AN OVERVIEW ABOUT PHARMACOLOGICAL ACTIONS,TOXICITY PHARAMETERS,GUIDELINES FOR SAFE DRINKING,CLINICAL USES,METHYL ALCOHOL.THIS FOR ALL MEDICAL AND PHARMACY STUDENTS.
Ethanol acts as a central nervous system depressant by enhancing the effects of the inhibitory neurotransmitter GABA at GABA-A receptors. It is metabolized in the liver by alcohol dehydrogenase and aldehyde dehydrogenase. Acute intoxication can cause impairment, loss of coordination, and respiratory depression, while chronic use is associated with conditions like cirrhosis of the liver and cardiomyopathy. Treatment for acute intoxication involves maintaining airway and circulation, gastric lavage, glucose supplementation, and benzodiazepines for seizures. Chronic alcoholism is treated with supervised withdrawal, benzodiazepine substitution, psychotherapy, and disulfiram to produce an aversive reaction if alcohol is consumed. Methanol poisoning is treated
This document summarizes key information about alcohols presented by Dr. Pravin Prasad to MBBS Sem IV students. It describes the effects of alcohol on the central nervous system and different organ systems. It explains that alcohol is metabolized in the liver and lists its uses, toxicity, and contraindications. The document provides details on the pharmacokinetics and metabolism of ethanol and outlines the local and systemic effects of alcohol consumption.
1. Ethanol is absorbed from the intestine and reaches peak levels after 30 minutes from an empty stomach. It undergoes first-pass metabolism in the liver, where 90-98% is oxidized to acetate.
2. Effects of ethanol include CNS depression in a dose-dependent manner, relieving anxiety but also causing behavioral disinhibition. Toxic doses can cause respiratory depression and coma.
3. Long-term heavy drinking is associated with increased risk of hypertension, cardiomyopathy, strokes, skeletal muscle damage, nutritional deficiencies, anemia, and impaired immune function. Tolerance and dependence can develop with chronic use.
This lecture covers all the effects of alcohols on various systems of the body.
It also covers the management of acute alcohol intoxication, withdrawal syndrome and alcohol dependence.
Uses of Methanol as well pharmacology of its toxicity is also explained.
This document discusses the pharmacokinetics and pharmacodynamics of alcohol. It covers the absorption, distribution, metabolism and elimination of alcohol. It describes the effects of alcohol on various body systems including the central nervous system, cardiovascular system, gastrointestinal system, and reproductive system. It also discusses tolerance, dependence and drug interactions related to alcohol.
Methanol poisoning causes metabolic acidosis, optic neuritis, renal toxicity, and CNS depression. Symptoms include odor on breath, acid urine with acetone and albumin, retinal ganglion cell degeneration, and convulsions. Death is mainly due to metabolic acidosis from formic acid production and respiratory depression from CNS effects.
This document discusses the toxicity of ethanol. It is a colorless, volatile liquid that readily diffuses through membranes and is metabolized in the liver. Chronic ethanol consumption can lead to malnutrition, oxidative stress, production of toxic metabolites like acetaldehyde, and increased risk of cancer. Clinical effects include inebriation, respiratory depression, hypothermia, and dysrhythmias. Blood tests can assess electrolyte abnormalities. Treatment involves stabilization, fluid/electrolyte correction, and occasionally hemodialysis. Ethanol metabolism can also cause hypoglycemia or alcoholic ketoacidosis in malnourished chronic drinkers.
Ethanol acts as a central nervous system depressant by enhancing the effects of the inhibitory neurotransmitter GABA at GABA-A receptors. It is metabolized in the liver by alcohol dehydrogenase and aldehyde dehydrogenase. Acute intoxication can cause impairment, loss of coordination, and respiratory depression, while chronic use is associated with conditions like cirrhosis of the liver and cardiomyopathy. Treatment for acute intoxication involves maintaining airway and circulation, gastric lavage, glucose supplementation, and benzodiazepines for seizures. Chronic alcoholism is treated with supervised withdrawal, benzodiazepine substitution, psychotherapy, and disulfiram to produce an aversive reaction if alcohol is consumed. Methanol poisoning is treated
This document summarizes key information about alcohols presented by Dr. Pravin Prasad to MBBS Sem IV students. It describes the effects of alcohol on the central nervous system and different organ systems. It explains that alcohol is metabolized in the liver and lists its uses, toxicity, and contraindications. The document provides details on the pharmacokinetics and metabolism of ethanol and outlines the local and systemic effects of alcohol consumption.
1. Ethanol is absorbed from the intestine and reaches peak levels after 30 minutes from an empty stomach. It undergoes first-pass metabolism in the liver, where 90-98% is oxidized to acetate.
2. Effects of ethanol include CNS depression in a dose-dependent manner, relieving anxiety but also causing behavioral disinhibition. Toxic doses can cause respiratory depression and coma.
3. Long-term heavy drinking is associated with increased risk of hypertension, cardiomyopathy, strokes, skeletal muscle damage, nutritional deficiencies, anemia, and impaired immune function. Tolerance and dependence can develop with chronic use.
This lecture covers all the effects of alcohols on various systems of the body.
It also covers the management of acute alcohol intoxication, withdrawal syndrome and alcohol dependence.
Uses of Methanol as well pharmacology of its toxicity is also explained.
This document discusses the pharmacokinetics and pharmacodynamics of alcohol. It covers the absorption, distribution, metabolism and elimination of alcohol. It describes the effects of alcohol on various body systems including the central nervous system, cardiovascular system, gastrointestinal system, and reproductive system. It also discusses tolerance, dependence and drug interactions related to alcohol.
Methanol poisoning causes metabolic acidosis, optic neuritis, renal toxicity, and CNS depression. Symptoms include odor on breath, acid urine with acetone and albumin, retinal ganglion cell degeneration, and convulsions. Death is mainly due to metabolic acidosis from formic acid production and respiratory depression from CNS effects.
This document discusses the toxicity of ethanol. It is a colorless, volatile liquid that readily diffuses through membranes and is metabolized in the liver. Chronic ethanol consumption can lead to malnutrition, oxidative stress, production of toxic metabolites like acetaldehyde, and increased risk of cancer. Clinical effects include inebriation, respiratory depression, hypothermia, and dysrhythmias. Blood tests can assess electrolyte abnormalities. Treatment involves stabilization, fluid/electrolyte correction, and occasionally hemodialysis. Ethanol metabolism can also cause hypoglycemia or alcoholic ketoacidosis in malnourished chronic drinkers.
alcohol perturbs the balance between excitatory and inhibitory influences in the brain, resulting in Anxiolysis. An increased reaction time, diminished fine motor control, impulsivity, and impaired judgement be come evident when the concentionof alcohol in the blood is 20-30mg/dl.
More than 50% of persons are grossly intoxicated by a conc. Of 150mg/dl.
The defintion of intoxication varies by country.
Alcohol can be measured in saliva, urine,sweat,and blood, level in exheled air remains the primary method of assessing the level of intoxication.
Ethanol (CH 3 CH 2 OH) is a water-soluble alcohol that rapidly crosses cell membranes.
Absorption of ethanol occurs via the gastrointestinal system, primarily in the stomach (70 percent) and duodenum (25 percent), with a small amount absorbed by the remaining intestine .
When the stomach is empty, peak blood ethanol levels are reached between 30 and 90 minutes after ingestion.
The document discusses ethanol (ethyl alcohol) and its effects as an inebriant substance. It defines alcohol and its origins, describes its production and metabolism in the body, acute and chronic effects on health, signs of alcohol poisoning and withdrawal symptoms, and treatments for alcoholism. Alcohol acts as a depressant on the central nervous system and can cause intoxication, coma and death in high doses.
Methyl alcohol is used industrially and is toxic to humans. It is metabolized to formaldehyde and then formic acid, which causes acidosis and is toxic. Symptoms range from dizziness and nausea to seizures, coma and death. Treatment involves correcting acidosis with bicarbonate, using ethanol to competitively bind to the metabolizing enzyme, and potentially haemodialysis. A case study describes a man with a history of alcoholism who was poisoned by methyl alcohol, developed seizures and metabolic acidosis, and died despite aggressive treatment including stomach washing and medications.
This document discusses different types of alcohols, specifically ethyl and methyl alcohols. It notes that only ethyl alcohol is drinkable, while methyl alcohol can cause poisoning. It then covers the pharmacological actions of ethyl alcohol on various body systems like the central nervous system, cardiovascular system, liver and others. It also discusses the pharmacokinetics of alcohol metabolism and some clinical uses of ethyl alcohol.
Methanol poisoning causes signs and symptoms within an hour of ingestion, including nausea, vomiting, abdominal cramps, headache, confusion and visual disturbances. Post-mortem findings include cyanosis, congestion of the lungs, liver and kidneys, and hemorrhages in the brain and GI tract. Treatment involves gastric lavage, activated charcoal, ethanol administration to compete for metabolism, hemodialysis for severe cases, and correcting acidosis and electrolyte abnormalities. Prognosis depends on prompt diagnosis and treatment to prevent metabolic acidosis and optic nerve damage from methanol and its toxic byproducts.
1) Alcohol is rapidly absorbed into the bloodstream and distributed throughout total body water, reaching peak blood levels around 30 minutes after ingestion when the stomach is empty.
2) Metabolism of alcohol occurs mainly in the liver by alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), accounting for 90-98% of ingested alcohol.
3) Acute alcohol intoxication can impair judgment and motor control at blood alcohol concentrations (BAC) of 20-30 mg/dL and cause gross intoxication over 50 mg/dL, presenting risks such as blackouts, vomiting, and aggression that require medical monitoring.
This document discusses ethanol toxicity and its effects both acutely and chronically. It covers the pharmacokinetics of ethanol including absorption, distribution, metabolism and elimination. Acute toxicity can range from mild euphoria to death depending on blood alcohol concentration. Chronic toxicity includes tolerance, withdrawal symptoms, liver damage, increased cancer risk and fetal alcohol syndrome. Management of acute toxicity focuses on supporting vital signs and increasing ethanol clearance. Chronic alcoholism treatment includes psychosocial support and nutritional supplementation.
This document summarizes the pharmacokinetics, toxicity, and clinical effects of various alcohols including ethanol, isopropanol, and methanol. Ethanol is rapidly absorbed through the stomach and intestine and metabolized in the liver. Common signs of intoxication include sedation, hypoglycemia, and respiratory depression. Methanol is metabolized to toxic compounds that can cause metabolic acidosis, visual impairment, and death. Treatment involves blocking metabolism using ethanol or fomepizole to prevent formation of toxic metabolites.
This document provides an outline and objectives for a group assignment on substance-related disorders involving alcohol. It discusses the definition, epidemiology, pharmacology, clinical presentation of intoxication and withdrawal, and treatment of alcohol use disorders. Regarding treatment, it describes pharmacological therapies like benzodiazepines for withdrawal and drugs like disulfiram, naltrexone, and acamprosate for dependence, as well as nutritional supplementation and settings for inpatient versus outpatient detoxification. Controversies around treatment and references are also noted. The four group members and their IDs are listed at the end.
Methanol is metabolized in the body to formaldehyde and then formic acid. Formic acid is responsible for methanol toxicity and causes acidosis, tissue hypoxia, and circulatory failure. Symptoms of methanol poisoning range from mild like dizziness and headache to severe like metabolic acidosis, convulsions, coma, and respiratory failure. Treatment involves correcting acidosis with sodium bicarbonate, giving ethanol to compete with methanol metabolism, and removing formic acid through hemodialysis or folinic acid. A case study describes a 58-year-old man with a history of alcoholism who was found unconscious after consuming alcohol and developed seizures, metabolic acidosis, and died from respiratory depression and cardiac failure
The document discusses various aspects of dopamine, neurotransmitters, and alcohol. It provides true/false and multiple choice questions about their roles and effects. Dopamine is responsible for mood, pleasure/reward, and alertness. Natural pain killers in the body are endorphins. Alcohol is metabolized in the liver and primarily impacts the limbic system of the brain. It can increase violence and accidents when misused. College binge drinking is common and negatively impacts academic and social functioning.
Clinical presentation of chronic alcohol useAli Alkabi
1. Chronic alcohol use can lead to alcohol use disorder, characterized by increased tolerance, withdrawal symptoms, and impaired control over drinking. Prolonged heavy drinking causes adaptive changes in the brain that can result in addiction.
2. Alcohol is broken down in the liver by enzymes, producing toxic compounds like acetaldehyde that can damage cells. Intoxication from high alcohol levels causes impaired behavior and thinking, while withdrawal can cause tremors, anxiety, and occasionally seizures.
3. Heavy long-term drinking is associated with increased risks of liver diseases like fatty liver, hepatitis, and cirrhosis as well as cancers, heart and digestive problems, immune system weaknesses, birth defects, and bone damage.
Alcohol refers to any organic compound containing a hydroxyl group bonded to a carbon atom. Ethanol is the type of alcohol found in alcoholic beverages and is produced through fermentation of sugars by yeast. All humans produce small amounts of alcohol endogenously through bacterial fermentation in the intestines. While ethanol consumption has risks, other alcohols like methanol are more toxic and can cause blindness or death if ingested.
1. Alcohol use disorder is defined as having difficulties in at least 2 of 11 life areas due to alcohol use over a 12-month period. The lifetime risk is 10-15% for men and 5-8% for women.
2. Consuming more than 3 standard drinks per day increases risks for cancer, vascular disease, and decreases life expectancy by about 10 years. Heavy drinking can also lead to alcoholic ketoacidosis, neurotransmission changes, and organ damage.
3. Treatment involves recognizing alcohol use disorder in at least 20% of patients, identifying and treating acute alcohol-related conditions, helping patients address their alcohol problems, and referring for additional treatment as needed.
Cocaine is derived from the coca plant and can be administered via smoking, insufflation, or injection. It acts by inhibiting the reuptake of dopamine, serotonin, and norepinephrine. Initial effects include euphoria and increased energy, but overdose can cause seizures, cardiac issues, and death. Regular use is associated with nasal damage, weight loss, dependence, and psychological issues. Treatment focuses on managing the acute effects of overdose and providing therapies for addiction.
A 25-year-old man was found by police acting wildly after injecting bath salts containing MDPV. He developed multiple organ failure including renal failure, hepatic failure, and rhabdomyolysis. His lab values peaked severely before gradually returning to normal over two weeks with intensive care. Bath salts contain stimulants like MDPV that cause dangerous effects by disrupting neurotransmitter systems, especially dopamine, in a similar but more potent way than cocaine and amphetamines. Their use can lead to severe physical and mental health emergencies that require supportive critical care.
Chocolate toxicity in animals by Dr.AmandeepAmen Deep
chocolate toxicity in pet animals is very common due to extensive use of chocolates and various beverages in daily food. Animals got ill by consuming these due to their indiscriminate habit of eating.....
this presentation includes causes, toxic doses, pathogenesis, clinical signs, differential diagnosis & treatment.......HOPE..... PPT WILL HELP :)
Introduction of hormone & Anterior pituitary drugs Manoj Kumar
The document discusses hormones secreted by the hypothalamus and anterior pituitary gland. It describes how these hormones regulate growth, metabolism, and sexual development/function by binding to receptor sites in target tissues. The hormones are released into the bloodstream and can affect multiple organs. The hypothalamus regulates hormone secretion through releasing or inhibiting factors. Some key anterior pituitary hormones discussed include growth hormone, prolactin, gonadotropins, and their functions.
This document discusses disorders of the endocrine system. It begins by describing the endocrine system and hormones. It then discusses the main groups of hormones and their general characteristics and effects. The document outlines various mechanisms that can cause hormonal alterations, including failures of feedback systems or endocrine glands. It provides details on specific disorders of the hypothalamic-pituitary system, anterior pituitary gland, and thyroid function. The major manifestations and mechanisms of onset are described for conditions like hyperthyroidism, hypothyroidism, Cushing's disease, and diabetes insipidus.
This document discusses alcohol use disorders and their treatment. It defines key terms like acute intoxication, withdrawal state, and dependence syndrome. It describes the major symptoms of alcohol withdrawal. It also outlines chronic health complications of alcohol use like Wernicke's encephalopathy and Korsakoff's psychosis. The document lists screening tools and treatments for alcohol dependence, including detoxification with benzodiazepines, vitamin supplementation, and approaches like psychotherapy, group therapy, and medications to reduce cravings or deter drinking.
This document provides information on the pharmacology of ethyl and methyl alcohol. It discusses that alcohols are hydroxy derivatives of aliphatic hydrocarbons and are manufactured by fermentation. Ethanol is produced by fermentation of sugar by yeast, while methanol is mostly produced synthetically. Ethanol can cause drowsiness at high amounts, while only a small amount of methanol is able to cause blindness. The effects of ethanol are dose dependent, while methanol is metabolized to toxic compounds that can damage the retina. Treatment for methanol poisoning involves inhibiting its metabolism using fomepizole or ethanol.
Pharmacology of Ethyl and Methyl AlcoholManoj Kumar
This document provides information on ethyl and methyl alcohol. It discusses that alcohols are produced by fermenting sugars and starches and the major commercial source is molasses. It then describes different types of alcoholic beverages and their alcohol contents. Key differences between ethanol and methanol are highlighted, including that ethanol is safe for consumption in moderation while methanol is highly toxic.
alcohol perturbs the balance between excitatory and inhibitory influences in the brain, resulting in Anxiolysis. An increased reaction time, diminished fine motor control, impulsivity, and impaired judgement be come evident when the concentionof alcohol in the blood is 20-30mg/dl.
More than 50% of persons are grossly intoxicated by a conc. Of 150mg/dl.
The defintion of intoxication varies by country.
Alcohol can be measured in saliva, urine,sweat,and blood, level in exheled air remains the primary method of assessing the level of intoxication.
Ethanol (CH 3 CH 2 OH) is a water-soluble alcohol that rapidly crosses cell membranes.
Absorption of ethanol occurs via the gastrointestinal system, primarily in the stomach (70 percent) and duodenum (25 percent), with a small amount absorbed by the remaining intestine .
When the stomach is empty, peak blood ethanol levels are reached between 30 and 90 minutes after ingestion.
The document discusses ethanol (ethyl alcohol) and its effects as an inebriant substance. It defines alcohol and its origins, describes its production and metabolism in the body, acute and chronic effects on health, signs of alcohol poisoning and withdrawal symptoms, and treatments for alcoholism. Alcohol acts as a depressant on the central nervous system and can cause intoxication, coma and death in high doses.
Methyl alcohol is used industrially and is toxic to humans. It is metabolized to formaldehyde and then formic acid, which causes acidosis and is toxic. Symptoms range from dizziness and nausea to seizures, coma and death. Treatment involves correcting acidosis with bicarbonate, using ethanol to competitively bind to the metabolizing enzyme, and potentially haemodialysis. A case study describes a man with a history of alcoholism who was poisoned by methyl alcohol, developed seizures and metabolic acidosis, and died despite aggressive treatment including stomach washing and medications.
This document discusses different types of alcohols, specifically ethyl and methyl alcohols. It notes that only ethyl alcohol is drinkable, while methyl alcohol can cause poisoning. It then covers the pharmacological actions of ethyl alcohol on various body systems like the central nervous system, cardiovascular system, liver and others. It also discusses the pharmacokinetics of alcohol metabolism and some clinical uses of ethyl alcohol.
Methanol poisoning causes signs and symptoms within an hour of ingestion, including nausea, vomiting, abdominal cramps, headache, confusion and visual disturbances. Post-mortem findings include cyanosis, congestion of the lungs, liver and kidneys, and hemorrhages in the brain and GI tract. Treatment involves gastric lavage, activated charcoal, ethanol administration to compete for metabolism, hemodialysis for severe cases, and correcting acidosis and electrolyte abnormalities. Prognosis depends on prompt diagnosis and treatment to prevent metabolic acidosis and optic nerve damage from methanol and its toxic byproducts.
1) Alcohol is rapidly absorbed into the bloodstream and distributed throughout total body water, reaching peak blood levels around 30 minutes after ingestion when the stomach is empty.
2) Metabolism of alcohol occurs mainly in the liver by alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), accounting for 90-98% of ingested alcohol.
3) Acute alcohol intoxication can impair judgment and motor control at blood alcohol concentrations (BAC) of 20-30 mg/dL and cause gross intoxication over 50 mg/dL, presenting risks such as blackouts, vomiting, and aggression that require medical monitoring.
This document discusses ethanol toxicity and its effects both acutely and chronically. It covers the pharmacokinetics of ethanol including absorption, distribution, metabolism and elimination. Acute toxicity can range from mild euphoria to death depending on blood alcohol concentration. Chronic toxicity includes tolerance, withdrawal symptoms, liver damage, increased cancer risk and fetal alcohol syndrome. Management of acute toxicity focuses on supporting vital signs and increasing ethanol clearance. Chronic alcoholism treatment includes psychosocial support and nutritional supplementation.
This document summarizes the pharmacokinetics, toxicity, and clinical effects of various alcohols including ethanol, isopropanol, and methanol. Ethanol is rapidly absorbed through the stomach and intestine and metabolized in the liver. Common signs of intoxication include sedation, hypoglycemia, and respiratory depression. Methanol is metabolized to toxic compounds that can cause metabolic acidosis, visual impairment, and death. Treatment involves blocking metabolism using ethanol or fomepizole to prevent formation of toxic metabolites.
This document provides an outline and objectives for a group assignment on substance-related disorders involving alcohol. It discusses the definition, epidemiology, pharmacology, clinical presentation of intoxication and withdrawal, and treatment of alcohol use disorders. Regarding treatment, it describes pharmacological therapies like benzodiazepines for withdrawal and drugs like disulfiram, naltrexone, and acamprosate for dependence, as well as nutritional supplementation and settings for inpatient versus outpatient detoxification. Controversies around treatment and references are also noted. The four group members and their IDs are listed at the end.
Methanol is metabolized in the body to formaldehyde and then formic acid. Formic acid is responsible for methanol toxicity and causes acidosis, tissue hypoxia, and circulatory failure. Symptoms of methanol poisoning range from mild like dizziness and headache to severe like metabolic acidosis, convulsions, coma, and respiratory failure. Treatment involves correcting acidosis with sodium bicarbonate, giving ethanol to compete with methanol metabolism, and removing formic acid through hemodialysis or folinic acid. A case study describes a 58-year-old man with a history of alcoholism who was found unconscious after consuming alcohol and developed seizures, metabolic acidosis, and died from respiratory depression and cardiac failure
The document discusses various aspects of dopamine, neurotransmitters, and alcohol. It provides true/false and multiple choice questions about their roles and effects. Dopamine is responsible for mood, pleasure/reward, and alertness. Natural pain killers in the body are endorphins. Alcohol is metabolized in the liver and primarily impacts the limbic system of the brain. It can increase violence and accidents when misused. College binge drinking is common and negatively impacts academic and social functioning.
Clinical presentation of chronic alcohol useAli Alkabi
1. Chronic alcohol use can lead to alcohol use disorder, characterized by increased tolerance, withdrawal symptoms, and impaired control over drinking. Prolonged heavy drinking causes adaptive changes in the brain that can result in addiction.
2. Alcohol is broken down in the liver by enzymes, producing toxic compounds like acetaldehyde that can damage cells. Intoxication from high alcohol levels causes impaired behavior and thinking, while withdrawal can cause tremors, anxiety, and occasionally seizures.
3. Heavy long-term drinking is associated with increased risks of liver diseases like fatty liver, hepatitis, and cirrhosis as well as cancers, heart and digestive problems, immune system weaknesses, birth defects, and bone damage.
Alcohol refers to any organic compound containing a hydroxyl group bonded to a carbon atom. Ethanol is the type of alcohol found in alcoholic beverages and is produced through fermentation of sugars by yeast. All humans produce small amounts of alcohol endogenously through bacterial fermentation in the intestines. While ethanol consumption has risks, other alcohols like methanol are more toxic and can cause blindness or death if ingested.
1. Alcohol use disorder is defined as having difficulties in at least 2 of 11 life areas due to alcohol use over a 12-month period. The lifetime risk is 10-15% for men and 5-8% for women.
2. Consuming more than 3 standard drinks per day increases risks for cancer, vascular disease, and decreases life expectancy by about 10 years. Heavy drinking can also lead to alcoholic ketoacidosis, neurotransmission changes, and organ damage.
3. Treatment involves recognizing alcohol use disorder in at least 20% of patients, identifying and treating acute alcohol-related conditions, helping patients address their alcohol problems, and referring for additional treatment as needed.
Cocaine is derived from the coca plant and can be administered via smoking, insufflation, or injection. It acts by inhibiting the reuptake of dopamine, serotonin, and norepinephrine. Initial effects include euphoria and increased energy, but overdose can cause seizures, cardiac issues, and death. Regular use is associated with nasal damage, weight loss, dependence, and psychological issues. Treatment focuses on managing the acute effects of overdose and providing therapies for addiction.
A 25-year-old man was found by police acting wildly after injecting bath salts containing MDPV. He developed multiple organ failure including renal failure, hepatic failure, and rhabdomyolysis. His lab values peaked severely before gradually returning to normal over two weeks with intensive care. Bath salts contain stimulants like MDPV that cause dangerous effects by disrupting neurotransmitter systems, especially dopamine, in a similar but more potent way than cocaine and amphetamines. Their use can lead to severe physical and mental health emergencies that require supportive critical care.
Chocolate toxicity in animals by Dr.AmandeepAmen Deep
chocolate toxicity in pet animals is very common due to extensive use of chocolates and various beverages in daily food. Animals got ill by consuming these due to their indiscriminate habit of eating.....
this presentation includes causes, toxic doses, pathogenesis, clinical signs, differential diagnosis & treatment.......HOPE..... PPT WILL HELP :)
Introduction of hormone & Anterior pituitary drugs Manoj Kumar
The document discusses hormones secreted by the hypothalamus and anterior pituitary gland. It describes how these hormones regulate growth, metabolism, and sexual development/function by binding to receptor sites in target tissues. The hormones are released into the bloodstream and can affect multiple organs. The hypothalamus regulates hormone secretion through releasing or inhibiting factors. Some key anterior pituitary hormones discussed include growth hormone, prolactin, gonadotropins, and their functions.
This document discusses disorders of the endocrine system. It begins by describing the endocrine system and hormones. It then discusses the main groups of hormones and their general characteristics and effects. The document outlines various mechanisms that can cause hormonal alterations, including failures of feedback systems or endocrine glands. It provides details on specific disorders of the hypothalamic-pituitary system, anterior pituitary gland, and thyroid function. The major manifestations and mechanisms of onset are described for conditions like hyperthyroidism, hypothyroidism, Cushing's disease, and diabetes insipidus.
This document discusses alcohol use disorders and their treatment. It defines key terms like acute intoxication, withdrawal state, and dependence syndrome. It describes the major symptoms of alcohol withdrawal. It also outlines chronic health complications of alcohol use like Wernicke's encephalopathy and Korsakoff's psychosis. The document lists screening tools and treatments for alcohol dependence, including detoxification with benzodiazepines, vitamin supplementation, and approaches like psychotherapy, group therapy, and medications to reduce cravings or deter drinking.
This document provides information on the pharmacology of ethyl and methyl alcohol. It discusses that alcohols are hydroxy derivatives of aliphatic hydrocarbons and are manufactured by fermentation. Ethanol is produced by fermentation of sugar by yeast, while methanol is mostly produced synthetically. Ethanol can cause drowsiness at high amounts, while only a small amount of methanol is able to cause blindness. The effects of ethanol are dose dependent, while methanol is metabolized to toxic compounds that can damage the retina. Treatment for methanol poisoning involves inhibiting its metabolism using fomepizole or ethanol.
Pharmacology of Ethyl and Methyl AlcoholManoj Kumar
This document provides information on ethyl and methyl alcohol. It discusses that alcohols are produced by fermenting sugars and starches and the major commercial source is molasses. It then describes different types of alcoholic beverages and their alcohol contents. Key differences between ethanol and methanol are highlighted, including that ethanol is safe for consumption in moderation while methanol is highly toxic.
This document discusses ethyl and methyl alcohols. It notes that ethyl alcohol is produced by fermenting sugars from sources like molasses. It is found in alcoholic beverages in varying concentrations depending on the type of beverage. The document also discusses the pharmacokinetics of alcohol metabolism and potential adverse effects ranging from mild symptoms to chronic conditions. Guidelines for safe alcohol consumption are provided. Methyl alcohol is also summarized as being toxic and potentially fatal even in small doses due to its metabolism producing toxic compounds that can cause blindness or death.
1. Ethyl alcohol is produced by fermenting sugars from sources like molasses and is used in alcoholic beverages.
2. Alcohol acts as a central nervous system depressant in a dose-dependent manner, affecting functions like sedation, sleep, and respiration.
3. Alcohol is metabolized in the liver but high doses can cause adverse effects like hypoglycemia, liver damage, and dependence.
The patient presented with difficulty breathing, blurred vision, vomiting, and abdominal pain after consuming cheap alcoholic beverages. The diagnosis is acute alcohol intoxication based on the history and symptoms. Ethyl alcohol is produced by fermenting sugars and can be found in beverages like beer, wine, and spirits in varying concentrations. At high doses, alcohol causes central nervous system and cardiovascular depression which can lead to coma and death. Treatment for acute intoxication focuses on airway support, glucose supplementation, and hastening alcohol metabolism.
This document discusses the pharmacology of ethyl alcohol and methyl alcohol. It provides details on the pharmacological actions of ethyl alcohol on various body systems like the CNS, CVS, liver, and others. It also discusses the pharmacokinetics of alcohol absorption, distribution, metabolism and excretion. Adverse interactions of alcohol with other drugs are mentioned. Treatment for methyl alcohol poisoning focuses on preventing further metabolism using ethanol, fomepizole or hemodialysis to remove toxic metabolites.
This document discusses the pharmacology of ethyl alcohol. It begins by describing how alcohol is produced through fermentation and its presence in various beverages. It then covers the pharmacological actions of alcohol throughout the body, including its effects on the central nervous system as both a stimulant and depressant. The document also discusses the pharmacokinetics of alcohol absorption, distribution, metabolism and excretion. It notes some drug interactions with alcohol and contraindications for its use. Adverse effects of both acute and chronic alcohol toxicity are described. Finally, treatment approaches for alcohol withdrawal and dependence are mentioned.
Alcohol (ethanol, EtOH) has pleiotropic actions and induces a number of acute and long-term effects due to direct actions on alcohol targets, and effects of alcohol metabolites and metabolism
Alcohol is by far the most frequently used and abused addictive drug, and therefore a detailed understanding of the molecular mechanisms of alcohol actions is important to human health and well-being
1. Local actions:-
Ethanol is a mild rubefacient (agent Produces redness of skin)
and counterirritant when rubbed on
the skin. By evaporation it produces cooling.
Applied to delicate skin (scrotum) or mucous membranes it produces irritation and burning sensation.
Concentrated alcohol (spirit) should not be applied in the mouth, nose, etc. Injected s.c. it causes intense pain, inflammation and necrosis.
Applied to the surface, alcohol is an astringent— precipitates surface proteins and hardens the skin, and antiseptic property.
Alcohol does not
kill bacterial spores
This document discusses alcohols, including ethanol and methanol. It covers the pharmacology of alcohol including its mechanisms of action in the body, metabolism, effects of acute and chronic consumption, toxicity, and treatment of alcoholism. Specifically, it describes how alcohol is absorbed and distributed in the body, metabolized primarily in the liver, and can cause intoxication, organ damage, and diseases with heavy long-term use such as cirrhosis and fetal alcohol syndrome.
This document discusses ethyl alcohol, including its production, forms, pharmacological actions, pharmacokinetics, interactions, toxicity, and clinical uses. Ethyl alcohol is produced by fermentation of sugars and is the active ingredient in alcoholic beverages. It has central nervous system depressant effects and impacts many organ systems. Chronic alcohol abuse can lead to serious health issues like cirrhosis of the liver and alcohol dependence.
The document discusses various types of alcohols such as ethyl alcohol and methyl alcohol, how alcohols like ethanol are manufactured through fermentation, and the pharmacological effects of acute and chronic alcohol consumption including intoxication, organ damage, and diseases like cirrhosis as well as the potential benefits and uses of alcohol in small amounts.
DISORDERS INDUCED BY USE OF ALCOHOL-1.pptxHappychifunda
This document discusses several alcohol-induced mental disorders including acute intoxication, withdrawal, alcoholic hallucinosis, and pathological jealousy or Othello's syndrome. Acute intoxication causes impairment that varies with blood alcohol concentration. Withdrawal can cause symptoms like anxiety, seizures, and delirium tremens. Hallucinosis involves auditory hallucinations during or after heavy drinking. Pathological jealousy involves delusions of infidelity related to issues like alcohol-caused impotence. Treatment focuses on managing symptoms, withdrawing alcohol use, and sometimes using antipsychotics.
1. Alcohol is produced by fermentation of sugars and its pharmacological actions include local irritation, effects on cardiovascular and respiratory systems, hypoglycemia, impacts on temperature regulation and more.
2. Chronic alcoholism can lead to complications like cirrhosis of the liver, hypertension, cardiomyopathy and more. Treatments include naltrexone, acamprosate, topiramate and disulfiram.
3. Methanol poisoning results in symptoms like vomiting, headache and can cause blindness or death if not treated. Treatments include gastric lavage, ethanol administration, fomepizole, hemodialysis and folate therapy.
This document discusses the pharmacology of alcohol. It begins by describing how drugs of abuse interact with the neurochemical mechanisms in the brain and alcohol's effects as a central nervous system depressant. It then covers the absorption, distribution, metabolism and excretion of alcohol as well as its pharmacological effects. Finally, it discusses the management of alcohol dependence, describing how Naltrexone and Acamprosate can be effective treatments by interrupting neurochemical mechanisms involved in alcohol reinforcement and preventing relapse.
1) Ethanol is produced commercially by fermenting sugars or starches with yeast. It is then distilled to produce spirits with 40-55% alcohol content.
2) Acute ethanol intoxication causes symptoms like slurred speech and impaired coordination above 80mg/dL blood alcohol content. Treatment focuses on airway protection and supportive care.
3) Chronic heavy ethanol use can lead to tolerance, dependence, and withdrawal symptoms like tremors or seizures upon cessation. Approved medications like naltrexone and acamprosate aim to reduce craving and ease withdrawal.
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.
This document discusses various alcohols including ethanol, isopropanol, and methanol. It provides details on:
- The pathophysiology of how each alcohol is absorbed and metabolized in the body. Ethanol is metabolized to acetaldehyde while isopropanol is metabolized to acetone.
- The signs and symptoms of intoxication for each alcohol, which generally involve central nervous system depression and inebriation. Isopropanol ingestion can also cause abdominal pain and vomiting.
- The treatment for alcohol intoxication, which is largely supportive care focusing on airway, breathing, and circulation. Gastric decontamination is rarely needed.
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This document provides an overview of syphilis, including its causes, transmission, stages, diagnosis, and treatment. It is caused by the Treponema pallidum bacterium, which can be transmitted sexually, from mother to fetus, or through blood transfusions. Syphilis progresses through primary, secondary, latent, and tertiary stages. It is diagnosed through clinical examination, demonstration of spirochetes, and detection of antibodies. Treatment involves benzathine penicillin or alternative antibiotics depending on the stage of syphilis. Prevention involves barrier methods and avoiding contact with infected individuals.
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1. Topic- Ethyl and Methyl Alcohols
By – Nilesh Sharma (pharm.d 2nd year)
2. Ethyl Alcohol (Ethanol)
Alcohols are Hydroxy deriatives of aliphatic hydrocarbons.
Alcohol is manufactured by fermentation of sugar.
C6H12O6 → 2 C2H5OH + 2 C02. ( PRESENCE OF ZYMASE ENZYME IN YEAST).
3. Alchololic beverages
A.Malted liquors – Obtained by fermentation of germinating cereals. Alcohol Content is low(3 to 6%)
Example – beers,Stout.
B.Wines – Produced by fermentation of natural sugars as present in grapes and other fruits.
There are 3 typs of wines .
1. Light wines – Alcohol content (9to12%) example .claret, cider. Cannot exceed 15%
2. Fortified wines-Alcohol content (16 to 22%) example port ,Sherry.
3. Effervescent wines – alcohol content (12 to 16%) example champagne.
C.Spirits- These are produced by distillation of the fermented broth. Alcohol content is (40 to
55%)example Rum,whiskey,vodka etc
4. Other forms of alcohol
1. Absolute alcohol - 99% w/w ethanol. (Dehydrated alcohol)
2. Rectified spirit - 90% w/w ethanol produced from fermented molasses,by distillation.
3. Proof spirit – 49.29% w/w ethanol.
4.Methylated spirit (industrial) – also called denatured spitit is produced by adding 5 parts of
wood naphtha (methyl alcohol) to 95 parts of rectified spirit so as to render it unfit for drinking.
It can be applied on the skin for antiseptic ,cleaning and astringent purposes.
5. Pharmacological Actions.
1. Local action –
ethanol is a mild rubefacient and counter irritant.
By evaporation it produces cooling .
Injected causes intense pain and inflammation.
Injected around nerve it produces permanent damage.
Alcohol is an astringent.
By precipitating bacterial proteins it acts as an antiseptic. this effect is predominant at 70-90%
alcohol.
6. 2.CNS
It is a neuronal depressant.
BAC (Mg/dl) Clinical effects
30-60 mg/dl Apparent excitation and euphoria.
100-150 mg/dl Impaired motor function , impairment of
memory , drowsiness.(feel high)
150-200mg/dl sloppy ,ataxic and drunk,black outs.
200-300 mg/dl Emesis , stupor.
300-400 mg/dl coma
>500 mg/dl Respiratory failure , death.
7. Meachanism of action .
1.It promotes GABAA Receptor mediated synaptic inhibition (through chloride
channel opening).
2.Inhibits NMDA type of excitatory amino acid receptor which has been implicated
in memory impairment cause by alcohol.
3.Ethanol can indirectly reduce neuro transmitter release by inhibiting voltage
sensitive neuronal calcium channels.
4.It also activates specific type of k+ channel in certain brain areas .
5.The activety and translocation channel/enzyme proteins in the membrane could
be affected by alcohol through protein kinase C (PKC) and (PKA) mediated alteration
in the state of their phosphorylation.
8. 3.CVS
The effects are dose dependent.
1.Small doses : produces cutaneous and gastric
vasodilatation. Skin is warm and flushed . BP is not
effected.
2.Moderate doses :causes tachycardia , mild rise in BP.
3.Large doses :cause direct myocardial as well as
vasomotor depression and fall in BP.
9. 4.Blood
• Regular intake of alcohol ( 1 to 2 drinks) has been found to raise HDL level and dec LDL level.
• This may be responsible for the (15 to 35%) lower incidence of CAD .
• Mild anaemia is common in chronic alcoholism is due to interference with folate metabolism.
5.Body temperature
• It produces a sense of warmth due to cutaneous and gastric vasodilatation , but heat loss is actually inc in
cold surrounding .
• High doses depress temp regulating system .
6.Respiration
• Alcoholic beverages acts as respiratory stimulant in collapse by irritating buccal and pharyngeal
mucosa.
• How ever it is better not to depend on this bcz the direct action of alcohol on respiratory center is
only a depressant one.
10. 7.GIT
1.Higher conc.(>20%) inhibit gastric secretions , cause
vomiting , mucosal congestion and gastritis.
2.Alcoholism is an imp cause of chronic gastritis.
3.LES tone is reduced by alcohol- bowel movement may be altered in either directions.
4.Acute pancreatitis is a complication of heavy drinkinf
8.Skeletal muscle
1. Fatigue is allayed by small doses.
2.Weakness and myopathy occurs in chronic alcoholism.
11. 9.liver
Causes alcoholic liver
cirrhosis
1. By alcohol metabolism acetaldehyde gets accumulated and damages the function of
liver.
2. It induces inflammation and damage the hepatocytes.
3. Regular intake induces microsomal enzymes present in liver.
12. 10.Kidney
1.Diuresis is often noticed after alcohol intake
2.Due to water ingested and alcohol induced inhibition of ADH secretion.
3.Alcohol does not impair renal function .
11.Endocrine effects
1.Alcohol increases adrenalin release which causes hyperglycemia.
2.Acute intoxification is often associated with hypoglycemia and depletion of hepatic
Glycogen , because gluconeogenesis is inhibited ,glucose must be given to counteract it.
3. Uterine contractions are suppressed at moderate blood levels.
13. 12. sEX
• Chronic alcoholism can produce IMPOTENCE,TESTICULAR ATROPHY ,GYNAECOMASTIA and
INFERTILITY IN BOTH Men and Women.
14. Pharmacokinetics
A absorption from intestine is very fast
Peak levels are attained after 30 min.
D distributed widely in the body.
crosses blood brain barrier (BBB)and also placenta.
conc.in brain =conc. in blood.
M gets oxidised in liver to an extent of 98%.
metabolism of alcohol follows zero order
kinetics
constant rate (8-12 ml /hr)
Eexcretion is through kidney and lungs.
Concentration in exhaled air is about 0.05% of blood concentration.
This is utilized for medico legal determination of drunken state using breath analyser.
15. Contraindication
1.Peptic ulcer , hyper acidity , and gastroesophageal reflux disease
(alcohol increases gastric secretion and reflex LES).
2.Epileptics : seizures may precipitated.
3.Severe liver disease patients.
4.Pregnant women :even moderate drinking cause foetal alcohol
syndrome resulting in intrauterine growth retardation, low IQ, facial and
other abnormalities.
16. Guidelines for safe drinking.
1.On an average 1-2 drinks per
day is usually safe.
2. Do not drive or engage in
hazardous activities after
drinking.
3. Do not drink if any
interacting
drug has been taken.
17. Clinical use
As antiseptic
1.Rubefacient and counter irritant for sprains , joint pains.
2.As appetite stimulant and carminative:30-50ml of 7-10% alcohol may
be taken as beverages and tinctures.
3.To treat methanol poisoning.
18. Aldehyde dehydrogenase inhibitor
Disulfiram
1. It inhibits enzyme aldehyde dehydrogenase probably after conversion into active metabolites.
Symptoms:
1. Flushing , burning sensation ,
throbbing headache ,perspiration,uneasiness,tightness in chest,dizziness,vomiting,mental
confusion.
Duration(1-4 hrs).
1. Disulfiram has been used in chronic
alcoholics who are motivated and
sincerely desire to leave the habit.
19. Methyl Alcohol
Methanol is also a CNS depressant as ethanol.
Even 15 ml of methanol causes blindness
30 ml causes death
75-100 ml is regarded as fatal dose.
Manifestations of methanol poisoning
Vomiting , headache , epigastric pain , uneasiness ,
bradycardia , hypotension
Methanol is metabolised to formaldehyde and formic acid.
The specific toxicity of formic acid is retinal damage.