorbed from the stomach.
When the level of ammonia is high, the animal cannot detoxify ammonia fast because the urea and glutamine synthesizing mechanisms are saturated.
Increased ammonia leads to inhibition of citric acid cycle.
There is an increase in anaerobic glycolysis, blood glucose and blood lactate.
A decreased energy production and cellular respiration leads to convulsions.
In animals that are not too ill, cold water-acetic acid treatment can be given. 19-38 litres of water and 3.8litres of 5% acetic acid can be administered to an adult cow
Intravenous fluids should be administered.
Toxicity of hydrocarbons can affect many organs but most commonly the lungs due to aspiration. Hydrocarbons are a diverse group of organic compounds including gasoline, oils, and solvents. Their physical properties like viscosity and volatility determine toxicity risk. Inhalation can cause pneumonitis while ingestion risks aspiration pneumonia. Symptoms include respiratory, CNS, cardiac, and GI issues. Treatment is supportive with monitoring for pulmonary or cardiac complications.
Ammonia is commonly used in household cleaners but also has many industrial uses including fertilizers, pharmaceuticals, and refrigeration. It is a colorless gas with a strong odor, molecular weight of 17.0, and boiling point of -28°F. Exposure to ammonia can occur through inhalation, skin contact, or eye contact and can cause burns, respiratory issues, and blindness. Proper precautions like PPE, ventilation, and training are needed when handling ammonia to prevent health hazards.
This document discusses drugs acting on the respiratory system. It begins by defining cough and its types. It then discusses common respiratory conditions like asthma and COPD in detail. The causes, symptoms and treatment options for cough, asthma and COPD are explained. Finally, it discusses various classes of drugs used for cough like expectorants, suppressants and adjuvents. Specific drugs like codeine, dextromethorphan, ammonium chloride, guaifenesin, bromhexine and bronchodilators are also explained in terms of their mechanisms, indications, doses and side effects.
Clinical symptoms and management of poisoningschiragmarwah1
The document discusses lead poisoning, including its causes, clinical features, diagnosis, and treatment. Lead poisoning occurs when lead is absorbed into the body, such as from lead-based paint, contaminated dust, or water. Symptoms depend on the amount of lead absorbed but can include abdominal pain, constipation, fatigue, and in more severe cases, damage to the nervous system. Diagnosis involves testing blood and urine samples to check for elevated lead levels. Treatment focuses on removing lead from the body through chelation therapy or other means while also preventing further exposure.
Ammonia is produced from urea in horse urine and feces and can cause respiratory issues in horses when present at high levels. The document discusses how ammonia levels vary in stables and can exceed recommended limits for humans. Prolonged exposure to ammonia can lead to inflammatory airway disease in horses and cause coughing, decreased stamina, and difficulty breathing. Preventing the buildup of ammonia through frequent mucking, adequate ventilation, and the use of ammonia-reducing products can help improve horse respiratory health.
This document discusses the toxicity of ethanol and methanol. Ethanol is commonly used as an alcohol ingredient but can cause intoxication in high amounts by depressing the central nervous system. Methanol is toxic and can cause blindness or death when metabolized into formic acid. Both ethanol and methanol are absorbed quickly and metabolized in the liver, with their toxicity resulting from metabolic byproducts. Proper diagnosis and treatment is needed for methanol poisoning due to its delayed onset and serious complications.
toxin
medicine
antidotes
medicolegal duties of a RMP
duties of a doctor
management of a case of poisoing
sources of poisons
gastric lavage
ideal homicidal poison
This document discusses anticholinesterase poisoning from organophosphorus compounds. It covers the clinical features of organophosphorus poisoning including signs and symptoms due to excessive acetylcholine levels. Management includes atropine to block muscarinic receptors, pralidoxime as an enzyme reactivator, and supportive care. Atropine has anticholinergic effects and specific contraindications. Some synthetic drugs are similar to atropine but have more selective effects and fewer side effects for uses like mydriasis, gastrointestinal spasms, asthma, and parkinsonism.
This document discusses poisoning from central nervous system stimulants like amphetamines and cocaine. It provides details on amphetamine poisoning including its mode of action, signs and symptoms, fatal dose, treatment, and post-mortem findings. For cocaine poisoning, it similarly outlines its introduction, routes of administration, mode of action, acute signs and symptoms, fatal dose, diagnosis, treatment, and post-mortem appearances. It also discusses chronic cocaine poisoning and its associated signs and symptoms.
This document discusses various chemical hazards found in pharmaceutical industries. It describes hazards associated with sulphonating agents like fuming sulphuric acid which can cause corrosion. Organic solvents like acetone, acetonitrile, toluene and xylene are commonly used but pose health risks if inhaled or absorbed in high quantities. Control measures for chemical hazards include designated areas, engineering controls like ventilation, exhaust systems and fume hoods. Personal protective equipment including protective clothing, gloves and respirators are also recommended. Proper storage, labeling and limiting lone work with hazardous chemicals can help manage risks.
Heavy metal poisoning can involve multiple systems and be caused by various metals like arsenic, lead, mercury, and copper. Arsenic poisoning presents with gastrointestinal symptoms like vomiting and diarrhea as well as skin lesions. Lead poisoning commonly affects the nervous system causing issues like decreased IQ and hyperactivity. Mercury poisoning can cause pulmonary toxicity and kidney damage. Copper poisoning results in liver injury and haemolysis. Diagnosis involves measuring metal levels in blood and urine. Treatment focuses on decontamination, chelation therapy, and supportive care.
This document discusses forensic aspects of alcohol, including the physiology of alcohol absorption and elimination in the body, effects of alcohol intoxication, and causes of death from acute alcohol intoxication and chronic alcoholism. It describes autopsy findings and specimens that should be collected, such as central blood and stomach contents. Cut-off levels for intoxication according to traffic rules are provided. Causes of death from acute alcohol intoxication include toxic brainstem depression, drowning, trauma, coronary events, hypoglycemia, and hypothermia.
MANAGEMENT OF CASE OF CODEINE OVERDOSE.pptxakash chauhan
A 23-year-old girl presented to the emergency department with headaches, nausea, vomiting, and drowsiness. Her history revealed she had ingested a large amount of tablets 3 hours prior. On examination, she exhibited symptoms of opioid poisoning including a characteristic odor on her breath, slow pulse, moist skin, pinpoint pupils, and respiratory depression. She was diagnosed with codeine overdose and treated symptomatically with naloxone.
Organophosphate poisoning management with medicolegal aspectsVikram Singh
Organophosphate poisoning is caused by insecticides and chemical weapons that inhibit cholinesterase, causing excess acetylcholine. It affects over 200,000 people annually and has acute cholinergic effects, intermediate syndrome 1-4 days later with respiratory muscle weakness, and sometimes delayed neuropathy weeks later. Treatment involves atropine to reverse cholinergic effects and pralidoxime to reactivate cholinesterase. Management also requires decontamination, supportive care, and monitoring for complications due to the risk of intermediate syndrome and delayed effects.
Disease related to aminoacid metabolosmVipin Kannan
This document discusses diseases related to amino acid metabolism, including alkaptonuria, phenylketonuria, and homocystinuria. It provides an overview of amino acid catabolism and degradation pathways. Specific genetic defects that cause these diseases are described, including symptoms and diagnostic criteria. Treatment options are mentioned for managing associated health issues.
Ammonia is commonly used for industrial refrigeration, and comes with associated risks. Here are 3 steps to ammonia emergency preparedness in industrial refrigeration.
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.
Hydrocarbons are organic substances composed of carbon and hydrogen that are commonly ingested through substances like gasoline, oil, and solvents. Inhalation of hydrocarbon vapors can cause lung damage and neurological effects. Symptoms vary based on the specific hydrocarbon but can include cough, hypoxia, headaches, and in some cases neuropathy or cardiac issues. Treatment involves supportive care, observation of symptoms, addressing any respiratory failure, and consideration of gastric decontamination for certain toxic hydrocarbons.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
The skin is the largest organ and its health plays a vital role among the other sense organs. The skin concerns like acne breakout, psoriasis, or anything similar along the lines, finding a qualified and experienced dermatologist becomes paramount.
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
10 Benefits an EPCR Software should Bring to EMS Organizations Traumasoft LLC
The benefits of an ePCR solution should extend to the whole EMS organization, not just certain groups of people or certain departments. It should provide more than just a form for entering and a database for storing information. It should also include a workflow of how information is communicated, used and stored across the entire organization.
Kosmoderma Academy, a leading institution in the field of dermatology and aesthetics, offers comprehensive courses in cosmetology and trichology. Our specialized courses on PRP (Hair), DR+Growth Factor, GFC, and Qr678 are designed to equip practitioners with advanced skills and knowledge to excel in hair restoration and growth treatments.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
Mercurius is named after the roman god mercurius, the god of trade and science. The planet mercurius is named after the same god. Mercurius is sometimes called hydrargyrum, means ‘watery silver’. Its shine and colour are very similar to silver, but mercury is a fluid at room temperatures. The name quick silver is a translation of hydrargyrum, where the word quick describes its tendency to scatter away in all directions.
The droplets have a tendency to conglomerate to one big mass, but on being shaken they fall apart into countless little droplets again. It is used to ignite explosives, like mercury fulminate, the explosive character is one of its general themes.
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1. DISEASES CAUSED BY
AMMONIA
DISEASES CAUSED BY
AMMONIA
DISEASES CAUSED BY
AMMONIA
BY: SOMIA TARIQ
TO: DR. OMM-E-HANY
Institute of Environmental
studies, University of Karachi.
2. OCCUPATIONAL
DISEASE:
Any illness associated with a
particular occupation or
industry.
Such diseases result from a
variety of biological, chemical,
physical, and psychological factors
that are present in the
work environment or are
otherwise encountered in the
course of employment.
3. AMMONIA
NH3
Ammonia is a naturally
occurring chemical in
the atmosphere, as well
as an essential man-
made chemical.
It is represented by
the chemical formula
NH3. Ammonia in
this form is also
known as ammonia
gas or anhydrous
(“without water”)
ammonia.
At room
temperature,
ammonia is a
colorless, pungent-
smelling gas and is
lighter than air.
At -33 degrees Celsius, ammonia
becomes liquid. In this form, it is
also known as liquid ammonia, In
water, most of the ammonia changes
to ammonium ions, NH4+.
4. Uses of
Ammonia
Ammonia is one of
the most widely
used industrial
chemicals. It is also
used as fertilizer.
Ammonia is also
used in large-scale
refrigeration
systems; to make
synthetic fibers,
plastics and glues.
It is used in a variety
of other chemical
production processes
and foods.
It is used in the
treatment and refining
of metals.
5. Ammonia in the human body:
About 17 grams (≈ 0.5 ounces) of ammonia are
produced by the body every day, of which
approximately 4 grams are absorbed into the
body’s circulation system. The rest is excreted
through urine.
External Exposures:-
The average human intake of
ammonia from external sources
is about 18 milligrams per day
(mg/day).
6. Daily ammonia intake:
• Total Production by the Body 17,000
• Eating a 7 ounce Steak 13,000 mg
• Food Additives 18 mg
• Drinking Water City 1.0 mg Rural 0.4 mg
• Normal Breathing City 0.4 mg Rural 0.1 mg
• Cigarette Smoking (one pack per day) 0.8 mg
7. Acute Health Effects
•Ammonia, in both its gaseous and liquid
form, can be irritating to the eyes,
respiratory tract and skin due to its alkaline
nature.
•The biological effects of ammonia in
humans after acute exposures are dose-
related – they depend on the ambient
concentration, the amount taken in by the
body and the duration of exposure.
8.
9. Work place exposure limit:
• According to OSHA, the smallest amount of ammonia that
has been found to be irritating to the eyes, nose and throat
of the most sensitive individuals is 50 ppm.
• OSHA also sets 300 ppm as the exposure concentration of
ammonia causing no escape-impairing symptoms and no
irreversible effects.
• Breathing 700 to 1,700 ppm results in coughing,
bronchospasm and chest pain along with severe eye
irritation and tearing
•At levels greater than 5,000 ppm,ammonia causes
chemical bronchitis, fluid accumulation in the lungs,
chemical burns of the skin and is potentially fatal
10. Effects of Ammonia Exposure for “A Few Minutes” (without protective equipment)
11. • Persons who suffer from severe liver or kidney disease
may be more sensitive to exposure to higher
concentrations of ammonia, because of the importance of
these organs in transforming and excreting ammonia.
• Because ammonia is a respiratory tract irritant, persons
who are hyperreactive to other respiratory irritants, or who
are asthmatic, would be expected to be more susceptible
to inhalation of high concentrations of ammonia.
Effects on Sensitive Individuals
12. •Hyperammonemia:
Elevated concentrations of ammonia in the
brain as a result of hyperammonemia leads to cerebral
dysfunction
involving a spectrum of neuropsychiatric and neurologi
cal symptoms (impaired memory, shortened attention
span, sleep-wake inversions, brain edema, intracranial
hypertension, seizures, ataxia and coma).
Diseases caused by ammonia
13. •Hepatic encephalopathy,
Hepatic encephalopathy is a decline in brain function that
occurs as a result of severe liver disease. In this condition,
your liver can’t adequately remove toxins from your blood.
This causes a buildup of toxins in your bloodstream, which
can lead to brain damage. It is a condition that happens
when the liver is too diseased or damaged to properly
process ammonia. In this disorder, ammonia builds up in
the blood and travels to the brain. It can cause confusion,
disorientation, coma, and even death.
Diseases caused by ammonia
14. symptoms
• Symptoms of hepatic encephalopathy differ depending on the
underlying cause of the liver damage.
• Symptoms and signs of moderate hepatic encephalopathy may
include:
• difficulty thinking
• personality changes
• poor concentration
• problems with handwriting or loss of other small hand movements
• confusion
• forgetfulness
• poor judgment
• a musty or sweet breath odor
15. Severe symptoms
• Symptoms of severe hepatic encephalopathy are:
• confusion
• drowsiness or lethargy
• anxiety
• seizures
• severe personality changes
• fatigue
• confused speech
• shaky hands
• slow movements
• Get emergency medical help right away if you develop symptoms of
severe hepatic encephalopathy. These symptoms can lead to
a coma if they’re not treated quickly.
16. What are the different stages of
hepatic encephalopathy?
• Hepatic encephalopathy is divided into stages based on the severity
of the symptoms. Common classification systems include the West
Haven Criteria and the Glasgow Coma Scale.
• The five stages of hepatic encephalopathy, according to the West
Haven Criteria, are:
• Stage 0. At this stage, symptoms are minimal.
• Stage 1. Symptoms are mild. They may include a shortened
attention span and changes to your sleep habits, such
as hypersomnia or insomnia.
• Stage 2. Symptoms are moderate. At this stage, you may
feel disoriented or lethargic.
• Stage 3. Symptoms are severe. You’ll be unable to perform basic
tasks. You’ll also feel confused and experience personality changes.
• Stage 4. This stage is characterized by coma.
17. How to Protect Yourself Before working with ammonia,
• Personnel should review the material safety data sheet.
• Personnel handling anhydrous or strong aqua ammonia
where skin or eye contact is likely to occur should wear
gloves, shoe covers and aprons impervious to
ammonia.
• Unless eye and face protection is afforded by a
respirator hood or face piece, chemical goggles and
face shields should be worn at all times.
• The National Institute for Occupational Safety and
Health recommends wearing gloves made of Butyl,
Teflon or Viton for up to eight hours of exposure and
Nitrile gloves for up to four hours of exposure.